August 2014

Living with Ehlers Danlos is Hell

12849 views

I have Ehlers Danlos. On top that disease, I was given fluoroquinolone antibiotics and suffered a severe reaction which then lead to a rare and deadly fungal infection called Glabrata. This is what I have lived through over the three years.

Ehlers Danlos

Ehlers Danlos Syndrome (EDS) are genetic mutations that cause a lack of several types of collagen found throughout the body (skin, muscle, tendons, tissues, nerves and blood vessels). I have types I, II, & IV and crossover variations into several other forms. The type IV form that I have, also known as the vascular form, is a rare mutation form rarely ever seen (as of to date only three families including mine) and this is the most severe form that the NIH and John Hopkins has ever seen. This along with having more than one form (which is also extremely rare) has affected every part of my body and every system I have. It has left me with several other sub-illnesses, (some of them are common to all EDS sufferers and others not so common) such as hyperadrenergic dysautonomia, systemic mastocytosis, myalgic encephlamylitis (ME), pelvic congestion syndrome (PCS) and if God did not think he gave me enough to fight he threw in seronegative spondyloarthpathy with Crohns, which is seen in 35% of all female EDS patients. I also developed secondary Sjorgen’s Disease.

Ehlers Danlos plus Fluoroquinolones – Exploding Collagen

On top of all this crap I was given a fluoroquinolone drug by mistake, which is a collagen depleting drug!

After taking only four pills, my life turned upside down on a dime. I spent 64 days in the hospital fighting for my life, as my defective collagen exploded in every part of my body. Since then I have been fighting a daily battle of severe pain and organs and blood vessels that no longer know how or have the capabilities of functioning normally. It has now been almost three years since the fluoroquinolones and my body is still deteriorating.  Fluoroquinolones, as all my floxy friends know, is a nuclear bomb that slowly kills through DNA adduction and mitochondrial destruction.

The fluoroquinolones have left me with no immune system to speak of, so I am constantly fighting one infection after another. Last year, I fought the hardest battle of my life with a rare drug resistant fungal infection known as Glabrata; leaving me to spend 120 plus days in the hospital plus five months of home nursing care and daily IV’s of poison that nearly wiped out my liver. While fighting the Glabrata infection, I was also fighting the Crohn’s, liver damage, fluoroquinolone symptoms, sublexes, dislocations of my ribs from my sternum and a host of organ, nerve and blood vessel issues.

Pelvic Congestion Syndrome with Ehlers Danlos

One of the most painful issues is the pelvic congestion syndrome (PCS). The easiest way to explain this awful part of vascular EDS is to think of varicose veins the legs; the kind that when the person stands the blood begins to pool in their legs, the veins bulge out like thick blue ropes and begin to swell. After standing for a short period of time these people begin to suffer horrific pain down their legs to the point that they have to sit and put their legs up because it feels like razor blades cutting through them. Well, pelvic congestion syndrome is the exact same thing only it is the blood vessels in your abdomen. It can be the major arteries or the smaller ones known as the feeder veins, the ones that feed your organs.

For some of us with Ehlers Danlos, PCS affects only one or two veins and for others, like me, it affects several or all. For me, it is the feeders and the major mesenteric artery that are damaged. Every time I am in an upright position for any length of time the blood vessels dilate and fill with blood. This puts pressure on my organs and all the nerves that surround them. So, I suffer from both organ inflammation and dysfunctional organs because of the Ehlers Danlos. I also have severe nerve pain that can only described as a screaming pain. It makes me want to jump out of my own skin and run. The pain is so bad, I want to run to the nearest ER and beg for someone to help or end my life.

Unfortunately, there is no way to fix this other than to take enough pain meds to knock me out for days. Life with Ehlers Danlos, and especially PCS, revolves around being drugged with the strongest pain meds on the market and only getting up to shower and then back to lying down flat again. It leaves me unable to walk. Many people with Ehlers Danlos are in wheelchairs, but even that has its time limits.

Ehlers Danlos Specialists – Good Luck

In an attempt to hold on, people with Ehlers Danlos reach out to other patients, looking for any help they can. We search out specialists around the country, always praying that we will find that one doctor that is going to have the miracle we need. Because this is such a rare illness and my form of it is particularly rare, there is no protocol or research to follow. We are all on our own. Every one of us with Ehlers Danlos, no matter where we live in the country, have at some point, seen the same handful of doctors and received the same response – ‘there is nothing we can do.’

My journey has lead me to specialists from Chicago to Washington DC to Michigan and to Mayo, both my doctors and I have consulted with doctors from the NIH, John Hopkins to UCLA, and of course, every one of them tells me the same thing: ‘You can’t fix this [the exploding veins]. If you try [surgery]you will surely cause more severe damage to the remaining blood vessels or the surrounding nerves, which could, and has in some who have attempted it, left them in what is known as intractable nerve pain that is not treatable.’

Surgery to Repair Veins and Arteries Damaged by Ehlers Danlos

For people with Ehlers Danlos, healing is difficult and complications to surgery are very real and dangerous; attempts to stint, remove, bypass or replace the veins only causes other veins to erupt. Surgery is a bit like a dog chasing his tail. I have seen these complications first hand in others who have tried these surgeries, but there are a few, a very few people, who have succeeded and healed.

I know the risks and have spent the last two years searching out a doctor willing to attempt to repair my veins. I have begged and pleaded him to try it on me. Surgery to fix the faulty veins is very risky. The 80% failure rate is 80% and the repeat rate, 100%, meaning additional surgeries. And yet, I am willing to pursue the surgery anyway. What else can I do? There are no other treatments. My one feeder vein, which should have the circumference of a piece of pencil lead, now has the circumference of a quarter and is only getting bigger by the month. It is a feeder vein to my lower colon and rectum and is no longer allowing the organ to function normally. The pain is beyond anything I can take, even on pain meds. It is going to blow at some point and I am not willing to go there or lose my organs, so after much consideration, and two years of working with a surgeon, we are going to go in after this vein and we’re going to clamp it off and bypass it.

This vein is embedded in not only feeder nerves to the colon and rectum, but also, a ganglion of autonomic nerves. This surgery is extremely risky. If any of these nerves are damaged in the process, I would suffer not only intractable nerve pain, but also, loss of control of the bowel or bowel paralysis. This could also happen to my bladder, which eventually may cause me to lose the colon and the rectum (or as we Cronnies like to call it a “Barbie butt”, which is where they remove it all, put a bag on your side and sew up your butt like a Barbie doll).  On top of this, because of the autonomic nerves connect there; I could lose control over my heart rate, blood pressure and respiration. With all this being said, I’m willing to take my chances.

This surgery will leave me in severe pain for about 10 to 30 days. I will be bed ridden for those 30 days. This surgery will not get me off the pain meds but should reduce them dramatically. We’re only working on one vein right now; however, we may need to work on another.

Last Saturday, I woke up to filling the toilet with blood, a sign that something else has gone wrong. I took my pain meds, took my BP and heart rate and decided I was going to live. I went to the bathroom again, again later that day and this time I bleed out so bad that even after standing up I was still trickling blood and clots down my leg. It was off to the ER again.  After several hours they could not figure out where it was coming from but my hemocrit was high enough that I did not need a transfusion, so I told them I was going home and did.

The bleeding had stopped as usual, but I called the doctor, and spent the day at Northwestern with my doctor trying to figure out which vein blew. We think it came from the kidney and that was a self-contained bleed; it busted open and then clotted itself off. This is not my first bleed. I am constantly in the hospital for bleeds. My doctor says I need to come in and STAY in the hospital. I looked at her and said, “I spent just over 200 days in the hospital in 2012 and over 120 in in 2013 and I’m somewhere around 50 plus this year, I’m not going in anymore unless I’m dying.” It is not that I am giving up the fight but I’m tired damn it! So, I’m living and letting God take care of the rest.

Living Chronically Ill with Ehlers Danlos: Children and Spouses

This is only one of the many things I live with daily from EDS. The saddest part of all of this is now watching my babies go through this journey. The heart break and guilt runs deep and not being able to save them from this hell, is hell itself.  All we can do is to teach them how live with this horrible disease and be guinea pigs ourselves to help find ways to eventually treat them.

