What does my progesterone level mean?
My husband and I have been ttc for 5 months now and I took my first round of Clomid (50 mg days 3-7) this month. On cycle day 20 (Tuesday) I went in and had blood work to test my progesterone levels. I got my results this morning and it was 18.7 and they said that’s good. I was wondering what that means more specifically. I have an appt. with my dr. next Tues. and we will discuss it more in depth then but I was curious now. Any help would be greatly appreciated.
I know that means I ovulated which is great. Are those levels high enough that I could be pregnant?
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They just told me that I ovulated. They didn’t tell me my level. I wish they did because it would be nice to compare. It really sucks that they can’t give you more info. When you are trying you want to know every possiblility….so can you tell when I ovulated? Best of luck and I’m sure you’ll get the answers that you need when you go to the dr. but I don’t believe that a progestrone test can tell you anything about an early pregnancy.
Best of luck!
Anything over 15 on medicated cycle means ovulation occurred. Progesterone level has nothing to do with the odds of being pregnant, it is simply a test to ensure you are responding to the meds.
I am not sure about when you are ttc but once you get pregnant, your progesterone keeps the baby growing until the placenta is developed and ready to feed the baby. Over 10 is good but the higher the better.
Progesterone is a hormone naturally found in pregnate women. However, the hormone is used in the morning after pill to stop women from becoming pregnate because it stops fertilization from occuring. If levels are too high before you are carrying a baby it might be difficult for you to become pregnate.
It is an indicator if there is enough of this hormone, which is vital to the fertilized ovum.
The word "natural," when used to modify the meaning of a word which names one of the hormones, means that the hormone under consideration is an exact replication of the hormone as it is found in the human body. In the case of progesterone, it is found in a variety of plants, including the European mistletoe and in the Mexican wild yam. This does not mean you should try to supplement from plants. Supplementation should be done using pharmaceutical grade bio-identical (orthomolecular) hormones with doses prescribed by an experienced doctor based on the results of precise testing of your current hormone status. Anything less and you are asking for trouble.
The word "phyto-hormone" is used to denote the fact of plant origin. "Phyto" means "plant." The FDA is well aware of the presence of phyto-hormones in nature; that is why they have issued proclamations declaring certain plants "toxic." This can be interpreted to mean, "toxic to the capitalist interests of the medical/pharmaceutical superstructure for which the FDA is the unofficial guardian." These plants are sources of natural hormones, which can be extracted and sold at a fraction of the cost of competing synthetic (and therefore toxic) hormones. It is well-known that the FDA is committed to the financial health of the American pharmaceutical industry.
A fact of life is that aging results in the progressive decrease in the body’s ability to manufacture hormones at youthful levels. Many of the physical changes people experience with aging are not inevitable, but are correctable with hormone therapy. Of course, the pharmaceutical industry has long since realized this, but they have a large problem: if they don’t make it, they cannot patent it and, if they cannot patent it, they cannot make a large profit on it. In the case of phyto-hormones, the pharmacy of origin is nature, and the pharmaceutical scientist is God. It is hard to compete with God. God makes good stuff!
During childbearing years, progesterone is made by a succession of short-lived glands. Each successive gland is called a "corpus luteum." The corpus luteum develops from the cells surrounding that place on the ovary from which the recently departed egg was extruded to make its journey down the Fallopian tube. This tiny gland lives through the last half of the menstrual cycle, until menstrual flow begins, then it shrivels up and dies, unless pregnancy intervenes. Therefore, in the absence of pregnancy, a woman has an abundant supply of progesterone for the last half of each cycle and relatively little through the first half.
If the egg is fertilized and implanted, the corpus luteum continues to function and increases its output of progesterone through pregnancy. The function of progesterone is to nourish and prepare the wall of the uterus for implantation of the fertilized egg and to continue this nourishment through pregnancy.
Progesterone production from the corpus luteum begins two days before ovulation and has the effect of increasing sex drive, making intercourse and fertilization more likely. If fertilization and implantation do not take place, this particular corpus luteum withers and dies, and progesterone level falls to a low level until the next corpus luteum appears from the next ovulation.
Therefore, progesterone levels are low from day 26 until ovulation, usually around day twelve. Then levels are high until day 26, unless pregnancy occurs in which case, levels are even higher throughout pregnancy.
Another function of progesterone is known only by what happens when it is no longer present in youthful levels. Because most progesterone is produced by the corpus luteum, and because there is no further corpus luteum formation after menopause, progesterone levels fall precipitously at menopause and remain low for the rest of a woman’s life.
Not by coincidence, another thing happens concurrently around menopause and especially the next five to six years: demineralization of bones, which is called "osteoporosis." Osteoporosis can be prevented with the use of natural progesterone. It also can be reversed with the use of natural progesterone.
Much attention has been paid to the largely unsuccessful, or partially successful, attempt to prevent osteoporosis with estrogens. Because there is no large profit in natural progesterone, the drug companies have not alerted physicians to the value of this good medicine. Consequently, docs are out there following the party line: horse estrogen (Premarin), vitamin D and calcium for osteoporosis prevention.
Many women, who now are disabled with hip fractures and other debilitating complications of osteoporosis, followed that advice. That regime can slow down osteoporosis in some cases but has nothing like progesterone’s power to prevent demineralization of bones and remineralize osteoporotic bones.
The fact that osteoporosis can be prevented and reversed with natural progesterone is not something which drug companies want you to know about, because there is not much money in natural progesterone. However, they would love to have you know about all the possible uses of their synthetic (patented) estrogens.
The major use of synthetic estrogens is, of course, for birth control, and they are combined with synthetic progesterone-like substances (called "progestins"). It is important to realize that progestins are synthetic — made in labs other than nature’s lab — and are profoundly incompatible with the human body, as any woman who has taken BCPs can tell you. Here is a partial list of warnings to be found for your friendly BCP, found on the package insert and caused by the progestin content.
