THE SICK CULT OF METFORMIN NEEDS TO GET OUT OF THE WAY AND ALLOW PEOPLE TO FIND A CURE FOR PCOS.
This is an epidemic. There are too many women running around with a disease we never asked for which is putting our lives and the baby's life at risk.
THIS IS A LIFE AND DEATH ISSUE.
It's dangerous to the unborn baby; most women cannot conceive with PCOS and the cases of MISCARRIAGES is rather high.
If that's not concern enough for Big Pharma...
There are so many connections between PCOS and CANCER. There are connections between PCOS and BREAST CANCER, theres' a connection between PCOS and OVARIAN CANCER.
DON'T SAY PCOS-sarcasm. PCOS IS AN IMMUNE RELATED DISORDER, NOT CAUSED BY INSULIN RESISTANCE.
"But if ovarian cancer does prove to have an AUTOIMMUNE component, Luborsky says it could one day be possible to give a woman at risk a drug that could REDUCE HER RISK OF OVARIAN CANCER BY TURNING OFF THE IMMUNE ATTACK."
"AUTOIMMUNE OOPHORESIS is known to cause infertility, and researchers think it may also lead to some cases of ovarian cancer, though it's not clear how.
"PREVIOUS CASE REPORTS HAVE DEMONSTRATEDOVARIES WITH MULTIPLE CYSTS IN PATIENTS WITH AUTOIMMUNE OOPHORITIS."
"That's the 64 million dollar question," says study researcher Judith L. Luborsky, PhD, professor of pharmacology, obstetrics and gynecology and preventive medicine at Rush University Medical Center in Chicago."
-NO KIDDING. FOLLOW THE HIPPOCRATIC OATH AND THE MEDICAL CODE OF ETHICS AND GET RID OF YOUR CONFLICTS OF INTEREST AND LET THE IMMUNE DRUGS ON THE MARKET. METFORMIN WILL LIVE.
"The question we don't have an answer to is what role the immune system actually plays in the initiation [of cancer]," she tells WebMD.
While the idea is interesting, experts who were not involved in the research say the study only looked at one moment in time, so it's tough to draw conclusions about what elevated antibody levels may mean and it doesn't prove that elevated antibodies cause cancer."
-BULLSH*T. THYMUS GLAND=T-CELLS=IMMUNE SYSTEM.
THERE'S A DIRECT CONNECTION
""A study of female mice is suggesting that ovarian cysts may at least partially be the result of an immune system dysfunction. The gland involved is the thymus gland, which is responsible for the management of major aspects of your immune system. One of the functions of the thymus gland is to produce T-cells, which are white blood cells that help protect you from infection and also perform other important activities.
The researchers reported that ovarian cysts in the female mice did not develop unless there was an absence of regulatory T-cells."
http://www.ovarian-cysts-pcos.com/news81.html
-I SUCK AT MOLECULAR AND CELLULAR BIO-CHEMISTRY. AND I CAN STILL FIGURE THAT MUCH OUT. WHY DOES BIG PHARMA INSIST ON PULLING THE WOOL OVER OUR EYES?
They just called Autoimmune oophoritis a "rare occurance" yet PCOS is so common.
Autoimmune Oophoritis / Premature Ovarian Failure
Autoimmune Oophoritis is an autoimmune of the ovaries that can cause premature ovarian failure in women still in their childbearing years. It can strike at any age between 15 and 39 years, and the initial symptoms might include irregular, heavier periods that are more painful, reduced sex drive, vaginal discharge, pain when having sex, mood swings and insomnia. The low estrogen levels can also cause other complications such as osteoporosis, anxiety and depression (from the lower estrogen and possibly at the thought of infertility in young women).
The attack on the ovaries results in the destruction, wasting away (atrophy) and scarring of the ovarie, which reduces the production of the female hormones required to release eggs from the ovaries. Autoimmune Oophoritis can be a primary condition, or secondary to other autoimmune conditions such as Thyroiditis, Addison's Disease, Hypothyroidism, Diabetes, Myasthenia Gravis, Vitiligo and Pernicious Anemia. It is also commonly found in combination with inflammation of the fallopian tubes (Salpingitis). There is no cure, but it is treatable.
Symptoms:
Absence of period
Changes in mood
Difficulty falling asleep
Difficulty staying asleep
Heavy, long periods
Hot flashes
Infertility
Insomnia Irregular periods
Low sex drive
Night sweats
Pain when having sex
Severe menstrual cramps
Vaginal discharge
Diagnosis:
Diagnosis is usually based on the menstruation history combined with an elevated Follicle Stimulating Hormone (FSH) blood test.
Treatment:
The only treatment available is hormone replacement therapy, usually containing both estrogen and progestin hormones.
Prognosis:
With effective hormone replacement therapy, it is possible to to restore the hormone balance and return to a normal menstrual cycle. Untreated, Autoimmune Oophoritis will cause premature ovarian failure and eventually infertility.
The aim of the present study was to investigate whether dietary advanced glycation end-products (AGEs) can be detected in the ovarian tissue of normal female rats and whether they can affect their metabolic or hormonal profile. Sixty normal rats (20 animals in each group) were randomly assigned to regular diet, either high (H-AGE) or low (L-AGE) in AGE content for 6 months. H-AGE rats demonstrated higher levels of fasting glucose (P < 0.001), insulin (P < 0.069), and serum AGEs (P < 0.001) than control and L-AGE rats. Additionally, the H-AGE group showed increased AGE localization in the theca interna cells of the ovarian tissue compared to control/L-AGE rats (P = 0.003). Furthermore, increased receptor for AGE (RAGE) staining was also observed in granulosa cells compared to control/L-AGE samples (P = 0.038). In the H-AGE group, plasma testosterone was higher than in control rats (P < 0.001) and in the L-AGE group (P < 0.001). However, H-AGE rats did not exhibit higher body weight compared with normal (P = 0.118) and L-AGE-fed rats (P = 0.35). These results demonstrate for the first time that administration of high AGE diet in female rats for a prolonged period is associated with increased deposition of AGEs in the theca cells and of RAGE in the granulosa and theca interna cells of the ovarian tissue compared with the corresponding ovarian compartments of the control and L-AGE-fed animals. The metabolic alterations in conjuction with the increased deposition in ovarian tissues of dietary glycotoxins and elevated levels of testosterone in H-AGE-fed animals compared to the controls suggest an impact of environmental factors on ovarian tissue and these findings need further exploration.
First of all, we clearly see that PCOS is an autoimmune disease.
Before we go on any further, I need to go on a tangent. THIS STUDY WAS DONE IN ATHENS GREECE.
Greece is under attack by Wall Street through the use of Interest rate swaps and Credit default swaps. (My background isn't in medicine, it's in finance).
As we can clearly see here, Greece's bonds are way undervalued. This is incredibly sophisticated research, one that the researchers were free to conduct because they seemed to lack a conflict of interest between Big Pharma and doctors of medicine.
It was the Greeks who came up with the Hippocratic Oath.
The Modern Version:
I swear to fulfill, to the best of my ability and judgment, this covenant:
I will respect the hard-won scientific gains of those physicians in whose steps I walk, and gladly share such knowledge as is mine with those who are to follow.
I will apply, for the benefit of the sick, all measures [that] are required, avoiding those twin traps of overtreatment and therapeutic nihilism.
