BioIdentical Hormones Relieve Anxiety by Jeffrey Dach MD

Anxiety_fear_panic_estradiolBioIdentical Hormones
For Anxiety and Depression
 

by Jeffrey Dach MD

56 year old Susan suffered from anxiety and panic attacks, and had been prescribed  Valium, Effexor and Wellbutrin by her primary care doctor.  The drugs had adverse side effects and didn't seem to be helping, so she stopped taking them.  After further discussion, she  told me that symptoms started a few years ago after monthly cycles stopped and the onset of menopausal hot flashes.  She noticed that the anxiety and panic attack seems to precede an episode of hot flashes.

Left Image: Anxiety, Fear and Panic courtesy of Wikimedia commons

Estrogen Deficiency Causes Anxiety

We sent Susan to the lab for a hormone panel, and sure enough, Susan's estrogen level was low. Susan's symptoms were caused by menopausal estrogen deficiency, a finding commonly seen in the post menopausal age group. Symptoms are promptly relieved with bioidentical estradiol applied as a topical cream twice a day.  Additionally, Susan's tests revealed vitamin and mineral deficiencies which were, no doubt, aggravating the anxiety attacks.

Susan was started on her bioidentical hormone program which included estradiol and progesterone as a balanced topical cream. She was also started on vitamin B12 and Magnesium supplements.  Six weeks later, Susan reported that her anxiety and panic attacks had improved and were almost gone.  She also noticed better sleep and more clarity of mind, and her night sweats and hot flashes had resolved as well.

Anxiety is Associated with Hot Flashes

Dont Panic estradiol AnxietyA study published in 2005 Menopause reported that anxiety is strongly associated with menopausal hot flashes, and usually precedes the hot flash episode. (13)  Hot flashes are caused by estrogen deficiency, and are treated with bioidentical estradiol, which virtually eliminates them.(15)(16)(17)

above image: dont panic courtesy of wikimedia commons

The Benefits of Bioidentical Estrogen

My previous articles discuss the safety and the importance of bioidentical hormones.

Uzzi Reiss's new book Natural SuperWoman contains an excellent discussion of bioidentical hormones.  Chapter 4 covers anxiety, panic attacks and relief with bioidentical estrogen.(1)  Numerous articles (see below) summarize the medical literature showing that low estrogen levels cause anxiety and depression in humans and animals.  Estrogen treatment relieves anxiety and depression as well as virtually eliminates the hot flashes.

tryptophan_serotonin_5htp

What is the Mechanism of Action Of Estrogen in Eliminating Anxiety and Depression?

Estrogen receptors have been found in the brain, and estrogen increases the expression of an enzyme in the brain called tryptophan hydroxylase-2 (TPH2).  This enzyme converts tryptophan to serotonin, an important neurotransmitter responsible for an anti-anxiety and calming effect in the brain.  These estrogen receptors have been isolated to specific areas of the brain call the DRN, or the dorsal raphe nuclei (2)(3)(4)(5)(6).

Dorsal Raphe Nuclei Estrogen SerotoninEstrogen Effective for Perimenopausal Depression

A study published in the 2001 Archives of General Psychiatry evaluated bioidentical estrogen as treatment for peri-menopausal depression.  They evaluated fifty women ages 40-55 years, suffering from a depressive disorder and irregular menstrual periods (FSH >25 IU/L).  These women were treated with bioidentical estrogen or placebo over 12-weeks.  Remission of depression was observed in 17 (68%) women treated with bioidentical estradiol compared with only 5 (20%) in the placebo group.  The authors concluded,  "Transdermal estradiol is an effective treatment of depression for perimenopausal women."(7)

Above left image: Brain Anatomy of DRN: The formatio reticularis of the medulla oblongata, shown by a transverse section passing through the middle of the olive of the midbrain showing (4) DRN Dorsal Raphe Nucleus courtesy of wikimedia commons  4. Raphe.

Estrogen Effective for Post-Partum Depression (after child birth)

Postpartum depression is seen in approximately 13% of women who have recently given birth, and often remains untreated. (10) Various treatments have been tried, including antidepressant drug therapy (SSRI's), bioidentical estrogen, individual psychotherapy, and group psychotherapy. (10)

Mother and Child By GilmanA study published in the 2001 Journal of Clinical Psychiatry showed that bioidentical estrogen is effective for post-partum depression.(8) Twenty-three women suffering from postpartum depression were recruited from a psychiatric emergency unit.  The women were treated over 8 weeks with bioidentical estradiol (sublingual form).  Baseline serum estradiol levels were very low with a mean of 80 pmol/L, or even lower suggesting ovarian failure. During the first week of estradiol treatment, depressive symptoms resolved rapidly, and serum estradiol levels increased to 340 pmol/L.  By the  second week of treatment, 83% of patients showed clinical recovery.

Left image: Harold Gilman (1876 - 1919). Mother and Child, 1918, oil on canvas. Auckland Art Gallery, courtesy of Wikimedia Commons.

A second earlier study published in 1996 Lancet showed that bioidentical estrogen is an effective treatment for post-partum depression.  Sixty One women suffering from post partum depression were given transdermal estradiol (0.2 mg daily), and rapid improvement was reported during the first month of treatment.(9)

Many women with post-partum depression are treated with SSRI antidepressants which does not address the underlying estrogen deficiency and ovarian failure.  In my opinion,  bioidentical hormone treatment is a more effective and safer treatment alternative.    Bioidentical estrogen has none of the adverse effects associated with SSRI antidepressants which, after all,  may end up in mother's milk, and may have adverse effects on the breast feeding baby.

Estradiol for Post Partum Psychosis

While post partum estrogen deficiency causes depression in 13%  of patients, a smaller subset go on to develop full blown post partum psychosis. Bioidentical estrogen is also effective for this more severely effected group.  A study done in Finland published in the 2001 Journal of Clinical Psychiatry evaluated 10 women suffering from post partum psychosis.  All had low serum estradiol (mean of 50 pg/ml) indicating gonadal failure.  All were treated with bioidentical estradiol, with serum estradiol levels rising to normal.  Remarkably, estradiol treatment reversed psychiatric symptoms in all patients. (11)

Estradiol  Improves Cognition for Alzheimer's Dementia

In a study published in 2001 Neurology, twenty postmenopausal women with Alzheimer's dementia were treated with bioidentical estradiol (0.10 mg per day, topical) and compared to placebo.  Sophisticated neuropsychological tests showed improvement in attention, and in verbal, visual and semantic memory compared with subjects who received a placebo.(12)

Estradiol Reduces Anxiety in Mouse Model

Estradiol in Lab Mice prevents anxietyAlicia A. Walf examined a mouse model in which Estradiol reduces anxiety- and depression-like behavior of aged female mice. Her findings were justpublished in   Neuroscience Research in Feb 2010.  Matthew N. Hill investigated the mechanism of estradiol as an anxiolytic, and he implicated the enzyme, fatty acid amide hydrolase (FAAH), which  degrades the endocannabinoid anandamide.  FAAH is regulated by estrogen.  Obviously, this is a fertile area for new research, as the exact mechanism has not yet been elucidated.

