July 2014

Fluoroquinolone Antibiotics Damage Mitochondria – FDA Does Little

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Most people assume that antibiotics kill bacteria, but leave human (and other eukaryotic) cells unscathed. Unfortunately, this assumption isn’t correct. Bactericidal antibiotics have been found to damage the mitochondria of human cells.

Mitochondria are present in almost every cell in the body (except for red blood cells and sperm). They are responsible for cellular energy production, cell signaling, apoptosis (the process through which the body kills unhealthy cells), and aging. Mitochondria are vitally important organelles and malfunctioning mitochondria have been linked to many diseases including fibromyalgia, chronic fatigue syndrome / M.E., autism, Gulf War Syndrome, Alzheimer’s Disease, Parkinson’s, diabetes, cancer, and others.

Focusing on Fluoroquinolones

Though several kinds of bactericidal antibiotics have been shown to damage mitochondria, I’m going to focus this article on fluoroquinolone antibiotics because, a) there are multiple journal articles that note that fluoroquinolone antibiotics damage mitochondria, b) fluoroquinolone antibiotics have been shown to not just damage mitochondria, but to deplete mitochondrial DNA as well, and c) adverse reactions to fluoroquinolones involve multi-symptom, chronic illness that typifies mitochondrial injury.

Fluoroquinolone antibiotics – cipro/ciprofloxacin, levaquin/levofloxacin, avelox/moxifloxacin and floxin/ofloxacin – are damaging human mitochondria. This has been shown repeatedly, and even the FDA (never first to the party) acknowledges that the mechanism for damage done by fluoroquinolones is mitochondrial damage and the ensuing oxidative stress that occurs when mitochondria are damaged.

FDA Report Notes that Fluoroquinolones Damage Mitochondria

In their April 27, 2013 Pharmacovigilance Review, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure,” the FDA notes that the mechanism for action through which fluoroquinolones induce peripheral neuropathy is mitochondrial toxicity. The report says:

Ciprofloxacin has been found to affect mammalian topoisomerase II, especially in mitochondria. In vitro studies in drug-treated mammalian cells found that nalidixic acid and ciprofloxacin cause a loss of motichondrial DNA (mtDNA), resulting in a decrease of mitochondrial respiration and an arrest in cell growth. Further analysis found protein-linked double-stranded DNA breaks in the mtDNA from ciprofloxacin-treated cells, suggesting that ciprofloxacin was targeting topoisomerase II activity in the mitochondria.

The FDA Pharmacovigilance Report also notes that mitochondrial damage (and the ensuing oxidative stress that occurs when mitochondria are damaged) is related to multi-symptom, chronic diseases like optic neuropathy, neuropathic pain, hearing loss, muscle weakness, cardiomyopathy, lactic acidosis, Parkinson’s, Alzheimer’s and amyotrophic lateral sclerosis (ALS).

Bactericidal Antibiotics Damage Mitochondria

A study entitled “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells” that was published in Science Translational Medicine in 2013 notes that:

Clinically relevant doses of bactericidal antibiotics – quinolones (fluoroquinolones), aminoglycosides, and Beta-lactams – cause mitochondrial dysfunction and ROS overproduction in mammalian cells. We demonstrated that these bactericidal antibiotic-induced effects lead to oxidative damage to DNA, proteins and membrane lipids. Mice treated with bactericidal antibiotics exhibited elevated oxidative stress markers in the blood, oxidative tissue damage, and up-regulated expression of key genes involved in antioxidant defense mechanisms, which points to the potential physiological relevance of these antibiotic effects.

Fluoroquinolones Deplete Antioxidants

Fluoroquinolone antibiotics damage the cellular mechanisms that are needed to repair mitochondrial damage – namely intracellular antioxidant production. The FDA report notes that, “Under normal circumstances, there is a mechanism to remove or prevent the generation of ROS to avoid cellular damage such as lipid peroxidation, mtDNA mutations, and DNA strand breaks; if this does not happen, it can then lead to even more oxidative damage.”

A 2011 study of Indian patients who took various fluoroquinolones to treat urinary tract infections found that, “There was substantial depletion in both SOD and glutathione levels particularly with ciprofloxacin.” SODs are superoxide dismutases – enzymes that are necessary for converting superoxide – a powerful oxidant – into oxygen and hydrogen peroxide. Without adequate SOD, superoxide wreaks havoc on every cell in the body. Glutathione is often called the “master antioxidant” and without proper levels of it, oxidants damage cells. (Additionally, “Glutathione (GSH) has a crucial role in cellular signaling and antioxidant defenses either by reacting directly with reactive oxygen or nitrogen species or by acting as an essential cofactor for GSH S-transferases and glutathione peroxidases. GSH acting in concert with its dependent enzymes, known as the glutathione system, is responsible for the detoxification of reactive oxygen and nitrogen species (ROS/RNS) and electrophiles produced by xenobiotics. Adequate levels of GSH are essential for the optimal functioning of the immune system in general and T cell activation and differentiation in particular.” source)

As the FDA noted, when damaged mitochondria produce too much ROS, and the mechanisms to limit the damage (cellular production of antioxidants) aren’t working properly, an increasing amount of oxidative damage is done. This is often referred to as the “vicious cycle” of mitochondrial damage – damaged mitochondria produce excess ROS (reactive oxygen species – often called oxidative stress), those ROS further damage the mitochondria, the further damaged mitochondria produce more ROS, and so on, and so on. As noted above, mitochondrial damage, oxidative stress, and the vicious cycle between them has been linked to every chronic disease that plagues people – diabetes, Alzheimer’s, autism, etc.

Fluoroquinolone antibiotics damage mitochondria and cause an increase in ROS/oxidative stress. They also deplete cells of antioxidants such as SOD and glutathione, leaving the cells unable to neutralize ROS / oxidative stress. Excess cellular ROS / oxidative stress is related to every chronic disease there is.

See Evil, Hear Evil, but do Nothing About It

Rather than utilizing the FDA’s vast databases and the hundreds of Ph.D. scientists and statisticians on their payroll to determine whether or not fluoroquinolones – which have been shown to cause mitochondrial damage and oxidative stress, are related to the many chronic diseases that plague Americans – diseases that have been shown to be caused by mitochondrial damage and oxidative stress; the FDA simply added one more thing to the 43 PAGE warning label for fluoroquinolones – PERMANENT PERIPHERAL NEUROPATHY. They could have, and probably should have, added warnings that noted that fluoroquinolone use increases the risk of every disease that is linked to mitochondrial damage and oxidative stress – Alzheimer’s, Parkinson’s, ALS, diabetes, autism, depression, etc.

But they didn’t. They just added another warning that few physicians will read let alone understand and left these drugs on the market.

Fluoroquinolone antibiotics – cipro/ciprofloxacin, levaquin/levofloxacin, avelox/moxifloxacin and floxin/ofloxacin – are damaging human mitochondria and inducing large amounts of oxidative stress that wreaks havoc on many areas of health. The FDA knows about this, and they are doing nothing about it. Actually, worse than doing nothing, they are increasing the length of the warning label, so that when victims go to sue the companies (Bayer makes Cipro and Avelox and Johnson & Johnson makes Levaquin) that damaged their cells and gave them a multi-symptom, chronic disease, they are told that their symptoms are on the warning label and thus they gave informed consent to be crippled by an antibiotic.

It is absurd. Fluoroquinolones do severe damage to human cells, and the FDA is looking the other way. They’re not protecting our mitochondria, and they’re not protecting us.

Sources:

  1. Department of Health and Human Services Public Health Service Food and Drug Administration Center for Drug Evaluation and Research Office of Surveillance and Epidemiology, Pharmacovigilance Review, April 17, 2013, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure
  2. Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells”
  3. Journal of Young Pharmacists, “Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients
  4. Molecular Pharmacology, “Delayed Cytotocicity and Cleavage of Mitochondrial DNA in Ciprofloxacin Treated Mammalian Cells
  5. Molecular Neurobiology, “The Glutathione System: A New Drug Target in Neuroimmune Disorders

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.

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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.

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The Dangers of Glyphosate Herbicides

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Do we know what we’re eating? That’s the question that I constantly ask myself, because I know that at this point in time, my own regulations are the only thing protecting my health. It seems that the moment I become lax with my rules, I am quickly reminded why I must enforce them.

