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Congenital General Anosmia

The most well studied group of syndromic CGA is related to the Kallmann syndrome. Such patients exhibit hypogonadotropic hypogonadism and anosmia, secondary to failure of gona-dotropin-releasing hormone (GnRH)-producing neurons to migrate from the olfactory placode to the brain, and to agenesis of the olfactory bulbs. The prevalence of the disease has been estimated at 1 in 10,000 in males and five to seven times lower in females. Three different modes of inheritance have been reported in familial cases of Kallmann Syndrome, X chromosome-linked, autosomal dominant, and autosomal recessive (39). The X-linked form of the Kallmann Syndrome has been well characterized, being caused by mutations in the gene KALI (chromosome Xp22.3) (40-42). The KALI protein, anosmin-1, is a locally restricted component of basement membranes and or extracellular matrices during the organogenesis period (39). It has been found to enhance axonal branching from olfactory bulb output neurons (43) and to affect...

Detection and Assessment

A physical examination and laboratory screening (e.g., complete blood count, liver function, serum testosterone level, serum vitamin B12, thyroid function) may be performed to exclude potential systemic causes of depressive symptomatology. Testosterone deficiency associated with depressive symptomatology (e.g., anhedo-nia, fatigue, and sexual dysfunction) has been described in males with PD and may possibly be managed with testosterone replacement therapy (120). Likewise, symptoms of hypothyroidism (e.g., anxiety, difficulty with concentration, dysphoria, fatigue, irritability, and motor retardation) resemble depressive symptomatology and are treatable with thyroid replacement. It is also important to ensure that patients are on optimal doses of antiparkinson drugs to minimize motor fluctuations that may contribute to mood fluctuations.


In addition to HIV infection, other factors such as malnutrition, diminished fat tissues, steroid treatment, hypogonadism, immobilization and treatment with PIs and NRTIs, seem to play a role in the pathogenesis of this disorder. Osteopenia and osteoporosis are often asymptomatic. Osteoporosis occurs mainly in the vertebrae, lower arms and hips. The following tests should be performed on all patients with AIDS a lumbar spine X-ray in the standard anteroposterior and lateral views, bone density measurement (DEXA scan) of the lumbar spine and hip and laboratory blood tests, including calcium, phosphate and alkaline phosphatase. Osteopenia should be treated with 1000 I.E. vitamin D daily and a calcium-rich diet or calcium tablets with a dose of 1200 mg day. Patients should be advised to exercise and give up alcohol and nicotine. In cases with osteoporosis, bisphosphonates (e.g. alendronat 70 mg once a week) should be added. The tablets should be taken on an empty stomach 30 min before...

The Endocrinology Of Birds Vocalization

In relation with these testosterone-dependent vocalizations, seasonal changes in song structure correlate with periods of dramatically increased testis size and testosterone production (Leitner et al., 2001). Although the overall relationship between testosterone and singing is well established, there are only a few studies of how variation in steroid levels relate to individual variation in song. Experimental manipulations show that testosterone levels in the dark-eyed junco (Junco hyemalis) (Ketterson et al., 1992) influence song rates. However, two correlative studies provide negative evidence for such a relationship in other species testosterone levels are not related to song output in the barn swallow (Hirunda rustica) (Saino and Moller, 1995) or to repertoire size in the red-winged blackbird (Agelaius phoenicus) (Weatherhead et al., 1993). This lack of correlation is to be expected if there are individual differences in the responsiveness of the brain vocal systems to...

Neuroendocrine Studies

The neuroendocrine circuitries that serve as convergence points between the body weight and reproduction systems have been recently explored.57 Rare mutations in both the leptin gene and its receptor have been identified in patients with hypogonadotropic hypogonadism and morbid obesity.58 Interestingly, the administration of kisspeptin can correct the hypogonadism of leptin deficient animals, suggesting that the kisspeptin GPR54 pathway may serve a converging function between the reproductive and nutritional systems.59

Gpr54 and kissl Knockout Mice

Gpr54 and kiss1 knockout mice have been generated by different groups of researchers.7,67-70 The phenotype of these animals is in general similar, with slight variations, which were attributed to the type of mutation carried by each line.70 Both the gpr54 and kiss1 knockout mice fail to undergo pubertal maturation and show poor development of the gonads, hypogonadotropic hypogonadism and infertility. Spermatogenesis and ovulation are severely impaired and mutant females do not showestrous cycling. Nevertheless, GnRH neurons were anatomically intact in these animals, with normal hypothalamic GnRH content, indicating that migration of GnRH neurons occurs normally. Apart from the reproductive system, no alterations have been described in other organs or systems. The gonads and the anterior pituitary retain functional responses to exogenous GnRH stimulation, consistent with the primary defect being a failure to secrete GnRH from the hypothalamus.70 When injected with kisspeptin, gpr54...

