March 2014 - Page 2

Endometriosis Research and Lipoxin A4: A Biologist’s Perspective

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Geraldine Canny

My scientific training is in mucosal immunity and I have been interested in lipids which help to dampen inflammation in the body for over a decade. One of these anti-inflammatory lipids is called Lipoxin A4. Some such lipids are made at sites of inflammation and others are metabolized from fats taken in the diet. Inflammation is a natural response to a wound or an infection and should stop or “be resolved”. Otherwise, inflammation becomes chronic, surrounding tissue becomes damaged and dysfunctions occur, which can manifest in symptoms such as pain. Inflammation was first described many centuries ago but we still do not understand how it resolves. This is a fascinating field and deserves more attention as it could help further our understanding of major chronic diseases, including diabetes type 2, obesity, cardiovascular disease, cancer and endometriosis. However, inflammation is necessary for implantation to occur and it is also an integral part of menstruation, when the endometrium (lining of the uterus) degrades and is shed. Such processes must involve the resolution of inflammation and this is one of the reasons I consider the uterus a fascinating organ.

Endometriosis and Lipoxin A4 – New Possibilities

I first became interested in endometriosis in 2008 and began this research in 2009. It struck me that a good deal of endometriosis research is of relatively poor quality, with small study numbers and not very novel. Medical treatments for endometriosis are lacking and practically all target the hormonal system, resulting in unpleasant side effects. Medical treatments include progestagens, gonadotropin-releasing hormone agonists (for example Lupron) and oral contraceptives. However, the use of these therapeutics is limited due to the high cost, significant side effects (including premature menopause, decreased bone density and libido) and do not prevent disease recurrence after discontinuation of treatment. Additionally, each of these treatments preclude pregnancy. Therefore improved therapies, with fewer side effects, are necessary.

My group had been working on estrogen signaling and we observed, by chance, that Lipoxin A4, an anti-inflammatory molecule derived from the metabolism of fatty acids, had estrogenic properties. This was completely unexpected but when we looked at the structure of Lipoxin A4 it resembled that of Estriol, a weak estrogen. Using several different methods we confirmed that Lipoxin A4 did indeed act like an estrogen in the cells that line the uterus (endometrial epithelial cells) in vitro and that it also mediated effects similar to the most potent estrogen, estradiol, in the mouse uterus in vivo.  So this was the discovery of a new hormone. Over twenty years ago, estriol had been shown to inhibit certain actions of estradiol. This is because they compete for the same receptor. Picture the hormone as a key and the receptor as a lock, in this case there are two keys trying to fit into the same lock. Lipoxin A4 also inhibited certain actions of estradiol.

As these dual characteristics, anti-estrogen actions and anti-inflammatory properties, are relevant to endometriosis, we decided to examine the effect of Lipoxin A4 in a mouse model of disease.

Lipoxin A4 and Endometriosis – The Research

Mouse models, though they do not mimic every aspect of the human disease, are useful to test potential drugs. These preclinical studies showed that Lipoxin A4 prevented endometriosis progression. We induced endometriosis in mice by transferring uterine tissue into donor mice. When looked at under a microscope these “lesions” resemble human lesions. We randomly divided mice into two groups: mice receiving Lipoxin A4 and mice receiving a vehicle, this is the liquid in which the drug (in this case Lipoxin A4) had been dissolved, which should not have an effect. Endometriotic lesions were smaller and inflammation was decreased in mice that had been administered Lipoxin A4 versus mice who had received vehicle. Many molecules involved in inflammation and cellular proliferation, which are also increased in endometriosis patients, were decreased by Lipoxin A4. Also, estrogen signaling was blunted. It is noteworthy that Lipoxin A4 did not alter the cycling of the mice, their cycle is shorter than the human menstrual cycle, and no other adverse effects were observed. Lipoxin A4 is an interesting molecule as it has never been associated with harmful effects and in this context can reduce inflammation and also impact estrogen-mediated signaling. These are two major components in the pathology of endometriosis.

Current research collaborations have as a goal to understand the role of Lipoxin A4 in human endometriosis; is more or less of it made? What is it doing and how?

The main problem here is that Lipoxin A4 is a short-lived molecule and is rapidly broken down. I hope that a more stable analog with the same functions can be synthesized which might eventually become a new, improved endometriosis therapy. I also hope that more discoveries regarding it’s role in the female reproductive tract will be made as it is almost certainly a significant player in this environment.

