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Anabolic Running Review

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Anabolic Running Review Summary


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Juicing for your manhood Cure Ed

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Juicing for your manhood Cure Ed Summary

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Author: Olivier Langlois
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Juicing for Your Manhood

Juicing for Your Manhood is a program that employs natural methods in fighting erectile dysfunction that comes about as a result of low testosterone levels. It puts focus in rejuvenating this hormone within the bodies of the affected individuals, transforming them back to the persons they used to be before. It is a creation of Olivier Langlois, a guy who used to be overweight with no energy to satisfy his partners. He was diagnosed with Limp Libido Syndrome due to the reduced level of testosterone hormone within his body. It is this condition that motivated him to carry out extensive research on how he could bring to an end this problem. The ingredients are scientifically and therapeutically verified. Isn't this the most important aspect of a program you may wish to undertake? Definitely yes! The program was designed following a wide-ranging study that is scientifically based. Unlike many programs based on theories, the techniques employed in this guide and been tested and verified practically. The program has no side effects. The techniques used in the guide to upsurge libido are safe, unlike prescriptions. As pointed out at the onset, the program uses natural methods. If you need to regain your manhood, this is a perfect product for you. Read more...

Juicing for Your Manhood Summary

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Other signalling pathways

In addition to SCF and Epo, recent observations have shown that stimulation of the nuclear hormone receptors for dexa-methasone (glucocorticoid receptor) and oestrogen (oestrogen receptor) produces sustained proliferation of erythroid progenitors. Furthermore, the nuclear hormone receptors for thyroid hormone (c-ErbA thyroid hormone receptor), all-trans retinoic acid (retinoic acid receptor) and 9-a's-RA (RXR) were found to promote erythroid differentiation. Such observations are consistent with previous reports showing that patients with a wide range of endocrine disorders (hypothyroidism, hypopituitarism, Addison's disease and male hypogonadism) all have variable degrees of normochromic normocytic anaemia. It appears, therefore, that many hormones of the endocrine system can modify erythropoiesis.

Lowfat diets and dietary factors

Just as high-fat and high-caloric diets seem to be promoters of some cancers, low-fat diets are protective. This has been demonstrated for prostate cancer in the laboratory. Wang et al. reported that there was less growth of prostate cancer cells implanted in nude mice fed low-fat diets.64 A recent clinical report described that dietary modification of fat intake could lower prostate specific antigen (PSA) levels without affecting overall testosterone levels, although it is not clear whether this influenced the prognosis.65

Symptomatic treatment

Well-transfused children maintained on a good diet do not usually develop important vitamin deficiency states. However, folic acid deficiency occurs in poorly transfused children or in those with thalassaemia intermedia, and it is probably better to maintain these patients on regular folate supplements. In those who develop iron loading with end-organ failure, endocrine replacement therapy may be necessary to improve growth and secondary sexual development and, if necessary, to treat diabetes mellitus. These children require expert endocrinological assessment before treatment. Because the occurrence of osteoporosis is also likely to be due to hypogonadism, similar precautions should be followed. In those who develop cardiac abnormalities, intensive chelation therapy may improve cardiac function.

Gonadotropin Releasing Hormone Analogs

Gonadotropin releasing hormone analogs (GnRH) cause a temporaty medical menopause resulting in hypogonadism and hypoestrogenism by acting on the pituitary to reduce gonadotropin synthesis and secretion. Most of the side effects experienced occur because of the hypoestrogenic state including hot flashes, vaginal dryness, mood lability and decreased libido. The GnRH agonists have been shown to work well in reducing pain symptoms associated with endometriosis such as dys-menorrhea, dyspareunia, and noncyclic pelvic pain. GnRH agonists are often initiated with the onset of menses, but a more rapid response is observed with mid-luteal administration. A limit of 6 months per treatment course is required due to loss of bone mineral density during therapy, but this can be extended via the addition of 'add-back' therapy with estrogens. Retreatment with these drugs is supported by limited data. Several investigators have studied the use of GnRH agonists as surgical adjuncts. Their use...

