ShirleysWellnessCafe.com
Oral birth control pills are mostly the hormone estrogen. Supplemental estrogen in the synthetic form has been found to promote the growth of yeast. Several years ago the Great Smokies Medical lab published studies showing that hormones could effect intestinal bacteria. A common compliant of women on birth control pills is yeast infection. The copper IUD is another possible yeast promoter. It has been observed by David Watts, Ph.D., that copper promotes the growth of yeast. Often copper IUD users develop excessive levels of copper in their tissues. Excess copper can depress the adrenal, thyroid and immune systems of the body. This can make it more difficult for the body to resist yeast.
http://www.shirleys-wellness-cafe.com/candida.htm
National Candida Society
Mandy Smith (then Bill Wyman's wife) was the first UK public person reported in the press to be suffering from candida, which was attributed to her continuous use of the contraceptive pill from puberty. In fact, it still seems likely that hormonal pills are the major factor in women developing candida. The factors are:
contraceptive pill or HRT including 'natural' progesterone cream
other corticosteroids (hydrocortisone, beconase, prednisolone etc.)
hormonal changes e.g. puberty, sexual maturity, pregnancy, sterilisation, menopause including peri- and post-menopause
broad-spectrum antibiotics
dental mercury amalgam poisoning
chemical poisoning in the home or office
stress (usually as a contributory factor).
The exact effect is unknown. Depending on which receptors are blocked and what activity the receptor was governing, the net result could be excess or insufficient oestrogen. Excess oestrogen is a cancer risk e.g. for breast cancer. Progesterone dominance (low oestrogen) can cause headaches, migraines, depression, blood sugar irregularities leading to asthma and adrenal gland exhaustion leading to allergies particularly environmental allergies. (!!!!!!!!!!!!!! They obviously know nothing about progesterone, as these are all oestrogen symptoms!! Dr Dalton used to give progesterone injections to her patients when they had asthma and the attack goes instantly!!! One of the roles of progesterone in the body is to help control blood sugar!!!). Low body temperature (but normal thyroid tests) are another sign of adrenal dysfunction. So we find that all of our symptoms listed earlier are signs of an endocrine disorder. Interesting!
http://www.candida-society.org/ncs/digestv1i3.htm
Worldhealthmall.com
Hypoglycemia Symptoms begin to show up and are usually viewed as individual diseases themselves.
The fungus in seeking its main food of SUGAR upsets the body's whole sugar system. The person deprived of the chaperone minerals needed to escort sugar and insulin into the cells…… becomes hypoglycemic .
They now have low cellular sugar, a perfect playground for fungus to feed. However, now the cells do not have enough sugar to burn for energy so we become weak if we do not eat often and we surely do not have enough sugar to keep us alive during the night!
The brain now signals the adrenal gland to send out adrenal hormones to keep the body functioning during the night, which it does. But the side effect is that during the night the person may get hot or they may even have night sweats! The adrenal gland is now working 24 hours per day!
All diabetics come from this type of person. All diabetics develop from a hypoglycemic individual. If the lacking chaperone minerals are not supplied and the person has a weak gene they become diabetic.
By now the person tends towards constipation or diarrhea or both due to the fungus and they either bloat or produce gas whenever they eat high glycemic carbohydrates, grains or beans. This is because these foods are the main source of fast sugars which the fungus thrives on.
Bloating is an improper fermenting process instead of a digestion process.
Mal-absorption is the result of fungus in the small intestine.
Progesterone: Ever wonder why so many women have to use progesterone cream? It is because fungus devours it and changes it into prednisone. In fact, I have heard that drug companies farm fungus colonies, feeding them progesterone to make the drug prednisone which they then sell to consumers as a remedy for everything. (Not heard of this!!!!!!!! This misinformation irritates me: “I have heard” and “drug companies farm fungus colonies,” what fungus?!?!!?)
Prednisone is just one of the many powerful mycotoxins of the fungus that can kill bacteria.
This explains why most women are estrogen dominant. Not that they have a lot of estrogen but they lack progesterone due to fungus.