The men in our lives suffer right along with us. They feel helpless during our suffering. They have to pick up the household duties on top of working, and then there are the countless ER visits, the surgeries, the endless nights sleeping in chairs next to our beds in the ER, ICU or hospital, holding our hands and praying that we will get through this one too. They too have to deal with our screaming pain that many times leaves us unable to even hold a conversation. When we reach that screaming pain level, these poor spouses know it’s going to get ugly because it is all we can do to breathe. God help them if they even breathe too loudly because we are likely to snap the F@#k off and that’s when the crazy person comes out, the kind of crazy that even their mothers never warned them about because no one ever knew that level of crazy existed. They have learned the code words for it’s a really bad day, which means make sure I have a tall glass of water, my pain pill bottle and then leave me alone until I am either drugged enough or my body has adjusted to the pain level. My poor Tom not only deals with me but also my daughter who is now experiencing the pain and fatigue on levels that are leaving her to fight the crazy nasty pain devil that comes with this illness and that’s not to mention all the problems my boys have gone through because of this disease. God love these men and any faults they may have because they are angels to go through this.

Ehlers Danlos is a genetic disease that affects every part of our bodies, it affects every system and it disables us at every turn. There is no cure or treatment, there are few doctors who even know about this illness and even fewer that are willing to treat us. We actually get turned away as soon as they find out what we have. Our pain is so severe and incapacitating that most of the time there is not much that can be done other than to put us in the hospital and sedate us into oblivion! Those with the vascular form walk around with a cloud hanging over our heads not knowing when the next bleed is going to happen and whether it will be the one that finally takes us out.

I live with aneurisms in my brain, spinal cord and mesenteric artery. They will blow eventually just like the feeder veins. Some of us take palliative care, not that we are giving up the fight but because we hope they offer us something that helps. After being a hospice nurse for nearly 20 years, I could not do this. I walked out of the hospital and have chosen not to go there anytime soon. My head just cannot comprehend that yet.

Ehlers Danlos – We Look Normal

The worst part of this disease is that from the outside we look like everyone else, so no one can see our pain or what is happening to our bodies on the inside, so very few understand what our lives are like or what it takes for us to just get dressed. They can’t understand how different we are, only those that live with us, and unfortunately, our children who are now walking our path and the other EDS sufferers. It is also hard for some to not understand how one child in a family plagued with this illness can be so sick while another who has it too only suffers some minor problems or nothing until one of their arteries burst in the 5th decade of life. This is still being researched, the only thing they do know is that it is dominant gene and the mutation is true to the family, but the symptoms vary in degrees and systems from one person to another. It is a horrific disease that robs us of our lives and hides inside so others cannot see what we live with daily. At the bottom of this page I posted a pic from the National EDS foundations site to try and make people aware of what we look like on the inside, this is what EDS does to our bodies, organs, bones, nerves. If people could see what we really look like maybe then they could understand our pain, then maybe they would not criticize but instead praise us for continuing to fight, to get out of that bed, to continue to keep living despite the destruction! For me I continue to fight for my kids, I offer myself up for research, hell I’ll be a guinea pig like so many of us Ehlers Danlos sufferers. I will continue to get my ass knocked out by this disease but I refuse to stay down. No, I will get up and I will put a smile on my face I will laugh. I will go out and join the rest of the world, because that’s what we do!!

Postscript: Debra enters surgery today, August 28, 2014. We wish her well.

Ehler's Danlos

Fluoroquinolone Antibiotics Linked to Diabetes Onset

6529 views

What are the risk factors for type 2 diabetes? Obesity and a high-sugar diet, right?  Those are the most highly publicized factors that can lead to an onset of type 2 diabetes – but they’re not the whole picture.

Numerous studies have linked magnesium deficiency to type 2  diabetes. While the magnesium levels in one’s diet are a large factor in determining cellular magnesium content, there are things other than not eating magnesium-rich foods that can lead to depleted cellular magnesium. Namely, many pharmaceuticals and environmental toxins (especially glyphosate) have been shown to deplete magnesium from cells, leading to intracellular magnesium depletion and, potentially, diabetes and other diseases related to magnesium deficiency.

Fluoroquinolones are Linked to Diabetes – By Way of Magnesium Depletion

In an article published in the journal Medical Hypothesis entitled “Fluoroquinolone Antibiotics and Type 2 diabetes Mellitus,” it was found, through statistical analysis of the rates for both diabetes diagnosis and fluoroquinolone antibiotic (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/Ofloxacin and a few others) prescriptions, that “the probability of developing diabetes following a fluoroquinolone prescription is thus estimated at 3.5 percent.”

3.5 percent. Who would think that a commonly prescribed class of ANTIBIOTICS could affect diabetes rates?

Fluoroquinolone antibiotic use is a completely unrecognized risk factor for future development of type 2 diabetes. In taking Cipro, Levaquin, Avelox or another fluoroquinolone to treat a sinus infection, urinary tract infection, prostatitis, etc., patients are increasing their risk of developing type 2 diabetes significantly. It is postulated in “Fluoroquinolone Antibiotics and Type 2 diabetes Mellitus” that fluoroquinolones are “responsible for much of the increase in the prevalence of type 2 diabetes in the United States from 1990 to the present day.”  (The article was published in May, 2014.)

Fluoroquinolone antibiotics increase the risk of diabetes because they “can penetrate cell membranes inducing an intracellular magnesium deficiency that increases the probability of insulin resistance. This can lead (when accompanied by other risk factors) to type 2 diabetes.”

Cellular magnesium deficiency, brought on by fluoroquinolone antibiotics – antibiotics used to treat common infections – can lead to type 2 diabetes.

To support the hypothesis that much of the increase in prevalence of type 2 diabetes in the United States since 1990 is due to the use of fluoroquinolones, the study notes that the correlation between the rates of type 2 diabetes and fluoroquinolone prescriptions is strong.

Correlation between fluoroquinolone use rates and prevalence of diabetes.
(A) Incidence of diabetes in the non-institutionalized U. S. population aged 18–79. (B) U.S. national outpatient prescription rates of fluoroquinolone antibiotics from Refs. [3] and [27] (squares) and [28] (diamonds). (C) Correlation between incidence of diabetes in a given year and outpatient fluoroquinolone prescription rate 2years previously. (D) Prevalence of diabetes in the whole U.S. population plotted with prevalence of obesity. Posted with permission of the author.

While the tracking of the dramatic increase in type-2 diabetes rates (from 3.5/1000 in 1991 to 9/1000 in 2009) with increasing fluoroquinolone prescription rates is alarming, the more interesting correlation is the downturn in type-2 diabetes rates that corresponds to the decrease in fluoroquinolone prescriptions after a black-box warning of tendon ruptures was added to the warning label for all fluoroquinolones in 2008. (Though correlation does not mean causation, statistical tools and analysis were utilized in the study to analyze the data and remove some of the cross-correlations. The R-squared for the correlations are high – indicating that the correlation is strong and that the data fits well.)

History of Dysglycemia with Fluoroquinolones

The link between fluoroquinolones and type 2 diabetes should not come as a surprise to the FDA or anyone who has studied fluoroquinolones.  Gatifloxacin, a fourth generation fluoroquinolone sold under the brand name Tequin, “was withdrawn from clinical use after reports of drug-induced hyperglycemia.” Additionally, “other fluoroquinolones have been reported to interfere with glucose homeostasis.” Severe dysglycemia has been induced in already diabetic patients when they have been exposed to fluoroquinolones.

Despite the fact that Tequin/gatifloxacin was removed from the market because it caused severe dysglycemia, and that fluoroquinolones have been shown to adversely affect glycemic indicators at rates much higher than those of other antibiotics, more than 26 million prescriptions for fluoroquinolones were given out to the American public in 2011 alone. And though both hyper and hypo-glycemia are noted as adverse reactions on the Cipro/ciprofloxacin warning label, there is nothing on the label that warns of increasing the risk of type 2 diabetes.

Repairing the Damage

Multiple studies have shown that a high-magnesium diet and high intracellular magnesium levels are protective against both diabetes and fluoroquinolone toxicity, but clinical experiments where magnesium is supplemented in order to treat diabetes shows mixed results. Although magnesium is protective, once it is depleted, it takes more than supplementation and eating leafy greens to repair the damage. Additional research shows that thiamine, which works in conjunction with magnesium, improves mitochondrial function and diabetic outcomes.

