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Thread: Prolactine (sp)?

  1. #11
    Quote Originally Posted by Steven Edwards
    Sex also increases prolactin levels.
    Well, increased prolactin levels certainly don't make you want to have sex. At least not me. An abnormally high level of prolactin is one of the issues my endocrinologist is helping me with.

    C.

  2. #12
    Prolactin & Spinal Cord Injury

    Prolactin is a pituitary hormone. In women, it stimulates the breasts to enlarge and produce milk. It is also said to produce feelings of sexual gratification after intercourse, by repressing the effects of dopamine that causes sexual arousal. It is believed to be responsible for the male's refractory period. High levels of prolactin can cause impotence and loss of libido, a condition called hyperprolactinemia. Prolactin levels increase during ovulation, pregnancy, during breast feeding, and intercourse.

    Prolactin is a polypeptide with 199 amino acids (24 kD) and the molecule can be variously glycosylated, phosphorylated, sulfated, as well as fragmented, after release from the pituitary. The transcription factor that stimulates prolactin production is Pit-1 and it is regulated by estrogens that enhance prolactin production and suppress dopamine effects. High prolactin levels suppresses ovulation by inhibiting FSH and GnRH secretion. Prolactin has been implicated in surfactant synthesis in fetal lungs at the end of pregnancy and also immune tolerance of the fetus by the mother during pregnancy (Source).

    In women with spinal cord injury, hyperprolactinemia (high prolactin blood levels) is associated with galactorrhea (breast secretions) and amenorrhea (abnormal low or absent menstrual flows). Berezin, et al. (1989) in Israel, described six women who developed hyperprolactinemia, amenorrhea, and galactorrhea after spinal cord injury. Two were postpartum and one was pregnant at the time of injury. One had transient diabetes insipidus. Treatment of bromocriptine reduced the prolactin levels and restored ovulatory cycles. The authors suggested that being pregnant or early postpartum can predispose women with spinal cord injury to have this problem. Yarkony, et al., (1992) likewise reported galactorrhea in four women with SCI. In fact, the inhibitory effect of breast-feeding on fertility is attributed to breast-feeding elevation of prolactin causing amenorrhea during the first 6 months after delivery.

    In men, prolactin levels may be higher than normal during the first 3 months after injury and returned to normal thereafter in one early study (Cortes-Gallegos, et al., 1982). Campangolo, et al. (1999) reported no difference of prolactin levels between subjects with spinal cord injury and control subjects. However, in tetraplegic subjects, prolactin correlated highly with dehydroepiandrosterone sulfate levels, suggesting that low prolactin levels is associated with hypogonadism (low testosterone levels) in males. However, high prolactin levels are also associated with hypogonadism and erectile dysfunction in men. Elevated prolactin levels are also associated with abnormally low parathyroid hormone in men with spinal cord injury, compared to those with traumatic brain injury (Mechanick, et al., 1997). High prolactin levels probably the cause gynecomastia (excessive development of the mammary gland) that can occur in men during the first 6 months after spinal cord injury (Heruti, et al., 1997).

    Huang, et al. (1998) examined the hypothalamic-pituitary-adrenal axis in 25 men with spinal cord injury. Compared against age-matched male non-injured volunteers, they found 3 of the 25 men had hyperprolactinemia, 3 had elevated basal follicle-stimulating hormone levels, one had elevated basal luteinizing hormone levels, and four had low testosterone levels. In general, the men had lower ACTH response to CRF stimulation, suggesting depressed pituitary response. Eleven of the spinal-injured subjects had abnormally low cortisol response to insulin-induced hypoglycemia. These findings suggest that many men with spinal cord injury have altered hypothalamic-pituitary-adrenal axes. Similarly, three of 16 women with spinal cord injury had elevated prolactin levels. Over 81% of women with SCI had at least one axis abnormality of their hypothalamus-pituitary-ovary-thyroid axis.

    Many drugs increase prolactin levels, including anti-psychotic medications. Such drugs include chlorpromazine, haloperidol, clozapine, and others. Excessive thyrotropin-releasing hormone (TRH) can also elevate prolactin levels. Of course, breast feeding elevate prolactin levels. Of course, pituitary tumors can cause very high levels of prolactin and is treated with bromocryptine. Hypothyroidism is associated with hyperprolactinemia and treatment of the hypothyroid condition may resolve the increased prolactin. Interestingly, surgical scars on the chest all and other chest wall irritation (shingles for example) can trigger excessive prolactin secretion. Certain tranquilizers, high blood pressure medications, and anti-nausea medication can lead to excessive prolactin secretion. Oral contraceptives and marijuana may also cause mild prolactin excess (ASRM Fact Sheet: Prolactin Excess (PDF)).

    In summary, this is not a hormone that one wants to take if one doesn't have low prolactin levels. It has many side-effects and is not innocuous. Hyperprolactinemia is associated with infertility and impotence, as well as other undesirable side-effects, such as gynecomastia. Given that many people with spinal cord injury have had high prolactin levels (due to medication or other causes) and there is no report of improved recovery, prolactin probably does not promotes neurological recovery. I was unable to find any animal study that suggested beneficial effects of prolactin on spinal cord injury or recovery.