Myotonic Dystrophy DMPK

Similar to FRM1, DMPK is an autosomal dominant dynamic mutation in chromosome 19 (19q13.2-13.3), resulting from the expansion of triplet repeat, with a prevalence of 1 in 8000 live births. This is a severe neurodegenerative disorder chalacterized by myotonia, muscle wasting in the distal extremities, cataract, hypogonadism, defective endocrine functions, and cardiac arryth-mias. As mentioned in Chapter 3, DM was one of the most frequent indications for PGD, which also provided the possibility for obtaining affected embryos for the establishment of the ES cell lines with DMPK. One of the PGD cycles for the maternally derived mutation is presented in Figure 7.7, showing the results of blastomere biopsy of six embryos, which resulted in the transfer of two mutation-free embryos (embryos 5 and 7). Two of the remaining four embryos were with aneuploidies, monosomy 16 in embryo 8 and monosomy 22 in embryo 10, and two affected embryos were donated for research and resulted in the...

Growth factors the cell cycle and apoptosis

Estramustine phosphate, a nitrogen mustard derivative of 17 P-estradiol, has been used for treatment of prostate cancer patients since the 1960s. Mechanisms of action include inhibiting microtubule assembly and promoting disassembly of polymerized microtubules by interacting with microtubule-associated binding proteins, in addition to decreasing serum testosterone levels.167,168 Cytotoxic effects derive mainly from microtubule polymer inhibition required in the formation of the spindle pole apparatus during mitosis. Multiple agents that inhibit microtubule polymers have been used together and colchicine with estramustine phosphate is cytotoxic in vitro in PC-3 cells.169 Clinically, estramustine phosphate has been used in combination with another microtubule inhibitor, vinblastine, without additive side affects and modest results were observed.170 One video microscopy study suggests that estramustine phosphate mostly stabilizes microtubules in an attenuated state, perhaps explaining...

In Vivo Functional Activity

Sometimes there is no adequate or usable disease model however, a suitable surrogate marker may be available to give an approximate readout of potential in vivo efficacy. Surrogate markers also serve to simplify and speed-up compound evaluation because they avoid the need to use a full-blown disease model. An example of this is the GnRH field described previously. Here, rather than use models of prostate cancer or endometriosis or some other indication for GnRH agonists or antagonists, one need only monitor testosterone levels in male animals or estrogen levels in females to see whether the compounds are effective or not.

Prostate Development and Carcinogenesis in Prostate Specific ARKO Mice

Genotyping, RT-PCR and immunohistochemistry (IHC). Hormonal studies revealed normal serum testosterone levels in prostate-specific ARKO as compared to wild-type (WT) mice. The growth of urogenital organs other than prostate remained unchanged after the prostate epithelium no longer has a functional AR, however the size and weight of prostate glands were slightly decreased. The secretion proteins, probasin and prostatic secretory protein 94 (PSP94), were dramatically decreased in prostate-specific ARKO mice. When androgen ablation by castration was induced at 12 weeks old, both WT and prostate-specific ARKO mice showed dramatic regression of prostate and seminal vesicle growth. This model implies that the AR plays specific roles in epithelium and in stromal development. By crossing male probasin-cre mice to flox AR TRAMP female mice, the prostate-specific ARKO TRAMP mice were generated. This model will add more clues about the role of AR in the prostate cancer carcinogenesis and...

Aggression and Body Chemistry

In most species, including humans, males are more aggressive than females. This is thought to be because of the testosterone levels present in varying degrees in males. The higher the testosterone level, the more aggressive the male. Aggressive behavior that threatens the welfare of the species is often controlled in humans by medication that reduces the testosterone levels and pacifies aggressive men. It is notable that young men tend to be considerably more aggressive than older males, presumably because as men age, their testosterone levels decrease considerably. Prisons are filled with young men unable to control their aggressions sufficiently to stay out of trouble with the law. Many of these prisoners mellow into relatively benign older men, not because prison has reformed them but because their body chemistry has undergone significant changes through the years.