Cells that are depleted of magnesium enter cycles of self-perpetuating damage and further magnesium depletion.  ATP, the enzymatic process of cellular energy production, is dependent on magnesium. It has been suggested that insufficient magnesium, because of depletion by pharmaceuticals (especially fluoroquinolones), environmental toxins, or a deficient diet, cells do not have enough energy to renormalize their magnesium levels, and the deficiency becomes chronic.

When magnesium is depleted, other cellular mineral balances are also disturbed.  In “Magnesium:  the Forgotten Electrolyte,” it is noted that “Magnesium is needed for the proper functioning of the Na+/K+—ATPase pump, so a deficiency causes an increase in intracellular sodium and allows potassium to leak out of cells.”  Intracellular magnesium deficiency also disrupts intracellular calcium homeostasis. The proper balance of magnesium, sodium, potassium, calcium and other minerals within cells is quite important, and restoring the balance of these vital minerals is difficult.

Magnesium Depletion and Chronic Diseases of Modernity

When are the connections between magnesium depleting pharmaceuticals and the “diseases of modernity” (such as diabetes, autoimmune diseases, and others) going to be realized?  Depletion of intracellular magnesium can lead to a spiral of ill-health effects.  After all, magnesium is necessary for more than 300 enzymatic reactions.  Without proper levels of intracellular magnesium, ATP doesn’t work properly and mitochondrial dysfunction can result. Mitochondrial dysfunction leads to an over-production of reactive oxygen species (ROS) / oxidative stress. An over-production of ROS has been linked to almost every chronic disease there is, from Gulf War Syndrome to Autism. Liver enzymes are dependent on magnesium and when magnesium is depleted, the liver’s detoxification processes malfunction. This leads to toxic metabolites circulating through the body, which is connected with autoimmune diseases and many other chronic illnesses. Sufficient levels of magnesium are necessary for the proper metabolism of many vitamins and nutrients, including the B vitamins. Taking fluoroquinolone antibiotics or other magnesium depleting pharmaceuticals can lead to a spiral of ill-health and disease.

The correlation between fluoroquinolone prescriptions and diabetes is clear, however, longitudinal studies would be necessary to show causation. Similar studies should be done for all of the diseases of modernity that have been on the rise since fluoroquinolones were introduced. Though fluoroquinolones aren’t the only toxic chemicals that can deplete cellular magnesium, they are common and frivolously over-used.  Fluoroquinolones (chemotherapeutic agents masquerading as simple antibiotics) cause magnesium depletion and mitochondrial damage, which in turn lead to massive, progressive, sometimes irreversible, cellular damage and many chronic, poorly understood diseases.

Type 2 diabetes is a serious, debilitating, and sometimes fatal disease. It is unconscionable to give patients a drug that increases their chances of developing type 2 diabetes when there are other, safer drugs available.

Recognition of the connection between fluoroquinolone antibiotic use and the onset of type 2 diabetes requires a re-examination of the prevalent assumptions about the causes of diabetes. The findings in “Fluoroquinolone Antibiotics and Type 2 Diabetes Mellitus” may revolutionize our paradigms.

Credit for the graphical image: Fluoroquinolone antibiotics and type 2 diabetes mellitus; Telfer, Stephen J., Medical Hypotheses, Volume 83, Issue 3, 263 – 269. The graphic was used with the author’s permission.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

Write for Us

Patient stories are important. Help spread awareness. Write for us.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

To support Hormones Matter and our research projects – Crowdfund Us – Buy an Unsubscription.  

High Blood Pressure in Women: Could Progesterone be to Blame?

77731 views

High blood pressure develops for a number of reasons, with poor diet, lack of exercise and medication key contributors to chronic hypertension. Explaining high blood pressure in young, otherwise active, athletic and healthy individuals is difficult at best, but when the blood pressure seems to wax and wane for no obvious reason, diagnosing and treating this form of hypertension can be downright impossible.

This is where an good percentage of the female population find themselves; with treatment refractory high blood pressure, that worsens across the menstrual cycle, during pregnancy and in response to certain formulations of oral contraceptives. Unbeknownst to many of these women and their doctors, they are carriers of a genetic mutation that raises their blood pressure relative to circulating progesterone concentrations. For these women, when progesterone concentrations are high, as during the luteal phase of menstrual cycle, and especially during pregnancy, blood pressure skyrockets uncontrollably. When progesterone concentrations are low and provided lifestyle variables are in check, blood pressure is more manageable.

Mineralocorticoids and Blood Pressure

Blood pressure is controlled in large part by what is called the mineralocorticoid system. This is a set of both steroid and peptide hormones that interact with the vasculature and the kidneys to increase or decrease blood flow. The mineralocorticoid hormone receptors are at the center of this system. Binding to these receptors is the mineralocorticoid hormone called aldosterone. Aldosterone regulates salt homeostasis and whether the kidneys store salt and water or release it.

Sensors within the kidneys monitor sodium concentrations. When there is not enough salt, they release the peptide hormones renin and then angiotensin I and II. The renin-angiotensin system then activates the release of the steroid hormone aldosterone. Aldosterone binds to the mineralocorticoid receptors and signals the kidney to reabsorb more salt. More water is also reabsorbed, and with those changes, plasma volume increases. Increased plasma volume, increases vascular volume which in turn requires a higher cardiac output. Increased cardiac output then leads increased blood pressure. The reverse is also true, decrease salt reabsorption and we get hypotension or low blood pressure.

Regulating Blood Pressure

At every junction there can be errors or mutations in this system and compensatory reactions to environmental or dietary changes. Add those possibilities to the variety of other factors that control blood pressure (baroreceptors, natriutetic peptides, kinin-kallikrein, adrenergic receptors, nitric oxide and endothelin) and it is easy to see why hypertension is sometimes difficult to manage. Women, however, have the added bonus of constantly changing hormone concentrations, across the menstrual cycle, pharmaceutically, across pregnancy and across menopause. Since the mineralocorticoid receptors, like all steroid hormone receptors, bind promiscuously to a bunch of different hormones, it is easy to see how drastically changing hormone concentrations can impact salt and water homeostasis (premenstrual swelling, pregnancy swelling, oral contraceptive swelling), and ultimately, blood pressure. Add a little stress to this mix and we have a recipe for hypertension. Indeed, it should be noted that both cortisol, the stress hormone, and progesterone, bind more strongly to the mineralocorticoid receptor than aldosterone.

Progesterone Binds to Mineralocorticoid Receptors

Progesterone, the reproductive hormone that prepares the endometrium for implantation during the luteal phase of the menstrual cycle and supports the pregnancy once underway, binds to mineralocorticoid receptor. The relationship between progesterone and blood pressure is complex, but mostly progesterone blocks the mineralocorticoid receptors and lowers blood pressure. In some women, however, the shape of the mineralocorticoid receptor is altered, allowing for increased progesterone binding in such a way that it activates the signals sent from the receptor. So rather than block the mineralocorticoid-aldosterone pathway, it launches it. Progesterone then becomes the conduit for increasing salt and water retention and increasing blood pressure.

Progesterone and High Blood Pressure

For women who carry this gain-of-function mineralocorticoid receptor mutation, high blood pressure emerges early, before the age of 20 and, for all intents and purposes, is refractory to the normal lifestyle changes and many medications that reduce blood pressure, except perhaps diuretics. The high blood pressure often becomes severe during pregnancy. It may also become severe with any drug that increases progesterone or decreases aldosterone including with oral contraceptives, synthetic progestins (medroxyprogesterone, micronized progesterone, prempro and related), and blood pressure medications that block aldosterone (spironolactone) and are derived from 17a- spirolactone. Fourth generation progestin, contraceptives or hormone replacement therapies (HRT) containing drospirenone are particularly dangerous, as they both bind to progesterone receptors strongly and block mineralocortiocoid activity simultaneously.

It should be noted that boys and men also carry this mutation and are susceptible to early onset hypertension.