As referent biologist for a patient association I am saddened by how much women suffering from endometriosis endure and hope they can be heard and that they can participate in transdisciplinary research. For such a chronic and complex disease this would seem logical in order to move the field forward.

The full story: Lipoxin A4 Prevents the Progression of De Novo and Established Endometriosis in a Mouse Model by Attenuating Prostaglandin E2 Production and Estrogen Signaling.

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Endometriosis: A Husband’s Perspective

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Jeremy Bridge-Cook

For the third time this week, I’m on my own helping the kids with their homework, driving them to and from sports activities, feeding them dinner, cleaning up the kitchen, and putting them to bed. My wife is upstairs in bed, in pain that is so excruciating that the only way she can cope by the end of the day is to load up on painkillers and sleeping pills and go to bed as early as possible. While ferrying the kids to their activities, I spend the drive worrying about how my wife is holding up, particularly emotionally. This is not an unusual occurrence for her. And for me, worrying about my wife is part of the life of being an endo husband.

My wife has had endometriosis since she was 13, but it only became debilitating when she was in her 30s. In the last decade or so, she has tried every type of medical and alternative treatment available, searching for solutions to her pain and many other related symptoms and secondary complications. Every day, we talk about how she’s doing that day. She rates her various organs on a pain scale of one to ten. “My bladder is a 7 this morning, unfortunately, but my gastrointestinal system is only a 3, and my uterus and chest pain are barely noticeable, so today isn’t too bad so far.” After the morning pain report, we often discuss medication strategy and any other health-related topics, trying to come up with the best plan for that day for my wife to minimize pain and get the most out of her day. This type of conversation is also part of being an endo husband.

Endometriosis is a particularly complex disease because it can affect almost any organ in the body. Every patient experiences it in her own unique, but usually excruciating, way. An implication of this fact is that, ideally, a team of specialists (especially surgeons) is needed to provide the best care possible for this disease, led by a highly trained laparoscopic excision surgeon/gynecologist. Unfortunately, this type of care is rarely available. More typically, women are simply prescribed one type of hormone therapy or another, and sent home to cope as well as they can. Their pain is often explained away by doctors as being either hypochondriacal, or drug-seeking. Considering how common and debilitating this disease is, the quality of care for most women is truly appalling. As a husband who has watched his wife suffer terribly for years, I have had a close-up, but second-hand, education in what it is like to have a chronic disease that the medical system doesn’t care much about.

Years ago, my wife and I would have discussions about how she should handle conversations with friends and colleagues about her disease. As a naturally introverted person, it went against my wife’s instincts to talk about her body and symptoms in a frank way, especially since her period or ovulations were inherently involved in her symptoms, not to mention organs such as bladder and bowels. My position was always the same: “Just tell them the truth. Don’t hide anything or gloss over anything. Why should you? You haven’t done anything wrong!” Eventually, my wife got used to having these types of conversations. It makes some people uncomfortable, but that’s their problem, not hers.

As an endo husband, I have gradually come to feel a sense of disgust and outrage at how ignored this disease, and the women who suffer from it, are. Research is virtually non-existent compared to other major diseases.  Coordinated care is rare. Misconceptions and misinformation, even among gynecologists, is rampant. There is no standard of care, no evidence-based treatment guideline. Women are left to figure it out largely on their own.

Incredibly, my wife is in many ways one of the luckier victims of this disease. She is a Ph.D. scientist, so she can research the scientific and clinical literature while trying to determine the best care possible. She has a strong network of family and friends (including many women with endo).  She was able to keep a half-time job until recently. And we have three beautiful children to help keep her motivated to fight this disease tooth and nail, even when it’s at its most discouraging and hopeless.

When my wife asked me if I would be interested in writing a brief article about endo from the perspective of a support person, I quickly agreed. I welcomed the opportunity to make the same plea to all women with endo that I made years ago to my wife. Please, tell anyone who asks how you are doing the whole truth. Don’t hide anything or gloss over anything. After all these years of watching my wife struggle and suffer, there’s one thing I’ve learned the hard way: The only way this disease will stop being invisible and ignored is if all women affected by it (and their partners) speak up together, and demand change. This is what endometriosis awareness month is all about. And this is my fervent hope as an endo husband.

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Million Women March for Endometriosis – MWMFE

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Million Women March for Endometriosis

Did you know that March is Endometriosis Awareness Month? Did you know that the yellow ribbon is the color for endometriosis awareness and support? The sponsors of the Million Women March for Endometriosis (MWMFE) have funded and organized a worldwide event to empower, educate and effect change.