Risk of DHT Formation

Men castrated at a young age and patients with male hypogonadism seldom experience prostate cancer. Ethnic differences in the incidence of clinical prostate cancer are evident, although differences in the incidence of latent cancer among the races are small. Therefore, the activity of 5a-reductase in the formation of DHT may be an etiological and or progressive factor in clinical cancer.42 The levels of total and free testosterone in African-Americans were 19 and 21 higher than those in whites (both p 0.02), respectively.43 Three reports, in which testosterone, DHT, estradiol, and sex hormone-binding globulin were measured in prospective cohort studies, were reviewed by meta-analysis.44 Men whose total testosterone level was in the highest quartile were 2.34-fold more likely to develop prostate cancer than men in the lowest quartile. Levels of DHT and estradiol did not differ significantly, but low sex hormone-binding globulin was revealed as a

Type 2 juvenile haemochromatosis

Juvenile haemochromatosis is a rare autosomal recessive disease, with clinical symptoms appearing in the second and third decades of life, characterized by cardiomyopathy and hypogonadism. The hemojuvelin locus has been mapped to chromosome 1q21. Iron absorption is greater than in type 1 haemochromatosis. Like hepcidin, hemojuvelin modulates hep-cidin expression and hepcidin levels are low in homozygous individuals with hemojuvelin mutations. Mutations were found in Greek, Canadian and French families with G320V, accounting for two-thirds of these mutations. Like HFE, hemojuvelin modulates hepcidin expression and serum hepcidin was low in homozygous affected individuals with hemojuvelin mutations.

Racial Differences

On the other hand, is there a biologic factor, or factors, such as testosterone, that is making these tumors grow bigger more quickly Studies in younger men have shown that Blacks had testosterone levels 10-15 higher than age-matched Whites.59 Furthermore, a more recent study has found genetic variation in the androgen receptor (AR) gene that may make the receptor more active in African American men.60 Specifically, the CAG polymorphic repeat in exon 1 of AR is shorter in Black men and theoretically could potentiate the effect of testosterone in prostatic cells. Alternatively, is it a combination of behavior and biology that is responsible for the observed differences Despite not knowing the exact cause, what can we do now

IMAGe association

Features include intrauterine growth retardation, Metaphyseal dysplasia, Adrenal hypoplasia congenita, and Genital anomalies. Patients present shortly alter birth with growth retardation and severe adrenal insufficiency, mild dysmorphic features, bilateral cryptorchidism, micropenis, and hypogonadotrophic hypogonadism. Skeletal surveys show metaphyseal dysplasia with or without epiphyseal dysplasia. Patients have documented or suspected hypercalciuria and or hypercalcaemia, which may result in nephrocalcinosis, or visceral calcification.

Robinow syndrome

Features include costovertebral anomalies with mesomelia, brachydactyly, bifid thumbs with abnormal orientation. There are characteristic facial features including large mouth and tongue, frontal bossing, wide downslant-ing palpebral fissures, hypertelorism with depressed nasal bridge, small low-set ears, gingival hypertrophy. Patients may have cleft lip palate (not midline). Genital anomalies include hypoplastic genitalia, hypospadias or cryptorchidism. Intelligence may be normal. Inheritance can be autosomal recessive or dominant. The autosomal recessive form of Robinow syndrome is caused by homozygous mutations in the ROR2 gene (ROR2 gene on chro-mosme 9q22 affecting cartilage and bone formation). Heterozygous mutations in the same gene cause autosomal dominant brachydactyly B. Adult males show partial primary hypogonadism, whereas gonadal function and fertility in females seems to be normal which may explain a lack of male-tomale transmission in the dominant form. The recessive...