Monsanto is a corporation that manufactures herbicide and genetically engineered plants. Today, I learned that Roundup and other herbicides from the Monsanto corporation are made with a chemical ingredient called glyphosate. Glyphosate has been linked to a number of health-related issues ranging from birth defects to endocrine disruption (the endocrine system regulates the hormones in our body). Unfortunately, Monsanto’s products are used around the world. Products like Roundup are not just used to kill weeds in homes and the agricultural industry, but also to deter plant growth on railroad tracks, sidewalks and roads. This means that farmers, government workers and consumers are constantly spraying glyphosate on the ground, which is why it should come as no surprise that scientists are finding increasing levels of glyphosate in our groundwater. Even if we choose organic food (which is still recommended, since glyphosate is absorbed by plants treated with Roundup), our water cycle, including our drinking water, is being contaminated. In fact, glyphosate was detected in 60% to 100% of rain samples in Mississippi and Iowa.

Monsato, Malformations, Miscarriages and More

Consumers, workers and bystanders alike are affected by the use of glyphosate. Uninformed consumers purchase glyphosate-sprayed products and are exposed to the toxin. Agricultural workers handle the chemical directly. And then there are those that do not use the herbicide or consume the treated products, but are exposed to glyphosate nonetheless. This is particularly the case for those that live in close proximity to agricultural businesses that use Monsanto’s herbicides, such as Roundup.

Residents and doctors of Argentina and Paraguay began reporting a host of serious health effects, including birth defects, miscarriages, infertility and cancer. Those affected lived in regions where glyphosate was regularly used, linking abnormal health conditions to the pervasive chemical.

Argentinian scientists took this cue and began to study glyphosate, finding that exposure to glyphosate did cause birth defects in the embyros of chickens and frogs. Glyphosate has even been tied to an increase in spontaneous abortion and infertility among the cattle that are fed Roundup treated alfalfa.

Scientists from the University of Caen, in France, conducted an experiment using glyphosate doses that were less than the maximum residue limit (legal limit) and discovered that the chemical caused endocrine disruption. More specifically, the scientists found estrogen receptors were inhibited (blocking estrogen hormones from activating cells) with just 2 ppm (2mg/kg). The legal limit in the US is 5 ppm.

Dr. Don M. Huber, a plant pathologist who is part of the USDA National Plant Disease Recovery system, stated that there are, “more than 40 diseases reported with the use of glyphosate, and that number keeps growing as people recognize [glyphosate’s] association [with disease].”

Clearly, we should be concerned.

What about Government Health Regulations?

While only 2.03 mg/kg of glyphosate is needed to cause birth defects in chicken and frog embryos, government regulations, referred to as the maximum residue limit, allow 5 mg/kg of glyphosate residue in the US and a whopping 20 mg/kg in the European Union. The question isn’t how does this protect, but rather, who does this protect?

Unfortunately, government regulations are often set in place to protect corporations from liabilities. When citizens attempt to sue, corporations can state that they have complied with the law and that toxins are within the legal limit. Concerned parties may seek retribution from the government, but at this point, our tax dollars are being used for litigation.

What’s a Girl to Do? Take Action!

We start by sharing information with others to make a change. Litigation may be costly, but changing government regulations is not. (Corporations take the financial hit). Tell your friends, tell your co-workers, tell your neighbors.

This isn’t just a female-specific matter (though miscarriages and infertility concern us), since glyphosate is associated with a myriad of health issues and wreaks havoc on our crops by promoting plant diseases. Contact your senators and house representatives and let them know that you want regulations that protect your crops, your water resources, and your well-being. CLICK HERE to sign the petition to ban glyphosate-based herbicides.

Of course, if you’re worried your voice won’t be heard, the best way to make a statement is with your consumption habits. Every time you make a purchase, you cast a vote. Pay extra special attention to labels, buy organic and avoid products sprayed with glyphosate-based herbicide. Remember that corn chips may be processed from corn that has been treated with glyphosate. Let your money show that you don’t support the use of glyphosate, because money speaks.

Glyphosate Petition Review

The current petition against glyphosates was created on SignOn.org. I have recently been informed that emails associated with SignOn.org may start to pile up in your inbox. If this is the case, feel free to unsubscribe at any time to eliminate the onslaught of emails. Any recommendations for sites that create petitions without the spam would be greatly appreciated. Thanks for your support!

Hysterectomy in America

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Women suffer in childbearing, many women suffer during their periods, and many more women suffer from various methods of birth control. They also suffer from fibroids, leiomyoma, uterine prolapse, immobilizing pain, bleeding, migraines, endometriosis, uterine cancer, and are immobilized, squirming in bed, and crying out for mercy before they die or  sadly seek suicide as what they see as the only definitive option. After seeing doctor after doctor, after immeasurable doctor, hysterectomy is offered as an escape for each and every of these problems. After Cesarean Section, hysterectomy is the second-most popular surgery in American women, providing 600,000 procedures per year, and 20 million procedures to date (Keshavarz, 2012), with 55% having both ovaries removed.

Given that an astounding 40% of American women have had a hysterectomy by age 45, and about one-half have had both normal ovaries removed, if you are a woman, and you have had menstrual problems, it is likely that you have talked to your doctor about hysterectomy. You may even have considered scheduling it, particularly if the pain persists as so often it does.

Gynecologists and Hysterectomy

For many women, the gynecologist drives conservation. He thinks you’re ready for the hysterectomy now. It’s the only solution to your problems. There’s an ever-so-subtle pressure for you to pick a date for your hysterectomy already.  And so, you pick the date, and he practically stumbles out of the room to go get it on the Schedule.

As he’s leaving and just before the heavy door closes, he says his nurse will give you the details. Not knowing any better, you sit in your blue, stiff paper garb, freezing cold and still bleeding from your fibroids. You feel like he just told you that all your problems will melt away, and your life will start over again.

Did I Consent to this?

You are just too busy smelling the roses to stop and ask yourself, “Wait. What does this mean?” But really, it nags at you. You further contemplate: what’s wrong with this picture? Several huge and glaring things suddenly hit you like a smack in the face. It’s like you just heard the buzzing of a bee in the middle of the rose you are about to sniff.

No Informed Consent was given, and you don’t even know the risk: benefit ratio (Aranda, 2013).

Hysterectomy Second Opinion

You haven’t had a Second Opinion from another surgeon (eHow, 2014; Cornforth, 2014). Big Boo-Boos, because maybe you don’t need the surgery at all. “C’mon me. Get a hold of ourself.”  “I have to know that getting a hysterectomy isn’t like getting my tooth pulled out.” It is this author’s personal opinion is that surgery should be used as a ‘last’ resort, not a ‘first’ resort. Additionally, alternatives should be sought and tried before resorting to any surgery that requires general anesthesia. I was an anesthesiologist. My opinion. Take the time to get a second opinion and maybe even a third before finalizing the hysterectomy.

In my case, my second opinion Ob/Gyn was female, had two children of her own, the last one by C-section. She knew the drill, and gave a detailed analysis of the algorithm she would use; it led to my decision to have an open hysterectomy. I agreed, and scheduled it with her, later cancelling with the first doctor.

She told me that the risks of surgery are about 10% for complications related to infection, inability to see structures and a need to operate with an “open” (large) incision, bleeding, transfusion(s), adverse drug reactions, death, etc. Informed consent includes (a) the general risks of the procedure, and (b) the specific risks for me. If the doctor does not discuss the risks of the surgery specific to you run, don’t walk, out the door and find another doctor. For more information on what an informed consent should include: Informed Consent is the Law: Stop, Talk and Show Should be the Standard.

I should note that this conversation has to be between patient and the surgeon, not the patient and a nurse, not the patient and a doctor-in-training.

In my case, I happen to be both a patient and an anesthesiologist. I know the general and the specific risks of anesthesia; most women do not. We’re talking general anesthesia, a breathing tube down the windpipe, anesthetic gases breathed in from a ventilator, a high chance of vomiting afterwards; the whole shebang.

I knew that I would be bloated and blown up like a 7 month old pregnancy for a matter of days. Or could it be it weeks? Or…could it be months?  Most women do not know this and sadly many surgeons do not discuss this with the patients either.  She reminds me to bring gym pants with an elastic waist.