I will remember that there is art to medicine as well as science, and that warmth, sympathy, and understanding may outweigh the surgeon's knife or the chemist's drug.
I will not be ashamed to say "I know not," nor will I fail to call in my colleagues when the skills of another are needed for a patient's recovery.
I will respect the privacy of my patients, for their problems are not disclosed to me that the world may know. Most especially must I tread with care in matters of life and death. If it is given to me to save a life, all thanks. But it may also be within my power to take a life; this awesome responsibility must be faced with great humbleness and awareness of my own frailty. Above all, I must not play at God.
I will remember that I do not treat a fever chart, a cancerous growth, but a sick human being, whose illness may affect the person's family and economic stability. My responsibility includes these related problems, if I am to care adequately for the sick.
I will prevent disease whenever I can, for prevention is preferable to cure.
I will remember that I remain a member of society, with special obligations to all my fellow human beings, those sound of mind and body as well as the infirm.
If I do not violate this oath, may I enjoy life and art, respected while I live and remembered with affection thereafter. May I always act so as to preserve the finest traditions of my calling and may I long experience the joy of healing those who seek my help.
Dioscorides wrote a five-volume book in his native Greek,Περὶ ὕλης ἰατρικής, known in English by its Latin titleDe Materia Medica("Regarding Medical Materials") that is a "precursor to all modernpharmacopeias"."
Apparently the grounds to develop mathematical, medical and scientific achievements, cures, etc. were only possible under a democratic reign. Greece was the inspiration to the Romans who adopted their culture in a Republic, and we adopted many of Greeces' concepts to build the modern world in the U.S.
Pray for Greece. Wall Street is attacking it with subprime derivatives to get their assets for cheap, I feel that I owe Greece a world of thanks for a genuine understanding of this horrible problem and hopefully a cure for it. Remember, money is just a bartering tool. Money can't cure people, doctors, God and you can.
This study was done in NY?
"An examination of the literature indicates a strong likelihood
of thymus involvement in estrogen and/or testosterone-
induced anovulation in other animal species. For
example, Kincl et al. [24,25] reported that anovulation in
E2- and T-injected female rats could be prevented by thymocyte
infusion. Notably, only thymocytes from adult
donors were effective. Thymocytes from 5-day-old animals
did not prevent anovulation. In primates the thymus
undergoes its final development prenatally [7]. Steroid
action would thus occur in utero. This could explain why
injections of testosterone propionate (TP) given to pregnant
rhesus monkeys on gestational day's 40–55, produces
anovulatory female offspring [26,27]. The female
offspring have enlarged ovaries with multiple small follicles;
an elevated LH/FSH ratio; and, high levels of serum
17αOH-progesterone and testosterone.
Additional evidence of steroid influence in utero is
detailed in reports of the consequences of using DES in
pregnant women [28-35]. Prescribed from the 1940s until
1971, DES was banned by the FDA due to the large
number of reproductive problems in daughters exposed in
utero. Problems included an increased rate of primary
infertility, oligomenhorrhea, amenorrhea, high levels of
androstenedione and testosterone, facial hirsutism, and
an elevated LH/FSH ratio. These symptoms are all associated
with the formation of cysts [36,37]. Notably, exposure
to DES on gestational weeks 9 through 12 produced
the highest rate of infertility [35]. This timeframe is coincident
with the final developmental stages of the thymus
[7].
The identity of the self-antigen(s) that CD8+
Autoreactive T
cells regard as nonself, is at present, a matter for conjecture.
MECs synthesize approximately 300 ectopic tissue
proteins [20]. At least two are involved in autoimmune
disease. A peptide epitope of insulin initiates CD8+
Autoreactive
T cell destruction of pancreatic β cells [38], and zona
pellucida glycoprotein 3 (ZP3) is implicated as the selfantigen
involved in ovarian dysgenesis [39]. Synthesized
in the ovary by the oocyte and granulosa cells [40], ZP3 is
a prime candidate for the self-antigen involved in the formation
of follicular cysts. Destruction of granulosa cells
by CD8+
Autoreactive T cells would seriously impair the follicle's
capacity to synthesize estrogen. Restoration of this
ability might explain why injections of FSH cause ovulation
in clomiphene-resistant PCOS women without intervention
by either exogenous LH or hCG [41].
In conclusion: we have proposed that follicular cysts
formed in a popular animal model of PCOS represent an
autoimmune disease initiated by steroid administration.
An increased incidence of autoimmune disease in DESexposed
women [42], lends further support for the
autoimmune nature of PCOS. As maternally derived
androgens and estrogens diffusing into the fetal area are
limited by the amnion [43], and are normally at nanogram
levels, it is unlikely that this source of steroid causes
PCOS. The reproductive problems observed with DES
came from milligram levels [44]. Potential sources of steroids
at this level are phytoestrogens, contained in food
supplements and ingested by some pregnant women. The
Centers for Disease Control and Prevention, for example,
report that 10% of representative samples of women in
the United States contain urinary levels in the milligram
range, of phytoestrogens found in flax seed [45]. Flax seed
and soy bean products cause reproductive problems in
female rats [46] and mice [47], and mice suffer thymocyte
loss and thymic atrophy when given genistein, the phytoestrogen
contained in soy beans [47]. Our future
research will determine whether or not phytoestrogens
cause anovulation and follicular cysts when administered
to female mice during the thymus' critical period. We will
also be investigating the impact of adrenal corticoids.
While the bulk of this paper has concentrated on the role
of gonadal steroids, the observation that adrenal steroids
diminish thymic/spleen weight and numbers of thymocytes/
splenocytes (Table 2), and can instigate cyst formation
[6], raises the possibility that severe stress during
“We propose that in utero exposure to excessive levels of steroids such as estrogen has a long-term effect on the ability of the thymus to produce regulatory T cells. In female offspring this can lead to PCOS.”
Researchers from Binghamton University in New York published an article on 18 May 2009 in the Journal of Reproductive Biology and Endocrinology hypothesizing a new cause for PCOS.
Essentially they suggest, and their study supports, the theory that exposure of a foetus to high levels of steroids (such as eostrogen, testosterone or corticosteroids) whilst it is in utero may cause a cascade of auto-immune dysfunctions involving the thymus gland and it’s production of regulatory T-cells, eventually resulting in polycystic ovarian syndrome if the child is female. Sources of steroid exposure are likely to be from dietary phytoestrogens in the case of oestrogen or severe maternal stress whilst pregnant in the case of corticosteroids.
In the study, mice were injected with oestrogen at between 5 & 7 days old. This is known to cause anovulation and follicular cysts, a disease model that bears a similarity to PCOS in humans.
It is generally believed (but not proven) that this response is due to the hypothalamus responding to the excess oestrogen and a disruption in the GnRH delivery system.
This group of researchers, however, had a new idea which they sought to prove, namely that the anovulation and follicular cysts may be part of an immune response to the oestrogen and involving the thymus gland and it’s production of a specialised type of white blood cells called T cells and which help to fight infection or potential infection and also have a regulatory effect. High levels of oestrogen appear to prevent the thymus gland from producing fully developed regulatory T-cells. The absence of T-regulatory cells is known to cause a number of auto-immune diseases.
The researchers found that mice who had their thymus gland removed when they were 3 days old, prior to the injection of oestrogen, they did not develop follicular cysts and anovulation. When these mice later received an infusion from older mice who had been exposed to oestrogen, they found that the disease was transferable in a large percentage of the mice through the lymphocytes. Thus it would appear that the absence of regulatory T-cells is a prerequisite for the formation of follicular cysts.