Left image : lab mice courtesy of wikimedia commons

Links to Associated Content:

The Importance of Bioidentical Hormones

The Safety Of Bio-Identical Hormones by Jeffrey Dach MD

The Battle for BioIdentical Hormones by Jeffrey Dach MD

Breast Cancer Prevention and Iodine Supplementation by Jeffrey Dach MD


Jeffrey Dach MD
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Links and References

1) http://www.uzzireissmd.com/refs/04.html
Uzzi Reiss MD and Yfat Reiss Gendell- The Natural SuperWoman, references for Estrogen chapter.

Estrogen B Receptor in the Brain, 5 HTP  and Anxiety

2)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2667128
Neuroscience. 2009 January 23; 158(2): 456–464.

Estrogen decreases 5-HT1B autoreceptor mRNA in selective subregion of rat dorsal raphe nucleus: inverse association between gene expression and anxiety behavior in the open field. by Ryoko Hiroiab and John F. Neumaierb a Department of Psychology, University of Washington, Seattle, WA 98195

We have recently shown that estrogen decreases anxiety and increases expression of tryptophan hydroxylase-2 (TPH2), the rate-limiting enzyme for serotonin synthesis. 

The paradigm used in the present study, nevertheless, closely resembles menopausal women undergoing hormone replacement therapy and may have clinical significance, since anxiety disorders are associated with relatively low serum estrogen levels in several conditions, including menopause, and are often relieved by estrogen treatment (Best et al., 1992, Sichel et al., 1995, Arpels, 1996, Gregoire et al., 1996). Antidepressants targeting the serotonin system, collectively known as selective serotonin reuptake inhibitors (SSRIs), also successfully treat some symptoms of menopause, yet there is evidence that a lower response rate is augmented by estrogen treatment. These studies suggest a possible interaction of estrogen and serotonin in regulating anxiety and thus elucidating the exact mechanisms of the effects of estrogen on anxiety via the DRN serotonergic system may lead to further advancement in treating affective disorders.

3) http://endo.endojournals.org/cgi/content/full/endo;146/2/797
Endocrinology Vol. 146, No. 2 797-807, 2005 by The Endocrine Society

Novel Actions of Estrogen Receptor-ß on Anxiety-Related Behaviors by Trent D. Lund, Tomislav Rovis, Wilson C. J. Chung and Robert J. Handa

ESTROGENS ARE WELL-ESTABLISHED regulators of mood in humans and animals. Its effects, however, are varied, with both anxiolytic and anxiogenic actions, depending on factors such as age and stage of the reproductive cycle. In women, reduced estrogen levels, particularly at the menopause, are associated with depression, sleep disturbance, irritability, anxiety, panic disorders, and cognitive dysfunction (1, 2, 3). Estrogen replacement therapy in postmenopausal women is consistently reported to improve mood, feelings of general well being, and learning as well as increase general activity levels (3, 4). In contrast, an anxiogenic role for estrogens is suggested by the significantly higher level of depression reported in women compared with men (5, 6, 7), a sex difference that emerges at the time of puberty (5, 6, 7). Furthermore, research by Schmidt et al. (8) identified that women with severe premenstrual dysphoria developed anxiety and other mood symptoms when treated with estradiol in combination with leuprolide, an agonist analog of GnRH.

Similar effects of estradiol on anxiety and mood have been reported in rodents. For example, elevated levels of estradiol achieved during rodent proestrus, or after exogenous hormone injections to ovariectomized (OVX) females, exert anxiolytic actions in the elevated plus maze (9, 10); consistently, when endogenous estrogens are removed, via OVX, behavioral indices of anxiety increase (10, 11, 12, 13, 15).

DRN- Dorsal Raphe Nucleus in Midbrain E2 receptors regulate 5HT synthesis

(4) http://www.ncbi.nlm.nih.gov/pubmed/15820717?dopt=Abstract
Biol Psychiatry. 2005 Apr 15;57(8):938-42.

Estrogen receptor-beta regulates tryptophan hydroxylase-1 expression in the murine midbrain raphe. Gundlah C, Alves SE, Clark JA, Pai LY, Schaeffer JM, Rohrer SP. Synaptic Pharmaceutical Corporation, Paramus.

BACKGROUND: Distinct expression patterns of estrogen receptor (ER)-alpha and ER-beta are displayed in the murine central nervous system. ER-beta is the predominant form of the receptor expressed in the murine midbrain dorsal raphe nucleus (DRN). Tryptophan hydroxylase (TPH) is abundantly expressed in the serotonergic neurons of the DRN and is regulated by estrogen in both the monkey and the guinea pig.

METHODS: In this study we used immunocytochemistry to show that ER-beta and TPH are colocalized in the serotonergic cells of the murine DRN. We utilized the ER-alpha and ER-beta gene deletion mouse models and in situ hybridization to demonstrate that ER-beta is responsible for regulating TPH1 mRNA expression.

RESULTS: Estrogen increased TPH1 mRNA expression in the DRN of wild type and ER-alpha knockout mice (alpha-ERKO) but not ER-beta knockouts (beta-ERKO).

CONCLUSIONS: These data indicate that ER-beta is responsible for mediating estrogen regulated TPH1 expression in the murine DRN.

(5) http://www.ncbi.nlm.nih.gov/pubmed/19559077
Neuroscience. 2009 Oct 6;163(2):705-18. Epub 2009 Jun 23.

Estrogen receptor beta regulates the expression of tryptophan-hydroxylase 2 mRNA within serotonergic neurons of the rat dorsal raphe nuclei.

Donner N, Handa RJ. Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80526, USA.

Dysfunctions of the brain 5-HT system are often associated with affective disorders, such as depression. The raphe nuclei target the limbic system and most forebrain areas and constitute the main source of 5-HT in the brain. All 5-HT neurons express tryptophan hydroxylase-2 (TPH2), the brain specific, rate-limiting enzyme for 5-HT synthesis. Estrogen receptor (ER) beta agonists have been shown to attenuate anxiety- and despair-like behaviors in rodent models. Therefore, we tested the hypothesis that ER beta may contribute to the regulation of gene expression in 5-HT neurons of the dorsal raphe nuclei (DRN) by examining the effects of systemic and local application of the selective ER beta agonist diarylpropionitrile (DPN) on tph2 mRNA expression.