    References
    1. Berezin M, Ohry A, Shemesh Y, Zeilig G and Brooks ME (1989). Hyperprolactinemia, galactorrhea and amenorrhea in women with a spinal cord injury. Gynecol Endocrinol 3: 159-63. Six women with a traumatic spinal cord injury (SCI) developed hyperprolactinemia, amenorrhea and galactorrhea. Five of them had thoracic level lesions and 1 had a lumbosacral lesion. Two were postpartum and 1 was pregnant at the time of injury. Transient diabetes insipidus developed in 1 patient. Temporary administration of bromocriptine decreased prolactin levels, caused cessation of lactation and restored ovulatory cycles. The syndrome disappeared spontaneously in all 6 patients. Pituitary stalk concussion resulting from the trauma might cause this phenomenon, with the level of the cord injury playing a role. Being pregnant or early postpartum can predispose women to develop this syndrome. Institute of Endocrinology, Chaim Sheba Medical Center, Tel-Hashomer, Israel. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=2510463
    2. Campagnolo DI, Bartlett JA, Chatterton R, Jr. and Keller SE (1999). Adrenal and pituitary hormone patterns after spinal cord injury. Am J Phys Med Rehabil 78: 361-6. Current evidence indicates that the neuroendocrine system is the highest regulator of immune/inflammatory reactions. We hypothesized that immune alterations, which were related to the level of injury, found in a cohort of spinal cord-injured subjects may be influenced by altered hormonal patterns postinjury. Therefore, we investigated aspects of both pituitary and adrenal function in the same cohort of spinal cord-injured subjects. We found significant elevations in both cortisol and dehydroepiandrosterone sulfate in chronic spinal cord-injured survivors compared with their able-bodied age- and gender-matched controls. Levels of dehydroepiandrosterone, adrenocorticotropin, and prolactin were not different in spinal cord-injured subjects overall compared with their controls. Both dehydroepiandrosterone sulfate and dehydroepiandrosterone were higher in tetraplegics compared with their controls, but we found no such differences in paraplegics compared with their controls. When the two groups of spinal cord-injured subjects were compared with each other, we also found differences between these two subject groups in dehydroepiandrosterone sulfate and dehydroepiandrosterone (higher in the tetraplegics compared with paraplegics). We found no differences between either group of spinal cord-injured subjects and their controls for adrenocorticotropin, prolactin, or cortisol. These data suggest that some hormonal differences between subjects and their controls may be further related to the level of injury (specifically dehydroepiandrosterone and dehydroepiandrosterone). Finally, we investigated correlations within subjects for the above hormones. Dehydroepiandrosterone sulfate and prolactin were highly correlated (the higher the dehydroepiandrosterone sulfate, the higher the prolactin) but only in the tetraplegic subjects. Department of Physical Medicine and Rehabilitation, UMDNJ-New Jersey Medical School, Newark, New Jersey 07103-2406, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10418843
    3. Cortes-Gallegos V, Castaneda G, Alonso R, Arellano H, Cervantes C and Parra A (1982). Diurnal variations of pituitary and testicular hormones in paraplegic men. Arch Androl 8: 221-6. The effect of the neuro-spinal cord injury upon testicular physiology was evaluated in six adult paraplegic (PPG) men by measuring the circulating levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), androstenedione, testosterone, and dihydrotestosterone every 4 hr throughout a 24-hr period. Three PPG men were studied within the first 3 months (acute period) and the other three patients 39-79 months (stabilized period) after trauma. Hormonal values were compared with eight age-matched normal adult males. Plasma FSH and LH were constantly above normal concentrations regardless of the sampling time and period of observation, whereas prolactin was higher than normal only during the first two months after trauma, returning to normal afterwards. Plasma androgens were consistently below normal during the first 3 months after injury, and returned toward normal thereafter. There may be a direct relationship between the time elapsed after the spinal cord injury and the plasma androgens concentrations. A possible role of PRL in testicular steroidogenesis is suggested. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=6808942
    4. Heruti RJ, Dankner R, Berezin M, Zeilig G and Ohry A (1997). Gynecomastia following spinal cord disorder. Arch Phys Med Rehabil 78: 534-7. Gynecomastia, an excessive development of the mammary glands in men, is a known phenomenon among patients with spinal cord disorder, yet in the last 50 years it has not been fully described in relation to spinal cord disorder. Over a period of 2 years, six patients with spinal cord disorder (4 secondary to a traumatic injury, 1 to decompression sickness, and 1 to transverse myelitis) manifested gynecomastia. The onset of gynecomastia occurred between 1 to 6 months after injury. These patients are presented along with a review of the possible causes for gynecomastia and a suggested workup routine. A clinical examination for the presence of gynecomastia should be performed for every patient with spinal cord disorder and a thorough endocrinological workup should follow to rule out malignancy and reassure the anxious patient undergoing a disruption of his body image. Department of Neurologic Rehabilitation, Sheba Medical Center, Tel-Hashomer, Israel. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9161376
    5. Huang TS, Wang YH, Lai JS, Chang CC and Lien IN (1996). The hypothalamus-pituitary-ovary and hypothalamus-pituitary-thyroid axes in spinal cord-injured women. Metabolism 45: 718-22. Sixteen women with spinal cord injury (SCI) underwent studies of the hypothalamus-pituitary-ovary (HPO) and hypothalamus-pituitary-thyroid (HPT) axes with luteinizing hormone (LH) releasing hormone (LHRH) and thyrotropin (TSH) releasing hormone (TRH) stimulation tests during the early follicular phase. The mean interval from injury to participation in this study was 7.5 years (range, 1.5 to 13.1). All subjects were menstruating regularly. Five (35.7%) SCI subjects who were menstruating before injury had postinjury amenorrhea for 1 to 12 months, and the other nine (64.3%) SCI subjects had no interruption of menstruation after injury. Two SCI subjects whose injury occurred in preadolescence proceeded to menarche without any delay. The amount of menstrual flow was noted to be reduced in nine (64.3%) SCI subjects. Two and three SCI subjects had elevated follicle-stimulating hormone (FSH) and prolactin (PRL) levels, respectively. LH responses to LHRH were significantly higher in the SCI group (P < .001). Ten (62.6%) SCI subjects had enhanced LH responses to LHRH. The mean TSH, PRL, and FSH responses to TRH and LHRH of the SCI group were not significantly different from those of age-matched controls. However, five (31.2%), four (25.0%), and five (31.2%) SCI subjects had enhanced TSH, PRL, and FSH responses to TRH and LHRH, respectively. Six (37.5%) SCI subjects had a delayed FSH response to LHRH. In total, 13 (81.2%) SCI subjects had at least one axis abnormality. These findings are consistent with the hypothesis that changes of central neurotransmitters may occur after SCI. Department of Medicine, National Taiwan University Hospital, Taipei, Republic of China. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8637446