Possible side effects:
Birth defects
Loss of vision
Thrombophlebitis, embolism, cerebral thrombosis
Liver dysfunction, cholestatic jaundice
Breast or genital malignancy
Fluid retention, migraine, asthma, epilepsy
Heart and kidney dysfunction
Menstrual irregularities
Depression, nervousness, fatigue
Decreased glucose tolerance, may exacerbate diabetes
Breast tenderness, galactorrhea (flow of milk)
Skin eruptions
Acne, alopecia, hirsutism
Edema, weight changes
Cervical erosions
Pyrexia, nausea, insomnia, somnolence
Anaphylactic reaction (sever, life-threatening allergic reaction)
Hypertension
If you bother to read the fine print, you will see that almost every synthetic drug is sporting such a warning. Man’s lab is just unable to compete with nature’s lab. In the case of natural progesterone, given in proper doses, here is a list of possible adverse side effects:
None.
It is a short list; a list of nothing. There are no side effects — hard to believe, but true. The first tenet of medicine, part of the Hippocratic Oath, an oath taken by all doctors when they graduate from medical school, is, "First, do no harm," or Premum non nocere in the original Latin. Many doctors have forgotten this basic tenet of medicine under the hypnotic influence of a blizzard of propaganda from pharmaceutical companies touting their latest patented, money-making, synthetic nightmare.
Estrogen and progesterone exist and do their respective jobs in relation to each other and must be in a certain proportion to each other to work best. Estrogen acting in the absence of progesterone goes out of control in certain ways. Estrogen and progesterone mutually antagonize the effects of each other, thus making possible the cyclic nature of ovulation, fertilization, implantation and gestation in human reproduction. If fertilization and/or implantation do not occur, estrogen and progesterone are involved in resetting the system to try again one month later.
At around age 45 to 50, the woman’s supply of oocytes (eggs cells) diminishes from millions at birth to around 1000. Because the major source of estrogen is the oocytes, this depletion of oocytes induces a condition of hypoestrogenemia — and thus menopause. So, age itself does not account for menopause, but rather the falling estrogen levels from the depletion of oocytes. Proper nutrition and avoidance of toxins delay menopause by preserving greater numbers of viable oocytes.
Even though estrogen levels fall at menopause, progesterone falls even more, because there is no longer the monthly creation of a corpus luteum to make progesterone. Because estrogen and progesterone balance each other, there comes to be a condition of estrogen dominance after menopause. The regulating hormones of the pituitary gland sense this imbalance and give the neurochemical command for more estrogen and progesterone. This creates an even larger imbalance, because the ability to make progesterone is so extremely compromised while there still are around 1000 eggs left to make estrogen. This imbalance accounts for the myriad symptoms and complaints seen in the doctor’s office at this time of a woman’s life.
The solution for this situation is natural progesterone along with a good diet and avoidance of toxins. Progesterone supplementation should be considered when there are signs of estrogen dominance: edema, swelling of breasts or fibrocystic disease, loss of sex drive, mood swings with depression, uterine fibroids, irregular or heavy menses, weight gain around hips and thighs and craving for sweets.
For the premenopausal woman who may be experiencing anovulatory (no eggs traveling down the Fallopian tubes) cycles, progesterone provides relief from estrogen dominance/progesterone deficiency between days twelve and 26. For the premenopausal woman, the symptoms of hot flashes, mood swings, etc., are eliminated. For the postmenopausal woman, the advantage of progesterone is a continuing good sex drive.
It is unlikely that estrogen supplementation will be needed since a good diet includes a number of phytoestrogens (estrogens of plant origin) and everyone is exposed to xenoestro-gens of petrochemical origin from the environment. Also, progesterone sensitizes all estrogen receptors, so that there is a heightened response to estrogen which is present. If, after three months, there are neither hot flashes nor vaginal dryness, there is no need for estrogen.
The sources of progesterone are the wild yam and placentas harvested at birth. The synthetic substitutes for progesterone (the progestins) are made from the wild yam. The progesterone molecule is altered so that it can be patented.
Few doctors are even aware that natural progesterone is available and far safer than the pharmaceutical attempt at substitution for the real thing. At present, you cannot obtain USP progesterone from standard pharmacies. For this, you must find a compounding pharmacist. Most docs don’t know how to find a compounding pharmacist, or even what they are!
Many pelvic diseases improve with progesterone therapy given before menopause. These include pelvic inflammatory disease (PID), vaginitis, Mittelschmerz (pain on ovulation), ovarian cysts and endometriosis.
PMS
Premenstrual syndrome (PMS) is a problem for many woman (and therefore many men) and involves physical and mental changes. PMS begins around seven to ten days before menses and brings a tidal wave of negative emotions for which husbands and boyfriends are sometimes blamed. The mental effects of PMS are so severe that they even have been used as a defense in court against the charge of murder! Some of the physical effects are a loss of interest in sex, headache, weight gain, back ache, breast tenderness and fatigue.
The treatment of PMS is notoriously unsuccessful. The need for an effective treatment is made clear by the many vitamin/mineral/supplement entries on the market for treatment of PMS. The symptoms of PMS read like a catalog description of estrogen dominance. If estrogen levels are higher than normal, or if progesterone levels are lower than normal, the stage is set for estrogen dominance. If there is an anovulatory cycle, the woman is exposed to an abnormal full month of estrogen effects, relatively unopposed by progesterone.
That PMS should occur at all, even in the absence of anovulatory cycles, is a comment on the effects of the industrial age on our immune systems and on our hormone systems as well. Nature did not design women to become physically and emotionally unstable every month. You can be sure that this syndrome has its origins in the toxic chemical soup in which we live in the modern world. (A similar situation holds for men in that progressively decreasing sperm counts and infertility among men is related to pollution.)
The treatment of PMS with progesterone is 100 to 200 mg. transdermally or 25-50 mg. by mouth from day fourteen to day 25 of the cycle.
Osteoporosis
Osteoporosis, the progressive demineralization of bone, causes 1.3 million fractures per year in the U.S., at an estimated cost of $10 billion. Thin white women fare worst and risk factors include smoking, vitamin D deficiency, calcium and/or magnesium deficiency, a meat-based diet, alcohol consumption and lack of exercise. Until now, the most effective therapy was "estrogen" (not the real human variety) with vitamin D replacement, and the best one could hope for was to slow the disease down and maybe even prevent it.