Ovariectomized (OVX) female rats were injected s.c. with DPN or vehicle once daily for 8 days. In situ hybridization revealed that systemic DPN-treatment elevated basal tph2 mRNA expression in the caudal and mid-dorsal DRN. Behavioral testing of all animals in the open field (OF) and on the elevated plus maze (EPM) on days 6 and 7 of treatment confirmed the anxiolytic nature of ER beta activation.

Another cohort of female OVX rats was stereotaxically implanted bilaterally with hormone-containing wax pellets flanking the DRN. Pellets contained 17-beta-estradiol (E), DPN, or no hormone. Both DPN and E significantly enhanced tph2 mRNA expression in the mid-dorsal DRN. DPN also increased tph2 mRNA in the caudal DRN. DPN- and E-treated rats displayed a more active stress-coping behavior in the forced-swim test (FST). No behavioral differences were found in the OF or on the EPM.

These data indicate that ER beta acts at the level of the rat DRN to modulate tph2 mRNA expression and thereby influence 5-HT synthesis in DRN subregions. Our results also suggest that local activation of ER beta neurons in the DRN may be sufficient to decrease despair-like behavior, but not anxiolytic behaviors.

(6) http://www.albany.edu/~cafrye/papers/walfFrye06review.pdf
Neuropsychopharmacology (2006) 31, 1097–1111,  2006 Nature

Perspective - A Review and Update of Mechanisms of Estrogen in the Hippocampus and Amygdala for Anxiety and Depression Behavior by Alicia A Walf1 and Cheryl A Frye

Estrogen (E2) has many effects in the central nervous system, including effects on anxiety and depression behavior. This review will address effects of E2 on behaviors related to anxiety and depression in women and animal models and include recent findings from our laboratory related to this topic. E2’s antianxiety and antidepressant-like effects may depend upon many factors, including the regimen of
E2 utilized and interactions with the hypothalamic–pituitary–adrenal axis. Brain targets for E2’s effects on anxiety and depression include the hippocampus and amygdala.

Administration of E2, compared to vehicle, subcutaneously or to the hippocampus or amygdala of ovariectomized rats decreases anxiety and depressive behavior. Intracellular estrogen receptors (ERs) may be important for E2’s anxiolytic and antidepressant-like effects. Administration of an ER antagonist to the hippocampus, but not amygdala, increases anxiety and depression behavior of naturally receptive female rats.  Studies utilizing ER knockout mice or selective ER modulators suggest that
ER-mediated effects of E2 on anxiety and depressive behavior may require ERb.


Estradiol Treats Depressive Disorder- Clinical Studies
 

Perimenopausal Mood Disorder and Depression

https://www.healthsystem.virginia.edu/
internet/neuroscience/BehavioralNeuroscience/soares-et-al.pdf

(7) http://www.ncbi.nlm.nih.gov/pubmed/11386980
Arch Gen Psychiatry. 2001 Jun;58(6):529-34.

Efficacy of estradiol for the treatment of depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. by Soares CN, Almeida OP, Joffe H, Cohen LS. Perinatal and Reproductive Psychiatry Clinical Research Program, Massachusetts General Hospital, Harvard Medical School, 15 Parkman St, WACC 812, Boston, MA

BACKGROUND: Results of previous studies suggest that estrogen improves somatic and mild depressive symptoms experienced by perimenopausal women. This study investigated the efficacy of 17beta-estradiol for the treatment of clinically significant depressive disorders in endocrinologically confirmed perimenopausal women.

METHODS: Perimenopausal women (aged 40-55 years, with irregular menstrual periods and serum concentrations of follicle-stimulating hormone >25 IU/L), meeting criteria for major depressive disorder, dysthymic disorder, or minor depressive disorder, according to DSM-IV, were randomized to receive transdermal patches of 17beta-estradiol (100 microgram) or placebo in a 12-week, double-blind, placebo-controlled study. A 4-week washout period followed the 12-week treatment phase. Outcome measures were the Montgomery-Asberg Depression Rating Scale and Blatt-Kupperman Menopausal Index scores.

RESULTS: Fifty women were enrolled in the study; 26 met DSM-IV criteria for major depressive disorder, 11 for dysthymic disorder, and 13 for minor depressive disorder. Remission of depression was observed in 17 (68%) women treated with 17beta-estradiol compared with 5 (20%) in the placebo group (P =.001). Subjects responded similarly to estradiol treatment, regardless of DSM-IV diagnosis. Patients treated with estradiol sustained antidepressant benefit of treatment after the 4-week washout period, although somatic complaints increased in frequency and intensity. Treatment was well tolerated and adverse events were rare in both groups.

CONCLUSION: Transdermal estradiol replacement is an effective treatment of depression for perimenopausal women.

Estrogen Treatment in Post Partum Depression in pts with low serum estrogen

(8) http://www.ncbi.nlm.nih.gov/pubmed/11411813
J Clin Psychiatry. 2001 May;62(5):332-6.

Estrogen deficiency in severe postpartum depression: successful treatment with sublingual physiologic 17beta-estradiol: a preliminary study.by Ahokas A, Kaukoranta J, Wahlbeck K, Aito M. Psychiatric Research Unit, Mehilainen Clinic, University of Helsinki, Finland.  

BACKGROUND: The postpartum period is a time when women are vulnerable to depressive disorders, which can be severe and have long-lasting adverse sequelae. In spite of multiple contacts with health care providers, women with postpartum depression often remain unrecognized and untreated. To evaluate the association between estradiol and postpartum depression, we measured serum estradiol concentration and performed an open-label study of physiologic 17beta-estradiol.

METHOD: Twenty-three women fulfilling ICD-10 criteria for major depression with postpartum onset were consecutively recruited from a psychiatric emergency unit. Serum estradiol concentrations were measured at baseline and weekly during sublingual 17beta-estradiol treatment for 8 weeks. The treatment effect was assessed using a clinician-rated depression symptom scale, the Montgomery-Asberg Depression Rating Scale (MADRS).

RESULTS: At baseline, all patients were severely depressed (mean MADRS total score = 40.7; range, 35-45) and had a low serum estradiol concentration (mean = 79.8 pmol/L; range, 23-140 pmol/L); in 16/23 patients, the concentration was even lower than the threshold value for gonadal failure. During the first week of estradiol treatment, depressive symptoms diminished significantly, resulting in a mean MADRS score of 11.0 (Z = -4.20, p < .001), and serum estradiol concentrations approached those of the follicular phase (mean +/- SD = 342 +/- 141 pmol/L). At the end of the second week of treatment, the MADRS scores were compatible with clinical recovery in 19/23 patients.

CONCLUSION: This preliminary study shows that depression symptoms may be rapidly reduced in patients with postpartum depression who have documented estradiol deficiency by treatment with 17beta-estradiol and suggests that estradiol can have significance in the pathophysiology of this condition and may be an option in the treatment of women vulnerable to postpartum depression.