    6. Huang TS, Wang YH, Lee SH and Lai JS (1998). Impaired hypothalamus-pituitary-adrenal axis in men with spinal cord injuries. Am J Phys Med Rehabil 77: 108-12. Twenty-five men with spinal cord injuries were studied for evaluation of the hypothalamus-pituitary-adrenal axis, using corticotropin-releasing hormone and insulin-induced hypoglycemia. Twenty-five age-matched healthy male volunteers served as controls. Three spinal cord-injured subjects had hyperprolactinemia, three had elevated basal follicle-stimulating hormone levels, one had an elevated basal luteinizing hormone level, and four had hypotestosteronemia. The mean plasma adrenocorticotropin response to corticotropin-releasing hormone of spinal cord-injured subjects was smaller than that of the healthy controls but did not reach a statistical significance. The cortisol response to corticotropin-releasing hormone of the spinal cord-injured subjects was significantly lower than that of healthy controls. However, the difference disappeared if a correction was made for baseline values. Six spinal cord-injured subjects did not have a cortisol response to insulin-induced hypoglycemia, and they had either a minimal or no adrenocorticotropin response. Another 11 spinal cord-injured subjects had a maximal cortisol response to insulin-induced hypoglycemia below the lowest limit of normal, i.e., 0.5 micromol/l. Among these spinal cord-injured subjects, three had a less than 50% increase of plasma adrenocorticotropin after insulin-induced hypoglycemia. These findings are consistent with the notion that spinal cord-injured subjects have an altered central neurotransmitter tone and substantiate the hypothesis that an afferent neural pathway exists between the adrenal and hypothalamus and may modulate stress-induced secretion of adrenocorticotropin. Long-term abnormal adrenocorticotropin secretion may cause mild adrenocortical atrophy and, thereby, a reduced cortisol response. Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Republic of China. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9558010
    7. Mechanick JI, Pomerantz F, Flanagan S, Stein A, Gordon WA and Ragnarsson KT (1997). Parathyroid hormone suppression in spinal cord injury patients is associated with the degree of neurologic impairment and not the level of injury. Arch Phys Med Rehabil 78: 692-6. OBJECTIVE: To demonstrate that after spinal cord injury (SCI) suppression of the parathyroid-vitamin D axis is associated with the degree of neurologic impairment and not the level of injury. DESIGN: A retrospective analysis of clinical and biochemical data obtained from hospital records of patients with SCI compared to a control group of patients with traumatic brain injury (TBI). SETTING: The inpatient rehabilitation unit of a tertiary care hospital. SUBJECTS: The medical records of 82 consecutive admissions to the rehabilitation unit with a diagnosis of SCI or TBI were reviewed. Patients with SCI were classified by the American Spinal Injury Association (ASIA) impairment scale and then grouped based on the completeness and level of injury. MAIN OUTCOME MEASURE: Comparisons of serum parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D (1,25-D) were planned. Multiple comparisons were performed for total and ionized serum calcium levels, serum phosphorus levels, and 24-hour urinary calcium excretion rates to reflect changes in mineral homeostasis. Multiple comparisons were also performed for serum albumin, prolactin, thyroid function tests, and AM cortisol levels, as well as 24-hour urinary urea nitrogen and cortisol excretion rates to reflect metabolic responses to stress. RESULTS: Patients with SCI had significant suppression in PTH (p < .000009) and 1,25-D (p < .02) levels with elevated phosphorus (p < 0.03) and prolactin (p < .03) levels compared to patients with TBI. Also, more patients with SCI were hypoalbuminemic (p < .003) than patients with TBI. Patients with complete SCI (ASIA A) had more suppressed PTH (p < .03) and higher urinary urea nitrogen (p < .05) levels than SCI patients with incomplete injuries (ASIA B-D). Patients with complete, but not incomplete, SCI had lower albumin levels than patients with TBI (p < .05). These differences were not found between patients with tetraplegic and paraplegic SCI. ASIA motor scores did not correlate with any of the measured parameters but when used as a covariate did abolish differences in PTH and 1,25-D among the study groups by ANOVA. CONCLUSION: In patients with SCI, the degree of neurologic impairment, and not the level of injury, is associated with PTH suppression and markers of metabolic stress. Division of Endocrinology and Metabolism, Mount Sinai School of Medicine, New York, NY 10029, USA. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9228870
    8. Wheeler GD, Ashley EA, Harber V, Laskin JJ, Olenik LM, Sloley D, Burnham R, Steadward RD and Cumming DC (1996). Hormonal responses to graded-resistance, FES-assisted strength training in spinal cord-injured. Spinal Cord 34: 264-7. Functional electrical stimulation (FES) assisted resistance training has been effective in increasing muscular strength and endurance in spinal cord injured men and women in preparation for FES-assisted cycle programs and for FES-assisted standing and walking. Increases in blood pressure and a concomitant bradycardia suggestive of autonomic dysreflexia have been reported during FES-assisted resistance training. Self-induced autonomic dysreflexia in athletes who use wheelchairs suppressed the normal exercise induced serum testosterone increase. We, therefore, examined the changes in hematocrit and circulating levels of testosterone, sex hormone binding globulin (SHBG), cortisol, prolactin, norepinephrine and epinephrine during FES assisted resistance exercise in five high spinal cord injured men (SCI) and comparable maximal exercise in five able bodied controls (AB). Mean serum testosterone levels significantly increased with FES-assisted resistance training in SCI and maximal resistance exercise in AB with no significant change in hematocrit or SHBG. Prolactin, cortisol and epinephrine levels were unchanged while norepinephrine levels were significantly increased in SCI and AB. These findings suggest that there is no concern over inadequate physiological androgen response to an exercise stimulus in SCI. The data do not support the previous findings that elevated levels of norepinephrine in autonomic dysreflexia suppress testosterone response to exercise. Rick Hansen Centre, University of Alberta, Edmonton, Canada. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8963972
    9. Yarkony GM, Novick AK, Roth EJ, Kirschner KL, Rayner S and Betts HB (1992). Galactorrhea: a complication of spinal cord injury. Arch Phys Med Rehabil 73: 878-80. Galactorrhea, a secretion of milk or milk-like products from the breast in the absence of parturition, has been reported to occur in women with spinal cord injuries in association with amenorrhea and hyperprolactinemia. Four cases of galactorrhea in association with spinal cord injury are reported. Galactorrhea developed in four spinal cord injured women who had thoracic paraplegia. The onset of galactorrhea was from one month to five months after injury. Although the onset of galactorrhea may have been related to prescribed medications in all four cases, insufficient data exist to draw conclusions. The three women whose galactorrhea persisted declined treatment and galactorrhea continuing for more than two years in one instance. We conclude that galactorrhea with or without amenorrhea may develop after a spinal cord injury and that spinal cord injured women may have an enhanced sensitivity to medication-induced galactorrhea. Department of Rehabilitation Medicine, Northwestern University Medical School, Chicago, IL. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1514898
    Last edited by Wise Young; 02-22-2007 at 12:05 AM.