No hope has been offered to reverse osteoporosis with "estrogen" therapy. Also, the risk of cancer, as well as a panoply of other symptoms of estrogen dominance, mars the use of horse estrogen (Premarin) as well as synthetic estrogens. Despite the clear warnings attached to estrogen therapy, even outlined in the best textbooks of medicine, mainstream establishment medicine has stayed with "estrogen" therapy. This is a tribute to the power of pharmaceutical company propaganda. To handle a part of the risk of osteoporosis — which could be handled safely with natural human progesterone — the drug companies recommend that you take their products and increased your chances of dying of cancer.
Although there have been many therapies for osteoporosis over the years, the fact that none of them could reverse the condition gave testament to the fact that the cause of osteoporosis was simply not understood. Now, it appears that, in women at least, the cause is the loss of adequate progesterone supplies at menopause. This conclusion is arrived at by reverse logic, because replacement of progesterone has the power to reverse osteoporosis, and strengthen and remineralize fragile bone in the older woman.
Of course, the progression of osteoporosis is much more of a problem for women than it is for men. Men also experience osteoporosis, but typically about twenty years later than women and even then not to the extreme degree seen in women. We can hardly say that loss of progesterone is the problem in men, because men do not produce large quantities of progesterone in the first place.
Apparently, in men, the hormone which has the most to do with bone mineralization is testosterone. However, although testosterone does decline gradually in men, there is not a precipitous drop in level comparable to the drop seen in a woman’s progesterone level with menopause. Nevertheless, men are protected from osteoporosis by supplemental testosterone in their autumn and winter years of life.
Osteoblasts and Osteoclasts
There are two types of cells responsible for bone maintenance. They are called "osteoclasts" and "osteoblasts." The root word "osteo" refers to bone. The root words "clast" means to break down, and "blast" means to construct. Therefore, osteoclasts break down old bone and clean up the mess, so that the osteoblasts can come in and build new bone. This is happening at a microscopic level at all times. Progesterone (and testosterone) activate osteoblasts. The turnover time for complete renewal of bone is ten to twelve years, so the development of osteoporosis is a slow affair, and the complete reversal can require a decade or more. Improvement, however, is sooner — six months to one year.
When all of these facts are considered together, it is obviously wise to begin progesterone therapy at menopause (and testosterone at male menopause) to achieve prevention of the disease. Bone density changes in the negative direction accelerate at menopause, and within five years most of the damage is done. This is the critical time for prevention.
Supplementation
Although vitamin and mineral supplementation in the absence of progesterone therapy are relatively useless in reversal of osteoporosis, when used as an adjuct to progesterone they make for more rapid rebuilding of bone structure. Here are the essential nutrients for bone reconstruction, along with suggested daily dosage levels for adult women:
Calcium: premenopausal: 800 mg., postmenopausal 1500 mg. (same for men over 65)
Phosphorus: 1.5 times the calcium intake (for example, if calcium is taken at 800 mg. per day, phosphorus supplementation should be 800 x 1.5 = 1200 mg.)
Magnesium: 300 mg.Beta-carotene: 50,000 IU
15 mg. Vitamin C: 2000+ mg.
Vitamin D: 300-400 IUVitamin B6: 50-100 mg.
Progesterone Even Earlier?
It also is true that bone density begins to decrease at about one percent per year beginning at age 35. Therefore, a case can be made for progesterone therapy in an asymptomatic woman beginning at age 35. Nevertheless, it is never too late to begin, because osteoporosis is now a reversible, not only a preventable, disease.
Other Factors in Bone Regeneration
Of course, there are other factors in the regeneration of bone. If a woman invests in progesterone therapy (or a man in testosterone therapy) and wants it to work in the best possible way, sup plementation with calcium, phosphorus, magnesium, all the trace minerals, vitamins A, C, D, K and B6 is in order.
Exercise
The other factor, which is very important, is exercise. Even mild, but daily, exercise has an effect on bone remineralization. Somehow bone tissue is able to detect the stress of exercise and knows that it must respond by building a stronger structure to stand the stress. This is especially true for weight lifting exercises.
What To Avoid
Diuretics remove calcium and should be avoided. Long term antibiotic therapy kills off normal intestinal bacteria which make vitamin K for us. If antibiotics are used, it is best to supplement with vitamin K also. Fluoride in all forms should be avoided. Metabolic acidosis, such as that caused by lung disease typical to smokers, also demineralizes bone and should be avoided. Alcohol abuse also is known to cause osteoporosis, as does hyperthyroidism.
When progesterone levels fall at menopause the woman is left with all the effects of unopposed estrogen. Two of these effects are increased risks of uterine (endometrial) and breast cancer. Of the three estrogens in the human body, two are known to be procarcinogenic: estrone and estradiol. These need to be balanced by progesterone and/or estriol (which is anti-carcinogenic) in order to reduce the risk of these two types of cancer. So here is one more benefit to the use of natural human estrogen: it has the proper balance between estrone, estriol and estradiol.
Progesterone may be taken as a capsule form or as a gel, which is rubbed into the skin. The cost is only about $18 per month for the transdermal gel and slightly more for the oral form, depending on the dosage. Some people believe the oral form is somewhat inferior to the transdermal route of administration, in that whatever is taken orally and absorbed through the stomach and intestines goes directly to the liver through the portal venous system and there 75% of it is quickly deactivated and prepared for excretion through the bile duct, right into the small intestine and thus on out of the body.
Parenthetically, let me add that from time to time I hear that fluoride makes strong bones and strong teeth. I doubt either is true, but the scientific evidence is now solidly lined up against this assertion regarding bones. The incorporation of fluoride into bone structure makes it weaker, not stronger, much to the chagrin of the aluminum industry, which has been selling this side product of aluminum production to be dumped in our water supply for over forty years now.
The time was, not long ago, when menopause was a time in life for a woman to fear. Men who were fully informed about the medical dangers of being a woman were glad to have been born male. With the discovery of the myriad benefits of progesterone therapy, a man can now secretly envy women who have the possibility to slow aging and prevent disease with this very powerful, inexpensive and, best of all, natural treatment.