These imbalances can cause the face to break out, breast to lose firmness, hair problems and the most significant…. Depression even migraines . Aside from these problems a woman's skin can become so sensitive she can't stand to be touched. The skin can become so painful intimacy becomes impossible.
http://worldhealthmall.com/new/candida.html
Polaris.net
Candida Albicans
The human intestinal tract harbors just over 400 different species of bacteria, of which there are thousands of strains. They are divided into two general groups, "friendly" and "unfriendly". While both play an important role in overall health, an imbalance of the normal ratios of these bacteria may result in a wide variety of symptoms which range from anxiety to hypoglycemia.
Antibiotics, Birth Control Pills , mercury (from fillings), antacids, Stress and many other over the counter/prescription medications kill significant levels of "friendly" bacteria, allowing "unfriendly" bacteria to proliferate and overgrow the gut. Among the "unfriendly" bacteria, the most aggressive and opportunistic strain is Candidiasis Albicans, a.k.a., Candida.
If this overgrowth invades the bloodstream and infects other parts of the body, it is then referred to as Systemic Candidiasis.
Next, Candida usually migrates to the tract shared by the reproductive and urinary systems.
Because of the proximity of the vaginal tract to the anus of a female, women often experience vaginitis in the early stages of development and in men, jock itch is common.
An article published in The Journal of the American Medical Association (1977) states:
"Vaginal Candidiasis does not occur naturally without infection of Candida Albicans within the large bowel and that a cure is not likely as long as the vagina remains the only treatment target"
It is also common for males to end up with candida spores in their lungs!
As Candida matures it can then permeate the intestinal membrane directly into the blood stream and be a primary cause of Leaky Gut Syndrome which in turn leads to a myriad of other, often misdiagnosed, health problems
http://www.polaris.net/~health/candida_albicans.html
Healthy Awareness
Candida may complicate other diseases and conditions.
If PMS occurs during the later two weeks of the cycle, there is usually too much estrogen compared to progesterone during this part of the cycle. In this case, people often suggest zinc, B6 and natural progesterone to relieve symptoms. If PMS occurs during the first two weeks of the cycle, it is dubbed “reverse PMS” and will sometimes respond to a small amount of estrogen.
http://www.healthyawareness.com/
http://www.healthyawareness.com/
The Journal of Infectious Diseases , volume 184 (2001), pages 1489-1493
Growth Inhibition of Candida albicans by Human Vaginal Epithelial Cells
Vulvovaginal candidiasis (VVC) is a common mucosal infection caused by Candida species in women of childbearing age. Although acute VVC affects a large number of women and is often precipitated by hormonal fluctuations involving high estrogen levels, recurrent VVC (RVVC) affects another 5% 10% of women without any known predisposing factors. We have recently reported that vaginal epithelial cells from nonhuman primates and mice inhibit the growth of Candida albicans in vitro, which may represent an innate host defense mechanism against C. albicans at the vaginal mucosa. In the present study, we show that vaginal epithelial cells collected from healthy women with no history of VVC also exhibit anti- Candida activity, with no differences in activity at various stages of the menstrual cycle. Women diagnosed with RVVC, on the other hand, have reduced epithelial cell anti- Candida activity. These results are further evidence that vaginal epithelial cells provide an innate host resistance mechanism against Candida and that reduced activity may contributeto RVVC.