  3. #13

    Pregnancy Hormone May Offer Treatment For Multiple Sclerosis

    Pregnancy Hormone May Offer Treatment For Multiple Sclerosis

    Main Category: Neurology / Neuroscience News
    Article Date: 26 Feb 2007 - 8:00 PST
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    A hormone produced during pregnancy spontaneously increases myelin, which enhances signaling within the nervous system, and helps repair damage in the brain and spinal cord, according to new animal research.

    The findings, published in the Journal of Neuroscience, indicate that the hormone prolactin promotes an increase in myelin production and may have a use in treating multiple sclerosis (MS).

    In MS, affecting about 2.5 million people worldwide, the body's own immune system attacks myelin, which insulates nerve cells and plays a critical role in the speed at which messages are transmitted from cell to cell. Reduction in myelin leads to a progressive loss of sensation and movement in MS patients.

    "Agents promoting remyelination will be beneficial not only for typical demyelinating diseases like MS," says Fred Gage, PhD, of the Salk Institute, "but also for many other neurological disorders, such as spinal cord injuries and stroke." Gage did not participate in the study.

    The research was based on evidence showing that multiple sclerosis, which is more common in women than men, goes into remission when women become pregnant. "It was thought that during pregnancy, their immune systems no longer destroyed the myelin," says study author Samuel Weiss, PhD, at the Hotchkiss Brain Institute of the University of Calgary. "But no previous study has tested whether pregnancy actually results in the production of new myelin, which may explain improvement of symptoms."

    Comparing pregnant and virgin female mice of the same age, Weiss's team counted hundreds of cells in their brains and spinal cords. They found that the pregnant mice had twice as many myelin-producing cells, called oligodendrocytes, and continued to generate new ones during pregnancy. After giving birth, these mice also had 50 percent more myelin coating their nerve cells.

    The researchers also showed that pregnancy repaired nerve cells faster where the myelin had been chemically destroyed: Pregnant female mice had twice as much new myelin two weeks after damage. Finally, they found that prolactin mimicked the effects of pregnancy, increasing both myelin production and repair. This suggests prolactin, which increases during pregnancy, may help induce the making of new myelin.

    Should future tests of prolactin in animal models of MS prove successful, Weiss says the hormone will be ready for testing as a treatment for people with MS.

    ###

    The work was supported by the Canadian Institutes of Health Research, Multiple Sclerosis Society of Canada, Alberta Heritage Foundation for Medical Research, and Stem Cell Network.

    The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 36,500 basic scientists and clinicians who study the brain and nervous system.

    Contact: Sara Harris
    Society for Neuroscience










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  4. #14
    Senior Member litespeed4's Avatar
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    Pregnacy and Remyelination

    Original article published in Nature Reviews Neuroscience
    "White matter plasticity and enhanced remyelination in the maternal CNS"

    PubMed Link
    http://www.ncbi.nlm.nih.gov/entrez/q...arch&DB=pubmed

    This study was primarily for MS but the investigators studied the effect on the spinal cord as well.
    It's been known that people (women) suffering from MS often experience a remission during pregnacy. A Canadian team has shown that remyelination and the generation of new oligodendrocytes is involved. The hormone prolactin (PRL) seems to be the driving force behind the generation of new OPC cells and the remylination.