Lossof Function Mutations of GPR54

Congenital isolated hypogonadotropic hypogonadism (IHH) is defined as a deficiency of the pituitary secretion of LH and FSH, which results from defects in the synthesis, secretion, and action of GnRH, leading to impairment of pubertal maturation and reproductive function.71 It is characterized by low levels of sex steroids in the presence of low or inappropriately normal LH and Since then, four other inactivating GPR54 mutations were described in patients with normosmic IHH (Table I). Semple et al.11 described one sporadic case of normosmic IHH harboring a compound heterozygous mutation in GPR54. The boy had micropenis and undescended testes at birth and undetectable serum gonadotropins at 2 months of age. The first variant was a transition c.667T > C in exon 4, leading in a substitution of a cysteine near the cytoplasmic end of the fifth transmembrane helix for arginine (C223R), while the second mutation was a transversion in exon 5, c.891 G > T, resulting to the substitution of...

Molecular Mechanisms And Defects Hypothalamus

Two animal models of GHRH deficiency have been described. In one, administration of monosodium glutamate (MSG) to mice causes a selective loss of arcuate nuclei neurons (14,15). MSG-exposed rodents have impaired growth, obesity, hypogonadism, and hypothyroidism (16). The other animal model of GHRH deficiency is the Gsh-1 homeobox gene knockout mouse (17). Homeobox genes encode a family of DNA binding proteins, and the Gsh-1 gene encodes a product necessary for GHRH gene transcription and translation. Gsh-1 knockout mice have extreme postnatal dwarfism, sexual infantilism, leukopenia, significant perinatal mortality, a shortened life span, and biochemical evidence of GHRH deficiency. Their anterior pituitary glands are one-third normal size and possess decreased numbers of somatotrophs and lactotrophs.

The Myotonic Dystrophies an Overview

Myotonic dystrophy (dystrophia myotonica, DM) is a dominantly inherited neuromuscular disease that is characterized by a distinctive combination of clinical features, including skeletal muscle myotonia and weakness wasting, cardiac muscle arrhythmias and conduction defects, unusual ocular cataracts, insulin insensitivity, male hypogonadism, balding and hypogammaglobulinemia (Harper 2001). Moreover, the genetic basis of DM is novel because this disease is caused by the expansion of different, but structurally similar, microsatellite repeats in two unrelated genes. Type 1 DM (DM1) is associated with the expansion of a d(CTG) repeat poly r(CUG) positioned in the 3'-untranslated region (UTR) of the DMPK gene, while type 2 disease (DM2) results from a d(CCTG) expansion poly r(CCUG) in the first intron of ZNF9 (Brook et al. 1992 Liquori et al. 2001). Congenital DM (CDM), which is the most severe form of this disease, is exclusively associated with very large d(CTG) expansions in the DMPK...

The choice between Thl and Th2 responses in humans nature versus nurture

Neuroendocrine factors have a powerful effect on immune responses. Populations stressed by war or natural disasters have an increased incidence of infections such as tuberculosis and typhus, but under these circumstances it is difficult to estimate the relative contributions of defective public health and of increased host susceptibility to infection. Bernton et al (1995) studied the immunological and endocrine changes in military recruits under conditions of 'mental and physical stress approaching that found in combat', and found raised cortisol levels and reduced DHEA cortisol ratios in these recruits. Testosterone levels, delayed-type hypersensitive responses and T cell mitogenic responses decreased, while IgE levels increased. The authors suggested that stress induced a Th1 to Th2 shift.

The Prader Willi Syndrome

An excellent clinical summary of Prader-Willi syndrome (PWS) is provided in the literature (Holm et al., 1993 Cassidy, 1997). PWS is a multisystemic disorder with numerous manifestations of hypothalamic insufficiency. The neonatal and infantile period is marked by hypotonia, poor suck, feeding problems, and poor weight gain with a failure to thrive. In contrast, between 1 and 6 years of age, excessive weight gain with central obesity occurs, resulting from a voracious appetite. There is global developmental delay, mild to moderate mental retardation, and various learning problems. Characteristic cranio-facial features include dolichocephaly, narrow face or narrow forehead, almond-shaped eyes, small mouth with thin upper lip and downturned corners. Hypogonadism is marked, with hypoplasia of the genitals in both sexes and hypomaturity later on.