Sources
Lee JR Natural Progesterone: The Multiple Roles of a Remarkable Hormone BLL Publishing, Sebastopol, CA 1993
Nelson DR, Zhang Y, Hannan MT, et al. The effect of postmenopausal estrogen therapy on bone density in elderly women. N Eng J Med 1993;329:1141-1146.
Stevenson JC, Ganger KF, et al. Effects of transdermal versus oral hormone replacement therapy on bone density in spine and proximal femur in postmenopausal women. Lancet 1990;336:265-269.
Prior JC, Vigna YM Spinal bone loss and ovulatory disturbances. N Engl J Med 1990;223:1221-1227.
Reported in article Sperm-count drop tied to pollution rise. Medical Tribune 1992;March 26
Rudy DR Hormone replacement therapy. Postgraduate Medicine 1990;Dec.:157-164.
Johansen JS, Jensen SB, Riis BJ, et al. Bone formation is stimulated by combined estrogen, progestagen. Metabolism 1990;39:1122-1126.
Kleerekoper ME, Peterson E, Phillips E, Nelson D, et al. Continuous sodium fluoride therapy does not reduce vertebral fracture rate in postmenopausal osteoporosis [abstract] J Bone Miner Res 1989;Res 4 (Suppl. 1):S376.
Hedlund LR, Gallagher JC Increased incidence of hip fracture in osteoporotic women with sodium fouoride. J Bone Miner Res 1989;Res 4:223-225.
Follingstad AH Estriol. The forgotten estrogen? JAMA Jan. 2 1978;Vol 239, No. 1:29-30.
am 7 weeks pregnant now and a bit confused. I had a blood test done for progesterone and hcg on 1/26 with levels of 70 and 970 respectively, and at this point I was just 5 weeks pregnant. I again had blood work done on 1/30 and hcg came back 4350. The office called to schedule an ultrasound for tomorrow. I am a bit concerned about the progesterone level however. I seems incredibly high for this point in my pregnancy. I am very nervous because I miscarried in Sept, however at my doctors visit 1/29 he did not seem concerned about the high progesterone level. In your experience what does a progesterone level such as this indicate
Progesterone levels fluctuate with your cycle. A level of less than 10 is low. A level of 24.7 is excellent. That does not mean that you will conceive, but does mean that your luteal phase (the number of days from ovulation to the next period) is good and that you have enough progesterone to maintain a pregnancy if, indeed, you do ovulate and conceive. The Clomid may help you ovulate. A pregnancy test will let you know if you are pregnant. If it is positive, it means that you have HCG and are pregnant. If it is negative, it meanse that you do not have HCG and are not pregnant. Progesterone levels do not indicate pregnancy
have been trying to find information about normal progesterone levels.
I am currently on Clomid (month #3). The first month, I appeared to ovulate
and had a progesterone level of 16. I did not ovulate during the second round
so took provera and began Clomid again. This month, my progesterone level
was 30.6. I understand that it is good to have levels >15 but does it mean
anything when it almost doubles? What are the typical upper ranges for
progesterone? Also, are progesterone levels good indicators of pregnancy?
Thanks for your help!!
__________________________________________________
DearAlyssa:
In the luteal phase, a progesterone level >10 ng/ml is normal. Some people make the level slightly higher (12 ng/ml) when using clomiphene. In early pregnancy, the level is expected to be above 15 ng/ml.
There is no upper limit on progesterone. The level is higher with multiple pregnancy, it rises progressively as the placenta grows, and near the end of pregnancy, 250 mg/day is being produced.
Progesterone is not a pregnancy test. Progesterone is produced both during the menstrual cycle and during pregnancy. The level of progesterone, when above 15 ng/ml, is associated with a normal pregnancy but it does not assure normality.
This information is provided for education purposes and is not a medical consultation. If you have specific questions, please speak with your healthcare provider.
Natural Progesterone is NOT a synthetic prescription Progestin such as Provera, and Megestrol.
First of all, Natural Progesterone is NOT a synthetic prescription Progestin such as Provera, and Megestrol. Brand Name prescription synthetic Progestins CAUSE cancer according to a recent copy of the Physicians Desk Reference (PDR). Natural Progesterone PREVENTS endometrial hyperplasia according to Solvay Pharmaceuticals. Endometrial Hyperplasia untreated leads to endometrial cancer. Provera and Megestrol are chemically modified from Natural Progesterone so that drug companies can patent Provera and Megestrol and charge high prices. High prices mean high profits and drug representitives can push Brand Name prescription synthetic Progestins onto unsuspecting physicians. Because of these molecular changes, these progestins have side effects that are documented in any Physician’s Desk Reference such as breast tumor formation in Beagle dogs, mental depression, nausea, insomnia, edema, asthma, migraine, thrombophlebitis, etc. Read about this at http://www.fibrocystic.com under Progestins.
Natural Progesterone is bioidentical to the progesterone your body produces. In other words, it is the same molecule your body makes. Your body does NOT make Provera and Megestrol.
The cause of many of the female diseases is chemicals in the environment that mimic estrogen. Since 1990, the study of chemical hormone disrupters has become a hot topic in scientific circles. The key is to cut out the chemical estrogens, xenoestrogens, and use Natural Progesterone. Recently, as early as 1991, many synthetic chemicals have been found to have estrogen mimicking effects at very low concentrations. These estrogen mimicking chemicals may be found in every day materials such as varnish coating the inside of food cans, laundry detergent, and plastic water bottles. Dr. Lee and other researchers around the world believe that these estrogenic chemicals have created an environment where people are exposed to too much estrogen in their daily lives. This would account for increases in endometriosis, PMS, fibrocystic breast disease, uterine fibromas, prostate cancer and benign prostatic hypertrophy.
John Lee, MD claims that Natural Progesterone opposes the effect of estrogen and chemical estrogens. It is like a tug of war. Estrogen pulls on one side and Natural Progesterone pulls on the other side. John Lee, MD claims that the hormones must be balanced.
However, the real culprit of many female woes is the "estrogen" effect of these chemical estrogens or xenoestrogens. The xenoestrogens do not look like estrogen at all and when they go into the receptor and stimulate the body, they kind of act like estrogen, but sometimes do not exactly act like estrogen.