The Problem with Progesterone Mediated Blood Pressure

The problem with progesterone mediated high blood pressure is one of recognition. High blood pressure in general is not recognized in young women. Blood pressure mediated by progesterone concentrations, whether via endogenous and menstrually-related changes or the use of synthetic progestins, is all but completely unrecognized. Genetic testing in this population is unheard of. Consequently, many young women are at risk for cardiac and thromboembolic events and do not know it. Could the sudden deaths reported in association with drosperinone oral contraceptives be related to unrecognized gain of function mineralocorticoid mutations? Possibly.

During pregnancy, the risk is magnified exponentially as progesterone concentrations increase several hundred fold. Hypertension accounts for 6% of all pregnancy complications, one wonders what percentage are related to progesterone? No one knows, because it is not studied.

For older women, though blood pressure is routinely monitored, connections between synthetic progestins in HRT and blood pressure elevations may only be cursorily understood, leaving many women open to inadvertently increasing their risk for heart attack and stroke coincident with attempts to manage menopausal symptoms. Although, hormones naturally decline during menopause, the re-supplementation of progesterone and progestins can be problematic for these women.

Fourth Generation Progestins: The Dangers of Drospirenone

For women with the gain of function mutation, certain forms of oral contraceptives and HRT can be deadly. The 4th generation progestins contained the Yas, Yasmin, Ocella series of birth control pills and in the Angeliq brand of HRT, are derived from a synthetic progestin that blocks the mineralocorticoid receptor directly.

Drospirenone is a progestin and mineralocorticoid antagonist derived from 17a- spirolactone. 17a- spirolactone blocks aldosterone. Under normal circumstances, blocking aldosterone’s ability to bind with mineralocorticoid receptors might be a good thing and reduce high blood pressure, particularly in folks who have aldosterone based hypertension or who are in heart failure. In other populations, however, blocking aldosterone might not be such a great idea.

Drospirenone based oral contraceptives and HRT formulations contain progestins that bind with equal affinity to the progesterone receptor compared to endogenous progesterone, but bind 500X more strongly to the mineralocorticoid receptors  than aldosterone. This is problematic for most women, even if they don’t carry the gain-of-function mutation. Drospirenone based contraceptives increase the rate of serious cardiovascular events by as much as 6X compared to the older contraceptives. In women who carry the gain of function mineralocorticoid receptor mutation, taking a drosperinone based oral contraceptive or menopausal replacement therapy, the results can be deadly.

Drospirenone – Mineralocorticoid Receptor Connection

If one has the gain of function mutation, where the mineralocorticoid receptors preferentially bind with progesterone and its metabolites, blocking what remaining aldosterone controlled feedback loops of salt/water balance, skews the receptor activity in such a way that it is always on, and always telling the kidneys to reabsorb more salt and water. Similarly, increasing progesterone concentrations unnaturally, with drosperinone, or any other progestin, quantitatively increases binding with the mineralocorticoid receptors, displacing aldosterone, removing important feedback controls and creating a state of perpetual progestin-mineralocorticoid activation.

Epigenetic Factors in Blood Pressure

Environmental toxicants and pharmaceuticals induce what are called epigenetic changes in protein expression. Epigenetic means beyond genetics. These types of changes don’t alter DNA per se, just alter whether a certain protein codes are activated or deactivated. There are number technical mechanisms by which epigenetic variables can alter receptor expression and function. For other receptors, especially the glucocorticoid and estrogen receptors, many of these epigenetic mechanisms have been elucidated. Not so for the mineralocorticoid receptors. Certainly, with environmental exposures, which are all endocrine disrupting in some manner or another, it is possible to create constitutively open mineralocorticoid receptors, much like the gain of function mutations. This would mean that millions of women could be a great risk when using drospirenone based oral contraceptives or HRT, progesterone increasing or mimicing drugs (most oral contraceptives and HRT), aldosterone blocking agents from spirolactone and during pregnancy. Even across the menstrual cycle, blood pressure would be expected to wax and wane relative to circulating progesterone concentrations.

Final Thoughts

Maybe it is time to move beyond the one hormone, one receptor, one function view of endocrinology. It’s certainly time to address the role of cycling hormones on human physiology. Cycling progesterone concentrations impact blood pressure; recognizing this simple fact would help women and their physicians develop more reasonable and effective approaches to managing high blood pressure.

 

 

Red Raspberry Leaf Tea to Relieve Menstrual Pain

13453 views

My alarm goes off at 0600 every morning. I groggily put on my sports bra and tennis shoes and start one of my many work-out DVDs to start my day. I do push ups, pull ups, lunges and squats all in order to build lean muscle tissue. The science behind this equation is easy – use your muscles to build muscle. But how can you tone muscles in your body that can’t be toned with weights or treadmills? The muscle I’m talking about is the uterus. The uterus or womb is lined with muscles that are primarily designed for childbearing which as we all know gives way to that monthly visitor that brings a suitcase full of cramps, bloating, heavy cycles and more. What if I told you that there is an all natural remedy with no side effects that also helps regulate menstrual cycles, treat cramps, aid in fertility, even lessen the chance of miscarriage, and help labor? Interested?

While there have been very few studies on the effects of red raspberry leaf tea (tea made from the leaves of the raspberry plant), it has been used for thousands of years to tone the uterus for fertility and menstrual problems. Studies have concluded that there are no side effects of this natural remedy. Raspberry leaf tea is full of nutrients including iron, calcium, manganese and magnesium, vitamins B1, B3, C, and E.

In the past, I have tried synthetic hormone treatments to deal with irregular periods, heavy bleeding, and cramps. I suffered through severe side effects including heavy bleeding in between cycles, severe depression and of course, cramps. I decided to try raspberry leaf tea because it had no side effects, could be bought at the grocery store or online, and even if it didn’t work for my specific problems it was still very nutritious. After drinking 1-2 cups a day for about two months I noticed a significant change in the regularity and severity of my cycles.

While I can tone my arms, legs and abdominal muscles through weight and cardio routines, I continue to use red raspberry leaf tea to tone my uterus and reproductive system. Does anyone have other experiences with raspberry leaf tea to share? Any successful fertility stories through this ancient elixir?

Bonus: For an all natural beauty product try applying cold tea or tea bags to your face as an astringent to tone your skin and treat acne.

Walking on the Edge of a Sword: Cervarix Injury in Japan

3486 views

This is the story of my teenage daughter who, beginning in 2010, received a series of vaccinations that culminated with the three shot HPV vaccine, Cervarix (Gardasil in the US). Although she had some health issues as an infant and child, she was thriving and doing well prior to the vaccine. After the Cervarix vaccine series this all changed.

Sharne was born in 1998. Her health issues pre-vaccine included: pervasive developmental disorder (PDD), a form of Aspergers, infantile asthma, atopic dermatitis, pyelitis, otitis media, Candida, hemolytic streptococcus, pneumonia, wart, FMF (periodic fever syndrome), agrochemical sensitivity and repeated stomatitis. Her immunization history was as follows:

  • 15 May 2010 DT BIKEN (Lot. No. 2E007 2011.6.8, 0.1ml) left arm
  • 19 March 2011 Japanese encephalitis BIKEN (JR059 2012.5.18, 0.5ml) left arm
  • 25 June 2011 Measles and Rubella Takeda (Lot. No. Y116 2012.2.24, 0.5ml) left arm
  • 27 July 2011 HPV  Cervarix  1st shot (Lot. No. AHPVA129CA, 0.5ml) left arm
  • 17 October 2011  Cervarix  2nd shot (Lot. No. AHPVA143AA, 0.5ml) right arm
  • 26 March 2012  Cervarix  3rd shot (Lot. No. AHPVA161BA 0.5ml) left arm

Before the Cervarix Vaccine

Sharne was born October 02, 1998. Prior to Cervarix vaccine, she enjoyed her school life. She liked to be in the school rather than being home, including going to an evening school for extra study.  As she wanted to gain accreditation to a high school, she tried to go to school even when she had a fever of 40 degree centigrade because in order to get the accreditation she was allowed to be absent from school only up to 5 days

Prior to the HPV vaccine, Sharne did not need to sleep for a long time, and she woke up early even when she went to bed late the day before. Before the symptoms occurred, she used to wake up at five o’clock in the morning. She’d read her favorite books, and then went to run around the house for about 10 minutes.