Biological Correlates of Gender

Although the effects of testosterone on aggression in humans are not as clear as they are in other animals, a weak correlation between the two variables has been found. However, this finding does not necessarily mean that high testosterone levels cause aggressive behavior the result can also be interpreted as indicating that repeated aggression increases the level of testosterone in the blood (Archer, 1991). With respect to the female hormone estrogen, Hampson (1990) and Kimura and Hampson (1993) reported that women perform better on tests of motor coordination and verbal facility but poorer on tests of spatial reasoning during times of the month when estrogen levels in the blood are highest.

Information from Human Studies

Due to the powerful multisystem effects linked to oxytocin and vasopressin in regard to social phenomena, intervention research examining effects of increases in oxytocin in humans has recently burgeoned, including studies linking oxytocin to increased interpersonal trust, greater recognition of faces and decreased fear (Meyer-Lindenberg, 2008). For example, Ditzen and colleagues (2009) compared effects of intranasal oxytocin versus placebo in couples during conflict discussion, finding that oxytocin reduced cortisol and increased positive communication. Zak and colleagues observed that intranasal oxytocin increased experimentally assessed trust, reciprocity, and generosity behaviors (assessed by monetary transfer to strangers), and they also found that exposure to either deep massage or empathy-evoking film clips likewise increased both circulating oxytocin levels and such reciprocating or generous money sharing (Barrazza and Zak, 2009 Morhenn et al, 2008 Zak et al, 2007). As...

Are Female Gender and Sex Hormones Associated with a Higher Prevalence of HAND

The influence of sex hormones particularly testosterone on cognition is complex. Endocrine abnormalities are common in HIV-1 infected patients (119) and testosterone deficiency has been reported as the most common one (120-122). Usually, testosterone level is investigated in HIV-infected men, but recent data, using a more sensitive measure have shown that HIV-infected women also had lower free testosterone than seronegative women (123). Symptoms include depressed mood, decrease libido and energy, loss of weight, and muscle mass (124). Testosterone deficiency has been associated with higher occurrence of opportunistic infections, a CD4 cell count below 200 cells mm3 and treatment with megestrol acetate (125). However, other studies did not replicate these results and could not find any relation with HIV illness markers (126). Testosterone supplementation in HIV-1 infected individuals induces a positive effect on depression (127), libido, energy and weight, and muscle mass (124,...

Clinical Description Of The

The condition was first described some 40 years ago (Prader et al., 1956). The clinical phenotype of PWS is characterized by neonatal hypotonia and developmental delay, followed by hyperphagia and major obesity, short stature, secondary hypogonadism, mild dysmorphism, small hands and feet, and mild to moderate mental retardation with learning disability. Consensus diagnostic criteria have been established and proven to be satisfactory for the clinicians (Holm et al., 1993). The frequency of the syndrome is on the order of 1 in 10,000 to 1 in 15,000 (Cassidy, 1984). Aside from a ravenous appetite, several behavior problems are noted, such as frequent temper tantrums, obsessive-compulsive behavior, stubbornness. There is a variable degree of mental retardation, usually not severe the average IQ is around 60, with a range of 20-80. Obesity is the main clinical and psychosocial problem. As a result, a tendency to develop type II diabetes mellitus is seen in adolescence, and cardiovascular...

Fertility and Aging Men An Introduction to the Male Biological Clock

The levels of sex hormones in men decline with age. The roughly 1 per year decline in testosterone levels after age 30 has been termed andropause, or ''symptomatic hypogonadism in the aging male.'' Rhoden and Morgentaler estimate that between 2 and 4 million men in the United States alone suffer from hypogonadism, but only 5 of men are getting treatment for their symptoms.

Adult Onset GHD and Osteoporosis

One study of 95 adults, ranging in age from 21-74 yr and identified as GH deficient on the basis of provocative tests, showed low bone density of the lumbar spine compared to normal controls. This significant deficit in bone density persisted when patients with untreated hypogonadism were excluded (20). Two smaller studies showed reduced bone density of the total body (21), femoral neck, Ward's triangle, and greater trochanter (22) in patients with adult-onset GHD compared to normals. In both of these studies, a significant correlation was found between bone density and serum levels of IGF-1, an integrated marker of GH secretion. Because patients with adult-onset GH deficiency were by definition endocrinologically intact through adolescence, they presumably had normal skeletal development and reached a normal peak bone mass. Therefore, osteopenia in such patients, can only be explained on the basis of accelerated loss of bone during adulthood.