The researchers concluded that exposure in utero to steroid hormones such as oestrogen or testosterone are unlikely to be derived from the mothers’ own hormones as these are usually only present in nanogram levels, whereas milligram levels are required to produce these effects. Therefore, the researchers hypothesize that it is more likely that these levels are achieved through the ingestion of phytoestrogens from the mothers’ diet, such as are found in soy and flaxseed products. Although it wasn’t covered in depth in the present study, the researchers highlighted that severe stress in pregnancy would raise levels of corticosteroids which are also known to negatively affect the spleen and thymus development of a foetus and the subsequent production of lymphocytes/thymocytes respectively.
A few more ideas on hormone control (I still have to research these):
HORMONES Estrogen (female hormone) and Testosterone (male hormone). This page is still under construction/research
UPDATE 12 minutes of Cardio Vascular Exercise a day (non-stop), be it mild walking, or more strenuous, will get the Adrenalin glands going, which in turn stimulate the Pituitary (master gland, which regulates the other glands). .
BLOOD TYPE AND DHEA (and hormones)
typo corrected: (blood type O and type A must not have Yams, type B and type AB may enjoy both Yams and Sweet Potatoes
1) DHEA helps both genders, and is available in most health food stores. It comes in various dosages, up to around 50 mg. And it naturally occurs in Yams and Sweet Potatoes. Blood type O and type A must not have Yams, type B and type AB may enjoy both Yams and Sweet Potatoes. DHEA helps both female and male hormones, very excellent stuff. I would start out with a pill supplement AND either Yams or Sweet Potatoes (depending on type), then discontinue the pills after a couple of months, maintaining the Yams/SweetPotatoes once or twice a week. . 2) For Estrogen (female hormone), Boron apparently helps. I (a male) get "Boron-ates" by Natures Plus vitamins for another reason, good for the bones. I don't take it every day, but Shari Liebermans "Real Vitamin & Mineral Book" advises it as good for Estrogen. . 3) Melatonin hampers Estrogen (female hormone), info source? (forgot where I got that info, I hope to ivestigate this further) Contrary to that image (even if slightly different), wikipedia.org says.... http://en.wikipedia.org/wiki/Melatonin#Fertility "Recent research has concluded that melatonin supplementation in perimenopausal women produces a highly significant improvement in thyroid function and gonadotropin levels, as well as restoring fertility and menstruation and preventing the depression associated with the menopause." I used to take Melatonin, to help me sleep. And as of April 2007 have restored my interest in Melatonin, initially for sleep, which led to better music the next morning (music with more depth, more meaning, more mystery, more inspirations). See my article on Melatonin at http://www.archure.net/minds/bonintel.html#melatonin The body naturally makes Melatonin, until around age 40 (thats why older people have a hard time sleeping), but I found that instead of replacing the bodies natural Melatonin with an artificial source, I could instead take DHEA to get my hormones going again, and it worked, made me quite horny of course, not that I wasn't to begin with, but I was then able to sleep. . 4) Sex also helps the hormones, as it stimulates the Hypothalamus, which stimulates the Pituitary, which stimulates the ovaries and testis, it sort of gets the whole Endocrine System revitalized (with the Pituitary being the key to the Endocrine system). Vitamin E supplements (400 IU to 800 IU, or even up to 1200 IU per day), is good for sexuality, which helps the Endocrine system. UPDATE: However, expert nutritionist Dr Shari Liberman says, in "The Real Vitamin and Mineral Book" that Vitamin E does NOT help anything to do with Sex. So I guess we can negate that common missunderstanding. HOWEVER, Vitamin E is very good for you, and very hard to get from Natural Sources (Vit A eat a carrot, Vit C eat an apple, Vit E drink 10 gallons of vegetable oil? no way). I stand coerrected
STILL IN DEBATE Vitamin E Update: a local Las Vegas doctor has advised me to limit my Vitamin E, as it can cause heart issues, I have investigated that claim, but have found nothing yet. I have read that Vitamin E deficiencies are rare, however, I think I have personally observed that less Vitamin E diminishes sexual function, so I am still investigating everything (perhaps the doctor or the study which the doctor refered to, was done by someone with a low libido?).
STILL TRUE: Sex is good for your health in general, in that it helps the Endocrine system, which maintains your body in many ways, not just sex. . 5) For everyone, and especially for Blood Type O persons (the most common type), get an Iodine supplement (liquid drops, seaweed, or pills, at your Health Food Store). The Iodine gets the Thyroid going, very important in type O blood types like myself. The Thyroid affects the Endocrine System (the bodies Glands, and they all interact directly or indirectly). 1,000 mcg/day of Iodine for blood type O, and 225 mcg/day for all other blood types. . 6) Low pH (acidity) attacks your organs, so easy on the Alcohol (and mix it with large quantities of water when you do drink), avoid all sodas, avoid orange juice and oranges; Do eat lots of raw vegetables (big salad daily), and drink lots of Water (not near a mealtime). This will increase your pH, helping your Endocrine system. . 7) ZINC (50 mg per day for men, while women need only 15 mg), creates Testosterone, the male hormone. A plate of oysters (sometimes toxic) has around 40 mg of Zinc, but you can just go to any store which sells vitamins (grocery, pharmacy, health food store), and get a 50 mg supplement (per day, for men). Its fairly inexpensive.
http://www.archure.net/salus/hormones.html
BLOOD TYPE
???
O = 45% of population 26% of PCOS A = 40% ............"...... 32% " " B= 11% ......... "....... 10% of PCOS AB= 4% ........ " ....... 5% " "
"Syndrome X is most common for Type As, followed by Type Bs. Individuals of these blood types often have more problems with elevated fasting blood sugar levels, impaired glucose tolerance, hypertension, and high cholesterol and triglycerides. Although no study exists, to my knowledge, I've observed an inordinately high incidence of Syndrome X in Type Bs of African descent, often leading to adult onset diabetes in this special group.
To add to the problem, high cortisol levels, seen in Type A and Type B, actually produce a very similar carbohydrate and lipid metabolism profile as that found in individuals with Syndrome X. These findings don't leave Type Os and Type ABs entirely off the hook,since certain foods will set a pattern of insulin resistance in motion. In fact, every blood type is vulnerable to Syndrome X, given a regular diet of the wrong foods, a sedentary lifestyle, and lack of exercise."
AMH has been synthesized. Its ability to inhibit growth of tissue derived from the Müllerian ducts has raised hopes of usefulness in the treatment of a variety of medical conditions including endometriosis, adenomyosis, and uterine cancer. Research is underway in several laboratories.
AMH assessment is also useful in fertility assessment as it provides a guide to ovarian reserve and identifies women that may need to consider either egg freezing or trying for a pregnancy sooner rather than later if their long-term future fertility is poor.[11] Measuring AMH alone may be misleading as high levels occur in conditions like polycystic ovarian syndromeand therefore AMH levels should be considered in conjunction with a transvaginal scan of the ovaries to assess antral follicle count.[12]
It also has the potential to rationalise the programme of ovulation induction and decisions about the number of embryos to transfer in assisted reproduction techniques to maximise pregnancy success rates whilst minimising the risk of ovarian hyperstimulation syndrome (OHSS) [13][14] AMH can predict an excessive response in ovarian hyperstimulation with asensitivity and specificity of 82% and 76%, respectively.[15]
I was able to get my estrogen balance down, My own TSH and FSH were low. Estrogen dominance causes all the fun, ranging from PCOS, Endometriosis and probably breast cancer too.