    The present study suggests that white matter changes occur in the maternal CNS. These changes are initiated during early pregnancy and include increases in OPC proliferation, oligodendrocyte generation, MBP expression, and, ultimately, an increase in the number of myelinated axons. Remarkably, we find that this process is associated with an enhanced capacity to regenerate myelin damage. PRL signaling is necessary and sufficient for the pregnancy-induced increase in OPC proliferation, and PRL treatments mimic the regenerative effects of pregnancy on myelin damage in virgin females. These results identify a novel form of white matter plasticity in the adult CNS and suggest that PRL may have therapeutic potential for the treatment of white matter damage.
    The researchers also extensively examined the effects on the spinal cord.
    To test whether pregnancy-induced OPC proliferation enhances the intrinsic capacity of the maternal CNS to repair demyelination, we used a spontaneously remyelinating model of acute demyelinating injury in which the detergent lysolecithin is injected directly into the dorsal funiculus of the spinal cord (Jeffery and Blakemore, 1995; Larsen et al., 2003). Remyelination in this model has begun by 7 d after lesion, is primarily completed after 23 d (Jeffery and Blakemore, 1995), and can be assessed by measurements of the lesion size (Larsen et al., 2003).
    Furthermore, results of recent studies have clearly demonstrated that enhancing remyelination after spinal cord injury through the transplantation of OPCs significantly improves recovery (Bambakidis and Miller, 2004; Cao et al., 2005; Lee et al., 2005; Karimi-Abdolrezaee et al., 2006). Moreover, efforts are underway to derive OPCs from human embryonic stem cell lines for the clinical treatment of spinal cord injury (Faulkner and Keirstead, 2005; Keirstead et al., 2005). Together, these studies suggest that a molecule such as PRL, which can be systemically delivered to mobilize endogenous OPCs and promote intrinsic myelin repair, may have potential for the treatment of several neurological disorders associated with white matter pathology.
    As for us guys - we might be screwed

  5. #15
    Senior Member rvr's Avatar
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    great news. now all I have to do is figure out how to get knocked up.
    rob

  6. #16
    So estriol is the culprit, not prolactin.

    http://www.sciencedaily.com/releases...0323104949.htm

    I would hope that the women can begin taking the drug now and not have to wait until the next series of trials is complete and the results are in. The drug is already FDA approved.

  7. #17
    Quote Originally Posted by antiquity
    So estriol is the culprit, not prolactin.

    http://www.sciencedaily.com/releases...0323104949.htm

    I would hope that the women can begin taking the drug now and not have to wait until the next series of trials is complete and the results are in. The drug is already FDA approved.
    Antiquity,

    I did a literature search on esteriol and multiple sclerosis. The possible beneficial effects of estrogen and estrogen derivatives have long been posulated for multiple sclerosis. In 1994, Janssen, et al. reported that estrogen itself prevents experimental autoimmune encephalomyelitis induced arthritis in mice. In 1998, Correale & Gilmore reported that estradiol (E2) modifies cytokine secretion by CD3+ T cells ioslated from patients with demyelinating diseases, multiple sclerosis, and also normal control subjects. They found that estrone (E1) and esteriol (E3) also enhance secretion of anti-inflammatory IL-10. In 1999, Kim, et al. reported that estriol ameliorates autoimune demyelinating disease in animal models. In 2000, Drew & Chavis showed that female sex steroid homones (estrogen and progesterone) inhbited production of ntiric oxide synthetase (iNOS) and microglial cell activation. Zang, et al. (2002) found that estriol inhibits the pro-inflammatory transcription factor NF-kappa-B.

    On the other hand, it is well known that women are more susceptible to mutliple sclerosis than men, even though they have higher resting levels of estrogen and progesterone. Although females are less susceptible during pregnancies (Voskuhl & Palazynski, 2001; Voskuhl, 2002), one question that has not been asked is whether this simply returns their susceptibility to the same as men.

    In 2002, Sicotte, et al., treated female MS patients with estriol (8 mg/day) and found that this significantly reduced delayed hypersensitivity responses to tetanus, decreased interferon-gamma levels in peripheral blood mononuclear cells, and shrank gadolinium enhancing lesion numbers and volumes on MRI. When estriol treatments were stopped, the lesions increased back to pre-treatment levels. In 2003, Soldan did a second study and found that estriol treatment reduced cytokines and reduction of enhancing lesions in patients with relapsing, remitting multiple sclerosis. In 2004, Palazynski, et al. found that estriol ameliorates disease in male mise with experimental autoimmune encephalomyeltis and suggested that esteriol may be useful for treating males with multiple sclerosis as well.

    Based on these kinds of results, doctors are already using a variety of treatments that are not FDA approved for MS, to treat people with relapsing MS. For example, drugs that are now prescribed by doctors to treat relapses include the statins, mycophenolate mofetil, monoclonal antibodies (alemtuzumab, daclzumab, natalizumab, and rituximab), antibiotics, antivirals, and estriol, and combinations (Rizvi & Bashir, 2004).

    By the way, the article that you cited referred to esteriol which is different from estriol. What is the difference between estriol and esteriol? Here is a picture of estriol.



    I think that esteriol is 17-beta-estradiol:



    Wise.