Congenital leptin deficiency

In 1997, we reported two severely obese cousins from a highly consanguineous family of Pakistani origin who had undetectable levels of serum leptin and were found to be homozygous for a frameshift mutation in the ob gene (AG133), which resulted in a truncated protein that was not secreted (Montague et al., 1997). We have since identified four further affected individuals from three other families who are also homozygous for the same mutation in the leptin gene. All the families are of Pakistani origin but not known to be related over five generations. A large Turkish family who carry a homozygous missense mutation have also been described (C105T) (Strobel etal., 1998). All subjects in these families are characterised by severe early onset obesity and intense hyperphagia. Some of the Turkish subjects who are adults failed to undergo pubertal development with biochemical evidence of hypogonadotropic hypogonadism (Ozata et al., 1999).

Dietary Prostate Cancer Risk Factors

There are at least seven major dietary macro- or micronutrients that are under intense scrutiny currently as dietary risk or protective factors (Table 15.1). Prominent among these is dietary fat or some component of fat (e.g., saturated fat), which first received attention as a mechanism to possibly explain the low risk in native Asian populations and the apparent rapid shift in risk upon migration of Asian populations to the United States. There are suggestive data that increased fat consumption is associated with higher circulating testosterone levels, providing a possible mechanism for a fat-prostate cancer relation

Nondietary Prostate Cancer Risk Factors

Of an androgenic profile associated with prostate cancer development.27 Smokers have higher circulating testosterone levels than nonsmokers.28 While there is no direct link between androgen levels and sexually transmitted diseases, androgen levels may be modestly correlated with indices of sexual activity.29

Organ Systems Affected By Low T Levels

Cognitive function decreases with aging. Most of the age-related changes in cognition are associated with vascular and or degenerative diseases that cause anatomic changes in the central nervous system. The possibility that an age-related fall in T causes functional changes in cognition is of great interest. In a study involving 407 men aged 50 to 91 years at baseline and followed for an average of 10 years, Moffat and colleagues showed that higher free T indices were associated with better scores on visual and verbal memory, visuospatial functioning, and visuomotor scanning, and a reduced rate of decline in visual memory (Moffat et al., 2002). On the other hand, men classified as hypogonadal had significantly lower scores on measures of memory and visuospatial performance and a faster decline in visual memory. Of course, changes in the CNS could cause hypogonadism rather than be caused by hypogonadism. In another study by Barrett-Conner and associates, low...

Diagnosis of sexual dysfunction

Low testosterone level requires maesurement of LH and FSH. Further work-up may require an LH or FSH stimulating test, usually handled by an endocrinologist, to exclude secondary hypogonadism. NPT (nocturne penile tumescence measurement) is considered minimally invasive and measures nocturnal erections. 3-6 erections per night of at least 70 rigidity, lasting 10 minutes, are considered normal values. The question of morning erections can serve as critical criterion for the sexual anamnesis.

Clinical Progression Of Ws

The progression of clinical changes in WS can usefully be thought of as having three distinct phases. The first of these comprises the absence of an adolescent growth spurt followed over the subsequent decade by the appearance of graying and loss of hair, the development of skin changes, and of cataracts. A second wave of changes, often first seen late in the third or in the fourth decades of life, include skin ulceration, hypogonadism, and reproductive failure, together with a progressive worsening of the primary changes. A third phase may follow with the development of clinically important disease processes such as atherosclerosis, osteoporosis, diabetes mellitus, and cancer. These diseases occur proportionately earlier in WS patients than in otherwise normal individuals of comparable age, and are an important cause of premature morbidity and mortality. The three leading causes of death in WS patients are atherosclerotic cardiovascular disease, neoplasia, and, in a minority of...

Potential endocrine causes of hypoactive sexual desire disorder

In Chapter 5, I made clear that adequate blood concentrations of androgens are necessary for maintaining a functional central motive state in both men and women. Therefore, it is not startling that several studies have determined blood androgen concentrations in women diagnosed with hypoactive sexual desire disorder. Early studies failed to detect any difference between women reporting an adequate level of desire and those diagnosed with hypoactive desire disorder (Stuart et al., 1987 Schreiner-Engel et al., 1989). In contrast, a group of women with life-long hypoactive sexual desire disorder were found to have a lower free testosterone blood concentration than controls (Riley and Riley, 2000). This is a very interesting observation, suggesting that the life-long variant of desire disorder can be attributed to reduced reactivity of the central motive state because of insufficient androgen stimulation. Later studies have extended these findings. Premenopausal, regularly cycling women...