http://www.journals.uchicago.edu/cgi-bin/resolve?id=doi:10.1086/324532&erFrom=1653107012841874889Guest
Braz. J. Microbiol. vol.36 no.2 São Paulo Apr./June 2005
Isolation of Candida spp from vaginal microbiota of healthy canine females during estrous cycle
The high incidence of Candida spp during dioestrus (62 %) may be linked to high progesterone levels in this phase (17) Candida -specific cell-mediated immunity, acquired by exposure to Candida as a commensal early in life, has been considered the predominant host defense mechanism against mucosal Candida infections (11), acting as cellular immunity suppressor, and promoting the expression of a gene that favours synthesis of an epithelial receptor able to bind certain fungi (38). Studies suggest that estrogen, but not progesterone, is important in the reproductive-hormone-associated susceptibility to vaginal C. albicans infection (10,11). The high estrogen levels in proestrus (18,28,35) can account for Candida isolation in this phase. Fungi development is enhanced by this hormone which increases glycoproteic epithelial complexes exposition acting as receptors for fungi agents (38). Estrogen or also stimulate glycogen collection (15), and the decrease of the vaginal pH due to its metabolization to lactic acid supports to lactobacillus and yeasts growth (22,27). Immunoglobulin A (IgA) and IgG are the predominant Ig classes found in vaginal washes, suggesting that they represent the dominant Igs in the female genital tract (29). Decrease of these immunoglobulines in proestrus due to high estrogen levels is also considered as a factor that could influence yeast growth (37). Sex steroid hormones regulate the movement of mucosal IgA antibody and its transporter, polymeric immunoglobulin receptor, from uterine tissues into secretions (34). Biological models demonstrated that estrogen and progesterone levels are high in oestrus, increasing uterine and reducing vaginal immune function, what could justify Candida spp isolation in this phase (37). Basal hormones concentration (4,8,35), and alkaline vaginal pH are adverse conditions to fungi development (27) and could, probably, account for little Candida spp isolation in anoestrus.
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1517-83822005000200018
Infection and Immunity, February 2000, p. 651-657, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000 ,American Society for Microbiology . All rights reserved.
Effects of Reproductive Hormones on Experimental Vaginal Candidiasis
Paul L. Fidel Jr., *Jessica Cutright, and Chad Steele
Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, Louisiana
Received 28 June 1999/Returned for modification 30 September 1999/Accepted 30 October 1999
Vulvovaginal candidiasis (VVC) is an opportunistic mucosal infection caused by Candida albicans that affects large numbers of otherwise healthy women of childbearing age. Acute episodes of VVC often occur during pregnancy and during the luteal phase of the menstrual cycle, when levels of progesterone and estrogen are elevated. Although estrogen-dependent experimental rodent models of C. albicans vaginal infection are used for many applications, the role of reproductive hormones and/or their limits in the acquisition of vaginal candidiasis remain unclear. This study examined the effects of estrogen and progesterone on several aspects of an experimental infection together with relative cell-mediated immune responses. Results showed that while decreasing estrogen concentrations eventually influenced infection-induced vaginal titers of C. albicans and rates of infection in inoculated animals, the experimental infection could not be achieved in mice treated with various concentrations of progesterone alone. Furthermore, progesterone had no effect on (i) the induction and persistence of the infection in the presence of estrogen, (ii) delayed-type hypersensitivity in primary-infected mice, or (iii) the partial protection from a secondary vaginal infection under pseudoestrus conditions. Other results with estrogen showed that a persistent infection could be established with a wide range of C. albicans inocula under supraphysiologic and near-physiologic (at estrus) concentrations of estrogen and that vaginal fungus titers or rates of infection were similar if pseudoestrus was initiated several days before or after inoculation. However, the pseudoestrus state had to be maintained for the infection to persist. Finally, estrogen was found to reduce the ability of vaginal epithelial cells to inhibit the growth of C. albicans . These results suggest that estrogen, but not progesterone, is an important factor in hormone-associated susceptibility to C. albicans vaginitis.
*Corresponding author. Mailing address: Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112. Phone: (504) 568-4066. Fax: (504) 568-4066. E-mail: pfidel@lsumc.edu .
http://iai.asm.org/cgi/content/abstract/68/2/651
Gynecologic and Obstetric Investigation 2000;49:57-61 (DOI: 10.1159/000010214)
Vol. 49, No. 1, 2000
Original Paper
Protective Effect of the Selective Estrogen Receptor Modulator LY117018 on Rat Vaginal Candida albicans Colonization
Michael Essmann, Bryan Larsen
Infectious Disease Research Laboratory, University of Osteopathic Medicine and Health Sciences, Des Moines, Iowa, USA
Abstract
Although we know that estrogen promotes vaginal colonization with Candida albicans in oophorectomized rats, the availability of selective estrogen receptor modulators (SERMs) raises the question of whether these compounds may influence the susceptibility of vaginal epithelium to Candida colonization. We inoculated rats with viable C. albicans 2 days after treatment with oil vehicle (controls), estradiol cypionate or the proprietary SERM, LY117018. LY117018 prevented colonization by a clinical isolate of C. albicans . In contrast, rats treated with estradiol cypionate remained colonized for up to 10 days after initial inoculation with viable yeast. In vitro tests demonstrated that both estradiol-17 and LY117018 promoted growth at a 1 _ 10 -9 Mconcentration, whereas both compounds suppressed yeast growth at a higher (1 _ 10 -6 M) concentration. The effect of LY117018 on vaginal colonization could not be predicted on the basis of in vitro investigation. We conclude that the protective effect of LY117018 resulted from an indirect effect on the host and not from its effect directly on the microorganism.