About the Hysterectomy: In the Operating Room

The doctor will fill her belly up with CO2 gas, and will leave it blown up for the duration of the surgery. She will be in ‘extreme’ lithotomy and ‘extreme’ Trendelenburg position. Legs wide open, head down, feet to the sky. The anesthesiologist will have to add positive airway pressure (PEEP) to push her lungs opened to fill with oxygen, and sometime the surgeon argues saying, “Hey, anesthesia, I can’t see anything.” Then a classic argument ensues: lungs for the patient vs. visibility for the surgeon. So they both work together, sometimes screaming, to get it done for the patient. Anesthesia always wins. No one wants a pneumothorax, a popped lung on the O.R. table. Then it will become a blame game and both of them are responsible. Sometimes the poor patient needs a chest tube and an ICU stay instead of going home.

Some people get shoulder blade pain that hurts like the dickens, and she already knew that if your shoulder blade hurts afterwards, it is ‘referred’ pain coming from your belly. Most of my patients had not been told that information by their surgeon, but if they are lucky, a good anesthesiologist will give her the down low.

Who will be Performing the Hysterectomy and How?

The types of hysterectomy procedures themselves aren’t always explained to the patient (Aranda, 2012). Admit it. You were so eager and desperate to have your uterus out, that you didn’t really even care how it came out; as long as it was gone by the time you woke up. You didn’t care if a medical student, resident, intern, Fellow, or Attending did it with or without a morcellator. Oh. A morcellator. What’s that (Fulton, 2014) ? Or the daVinci robotic hysterectomy robotic machine ~ Are they using that on me? Uhm. Each of these technologies carries with it discrete risks. You should know those risks to make the decision most appropriate for your health.

The Morcellator Problem

It wasn’t generally known until recently, but in order to get the ball of the uterus out of the large straw of the laparoscopic instrument, Ob/Gyn surgeons have been using, for the last 20 years, what is called a power morcellator once you are good and asleep. It pretty much goes into the laparoscopic scope and into the uterus to churn and blend it up like a garbage disposer, so it can be sucked up the tube.

Problem is…no one can possibly know if you have uterine cancer or not, until after the whole uterus is out. It is simply undetectable until then. Some women, like Amy Reed, M.D., an anesthesiologist and internist at Harvard, got her uterus, along with undiagnosed uterine cancer, splatted all over the abdomen at the same time (Reed, 2014). Now that was a big Oops.

As it turns out, they’ve been doing it to our mothers, aunts, and sisters for decades, and even invented the daVinci robot to do the hysterectomy instead of a surgeon. What do you think the Ob/Gyn Associations have let their surgeons do? No one knows if it’s 1:1000, or 1:500, or 1:400, or 1:315 women that actually does have uterine cancer, but splat!splat!splat! There it all goes! All over the woman’s abdomen, it is upstaged from a Stage I to a Stage IV cancer because the doctor has now iatrogenically done the bad deed. Never should have happened. Never should have been allowed. Ethics Committee should have been involved. One woman in the same hospital as Dr. Reed had also been upstaged to uterine Stage IV cancer, one year before. “Hush! Hush!” There was no need for Dr. Reed to be placed in this position. But “Hush! Hush!” She was. An “n” of 1 is too much. We don’t want one woman to ever suffer this known fate.

No one knew this was really happening until Dr. Amy Reed’s husband, Dr. Hooman Noorchasm, and his love for his wife and family of six children, that he took this to Change.org, then the Senate, then to the FDA.

The July 10-11, 2014 FDA Hearing where Dr. Noorchasm spoke, resulted in these conclusions by the FDA:

  1. Little to no evidence that morcellation can be performed without spreading cancer to other parts of the body;
  2. Informed consent, including the risk of spreading an unknown cancer, should be included from now on;
  3. There is no evidence that the bags…prevent the outcome we are trying to prevent.”
  4. “There is at present no safe way to offer morcellation as part of gynecological surgery.”

Watch the video of Dr. Noorchasm’s testimony to the FDA.  Now, he has accomplished the seemingly impossible for all women: he has all but put a ban on most uses of the morcellator. ROCK ON, Dr.Hooman Noorchasm! There’s always more work to be done, but once the people have a heart, a Movement has started.

What about the Ovaries?

Are they planning to keep your ovaries in? And the Fallopian tubes? If they take the ovaries out, you will not only have your uterus out when you wake up, but you will be in surgical menopause.  Surgical menopause sounds benign enough, but really it isn’t. The rapid depletion of hormones can cause serious mental health issues, along with a compilation of physical health issues that will be with you for the rest of your life. And although hormone replacement is available, hormone management is never as easy as popping pill or pasting a patch on your abdomen.

If the ovaries are removed with the hysterectomy, women enter surgical menopause overnight, leaving them with huge fluctuations in the estrogens, progesterone and the androgens. There’s no ‘gradual’ menopause for them over the course of 1-10 years, as other women naturally have. They hit the menopause wall POOF! When they wake up and oh! Eeeh! Was surgical menopause part of the Informed Consent? These ladies are ready to throw in the towel by now, as they are living in “hell”.

Symptoms range from precipitous drops in hormones if the ovaries were taken out: hot flashes, night sweats, they can’t sleep with their husbands any more, thinning hair, pain on intercourse, insomnia, disturbance in day/night cycles, depression, irritability, and with the uterus gone. Hormones need to be tested and hormone replacement is used on an individual basis, in light of lab results, contraindications to hormones, family history, and other risk factors.

It is important to note that surgical menopause also means faster aging, increased risk of heart attack, cognitive dysfunction, osteopenia, osteoporosis, a fractured hip from a fall.  Ask any woman who has had her ovaries removed about the complications and health issues she has faced. It might just change your mind.

Making the Hysterectomy Decision

Weigh the pros and cons and above all realize that your health matters. Whatever you do, speak up! Ask questions. You are expected to ask questions, like ordering food at a restaurant. So ask them.

Your body belongs to you. It is your temple, meant to be treated with respect and care. Ask if the if the daVinci robotic and morcellator will be used. Make sure you understand. The choice is yours, and no one can take it away from you.

Hysterectomy Research

Hormones Matter is conducting research on hysterectomy outcomes. If you have had a hysterectomy, please take a few minutes to complete The Hysterectomy Survey.

References

Maternal Vitamin B: From Periconception and Beyond

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A wise midwife recently told me that in 1960’s the B vitamins were part and parcel of a healthy pregnancy, not just folate (vitamin B9), that we stress now, but the entire complex of B vitamins, including: thiamine (vitamin B1), riboflavin (vitamin B2), niacin (vitamin B3), pantothenic acid (vitamin B5), pyridoxine (vitamin B6), biotin (B7), folate (B9) and the cobalamins (vitamin B12). Thiamine (also referred to as thiamin) was viewed as critical for maternal and fetal health and used within the midwifery community to ensure not only a healthy pregnancy, but a healthy postpartum. In many non-industrialized regions, thiamine is still supplemented for maternal and fetal health and maternal thiamine deficiencies are still recognized as critical impediments to health. Not so in the Western, industrialized world. Here, most resources and education seem set on prenatal folate; so much that it is difficult to escape folic acid supplementation in everyday foods.  Despite heavy fortification and regular use of prenatal vitamins, we see increasing evidence of nutrient deficiencies in pregnant mamas and most especially, in their children. Some of these deficiencies are visibly obvious, as least to those who look, such as the increased incidence of neural tube defects in children of women who are low in vitamin B12, but sufficient, even abundant in folate or B9. While other deficits are not so obvious, at least not immediately.

Maternal vitamin B status is important to the pregnancy at hand but also for the child’s long term health, as many of the B vitamins are capable of activating or deactivating gene programs in the children. Maternal vitamin B deficiencies can induce long-term epigenetic changes in the children, and likely, grandchildren. Maternal (and probably paternal too) vitamin B deficiencies silence genes in their off-spring that significantly increase the risk of insulin resistance, high blood pressure and a host of metabolic disorders through adulthood. Nutrition, in addition to its vital role as a source of energy for our cells, is the guidepost for DNA activation and inactivation. The balance of nutrients tell our cells how to function or not function, as the case may be. This information is carried from parents to offspring, across generations. It is this genetic control derived from lifestyle and nutrients that forms the basis of health for our children, and so it becomes something as parents we must pay attention to.