Diseases of genomic imprinting

Neurobehavioral disorders with distinct clinical manifestations (Ferguson-Smith et al., 2004 Nicholls and Knepper, 200l). Patients with PWS present with hypotonia at birth, obesity, short stature, mental retardation, hypogonadism and a characteristic facial appearance. AS is characterized by microbrachycephaly, large mouth with tongue protrusion and prognathism mental retardation is severe with absence of speech. Both diseases are associated with deficiencies in the same region of human chromosome 15q11-q13 due to an unequal crossing over between low copy repeats. These deletions are of paternal origin in PWS

Prohormone convertase 1 deficiency

Further evidence for the role of the melanocortin system in the regulation of body weight in humans comes from the description of a 47-year-old woman with severe childhood obesity, abnormal glucose homeostasis, very low plasma insulin but elevated levels of proinsulin, hypogonadotropic hypogonadism and hypocortisolemia associated with elevated levels of POMC (O'Rahilly et al., 1995). This subject was found to be a compound heterozygote for mutations in prohormone conver-tase 1, which cleaves prohormones at pairs of basic amino acids, leaving C-terminal basic residues which are then excised by carboxypeptidase E (CPE) (Jackson et al., 1997). We have also recently identified a child with severe, early-onset obesity who was a compound heterozygote for complete loss of function mutations in PC1 (Jackson et al., 2003). Although failure to cleave POMC is a likely mechanism for the obesity in these patients, PC1 cleaves a number of other neuropeptides in the


Most of the etiologic and epidemiologic associations appear to point to an origin in atypical germ cells. The association of testicular maldescent and the formation of testicular tumors has been known for more than 200 years,84,85 and atypical germ cells have been identified in cryptorchid testicles.22 Similarly, testicular cancer is found more commonly in patients with testicular dysgenesis, infertility, and Kleinfelter's syndrome (with expression of an XXY chromosome). Additional epidemiologic associations include reduced body muscle mass and a lower prevalence of male pattern baldness, which may imply lower circulating testosterone levels, as either a cause or an effect of testicular cancer.86 Although testicular trauma and mumps orchitis have largely been discounted as antecedents of GCTs,87,88 earlier studies suggested that both could have mechanisms of oncogenesis predicated on testicular atrophy and the consequent evolution of atypical germ cells. Similar mechanisms have been...


Possible associations with androgen levels have been explored, using proxies. Two presumed proxies for testosterone levels are a history of severe acne during puberty and male pattern baldness as both are associated with somewhat higher testosterone levels. A history of both conditions may be less frequent among men who develop testicular cancer.84 In addition, testicular germ cell tumors and CIS are observed in patients who are in a low-androgen state.89 While animal experiments show that androgen is required for testicular descent,90 a limited number of epidemiologic studies suggest that a high proportion of boys with cryptorchidism have normal androgen action and response.91,92 Some cases of hypospadias have been attributed to defects of androgen action or response, but this mechanism appears to account for only a small proportion of


Patients should routinely be questioned and examined for cardiovascular risk factors, such as smoking, hypertension, adiposity, type 2 diabetes, and family history. For an accurate assessment of blood lipid levels, it is recommended to obtain blood after a fasting of at least 8 hours. Total cholesterol and triglycerides together with LDL and HDL cholesterol should be obtained prior to the initiation of, or switch to, a new potent antiretroviral therapy and repeated 3 to 6 months later. Fasting glucose should be assessed with at least a similar frequency. The oral glucose tolerance test (OGTT) is a reliable and accurate instrument for evaluating insulin resistance and glucose intolerance. An OGTT may be indicated in patients with suspected insulin resistance such as those with adipositas (BMI > 27 kg m2), a history of gestational diabetes and a fasting glucose level of 110 to 126 mg dl (impaired fasting glucose). The diagnosis of diabetes is based on fasting glucose levels > 126 mg...