The March for Endometriosis

On March 13th, 2014 women battling endometriosis and their supporters will take a stand against endometriosis. The goals are simple; to raise awareness about endo and the lifelong effects it has on both girls and women of all ages. Early diagnosis is key to winning the battle against endometriosis and non-invasive diagnostic tests are needed to make this possible. Currently, the only way to diagnose endometriosis at any stage is to have a surgeon perform an exploratory laparoscopic surgery.

What is Endometriosis?

Endometriosis is a serious and sometimes severely debilitating disease that no one is talking about and some people have never even heard of. In North America estimates are that over 8 million women are currently battling this devastating disease. Worldwide there are close to 176 million women who are suffering the chronic pain of endometriosis. Let’s start with the basics; what is endometriosis?

I assure you it is not contagious like a cold and it’s not an STD from unprotected intercourse. “Endo” as it is commonly referred to; is a disease in which cells similar to the endometrial cells inside the lining of the uterus are growing outside of the uterus. These cells are under the constant influence and control  of a woman’s hormones so as a woman gets her monthly cycle, these cells are stimulated, create inflammation, and may cause bleeding in the surrounding tissue. This means that wherever the endometriosis cells have started growing (the ovaries, the cervix, the bladder, the bowel, the colon, the appendix, the diaphragm, the sciatic nerve, the lungs) these areas can become extremely painful due to inflammation, and can develop painful adhesions (scar tissue) that attaches organs together and cause organ dysfunction.

Simple everyday bodily functions are compromised such as urinating and defecating. In extreme cases where endometriosis cells are found in the lungs, thoracic endometriosis causes shortness of breath, asthma-like symptoms and collapsed lungs. Hence the reason that-like cancer-endometriosis is classified by 4 stages. Endometriosis stages (I-minimal, II-mild, III-moderate, and IV-severe) are classified as such depending on the location, extent, and depth of the endometriosis implants and the extent of the adhesions. However, the stage of the disease does not necessarily correlate with the level of pain.

Every woman with endometriosis can make a difference by using her voice! All of our voices have power but only if we use them. This goes for the family, friends, acquaintances, neighbors, significant others and medical professionals who have a woman in their life battling this horrific incurable disease.

What is MWMFE?

The MWMFE is an internationally-coordinated awareness campaign that will occur worldwide on Thursday, March 13, 2014, in dozens of international capitals, including Amsterdam, Belfast, Berlin, Brasilia, Buenos Aires, Copenhagen, Dublin, Helsinki, Kingston, Lisbon, London, Madrid, Oslo, Reykjavik, Rome, Stockholm, Valleta, and Washington, D.C., just to name a few. An internationally coordinated campaign is absolutely necessary to effect the changes that are needed to overturn the status quo.

One person truly can make a difference but together-we can really make a difference in the lives of girls and women who currently battle endo and it’s crippling effects on the body. The 1st annual Million Women March for Endometriosis (MWMFE) will be held at the National Mall in DC and registration and attendance is FREE!

This unprecedented worldwide peaceful demonstration to raise awareness is an amazing opportunity for endo warriors and the people who love them to come together to effect real change. There will be live music and guest speakers as well as men, women, children, celebrities and medical professionals all focused on Endometriosis Awareness.

Please help us end the silence about endometriosis and get the proper care and cure we need before it’s too late.

How to Get Involved

Don’t wait, visit our website today! The event is less than 2 months away! Million Women March 2014. The website will help you:

  • Register to attend the event in DC on March 13th, 2014
  • Register to be a volunteer on the day of the event…..there could never be too many participants or volunteers!
  • We have precinct managers in every state who can help with hotel discounts, flight discounts and event day information if you are planning to attend. They can also help you can make a difference in your own community. Contact us today and we can put you in touch with someone in your area.
  • If you are unable to attend you can still use your most powerful weapon…..your voice. Get the conversation started! Please help us end the silence about endometriosis and get the proper care and cure we need before it’s too late. We would be honored to have you join the campaign in any way that works for you, even if it’s just a post about the event details on your Facebook/Twitter/Blog.

Feel free to contact us here at MWMFE so we can assist you in getting involved. Email:endomarch.information@gmail.com; Phone:  (408) 28-MARCH; (408) 286-2724

Endo is widely recognized as one of the top 10 most painful diseases on Earth. It’s time to end the suffering in silence!