The B Vitamins are Important for Mom’s Health

For the moms, latent deficiencies in core nutrients will become unmasked with the increasing energy demands of pregnancy as many nutrients are shuttled preferentially toward placental and fetal needs, depleting maternal stores. Following delivery, the demands of lactation will further deplete maternal nutrient status and depending upon the vitamin in question, adversely affect her health and/or her child’s health.  Reports link maternal thiamine deficiency to hyperemesis gravidarum – severe vomiting across the pregnancy, in some instances leading to a full blown Wernicke’s Encephalopathy. Maternal vitamin B12 deficiency is linked to an increased risk of developing preeclampsia, intra-uterine growth retardation, preterm labor, but also, low vitamin B12 puts mom at risk for developing a myriad of neurocognitive, neuromuscular and psychiatric symptoms associated with B12 deficiencies both during pregnancy and postpartum.

How Prevalent is Maternal Vitamin B Deficiency?

Since there are few reference ranges for vitamin status during pregnancy, with most ranges based upon non-pregnant women, and since much of the research in nutrition is conducted in non-industrialized, poorer countries, it is difficult to assess how many outwardly healthy, western women carry nutritional deficiencies into pregnancy and postpartum. A 2002 study reported the vitamin profile in 563 pregnant New Jersey women at different points across the pregnancy. They found a trend towards too much folate, riboflavin, biotin and pantothenate (vitamin B5) and too little niacin, thiamin, vitamins A, B6, B12, suggesting that prenatal vitamins neither appropriately nor sufficiently address maternal nutrient demands.

A study of healthy pregnant women in Spain found that 32-68% of the women tested were deficient in thiamine, riboflavin or pyridoxine. Interestingly, the severity of deficiency correlated with oral contraceptive use, specifically with the length of oral contraceptive washout period prior to becoming pregnant. That is, when the woman became pregnant shortly after stopping oral contraceptives, she was more likely to exhibit a vitamin deficiency than if she had to waited to become pregnant and allowed her body to readjust to the non-oral contraceptive state. Additionally, the researchers found that if the woman was deficient in one of these nutrients, she was more likely to be deficient in each of them. Although not measured in this study, we know from other studies that many medications, including oral contraceptives, metformin and statins, decrease vitamin B12 significantly.

These reports, combined with the current trends in obesity, type 2 diabetes and the inherent nutritional shortcomings in the Western diet, suggest that it is likely that nutritional deficits and even nutritional imbalances are more common than are recognized.

Maternal Vitamin B Status Before Pregnancy Affects Health of the Male Offspring

A study carried out in sheep found clear evidence linking maternal vitamin B9 and B12 status pre-conception to the health the male offspring later in life. This particular study compared the offspring from sheep fed a nutritionally normal diet to those fed a slightly deficient diet, but one that was still within accepted nutritional parameters, from eight weeks before conception, throughout the pregnancy and six days postpartum. While the pregnancy proceeded normally in both groups and both male and female offspring appeared normal and healthy at birth, continued monitoring across the lifespan of the sheep, showed remarkable changes in the health of the adult males conceived on the nutritionally deficient diets. These males were heavier, had significantly disrupted immune function, impaired glucose metabolism and increased blood pressure, than the females and in comparison to the offspring whose moms had more nutritionally sound diets. This slight change, towards the lower end of what is considered a nutritionally normal diet, had significant influence on long term health in the male offspring. This study also identified clear epigenetic markers in the offspring conceived with dietary deficiency.

Maternal Vitamin B Status, Breast Milk and Infant Health

Maternal vitamin demands do not end postpartum. Lactation increases the demand for maternal nutrients. Deficits in maternal vitamin status impacts infant health and development as well as maternal health and recovery. It should be clear that maternal vitamin deficiencies negatively affect maternal health. Even so, there has been some contention regarding the relationship between maternal vitamin status, fetal development, the quality of breast milk and subsequent infant health and development.

A review of studies assessing vitamin status in breast milk found widespread deficiency, with levels below what is considered adequate intake for proper infant development in most of the samples. The B vitamins (thiamine, riboflavin, B6, B12 and choline) were particularly inadequate.

What was particularly interesting about this study is that researchers found that nutrient deficiencies affect maternal health more so than infant health. Nutrients can be categorized into two groups, those that respond favorably to maternal supplementation with higher milk concentrations (Group 1) and those that do not (Group 2). Group 1 nutrients included thiamine, riboflavin, B6, B12, choline, retinol, vitamin A, vitamin D, selenium and iodine. These nutrietns are secreted into breast milk and depleted rapidly in breast milk when maternal nutrient status is low. Deficiencies in these nutrients can be supplemented and passed on through the breast milk. In this way, maternal nutrient status directly affects the quality of the milk. Group 2 nutrients (folate, calcium, iron, copper and zinc), on the other hand, do not respond as well to supplementation. Breast milk concentrations of these nutrients remain relatively unchanged by maternal status, even when maternal status is declining. Supplementation with Group 2 nutrients affects maternal health more so than infant health.

Take Away

Fetal and infant health and development can be severely impaired by maternal nutrient deficiencies during pregnancy and during breastfeeding. The period across which maternal nutrient status affects the health of her offspring should be extended to well before conception. The B vitamins are especially important to proper development and long term health and appear to regulate genetic expression via epigenetic mechanisms. Recognizing and treating the potential nutritional deficiencies in modern, western diets, may go a long way towards reducing maternal illness while improving fetal, infant, child and adult health for generations. A growing body of evidence, and indeed, common sense suggest that while vitamin B9 or folate is critically important to maternal and fetal health, deficiencies in the remaining B vitamins and other nutrients may be equally important.

Physical Therapy for Endometriosis Adhesions and Symptoms

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As a women’s health physical therapist specializing in pain and scar tissue, I frequently see patients in clinic with intense, often debilitating pain caused by endometriosis.  These women have often tried every treatment made available to them:  surgery to cut adhesions and remove endometrial growths, hormone treatments, and symptom control (usually in the form of strong pain killers, anti- nausea, anti-depressant, and anti-anxiety medications).  Despite these interventions, some patients report continued or even worsening pain.  In the worst cases, their quality of life has been disrupted to the point of suicidal thoughts.

Endometriosis and Adhesions

How does it get so bad? It has to do with the chronic inflammation that endometriosis causes wherever it resides in the body.  Inflammation is a natural part of the body’s healing process. In normal healing inflammation is followed by the re-building processes to form new tissue, for example scars, that repairs the area. In chronic inflammation such as endometriosis, this scarring process continues, continuously build scars, or adhesions, that are not needed by the body.  As these adhesions form they can limit normal mobility of organs and connective tissue, put pressure on pain sensitive structures, and disrupt the function of the tissues they restrict. Because endometriosis continues to remain in the body, these symptoms can get worse over time. If the endometriosis or adhesions are surgically removed, the surgery itself may cause new adhesions and scar tissue to form.

With the chronic pain and chronic inflammation caused by endometriosis, other issues may develop. The muscles of the pelvic floor may go into spasm or constantly be too tight. This can cause pain with intercourse, difficulty using tampons, or difficulty controlling bladder or bowel function.  The nerves in the skin of the groin and genitalia may become over stimulated and confuse light touch with pain.  Bladder issues, gastrointestinal symptoms, postural changes, even lower back and neck pain can occur as the body deals with the chronic inflammatory process and pain.

Physical Therapy for Endometriosis Adhesions

When I feel the abdomen and pelvis in my patients with endometriosis, the tissue texture and mobility of the organs is often very different from that of unaffected tissue. Sometimes this is throughout the pelvis, other times it is only in very focal locations. The restrictions are not always in the same location as the primary area of pain. Because everything in the body is connected through the fascia (another name for connective tissue), restriction in one area can pull into other more distant areas. Imagine a spider web: tension at one point in the web can pull across to multiple other points.

Using specialized manual therapy techniques these adhesions and fascial restrictions can be softened or released, so that the pressure they put on surrounding areas is relieved (research on this is aspect of treating endometriosis adhesions is ongoing by the Clear Passage physical therapy group[i]).  If the endometriosis is active, it is always possible that new fascial restrictions will reform, due to the continued chronic healing process that is ongoing in the body.  However by learning self-treatment techniques patients can often manage their own symptoms quite well.