One of the great mysteries of human biology is what initiates puberty. Definitely, we currently know that gonadotropin-releasing hormone (GnRH) is a decapeptide central to the initiation of the reproductive hormone cascade. It is produced by hypothalamic neurons in a pulsatile manner and released into the hypophyseal portal circulation to stimulate the biosynthesis and secretion of the pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The pituitary gonadotropins stimulate gonadal function, including gametogenesis and steroid hormone synthesis. However, little is known about the precise mechanisms underlying the maturation and function of GnRH neurons and the regulation of GnRH secretion.5 The episodic release of GnRH seems to be modulated by excitatory and inhibitory signals transmitted by neurohormones and neurotransmitters acting at the level of the hypothalamus. The complex composed of a G protein-coupled receptor, GPR54, and its endogenous...

Major Risk Factors

In the late 1980s and early 1990s, we initiated a series of studies to determine whether there was any evidence ofunderlying differences in the androgen milieu among populations at widely varying risk of PCA, i.e., African-Americans, USA whites, and rural Japanese, that might suggest an androgen role in this variability. We found that African-American men have substantially higher testosterone levels at a young age than young men in the other two groups (12), and that Japanese men, while not having lower testosterone than whites as anticipated, have substantially lower circulating levels ofandrostanediol glucuronide (13). This hormone is a whole body index of the enzyme required to bioactivate

Case 11

In another abstract, a 12-year-old boy of normal intelligence, with an early history of hypotonia, failure to thrive, developmental delay, and hypogonadism, followed by precocious puberty and obesity was reported to carry a familial balanced, t(13 14) Robertsonian translocation (Linck et al., 1996). He had inherited his single ''free'' chromosome 14 from his mother and preliminary results from the analysis of DNA polymorphisms demonstrated maternal UPD14 (heterodisomy). The phenotype in this case included short stature, small hands and feet, mild developmental delay, hypotonia, premature puberty, hypogonadism, scoliosis, and mild dysmorphic features.


Lanfranco F, Gromoll J, von Eckardstein S, Herding EM, Nieschlag E, Simoni M. Role of sequence variations of the GnRH receptor and G protein-coupled receptor 54 gene in male idiopathic hypogonadotropic hypogonadism. Eur J Endocrinol 2005 153 845-52. Seminara SB, Messager S, Chatzidaki EE, Thresher RR, Acierno Jr JS, Shagoury JK, et al. The GPR54 gene as a regulator of puberty. N Engl J Med 2003 349 1614-27. de Roux N, Genin E, Carel JC, Matsuda F, Chaussain JL, Milgrom E. Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54. Proc Natl Acad Sci USA 2003 100 10972-6. Tenenbaum-Rakover Y, Commenges-Ducos M, Iovane A, Aumas C, Admoni O, de Roux N. Neuroendocrine phenotype analysis in five patients with isolated hypogonadotropic hypogonadism due to a L102P inactivating mutation of GPR54. J Clin Endocrinol Metab 2007 92 1137-44. Teles MG, Trarbach E, Guerra G, Costa EMF, Baptista MTM, Castro M, et al. In 89th Endocrine Society Annual Meeting,...

Biological Factors

Biological and biosocial risks are also involved in persistently delinquent and particularly aggressive adolescents (Raine, 1997 Rowe, 1994). Genetic factors play a significant role in differences in temperament and cognitive functions (Plomin, 1994). Biological dispositions for criminal behaviour can also emerge prenatally through alcohol abuse and smoking during pregnancy, perinatally through birth complications or post-natally through deprivations in emotional care, stimulation, and nutrition during infancy (Hodgins, Kratzer and McNeil, 2002 Moffitt, 1993 Raine, 1993). However, biological risks should not be viewed in too isolated a manner. For example, prenatal and perinatal complications seem to become only significant for specific forms of delinquency when they are accompanied by social risks such as lower-class milieu, parental rejection, or family instability (Brennan, Mednick and Raine, 1997 Hodgins et al., 2002). A deprived relationship with the primary caregiver can impair...


Megestrol acetate, a synthetic gestagenic hormone, shows some benefit as an appetite stimulant in wasting syndrome (Von Roenn 1994, Mulligan 2006). Its main problems are typical steroidal side effects, including hypogonadism - which should really be avoided in cases of wasting syndrome and which is not necessarily improved by concurrent administration of testosterone (Mulligan 2006). We therefore do not currently recommend the use of this drug. Hypogonadism is a frequent problem in patients with wasting syndrome. It is therefore useful to determine testosterone levels (age-dependent ). If levels are low, testosterone substitution is useful, both for weight gain and quality of life (Grinspoon 1998). A dose of 250 mg testosterone is given i.m. every 3-4 weeks, and there is a variety of less expensive generics. The effect is sustained, even with long-term use (Grinspoon 1999). If testosterone levels are normal, substitution in cases of wasting syndrome is not indicated. In women, one...