For instance, low level dioxin was recently found to create endometriosis.
Here is an excerpt from John Lee, MD’s book, "What Your Doctor May Not Tell You About Breast Cancer":
"Gerhard and Runnebaum (1992) first brought attention to the link between the high levels of dioxins in blood and endometriosis ( adenomyosis is similar to endometriosis ). Scientific research with female rhesus monkeys fed different amounts of dioxin in their diet for four years. One group of seven animals was fed as usual without dioxin in their food, a second group had 5 parts per trillion dioxin, a third group was fed 25 parts per trillion dioxin. Ten years following dioxin administration, five of the seven animals (71 percent) given the high does of dioxin developed moderate to severe endometriosis [ adenomyosis ]. In the group receiving the intermediate dose three of the seven animals (43 percent) developed endometriosis [ adenomyosis ]. And in the group receiving no dioxin only about 33 percent developed any level of endometriosis [ adenomyosis ], which is consistent with the expected frequency of endometriosis [ adenomyosis ] in rhesus monkeys in captivity."
Progesterone,
The Forgotten Hormone
Overview (Exerpt from Listen To YOUR Hormones- new book by Dr. Kryger )
Steroids are the basis of the sex hormones, which are conventionally divided into three groups: the male sex hormones or androgens, the female sex hormones or estrogens, and the pregnancy hormones or progestins. The principal androgen hormone is testosterone, which is produced in the testes. Estradiol is the principal female sex hormone produced by the ovaries. The first few milligrams of estradiol to be isolated were obtained from four tons (!) of sow ovaries. Estradiol is responsible for the development of secondary female characteristics and participates in control of the menstrual cycle.
Progesterone is the most important progestin in human beings. It is synthesiszed in the ovary, testes, and adrenal glands from cholesterol and pregnenolone. Women need increasing in amounts of progesterone with pregancy as the uterus prepares for implantation of a fertilized egg. Progestins have an interesting metabolic conversion as Progesterone is involved in the production of Cortisol, Aldosterone, Estradiol, DHEA, Testosterone, Estriol and Estrone as well as Androstenedione.
Normal males secrete 1-5 mg of progesterone daily, and the level is only sligthtly higher in females during the egg releasing stage of the cycle. During the Luteal phase, progesterone amounts of 20-30 mg/day are released into the circulation to signal fertility and preparation for implantation in the stage known as the Premenstrual period. This phase of the menstrual cycle occurs from about 10 days to one weeks before menstruation. This monthly cycle occurs only if the egg does not implant into the uterus.
Menstruating women start to produce progesterone in their ovaries after the lutenizing hormone ( LH ) surge around the time of ovulation (usally 14 days after the first day of the cycle). The progesterone level rises and falls just before the bleeding begins. This premenstrual time is called the progesterone withdrawl phase. For some women this period is felt as an exteremely anxious, nervous, "tempermental mood." Some women find it to be an extremely depressing time with tears and feelings of low self-esteem.
Until recently, progesterone given in the form of vaginal or rectal suppositories was widely prescribed for PMS. This treatment was based on results of uncontrolled studies indicating that some women had a decreased level of progesterone during this time and experienced a range of unpleasant symptoms called Premenstrual Syndrome (PMS).
This time of the month ranges in symptoms from mild cramps to wild emotion al swings that somewomen report can drive a woman nuts and even to murder. PMS has been attempted as a defence for a murder in the UK. However, not all women suffer forom this condition. PMS is more common in women with irregular menstrual cycls, little exercise and creates cravings for salt and/or sugar. More recently, natural progesterone has been shown to be more effective than placebo or synthetic forms in treating PMS symptoms. Calcium supplements have also been found to abolish the moods and cravings. Moreover, there is also evidence that both the physical and emotional symptoms of PMS may be progesterone-induced in these women.
In controlled studies, the administration of synthetic progesterone to normal women commonly resulted in increased breast tenderness, bloating of the abdomen and extremities, and emotional lability. These symptoms of excess are almost identical to the symptoms of deficiency of Progesterone. Therefore, the use of synthetic progesterone, Provera or medroxyprogesterone in the treatment of PMS cannot be advocated in the treatment of PMS. Natural Progesterone sold OTC in health stores as Progest® or by prescription as found in the WellnessMD product EstroCreme®. Natural progesterone in small doses of 25-100 mg per day boosts the low levels which might induce swelling.
In a 25 year study on women in England reported in the Lancet in 1983, it was reported that at least 13 days of progesterone were needed each month to provide protection against breast cancer. Even women who took only 10 days of progesterone, from the 16-25 day of each cycle ran a slightly higher risk of breast cancer and had less protection than the women who took progesterone for a full 13 days.
Progesterone competes with Aldosterone, the salt regulating hormone. Progesterone can prevent salt from being absorbed leading to fluid retention. Progesterone raises the temperature in man and and has hypnotic effects on the brain. Progesterone also acts on the respiratory system to decrease carbon dioxide levels in the blood and in the lungs. One can see how a deficiency of progesterone might aggravate the PMS symptoms. Many women benefit from small amounts of extra progesterone during the premenstrual time of the month. Raising progesterone slightly also prevent cravings for sweets which occur with huge swings of progesterone. Progesterone even affects levels of amino acids and lipid metabolism. Increasing calcium to 1500mg a day for one week premestrually, helps to stimulate progesterone production and decreases PMS symptoms considerably.
Which Androgen Replacement Therapy for Women?
Although the postmenopausal ovary remains an important source of testosterone (T) production, there is nevertheless a decline in total circulating androgen levels with age. A role for androgen replacement in addition to estrogens in some postmenopausal, particularly ovariectomized, women is increasingly gaining acceptance.
Two existing testosterone preparations, oral testosterone undecanoate (TU) and subcutaneous testosterone implants, with a new matrix transdermal delivery system for T were compared in a UK study. T Levels rose regardless of mode of intake, oral, transdermal or implants. TU produced inappropriate high T levels at all doses, with wide variations between subjects, confirming that TU is unpredictably absorbed and unlikely to be satisfactory for use in women. Subcutaneous testosterone implants produce unphysiological T levels for at least 1-2 months.