She was an athlete and was the fastest 1000 meter runner in her class when she was in 7th grade. She had strong lungs, and her respiration rate and pulse rate had been low since she was a little girl, but it is now is much higher. Her pulse is averages 70-80 beats per minute; average for some, but several points higher for her.

She used to prepare breakfast by herself, do homework and go to school. She was really independent, managed her own schedule, found whatever she wanted to do, and when she needed to be taken to or picked up she just told me the time to be taken to or picked up.  She never conflicted with others, avoided any dispute, and was a very quiet, gentle and good natured child.

After the Cervarix Vaccine

Now she cannot do what she could do previously. She has difficulties remembering things. She cannot remember what she has done. She cannot manage her own things, stationary, notebooks, glasses.  She used to look after her things very carefully, and never asked where they were. She’d never forgotten what she needed to take to school, but now she leaves her glasses on the floor of her bedroom or in a washing bowl even for two weeks. She cries when she cannot find her notebook, and she cannot remember what she did in the past.

Her IQ and test scores have dropped a lot and continue to drop.

She says impolite things to teachers or family members and becomes violent like an insane person. She hates most of people around her.

Recently, she cannot understand what she is going to do or where she is. In addition, she has muscle weakness in legs, and cannot raise her left foot. Her grip strength dropped from about 30 kgf to 5 or 6 kgf.

The Progression of Symptoms Post – HPV Vaccine

Looking back now, it seemed to have started after the first Cervarix shot, but it gradually worsened for about two weeks after the third shot, and half a year later she could not get up at all. Symptoms:

  • After 1st shot: asthma attack (the first time for seven years).
  • After 2nd shot: malaise, long-lasting urticaria, repeated nosebleed
  • After 3rd shot: in MRI, extension of T2, cerebral blood flow decrease, atrial rhythm, arrhythmia, increase of eosinophil, IgE, IgD, and complement titer, abnormal malaise, chronic slight fever, clouding of consciousness, hypersomnia, brain function deterioration such as memory, comprehension, calculation, and execution functions, personality change, irritability, aggression, depression, childishness, behaving like a baby, hyperpnea, respiratory distress, muscle weakness, back pain, headache, parotitis, temporomandibular arthritis, dysphagia, stomatitis, abdominal pain, vomiting, diarrhea, back pain, muscle pain, abnormal vision, photophobia, double vision, reduced vision, etc.

Timeline of Symptoms Post Cervarix Shots

2012

April: about 2 weeks after the third shot (March 26), exertional hyperpnoea and muscle weakness occurred.

May or June: started experiencing malaise, gastrointestinal symptoms such as vomiting, headache, chest pain, and anginal symptoms during nocturnal rest. There was muscle weakness when getting off from her bicycle in the school and could not stand up.

September: could not get up, altered state of consciousness lasted for a long time, there were anginal symptoms, atrial rhythm, arrhythmia, blood flow decrease, extension of T2 in MRI, and leukoaraiosis.

October to December: treated with steroid. Although malaise had dramatically improved, brain blood flow did not improve, accumulation was observed in the hippocampus, and the treatment was stopped.

 2013

January: malaise worsened seriously. There were depression, suicidal thought, and personality change (irritability, excitability, persecutory delusion).  Even in school she cried loudly like a one-year old baby and dashed out from the classroom.

June: we noticed the association with the vaccine when watching a TV news about suspension of recommendation of HPV vaccine.  Around this time, she became violent at night. Cried loudly like roaring. Sharne threw her younger brother by the full force. (This violence disappeared soon after IVIG.)

August: we saw Dr. Sasaki, and he proposed three treatments, that included, steroid pulse, IVIG, and an immunosuppressive agent.

September: immunoglobulin (due to fever, discontinued on the 3rd day, she became cheerful on the 2nd day, and the sensation of toes returned. Malaise also improved a little.  Blood flow increased, and the best results for SPECT so far), but involuntary movement gradually intensified.

2014

February: steroid pulse (after about 2 weeks, headache and back ache, etc. decreased, cognitive function and facial expression a improved slightly, the time of sleep during day decreased, but after about 20 days new systemic joint pain and excruciating pain started, and malaise, gastrointestinal symptoms, etc. also restarted.)

Her sensitivity to glare and the double vision disappeared.  Involuntary movement started to appear.

March: 2nd cycle of steroid pulse (this time, there were no effects on mental strength and malaise, and there was a symptom like muscle weakness, which had appeared with the altered state of consciousness in the autumn 2012), involuntary movement and muscle weakness seemed to increase, and IgG decreased.

May: she was depressed. She received immunoadsorption therapy, involuntary movement decreased, but spasm and tremor have started. Mental motivation improved, and gentle character has returned. Malaise has alleviated, and daily life became almost normal.

June: malaise returned in one week after discharge from the hospital, and IgG decreased.

July: motivation dropped. Mental symptoms have started.

Lab Tests and Other Diagnostic Results

  • Cerebrospinal fluid test results: autumn 2013: contaminated with blood, but IgG was as high as 5.8 (this is not influenced by serum contamination)
  • February 2014: cell count 12, CD4 64.9, CD8 31.4, cytotoxic T cell, granzyme B 1.3
  • Diagnosed as a possibility of subacute encephalitis.
  • April 2014: abnormal values for various types of interleukins, etc.
  • June 2014: antiganglioside antibody positive

The Lesson I Learned too late

‘We need question even what the government is doing.’ This is what I learned with this huge and irreparable mistake. I tell our story because I do not want to other parents to make the same mistake and because we need help understanding the post-vaccine reactions, so that our children, already injured by the Cervarix vaccine can recover.

Vaccination of boys has already started in some countries, and clinical trials have begun in Japan. In order to protect the future of children, please think and research before you vaccinate. I will let my voice be heard in order for many people to receive information about the dangers of the HPV vaccine.

Cervarix Adverse Effects in Japan

There are more than 2000 reports about adverse effects in Japan, but some doctors refuse to report. There have been more than 1000 contacts to the network of HPVW injured people in Japan, the number of people registered exceeds 255, but still there are only a few medical institutions that care for injured.  The government should support and subsidize medical institutions that exert themselves for elucidation of the mechanisms of the cause and establishment of the way to treat underlying causes.

Postscript: This article was written originally in Japanese and translated to English by a friend of Hormones Matter.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with Gardasil and its counterpart Cervarix. If you or your daughter has had either HPV vaccine, please take this important survey. The Gardasil Cervarix HPV Vaccine Survey.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

To support Hormones Matter and our research projects – Crowdfund Us.

A Matrifocal View of Endocrine Disruptors and Premature Birth

2391 views

In the spring of 2012, the results of a long-term study on one of the most overlooked problems in the human experience was released. Born Too Soon: The Global Action Report on Preterm Birth, jointly sponsored by The March of Dimes Foundation, The Partnership for Maternal, Newborn & Child Health, Save the Children and The World Health Organization revealed an annotated selection of possible causes as well as detailed plan for actions intended to reduce premature birth and death. It also presented a dismal report card of the childbearing management and outcomes of the world’s countries; the United States ranked shamefully at 131st in preterm births.

The United States’ ranking is particularly shocking in that the primary causes of premature birth and death have supposedly been ameliorated. Since the 1990’s, lung maturity has been addressed through use of steroid injections at the first signs of labor. Nutrition has been addressed since the 1980’s through increased maternal resources (Women, Infants and Children or WIC ). Issues of ill-health, notably under/overweight, diabetes, high blood pressure, smoking, infection, age, genetics, multiple pregnancy and closely spaced pregnancy are supposedly mitigated through our mind-boggling 35% average, surgical intervention rate.

The US is unique in that its obstetrical practices include a substantial number of pregnancies are introduced by in vitro fertilization (IVF) and artificial insemination (AI) (increasingly performed in other countries, with birth occurring within the US borders). Additionally, first time moms in the US are often older and cesarean sections, either elective or for perceived complications, add to the increasing rate of prematurity in the US. These facts are presumed to explain the dismal state of maternal health and rise of premature births seen over the last decades in the US. Using these circumstances to disregard a troubling trend, however, negates the fact that this same population where premature birth is increasing, represents some of the best fed and medically attended women in the world. And yet, our premature birth rate continues to increase, along with births in which unusual defects of placenta, cord and newborn become more prominent. Why is this?