Since we need to combat the estrogen (with progesterone); it's probably a good idea to look at what's going to increase progesterone levels.
Improving Progesterone Balance So how can you improve these levels? The reality is that hormone therapy is only a small part of the process; the rest is up to you.
Saliva Hormone Level Imbalance Testing Kit 1. Exercise: Exercise is essential to maintaining good overall health and as it turns out in maintaining or increasing hormone levels when they are imbalanced. Get up and stay active to get your body to follow suit. 2. Eat Right: Eating more of foods that boost progesterone levels in the body can go a long way toward increasing progesterone levels. Foods such as walnuts, cherries, chicken, red meat, wild yams, soy milk, whole grains and herbs such as turmeric, oregano and thyme are all good progesterone boosters. 3. Get Your Vitamins: Zinc, magnesium and vitamins such as Vitamin B-6 and Vitamin C, are generally found to be lower in women who have low progesterone. Getting more of these vitamins in your diet and vitamin intake can help boost your levels. 4. Reduce Stress: The less stress there is in your life the less fluctuation your hormones will go through in your daily life. Lowering the damage that can occur from excess levels of cortisol and estrogen. 5. Stop Smoking: No seriously! Smoking has been shown to bring on premature menopause and increase infertility in younger women. The more you smoke and longer the higher risk there is to bring on these side effects. 6. Consider Hormone Therapy: Whether you use all natural methods or synthetics it’s important that you begin some sort of therapy to help balance your hormone levels, without it there’s a strong chance that the effects of hormonal imbalance will increase. 7. Try Natural Supplements: Chasteberry is one of several supplements you can get that may boost progesterone levels. 8. See Your Doctor: Seeing your doctor and getting your hormonal levels tested regularly are important to maintain desired levels as well as check up on the effectiveness of what you’re doing.
THIS is a good read: Caffine also depletes progesterone development. Car exhaust, petrol-chemical derived pesticides are just some examples of how these estrogen-like compounds can behave like estrogen once inside the body. http://www.drlam.com/articles/Jane_Story.asp?print=yes&page=3
I haven't had the ample time to dedicate to the blog and research, but I'm still running across evidence of links between inflammation and PCOS.
Some women with PCOS have other signs of inflammation (as written in one of my former blogs)., one being Lupus.
Association of estrogen receptor alpha gene polymorphisms with cytokine genes expression in systemic lupus erythematosus
Abstract
AIM:
To analyze the association of estrogen receptor alpha (OR alpha) gene polymorphisms with cytokine genes expression in patients with systemic lupus erythematosus (SLE) and controls.
METHODS:
Genomic DNA was extracted and polymorphisms of XbaI, Ukrainian (XX, Xx, or xx genotype) and PvuII (PP, Pp, or pp) in intron 1 of OR alpha gene were detected by polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) method. The messenger RNA (mRNA) levels of interleukin (IL)-10, IL-4, interferon (IFN)-gamma, and IL-2 were assessed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR).
RESULTS:
In patients with SLE with PpXx genotype, IL-10 and IL-4 mRNA expression was higher (P < 0.001 and P = 0.013, respectively), while in patients with SLE with Ppxx genotype IFN-gamma and IL-2 mRNA expression was lower than in controls (P < 0.001). There was no significant difference in mRNA expression of 4 cytokines among controls with various genotypes.
CONCLUSION:
OR alpha gene polymorphism may be associated with the expression of IL-10, IL-4, IL-2, and IFN-gamma in patients with SLE.
Estrogen Receptor Signaling and Its Relationship to Cytokines in Systemic Lupus Erythematosus E. Kassi1,2 and P. Moutsatsou1 1Department of Biological Chemistry, Medical School, University of Athens, 75 M. Asias, Goudi, 11527 Athens, Greece 2Laboratory of Clinical Biochemistry, “Attikon” University General Hospital, 1 Rimini, Haidari, 12462 Athens, Greece
Received 15 January 2010; Revised 18 March 2010; Accepted 31 March 2010
Dysregulation of cytokines is among the main abnormalities in Systemic Lupus Erythematosus (SLE). However, although, estrogens, which are known to be involved in lupus disease, influence cytokine production, the underlying molecular mechanisms remain poorly defined. Recent evidence demonstrates the presence of estrogen receptor in various cell types of the immune system, while divergent effects of estrogens on the cytokine regulation are thought to be implicated. In this paper, we provide an overview of the current knowledge as to how estrogen-induced modulation of cytokine production in SLE is mediated by the estrogen receptor while simultaneously clarifying various aspects of estrogen receptor signaling in this disease. ...
Although estrogens have been proposed as obvious candidates to explain this sexual dimorphism [17], measurement of plasma estradiol levels did not reveal significant differences between normal women and women with SLE; nevertheless, abnormal levels of estrogenic metabolites have been identified in the latter. These metabolites include 2-hydroxy- and 16-hydroxyestrone and their derivatives produced by the enzymatic oxidation of estrogen. Additionally, pregnancy is frequently associated with flares of the disease in SLE patients [17]. Of note, pregnancy can disturb the balance in favor of the highly feminizing 16-hydroxy metabolites, thus predisposing to SLE, while exercise or consuming specific foods that inhibit the 16-hydroxylase can have opposite effects [18]. ...
SLE is characterized by numerous immune system disturbances including alterations in cytokine regulation. Estrogens are known modulators of immune system functions, influence cytokine production and are involved in the lupus disease process. Accumulating evidence on the molecular and cellular actions of estrogens via the estrogen receptor subtypes ER and ER adds to the depth of our understanding of estrogen-estrogen receptor mediated signaling. Both estrogen receptor proteins have been detected in immune cells, while increasing information points to their possible involvement in cytokine expression. However, in spite of the clinical significance of the estrogen-induced changes in cytokine production in SLE disease, many of the key elements in the underlying molecular mechanisms remain largely unknown. Existing data show an estrogen receptor-mediated effect in the production of cytokines and other cytokine regulatory molecules (such as calcineurin and CD40L) in humans and animal models of SLE disease. A possible correlation of ER gene polymorphisms and of quantitative and qualitative changes in the receptor proteins to cytokine production and to disease aetiopathogenesis have also been reported. Clearly, further elucidation of ER signaling in SLE awaits characterization of the interactions of ER with the many other intracellular molecules and/or its interplay with other signaling pathways.
Recent evidence indicates a role of estrogens in mitochondrial function in immune cells along with cytokine regulation, while the existence of mitochondrial ER in human cells has been associated with stimulation of mitochondrial encoded enzymes."
http://www.hindawi.com/journals/jbb/2010/317452/
"BACKGROUND: Recent research shows that polycystic ovary syndrome (PCOS) may have an association with low-grade chronic inflammation, and that PCOS may induce an increase in serum interleukin-18 (IL-18) levels. [2010]"
"This article reviews the literature available on the role of T helper cytokines and IL-1, IL-11 [?], LIF [?], IL-12 and IL-18 in infertility and recurrent miscarriage, with particular emphasis on the role that endometrial cytokines may play. [2006]" http://www.ihop-net.org/UniPub/iHOP/gs/89488.html
We aimed to study if the changes observed in the insulin sensitivity of PCOS patients during treatment with oral contraceptives or metforminassociate changes in the serum inflammatory markers interleukin-6 (IL-6) and interleukin-18 (IL-18). [2010]
Fast Facts An imbalance in thyroid and adrenal hormones, testosterone, the estrogen’s (estrone, estradiol, estriol), and progesterone can affect the immune system.