Copyright © 2000 S. Karger AG, Basel
Author Contacts
Bryan Larsen, PhD
Dean for University Research
University of Osteopathic Medicine and Health Sciences
3200 Grand Avenue, Des Moines, Iowa 50312 (USA)
Tel. +1 515 271 1559, Fax +1 515 271 1644, E-Mail blarsen@uomhs.edu
Candida albicans morphogenesis is influenced by estrogen
Cellular and Molecular Life Sciences (CMLS)
Publisher Birkhäuser Basel
ISSN 1420-682X (Print) 1420-9071 (Online)
Volume 53, Number 9 / October, 1997
DOI 10.1007/s000180050094
Pages 744-749
Thursday, February 19, 2004
Authors
S. White, B. Larsen
Abstract
Conversion of Candida albicans from yeast to mycelial growth is believed to be associated with the organism's virulence. We investigated the role of mammalian hormones in initiating this transformation. Three clinical isolates of Candida albicans were tested for their ability to produce germ tubes under various conditions. Controlled hormonal conditions were provided by stripping rabbit serum with activated charcoal. Steroid compounds under investigation were added back to the stripped serum and yeast were inoculated into the test materials. Microscopic counts of germinated versus ungerminated cells were used as an indicator of morphogenic transformation. The percent of yeast cells germinating was profoundly reduced in stripped compared to unstripped serum. The addition of 1 wM estradiol, cholesterol or testosterone only slightly increased levels of germination above that seen in controls. Estradiol at concentrations 100 times less, however, proved a strong inducer of germination. Cholesterol did not synergize germination when combined with estradiol and the alpha isomer of estradiol had almost no activity as an inducer of morphogenic change in Candida albicans . We conclude that beta estradiol was a morphogenic inducer in three clinical isolates of Candida albicans but only at concentrations typical in vivo.
http://www.springerlink.com/content/43wu073yp6k39h6a/
J Infect Dis. 1983 Jan;147(1):160. Links
Inhibition of monocyte-mediated damage to fungal hyphae by steroid hormones.
Diamond RD .
Human monocytes can damage hyphal forms of C. albicans [1], R. oryzae [2], and A. fumigatus [3]. Because corticosteroids can inhibit phagocytosis and killing of bacteria by monocytes, the effects of steroid hormones on interactions of monocytes with hyphae were studied. Monocyte-mediated hyphal damage was inhibited by 10 microM hydrocortisone; inhibitory effects of lower concentrations of hydrocortisone were less marked with Rhizopus than with Candida or Aspergillus hyphae. Addition of 10% normal human serum to hyphae and monocytes did not affect the inhibitory effects of hydrocortisone (data not shown). Comparable inhibitory effects were obtained using 0.3-1.0 microM dexamethasone (data not shown). Estrogen and progesterone also inhibited damage to Candida or Rhizopus. However, inhibition occurred at concentrations which are readily achievable in vivo by pharmacologic doses of hydrocortisone, but not by other steroid hormones. Thus, pharmacologic doses of corticosteroids might produce serum hormone concentrations which could interfere with activity of host monocytes against the tissue-invasive forms of C. albicans and A. fumigatus in vivo. However, higher pharmacologic doses of these hormones may be required to inhibit leukocyte-mediated damage to Rhizopus hyphae. In contrast, predisposition of women to superficial candidal infections cannot be explained solely by direct effects of estrogens or progesterone on leukocyte-mediated hyphal damage.