(9) http://www.ncbi.nlm.nih.gov/pubmed/8598756
Lancet. 1996 Apr 6;347(9006):930-3.

Transdermal oestrogen for treatment of severe postnatal depression. by Gregoire AJ, Kumar R, Everitt B, Henderson AF, Studd JW. Mental Health Services, Salisbury Health Care, Salisbury, UK.

BACKGROUND
postnatal depression can have long-term adverse consequences for the mother, for the marital relationship, and for the infant's psychological development. Such depressions can be severe and resistant to both support and counselling and to therapy with antidepressant drugs. We investigated the antidepressant efficacy of oestrogen given transdermally.

METHODS: In a double-blind, placebo-controlled study, 61 women with major depression, which began within 3 months of childbirth and persisted for up to 18 months postnatally, were allocated randomly active treatment (n=34; 3 months of transdermal 17 beta-oestradiol 200 micrograms daily alone, then 3 months with added cyclical dydrogesterone 10mg daily for 12 days each month) or placebo (n=27; placebo patches and tablets according to the same regimen). The women were assessed monthly by self-ratings of depressive symptoms on the Edinburgh postnatal depression scale (EPDS) and by clinical psychiatric interview (schedule for affective disorders and schizophrenia [SADS]-change scale).

FINDINGS: On pretreatment assessments the women in both groups were severely depressed (mean EPDS score 21.8 [SD 3.0] active group, 21.3 [2.9] placebo group; SADS scores, 66.3 [11.4] and 64.3 [10.7]). During the first month of therapy the women receiving oestrogen improved rapidly, and to a significantly greater extent than controls (mean EPDS scores 13.3 [SD 5.7] vs 16.5 [5.3]. Patients receiving placebo also improved over time but, on average, their scores did not fall below the screening threshold for major depression for at least 4 months. The estimated overall treatment effect of oestrogen on the EPDS was 4.38 points (95% Cl 1.89-6.87). None of a range of other factors (age, psychiatric, obstetric and gynaecological history, severity and duration of current episode of depression, and concurrent antidepressant medication), influenced the response to oestrogen.

INTERPRETATION: This study has shown that transdermal oestrogen is an effective treatment for postnatal depression. Further studies are required to establish the minimum effective dose and shortest necessary duration of treatment as well as the mechanism of antidepressant action of oestrogen.

(10) http://www.jabfm.com/cgi/reprint/16/5/372.pdf

The Effectiveness of Various Postpartum Depression Treatments and the Impact of
Antidepressant Drugs on Nursing Infants Dwenda Gjerdingen, MD, MS (J Am Board Fam Pract 2003;16:372– 82.)

Background: Postpartum depression is seen in approximately 13% of women who have recently given birth; unfortunately, it often remains untreated. Important causes for undertreatment of this disorder are providers’ and patients’ lack of information about the effectiveness of various treatments, and their concerns about the impact of treatment on nursing infants. This article presents research-based evidence on the benefits of various treatments for postpartum depression and their potential risks to nursing infants.

There is evidence that postpartum depression improves with antidepressant
drug therapy, estrogen, individual psychotherapy, nurse home visits, and possibly group therapy.

Of the more frequently studied antidepressant drugs in breastfeeding women, paroxetine, sertraline, and nortriptyline have not been found to have adverse effects on infants. Fluoxetine, however, should be avoided in breastfeeding women. By administering effective treatment to women with postpartum depression,
we can positively impact the lives of mothers, their infants, and other family members. (J Am Board Fam Pract 2003;16:372– 82.)

72. Cizza G, Gold PW, Chrousos GP. High-dose transdermal estrogen, corticotropin-releasing hormone, and postnatal depression [letter]. J Clin Endocrinol Metab 1997;82:704.

73. Ahokas A, Kaukoranta J, Wahlbeck K, Aito M. Estrogen deficiency in severe postpartum depression: successful treatment with sublingual physiologic
17B-estradiol: a preliminary study. J Clin Psychiatry 2001;62:332– 6.

74. Ahokas AJ, Turtiainen S, Aito M. Sublingual oestrogen treatment of postnatal depression [letter]. Lancet 1998;351:109.

75. Gregoire AJ, Kumar R, Everitt B, Henderson AF, Studd JW. Transdermal oestrogen for treatment of severe postnatal depression. Lancet 1996; 347:930–3.

76. Ahokas A, Aito M. Role of estradiol in puerperal psychosis. Psychopharmacology (Berl) 1999;147: 108–10.

77. Ahokas A, Aito M, Turiainen S. Association between oestradiol and puerperal psychosis. Acta Psychiatr Scand 2000;101:167–70.

78. Granger ACP, Underwood MR. Review of the role Postpartum Depression Treatment 381 of progesterone in the management of postnatal mood disorders. J Psychosom Obstet Gynaecol 2001;22:49 –55.


Estradiol for Post Partum Psychosis

(11) http://www.ncbi.nlm.nih.gov/pubmed/10817099 
J Clin Psychiatry. 2000 Mar;61(3):166-9. Positive treatment effect of estradiol in postpartum psychosis: a pilot study. Ahokas A, Aito M, Rimón R. Department of Psychiatry, Helsinki City Hospital, Finland.

BACKGROUND: Postpartum illnesses with psychiatric symptoms and serious adverse sequelae are highly prevalent during the childbearing years. Despite multiple medical contacts, these illnesses often remain unidentified and untreated. To study the association between estradiol and puerperal psychosis, we measured serum concentration of estradiol and performed an open-label trial of physiologic 17beta-estradiol in women with this disorder.

METHOD: Ten women with ICD-10 psychosis with postpartum onset consecutively recruited from a psychiatric duty unit were studied. Serum estradiol concentration was measured at baseline and weekly during sublingual 17beta-estradiol treatment for 6 weeks. The treatment effect was evaluated by a clinician-rated psychiatric symptom scale (the Brief Psychiatric Rating Scale [BPRS]).

RESULTS: The baseline serum estradiol levels (mean = 49.5 pmol/L; range, 13-90 pmol/L) were even lower than the threshold value of gonadal failure, and the patients exhibited high scores on the psychiatric symptom scale (mean BPRS total score = 78.3; range, 65-87). During the first week of 17beta-estradiol treatment, psychiatric symptoms diminished significantly (BPRS score decreased to a mean of 18.8, p < .001). Until the end of the second week of treatment, serum estradiol concentrations rose to near the values normally found during the follicular phase, and the patients became almost free of psychiatric symptoms.

CONCLUSION: The reversal of psychiatric symptoms in all patients by treating documented estradiol deficiency suggests that estradiol plays a role in the pathophysiology and may have a role in the treatment of this condition. There was a rebound of psychotic symptoms in the 1 patient who discontinued estradiol treatment. Given the small number of patients, this area deserves further study.

