Birthing Bliss, Birthing Trauma, and the Role of the Perinatal Patient


KellyBroganMD.com
Dr. Kelly Brogan
February 8, 2020

I remember looking out of my living room window, drawing on my connection to all the women in the world who had felt this energy before, all that were in that moment, and all that would in time to come. This energy, this incredible power, was like a wave that I was riding for a brief window of my life, and sharing with my baby to move us through time into a new type of union. To me, this wasn’t anything to resist, to be afraid of, or to suppress. All I had to do was be there to witness, and keep my mind from getting in the way.

I came to a place of strong advocacy for homebirth because I am a tireless student of research, opinions, and “radical” theory espoused by critical thinkers. I believe in being an informed individual first and a patient second and surrendering my decision-making to a physician trained to perceive childbirth as a pathological process requiring management was not consistent with that perspective.  I knew that there were caregivers out there who believed in supporting the body’s natural process in a gentle way and who knew how to provide that support, actively and passively.  These are midwives.  They are the primary birth attendants in most of the 40+ nations in the world with more favorable maternal and infant mortality rates than our own.

So, how does a woman get to a place where she can turn her back on a society that teaches birth is a painful nuisance at best and a horror show of danger at worst?

Through active engagement in informed consent.  A careful review of some of the epidemiologic literature and an excellent book on the subject called Pushed by Jennifer Block will inform that prospective mother of the fact that countries with the best maternal/infant outcomes have 20-30% of their babies at home, and a caesarean rate of no higher than 15%.  In these healthy births, labor begins spontaneously, the woman is free to move about for whatever duration necessary, and she pushes in an intuitive position.

This soon-to-be-birthing reader might be prompted to question some of the casually accepted “rules” of hospital birth including induction of labor post-dates, the ban on eating and drinking, and active intervention after 24 hours after rupture of membranes.  She might note that continuous electronic fetal monitoring is a ubiquitous mandate in the hospital setting despite an absence of randomized, controlled studies demonstrating any benefit with regard to maternal/infant outcomes (and a noted higher association with caesarean section given the attendant immobilization and anxious interpretations of “the strip”).  Here is the informative Lamaze-sponsored handout I give my patients which highlights the discrepancy between known evidence (including Cochrane reviews, and even ACOG recommendations) and common practice, often militantly imposed.

Pushed discusses a WHO study which identified that only 10% of maternity care is justified by scientific evidence (as opposed to insurance constraints, convenience, liability, and habitual practice).  This wouldn’t be such a concern if the risks associated with interfering in a physiologic birth weren’t so troubling.  Here are some tidbits she reviews:

  • Infants born by caesarean are 3x more likely to die in the first month, and mothers are 2x more likely to die.  Caesarean carries risks of infection including necrotizing fasciitis, organ damage, adhesions, hemorrhage, embolism, hysterectomy, dehisance, poor respiratory adaptation for the baby, and future development of a major undesirable – placenta acreta (at an incidence of 1/533 in 2005 births from 1/19,000 births in 1970)
  • Epidurals decrease blood pressure, slow contractions, and lengthen labor, increasing the likelihood of tearing, fever, and instrumental delivery
  • Vaginal birth after caesarean has a rate of rupture of 1/200 which is comparable to the rate of miscarriage with an amniocentesis, but is all but impossible to obtain given the reflexive second, third, and fourth caesarean birth plans
  • Homebirth is comparably safe with lower intervention rates according to common sense and seminal studies.

The problem with the application of these interventions is that they serve to disempower the laboring woman, and force her to cope with the unintended consequences of the intervention domino effect.  Wresting autonomy from an individual in the interest of a questionably-evidenced system has feed-forward implications for generations.  Perhaps both psychiatry and obstetrics are guilty of pathologizing processes that scare us, and in our effort to subdue, we use crude and inexact implements in acute settings without consideration of the collateral damage.

Even the donning of a hospital gown on arrival puts a woman in the role of a sick patient rather than a conduit for life’s most transcendent contact with creation.  I hear frequent reviews from my patients, stating, “the room looked like a battle ground”, “I felt like I was drugged…like it wasn’t my baby”, “I was offered an epidural so many times, I thought I really needed one”.  This is not an arena in which we can expect Ina May Gaskin’s “sphincter law” to play out successfully – a woman needs a sense of calm, safety, and privacy open her body to the world and bring forth a baby.

Interfering with the sophisticated process of a physiologic birth may have unintended short, medium, and long-term effects.  Studies like this allude to the role of vaginal birth in the foundational seeding of the infant’s microbiome, but are there any benefits with regard to mom’s postpartum mood?  Does mode of delivery influence the risk of postpartum depression?  To my mind, it certainly seems possible that disruption in oxytocin feedback loops through interference with the hypothalamic-pituitary-adrenal-gonadal axis would set a woman up for near-term difficulty buffering the transition to new motherhood.  If a physiologic birth is interfered with, the woman is left to go through the motions unaided by appropriate hormonal cascades – like walking across hot coals without shoes.

Despite the intuitive connection between a mother’s birth-related trauma and postpartrum depression, data addressing the question of whether mode of delivery influences risk is equivocal: some propose no risk associated with caesarean, like this study in which depressive symptoms after caesarean were resolved by 6 months and this that suggested being a housewife with a history of depression were primary risk factors, and this metanalysis. Others, like this Armenian study, suggest that caesarean, and particularly elective caesarean, may put a woman at greater risk for postpartum mood disturbance.  A prospective cohort study in China found that, at two weeks, by Edinburgh Postnatal Depression Scale (EPDS), women were 2x more likely to be depressed if they had a surgical birth. Myriad confounders compromise this data, and I would argue that a woman’s psychological orientation toward self-empowerment – what an empowered birth looks like to her – may be more important than the disruption of the hormonal cascade.