Reproductive technology and other variables not-withstanding, the largest and most rapidly developing body of evidence suggests that being born too soon is just one of the consequences of long term chemical exposures from foods, medicines and environmental contaminants. Endocrine disrupting chemicals, whether by pharmaceutical or environmental exposure, elicit subtle but recognizable damage to broad swaths of mammalian cells; damage that is complex and chronic, likely spanning multiple generations. It is damage that we are only beginning to understand.

The Power of Small, Frequent Exposures to Endocrine Disruptors

February 19, 2013 – just 9 months after Born Too Soon was published, the massive 296 page, multi-continent report on the probable effects of endocrine disrupting chemicals (EDCs) was published in joint by the World Health Organization and The United Nations Environment Programme. Though it hardly made a whimper in the common press, State of the Science of Endocrine Disrupting Chemical-2012 is a shocking narrative into the damage being done to all mammalian cells, especially and most importantly by small, frequent exposures.

In the earlier 2002 version of this report, the Global Assessment of the State-of-the-Science of Endocrine Disruptors concluded that “there is weak evidence that human health has been adversely affected by exposure to endocrine-active chemicals.”  Under then-current testing, toxicity was most frequently measured by highest tolerable dose.  Despite early works such as Silent Spring, it was not until anecdotal insight gained through the popular book Our Stolen Future: Are We Threatening Our Fertility, Intelligence and Survival? that science began to wonder if it was asking the right questions.  While it is clear that massive doses of any chemical has a level at which cellular death is inevitable, is it possible that the living cell is more impacted by low, consistent doses?

With the release of the updated State of the Science the evidence is clear and the answer is yes; human health is indeed being adversely affected by exposure to endocrine-active chemicals at remarkably low and varied levels. Further, it is clear that we have been accumulating both exposure and cellular change for many years, certainly at least as long as the earliest pesticides and hormones at the turn of the century.  Although scientists cannot agree on specifics about identification of and protection from endocrine disrupting chemicals, the global scientific chatter indicates that the State of Science is an urgent warning that most endocrinologists are taking very seriously. We are changing cellular behavior from the mitochondria (the cells furnace) outward and the consequences are profound and growing (here) and (here).

So substantive is the insight contained within State of the Science  that ACOG followed in October 2013 with its own 17-page report, Exposure to Toxic Environmental Agents, reiterating the dangers of, and potential consequences to, exposure to toxic chemicals and EDCs, including risk of infertility, miscarriage, prematurity, deformity and stillbirth. Deeming reducing pregnant women’s exposure through education “critical”, the American College of Obstetricians and Gynecologists surveyed 2500 physicians over the following months and found that fewer than one in five ask patients about toxic exposure.

Citing lack of understanding of the issues and concerns over stressing pregnant women, doctors feel that they need to focus their time on other aspects of care, but these are precisely the issues that must be addressed if maternal and fetal health are to be protected. If doctors are not willing to protect maternal health, then others must step up. I would argue that midwives must fill that role. The first step is in understanding the role of endocrine disruptors in maternal fetal health.

Endocrine Disruptors and Preterm Birth

Consider the impact endocrine disrupting substances can have on reproduction and their potential relationship to prematurity. Women are born with all the eggs they will ever have, and thus, are particularly sensitive to any assault on individual cells. We understand this from dentistry where shields are required to prevent the cumulative damage of x-rays. In contrast, we have such difficulty considering that the minute doses of any endocrine disrupting chemicals or particles might change the course of human potential; but they can and do. Here are just a few examples of endocrine disruptors affecting maternal and fetal health.

Obesogens, Chronic Disease and Prematurity

Obesogens are compounds that can alter the lipid (fat) development and metabolic balance. They are present in plastic containers including bags, BPA, air fresheners, non-stick pans, pre-packaged foods, fructose, monosodium glutamate, nicotine, DES, Estradiol, pesticides, lead. They are found in plastic and melamine dishes and cups along with urea-formaldehyde resin.

Obesogens have a very specific relationship to fat, a relationship that has grown steadily and significantly over the past 50 years. The primary mechanism appears to be the transmutation of cortisone into the active hormone cortisol in the fatty tissues. Repeated trials indicated that it promotes adipgenesis; an energy component that processes substance into triglycerol, insulin, epinephrine, glucagon and ACTH in the body. They are time sensitive:  The longer a challenge is presented (exposure) the greater the impact; the greater the artificial exposure (such as chemical and EDC), the more complex the reaction at the cellular level.

They have been found in every fat cell in the body and their presence can have very far reaching consequences in the childbearing cycle. These compounds appear to create a profound deficiency in normal ratio of sex hormones, alter lipid regulation and derange glucose metabolism. Alone or combined these changes can have a profound relationship on maternal and fetal outcomes. Some have speculated a “probable link” between these endocrine disruptor initiated changes to pregnancy-induced hypertension.

There is evidence that exposure to obesogens can be epigenetic and heritable modifications to DNA, meaning that unchecked and uncontrolled continued exposure to obesogens may permanently alter our lipid and glycogenic biology progressively, and across current and future generations.

Flame Retardants and Preterm Birth

Polybrominated diphenyl ethers (PBDEs) are compounds that are uniquely disruptive to the neurological system through changes in the receptors. Their primary use is as flame retardants and have been used in building materials, electronics, household furnishings, motor vehicles, airplanes, plastics, polyurethane foam and textiles –including children’s sleepwear since the early 1970’s. PBDEs are dangerous in all forms but particularly insidious in one of their most readily found forms, dust, as they are taken up through both breath and skin absorption and moved throughout the body.  PBDEs have a profound effect on childbearing.

  1. PBDE reduces fertility at levels found in almost every household.
  2. PBDEs are indirectly associated with premature birth, low birth weight and stillbirth through first and second generation endocrine interruption.
  3. As little as a single dose has shown to impair neurodevelopment in the preborn and delayed development in young children including Autism spectrum disorders.
  4. PBDEs disrupt hormone levels in the thyroid gland of both mother and fetus.
  5. PBDEs evoke epigenetic dysregulation.

The EPA action plains have called for the removal PBDEs from our environment for years. Despite this, detectible levels remain high within the adult population; higher still in very young children.

Glyphosate Based Herbicides: A Danger to Maternal Fetal Health

Glyphosate is a glycine based broad spectrum kill-all herbicide which is, in large part, designed to work specifically with genetically modified organism which are tolerant of it.  Early and most on-going testing of this herbicide has tested the active ingredient in isolation. Very recent testing has shown the “inert” ingredients (adjuvants) to be aggressively toxic, one ingredient of which is extremely cytotoxic.

Unlike many of the other individual endocrine disrupting chemicals reviewed in State of the Science, the glyphosate substance has been slippery to fix within research. Many of the best research papers have been either dismissed out of hand or withdrawn from publication (a behavior which is rare indeed). The financial power of the major glyphosate producer (Monsanto) is well-connected in every government and research organization.

Of the studies that have been reasonably accepted and reviewed, glyphosate/adjuvant substances have been shown to be endocrine disruptors and further studies may confirm current research indicating the greatest danger in pregnancy to be:

  1. They are capable of vertebrate cranial faults during early gestation
  2. They have exhibited cytotoxic (cell killing) capacity in human cells at levels less than half the agricultural use
  3. Because of pure glyphosate’s ability to amplify the estrogenic effect of soy, gmo soy has shown to induce human breast cancer growth
  4. In 2013, the first solid evidence as to glyphosate’s impact on gut microbiome was released. Described as the “textbook example of exogenous semiotic entropy” it is shown to reduce or destroy tryptophan, tyrosine, phenylalanine, methionine, serotonin, Alzheimer’s, Parkinson’s, autoimmune diseases.
  5. Also in 2013, Interdisciplinary Toxicology released research documentation that glyphosate is “pathway to modern diseases: celica sprue and gluten intolerance”.

Today’s report of permanent kidney damage in the farm workers of South America seems to confirm that glyphosate is not just an endocrine disrupting chemical with epigenetic and mutagenic properties. As weeds become progressively resistant to glyphosate, it would seem that the increasingly high concentrations and applications of this chemical are linked to evidence of carcinogenic damage on a large scale.

