The first recorded reference to thrush infections was made by Hippocrates in 400 BC.1 The microflora of the human vagina has been meticulously scrutinized for over one hundred years, beginning with the Döderlein study of lactobacilli in 1892.2 The fact that glycogen in shed vaginal epithelial cells is the carbohydrate precursor of vaginal lactic acid, and the basis of vaginal pH, was established as early as 1897.3 Yet, none of this information is fundamental to present day gynecologic treatment of common vaginal disorders.
The newborn vulva and vagina exhibit the effects of residual maternal estrogens. At birth, the labia majora are well developed and the vaginal mucosa is rich in glycogen. The vagina becomes colonized with lactic acid-producing bacteria within the first 24 hours of birth. A normal white vaginal discharge is present, which may become tinged by slight endometrial bleeding as the concentration of residual maternal estrogen falls. These estrogenic effects dissipate by the fourth postnatal week. The vaginal epithelium loses its glycogen content, vulvar skin thickness recedes, and subcutaneous labial fat decreases.4
Beginning with menarche estrogen once again matures the structures of the vagina and vulva. Among menstruating women, low vaginal pH is the result of estradiol prompting the release of glycogen from the vaginal walls. Vaginal lactobacilli use glycogen to produce lactic acid, which helps maintain low pH and dominance of lactobacilli and other acid-loving bacteria. Certain strains of Lactobacillus produce hydrogen peroxide, which further repels unfriendly vaginal flora, particularly those that have low levels of free-radical scavenging enzymes. Candida albicans, Escherichia coli and Gardnerella vaginalis are examples of pathogenic vaginal microorganisms that are strongly inhibited by Lactobacillus. L. acidophilus was once believed to be the dominant species of Lactobacillus in the vagina, but the L. acidophilus group has recently been subdivided into a number of subspecies such as L. jensenii, L. crispatus, and L. vaginalis.5
Estradiol stimulates the maturation of vaginal epithelium and its production of glycogen. Glycogen is broken down into glucose, which in turn is metabolized by vaginal lactobacilli, leading to control of the growth of vaginal pathogens via hydrogen peroxide production. Antibiotic therapy, spermicide use, oral contraceptives, estrogen therapy, corticosteroids, diabetes mellitus, tight clothing and frequent sexual intercourse are factors that increase the risk of imbalance of vaginal microorganisms.
At menopause the production of vaginal glycogen comes to a gradual and complete halt. As estrogen levels decrease, glycogen is no longer secreted by the vaginal walls. Loss of lactobacilli creates a more alkaline environment, allowing for colonization of the vagina by fecal flora and other pathogens, resulting in a change in both quality and quantity of vaginal secretions. With estrogen loss, the vagina shortens and narrows due to the loss of elasticity and rugae and thinning of its walls. The vaginal surfaces become friable leading to ulceration and bleeding on minimal trauma. Dyspareunia and vaginal bleeding from fragile, atrophic skin are common problems.6
It is important to grasp that although the microbiology of the vagina has been well understood for over a century, a conscious choice was made by biochemists working with medical doctors in the 1930s to treat symptoms of vaginal atrophy with estrogen instead of glycogen. It was hoped the anabolic and feminizing effects of estradiol might reverse aspects of aging, keeping women sexually active and “forever young”, even as the dark side of exogenous estrogen surfaced soon after women were given these drugs.
There is no question that estadiol, or more accurately Estradiol-17B, results in an increased deposition of glycogen in cervical and vaginal tissues. Progesterone, cortisol, and testosterone do not elicit a vaginal glycogen response. In fact, cortical hormones repress the glycogen response, another reason stress intensifies vulvovaginal symptoms.7
Vaginal, vulva and cervical health is largely dependent upon the microorganisms that colonize their surfaces. Formidable strains of beneficial vaginal microorganisms are the best defense against pathogens including bacteria, yeasts, flagella, and viruses. A study in 1937 reported the success of using special glucose tablets in the treatment of gonorrheal vulvovaginitis.8 Shockingly, doctors have known for decades that glycogen in the squamous mucosa of the cervix and vagina is depleted in cases of cervical cancer.9
Glycogen is the animal form of complex carbohydrate. It can be considered a prebiotic on which vaginal microorganisms feed. Interventions for vaginal infection, atrophy and inflammation should be and should always have been focused at the prebiotic level. The marketplace is catching on to this fact and at least one new product, Luvena® vaginal moisturizer, contains a form of prebiotic. Unfortunately, this product also contains polypropylene glycol, a known toxin and irritant to mucous membranes, as its third most abundant ingredient.
Industry studies have elucidated that fructooligosaccharides and glucooligosaccharides promote the growth of the most beneficial strains of lactobacilli, while preventing overgrowth of pathogenic microorganisms such as Candida albicans, E. coli and Gardnerella vaginalis.10 “Designer” forms of these saccharides are being patented for use in new pharmaceutical vaginal products.
Fructooligosaccharides and glucooligosaccharides are found in a wide variety of foods, and research indicates they are found together in the most perfect of natural prebiotics, honey. Like glycogen, honey is a hydrophilic molecule, which means it draws water into cells, naturally moisturizing tissues. It feeds the most beneficial microorganisms so they multiply quickly and crowd out vaginal pathogens. The powerful, health-promoting qualities of honey have been recognized since Egyptian times. Honey is a prebiotic for the gut as well, balancing intestinal microorganisms and restoring moisture to the colon.11
While honey throat lozenges have been a favorite product of beekeepers for generations, vaginal suppositories made from honey are non-existent. I believe this is about to change as women begin to understand the level of well-being that can be obtained by returning to nature’s oldest remedies. Women and nature have always been intimately connected. Bee colonies are suffering terribly across Europe and the United States because of overwhelming pollution wrought by the medical/pharmaceutical/industrial/military complex. Women would never have created such an unhealthy world and it is time to do everything in our power to change it, beginning with our own vaginal health.
1 Hill, L Embril J Vaginitis: current microbiologic and clinical concepts. Canadian Medical Association Journal 134: 321-331 1986
2 Doderlein G Das Scheidensekret und seine Bedeutung fur das Puerperalfieber. O. Durr. Leipzig 1892
3 Cruickshank R Sharman A The biology of the vagina in the human subject. Journal of Obstetrics and Gynecology 41: 190-207 1934
4 Farage M Maiback H Lifetime changes in the vulva and vagina Archives of Gynecology and Obstetrics 273: 195-202 2006
5 Falagas M Betsi G Athanasiou S Probiotics for prevention of recurrent vulvovaginal candidiasis: a review. Journal of Antimicrobial Chemotherapy 58: 266-272 2006
6 Calleja-Agius J Brincat M Urogenital atrophy Climacteric 12: 279-285 2009
7 Wrenn T Wood J Bitman Brinsfield T Vaginal glycogen assay for oestrogen: specificity and application to blood and urine. Journal of Reproduction and Fertility 16: 301-304 1968
8 Little A The treatment of gonorrheal vulvovaginitis with a special glucose tablet. The Journal of Pediatrics 10(2): 202-203 1937
9 Das D Chowdury J The use of glycogen studies in the evaluation of treatment for carcinoma of the cervix uteri. Acta Cytologica 21(4): 578-587 1978
10 Rousseau V Lepargneur J Roques C Remaud-Simeon M Paul F Prebiotic effects of oligosaccharides on selected vaginal lactobacilli and pathogenic microorganisms. Anaerobe 11(3): 145-153 2005
11 Mei J Nordin M Norrakiah A Fructooligosaccharides in honey and effects of honey on growth of Bifidobacterium longum BB 536 International Food Research Journal 17: 557-561 2010