The transdermal organogel delivery system in TestoJel® used twice weekly , maintained relatively stable T levels within narrow ranges. The conclusion that reached was that transdermal systems may be of value for androgen therapy in postmenopausal women because they provide a highly controllable way of delivering T noninvasively and reliably, and achieve mean physiological levels not possible with existing methods.
Birth Control or Ovarian Function and Steroidal Regulation
Steroids are also the active ingredients of birth control pills, and they work by "tricking" the body into "believing" that it is pregnant, i.e. they chemically mimic pregnancy. One typical birth control pill contains 2.5 mg of norethynodrel as a main active ingredient. RU-486 has received a great deal of publicity as "the morning after pill", and it has been used in France since 1988. Its introduction into this country has been the source of controversy.
Steroid hormones regulate neuronal function, including behavior. Using rats as our model system, studies focusing on actions of the ovarian steroids, estradiol and progesterone, in brain regions (e.g., hypothalamus, preoptic area) that regulate female reproductive physiology. Estradiol and progesterone modify the way hypothalamic neurons respond to released neurotransmitter in humans as well during the PMS.
Pharmacologic Therapies for PMS: SSRI’s and BDZ’s
Dr. Mortola, Director of Reproductive Endocrinology at Cook County Hospital in Chicago, Ill. notes:
"At present, the most likely hypothesis of PMS pathogenesis is that ovarian steroids, acting through alterations in central neurotransmitters, are responsible for symptoms of PMS. In particular, serotonin (5-HT) and gamma-aminobutyric acid (GABA)-mediated mechanisms appear important in the syndrome. In the rat, serial injection of progesterone (P4) results in increased serotonin (5-HT) uptake in several areas of the brain as well as increased 5-HT turnover. During the normal estrous cycle, 5-HT receptors in the median forebrain undergo cyclic fluctuations, being upregulated following ovulation."
During the normal premenstrual phase in humans, decreased 5-HT uptake by platelets has been reported following ovarian steroid withdrawal. This fluctuation in 5-HT uptake has been correlated with the severity of some PMS symptoms. Differences in platelet 5-HT uptake mechanisms have also been noted in women with PMS. Similar alterations have been demonstrated in whole-blood 5-HT. In addition, the 5-HT metabolite, 5-HIAA, has been measured in urine throughout the menstrual cycle, with levels peaking at midluteal phase and declining in the late luteal phase. The new SSRI’s Prozac®, Paxil®, Zoloft®, Serzone®, Wellbutrin®, and Effexor® have been found effective in PMS, anxiety and depression. These agents act by increasing 5-HT levels and downregulating receptor sensitivity.
Newer, Successful Treatments for PMS
Fluoxetine vs imipramine. In humans, the 5-HT reuptake inhibitor, fluoxetine, has been demonstrated to be effective in the treatment of PMS in independent double-blind, placebo-controlled studies.[12,14,15] This proven efficacy as well as its safety profile make this agent effective therapy for women who meet the full criteria for PMS. Mortola and Moossazadeh[16] compared the effects of fluoxetine with those of the tricyclic antidepressant imipramine; the investigators demonstrated that the efficacy of fluoxetine in PMS is not due to the agent’s generalized antidepressant effects. When 30 women treated with fluoxetine were compared with 20 women treated with imipramine, a significant response was noted in 21 of 30 (70%) subjects treated with fluoxetine versus 5 of 20 (25%) treated with imipramine (P<.005). A uniformly high response to fluoxetine was noted in women presenting with either anxious or depressed symptoms of PMS and those presenting with a premenstrual appetite or sleep disturbance.
Although the majority of studies have utilized a regimen of daily administration of SSRIs throughout the menstrual cycle, there is evidence that limiting administration of fluoxetine to the luteal phase of the cycle is effective in treating PMS patients. When prescribed in this way, a 20-mg daily dose is given after the presumed time of ovulation (day 16 of the usual 28-day cycle) until the second day of the next cycle. Because the duration of side effects is shorter when fluoxetine is limited to the luteal phase of the cycle, this is the optimal starting regimen for PMS patients. However, although this treatment may be effective using fluoxetine, pharmacokinetic differences between fluoxetine and other SSRIs are too great to permit these results to be generalized to other drugs in this class.
Benzodiazepine Tranquilizers for PMS
The efficacy of alprazolam in the treatment of PMS at a dose range is 0.25mg 4 times a day during the luteal phase of the cycle. Occasionally, higher doses of 0.5mg up to 4 times a day are required. Although efficacy with this regimen has been demonstrated, clinically, many patients report significant improvement when the medication is taken as needed during the luteal phase.
Adverse effects of alprazolam. The side effect of greatest concern with alprazolam is its potential for addiction. For this reason, the use of this agent in the treatment of PMS should be carefully restricted to luteal phase administration in the reliable patient. Addiction to alprazolam has not been reported when restricted to use during this prescribed time interval.Administration of alprazolam has not been demonstrated to be safe in pregnancy and has been reported to cause lethargy in the infants of nursing mothers. Therefore, women taking this agent for PMS should be instructed to use reliable methods of birth control. Because of the variable effects of oral contraceptives on PMS symptoms, barrier methods are preferred.
According to Dr. Mortola, patients who present with PMS should be carefully evaluated to establish correct diagnosis. Those who meet all criteria for PMS, with the exception of an identifiable disruption in lifestyle, should be considered to have a subclinical form of the disorder. These women should first be prescribed an exercise regimen and be permitted to experiment with dietary modification. Although some dietary modifications, such as the addition of Calcium, Evening Primrose Oil, Vitamin B6, and Magnesium have shown positive results in clinical trials, some women who meet the criteria for PMS, including lifestyle disruption, may respond adequately to treatment with exercise alone, the majority require pharmacologic intervention for adequate symptom management.