About the author. Lindsay Murphy is a freelance writer currently focusing on Endometriosis Awareness. Lindsay’s battle against Stage 4 Endometriosis has resulted in four surgeries in less than two years. She has a BA in Broadcast Journalism and Mass Communications which comes in handy with writing assignments about endo warriors and their struggles with this disease. Lindsay is traveling the country, changing locations bi-weekly, in order to advocate for more endometriosis awareness and research. “Our voices have power but only if we use them.” – Lindsay Murphy

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Thyroid Hormones and Cardiovascular Function: New Research, New Neurons

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thyroid and cardiovascular function

Thyroid dysfunction affects approximately 12% of the US population and up to 30% of the world population, especially in iodine deficient regions.  According to the American Thyroid Association, women are eight times more likely to have thyroid disease than men and up to 60% of those with thyroid disease may be undiagnosed. The thyroid gland, located in base of the neck, produces two primary hormones thyroxine (T4) and triiodothyronine (T3) that travel throughout the body and bind to thyroid receptors that then control a myriad of physiological processes including temperature regulation, skeletal muscle, fat metabolism and cardiovascular function. Thyroid hormones also impact brain function and are linked to a range of neuropsychological functions including cognition, depression, anxiety and even psychosis.

Hypothalamic Pituitary Thyroid Axis

The thyroid hormones are controlled from a region in the brain about the size of an almond called the hypothalamus. The hypothalamus is the master regulator for all hormone systems and hormone related activity including feeding, sleeping, reproduction, fight, flight, energy usage – basically every aspect of human and animal survival. It sits at the interface between the central nervous system functioning and the endocrine system functioning.

To regulate thyroid function, the hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which signals the pituitary gland to release thyroid stimulating hormone (TSH). TSH then activates the thyroid gland to produce and release thyroxine or T4.  If all is well, T4 is converted to T3, which then binds to thyroid receptors located throughout the body and thyroid modulated functions are regulated appropriately. Too much or not enough circulating thyroid hormones, because of their broad reaching effects can, and often do, destabilize homeostatic balance throughout the body.

Thyroid Hormones and Cardiovascular Function

Thyroid hormones have a profound effect on cardiovascular function. Hyperthyroidism evokes heart palpitations, tachycardia, and high blood pressure. While hypothyroidism, elicits bradycardia and low blood pressure consistent with its slowing of metabolism in general. These effects were believed to be mediated solely through the thyroid hormone – thyroid receptor complex on the heart itself. New research shows that there may be an additional, more direct route for thyroid control of cardiovascular function – the brain’s autonomic system.

Researchers have identified a new set neurons in the anterior hypothalamus that suggest a site for central nervous system – autonomic control of thyroid mediated cardiovascular function. That is, these neurons directly control heart rate and blood pressure.

Anterior Hypothalamic Neurons Contain Thyroid Receptors

For over 50 years, researchers have known that lesions to this region of the hypothalamus cause heart rate and blood pressure to skyrocket. Conversely, stimulation causes heart rate and blood pressure to drop. What they didn’t know is how neurons in the anterior hypothalamus controlled cardiovascular function. It turns out, there are thyroid receptors in a set of nuclei called the parvalbuminergic neurons that directly control cardiovascular function. Mutations that specifically affect those thyroid receptors in the parvalbumiergic neurons have drastic affects on heart rate, blood pressure and thermosensation – the ability to sense temperature change and regulate the body’s response accordingly.

In the present study, mutations to the thyroid receptors located on the parvalbumiergic neurons in the anterior hypothalamus directly altered cardiovascular function, suggesting direct and specific autonomic control of cardiovascular function. The mutation to these thyroid receptors evoked high blood pressure and elevated heart rate in conjunction with thermosensation and in states of hypothyroidism. That is, temperature change evoked the cardiovascular effects. When animals with the defunct thyroid receptor in the anterior hypothalamus were exposed to cold, heart rate and blood pressure skyrocketed. In conditions where the ambient temperature was normal, only minimal tachycardia was observed. Since hypothyroid patients have difficulty maintaining core body heat, finding an association between cold exposure and impaired cardiovascular functioning, was particularly interesting.

Hypothyroidism, is not normally normally considered a risk for high blood pressure and high heart rate, at least initially. As other systems, affected by low thyroid hormones become damaged, however, high blood pressure can emerge.  The data from this study suggest a direct mechanism for high blood pressure in some hypothyroid patients. The mutation affecting the thyroid receptors in the hypothalamic neurons can elicit increased heart rate and blood pressure relative to cold exposure, irrespective of circulating thyroid hormone concentrations, adding yet another layer of complexity to thyroid disease management.