Adrenal Androgens

Sperm counts and concentrations are usually attained by that time and testosterone levels and muscle mass peak soon after. Whether the later phase of female reproductive maturation is properly understood as a part of pubertal development or as a different trajectory of adult reproductive function deserves fuller consideration.

Testosterone Decline

Or as sudden as that associated with menopause, but it can be equally significant for fertility and overall well-being. Recently, there has been a lot of interest in declining testosterone levels in men. The roughly 1 per year decline in testosterone levels after age 30 has been termed andropause and is associated with a plethora of congenital and acquired disease-syndromes (McLachlan, 2000). Previous longitudinal studies have demonstrated that abnormally low testosterone levels are present in elderly men (Sparrow et al., 1980 Harman et al., 2001 Feldman et al., 2002). Several large-scale studies in healthy, fertile men have evaluated mean values for serum testosterone (Ferrini et al., 1998). Additionally, there have been numerous cross-sectional investigations documenting lower concentrations of total testosterone and or free testosterone in older men (Vermeulen et al., 1972 Gray et al., 1991). Most recently, the Massachusetts Male Aging Study, a large population-based random-sample...

Prader Willi syndrome

Hypotonia, mental retardation, short stature, hypo-gonadotropic hypogonadism and hyperphagia (increased food intake) and obesity. Children with PWS display diminished growth, reduced lean body mass and increased fat mass - body composition abnormalities resembling those seen in growth hormone (GH) deficiency. GH treatment in these children decreases body fat, and increases linear growth, muscle mass, fat oxidation and energy expenditure (Carrel et al., 1999). One suggested mediator of the obesity phenotype in PWS patients is the enteric hormone ghrelin, which is implicated in the regulation of mealtime hunger in rodents and humans and is also a potent stimulator of growth hormone secretion. Several groups have shown that children and adults with PWS have fasting plasma ghrelin levels which are 4.5-fold higher in PWS subjects than in equally obese controls and thus may be implicated in the pathogenesis of hyperphagia in these patients (Cummings et al., 2002 Haqq et al., 2003).

Sex Steroids

In contrast to estrogen, well-designed and adequately powered interventional trials examining the effects of testosterone replacement on bone metabolism in elderly men are lacking. Therefore, the effects of androgen supplementation on BMD are largely unknown. Testosterone has been shown to retard atherosclerosis in rodent models however, prospective or cross-sectional studies have failed to reveal any consistent association of testosterone levels and coronary artery disease (Alexandersen et al., 1999). Similarly, there is no convincing evidence supporting an association of DHEA(S) with atherosclerosis. These studies suggest that estrogen, but not testosterone or DHEA(S), plays a key role in osteoporosis and atherosclerosis.

T Levels And Aging

The decline in T levels with aging when associated with symptoms and signs of androgen deficiency has been called andropause. This association also has been referred to as androgen deficiency in the aging male (ADAM), partial androgen deficiency in the aging male (PADAM), aging-associated androgen deficiency (AAAD) or late-onset hypogonadism. The term andropause is inaccurate because men do not have menses and because androgen secretion gradually decreases, and usually is

Ongoing research

The impact of PIs in SD was also seen by Collazos (2002) in a prospective study of 189 patients. No correlation could be found between measured sex hormone levels and incidence of SD. Interestingly, in subjects taking a PI-containing regimen, testosterone levels were significantly higher compared to NNRTI-containing regimens in which 17B-estradiol levels were significantly elevated. More recent research impressively underscores the positive effect of testosterone substitution in HIV-infected hypogonadotropic men (Rabkin 2000, Grinspoon 1998). Testosterone deficiency can cause weight loss, loss of muscle mass, osteopenia, and depression (Grinspoon 1996, Huang 2001).

Myotonic Dystrophy

CTG trinucleotide repeat expansion in the DM1 locus on chromosome 19q13.32 affects the expression of two adjacent genes DMPK and SIX5 and leads to myotonic dystrophy, an autosomal dominant disorder characterized by myotonia, muscular dystrophy, cataracts, hypogonadism, frontal balding, and electrocardiogram changes. Filippova et al. (55) demonstrated that CTCF binding sites flank the CTG repeat and act as insulator element between DMPK and SIX5. Similar to the H19 and Igf2 genes, methylation of these sites eliminates binding of CTCF. Thus, methylation of the DM1 locus in myotonic dystrophy disrupts the insulator function. The role of CTCF in the insulator function has been proposed also in establishing a regulatable epigenetic switch for X chromosome inactivation (56,57) and in cancer (58).