The first-line therapy for such patients should be fluoxetine given from day 16 of the menstrual cycle until the second day of menstrual flow. In cases where this treatment is ineffective or accompanied by undesirable side effects, treatment with either an SSRI given in a continuous daily fashion or alprazolam given on an as-needed basis is recommended. Patients who are unresponsive to these treatments are best treated with a GnRH agonist plus estrogen/progestin "add-back." Other agents, such as danazol and spironolactone, should be reserved for women with more specific symptoms, particularly headache and water retention. The use of synthetic progesterones or oral contraceptives has not been demonstrated to be effective in treating for PMS.
DHEA in Postmenopausal Women-Behavioral Effects
Aging in women and men is characterized by a progressive decline of circulating dehydroepiandrosterone (DHEA) levels and its sulfate ester (DHEAS). The improvement of well-being described in postmenopausal women treated with DHEA suggests that this steroid may exert specific actions on the central nervous system (CNS). The postmenopausal period is associated with several neuroendocrine modifications. The decrease of circulating levels of beta-endorphin is considered a hormonal marker of those changes. DHEAS (50 mg/day), orally with and without transdermal estradiol (50mg patch) mean basal serum DHEA, DHEAS, androstenedione, and testosterone levels significantly increased after treatment, while no changes were shown in the group receiving estradiol alone. Our EstroCreme® product contains both DHEA and estrogen and progesterone along with T for women.
Serum estradiol, estrone, GH and plasma beta-endorphin levels significantly increased progressively for the three months of treatment, with higher levels for estrone and estradiol in subjects receiving estradiol alone or plus DHEAS. In all women tested, the treatments were associated with similar and progressive improvement. After each of the treatments, the beta-endorphin response was completely restored and was similar, independent of the kind of therapy. Restoration of the beta-endorphin response to specific stimuli suggests that DHEAS and/or its active metabolites modulates the neuroendocrine control of pituitary beta-endorphin secretion, which may support the therapeutic efficacy of the DHEAS on behavioral symptoms.
The latest research in balancing estrogen/progestin action, the consequences of estrogen/testosterone loss, and the comprehensive benefits of menopausal hormone replacement with all hormones are discussed in the Practical Guide To Wellnesss 2000 series.
For more information on hormones, please go to our sister website, http://www.hormonenews.com.
References
Buckler HM, Robertson WR, Wu FC Which androgen replacement therapy for women? Department of Endocrinology and Medicine, University of Manchester, Hope Hospital, Salford, United Kingdom. J Clin Endocrinol Metab 1998 Nov;83(11):3920-4
Stomati M, Rubino S, Spinetti A, Parrini D, Luisi S, Casarosa E, Petraglia F, Genazzani AR. Endocrine, neuroendocrine and behavioral effects of oral dehydroepiandrosterone sulfate supplementation in postmenopausal women. Department of Reproductive Medicine and Child Development, University of Pisa, Italy.Gynecol Endocrinol 1999 Feb;13(1):15-25
Gillian S. Ashcroft, Joanne Dodsworth, Egon van Boxtel, Roy W. Tarnuzzer, Michael A. Horan, Gregory S. Schultz & Mark W.J. Ferguson from the University of Florida in 1997.
Estrogen accelerates cutaneous wound healing associated with an increase in TGF-beta1 levels. University Hospital of South Manchester, Withington, Manchester M202LR, UK/simultaneously with Department of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610, USA
Karkanias GB. Etgen AM. A thermodynamic analysis of estrogen regulation of a2-adrenoceptor binding. Brain Research. 647:26-32, 1995.
Fleischmann A. Makman MH. Etgen AM. GABAa receptor activation induces GABA and glutamate release from preoptic area. Life Sciences. 56(20):1665-1678, 1995.
Karkanias GB. Petitti N. Etgen AM Progesterone attenuation of alpha1-adrenergic receptor stimulation of phosphoinositol hydrolysis in hypothalamus of estrogen-primed female rats. Endocrinology 136(5):1993-1999, 1995.
Karkanias GB. Etgen AM. Estradiol reduction of the agonist high affinity form of the alpha 2-adrenoceptor in the hypothalamus of female rats: identification as the alpha 2D subtype. Molecular Pharmacology. 45(3):509-16, 1994
Etgen AM. Karkanias GB. Estrogen regulation of noradrenergic signaling in the hypothalamus. Psychoneuroendocrinology. 19(5-7):603-10, 1994
Saldivar-Gonzalez A. Fernandez-Guasti A. Etgen AM. Male rat sexual behavior induces changes in [3H]flunitrazepam binding. Brain Research. 611(2):326-9, 1993
Ungar S. Makman MH. Morris SA. Etgen AM. Estrogen uncouples beta-adrenergic receptor from the stimulatory guanine nucleotide-binding protein in female rat hypothalamus. Endocrinology. 133(6):2818-26, 1993
Vincent PA. Etgen AM. Steroid priming promotes oxytocin-induced norepinephrine release in the ventromedial hypothalamus of female rats. Brain Research. 620(2):189-94, 1993
Karkanias GB. Etgen AM. Estradiol attenuates alpha 2-adrenoceptor-mediated inhibition of hypothalamic norepinephrine release. Journal of Neuroscience. 13(8):3448-55, 1993
Petitti N. Karkanias GB. Etgen AM. Estradiol selectively regulates alpha 1B-noradrenergic receptors in the hypothalamus and preoptic area. Journal of Neuroscience. 12(10):3869-76, 1992
Fleischmann A. Makman MH. Etgen AM. Characterization of glutamate efflux from preoptic area synaptosomes. Neuropharmacology. 31(11):1171-8, 1992
Petitti N. Etgen AM. Progesterone promotes rapid desensitization of alpha 1-adrenergic receptor augmentation of cAMP formation in rat hypothalamic slices. Neuroendocrinology. 55(1):1-8, 1992