 

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Maternal Psychiatric Disturbances and Hormones

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postpartum depression anxiety psychosis

As a mom of young children, I was very much affected by the Andrea Yates case. If you recall she experienced successive bouts of psychosis and pursued multiple attempts at suicide following the delivery of each of her children. After her fifth child, she drowned her children, killing them all. The case was a heartbreaking, and I believe, a totally preventable tragedy had her psychosis been taken seriously by medical professionals, family and others in the community. In spite of her psychosis and suicide attempts she was sent home to care for her children, as if a woman with postpartum psychosis is somehow less ill than a man or than a woman whose psychosis develops unrelated to her pregnancies. Raising young children is difficult, even under the best of circumstances, but sending a severely depressed and psychotic woman home to care for young children is just downright negligent. Although there was blame to go around among the doctors, her family and community, I couldn’t but shake the feeling that this tragedy could have been averted if her illness had been taken more seriously.

Identifying the Biological Underpinnings of Maternal Psychiatric Disturbances

The Andrea Yates tragedy inspired me to research and identify the clinical and biological components of perinatal mental illness. My goal was to identify early warning markers; biological tests, that would give women, their physicians and family members a way to predict the possibility of illness and confirm that illness once it had arrived. I thought that if we could predict and identify the risk for this illness, then the families could prepare and maybe even lessen the severity the disease process. At the very least, tragedies like the Andrea Yates case could be prevented.

I knew hormones would be key to the onset and maintenance of perinatal psychiatric symptoms. What I didn’t know is which hormones, when, and related to which symptoms. It seems that no one else did either. Despite years of research and a clear temporal association between the onset of psychiatric distress and childbirth, only tenuous connections between maternal hormone concentrations and varying degrees of postpartum depression had ever been established. This was primarily because the research was focused so narrowly upon the relationships among what are often referred to as the female hormones, progesterone and estradiol, and depressive symptoms. Very little research had examined associations between a broader range of steroid hormones and the full spectrum of potential psychiatric symptoms. This didn’t make sense to me. Certainly, other hormones affected by pregnancy, might also impact brain chemistry; certainly, the range of clinical symptoms that women might experience would go beyond the blues and depression. Even when psychosis appeared, I wasn’t convinced that the psychosis of pregnancy and postpartum was clinically similar to the psychoses that developed irrespective of the vast biochemical changes that took place across pregnancy, parturition and in the weeks and months that followed. If the biochemistry was different, as it most necessarily had to be, wouldn’t everything else about maternal psychiatric disturbances be different as well?

Looking Beyond the Boundaries

And so began my research. For the first study: Beyond Progesterone and Estrogen: Maternal Psychiatric Disturbances Linked to Adrenal Androgens, I recruited healthy, medication free, first time moms, with no previous history of mental illness. This was no easy feat. I soon realized that many women, even pregnant women, were using antidepressants and anxiolytics and many other medications. It seems the old adage that pregnant women should not take medications lest it cross the placental barrier and affect the developing fetus, had fallen by the wayside.

To assess the psychiatric distress, I abandoned the singular blues, depression and anxiety scales used so often in this research and found a broad-based, standardized assessment of psychiatric distress called the Symptom Check List 90R (SCL90R). SCL-90R is a 90-item psychiatric self-report inventory designed to measure the severity and intensity of psychiatric symptoms in both inpatient and outpatient populations. Participants rate the severity of distress experienced during the prior seven-day period using a 0-4 Likert-type scale (0=no distress-“not at all” to 4=extreme). Symptoms measured included: anxiety, hostility (aggression, irritability, etc.) phobic anxiety, paranoid ideation, psychoticism, somatization (perceptions of pain or other physical disturbances), obsessive-compulsive behavior, interpersonal sensitivity (feelings of personal inadequacy), depression and the global severity index (GSI), which reflects the overall symptom severity.

Along with the clinical symptoms, I measured five hormones, progesterone, DHEAS, testosterone, estrone, estradiol and estradiol, using saliva based testing. Symptoms and hormones were assessed twice, first in late pregnancy at 37 weeks (n =32) and again within 10 days following the delivery of their children (n=28, four were lost to attrition). I also conducted a year long follow up of those same participants and will report those data soon.

It’s Not Just Depression and It’s Not Just Postpartum

As I suspected, symptoms were present in late pregnancy and in some cases, increased in severity postpartum, but in other cases, decreased in severity. For some women, pregnancy was more problematic than postpartum, especially those with obsessive compulsive symptoms.