Physical Therapy Treatment Possibilities

What might treatment by a women’s health physical therapist entail?  Treatment of scar tissue and fascia typically involves applying pressure to restricted areas, over a prolonged period of time.  This can sometimes be uncomfortable, and can even mimic the pain you feel from endometriosis. This is one reason that having a good rapport and open communication with your therapist is so important. Treatment of the pelvic floor typically involves internal vaginal work, and sometimes includes internal rectal treatment. This is almost like going to the gynecologist, in that the therapist will use gloved and lubricated fingers to evaluate and treat the pelvic floor muscles and other internal structures.  As you can imagine not every physical therapist does this kind of work!  It requires additional training beyond licensure and it is very important that your therapist has experience working patients with endometriosis specifically.  The patient should always feel confident in the expertise of their therapist and comfortable during treatment. They will be draped for modesty, educated on the evaluation and treatment to occur, and asked for feedback as treatment progresses.

Does it Work?

Endometriosis can cause life-altering pain and dysfunction. Fortunately, I have seen remarkable results using physical therapy, both to treat the scarring and adhesions associated with endometriosis, as well as the constellation of other symptoms that may develop.   Physical therapy techniques such as Barnes Myofascial Release (MFR) and the Wurn Technique™ can be used to treat fascial restrictions and adhesions. Techniques such as MFR, trigger point release, soft tissue mobilization, biofeedback, and others can be used to treat the pelvic floor. Very importantly, the physical therapist should be experienced in specifically treating patients with endometriosis.

The take-home message I would like to impart is this: have hope. Physical therapy is a powerful tool that can be used to help patients with endometriosis decrease pain, increase function, and improve their quality of life.

Reference

[i] Wurn, B., Wurn, L., Patterson, K., King, R., & Scharf, E. Decreasing dyspareunia and dysmenorrhea in women with endometriosis via a manual physical therapy: Results from two independent studies . Journal of Endometriosis, 3, 188-196.

Thiamine Deficiency and Aberrant Fat Metabolism: Clues to Adverse Reactions

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Over the last several months, the writers and researchers at Hormones Matter have posted a number of articles about mitochondrial dysfunction and thiamine deficiency.  Thiamin, or thiamine as the internet search engines prefer, is critical to mitochondrial function. We’ve learned that thiamine deficiency can emerge gradually due to dietary inadequacies or more suddenly as a result of a medication, environmental or surgical insult. Regardless of the cause, deficits in thiamine evoke devastating health issues that can be treated easily if identified. More often than not, however, thiamine deficiency is not assessed and symptoms are left to escalate, mitochondrial damage increases, and patient suffering continues. Because thiamine deficiency is rarely considered in the modern scientific era, mild symptoms are ascribed to other causes such as “an allergy” or “it’s all in the patient’s head”. If, however, the cause is not revealed, the same old dietary habits will continue and can be guaranteed to produce much more severe and difficult to treat chronic disease.

Although there are a myriad reasons why mitochondria are damaged, medication or vaccine reactions paired with latent nutritional deficiencies seem to be common. Predicting who and how the mitochondrial dysfunction might appear, however, is more complicated. Quite often, athletes and individuals considered healthy are hit harder by a stress factor such as a vaccine than those whom we might not regard as particularly healthy. There are several potential reasons for this, some of which have been outlined previously. In this post, I would like to add one more reason why highly active, high performing individuals might be hit harder and more quickly than their less active counterparts with vaccine or medication reactions that induce thiamine deficiency.

Mitochondria are the Engines of the Cell

To use an analogy, the usefulness of a car obviously depends upon its engine. Mitochondria are the “engines” of each cell within our bodies, all 70 to 100 trillion cells that make up an adult body. They are known as organelles and are so small that their structure can only be seen with an electron microscope. But we can take this analogy further by comparing each cell to a different car model. A high powered car uses more gasoline than a low powered one and there are many models of each type of car. So some cells in the body require more energy than others, depending on the special function of the cell.  The most energy consuming cells are in the brain, the nervous system and the heart, followed by the gastrointestinal system and muscles. That is why those organs and tissues are most affected in the disease known as beriberi, the thiamine deficiency disease that we have discussed previously in other posts. The function of other organs is affected by the deficiency because of the changes in the control mechanisms originating in the brain through the autonomic (automatic) nervous system.

It has been pointed out that this disease in its early stages affects the autonomic nervous system by causing POTS. Beriberi and POTS, both being examples of dysautonomia (abnormal activity of the autonomic nervous system), can only be distinguished by finding evidence of thiamine or other nutrient deficiency as a cause. Thiamine is but one factor whose deficiency causes loss of cellular energy, resulting in defective brain metabolism and dysautonomia.  Although the relationship with vaccination is conjectural, some individuals with post Gardasil POTS were found to be thiamine deficient and had some relief of symptoms by taking supplementary fat soluble thiamine, an important derivative that occurs in garlic and has been synthesized. Not all of these thiamine deficient individuals have benefited to the same degree, suggesting that other deficiencies might also be involved. This post is to provide some information about more recent knowledge concerning the action of thiamine and the incredible, far-reaching effects of its deficiency, particularly in the brain. Experimental work in animals has shown that thiamine deficiency will damage mitochondria, a devastating effect for an acquired rather than a genetic cause. Far too much research has been devoted to genetic cause without sufficient attention to the way genes are influenced by diet and lifestyle.

The Importance of Enzymes to Mitochondrial Function

Before I provide this new information, let me remind the reader that enzymes, like cogwheels in a man-made machine, enable bodily function to occur. The importance of thiamine is that it is a cofactor to many of the enzymes that preside over energy metabolism. Without its cofactor an enzyme becomes inefficient. Perhaps it might be compared with missing teeth in a cog wheel. With missing teeth the cog wheel may still function but not nearly as well as it would with all of its component parts.

In previous posts we have discussed how thiamine deficiency can be caused by an excess of sugar in the diet. I have likened this to a “choked engine” in a car where an excess of gasoline, relative to insufficient oxygen concentration in the mixture, makes ignition of the gasoline extremely inefficient. Bad diet, one that is rich in sugary, carbohydrate laden foods may be one of the more common contributors to latent thiamine deficiencies. Excessive intake of processed fats and the concomitant changes to mitochondrial function and energy metabolism may be another important contributor.

Thiamine and Fat Metabolism

All the enzymes affected by thiamine deficiency have a vital part to play in obtaining cellular energy from food by the process of oxidation. Most of them have been known for many years but in the nineties a new enzyme was discovered. It has a very fancy name that has been simplified by calling it HACL1.  Only in recent years has it been found that HACL1 is dependent on thiamine as its cofactor. Although not reported, it may mean that it is also dependent on magnesium. This is exceedingly important because it introduces the fact that thiamine is involved in fat as well as carbohydrate metabolism, something brand new, even to biochemists.

Here I must digress again to describe another type of organelle called a peroxisome that occurs in our cells.  Like mitochondria, they are infinitesimally small. Their job is to break down fatty acids and they have a double purpose. One purpose is to synthesize very important substances that construct and maintain cells and their function: they are particularly important in the brain. The other purpose is what might be called fuel preparation. As the fatty acids, consisting of long carbon chains, are broken down, the resulting smaller fragments can be used by mitochondria as fuel to produce energy.  Failure to break down these fatty acids can result in the accumulation of natural components that may be toxic in the brain and nervous system or simply result in lack of one type of fuel. That is why feeding medium chain triglycerides by administration of coconut oil has been reported useful to treat early Alzheimer disease. They can be oxidized in mitochondria.

The Important Use of Fatty Acids in Mitochondrial Health

Here, I want to use another analogy. Imagine a lake that admits water to a river through a sluice gate that has to be opened and closed by a farmer who regulates the supply of water. If the gate is open the river will supply water to the surrounding fields. If however the gate is closed, the river will begin to dry up and the crops in the fields will suffer. Perhaps the farmer half closed the gate during a rainy period and has forgotten to open it when a dry period follows. High temperatures in the dry period results in insufficient water to meet the growth needs of the crops.

In this analogy, the lake represents food, the sluice gate is the HACL1 enzyme and the farmer who controls the gate represents thiamine. The water in the river represents the flow of fatty acids to the tissues for the double purpose of cellular construction and fuel for oxidation. The half open gate represents a minor thiamine deficiency, more or less sufficient for everyday life but not enough when there is greater demand. A high temperature that increases the water needs for crops represents Gardasil and many other medications as a stress factor, placing a greater demand on essential metabolic action.  The analogy also implicates the nature of the crops, some of which require more water than others. The crops, of course, represent body tissues and organs.

If we consider high performing individuals, whether academically or athletically, like high performance cars or crops that demand more nutrients, we can see how a previously unrecognized minor deficiency might trigger clinical disease by the stressful demands of a vaccine or medication. Some pharmaceuticals can attack thiamine directly, like Gardasil and the fluoroquinolones, while others attack different pathways within the mitochondria.