Our chemical environment (xenoestrogens) and nutrition are both contributing factors to hormone imbalance “A hormone is a chemical substance which is produced in one location of the body and travels to another to convey, create, or generate a response”. Dr. Jesse Stoff (M.D.).
It’s also important to note that no hormone works in isolation from other hormones; they all function within a complex, subtle web of interconnectedness. Reference: Dr. John Lee Many hormones have an effect on the immune system, disease and each other.
Thyroid Hormone Imbalance and the Immune System “Thyroid hormone stimulates the activity of Natural Killer (NK) cells [cells in the immune system].” Dr. Jesse Stoff
What nutritional element does the thyroid need to function? Iodine. Janice Wittenberg, RN states that “Iodine in particular is important to the production of the thyroid hormone. Low to sub-clinical [not measurable through testing] thyroid function is very common. Soils in the mid-west and areas along the St. Lawrence have the lowest iodine concentrations and largest number of thyroid related problems in the world."
“Estrogen inhibits thyroid hormone activity and thus exacerbates thyroid deficiency. In contrast, progesterone, cortisol, and testosterone are thyroid allies.” Dr. John Lee
The most common symptoms (there are many) of a low functioning thyroid are fatigue and intolerance to cold according to Dr. James Balch.
Adrenal Glands and the Immune System Janice Wittenberg R.N. in her book, "The Rebellious Body", comments on adrenal glands by saying that they can, as a result of stress and nutritional deficiencies, produce hormones that inhibit the production of prostaglandins that interfere with immune response.
These hormones also deplete thymus [immune system] function. The thymus gland is responsible for training an immune system cell grouping called T cells. She says pantothenic acid is particularly important in strengthening the adrenals among other things. The hormone produced in excess is cortisol.
Testosterone, Estrogen & Progesterone - hormone balance The hormones testosterone, progesterone and estrogen can be found in both men and women, just in different amounts.
Estrogen is getting a lot of attention and rightly so as it’s a powerful hormone and found everywhere. Testosterone and progesterone balance its effects.
According to Dr. John Lee, MD, estrogen is a word that encompasses a class of three hormones; estrone, estradiol and estriol. It’s not one hormone. Of the estrogens, estradiol is the strongest and estriol is the weakest.
Estrogens come from different places. First, they are produced by the body in both men and women. Second, plants produce compounds with estrogen like qualities. They’re called phytoestrogens.
Xenoestrogens refer to the third kind which are environmental compounds (usually petrochemicals) and can be found everywhere – like in pesticides, meats or plastics.
The fourth kind are chemical estrogens made by pharmaceutical companies for use in things like hormone replacement therapy. Dr. Peter J. D’Adamo states that chemical estrogens are based on estradiol, the strongest, while phytoestrogens or plant based estrogens, are typically high in estriol, the weakest.
Estrogen Dominance Upsets Hormone Balance Estrogen dominance is a term that can apply to both women and men. It’s described by Dr. John Lee as “a condition where a woman can have deficient, normal, or excessive estrogen but has little or no progesterone to balance its effects in the body.”
He further states, “ A key to hormone balance is the knowledge that when estrogen becomes the dominant hormone and progesterone is deficient, the estrogen becomes toxic to the body…”
Progesterone is the “antidote” to the harmful effects of estrogen creating greater hormone balance. While a correct hormone balance between estrogen and progesterone is particularly important to women, it’s also important to men and just used in smaller amounts.
Testosterone for men also helps protect against the harmful effects of estrogen and the hormone imbalances it causes.
"The Hormone Replacement Debacle" by John Lee M.D. "xProstate Cancer Survival, Testosterone & Estrogen" by John Lee M.D.
Hormone Imbalance Causes 5 yr. Olds to Grow Breasts & Pubic Hair Hormone imbalance is not a small problem. The following is one example of what estrogens can do:
A couple of years ago, a clinic in Montana had several 5 year old girl patients who were developing breasts and exhibiting other signs of physical maturity way beyond their age.
After investigating the situation, the clinic director discovered that all the girls' families bought milk from the same dairy. It was then discovered that the advanced physical development these girls were experiencing were due to the hormones used in the dairy products.
This caused a hormone imbalance because the estrogen levels were too high. This is not isolated to Montana. This is a growing problem in this country and could be one of the causes of overweight children and adults as well.
Some of the things estrogen, testosterone and progesterone do with reference to the immune system and disease are as follows:
Estrogen, Progesterone and the Immune System Dr. Willian Hrushesky believes that natural killer cell activity and interleukin 2, both powerful immune system components, are compromised by estrogen dominance and promoted by adequate progesterone. His opinions were presented in the Journal of Women’s Health.
Dr. John Morrow, PhD and Dr. David Isenberg PhD say that estrogen has been shown to decrease the size of the thymus [depresses immune system] and to cause a reduction in the level of thymic hormone in the blood.
They also say it has been shown that the level of thymic hormone is markedly decreased in the blood of women who are either post-menopausal or who have had their ovaries removed and are undergoing estrogen therapy.
Estrogen, Progesterone and Cancer Dr. David Zava tested estrogen and progesterone levels in breast tissue specimens from several thousand women who had undergone breast cancer surgery. “Almost universally, they revealed a deficiency in progesterone relative to estrogen.”
John’s Hopkins published a study that showed that “the breast cancer incidence was 5.4 time greater in women with low progesterone than in women who had good progesterone levels…when the incidence of all types of cancer was looked at, they found that the incidence was 10 fold higher in women with low progesterone levels compared to women with good progesterone levels.”
“Estrogens in general tend to promote cell division, particularly in hormone sensitive tissue…” says Dr. John Lee. He also says that on a “gene” level, two genes figure prominently, Bcl-2 and p53. Bcl-2 production promotes cell proliferation (cancer). It is stimulated by estrogen. On the other hand, activation of gene p53 activated by progesterone, inhibits Bcl-2 shutting down cell proliferation.
Dr. Lauren Sompayrac states, “One indication of the importance of p53 (see above) is that this anti-oncogene is not activated in a large proportion of human tumors”. P53 is activated by progesterone according to Dr. John Lee.
Hormone Imbalance and Autoimmune Disease Drs. .Morrow and Isenberg also state, “There is little doubt that oral contraceptives, especially those with moderate or high doses of estrogen, can exacerbate or even induce a relapse of quiescent [latent, dormant] autoimmune disease.
” In addition they explain, “There are some reports of high estrogen levels in both females and males with this disease [lupus].
Male patients with lupus have also been shown to have lower levels of the male sex hormone testosterone.” Dr. John Lee also states that recent studies have shown that “women who use hormone replacement therapy containing estrogen are more likely to get lupus.”
Dr. John Lee says that “ Women are afflicted with autoimmune diseases at a much higher rate than men, which is a good clue that female hormone balance in involved in some way. …The onset of autoimmune disorders is often in middle age, when estrogen dominance becomes common.”
His conclusions are that estrogen dominance may have a hand in triggering the problem and thus correcting the estrogen dominance leads to gradual correction of the problem.