    References
    1. Jansson L, Olsson T and Holmdahl R (1994). Estrogen induces a potent suppression of experimental autoimmune encephalomyelitis and collagen-induced arthritis in mice. J Neuroimmunol 53: 203-7. We have earlier described a chronic relapsing experimental autoimmune encephalomyelitis (EAE) in B10.RIII mice induced with a peptide of myelin basic protein (MBP), mimicking the course of multiple sclerosis in man. We now show that estrogens ameliorate chronic EAE. Castration of female mice led to an earlier disease onset (day 9 +/- 2 postimmunization (p.i.) in castrated mice vs. day 16 +/- 4 p.i. in normal mice). Long-term treatment with high levels of 17 beta-estradiol (E2) given as Silastic implants led to a dramatically delayed onset of disease in both castrated and normal female mice (mean onset day was day 39 +/- 14 and day 50 +/- 3, respectively). Treatment of castrated females by injections of E2, at a concentration which induces the serum levels seen at late stage pregnancy, delayed the onset approximately 1 week (mean onset 21 +/- 8). In contrast, treatment with estriol (E3), which was also given at doses corresponding to those levels seen during pregnancy, delayed the disease onset for a longer time (mean onset day 31 +/- 5). Five times higher doses of E2, compared with those seen during pregnancy, were required to obtain similar effects as the low E3 dose. The same mouse strain (B10.RIII) is also susceptible to induction of collagen-induced arthritis (CIA). We show here that also CIA is suppressed by the same treatments with E2 and E3, suggesting that similar estrogen-mediated mechanisms may operate to suppress these T-cell-dependent autoimmune disease models. Department of Medical and Physiological Chemistry, Uppsala University, Sweden. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8071434
    2. Correale J, Arias M and Gilmore W (1998). Steroid hormone regulation of cytokine secretion by proteolipid protein-specific CD4+ T cell clones isolated from multiple sclerosis patients and normal control subjects. J Immunol 161: 3365-74. Steroid hormones have long been known to modulate immune function, and recent studies indicate that one of the means by which they do so involves effects on the secretion of immunoregulatory cytokines. Our laboratory has found recently that estradiol (E2) selectively modifies cytokine secretion in proteolipid protein (PLP)-specific, CD4+ T cell clones isolated from patients with the demyelinating disease, multiple sclerosis, and from normal control subjects. The data suggest that E2 may play a role in regulating the balance between pro- and antiinflammatory conditions, especially at concentrations typical of pregnancy. To determine whether other pregnancy-associated steroid hormones are capable of similar activity, we expanded our testing to include estrone (E1), estriol (E3), progesterone, and dexamethasone. The results indicate that E1 and E3 enhance secretion of Ag- or anti-CD3-stimulated IL-10 and IFN-gamma in dose-dependent fashion, almost identical to that of E2. The effect on IL-10 was more potent than occurred with IFN-gamma. In addition, E1 and E3, like E2, had a biphasic effect on TNF-alphabeta secretion, with low concentrations stimulatory, and high doses inhibitory. None of the estrogens influenced IL-4 or TGF-beta secretion. Progesterone enhanced secretion of IL-4, without affecting any other tested cytokine. Finally, dexamethasone induced TGF-beta secretion, but inhibited IFN-gamma and TNF-alphabeta. This differential effect of steroid hormones on the secretion of cytokines by CD4+ human T cell clones is consistent with the possibility that, collectively, they promote antiinflammatory conditions at high concentrations typical of pregnancy. Department of Neurology, University of Southern California School of Medicine, Los Angeles 90033, USA. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9759853
    3. Kim S, Liva SM, Dalal MA, Verity MA and Voskuhl RR (1999). Estriol ameliorates autoimmune demyelinating disease: implications for multiple sclerosis. Neurology 52: 1230-8. OBJECTIVE: To evaluate the use of estriol in the treatment of experimental autoimmune encephalomyelitis (EAE) and other cell mediated autoimmune diseases. BACKGROUND: Experimental autoimmune encephalomyelitis is a T helper 1 (Th1)-mediated autoimmune demyelinating disease that is a useful model for the study of immune responses in MS. Interestingly, both EAE and MS have been shown to be ameliorated during late pregnancy. METHODS: Estriol, progesterone, and placebo pellets were implanted in mice during the effector phase of adoptive EAE. Disease scores were compared between treatment groups, and autoantigen-specific humoral and cellular responses were examined. RESULTS: Estriol treatment reduced the severity of EAE significantly compared with placebo treatment whereas progesterone treatment had no effect. Estriol doses that induced serum estriol levels that approximated estriol levels during late pregnancy were capable of ameliorating disease. Estriol-treated EAE mice had significantly higher levels of serum antibodies of the immunoglobulin (Ig) G1 isotype specific for the autoantigen myelin basic protein (MBP). Further, MBP-specific T-lymphocyte responses from estriol-treated EAE mice were characterized by significantly increased production of the Th2 cytokine interleukin 10 (IL-10). T lymphocytes were shown to be the primary source of IL-10 within antigen-stimulated splenocyte populations. CONCLUSIONS: Estriol as a hormone involved in immune changes during pregnancy may provide a basis for the novel therapeutic use of estriol for MS and other putative Th1-mediated autoimmune diseases that improve during late pregnancy. Department of Neurology, University of California Los Angeles School of Medicine, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10214749