For midwifery and birth the single most remarkable statement about glyphosate’s impact in childbearing is the knowledge that glyphosate disrupts enzyme function the “cytochrome P450” enzymes regulate Vitamin D, cholesterol, sex hormones and stabilizes blood fibrinogen continuity, all important factors in healthy pregnancy. Glyphosate also causes cellular damage to the placenta, the one organ of regeneration everyone should care greatly about (here), (here),(here),(here).

The Precautionary Principle and Premature Birth

At the heart of the Born Too Soon report we are lead through the maze of what may be causing prematurity and then in State of the Science we are given an opportunity to reflect upon the cellular challenge of history; and quite possibly the single most important disturbances in our biological evolution. This is a critical moment in childbearing and one that we would do well to spend time in mindful consideration. If the research is even marginally accurate is there anything more important than understanding and putting a halt to the barrage of assaults to our mitochondria and cellular health?

Part of the global answer to this conundrum has been in place since 2005: The Precautionary Principle; “a strategy to cope with possible risks where scientific understanding is yet incomplete, such as the risks of nano technology, genetically modified organisms and systemic insecticides.” This UNESCO environmental mandate was ratified in 2005 and is part of the fundamental inquiry system outside the US. Something of a “prove its safe before you put it out there” perspective, the Precautionary Principle works antithetically to the American system of testing and releasing.

“The precautionary principle enables rapid response in the face of a possible danger to human, animal or plant health, or to protect the environment. In particular, where scientific data do not permit a complete evaluation of the risk, recourse to this principle may, for example, be used to stop distribution or order withdrawal from the market of products likely to be hazardous.”

Our work in the United States is complicated on a national level certainly as we are hindered by far too much by the politics of lobbies, big Agri-Business and Biotech companies. Evidence-based medical decision-making has been extremely slow in taking a position entirely because of the scientific corner it has boxed itself into. What then?

Born Too Soon and Midwifery: An Opportunity

Each individual world community is dealing with childbearing issues in unique ways; prematurity, birth defects and low birth weight have causal relationships that may look quite different from country to country, and yet, we are united in the truth that hunger, poverty, insufficient water, shelter and healthcare are an increasing problem worldwide.  The addition of the biochemical challenges of endocrine disrupting chemicals has turned childbearing toward a future none wants to see continue. Regardless of the promises made for more and better food through chemicals and genetic manipulation, we are watching a game-changing shift in human DNA through mitochondrial damage that is leading to more, not less, disease, disorder and childbearing loss.

Women and children are very much the canary in the coalmine of endocrinology.  If the choices we are making as a species so alter our potential for stable regeneration, we are ethically bound to not only study them without equivocation, but to soundly rebuke their presence in our world until their safety is assured.  Women are being labeled high-risk for high-blood pressure, obesity, thyroid imbalance, diabetes and reproductive challenges as consequences of the mitochondrial damage being inflicted by an indifferent industrial machine contaminating the environment with dangerous endocrine disrupting chemicals.

As midwives we are bound to stand beside women experiencing those challenges.  We have never been simply about birth. Midwifery has always been Matrifocal by definition; through our focus on the welfare of women and the communities we have stood beside in every issue.  It is time for us to remember that with or without scientific validation we are bound also by our role as teachers. We are called to educate toward sustainable behaviors, involve ourselves in community changes and focus our practices on least invasive technology, as we search for answers to the growing list of health problems within the community we serve.

Live without hesitation. Dwell not on outcome or reward. Act with full attention.

Midwives have been the guardians of the sacred in community and birth since the beginning of time. We have dared to speak the truth when none wanted to hear it; when the cost might have been our very lives. Despite the occasional feeling of loneliness, we have really never been alone in that journey and we are even less so today. There is a growing body of health practitioners asking the same questions, risking their reputations and often their livelihood in an effort to bring to light the path through the madness that is the current recklessness of science. Find resources within your area. Encourage and support their work. Comb the internet for research about hormone and endocrine disorders.  There are many online researchers that are asking good questions; endocrine research is becoming more approachable with websites like Hormones Matter. Women’s mental health is leaving the dark ages of toxic medications with a new breed of psychiatrists like Kelly Brogan, MD, providing the insight to make the shift.

There is a revolution brewing – in birth and in health – become part of it.

Fetal Hormone Protects Mom Against Preeclampsia

2581 views

Preeclampsia is a serious pregnancy complication that affects 2-6% of all pregnancies in the US and 5-14% worldwide. It is marked by maternal hypertension and protein in the urine, usually presenting after 20 weeks of pregnancy. Despite years of research to identify early maternal markers of preclampsia, no reliable early diagnostics have been developed. Perhaps we are looking in the wrong place.

Preeclampsia research has almost always focused solely on maternal health as the core component of the disease. While it is true that maternal health should be a consideration, as it is severely compromised with preeclampsia, it takes two to make a baby. What about the dad’s contribution to maternal, placental and fetal health during pregnancy? The absence of paternal contributions is curious, especially considering research shows that women with history of preeclampsia who change partners for subsequent pregnancies have a 30% reduction in the risk for preeclampsia. Conversely, women with no history of preeclampsia who change partners for subsequent pregnancies, increase their risk for preeclampsia by 30% – placing the dad’s contribution squarely in focus. Why is dad’s health not considered?

Truth be told, there is a line of research that suggests that a dysregulated maternal immune response to paternal semen causes preeclampsia.  A convenient remedy, greater exposure to one’s partner’s semen prior to pregnancy is postulated. Aside from the obvious chuckles with this line of reasoning e.g. that more sex prevents prevents preeclampsia, the deeper problem lay in the fact that this theory is still squarely focused on the mom’s health, or rather, her response to the semen. It takes no consideration of the healthiness of the semen itself.

What if paternal health contributes not only to fetal health (this should be obvious), but also, placental functioning?  What if the developing fetus, aided by paternal genetics, controls or contributes to placental health at least as much as the mom does?

In an interesting series of experiments conducted using rodents (here, here), researchers have identified a fetal hormone that reduces, maybe even prevents, the development of preelampsia. Although this doesn’t quite point to paternal health as contributing factor, it is a step in the right direction. That is, we’re finally moving beyond the mom as the sole contributor to a healthy pregnancy.

The hormone thought to protect mom from developing preeclampsia is called adrenomedullin or ADM for short. ADM is peptide hormone synthesized in a myriad of tissues including the heart, lungs, kidneys, the ovaries and testis, uterus and placenta. ADM is a vasodilator, meaning it dilates vasculature so that more blood and nutrients can flow to the tissue or organ. It’s also angiogenic, meaning it ‘grows’ new blood vessels. In normal healthy pregnancies ADM is elevated significantly. In preeclamptic pregnancies, it is not.  And this where it becomes interesting.

One of the tell-tale signs of preeclampsia is abnormal vascularization of the placenta. The maternal uterine spiral arteries must remodel and increase capacitance to support the nutrient and oxygen needs of the placenta and growing fetus. When they don’t remodel appropriately or are constricted in some way, placental, fetal and ultimately maternal health are compromised. The theory is, that as the primary recipient of the increased placental blood flow, in normal pregnancies the fetus signals its needs and in some way controls or contributes to uterine and placental artery remodeling and angiogenesis by releasing ADM. Fetal ADM then increases blood flow. This doesn’t appear to happen in preeclamptic pregnancies where ADM levels are diminished and uterine spiral arteries do not remodel appropriately. It is believed that if the fetus does not release sufficient ADM then maternal systems must hyper-compensate resulting in the preeclamptic pregnancy that places great physiological strain on the mom.  An interesting caveat though, ADM is increased in non-pregnant, usually male, patients with hypertension so the relationship may not be linear.

ADM interacts with other hormones as well. It enhances progesterone production, suppresses FSH induced estradiol production, and is thought to be involved with inhibiting uterine contractility during pregnancy. In the heart, ADM interacts with testosterone, estradiol and angiotensin-II to modulate heart vessel contractility.  Interestingly, it is testosterone that increases ADM in these cells, while estradiol has no direct effect on ADM. Through a complex interplay between estradiol and angiotensin II, however, estradiol can increase ADM (see here for details).

This is cool research and likely to open additional possibilities for preeclampsia treatment. It represents somewhat of a paradigm shift in recognizing the role of fetus, and indirectly the role of the dad in the development of preeclampsia. If taken just bit further, perhaps even more diagnostic and therapeutic opportunities would arise.