Or, since progesterone is the main precursor of corticosteroids, and in progesterone deficient women, restoration of normal progesterone levels may enhance normal corticosteroid production, thus suppressing the autoimmune attack. http://immunedisorders.homestead.com/Hormones.html
Both Endometriosis and Poly-cystic Ovarian Syndrome are caused by Estrogen Dominance.
This page demonstrates why insulin resistance is only part of the problem. Not the problem.
Note: cutting sugar will only help you feel better. It will not cure estrogen dominance. You need to cut out transfats (IN PROCESSED FOODS), eat omega 3's, Vitamin B's, and bromelain (enzyme in pineapples).
Like previously mentioned, cutting out sugar isn't enough.
First of all, without these T-cells, none of these ovarian cysts would happen. (I can't make this up.)
"A study of female mice is suggesting that ovarian cysts may at least partially be the result of an immune system dysfunction. The gland involved is the thymus gland, which is responsible for the management of major aspects of your immune system. One of the functions of the thymus gland is to produce T-cells, which are white blood cells that help protect you from infection and also perform other important activities.
The researchers reported that ovarian cysts in the female mice did not develop unless there was an absence of regulatory T-cells." http://www.ovarian-cysts-pcos.com/news81.html
The cellular biology is complex but this is incredibly good research. Diet is our only defense against it at this time, however if Big Pharma figures out how to combat the cause of inflammation, their products will be demand inelastic. It may be a bigger hit than a cancer cure.
Inflammatory issues and auto-immune disease are not limited to PCOS, inflammation also contributes to things like allergies (think about those sinuses) and celiac disease which is very common in women with PCOS.
NOTES:
PROSTAGLANDINS
Prostaglandins are like hormones in that they act as chemical messengers, but they do not move to other places in the body. They work right within the cells where they are made.
- any of a group of about a dozen compounds synthesised from fatty acids in mammals as well as in lower animals. Prostaglandins are highly potent substances that are not stored but are produced as needed by cell membranes in virtually every body tissue. Different prostaglandins have been found to raise or lower blood pressure and regulate smooth muscle activity and glandular secretions. One such substance, which stimulates contraction of the uterus, is used clinically to induce labour; another has been in experimental use as a birth control agent. Prostaglandins also control the substances involved in the transmission of nerve impulses, participate in the body’s defences against infection, and regulate the rate of metabolism in various tissues.
Several prostaglandins have been shown to induce fever, possibly by participating in the temperature-regulating mechanisms in the hypothalamus; they also play a part in inflammation. Many naturally occurring prostaglandins as well as many artificial forms have been synthesised in the laboratory
Chemical Messengers
Prostaglandins vary somewhat from one another based upon subtle differences in their chemical structures. These small variations are believed to be responsible for the immense diversity of effects they have on the body. In general, prostaglandins act in a manner similar to that of hormones, by stimulating target cells into action. However, they differ from hormones in that they act locally, near their site of synthesis, and they are metabolised very rapidly. Interestingly, thesame prostaglandins act differently in different tissue. (The in-built intelligence of the human body, that we will never understand)!
FUNCTION OF PROSTAGLANDINS
- Activation of the inflammatory responses at the sites of damaged tissue, and production of pain and fever. When tissues are damaged, white blood cells flood the site to try to minimise tissue destruction. Prostaglandins are produced as a result.
- Blood clots form when a blood vessel is damaged. A type of prostaglandin called thromboxane stimulates constriction and clotting of platelets. Also the opposite happens and protastaglandin 12 (PG12) is produced on the walls of blood vessels where clots should not be forming. ( The body is very, very clever. It knows what to do, where to do it and when.)
(Does anyone have Factor 2 or Factor 5 type blood? This might be WHY!)
- Certain prostaglandins are involved with the introduction of labour and other reproductive processes, and the role of fertility. PGE2 causes uterine contractions and has been used to induce labour.
- Prostaglandins are involved in several other organs and systems such as the gastrointestinal tract, cell growth and the immune system response.
Prostaglandins are a subset of a larger family of substances called eicosanoids
Other subgroups include thromboxanes, leukotrienes and lipoxins (just out of interest!)
Eicosanoids are localised tissue hormones that seem to be the fundamental regulating molecules in most forms of life
Prostaglandins are chemical mediators, or ‘local’ hormones. Whereas hormones circulate in the blood stream to influence distant tissues, prostaglandins act locally on adjacent cells
Prostaglandins serve as a catalyst for a large number of processes including -the movement of calcium and other substances into and out of cells (it's said that calcium and Vitamin D helps the uterus with contractions, Notice the mention of control of insulin release and elimination of bad free radicals in this source. Free Radicals contribute to inflammation.) -dilation and contraction -inhibition and promotion of blood clotting -regulation of secretions including digestive juices and hormones -control of fertility -cell division -growth
Prostaglandins are produced in the cells by the action of enzymes on essential fatty-acid
THE SERIES 1 and SERIES 2 PROSTAGLANDINS
Series 1 prostaglandins have the opposite effect of the Series 2 prostaglandins. Series 1 reduce inflammation, dilate blood vessels, and inhibit blood clotting. The strong anti-inflammatory properties help the body recover from injury by reducing pain, swelling and redness. -Beneficial prostaglandins are made from a fatty acid found mostly in marine plants and fish known as EPA (eicosapentaenoic acid) -EPA is the most important member of an exclusive group of three fatty acids called the "omega-3 fatty acids" -OMEGA-3 FATTY ACIDS - includes alpha linoleic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)
Series 2 prostaglandins play a role in swelling and inflammation at sites of damage or injury. They also play a role in inducing birth, in regulating temperature, lowering blood pressure, and in the regulation of platelet forming and clotting. The role of Series 2 Prostaglandins does serve a vital role for the body for without it you would bleed to death from the slightest cut. However, in excess, these prostaglandins are harmful and many diseases are directly linked to excessive inflammation and blood clotting. The Series 2 group is involved in intense actions, often in response to some emergency such as injury or stress. The Series 3 group has a modulating effect.
The Series 3 prostaglandins are formed at a slower rate and work to deal with excessive Series 2 prostaglandin production.
‘Antagonistic Prostaglandins’ - in simple terms this means unfriendly prostaglandins.
Antagonistic prostaglandins are made from a fatty acid called arachidonic acid. Aracidonic acid is obtained from animal products - meat and dairy. Arachidonic acid can also be made from another fatty acid linoleic acid, through the animal food chain consumption Linoleic acid is a fatty acid found in plant oils, such as corn oil, soybean oil, and other light vegetable oils. We also obtain linoleic acid from meat and dairy products (because the animals eat plants and store Linoleic acid)
Alpha Linoleic Acid (ALA)
-on ALA-it's made in the chloroplasts of green plants from linoleic acid.
-In mammals, linoleic acidis converted to arachidonic acid that is used to make the antagonistic prostaglandins.
-BUT, in the green plant the same linoleic acid is converted into the beneficial ALA -ALA is important because it serves as the building material for EPA
Eicosapentaenoic Acid (EPA)
-EPA is the most critical of the omega 3 fatty acids. It is the only material that our bodies use to make the beneficial prostaglandins that help reduce inflammation
Docosahexaenoic Acid (DHA)
-DHA is another omega 3 fatty acid. It is an integral part of eye and brain tissue.