Risk Factors

For prostate cancer, the most important risk factor is also prolonged exposure to steroid hormones, i.e. androgens. Early castration or genetic defects blocking androgen synthesis essentially eliminate the risk of prostate cancer, while more subtle abnormalities, such as qualitative differences in the levels of circulating androgens or qualitative differences in androgen receptor function or related signal transduction pathways due to various genetic polymorphisms may also alter the risk of prostate cancer in certain subpopulations.9 For example, genetic variations of 5a-reducatase may create more productive enzymatic conversion of testosterone to dihydrotestosterone (DHT), which has been suggested as one mechanism of increased prostate cancer risk.10 Studies have looked at the potential role of vitamin D receptor (VDR) polymorphisms in prostate cancer risk, particularly in African American men.11 It has also been noted that Black men of college age have 13 higher serum free...


Other pituitary conditions that can present with hyperprolactinemia are acromegaly and Cushing's disease. Acromegaly is caused by a growth hormone secreting adenoma. About 30-40 of such adenomas cosecrete prolactin. This is not a surprise given the common embryologic origin of the somatotrophic cells (GH secreting cells) and the mammotrophic cells (PRL secreting cells) of the anterior pituitary. The associated hyperprolactinemia partially explains the hypogonadism observed in acromegalic patients. Cushing's disease, caused by an ACTH secreting pituitary adenoma, can also be associated with hyperprolactinemia. Although the association is infrequent, mixed adenomas secreting both ACTH as well as PRL have been reported.


Osteoporosis in the male is a newly appreciated problem. Long associated with the aging woman, osteoporosis is now known to affect more than 2 000 000 American males over the age of 50 at this time, with another pool of 3100 000 men who are at risk for developing it.1-5 About one out of every eight men over the age of 50 will at some point have an osteoporosis-related fracture.6'7 Every year about 100000 men will suffer an osteoporosis-related hip fracture, one-third of which will die within the year. In addition tens of thousands of men will have a fracture of the wrist, spine or rib. Physicians who treat men need to be increasingly sensitive to this problem. Thirty-six per cent of the osteoporosis in men is due to low androgen levels, which can occur as a result of hypogonadism that is either congenital, as part of the aging process, or due to acute androgen deprivation, such as in the treatment of advanced carcinoma of the prostate.8 In the latter case, given the usually advanced...

Hormonal Therapy

LHRH agonists, like leuprolide and goserelin, decrease gonadotropin release, which suppresses testicular androgen production. LHRH agonists decrease sexual desire, sexual intercourse, and frequency, duration and rigidity of nocturnal erections when serum testosterone levels fall to castration levels.107 These agents are potent inhibitors of the male sexual response and must be used judiciously in younger patients who wish to preserve sexual function.

Ovulation Induction

Polycystic Ovarian Syndrome Etiology

Hypogonadotropic hypogonadism Eugonadotropic hypogonadism Hypergonadotropic hypogonadism Gonadotropin releasing hormone (GnRH) was first identified in 1971 and is the hypothalamic releasing hormone responsible for FSH and LH synthesis and release from the pituitary. While it is rarely used in clinical practice, it is the most physiological method of ovulation induction for WHO group I ovulatory disorders, namely women who have hypogonadotropic hypogonadism. These women typically do not have the pulsatile GnRH secretion required for the synthesis and release of gonadotropins from the pituitary that are responsible for ovarian folliculogenesis and regular, cyclic menses. GnRH is typically administered in doses from 2.5-20 ig every 60-120 minutes. GnRH pulsatile therapy may be administered intravenously (IV) or subcutaneously (SC) but appears to be more effective by IV route. The LH surge and subsequent ovulation occur spontaneously, therefore not requiring an injection of hCG to induce...

Females Males

Syndrome Albright

Precocious puberty may result in a decrease of final adult height so arresting the growth is an important objective. The history and physical exam are extremely important as are growth charts. A skeletal film of the hand for bone age is very important in assessing the severity of the disorder and need for treatment (Fig. 2.1). Premature thelarche may occur in girls 1-2 years old because of the GnRH pulse generator activity. Normally, this will not result in advanced growth and the bone age is consistent with chronologic age. No treatment is necessary, even though some girls may have follicular activity on ultrasound. Premature adrenarche without other signs of puberty is also a benign process, and if the bone age is normal, these patients can be followed expectantly. Patients with premature adrenarche tend to be taller and heavier than other children their age. These patients may be at risk for polycys-tic ovary syndrome in the future. If they have hirsutism, serum levels of total...