PMID: 6822752 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6822752&dopt=Citation
J Clin Microbiol. 1988 October; 26(10): 2110-2115
Dermatophyte-hormone relationships: characterization of progesterone-binding specificity and growth inhibition in the genera Trichophyton and Microsporum.
K V Clemons ,G Schär ,E P Stover ,D Feldman and D A Stevens
Department of Medicine, Stanford University School of Medicine, California 94305.
ABSTRACT
We reported previously that Trichophyton mentagrophytes contains a cytoplasmic macromolecule which specifically binds progesterone. Progesterone is also an effective inhibitor of growth of the fungus. We report here studies which characterize more fully the specific binding properties and the functional responses of T. mentagrophytes and taxonomically related fungi to a series of mammalian steroid hormones. Scatchard analysis of [3H]progesterone binding in both the + and - mating types of Arthroderma benhamiae and in Microsporum canis revealed a single class of binding sites with approximately the same affinity as that in T. mentagrophytes (Kd, 1 X 10(-7) to 2 X 10(-7) M). Trichophyton rubrum had a protein with a higher binding affinity (Kd, 1.6 X 10(-8) M). Characterization of the [3H]progesterone-binding sites in T. mentagrophytes showed the binder to be a protein which was destroyed by trypsin and heating to 56 degrees C. Previous examination of the steroid-binding specificity in T. mentagrophytes had demonstrated that deoxycorticosterone (DOC) and dihydrotestosterone (DHT) were effective competitors for [3H]progesterone binding. Expansion of this study to include other competitors revealed that R5020 (a synthetic progestin), androstenedione, and dehydroepiandosterone possessed relative binding affinities which were 20, 11, and 9% of that of progesterone, respectively. Other ligands tested were less effective. Competition studies for the binder in M. canis resulted in similar findings: DOC and DHT were effective competitors for [3H]progesterone binding. The growth of A. benhamiae + and -, M. canis, and T. rubrum were all inhibited by progesterone in a dose-responsive manner, with 50% inhibition achieved at concentrations of 9.8 x 10(-6), 1.2 x 10(-5), 1.5 x 10(-5), and 2.7 x 10(-6) M. respectively.
http://jcm.asm.org/cgi/content/abstract/26/10/2110
J Bacteriol. 1966 November; 92(5): 1285-1289
Copyright © 1966 American Society for Microbiology . All Rights Reserved.
Bacteriostatic Action of Progesterone on Staphylococci and Other Microorganisms
William Yotis and Ronald Stanke
Stritch School of Medicine, Loyola University, Hines, Illinois
ABSTRACT
YOTIS , W ILLIAM (Loyola University, Hines, Ill.), AND RONALD STANKE . Bacteriostatic action of progesterone on staphylococci and other microorganisms. J. Bacteriol. 92: 1285-1289. 1966.-Progesterone has been examined in vitro for antibacterial activity against 10 microorganisms. Turbidimetric and manometric techniques were used to assay the antibacterial activity of progesterone. The organisms tested consisted of Staphylococcus aureus, S. epidermidis, Gaffkya tetragena, Bacillus subtilis, Listeria monocytogenes, Candida albicans, Escherichia coli, Aerobacter aerogenes, Salmonella paratyphi , and Proteus vulgaris .Antibacterial action was shown by progesterone only against the gram-positive microorganisms when they were grown in tryptic soy broth containing 10 to 20 µg of progesterone per ml. Pregnenolone, 4-pregnen-20ß-ol-3-one, and 5 -pregnane also possessed antistaphylococcal properties, whereas pregnanolone, pregnandione, 11 -hydroxyprogesterone, and 17 -hydroxyprogesterone did not. The bacteriostatic action of progesterone on staphylococci was exerted primarily during the first 8 hr of incubation, and it was reduced in the presence of oxygen. In the presence of 20 µg of progesterone per ml, there was significant reduction in the oxidation by resting staphylococcal suspensions or utilization by staphylococci of pyruvate as an energy source during growth.
http://jb.asm.org/cgi/content/abstract/92/5/1285