This article was published previously on Hormones Matter.

Essure® Sterilization Coils: The Good, The Bad, and The Ugly

16368 views

The Essure ® Fallopian tube coils were manufactured by Conceptus, Inc. as a means for “permanent” birth control (click here for pictures). There was a need for something new and different that was a non-hormonal, non-invasive, and uncomplicated method of sterilization that did not require anesthesia. The surgical option, bilateral tubal ligation (BTL), had been introduced by Dr. Blundell in 1823 before the Medical Society of London, and while useful, was a drastic measure that many women were unwilling to take.

In the 1960’s, as the Women’s Liberation Movement first desired decreased numbers of children, and then no children at all, the need for permanent sterilization was rapidly evolving. Women were getting blood clots, weight gain and strokes from the pill. The IUD that released progesterone was falling out of favor.

The “T-shaped” Intrauterine Device (IUD) Mirena ® was approved by the FDA in 2000. In December 2009, The FDA sent a warning letter to Bayer, complaining that its campaign had “serious misrepresentations” of side effects including life-threatening ectopic pregnancies, uterine or intestinal perforations, internal scarring, serious infections, risk of pregnancy, organ damage, post-operative surgical complications, Streptococcal sepsis, intensive care unit stays, and more.

Enter Essure: The Solution for Permanent Birth Control

On November 4 2002, Bayer acquired the Essure coil product from Conceptus and its use was FDA approved through a “preemptive” process called “Expedited Review”. Expedited Review usually means that the product has already been in use (e.g., in another country).  The expedited review relies on data gathered from product use in other countries. The data presented to the FDA Panel are supposed to confirm the product’s use, safety, and effectiveness. We will see in subsequent posts that this was not the case for Essure. There were minimal data suggesting either the sufficient safety or efficacy to merit an expedited review.

The Good: How Essure was Supposed to Work

In an effort to offer a vaginal approach to permanent sterilization without hormone therapy or IUD complications, Essure was approved by the FDA in 2002.

Components of each tiny Essure coil include a spine of stainless steel, covered by 24 coils of expanding and elastic outer coil of nickel titanium. It is covered inside and out with polyethylene terephthalate (PET) fibers, that are wound in and around the inner coil of stainless steel. The specific goal of the Essure PET fibers is to cause inflammation, induce scar fibers, and thereby block fertilization of the egg with the sperm.

The proper placement of the Essure Fallopian tube coil is such that it is screwed into the tube from inside the uterus, in a counter – clockwise fashion with no screwdriver needed. To do this, a surgeon uses a surgical instrument by hysteroscopy so that the coil fills the fallopian tube, dangling into the uterus. Next an ‘ejector’ shoots the coil in a little further; a quick ‘tug’ is supposed to ‘prove’ that it is correctly placed and will not migrate.

A hysteroscope is too fat to fit past the cervical os, where the sperm travel up, often times the doctor cannot see the two holes where the Fallopian tubes empty into the uterus. So the doctor inserts the hysteroscope under IV sedation or local anesthesia block, to make the uterus numb. The doctor then tries to find two little holes, one on each side of the uterus, where the Fallopian tubes empty into the uterus.

Once the coil placements are confirmed, the procedure is complete. But this is just the beginning. The insides of Fallopian tubes still need to undergo a process fibrosis, a local inflammatory response around the coils, so the Fallopian tubes are blocked off, or occluded (See Illustration 3). The blockage needs to be double-confirmed, so a special procedure is done after three months.

The patient is instructed not to have unprotected sex for three months. Over these three months, an alternative form of birth control must be used.

At the end of the three-month period, a confirmation test must be done to show that the coils have done their job by fully occluding and blocking the Fallopian tubes. There is no other way to do this than to perform a  procedure called a hystero-salpingogram (HSG). The HSG uses dye injected past the vagina and cervix, past the uterus, and then hopefully it stops there, without going into the Fallopian tubes.

If the dye stays in the uterus and is blocked from going up both of the Fallopian tubes, the procedure is deemed a success and the patient is instructed that she can have unprotected sex now, because she can no longer have children.

If the contrast dye shows up inside the fallopian tube(s), however, then the patient can still get pregnant, and the coils have not finished doing their job at sclerosing the tubes shut. The doctor – patient relationship dictates what happens next; usually it is awaiting more time and then rechecking with another HSG at a later date. Although an area of controversy, removal of the coils is a possible choice.

The Bad: Side Effects of Essure

On the day of surgical placement, the most common side effects are: abdominal cramps, pain, and nausea/vomiting. Since the egg will still continue to be released each month at ovulation each month, the patient will still have her monthly period. The egg is simply reabsorbed into the body.

In 2013, Essure became a controversial procedure, with thousands of women complaining of complications leading to surgical removal, miscarriages with coils in babies’ ears, body hives, immune disease, coils breaking up into fragments, perforating the fallopian tubes, perforating the uterus, perforating the colon, pregnancies, severe abdominal bloating, pain on intercourse, general malaise, and even cancer. The first lawsuit against Bayer has been filed in 2014. Campaigner Erin Brockovich has taken Essure up as a cause, hosting her own website in the hopes of banning the product. Patients’ individual stories can be found here. Bayer continues to stand by its product, its safety, effectiveness, and reassures the public that it has a primary concern for public safety but that may not be enough.

If we look more closely at the Essure side effects, one thing becomes abundantly clear, they were predictable had anyone looked beyond the promise of ‘non-invasive’ sterilization. From the beginning, controlling the placement of the device within the Fallopian tubes was problematic and depended heavily on the surgical skill of the physician. Several studies indicate that correct placement occurred in only 84% to 98% of the cases. With perforation a likely outcome of a misplaced device, in a market of potentially millions of women, even a 2% failure rate is unacceptable. A 16% failure rate should give anyone pause; but it didn’t.

As difficult as that may be to accept, it seems that perforation may have been the least of the possible side effects. The chemical coating of the Essure device, meant by design to induce inflammation and scar tissue, was a toxicant itself; one that was inserted directly into the body.

The Ugly: Essure Chemical Coating

The Essure coils were coated in polyethylene terephthalate or PET fibers. PET fibers are plasticizers used in all sorts of commercial products. We recognize them by their brand names like Dacron (in the US), Terylene (in Briton) and Mylar under different conformational states. While these products are fantastic as outer coatings of materials to repel stains or water, as plasticizers that will degrade if exposed to heat and over time their usage in products that come in contact with food and/or are internalized is problematic to say the least.

The by-products of PET degradation, are acetaldehyde, a toxic intermediate in the metabolism of alcohol responsible for much of the liver disease in chronic alcoholics and antimony, a semi-metallic chemical element that is deleterious to health. Acetaldehyde is pervasive in airborne environments as a by-product wood smoke and other thermal reactions. Whether by inhalation or ingestion, acetyladehyde is a carcinogen. Should pregnancy occur in the presence of acetaldehyde exposure, it does cross the placenta and induce skeletal malformations, reduced birth weight, and increased postnatal mortality. Given its placement in the Fallopian tubes, follicular acetylaldehyde exposure could be predicted to induce changes in follicular morphology and perhaps even germ cell health for subsequent generations. Acetaldehyde is not something one wants leaching into the fallopian tubes, particularly when device placement is incorrect and pregnancy prevention nowhere near 100%.

Similarly problematic, Antimony leaching; antimony is a toxicant when applied topically. It induces local necrosis (cell damage and death). Systemically, continuous exposure to small amounts of antimony leads to an array of symptoms from cardiac to hepatic diseases similar to arsenic poisoning. Due to its very a very long half-life, antimony can induce reproductive disorders and chromosome damage. Antimony is toxic to reproduction with mutagenic and oncogenic potential.

Both degradation compounds have been found to leach into drinking water from plastic bottles exposed to heat (>65 degrees). Imagine how they might leach from a device placed into the Fallopian tubes where the temperature is ~98 degrees. There are no data regarding the degradation rate of the Essure coils or regarding the rate or risk of chemical exposure to women who used the device.  Even when the device is placed appropriately and skillfully, and sterilization reached, the potential local and systemic exposure to PET degradation products should give anyone pause, but it did not.