-It is made by marine algae, plankton, fish and mammals from EPA. Fish accumulate DHA in their oily tissue, along with EPA
Oleic Acid (EFA)
-found chiefly in olive oil and nuts
-will inhibit the prostaglandin pathway. But the block being set up is one which will inhibit the Series 2 prostaglandins (the ones which cause inflammation and swelling).
-Which is why women with endometriosis are advised to change the oil in their diet to only include the oils which will block Series 2.
Evening Primrose Oil
Fish Oils
Flax seed oil
Borage oil
ASPRIN- a non-steroidal anti-inflammatory, was discovered over 100 years ago.
It works by blocking prostaglandins that are produced in inflamed or injured tissues and cause the sensation of pain. It also acts centrally: the salicylate and acetate parts of aspirin's chemical structure (aspirin is acetyl salicylic acid) cross separately into the brain and spinal cord. There they act on prostaglandins in sites in the central nervous system known to be involved in both the perception and transmission of pain.
Prostaglandins are released by the endometrium during the menstrual cycle. Some women release more prostaglandin during menstruation than other women. These higher levels of prostaglandins in women with severe dysmenorrhea (painful periods) results in increased uterine contractions and muscular spasm.
"I define an activated essential fatty acid as any essential fatty acid that has this new double bond inserted by the delta-6-desaturase enzyme. This is because this new double bond starts bending the essential fatty acid to get the appropriate spatial configuration required to make an eicosanoid. Once this new double bond has been inserted into a short-chain essential fatty acid, then very small amounts of these activated essential fatty acids can profoundly affect eicosanoid balance in your body.
However, there are many factors that can decrease the activity of delta-6-desaturase enzyme. The most important factor is age itself. There are two times in your life during which this enzyme is relatively inactive. The first is at birth. For the first six months of life, the activity of this key enzyme in the newborn is relatively low. But this is also the time at which maximum amounts of long-chain essential fatty acids are required by the child since the brain is growing at the fastest possible rate, and these long-chain essential fatty acids are the key structural building blocks for the brain. Nature has developed a unique solution to this problem: mother's breast milk. Breast milk is very rich in GLA and other long-chain essential fatty acids such as the EPA and DHA. By supplying these activated essential fatty acids through the diet, this early inactivity of the delta-6-desaturase enzyme is overcome.
The second time in your life during which the activity of this enzyme begins to decrease is after the age of 30. Eicosanoids are critical for successful reproduction. Since the primary child-bearing years for women are between the ages of 18 and 30, it makes good evolutionary sense to start turning down the activity of a key enzyme needed to make the precursors of eicosanoids required for fertility after age 30.
The delta-6-desaturase enzyme can also be inhibited by viral infection. The only known anti-viral agents are "good" eicosanoids such as PGA1 because of their ability to increase cyclic AMP levels that keep viral replication under control. On the other hand, if you are a virus, then your number-one goal is to inhibit the formation of this type of eicosanoid. This is exactly what many viruses do by inhibiting the delta-6-desaturase enzyme. By doing so, the virus has devised an incredibly clever way to circumvent the body's primary anti-viral drug (i.e. PGA1).
The final factor that can decrease the activity of delta-6-desaturase is the presence of two types of fatty acids in your diet; trans fats and Omega-3 fats. Trans fatty acids don't exist naturally but are produced by food manufacturers. They are essential Omega-6 fatty acids that have been transformed by a commercial process (known as hydrogenation) into a new spatial configuration that is more stable to prevent oxidation.
The increased stability of these fatty acids makes them ideal for processed foods, but also makes trans fatty acids strong inhibitors of the delta-6-desaturase enzyme. Trans fatty acids occupy the active site of the delta-6-desaturase enzyme, thus preventing the formation of the activated essential fatty acids required for eicosanoid synthesis. In essence, trans fatty acids can be viewed as anti-essential fatty acids because of their inhibition of eicosanoid synthesis. This may be the reason why they are strongly implicated in the development of heart disease. How do you know if a food product you're consuming contains trans fatty acids?..... "It wasn't that insulin was a cause, but that it drove the metabolism of essential fatty acids to make more arachidonic acid, and therefore more "bad" eicosanoids. The more "bad" eicosanoids you make, the more likely you will promote platelet aggregation and increased vasoconstriction, the underlying factors for a heart attack."
AGAIN EVIDENCE. METFORMIN WILL NOT CURE ESTROGEN DOMINANCE OR PCOS.
BACK TO THE ORIGIONAL ARTICLE:
Prostaglandins and inflammation
Prostaglandins are known as local hormones - they are released from cells and bring about changes in neighbouring cells that carry specific prostaglandin receptors in their membranes.
The influence which prostaglandins have depends upon the type of tissue they are acting upon. Such action may be direct, or as a result of modifying the actions of other signalling molecules.
As well as signalling and influencing pain messengers to the brain, prostaglandins will interact with other chemicals in the body when there is damage. They will also intensify the effects of other chemical mediators such as histamine.
Acting in concert these substances can bring about vasodilatation and an increase in the permeability of capillaries supplying the damaged area, encouraging the migration of phagocytes (Phagocytes are leukocytes - white blood cells - that engulf invading micro-organisms, and then kill them. They are part of our natural defence against infection ) from the blood through capillary walls into the damaged tissue. As a result of these changes, the blood supply to the area increases, the tissues swell, causing inflammation and pain subsequently occurs.
Phagocytes in more detail
Phagocytes are large white cells that can engulf and digest foreign invaders.They include monocytes, which circulate in the blood, and macrophages, which are found in tissues throughout the body, as well as neutrophils, cells that circulate in the blood but move into tissues where they are needed. Macrophages are versatile cells; they act as scavengers, they secrete a wide variety of powerful chemicals, and they play an essential role in activating T cells (part of your immune system).
Neutrophils are not only phagocytes but also granulocytes: they contain granules filled with potent chemicals. These chemicals, in addition to destroying micro-organisms, play a key role in acute inflammatory reactions.
There are two main types of phagocytes: neutrophills and macrophages.
Neutrophils:
Are made in bone marrow throughout life.
Make up 60% of white blood cells.
Travel through the blood.
Are short lived.
Squeeze through capillary walls to patrol tissue.
Released in large numbers during infection.
Dead neutrophils make pus.
Macrophages:
Are made in bone marrow throughout life.
Leave bone marrow and travel in blood as monocytes.
Are longer lived than neutrophils.
Are found in organs such as: lungs, liver, kidney, spleen, lymph nodes.
Prostaglandins and womb contractions
Primary dysmenorrhoea (painful periods) is caused by cramping in the uterine muscles — the uterus is a muscle and like all muscles it contracts and relaxes! Women don’t usually feel these muscles contract, unless it is a particularly strong contraction. With endometriosis the pain associated with menstrual cramps is usually very intense and painful. During a contraction, blood supply to the uterus can be temporarily cut off. This deprives the muscle of oxygen, which causes pain. But why do the uterine muscles contract?
It is caused by the series two prostaglandins. Series two prostaglandins help the uterus to shed the womb lining during menstruation by causing the contraction of the uterine muscles. Understandably, if too many of these prostaglandins are produced, then the contractions will be more severe and cause painful menstrual cramps — primary dysmenorrhoea.