In terms of available evidence, the best treatment for elderly obese patients is exercise. Cardio-respiratory fitness is an important determinant of health status in the elderly and can be improved by exercise. The majority of elderly women actually achieve the currently recommended levels of exercise during activities of daily living, including housework. However, this level of activity does not appear to be protective against obesity and its consequences. There is now evidence from a large number of studies that exercise in the elderly is beneficial in terms of glucose tolerance, cardiac and respiratory function, improved function and quality of life. Patients have traditionally been instructed that aerobic exercise is most beneficial. Meaningful amounts of aerobic exercise may not be achievable in many with functional limitation and severe obesity. Furthermore, there is often a worsening of symptoms and well-being in the short term, and this may decrease adherence to programs of...

Sexual Dysfunction

Changes in both women and men decline on a steady slope with age. For women, a further incremental decline is related to falling estradiol levels probably more so than declines in testosterone levels (Dennerstein, Randolph, Taffe, Dudley, and Burger, 2002). The factors that affect a woman's sexuality include first and foremost aging, the length of her sexual relationship with her partner, her own or her partner's health problems, loss of a partner, and psychosocial stressors (Dennerstein, 2005). Moreover, sexual function or dysfunction in women is multidimensional. The problem may rest with desire, arousal, and inorgasmia. It is also nonlinear a woman can have responsive desire vs. innate desire (arousal before desire). Her sexual functioning at menopause or at any time along the lifespan is highly related to her previous behavior or level of interest, her feelings toward her partner, and her partner's status. Not surprisingly, a new partner puts a new set of variables in play for a...

Clinical Biology

A critical role in prostate development or car-cinogenesis. Despite the presence of elevated serum concentrations of adrenal androgens, patients with hypogonadotrophic hypogonadism have abnormal prostate development but do not develop prostate neoplasia. Males castrated at or prior to puberty seemingly never develop prostate cancer.

Gonadal Toxicity

In addition to impairment of spermatogenesis, injury to Leydig's cell function is a potential toxic effect of chemotherapy. Elevations of FSH levels were observed in 24 of a cohort of 32 patients who received platinum-based chemotherapy.54 Of these 24 patients, 15 had elevated LH levels. Two patients, each with a remaining testicle, had low testosterone levels. This underscores the problem of compensated (and sometimes uncompensated) Leydig's cell function. Testosterone replacement can be implemented if clinically indicated.

Female HIV infection

Fertility disorders in HIV-positive women seem to have a higher prevalence than in an age-matched HIV-negative population (Ohl 2005), but data still show some conflicting results. The reasons discussed include an increased rate of upper genital tract infections (Sobel 2000), menstrual disorders, and cervical infertility (Gilles 2005). Coll (2006) assumes the possibility of subclinical hypogonadism, potentially due to mitochondrial dysfunction. In some cases, women will only be able to conceive by assisted reproduction. Dependent on the fertility status of both partners, IVF and ICSI can be considered as methods of choice.

Bardet Biedl syndrome

Bardet-Biedl syndrome (BBS) is a rare (prevalence < 1 100000), autosomal recessive disease characterized by obesity, mental retardation, dysmorphic extremities (syndactyly, brachydactyly or polydactyly), retinal dystrophy or pigmentary retinopathy, hypogonadism and structural abnormalities of the kidney or functional renal impairment (Katsanis et al., 2001b). Bardet-Biedl syndrome is a genetically heterogeneous disorder that is now known to map to at least eight loci 11q13 (BBS1) (Mykytyn et al., 2002) 16q21 (BBS2) (Nishimura etal., 2001) 3p13-p12 (BBS3) (Sheffield et al., 1994) 15q22.3-q23 (BBS4) (Mykytyn et al., 2001) 2q31 (BBS5) (Young et al., 1999) 20p12 (BBS6) (Katsanis etal., 2000 Slavotinek etal., 2000) 4q27 (BBS7) (Badano et al., 2003) and 14q32.11 (BBS8) (Ansley et al., 2003). Although BBS had been originally thought to be a recessive disorder, Katsanis and colleagues proposed that clinical manifestation of some forms of Bardet-Biedl syndrome requires recessive mutations in...

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