Estradiol for Alzheimers Disease - Improves Cognition

(12) http://www.neurology.org/cgi/content/abstract/57/4/605
Neurology 2001;57:605-612, 2001 American Academy of Neurology

High-dose estradiol improves cognition for women with AD Results of a randomized study by S. Asthana, MD;, L. D. Baker, PhD;, S. Craft, PhD;, F. Z. Stanczyk, PhD;, R. C. Veith, MD;, M. A. Raskind, MD; and S. R. Plymate, MD From Geriatric Research, Education and Clinical Center (GRECC), Veterans Affairs Puget Sound Health Care System

Objective:— To characterize the cognitive and neuroendocrine response to treatment with a high dose of estrogen for postmenopausal women with AD.

Methods:— Twenty postmenopausal women with AD were randomized to receive either 0.10 mg/day of 17ß-estradiol by skin patch or a placebo patch for 8 weeks. Subjects were evaluated at baseline, at weeks 3, 5, and 8 during treatment, and again 8 weeks after treatment termination. During each visit, cognition was assessed with a battery of neuropsychological tests, and blood samples were collected to measure plasma estradiol as well as several other neuroendocrine markers of interest.

Results:— Significant effects of estrogen treatment were observed on attention (Stroop Color Word Interference Test), verbal memory (Buschke Selective Reminding Test), and visual memory (Figure Copy/Memory). In addition, women treated with estrogen demonstrated improved performance on a test of semantic memory (Boston Naming Test) compared with subjects who received a placebo. Estrogen appeared to have a suppressive effect on the insulin-like growth factor (IGF) system such that plasma concentration of IGF binding protein-3 was significantly reduced and plasma levels of estradiol and IGF-I were negatively correlated during estrogen treatment.

Conclusions:— Administration of a higher dose of estrogen may enhance attention and memory for postmenopausal women with AD.  

Anxiety is Strongly Associated with HOT Flashes


(13) http://www.ncbi.nlm.nih.gov/pubmed/15879914

Menopause. 2005 May-Jun;12(3):258-66.

The role of anxiety and hormonal changes in menopausal hot flashes.
Freeman EW, Sammel MD, Lin H, Gracia CR, Kapoor S, Ferdousi T. Department of Obstetrics/Gynecology, University of Pennsylvania, Philadelphia, PA 19104, USA.

OBJECTIVE: To estimate the association of anxiety with menopausal hot flashes in the early transition to menopause.

DESIGN: A randomly identified, population-based cohort of midlife women followed up for 6 years to assess reproductive hormones and other physical, emotional, and behavioral factors. At enrollment, the women were premenopausal, aged 35 to 47 years, and had regular menstrual cycles in the normal range. Enrollment was stratified to obtain equal numbers of African American (n = 219) and white (n = 217) women.

RESULTS: At the 6-year endpoint, 32% of the women were in the early transition stage and 20% reached the late menopausal transition or were postmenopausal. Reports of hot flashes increased with the transition stages, which were determined by bleeding patterns. At endpoint, hot flashes were reported by 37% of the premenopausal women, 48% of those in the early transition, 63% of women in the late transition, and 79% of the postmenopausal women. Anxiety scores were significantly associated with the occurrence of hot flashes and were also significantly associated with the severity and frequency of hot flashes (each outcome at P < 0.001). Compared with women in the normal anxiety range, women with moderate anxiety were nearly three times more likely to report hot flashes and women with high anxiety were nearly five times more likely to report hot flashes. Anxiety remained strongly associated with hot flashes after adjusting for menopause stage, depressive symptoms, smoking, body mass index, estradiol, race, age, and time. In a predictive model, anxiety levels at the previous assessment period and the change in anxiety from the previous assessment period significantly predicted hot flashes (P < 0.001).

CONCLUSIONS: Anxiety is strongly associated with menopausal hot flashes after adjusting for other variables including menopause stage, smoking, and estradiol levels. Anxiety preceded hot flashes in this cohort. Additional studies are needed to examine the duration of menopausal hot flashes and to determine whether treatments that target anxiety effectively reduce menopausal hot flashes.

Estradiol Reduces Anxiety in Mice

(14) http://www.ncbi.nlm.nih.gov/pubmed/19804793

Estradiol reduces anxiety- and depression-like behavior of aged female mice by
Alicia A. Walf and Cheryl A. Frye  Neuroscience Research, The University at Albany-SUNY, United States September 2009

Thus, an acute E2 regimen produced specific anti-anxiety and anti-depressant effects, independent of effects on motor behavior, when administered to aged female C57BL/6 mice.

Estrogen Inhibits Anxiety Through EndoCannabinoid System

http://science.iowamedicalmarijuana.org/pdfs/psych/Hill%202007.pdf
Estrogen recruits the endocannabinoid system to modulate emotionality
Matthew N. Hill, Eda S. Karacabeyli, Boris B. Gorzalka in Department of Psychology, University of British Columbia, 2136 West Mall, Vancouver, BC, Canada V6T1Z4

Estrogen administration elicits anxiolytic and antidepressant-like effects in female rats; however, the mechanism of this effect is unknown. Fatty acid amide hydrolase (FAAH), the enzyme which degrades the endocannabinoid anandamide, has been shown to be regulated by estrogen. Thus, we examined if the anxiolytic and antidepressant effects of estrogen implicated the endocannabinoid system. In the first experiment, ovariectomized female rats were administered a single injection of 17b-estradiol (10 mg) or oil, and 48 h later were given an injection of the cannabinoid CB1 receptor antagonist AM251 (1 mg/kg) or vehicle.

One hour after AM251 or vehicle administration, subjects were tested in either the open field test (OFT), elevated plus maze (EPM) or the forced swim test (FST). Estradiol treatment resulted in a significant increase in open arm entries in the EPM and time spent in the center quadrant of the OFT, which were reversed by co-treatment with  AM251, suggesting that endocannabinoids are integral to the anxiolytic effects of estrogen.

In the second experiment, administration of the FAAH inhibitor URB597 (0.1 and 0.3 mg/kg) increased open arm entries in the EPM and time spent in the center quadrant in the OFT as well as significantly reduced immobility in the FST. Collectively, these data demonstrate that estrogen may elicit changes in emotional behavior through an endocannabinoid mechanism, and suggest that inhibition of FAAH represents a therapeutic target for anxiety and depression in women.


(15) http://www.ncbi.nlm.nih.gov/pubmed/15474758
Maturitas. 2004 Oct 15;49(2):140-7.

A short study in the treatment of hot flashes with buccal administration of 17-beta estradiol. Gass MS, Rebar RW, Cuffie-Jackson C, Cedars MI, Lobo RA, Shoupe D, Judd HL, Buyalos RP, Clisham PR.