No matter the pathway, high performing individuals, with high energy needs not covered by diet, may be hit harder when a medication attacks mitochondrial energy.

The Outcome of Defective Fatty Acid Metabolism

Returning back to the HACL1 enzyme, we now know that HACL1 is the first thiamine dependent enzyme to be discovered in peroxisomes. It is research news of the highest importance, affecting us all. Its action is to oxidize a diet related fatty acid called phytanic acid and fatty acids with long carbon chains that cannot be used for fuel until they are broken down. Phytanic acid is obtained through consumption of dairy products, ruminant animal fats and some fish. People who consume meat have higher plasma phytanic acid concentrations than vegans. If the action of HACL1 is impaired because of thiamine deficiency the concentration of phytanic acid will be increased. The river in the analogy actually represents a series of enzymatic reactions that may be thought of as down-stream effects, whereas thiamine deficiency, being up-stream, affects all down-stream phenomena. One of the reasons thiamine deficiency is such an important contributor to illness is because its effects are broad.

These enzymatic reactions, known technically as alpha oxidation, involve four separate stages. It has been known for some time that if another enzyme at stage two is missing because of a gene defect, the result will be damage to the neurological system known as Refsum’s disease. Symptoms include cerebellar ataxia (also reported after Gardasil vaccination), scaly skin eruptions, difficulty in hearing, cataracts and night blindness. Other genetic mutations in alpha oxidation, resulting in various biochemical effects, result in a whole variety of different diseases. This places thiamine deficiency as a potential cause for all the down-stream effects resulting from defective alpha oxidation, for it has been shown in mice that this vitally important chemistry is totally dependent on presence of thiamine. Since its complete absence would be lethal, we have to assume that it is mild to moderate deficiency, equivalent to a partial closure of the sluice gate in the analogy.

Sources of Phytanic Acid: How Diet Affects Thiamine

In ruminant animals, our source of beef, the gut fermentation of consumed plant materials liberates phytol, a constituent of chlorophyll, which is then converted to phytanic acid and stored in fat. The major source of phytol in our diet is, however, milk and dairy products.  It raises several important questions. If thiamine deficiency is capable of causing an increase in phytanic acid in blood and urine, it might be a means of depicting such a deficiency in a patient with confusing symptoms. It might also explain why some individuals who have been shown to have thiamine deficiency by means of an abnormal transketolase test have symptoms that are not traditionally accepted as those of such a deficiency, perhaps because of loss of efficiency in HACL1.

If an excess of sugar in the diet gives rise to a secondary (relative) thiamine deficiency, we are provided with an excellent view of the extraordinary danger of empty simple carbohydrate and fat calories, perhaps explaining much widespread illness in Western civilization. Interestingly, it would also suggest that something as benign as milk could give rise to abnormal brain action in the presence of thiamine deficiency, because of phytanic acid accumulation. Our problems with dairy products may go well beyond lactose intolerance and immune dysregulation.

In sum, the discovery of HCAL1 enzyme and its dependence upon thiamine suggests one more mechanism by which thiamine deficiency affects mitochondrial functioning. As emerging evidence indicates a myriad of environmental and pharmaceutical insults impair mitochondrial functioning, thiamine deficiency ought to be considered of prime importance. Deficits in thiamine evoke devastating health issues that can be treated easily if identified.  If, however, thiamine deficiency is not identified and the same old dietary habits continue, the latent thiamine deficiency can be guaranteed to produce a much more severe and difficult to treat chronic disease. Moreover, individuals with thiamine deficiency who do not respond sufficiently to thiamine replacement might also have aberrant fatty acid metabolism. This too should be investigated and dietary changes adopted.

Do I Have Postpartum Depression? Case Scenario and Resources

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Postpartum depression may occur in up to 1 of every 8 pregnant women. Here, we produce a fictional representation of how it may present to you in real life, whether you are a family member, friend, or spouse. It is important to note that postpartum depression can also occur during pregnancy, and can occur as a seemingly ‘normal’ event of childbirth depression, yet postpartum depression carries more burdens and feelings of being totally overwhelmed, less in control of one’s life, anger, and rage. Gradiations of postpartum depression thus can be so subtle that you think nothing of it, yet with extreme postpartum depression, the mother is encompassed by hallucinations or voices incessantly talking to her, instructing her to harm herself and/or her child. The number one cause of death in new mothers is suicide, with thoughts of suicide and self-inflicted harm as very serious problems (Moses-Koldo, 2009; Lindahl, 2005)

Recognizing Postpartum Depression: A Case Scenario

Her name was Anna, little Anna. She soundly slept in the car all the way home, as if she was going to be a “good baby.” Her little hands scrunched up into balls every so often, and although she slept, her eyes moved just so, proving that she was in rapid eye movement sleep.

In the front seat, the mother with the straggly hair, Josephina, put on the smiling face of a clown. None of the doctors had noticed a thing that was wrong with her, even though she did complain to one good-looking young doctor in training. All he did was scoff at her. He made her feel ashamed and silly. But inwardly, she was petrified, just petrified, of being left alone with this little being that depended on her for everything.  Her thoughts of throwing the baby off the ledge and jumping in after her, like diving into a pool, continued to grow in their intensity, frequency, and enormity.  Josephine was scared to turn the lock and enter back into her apartment that represented loneliness, so she let her friend Marissa do it. Marissa stayed long enough to lay the baby in a clothes drawer on the floor, surrounded by blankets so soft that they still smelled like fabric softener.

As Josephine said her goodbyes and closed the front door with barely a squeak, she silently turned her back onto the white painted door. Slowly, ever so slowly, she slid down the door crying silent yet violent tears, body heaving, until at last she was sitting on the floor. All the thoughts continued to pound in her head: “Throw the baby out the balcony! Jump in and just dive in after her!” Her unkempt hands held her head, fighting the increasing enormity of the battle. “Do it!” “Do it!” Josephine grasped aloud at these intrusive thoughts that didn’t belong in her brain. She knew they didn’t belong there, and she felt cursed upon realizing what an ungrateful new mother she must be. Maybe she didn’t deserve to have this little Anna at all. Laden with guilt, she rocked herself on the floor and thankfully, the baby slept through it all.

She thought, as she wiped her tears for the millionth time, “Do all mothers feel this way? Do they all go through this? Aren’t I supposed to be happy?” Of course she was tired. No, she was exhausted. Of course she had continuing insomnia and her mood swings were unpredictable and covered the expanse of linear possibilities: one minute laughing and the next minute, crying. She looked at her hands and they were trembling as another layer of guilt fell over her like a black sheet at Halloween, showing only her eyes. She ran to the bathroom and threw up for the third day in a row. The thoughts turned into guilt and shame, chastising her very soul. She should be happy, but she wasn’t. She should be having happy thoughts, but she wasn’t. Another black sheet of guilt and remorse fell upon her, and her shoulders drooped with the heavy weight that she bore. She wanted to scream! She wanted to run! And yes! She wanted to jump over that balcony!

The exhaustion, insomnia, and the overwhelming state of mind were perfectly normal for any new or seasoned mother, indeed. Each pregnancy was different, but all pregnancies carry with them the dawning of another layer of new responsibilities, the screaming of a helpless being, the bursting of the mother’s eardrums, a hundredfold changes in circulating hormones, and concurrent inflammatory reactions that all but wreak havoc on a woman’s body. If she also suffers from poor nutritional status, this further compounds the biochemical reactions in her body, adding another twist of lime. When the baby cries, the breasts drip milk; it’s just automatic. Her body is a robotic machine, connected inexplicably to her baby, just as if the umbilical cord had never been cut. Mother and child are still tied together. Like a parasite of alien proportions, the baby sucks at her breasts and also sucks at her life.

Transition to Motherhood: When Postpartum Depression Rears its Ugly Head

For most women, this depression hits its worst on the day of the “Third Day” blues. Then it seemingly disappears just as quickly as it came. The blues gently fade away with day number four; they can last a week or two. Mom is smiling and laughing again. She has no thought of harm to herself or her baby.