Infertile Discharge

Using the patient's history and physical exam to guide the ordering of additional tests, the evaluation of amenorrhea can be both time efficient and cost effective. One such diagnostic approach is depicted in Figures 3.1-3.5. This management algorithm classifies patients by physical evidence of estrogen secretion and the absence of a Y chromosome. Because steroidogenesis is one of the basic functions of the intact gonad, the absence of breast development strongly suggests hypoestrogenemia and therefore, hypogonadism. However, the presence of breasts does not confirm normal estrogen levels or eugonadism. Breast development is only a marker for past exposure to estrogen. To obtain information on a patient's current estrogen status, it is necessary to evaluate the patient's reproductive organs. Upon speculum examination of the patient's vagina and cervix, a well-estrogenized vagina is characterized by pink, moist mucosa with multiple rugations and the presence of mucous discharge from...

Kallman syndrome

Characteristic features are hypogonadotrophic hypogonadism and anosmia. It can be associated with small penis, cryptorchidism (and absent postnatal rise in LH and testosterone, with blunted response to gonadotrophin-releasing hormone (GnRH) and human chorionic gonadotrophin (hCG)). Anosmia may be elicited in family history. Choanal atresia and cleft lip or palate have also been reported. Kallmann syndrome may represent the least severe form of the holoprosencephaly-hypopituitarism complex. patients have hypogonadism. Inheritance is autosomal recessive. 0

Specific Hormones

Kallmann Syndrome Penis

EXCESS May occur in prolactin-producing tumors, or with excess thyroid releasing hormone (TRI1) production, which stimulates prolactin secretion in addition to TSH secretion. Galactorrhea (excess milk secretion) results, as well as amenorrhea and anovulation secondary to disturbances of the menstrual cycle. Nursing also stimulates prolactin production and hence is associated with decreased fertility during the phase of nursing. Excess prolactin in males results in testosterone deficiency and impotence.

Endocrine Evaluation

Peripheral Follicles Polycystic Ovary

As PCOS is diagnosed after exclusion of other endocrine disorders, a work-up to assess for these other conditions is indicated. Table 5.2 summarizes the primary endocrine evaluation. Key to the differential diagnosis is to rule out late onset congenital adrenal hyperplasia due to 21-hydroxylase deficiency. This disorder mimics PCOS as it also presents at menarche and is associated with hyperandrogenism. Unlike PCOS the increased androgens in congenital adrenal hyperplasia are primarily from adrenal origin. A morning blood sample for 17-hydroxyprogesterone is a good screening test for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Samples should be drawn in the follicular phase if the patient is cycling. Generally levels less than 2 ng mL are not consistent with late onset 21-hydroxylase deficiency. Borderline values should be followed by an ACTH stimulation test. Androgen evaluation should include a serum total testosterone and DHEAS. Hormonal assays for free...


Several genetic diseases involve imprinted genes. The classic examples of diseases arising from imprinting are Prader-Willi and Angelman syndromes, which involve mutations on chromosome 15q11-q13. Prader-Willi syndrome (PWS OMIM 176270), which affects approx 1 in 10,000 to 1 in 15,000 newborns, is characterized by hypotonia, short stature, polyphagia, obesity, small hands and feet, hypogonadism, and mild mental retardation. Most cases of PWS are sporadic. In 70 of cases, a cytogenetically visible deletion of 15q11-q13 is present in the paternal chromosome in a region that includes the SNRPN gene, which is a candidate gene for this disease. Whether deletion of this gene alone is responsible for the disorder is presently uncertain. The maternal chromosome 15q is imprinted in this region, and therefore subjects with a deletion of this region of the paternal chromosome have no functional copy of the genes that are deleted.

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