Fully 50% of the women tested experienced symptoms during pregnancy and 57% postpartum. This means maternal psychiatric distress is far more common than generally ascribed. As a group the anxiety related symptom scales, particularly the anxiety and obsessive compulsive scales, had the highest individual scores at each test time and when combined with hostility, phobia and psychoticism contributed the largest increase in symptom severity from pregnancy to postpartum. So it wasn’t the blues and depressive type symptoms that were most troubling, but the agitated, anxiety and even psychotic type symptoms that were the most severe.

Current research suggests that for only 1-2 per 1000 pregnancies psychosis will develop. What I found with this research and from another study,  is that psychotic symptoms were far more prevalent than recognized and may be the symptoms that drive the depression. In this study, we found sub-threshold, but clinically relevant, psychotic symptoms present in several of the women postpartum. Their symptoms were absent concurrent elevations in paranoia (paranoia and psychosis often go hand in hand). The most frequently ascribed to symptoms within this cluster included fears of serious illness (n=8), loss of mind (n=7) and isolation (n=12). Surprisingly, three women showed mild to moderate distress about thought insertion and thought broadcasting, two were concerned about thought control and one woman indicated distress about auditory hallucinations. Interestingly, it was these very same women who had the most dysregulated hormone profiles.

In speaking with the women who indicated these symptoms, the visual hallucinations, involved their children suffering; usually graphic intrusive thoughts, seeing images of their children being burned, thrown out windows, cut with a butcher knife, strangled with the breast pump tubing and the like. When auditory hallucinations were present they berated the women for their weakness, bad mothering etc., inducing guilt and one can only assume, depression. We confirmed the prevalence of these types of symptoms in two subsequent studies, the first published here: Dimensions of postpartum psychiatric distress: preliminary evidence for broadening clinical scope, the second unpublished as of yet.

Aberrant  Androgen Metabolism may be to Blame for Maternal Psychiatric Symptoms

As I suspected and as much research had shown, no symptom clusters were correlated with progesterone, estrone or estriol either pre- or postpartum.  While expected to be a close correlate of postpartum psychiatric symptoms, estradiol was associated with very few symptom clusters in the present study. Instead, it was the androgens that were linked to the symptoms at both time periods and not in a way that might be expected.

Low late pregnancy testosterone was not only related to late pregnancy psychiatric symptoms, but significantly predicted postpartum symptom severity. In conjunction, and this is where the endocrinology gets interesting, elevated late pregnancy DHEAS and supra-elevated postpartum DHEAS were associated with pre – and postpartum symptoms, respectively. This was exciting, because in theory these two hormones should not be aligned. That is, high DHEAS should correlate with high testosterone and it didn’t. So somewhere between DHEAS>DHEA>androstenedione> testosterone there was a problem and I had pretty good idea where.

For now though, we had a pilot study that ripped open the notions that maternal psychiatric distress occurred only during postpartum, was depressive in nature, was rare and was related to the normal or expected hormone changes of pregnancy. It was none of these things. The psychiatric distress was present at both test points, was more agitated, included a spectrum of symptoms, and most importantly, was related to aberrant changes in hormones that were likely exacerbated by the normal or expected hormone disruptions of pregnancy.  I was very excited. If we could identify the problem, then we could fix it right?

Not so fast. I could never get the research published and though I carried on with research I could do without funding, including a long term follow-up of the same participants (to be self-published soon) and an online study of the symptoms of psychiatric distress, the hormone work was routinely and summarily rejected. I learned very quickly how controversial studying hormones in women’s health was. So there it stands, the work was good, it pointed to a biomarker that could be used to identify and then treat a group of women who suffer horribly, but the study needs to be replicated with a much larger and more diverse population of women. It is likely that this is but one of many potential markers along this hormone pathway that could be used to predict and prevent perinatal psychiatric distress. It is also likely that this pattern of metabolism is linked to a host of other mental health and physical health issues. It was because of this research that I began Hormones Matter and have worked so arduously to increase awareness about the need for more research in women’s health. Hormones ought to be measured consistently across a woman’s life span, they aren’t and we need to change that.

Here are the full study details and the article, now officially self-published: Beyond Progesterone and Estrogen: Maternal Psychiatric Disturbances Linked to Adrenal Androgens.

Another portion of this study included assessing cognitive changes: Mommy Brain: Pregnancy and Postpartum Memory Deficits.

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