Risk factors and symptoms for postpartum depression are broad and ill-defined. Some research focuses on the sadness, the lack of energy and the depression, while other research suggests postpartum depression is not really a depression in the classic sense, but an anxious feeling of unease, marked by increased intrusive thoughts, like those Josephina experienced. In truth, how and when women present with postpartum depression is highly variable. The symptoms can begin in pregnancy, 3-6 weeks after childbirth, or really anytime. For more information about pregnancy and postpartum psychiatric distress, the following articles may be helpful: Framing the Pregnancy Postpartum Hormone Mood Debate, Beyond Depression: Understanding Perinatal Mental Health,  Maternal Psychiatric Disturbances and Hormones, What Causes Postpartum Depression? You might also consider reading the personal stories listed on our blog about postpartum depression. If someone you know is suffering from postpartum depression after childbirth and you reach out, you may save a life.

Reaching Out to a Postpartum Woman

So you are the one that had met Josephina in the market before she had her baby, and you exchanged phone numbers with her. You are new in town, live comfortably with your husband and two toddlers, and are looking for a friend. You want another baby, but your husband does not. You decide to call Josephina to see how she is doing.

“Hi Josephina. This is Elena. Remember we met in the grocery store? My kids and I were wondering if we can stop by and visit. We have a gift for you and the baby. Call us back when you can, ok?” You leave a message on her cell phone, as Josephina did not pick up. She was too busy staring at the floor, feeling too sad and guilty to move.

You call her again the next day, after Josephina had awakened in a sweaty bed, had only two hours of sleep, and felt like a walking zombie. This time, Josephina picked up the phone and said you could come visit.

You and your children arrived to her apartment door knowing that it was the right one; you could hear the screaming baby all the way down the hallway. You, being so perceptive, also noted that you could not hear any words of consolation, no kisses, no whispers or singing of lullabies. Josephina answered the door, walking away without saying hello. She mumbled something about going to get the baby, and came back from the bedroom with little Anna. You let your children play with the baby laying in her portable car seat, while you pulled Josephina aside.

“What’s wrong, honey? You don’t look so good to me.” Clearly, Josephina was sorely depressed and had not yet bonded with her baby. She was thin as a rail, malnourished, unkempt to the extreme, and you sought immediate help for a diagnosis of Postpartum Depression. You told Josephina to go take a nice bath or shower, put on some clean clothes, and by the time she was finished, you would have a few phone numbers for her to call, a few resources for her to use so that she could get help and not be all alone with this beautiful baby girl.

Josephina stood still. She was catatonic. Immobilized. So you turned on the shower, took away the razor blades on the tub, and got her undressed. You went back and forth, checking on the baby, looking for baby formula, and watching Josephina shower. “Put the shampoo on first, Josephina.” You got internet access on your iPhone and did a search for Postpartum Depression. Finding a page full of resources, you checked on the baby and the children, then on Josephina again, saying, “Okay, Josephina, time to do shampoo number two!”

And you started making phone calls. You learned that Postpartum Depression is the #1 complication of childbirth. 1 in 8 women suffer from Postpartum Depression (that we know of), many going undiagnosed.

Approaches to Postpartum Depression

Treating postpartum depression presents unique challenges and concerns compared to treating depression or other mental health issues in non-pregnant women. In addition to the concerns about breastfeeding, new moms are sleep-deprived, sometimes feel isolated, have just undergone enormous hormonal changes and are often nutritionally deficient. Tackling these issues may require multiple treatment modalities. Here is an overview of the standard approaches to postpartum depression treatment.

  1. Counseling/Psychosocial Assessment and Support. This first-line road to better mental health helps with talking about your thoughts, coping mechanisms, and problem-solving; removal of solitude can make a huge difference. In addition to individual therapy, a number of postpartum and parenting support groups exist in every community, and many referral systems are in place through helpline resources, such as Resources International “Get Help”  http://www.postpartum.net/Get-Help.aspx .
  2. Anti-depressants, anxiolytics and/or other medications.  A common method to treat postpartum depression, but it is not without controversy and risk. If you are breastfeeding, be sure and talk to your doctor about which drug(s) to go on. Medications may pass from the mother through breast milk to the baby. It is crucial to note that with adolescents and young adults and postpartum women some antidepressants may lead to “…increased risk of suicidal thinking and behavior…” exacerbating the situation. (NIH; Package Insert). You may want to seek at least two opinions before starting antidepressant therapy.
  3. Hormone therapy. Still an area of controversy, some clinicians advocate attenuating the decrease in postpartum estradiol with transdermal estradiol (Moses-Kolo, 2009). The thinking is that if this hormone declines more gradually over time, the symptoms of postpartum depression may lessen or diminish completely. The research is mixed. Other research suggests declines in progesterone are linked to symptoms and thus, treating with progesterone may alleviate the symptoms. (It should be noted, however, that synthetic progesterone as is found in birth control pills, exacerbates postpartum depressive symptoms and should be avoided.) And yet, other research suggests that it is not the decline in estrogens or progesterone that spur postpartum symptoms, but rather abnormal fluxes in androgen hormones. It should be noted that undiagnosed thyroid conditions are common in women, especially during pregnancy and following childbirth, and so, thyroid disease might also be responsible for the onset of symptoms. With postpartum psychiatric issues, thyroid disease should always be tested for and treated if found, ideally prior to beginning other therapeutic interventions.
  4. Ongoing NIH Clinical Trial: If you are interested in participating in a clinical study on mood changes after childbirth whether or not you have had postpartum depression before, you can visit the NIH website here. This Screening Program to Evaluate Women with Postpartum-related Mood and Behavioral Disorders (Study 03-M-0138) is currently recruiting volunteers. Selected patients may be asked to participate in a follow-up study using estradiol for postpartum depression.
  5. Nutritional therapy. Emerging evidence connects nutritional deficits to postpartum psychiatric symptoms. With the added physical burden of pregnancy and childbirth, previously hidden nutritional deficits become unmasked and can initiate a cascade of psychiatric and inflammatory reactions.

From Postpartum Depression to Psychosis

“Put on your conditioner now, Josephina,” you instruct, as you sit and make some phone calls. Even your own hands are shaking now, because you don’t want her to lose her baby to the State, but you also don’t want her to take her baby and jump off the balcony. By this time, she has told you everything. It is almost too much. You are overwhelmed and you know that she needs professional help. You know that the next 15 minutes will be crucial, even staggering, in how you approach her illness. Your concern for how this will impact the rest of her life almost leaves you frozen, but you know that you know that you know that two lives hinge on your decisions. And to further confound matters, you know that none of your options will be optimal. No matter which path you choose, you could be perceived as ‘the bad guy’. The diagnosis may be made, but the treatment options are limited and wrought with controversy. There is no easy answer. Every choice comes with a consequence and you can only do your best.

Frightened at the unknown future results of your own actions, you begin to doubt yourself as pessimistic thoughts cry out: “What if I make the wrong decision?” You oscillate between worries, “If I do nothing and she hurts herself, it would be my fault.” On the other hand, “But if I call 911 and they take the baby from her, I would have to live knowing that I did that to her and the baby.” Back and forth you go. The reasonable, pragmatic side of you knows for a fact that Josephina can not take care of herself and can not be left alone with her baby. For one moment, the squeals of the baby break through the coo’s of your own children’s laughter, almost as a reminder, say yes! It is a reminder of how things are ‘supposed’ to be. Again, you internalize this conclusion, knowing that you need help yourself. You cannot bear this burden alone. You have no experience with this, you dread making a life-long or fatal mistake. You are smothered into a corner to do something NOW!

So you decide to call for help.

When Postpartum Depression Becomes an Emergency: Finding Help

Debating psychotic disorders and parenting, and the relevance of a mother’s children for general adult psychiatric services was, in 2000, Louise Howard’s project as a Research Fellow. She stated that women with psychiatric issues who become pregnant should be specifically identified for further study, assessment, and improved outcomes, considering their children. The impact of the parent’s illness on the children, as well as a need for supportive services, needed further study.

In 2000 in the UK, a woman could voluntarily admit herself to a the first psychiatric unit, the first women-only residential mental health crisis unit in Drayton Park, North London, where children could be admitted with their mothers (Killaspy, 2000).  Residential alternatives to inpatient ward care in England have since been shown to provide more patient autonomy, greater satisfaction, less coercion, more ‘voice’, less aggression, and less anger (Osborn, 2010). Since the 1980’s, these residential units have been rampant throughout the Australia, UK, Europe, and New Zealand.