OBJECTIVE: To assess the efficacy and safety of 17-beta estradiol buccal tablets in reducing hot flush frequency (HFF) in postmenopausal women. METHODS: Estradiol buccal tablets containing 0.05, 0.1, 0.2, or 0.4 mg or placebo were administered for 28 days to 99 postmenopausal women in a randomized, double-blind study; 19 premenopausal women were studied concurrently for comparison of laboratory data. Objective and subjective assessments of HFF were obtained along with measures of estradiol, estrone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). RESULTS: Measurements of HFF revealed significant decreases from baseline in all estradiol groups (P < 0.01). In the 0.4 mg group, HFF decreased significantly compared to placebo (P < 0.01). All estradiol doses produced similar improvement in the vaginal maturation index. Mean serum estradiol levels increased as doses increased but were lower than in the premenopausal subjects. Mean serum FSH and LH levels decreased in all estradiol groups but not to the levels of the premenopausal subjects; the greatest decrease occurred at the two highest estradiol doses. CONCLUSION: A numerical dose-response relationship with hot flushes was seen in this pilot study comparing 0.05, 0.1, 0.2, and 0.4 mg buccal estradiol. Only 0.4 mg 17-beta estradiol significantly reduced the occurrence of hot flushes compared to placebo.

(16) http://www.ncbi.nlm.nih.gov/pubmed/11400216
Menopause as a Measure of Population Health - Physiology of hot flashes Robert R. Freedman 1 2  Am. J. Hum. Biol. 13:453-464, 2001

Hot flashes are the most common symptom of the climacteric, although prevalence estimates are lower in some rural and non-Western areas. The symptoms are characteristic of a heat-dissipation response and consist of sweating on the face, neck, and chest, as well as peripheral vasodilation. Although hot flashes clearly accompany the estrogen withdrawal at menopause, estrogen alone is not responsible since levels do not differ between symptomatic and asymptomatic women. Until recently it was thought that hot flashes were triggered by a sudden, downward resetting of the hypothalamic setpoint, since there was no evidence of increased core body temperature. Evidence obtained using a rapidly responding ingested telemetry pill indicates that the thermoneutral zone, within which sweating, peripheral vasodilation, and shivering do not occur, is virtually nonexistent in symptomatic women but normal (about 0.4°C) in asymptomatic women. The results suggest that small temperature elevations preceding hot flashes acting within a reduced thermoneutral zone constitute the triggering mechanism. Central sympathetic activation is also elevated in symptomatic women which, in animal studies, reduces the thermoneutral zone. Clonidine reduces central sympathetic activation, widens the thermoneutral zone, and ameliorates hot flashes. Estrogen virtually eliminates hot flashes but its mechanism of action is not known. . © 2001 Wiley-Liss, Inc.

(17) http://jcem.endojournals.org/cgi/content/abstract/61/4/627
Journal of Clinical Endocrinology & Metabolism Vol. 61, No. 4 627-632

Treatment of Hot Flashes with Transdermal Estradiol Administration*
KENNETH A. STEINGOLD, LARRY LAUFER, RYSZARD J. CHETKOWSKI, JOHN D. DEFAZIO, DENNIS W. MATT, DAVID R. MELDRUM and HOWARD L. JUDD  Department of Obstetrics and Gynecology, University of California, Los Angeles, School of Medicine Los Angeles, California 90024

A randomized prospective double blind study was performed to assess the ability of a transdermal therapeutic system (TTS) delivering estradiol (E2) to suppress hot flashes (HFs) in symptomatic postmenopausal women. Patients were given placebo or E2 in four doses for a 20-day period, and serum gonadotropin and estrogen levels and the occurrences of HFs were measured.

Administration of placebo had no measurable effect on either estrogen or gonadotropin levels or the occurrence of HFs. A dose-response relationship was found between the rate of E2 administered and the circulating level of E2, with 25, 50, 100, and 200 µ/24 h dosages raising the mean E2 concentrations from mean baseline levels of 5-8 pg/ml to 18, 38, 73, and 100 pg/ml, respectively. Estrone levels also increased with TTS application, but to a lesser extent than did E2 levels. Doseresponse reductions of FSH and LH with increasing amounts of E2 administration occurred, but gonadotropin levels were not lowered in any of the patients into the ranges found in premenopausal women. TTS application significantly suppressed the occurrence of HFs at the 50 Mg/24 h dosage and higher. A significant negative correlation (r = 0.6045; P < 0.001) between E2 levels and the rates of occurrence of HFs was found during hormone administration. Based on this regression, 50% and100% reductions of HFs should occur at 61 and 122 pg/ml E2. These data indicate that the transdermal delivery of E2 with these systems significantly reduced the occurrence of HFs and allowed definition of the therapeutic range of hormone replacement in terms of lost ovarian function, as reflected by circulating E2 levels.



Jeffrey Dach MD
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  • 02-20-2010 susan wrote:

    Dr Dach,

    I had taken HRT drugs for 3 years until I was diagnosed with Breast cancer. I had the tumor removed, was node negative, had 1 shot of chemo, and went balistic. I did not want to take it but was pressured by doctors however I did not have further treatments, radiation or tomixifin which would have killed me. I was node negative, and the tumor did not have branches. I will never take a presciption drug again.

    My question is, I still have menopause symptoms, mainly restless sleep, hot flashes, moodiness. Can you recommend bioidentical hormones in my case, and which ones, or where can I get treatment.

    I live in canada near Toronto Ont. Thanks Dr. Dach,

    I got your name from Suzanne Somers.


    Susan

    _____________________________________________________________

    Dear Susan,

    In general, mainstream medicine is opposed to hormone replacement in breast cancer survivors for fear of inducing breast cancer recurrance.  However, a number of studies have looked at this question and have found no increased breast cancer recurrance, and no increased mortality in breast cancer survivors usintg bioidentical hormones. (see references below) 

    On the other hand, we know from many medical studies that synthetic hormones such as Prempro and provera are dangerous, and are to be avoided as they DO have increase cancer risk.  The synthetic hormones are chemically altered monsters to be avoided.

    References and links:

    http://www.ncbi.nlm.nih.gov/pubmed/9065117
    Am J Obstet Gynecol. 1996 May;174(5):1494-8.

    Hormone replacement therapy in breast cancer survivors: a cohort study.
    DiSaia PJ, Grosen EA, Kurosaki T, Gildea M, Cowan B, Anton-Culver H.

    Department of Obstetrics and Gynecology, University of California, Irvine Medical Center, Orange, CA 92668, USA.

    Comment in:

    Am J Obstet Gynecol. 2000 Aug;183(2):517.
    Am J Obstet Gynecol. 1997 Feb;176(2):493.