    4. Drew PD and Chavis JA (2000). Female sex steroids: effects upon microglial cell activation. J Neuroimmunol 111: 77-85. Multiple sclerosis occurs more commonly in females than males. However, the mechanisms resulting in gender differences in multiple sclerosis are unknown. Activated microglia are believed to contribute to multiple sclerosis pathology, perhaps in part due to production of nitric oxide (NO) and TNF-alpha, molecules which can be toxic to cells including oligodendrocytes. The current study demonstrates that the female sex steroids estriol, beta-estradiol and progesterone inhibit lipopolysaccharide (LPS) induction of nitric oxide (NO) production by primary rat microglia and by the mouse N9 microglial cell line. These hormones act by inhibiting the production of inducible nitric oxide synthase (iNOS) which catalyses the synthesis of NO. Estriol likely inhibits iNOS gene expression since the hormone blocks LPS induction of iNOS RNA levels. The pro-inflammatory cytokines IFN-gamma and TNF-alpha are believed to be important modulators of multiple sclerosis. Here, we demonstrate that estrogens and progesterone also inhibit NO production by microglial cells activated in response to these cytokines. Activated microglia elicit TNF-alpha in addition to NO and we further demonstrate that estrogens and progesterone repress TNF-alpha production by these cells. Finally, estriol and progesterone, at concentrations consistent with late pregnancy, inhibit NO and TNF-alpha production by activated microglia, suggesting that hormone inhibition of microglial cell activation may contribute to the decreased severity of multiple sclerosis symptoms commonly associated with pregnancy. University of Arkansas for Medical Sciences, Department of Anatomy, Slot 510, Shorey Bldg., Rm. 922, 4301 W. Markham St., 72205, Little Rock, AR, USA. drewpauld@exchange.uams.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11063824
    5. Voskuhl RR and Palaszynski K (2001). Sex hormones in experimental autoimmune encephalomyelitis: implications for multiple sclerosis. Neuroscientist 7: 258-70. For decades, it has been known that females are more susceptible than males to multiple sclerosis (MS). It has also long been appreciated that during late pregnancy there is a decrease in MS disease activity. Interestingly, these two observations have also been made in an extensively used animal model for MS, experimental autoimmune encephalomyelitis (EAE) in SJL mice. Female mice are more susceptible to disease than male mice, and there is an improvement in disease during late pregnancy. In this review, the role of sex hormones in each of these two observations is characterized in this EAE model using castration and exogenous hormone treatment strategies. The gender difference in EAE susceptibility is due primarily to a protective effect of testosterone in male mice. The decrease in disease severity during late pregnancy appears to be due at least in part to high levels of estriol, which characterize this time period. Department of Neurology, University of California, Los Angeles 90095, USA. rvoskuhl@ucla.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11499404
    6. Voskuhl RR (2002). Gender issues and multiple sclerosis. Curr Neurol Neurosci Rep 2: 277-86. Gender-related issues in multiple sclerosis include the important and widely accepted clinical observations that men are less susceptible to the disease than women and also that disease activity in multiple sclerosis is decreased during late pregnancy. This article reviews mechanisms underlying each of these clinical observations and discusses the role of sex hormones in each. Specifically, the protective role of testosterone in young men and the protective role of the pregnancy hormone estriol in pregnant women are discussed. Rationale for novel therapies in multiple sclerosis based on the protective roles of these sex hormones is presented. UCLA Department of Neurology, Reed Neurological Research Center, Room A-145, 710 Westwood Plaza, Los Angeles, CA 90024, USA. rvoskuhl@ucla.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11937007
    7. Zang YC, Halder JB, Hong J, Rivera VM and Zhang JZ (2002). Regulatory effects of estriol on T cell migration and cytokine profile: inhibition of transcription factor NF-kappa B. J Neuroimmunol 124: 106-14. The protective role of pregnancy in autoimmune conditions, such as multiple sclerosis (MS), is potentially associated with immune regulation by sex hormones produced during pregnancy. This study was undertaken to examine the regulatory effects of estriol on the T cell functions, including transmigration and the cytokine production. The results revealed for the first time that estriol significantly inhibited T cell transmigration at a concentration range typical of pregnancy, which correlated with decreased T cell expression of matrix metalloproteinase-9. Estriol was also found to alter the cytokine profile of T cells toward Th2 phenotype by up-regulating the production of IL-10 and inhibiting TNFalpha secretion of T cells. However, the inhibitory effects of estriol on T cells were not antigen-dependent. Further characterization indicated that estriol inhibited nuclear transcription factor kappa B (NF-kappa B), which controls a variety of immune-related genes. This study provides new evidence that estriol is a potent regulator for the T cell functions potentially through its interaction with the NF-kappa B signaling pathway. Multiple Sclerosis Research Unit, Baylor-Methodist Multiple Sclerosis Center and Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11958828
    8. Soldan SS, Alvarez Retuerto AI, Sicotte NL and Voskuhl RR (2003). Immune modulation in multiple sclerosis patients treated with the pregnancy hormone estriol. J Immunol 171: 6267-74. The protective effect of pregnancy on putative Th1-mediated autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis, is associated with a Th1 to Th2 immune shift during pregnancy. The hormone estriol increases during pregnancy and has been shown to ameliorate experimental autoimmune encephalomyelitis and collagen-induced arthritis. In addition, estrogens induce cytokine changes consistent with a Th1 to Th2 shift when administered in vitro to human immune cells and in vivo to mice. In a pilot trial, oral estriol treatment of relapsing remitting multiple sclerosis patients caused significant decreases in enhancing lesions on brain magnetic resonance imaging. Here, the immunomodulatory effects of oral estriol therapy were assessed. PBMCs collected longitudinally during the trial were stimulated with