In the USA, there are many ‘postpartum depression treatment centers’ that can serve as the initial call for help, and provide care in the outpatient clinic setting. This resource seems most appropriate for women with depression who are not hysterical, hallucinating, are overcome by intrusive thoughts, or are having visions or hearing voices. For a government department (i.e., Substance Abuse and Mental Health Services, or SAMHSA) that is continually updated and offers local, mental health referrals, use telephone 1-800-662-4357, 1-800-662-HELP, and/or website www.findtreatment.samhsa.gov .

During the week of August 11, 2011, the U.S.’s first treatment center based on the Drayton Park, London model of inpatient mother:child care opened. This was first inpatient facility for severe postpartum depression for both mothers and babies. It is still located at the University of North Carolina’s Chapel Hill hospital’s psychiatric ward. Brown’s University has a Postpartum Day Hospital opened for mothers and their baby’s weekdays from 9 am to 5 pm (Stampler, 2011).

A bipolar woman who gets pregnant has an increased chance of having postpartum depression leading to postpartum psychosis (Marks, 1992), but she may not seek care for her needs, for fear that her baby will be taken away from her (Howard 2000). When things have escalated to the point of Mom wanting to harm herself or the baby because of voices in her teeth telling her to do so, psychosis may exist and this demands immediate emergency care. Society still places a stigma on mental illness and it is unfortunate that an involuntary admission to a psychiatric unit is usually accompanied with separation from the child(ren).

In the United States, the most common route is for the woman to be rather forcefully taken by the police to determine her fate in jail or a psychiatric ward. Nonetheless, you must call 911 for any immediate danger to self or baby. When you do, a number of things may happen depending upon the state that you reside in.

As a useful tool to help you assess whether or not you have severe postpartum depression, Harvard Medial School’s “Edinburgh Postnatal Depression Scale” is an online test you can take in 5 minutes.

From Bad to Worse: When Postpartum Depression Risks Harming the Mom and Baby

Poor Josephina cannot dress herself. So you help, frequently checking on the baby and your own children who are happily playing in the living room. You ask Josephina several questions, “Do you have anyone to help you with the baby? Any relatives here?” Josephina just nods her head, “No.”  As you continue to help her get dressed, you ask her if she’s taking any medications. “No.” You ask her if she is still having these thoughts of jumping off the balcony and she slowly nods her head, “Yes” as her eyes widen and her eyes turn maliciously toward yours. “Get her away from me. Take her now. Please take her now and take care of her. I can’t take care of her. I beg you to please take her.”

You are in shock as you make her write it down on a piece of paper, dated and signed with her signature. You only left her for 15 seconds to check on the children, but already she had bolted with the car seat and the baby, and was trying to unlock the sliding glass door. You turn to Jimmy, the older boy and look him in the eyes. “Call 911 now.” He’s not sure why, but he can tell Mommy is in no mood for questions. As he picks up the phone, Josephina and Elena fight at the sliding glass door lock, each trying their own destination: Josephina to open it, and Elena to close it. The baby is suspended in mid-air and Elena says, “Put the baby down! Put the baby down now!” Josephina looks like a maniac now, bloodying up her fingernails on the door latch in a desperate attempt to jump off the balcony. They both hear, “Um. I’m not sure, but my Mom and a lady are fighting over a baby at the balcony.”

The little child of Elena, Cristal, starts crying. Mommy said, “Go and lock yourselves in the bathroom. Here, take the baby with you.” And in one final attempt and with all her bloody might, Elena kicked Josephina enough to sidetrack her for a microsecond. Elena forced the baby car seat out of Josephina’s grasp, and ran with all three children to the bathroom. As she turned the corner, she could see that Josephina was staring at her bloody fingernails, then looked up at her, then began to dart for the bathroom door. Elena got all the children in, and told Jimmy to lock the door. Now, the children were safe.

This 1 in 10,000 chance of a psychotic depression has turned into a police matter now, and Elena poses. She is ready to fight for all the babies. But she speaks in a calm tone, reminds Josephina of the calm shower, and gets her to sit down. Shortly thereafter, the police are at the door and they take Josephina away to book her for Child Endangerment and Danger to Self.

It’s not Josephina’s fault that her psychosis led her to this. If one person had listened to her earlier, she would have received help earlier, and this never would have happened. If she had known, she could have voluntarily turned herself in to a postpartum treatment center. If she had known, she could have taken the Edinburgh Postnatal Depression Scale test on her own, to self-diagnose and self-realize the extent of her own depression. If only…

But there is no pity for her, no blaming the biochemical changes in her brain, much like that described in people with a brain tumor who do aggressive things without realizing it. She is ostracized as a criminal instead of as a psychiatric patient, and is sentenced to 15 years in a Woman’s Prison. Being as there are no relatives that come forward, Elena gains first temporary and then permanent Custody of little Anna, then moves away to another city. Not something she had planned at that first chance meeting in the store.

If Josephina gets a proper diagnosis, showing that she was bipolar before the pregnancy, and receives proper treatment, her chances of recovery are 100%. But there’s a catch. She may never be able to go off her medications.

To learn more about resources for postpartum depression: Resources for Postpartum Depression.

About the Author: Dr. Margaret Aranda is a USC medical school graduate, as well as an anesthesiology resident and critical care Fellow graduate of Stanford. After a tragic car accident in 2006, she unfolded her passion of writing to advance the cause of health and wellness for girls and women. You can read more of her work on her personal blog, Dr. Margaret Aranda, her Pinterest page, a page on Postpartum Depression, her author’s page at Tate Publishing or follow Dr. Aranda on twitter @DrM_ArandaMD.

References

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  2. Killaspy, H., et al. Drayton Park, an alternative to hospital admission for women in acute mental crisis. Psychiatric Bulletin, 24, 101- 104. Abstract/FREE Full Text
  3. Lindahl, V., et al. Prevalence of suicidality during pregnancy and postpartum. Arch Womens Ment Health. 2005 Jun;8(2):77-87. Epub 2005 May 11. http://www.ncbi.nlm.nih.gov/pubmed/15883651 (Accessed June 26, 2014).
  4. Marks,  M.N., et. al. Contribution of psychological and social factors to psychotic and non-psychotic relapse after childbirth in women with previous histories of affective disorder. J Affect Disord, 1992: 29, 253-264.
  5. Moses-Kolo, E.L., et.al. Transdermal estradiol for postpartum depression: A promising treatment option.  Clin Obstet Gynecol.  Sep 2009; 52(3): 516-529. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782667/ (Accesed June 26, 2014).
  6. NIH. Transforming the understanding and treatment of mental illnesses. Depression. FDA Warning on Antidepressants. 2011. http://www.nimh.nih.gov/health/publications/depression/index.shtml. (Accessed June 26, 2014).
  7. Osborn, P.J., et. al. Residential alternatives to acute in-patient care in England: satisfaction, ward atmosphere, and service user experiences. Br J Psych 2010: 197:x41-s45. http://bjp.rcpsych.org/content/197/Supplement_53/s41.full (Accessed June 26, 2014).
  8. Package Insert. Fluoxetine hydrochloride. 1987. http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/018936s091lbl.pdf (Accessed June 26, 2014).
  9. Stampler, S. First U.S. Inpatient Clinic for Moms with PostPartum Depression Opens. Huffington Post: Parents. Oct 19, 2011. http://www.huffingtonpost.com/2011/08/19/americas-first-inpatient-postpartum-depression-unit_n_931179.html (Accessed June 27, 2014).
  10. Treatment Centers. Study examines postpartum depression. Psychiatry/Mental Health. May 24, 2010. http://www.treatmentcenters.net/psychiatry-mental-health/study-examines-postpartum-depression/ (Accessed June 27, 2014).

Resources for Postpartum Depression

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Postpartum depression can be frightening and devastating for some families, but it doesn’t have to be if you and your loved ones get help. Listed below are resources for postpartum families. If you suspect you or a loved one has postpartum depression, find help.

Resource Phone Numbers Available 24/7

  • Suicide Hotline 1-800-SUICIDE
  • National Suicide Prevention Hotline 1-800-273-TALK
  • Disorders.org (Postpartum Psychosis) 1-800-943-0566

Postpartum Depression Websites and Support

More about Postpartum Depression

To learn more about postpartum depression in all its forms, read the following articles.

If you have a postpartum story that you would like to share so that other women and families can navigate this condition, consider writing for us. We accept personal health stories to spread awareness and encourage openness. Write for Us.

If you know of additional resources for new moms and families, local, national or international, please add them to the comments section.