    OBJECTIVE: Our purpose was to measure any adverse effect (if one exists) of hormone replacement therapy administered to breast cancer survivors. STUDY DESIGN: Forty-one patients from a group of 77 patients who received hormone replacement therapy after therapy for breast cancer were matched with 82 comparison patients not receiving hormone replacement therapy. Both groups were taken from the same population on the basis of cancer registry of the Cancer Surveillance Program of Orange County and were compared with regard to survival results. RESULTS: An analysis of survival time and disease-free time revealed no statistically significant difference between the two groups. CONCLUSIONS: No obvious adverse effect of hormone replacement therapy could be shown in this pilot study. A case is made for a prospective randomized trial.


    http://www.ncbi.nlm.nih.gov/pubmed/12851510
    Menopause. 2003 Jul-Aug;10(4):277-85.

    Estrogen replacement therapy in breast cancer survivors: a matched-controlled series.
    Decker DA, Pettinga JE, VanderVelde N, Huang RR, Kestin L, Burdakin JH.

    Department of Medicine, William Beaumont Hospital, Royal Oak-Troy, MI 48073, USA.
    Comment in:  Menopause. 2003 Jul-Aug;10(4):269-70.

    OBJECTIVE: We prospectively administered estrogen replacement therapy (ERT) to control estrogen deficiency symptoms in breast cancer survivors as part of our clinical practice. We report the consequences of ERT compared with a historical matched-control group. DESIGN: Two hundred seventy-seven disease-free survivors received ERT. Controls were matched for exact stage, a recurrence-free period similar to the period to ERT initiation in the ERT group, approximate age, and duration of follow-up. The mean time from breast cancer diagnosis to initiation of ERT was 3.61 (+/- 0.25) years, with a median of 1.88 years. The mean duration of ERT was 3.7 (+/- 3.01) years, with a median of 3.05 years. RESULTS: Hot flashes were relieved in 206 of 223 women (92%), dyspareunia/vaginal dryness in 149 of 167 women (89%), and reactive depression/anxiety/mood change in 111 of 126 women (88%). Univariate analysis demonstrated no statistical differences between the groups for age, stage, pathology at diagnosis, progesterone receptor status, local therapy, breast at risk, prior chemotherapy, and duration of follow-up. The ERT group was more likely to be estrogen receptor negative (P = 0.01), to have received prior ERT (P < 0.001), and to have received no adjuvant tamoxifen (P < 0.001). There was no significant difference between the ERT and control groups in ipsilateral primary/recurrence (5/155 v 5/143; P = 0.85), contralateral breast cancers (10/258 v 9/260; P = 0.99), or systemic metastasis (8/277 v 15/277; P = 0.13). Noncause-specific deaths in the control group numbered 15 (of 277), and in the ERT group, 7 (of 277) (P = 0.03). Overall survival favored the ERT group (P = 0.02). CONCLUSIONS: In these selected patients, ERT relieved estrogen deficiency symptoms and did not increase the rate or time to an ipsilateral recurrence/new primary, contralateral new primary, local-regional recurrence, or systemic metastases.

    http://www.ncbi.nlm.nih.gov/pubmed/12193914
    Am J Obstet Gynecol. 2002 Aug;187(2):289-94; discussion 294-5.

    Estrogen replacement therapy in patients with early breast cancer.
    Natrajan PK, Gambrell RD Jr. Reproductive Endocrinologists, Augusta, GA 30910, USA.

    OBJECTIVE: Most physicians believe that estrogen replacement therapy is contraindicated once a patient is diagnosed with breast cancer. Recently, several studies have shown that estrogen replacement therapy may be safely used in patients with early breast cancer that has been treated successfully. These women can have severe menopausal symptoms and are at risk for osteoporosis. We reviewed the current status of women in our practice with breast cancer who received estrogen replacement therapy, who did not receive hormone replacement therapy, and who did not receive estrogenic hormone replacement therapy. STUDY DESIGN: The study group consisted of 123 women (mean age, 65.4 +/- 8.85 years) who were diagnosed with breast cancer in our practice, including 69 patients who received estrogen replacement therapy for < or = 32 years after diagnosis. The comparative groups were 22 women who used nonestrogenic hormones for < or = 18 years and 32 women who used no hormones for < or = 12 years. The group who did not receive estrogenic hormone replacement therapy received androgens with or without progestogens (such as megestrol acetate). Of the 63 living hormone users, 56 women are still being treated in our clinic, as are 15 of the 22 subjects who receive nonestrogenic hormone replacement therapy. Follow-up was done through the tumor registry at University Hospital; those patients whose tumor records were not current were contacted by telephone. RESULTS: There were 18 deaths in the 123 patients: 6 patients who received estrogen replacement therapy (8.69%), 2 patients who received nonestrogenic hormone replacement therapy (9.09%), and 10 patients who received no hormone replacement therapy (31.25%). Of the 18 deaths, 9 deaths were from breast cancer (mortality rate, 7.3%); 3 deaths were from lung cancer; 1 death was from endometrial cancer; 1 death was from myocardial infarction; 1 death was from renal failure; and 3 deaths were from cerebrovascular accidents. The 9 deaths from breast cancer included one patient who received nonestrogenic hormone replacement therapy (mortality rate, 4.5%), 6 patients who received no hormone replacement therapy (mortality rate, 11.3%), and 2 patients who received estrogen replacement therapy (mortality rate, 4.28%). The 9 non-breast cancer deaths included 4 patients who received estrogen replacement therapy (endometrial cancer [1 death], lung cancer [1 death], cerebrovascular accident [1 death], and renal failure [1 death]), 1 patient who did not receive estrogenic hormone replacement therapy group (myocardial infarction), and 4 patients who used no hormones (lung cancer, 2 deaths; stroke, 2 deaths). Carcinoma developed in one patient in the estrogen replacement therapy group in the contralateral breast after 4 years of hormone replacement therapy; she is living and well 2.5 years later with no evidence of disease. Metastatic breast cancer developed in one patient after 8 years of hormone replacement therapy; she is living with disease. CONCLUSION: Estrogen replacement therapy apparently does not increase either the risk of recurrence or of death in patients with early breast cancer. These patients may be offered estrogen replacement therapy after a full explanation of the benefits, risks, and controversies.


    http://www.ncbi.nlm.nih.gov/pubmed/11907916
    Climacteric. 1998 Jun;1(2):137-42.

    A cohort study of hormone replacement therapy given to women previously treated for breast cancer. Dew J, Eden J, Beller E, Magarey C, Schwartz P, Crea P, Wren B. Women's Health Institute, Royal Hospital for Women, Barker Street, Randwick, NSW 2031, Australia.