Fleischmann A. Etgen AM. Makman MH. Estradiol plus progesterone promote glutamate-induced release of gamma-aminobutyric acid from preoptic area synaptosomes. Neuropharmacology. 31(8):799-807, 1992
Vathy I. van der Plas J. Vincent PA. Etgen AM. Intracranial dialysis and microinfusion studies suggest that morphine may act in the ventromedial hypothalamus to inhibit female rat sexual behavior. Hormones & Behavior. 25(3):354-66, 1991
Petitti N. Etgen AM. Protein kinase C and phospholipase C mediate alpha 1- and beta-adrenoceptor intercommunication in rat hypothalamic slices. Journal of Neurochemistry. 56(2):628-35, 1991
Fleischmann A. Vincent PA. Etgen AM. Effects of non-competitive NMDA receptor antagonists on reproductive and motor behaviors in female rats. Brain Research. 568(1-2):138-46, 1991
Pleim ET. Cailliau PJ. Weinstein MA. Etgen AM. Barfield RJ. Facilitation of receptive behavior in estrogen-primed female rats by the anti-progestin, RU 486. Hormones & Behavior. 24(3):301-10, 1990
Etgen AM. Intrahypothalamic implants of noradrenergic antagonists disrupt lordosis behavior in female rats. Physiology & Behavior. 48(1):31-6, 1990
Fleischmann A. Makman MH. Etgen AM. Ovarian steroids increase veratridine-induced release of amino acid neurotransmitters in preoptic area synaptosomes. Brain Research. 507(1):161-3, 1990
Petitti N. Etgen AM. Alpha 1-adrenoceptor augmentation of beta-stimulated cAMP formation is enhanced by estrogen and reduced by progesterone in rat hypothalamic slices. Journal of Neuroscience. 10(8):2842-9, 1990
Etgen AM. Fadem BH. Ontogeny of estrogen binding sites in the brain of gray short-tailed opossums (Monodelphis domestica). Brain Research. Developmental Brain Research. 49(1):131-3, 1989
Petitti N. Etgen AM. Progesterone depression of norepinephrine-stimulated cAMP accumulation in hypothalamic slices. Brain Research. Molecular Brain Research. 5(2):109-19, 1989
Vathy IU. Etgen AM. Barfield RJ. Actions of RU 38486 on progesterone facilitation and sequential inhibition of rat estrous behavior: correlation with neural progestin receptor levels. Hormones & Behavior. 23(1):43-56, 1989
Pleim ET. Brown TJ. MacLusky NJ. Etgen AM. Barfield RJ. Dilute estradiol implants and progestin receptor induction in the ventromedial nucleus of the hypothalamus: correlation with receptive behavior in female rats. Endocrinology. 124(4):1807-12, 1989
Ng Cheong Ton JM. Gerhardt GA. Friedemann M. Etgen AM. Rose GM. Sharpless NS. Gardner EL. The effects of delta 9-tetrahydrocannabinol on potassium-evoked release of dopamine in the rat caudate nucleus: an in vivo electrochemical and in vivo microdialysis study. Brain Research. 451(1-2):59-68, 1988
Etgen AM. Robisch DM. Differential extraction of estradiol- and tamoxifen-receptor complexes from hypothalamic cell nuclei. Brain Research. 452(1-2):1-10, 1988
Vathy I. Etgen AM. Ovarian steroids and hypothalamic norepinephrine release: studies using in vivo brain microdialysis. Life Sciences. 43(19):1493-9, 1988
Etgen AM. Fadem BH. Estrogen binding macromolecules in hypothalamus-preoptic area of male and female gray short-tailed opossums (Monodelphis domestica). General & Comparative Endocrinology. 66(3):441-6, 1987
Etgen AM. Browning ET. Calcium dependence of vasoactive intestinal peptide-stimulated cyclic AMP accumulation in rat hippocampal slices. Journal of Neurochemistry. 49(1):303-9, 1987
Etgen AM. Petitti N. Mediation of norepinephrine-stimulated cyclic AMP accumulation by adrenergic receptors in hypothalamic and preoptic area slices: effects of estradiol. Journal of Neurochemistry. 49(6):1732-9, 1987
Etgen AM. Inhibition of estrous behavior in rats by intrahypothalamic application of agents that disrupt nuclear binding of estrogen-receptor complexes. Hormones & Behavior. 21(4):528-35, 1987
Glaser JH. Etgen AM. Barfield RJ. Temporal aspects of ventromedial hypothalamic progesterone action in the facilitation of estrous behavior in the female rat. Behavioral Neuroscience. 101(4):534-45, 1987
Vathy IU. Etgen AM. Barfield RJ. Actions of progestins on estrous behaviour in female rats. Physiology & Behavior. 40(5):591-5, 1987
Etgen AM. Barfield RJ. Antagonism of female sexual behavior with intracerebral implants of antiprogestin RU 38486: correlation with binding to neural progestin receptors. Endocrinology. 119(4):1610-7, 1986
Etgen AM. Petitti N. Norepinephrine-stimulated cyclic AMP accumulation in rat hypothalamic slices: effects of estrous cycle and ovarian steroids. Brain Research. 375(2):385-90, 1986
Etgen AM. Shamamian P. Regulation of estrogen-stimulated lordosis behavior and hypothalamic progestin receptor induction by antiestrogens in female rats. Hormones & Behavior. 20(2):166-80, 1986
Etgen AM. Effects of body weight, adrenal status, and estrogen priming on hypothalamic progestin receptors in male and female rats. Journal of Neuroscience. 5(9):2439-42, 1985
Glaser JH. Etgen AM. Barfield RJ. Intrahypothalamic effects of progestin agonists on estrous behavior and progestin receptor binding. Physiology & Behavior. 34(6):871-7, 1985
Vathy IU. Etgen AM. Barfield RJ. Effects of prenatal exposure to morphine on the development of sexual behavior in rats. Pharmacology, Biochemistry & Behavior. 22(2):227-32, 1985
Howard SB. Etgen AM. Barfield RJ. Antagonism of central estrogen action by intracerebral implants of tamoxifen. Hormones & Behavior. 18(3):256-66, 1984
Etgen AM. Progestin receptors and the activation of female reproductive behavior: a critical review. Hormones & Behavior. 18(4):411-30, 1984
Barfield RJ. Glaser JH. Rubin BS. Etgen AM. Behavioral effects of progestin in the brain. [Review] Psychoneuroendocrinology. 9(3):217-31, 1984
Progesterone level at that point is not an indication pregnancy. Mine was 33 when I was pg. with my son (@7dpo), but my friend recently had a 38, but was not pregnant. Both of those results were on Clomid.