mitogens, recall Ags, and glatiramer acetate. Cytokine profiles of stimulated PBMCs were determined by intracellular cytokine staining (IL-5, IL-10, IL-12 p40, TNF-alpha, and IFN-gamma) and cytometric bead array (IL-2, IL-4, IL-5, IL-10, TNF-alpha, and IFN-gamma). Significantly increased levels of IL-5 and IL-10 and decreased TNF-alpha were observed in stimulated PBMC isolated during estriol treatment. These changes in cytokines correlated with reductions of enhancing lesions on magnetic resonance imaging in relapsing remitting multiple sclerosis. The increase in IL-5 was primarily due to an increase in CD4(+) and CD8(+) T cells, the increase in IL-10 was primarily due to an increase in CD64(+) monocytes/macrophages with some effect in T cells, while the decrease in TNF-alpha was primarily due to a decrease in CD8(+) T cells. Further study of oral estriol therapy is warranted in Th1-mediated autoimmune diseases with known improvement during pregnancy. Department of Neurology, Reed Neurological Research Center, University of California School of Medicine, Los Angeles, CA 90095, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=14634144
    9. Sicotte NL, Liva SM, Klutch R, Pfeiffer P, Bouvier S, Odesa S, Wu TC and Voskuhl RR (2002). Treatment of multiple sclerosis with the pregnancy hormone estriol. Ann Neurol 52: 421-8. Multiple sclerosis patients who become pregnant experience a significant decrease in relapses that may be mediated by a shift in immune responses from T helper 1 to T helper 2. Animal models of multiple sclerosis have shown that the pregnancy hormone, estriol, can ameliorate disease and can cause an immune shift. We treated nonpregnant female multiple sclerosis patients with the pregnancy hormone estriol in an attempt to recapitulate the beneficial effect of pregnancy. As compared with pretreatment baseline, relapsing remitting patients treated with oral estriol (8 mg/day) demonstrated significant decreases in delayed type hypersensitivity responses to tetanus, interferon-gamma levels in peripheral blood mononuclear cells, and gadolinium enhancing lesion numbers and volumes on monthly cerebral magnetic resonance images. When estriol treatment was stopped, enhancing lesions increased to pretreatment levels. When estriol treatment was reinstituted, enhancing lesions again were significantly decreased. Based on these results, a larger, placebo-controlled trial of estriol is warranted in women with relapsing remitting multiple sclerosis. This novel treatment strategy of using pregnancy doses of estriol in multiple sclerosis has relevance to other autoimmune diseases that also improve during pregnancy. Department of Neurology, Reed Neurological Research Center, University of California Los Angeles, Los Angeles, CA 90095, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12325070
    10. Palaszynski KM, Liu H, Loo KK and Voskuhl RR (2004). Estriol treatment ameliorates disease in males with experimental autoimmune encephalomyelitis: implications for multiple sclerosis. J Neuroimmunol 149: 84-9. Estrogen treatment has been found to be protective in experimental autoimmune encephalomyelitis (EAE) and possibly multiple sclerosis (MS). We investigated whether the effect of estrogen treatment is gender-specific. Estrogen receptor (ER) expressions, ERalpha and ERbeta, were found to be equivalent in both genders. EAE disease severity in both females and males was decreased with estriol treatment as compared to placebo. Finally, proinflammatory cytokine production during autoantigen-specific immune responses was decreased with estriol treatment in both females and males. These data support a potential role for estriol treatment for men in addition to women with MS. Department of Neurology, Reed Neurological Research Center, University of California School of Medicine, 750 Westwood Plaza, Los Angeles, CA 90095, USA. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15020068
    11. Rizvi SA and Bashir K (2004). Other therapy options and future strategies for treating patients with multiple sclerosis. Neurology 63: S47-54. Research into therapy for multiple sclerosis (MS) is occurring at a rapid pace, and current treatment options approved by the FDA specifically target the inflammatory phase of MS. However, drugs that are not FDA-approved are routinely used to treat MS. One example is corticosteroids, which are commonly used to treat acute relapses. Other drugs that are commonly used to treat patients who do not respond to the FDA-approved agents include the following: methotrexate, azathioprine, cyclophosphamide, and pulse steroids. Drugs being studied as possible therapeutic agents include the statins, mycophenolate mofetil, various monoclonal antibodies (e.g., alemtuzumab, daclzumab, natalizumab, and rituximab), antibiotics and antivirals, and the pregnancy hormone estriol. Disease modifying agents (DMAs) that promote remyelination would be beneficial for preventing long-term disability, and such agents are also under active investigation (e.g., IV immunoglobulin G and stem cell transplantation). Combination therapy with DMAs with different mechanisms of action may be advantageous in the future for providing optimal treatment that both delays the progression of disability and promotes repair and remyelination. Department of Clinical Neurosciences, Brown University School of Medicine, 2 Dudley Street, Suite 555, Providence, Rhode Island 02905, USA. srizvi@lifespan.org http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15623671

  8. #18
    the pictures of estriol and esteriol are not showing up for some reason... but it doesn't matter. They are very similar to each other.

    Wise.

  9. #19
    low activity and rise of estrogens could be a reason of elevated prolactin too. Dostinex Carbengoline is great drug to use in such case. Vitamin B6 200-300 mg per day can help too.

  10. #20
    Quote Originally Posted by maxititer
    low activity and rise of estrogens could be a reason of elevated prolactin too.
    I thought that elevated levels of prolactin LOWERED estrogen levels.

    Dostinex Carbengoline is great drug to use in such case.
    It works, but it sure ain't cheap.

    C.

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