However, not all prostaglandins have this effect on the involuntary uterine muscles, which is why diet can play a big role in minimising the production of series two prostaglandins. The types of fatty acids included in your diet influence the types of prostaglandins made. For example, series two prostaglandin (the type that trigger powerful contractions of the uterus) levels are increased when animal fat is included in the diet. In contrast, series one and series three prostaglandins (the type that don’t cause uterine contractions) are produced when the diet is higher in linoleic acid, which is found naturally in tuna and salmon oil. Evening primrose oil and starflower oil are also rich sources of linoleic acid, which is why they are often recommended for women suffering from period cramps and are especially helpful for women with endometriosis.
Prostaglandins and infertility
I have to pause right there. This is incredibly good information so far. Now we know that both PCOS and Endometriosis are both caused by Estrogen Dominance?
The progtaglandins' relationship with Progesterone is where it gets interesting.
We have concluded that the progressive decline in prostaglandin production and the rise in progesterone output from luteinizing human granulosa cells occur independently of each other.
It was concluded that the co-operation of progesterone in theearlier stage and of prostaglandins in the later stage of thepreovulatory interval is required to mediate the action of hCGon ovulation.
"One major group of hormones secreted by the normal endometrium is that of prostaglandins. Prostaglandins are required for many bodily processes, including several stages of the menstrual cycle and pregnancy.
Prostaglandins are required for ovulation, regression of the corpus luteum (i.e., ending the monthly menstrual cycle), sperm motility, immune interaction, contraction of the uterus at birth and menstrual cramps. Endometrial implants and the endometrium of the uterus are the richest source of prostaglandin production in the body.
However, the problem with endometrial implants includes:
- Prostaglandins are released into the abdomen instead of inside the womb - Prostaglandins release by the implants seem to be out of phase with their release by the uterus - Prostaglandins are produced at the wrong time sending the wrong message
For instance, there is a normal surge in prostaglandin F production at the end of the menstrual cycle, causing the effect of the corpus luteum of the ovary to die down and signalling the start of a new menstrual cycle. The implants of endometriosis produce their own prostaglandin surge several days after that of the womb lining. This may be one of the main causes of very early miscarriage.
If a women is a few days pregnant then the endometriosis implants producing prostaglandin F would incorrectly signal the ovary to start a new menstrual cycle, causing the womb lining with the implanted egg to be expelled - and the consequence is an early miscarriage.
Prostaglandins also play an important role in the contractions of womb and fallopian tubes. During the normal menstrual cycle, the gentle contraction of the womb and fallopian tube aids the movement of egg and sperm to the outer third of the fallopian tube where fertilisation occurs. High concentrations of endometriosis implants may prevent fertilisation. An excess of PGF2 and PGE2 could cause contractions that are too strong and expel the egg too quickly.
Prostglandins and Diet
You should all have had it ‘drummed into you’ by now that the KEY way to shift the production of prostaglandins from the negative (inflammatory / pain messenger / womb contracting type) to the positive (anti-inflammatory / suppress womb contractions and pain messenger type), is through your diet, and most crucially by the types of fats and oils you include in your diet.
Several enzymes take part in the process that transforms fats into prostaglandins. These enzymes act as gatekeepers, channelling fats into the making of different prostaglandins. Like other enzymes in the body, they require specific nutrient coenzymes to do their job.
The enzyme delta-6-desaturase acts on linoleic acid - from most vegetable, nut and seed oils - to transform it to gamma-linoleic acid (GLA). GLA is used to make the anti-inflammatory series 1 prostaglandins and also supports healthy nervous system function.
The activity of delta-6-desaturase is affected by dietary factors. Trans-fatty acids from hydrogenated oils, too much saturated fat (found in meats, fried foods, junk foods and dairy products) in the diet, high stress, too much sugar or refined flours in the diet all slow down this enzyme down.
Trans-fatty Acids
Many processed foods contain trans-fatty acids. These fats slow down the activity of delta-6-desaturase. They are manufactured from vegetable oils in a process called hydrogenation, which involves the bombardment of liquid oils with hydrogen atoms to make them solid and prevent them going rancid.
These trans-fats have harmful effects on the stability of cell membranes and the structure of nerve and brain cells. They also interfere with the formation of anti-inflammatory prostglandins.
B Vitamins
The B vitamins are crucial for the conversion of linoleic acid to GLA, which is necessary to produce beneficial prostaglandins. Linoleic acid is an essential fatty acid (EFA), and it is found in foods such as fresh nuts and seeds, safflower oil, and Evening Primrose Oil.
The B vitamins are required to convert this essential oil into a form that can be used by the body to produce the good prostaglandins.
Bromelain and prostaglandins
The enzyme bromelain from the stem of the pineapple, is also effective in inhibiting the inflammatory prostaglandins. In an extensive five-year study of more than 200 people experiencing inflammation as a result of surgery, traumatic injuries and wounds, 75 percent of the study participants had good to excellent improvement with bromelain; a much higher rate than that afforded by drugs. Most of the people in this study were discharged from the hospital in only eight days—half the usual amount of time. They also experienced no side effects.
To conclude ….
Along with hormones, these are very powerful and complex substances and can be easily influenced by outside factors through diet. It could be that our emotions as well as stress could alter and influence the way these natural bodily chemicals work. Many of us have felt and witnessed the changes in our hormones brought about by stress and emotions.
‘You are what you eat’ - we have all heard that phrase. Our bodies react to what we eat. It sometimes seems incredible that the body can differentiate between the chemical and molecular structure of 2 different oils (its only food!) - but our bodies are very clever and NOTHING goes unnoticed. It may not show up immediately, but if you feed your body with things it does not like or need, eventually you will get signals.
Fortunately, due to huge advances in understanding the body and how it works, we now have a better awareness how correct diet is crucial to the health of the body. And women with endometriosis can take advantage of the discoveries and knowledge about the role of diet in controlling their symptoms and shifting the levels of prostaglandins from the bad ones to the good ones.
As it is mentioned above - we do need prostaglandins - both types - they are all part of the complex and intricate orchestra of the body. But it does seem apparent from research that women with endometriosis are producing too many of the negative prostaglandins, which is the cause of many symptoms.
If you take these findings on board then you are part way to taking control of this disease, rather than IT taking control of you."
Acronyms
AA
Arachidonic acid
COX
Cyclooxygenase
DHET
Dihydroxyeicosatrienoic acid
EET
Epoxyeicosatrienoic acid
HETE
Hydroxyeicosatetraenoic acid
HPETE
Hydroxyperoxyeicosatetraenoic acid
LTB, LTC
Leukotriene B, C, etc
LOX
Lipoxygenase
LXA, LXB
Lipoxin A, B
NSAID
Nonsteroidal anti-inflammatory drug
PGE, PGF
Prostaglandin E, F, etc
PLA, PLC
Phospholipase A, C
TXA, TXB
Thromboxane A, B
"REPRODUCTIVE ORGANS
Female Reproductive Organs
"Animal studies demonstrate a role for Prostaglandin E2 and Prostaglandin F2 in early reproductive processes such as ovulation, luteolysis, and fertilization. Uterine muscle is contracted by Prostaglandin F2, ThromboxaneA2, and low concentrations of Prostaglandin E2; PGI2 and high concentrations of Prostaglandin E2 cause relaxation. Prostaglandin
F2, together with oxytocin, is essential for the onset of parturition. The effects of prostaglandins on uterine function are discussed below (see Clinical Pharmacology of Eicosanoids)."
and ER
in early reproductive processes such as ovulation, luteolysis, and fertilization. Uterine muscle is contracted by