    Women who have been previously treated for breast cancer are usually advised to avoid hormone therapy for fear of increasing their risk of tumor recurrence. However, for some women, menopausal symptoms are so severe that their quality of life is poor. Because ethic committees are reticent to permit a double-blind randomized trial, we performed a cohort study of hormone therapy after breast cancer. METHODS: The study group comprised 1472 women with breast cancer. A total of 167 subjects had used an oral or transdermal estrogen after their treatment for breast cancer. Amongst these estrogen users, 152 (91%) had also used a progestin. In total, 106 other women had used a progestin alone as a treatment for menopausal flushes and not as a treatment for breast cancer. Cox regression analysis was performed using estrogen as a time-dependent covariate with disease-free interval as the outcome. RESULTS: The uncorrected hazard ratio for the estrogen-progestin users was 0.67 (95% confidence interval (CI) 0.38-1.16) and for the progestin alone users was 0.85 (95% CI 0.44-1.65). CONCLUSIONS: This study was unable to demonstrate a significant increase in risk of breast cancer recurrence for women who used HRT and suggests that the time is now appropriate for a randomized prospective trial of hormone therapy after breast cancer.


    http://www.ncbi.nlm.nih.gov/pubmed/16368466
    Maturitas. 2006 Jan 20;53(2):123-32.

    Menopausal hormone therapy (HT) in patients with breast cancer.
    Batur P, Blixen CE, Moore HC, Thacker HL, Xu M. Department of Internal Medicine, Section of Women's Health Cleveland Clinic Foundation, Crown Centre II, Independence, OH 44131, USA.

    OBJECTIVES: To assess the effect of menopausal hormone therapy (HT) on reoccurrence, cancer-related mortality, and overall mortality after a diagnosis of breast cancer. METHODS: We performed a quantitative review of all studies reporting experience with menopausal HT for symptomatic use after a diagnosis of breast cancer. Rates of reoccurrence, cancer-related mortality, and overall mortality were calculated in this entire group. A subgroup analysis was performed in studies using a control population to assess the odds ratio of cancer reoccurrence and mortality in hormone users versus non-users. RESULTS: Fifteen studies encompassing 1416 breast cancer survivors using HT were identified. Seven studies included a control group comprised of 1998 patients. Among the 1416 HT users, reoccurrence was noted in 10.0% (95% CI: 8.4-11.6%). Cancer-related mortality occurred at a rate of 2.6% (95% CI: 1.8-3.7%), while overall mortality was 4.5% (95% CI: 3.4-5.8%). Compared to non-users, patients using HT had a decreased chance of reoccurrence and cancer-related mortality with combined odds ratio of 0.5 (95% CI: 0.2-0.7) and 0.3 (95% CI: 0.0-0.6), respectively. CONCLUSIONS: In our review, menopausal HT use in breast cancer survivors was not associated with increased cancer reoccurrence, cancer-related mortality or total mortality. Despite conflicting opinions on this issue, it is important for primary care physicians to feel comfortable medically managing the increasing number of breast cancer survivors. In the subset of women with severe menopausal symptoms, HT options should be reviewed if non-hormonal methods are ineffective. Future trials should focus on better ways to identify breast cancer survivors who may safely benefit from HT versus those who have a substantial risk of reoccurrence with HT use.


    http://www.ncbi.nlm.nih.gov/pubmed/11776498
    Ann Surg Oncol. 2001 Dec;8(10):828-32.

    Estrogen replacement therapy after breast cancer: a 12-year follow-up.
    Peters GN, Fodera T, Sabol J, Jones S, Euhus D. The Center for Breast Care, The University of Texas Southwestern Medical Center at Dallas, 75390-9161, USA.

    BACKGROUND: In the United States, estrogen replacement therapy (ERT) is discouraged in breast cancer survivors because of concerns that hormones may reactivate the disease. Because ERT can improve quality of life and decrease morbidity from osteoporosis and cardiovascular disease, however, this policy is increasingly being challenged. METHODS: From February to August 1995, 607 breast cancer survivors were interviewed concerning ERT usage. Sixty-four patients indicated they received some form of ERT after their breast cancer diagnosis. Medical records for these patients were analyzed for disease stage, surgical treatment, adjuvant treatment, estrogen and progesterone receptor status, date of initiation of ERT, type of ERT, recurrence, and final outcome. Patients receiving ERT were followed prospectively. RESULTS: Eight patients were excluded because they had used only vaginal cream ERT. The remaining 56 received ERT as conjugated estrogens, an estradiol patch, estropipate, or birth control pills. The median follow-up from diagnosis was 12.8 years (range, 4.7-38.9 years). The median time on ERT since diagnosis was 6.4 years (range, 1.0-20.9 years); 38% of the patients initiated ERT within 2 years of diagnosis. Estrogen receptors were positive in 28 (74%) of the 38 cases with available information. Pathological disease stage at time of diagnosis and treatment was 0 in 15 cases (27%), I in 27 (48%), and II in 14 (25%). Twenty-six patients (47%) received adjuvant chemotherapy or hormonal therapy. One local recurrence and one contralateral breast cancer occurred during the follow-up period (13.5 and 9.6 years, respectively), with no regional or distant recurrences, for a 15-year actuarial disease-free survival rate of 92.5%. There were no breast cancer deaths. CONCLUSIONS: Use of ERT in a cohort of breast cancer survivors with tumors of generally good prognosis was not associated with increased breast cancer events compared with non-ERT users, even over a long follow-up period.

    http://www.power-surge.com/educate/hrt_breastcancer.htm 
    Hormone Therapy Possibilities for Breast Cancer Survivors and Women at High Risk for Cancer by Pete Hueseman R.Ph.,P.D., Consultant Pharmacist
    ____________________

    Jeffrey Dach MD 
    www.drdach.com   disclaimer


    Reply to this
  • 04-04-2010 DC wrote:
    I had a partial hyst in 1991 and anxiety depression, night sweats and can cry at a drop I am on Careplus.

    I need help and would like to find out more information on the bio identical hormone Blood test should be covered need to know how much office visit is and if ins covers anything.

    I really need some help I am only 52 but feel like Im on edge.

    Please call during day with any information.

    Thank You DC
    _________________________________________________________
    Please call the office for more information.

    regards from

    Jeffrey Dach MD 
    www.drdach.com   disclaimer

    Reply to this
  • 05-18-2012 AL wrote:
    Hi Dr Dach,

    just wanted check if the following testosterone lvls are considered low:-

    2 Apr: 9 nmol/L;
    16 May: 10.86 nmol/L?

    In between those dates,

    I've had a pit gland tumour removed and have just developed anxiety symptoms - out of nowhere!

    A.L.
    ---------------------------------------------------------------------------

    Hi A.L.,  Call the office and we will help you: 954-792-4663.  Dr D


    Reply to this

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