The mind is a powerful filter.  Perhaps the most provocative study I have come across is an fMRI evaluation of women responding, in multiple brain regions, to their own baby’s cry, and how this response is blunted after a surgical birth.  Could this evolve to be corrected for?  I would imagine so, but it suggests that surgical birth should be reserved for the <10% of true emergencies that could not otherwise have been prevented by allowing a woman to labor at her own pace, in her own comfort zone, without any interventions… the way it’s been done for millions of years.

Read More At: KellyBroganMD.com

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This post originally appeared on Mad in America as Birthing Bliss, Birthing Trauma and the Role of the Perinatal Patient.

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Kelly Brogan, MD

Kelly Brogan, M.D. is a Manhattan-based holistic psychiatrist, author of the New York Times bestselling book, A Mind of Your Own, and co-editor of the landmark textbook, Integrative Therapies for Depression. She completed her psychiatric training and fellowship at NYU Medical Center after graduating from Cornell University Medical College, and has a B.S. from MIT in Systems Neuroscience. View full bio. Want to share this article on your own blog? View our reposting guidelines.

Psycho-Neuro-Immunology: Uncovering the Roots of Mental Illness

KellyBroganMd.com
Dr. Kelly Brogan
Holistic Psychiatrist & Author Of A Mind Of Your Own
February 4, 2020

Nine months after the birth of my first daughter, I felt off. Flatness, forgetfulness, cold, and tired. If I hadn’t discovered my formal diagnosis of an autoimmune thyroid condition, I could easily have been offered an antidepressant. Instead, I delved into the complex physiology of the immune system and its relationship to seemingly unrelated areas like the gut and brain. I learned pathways and the role of nutrients in their optimization. I changed my lifestyle, and my life changed as a result. What if this diagnosis wasn’t just a result of chemical exposure, lack of sleep, and a horrendous diet? What if it meant something, specific, to me, for me, and about me?

• • •

Psychoneuroimmunology: Gut-Brain Science

According to my credentials, I have fellowship-level expertise in Psychosomatic Medicine. What does that phrase mean to you? Undoubtedly, it conjures notions of hysteria and attention-seeking illness fabrication. Almost in an effort to escape these implications, this advanced medical training has, at some sites, been rebranded as Consultation-Liaison Psychiatry, to invoke the seemingly more legitimate study of psychiatric symptoms emerging in medical and surgical patients.

Psychiatry has been seeking to scientifically substantiate itself for the better part of a century, and we have all fallen prey to the allure of the biological explanation, the organic cause, the mechanistic descriptor for a given pathology. Many a patient has felt relief at being told that they have a “chemical imbalance.” A chemical imbalance is, by definition not your fault. In fact, there’s nothing you can do about it, except, of course to fill your prescription and take it forever, like a good patient.

The Physical Origins of Mental Illness

Even with my left turn from conventional psychiatry, I have spent a decade steeped in vanguard biomedical models of depression, bipolar, and schizophrenia. Models that explore the contributions of various systems including endocrine, immune, and neurochemical. I have even been criticized by other psychiatry-dissenters as simply substituting one physiologic illusion for another that continues to pathologize what is appropriate human angst and response to trauma. These critics say, it’s all mind, not body.

What if there is a new conversation happening in the medical literature – one that encompasses the whole person, all at once?

Entitled Symbolic Diseases and “Mindbody” Co-Emergence. A Challenge for Psychoneuroimmunology, Broom et al take the progressive field of Psychoneuroimmunology to task and demand an even more nuanced and sophisticated approach to the human experience.

Gut-Brain: Just The Beginning

On many levels, psychoneuroimmunology is an exciting revelation simply because it decimates false boundaries between different systems and allows more cohesive assessments to be made. No longer are there many blind men feeling parts of the elephant describing a rope and a tree trunk. We begin to understand that the immune and endocrine systems appear to be mediating a dialogue – bidirectional – between the gut and the brain.

In this model, the gut influences the brain and the brain influences the gut but they are still two separate entities communicating through biochemical signals. Where are YOU in this relationship? Where are the elements of the human experience that reflect your deeply held beliefs, thoughts, and relationships? What about your history and experience of yourself up until this point? Are we still just reducing humanity to bubbles of substances?

Gut-Brain-Mind: Adding Another Dimension

The mind is invited into gut-brain physiologic conversation in the form of stress. Stress has been used as a cause-all vector of bodily illness, a perspective that still reigns in the literature including data that demonstrates that perceived stress mobilizes inflammatory immune cells in the bone marrow. But the mind is more than stress, isn’t it? Is the personal meaning of the stress relevant?

Dr. Candace Pert has confirmed as much through her discovery of the bodily opiate receptor and research on neuropeptides demonstrating that that emotions are literally encoded throughout organs and tissues. Her perspective seems to elucidate why and how one person could weep after 8 minutes of raised arms in a kundalini yoga class and another might barely find it challenging. We get closer to a more personal experience of the physical body that blurs the boundaries between mental and physical.

In fact, the interpretation of the physical by the mind can actually then lead to changes and shifts in the physical – this is called the placebo effect. An emergent phenomenon, the placebo effect is physical and mental and both in the context of your personal beliefs, history, and expectations. It is not a mental factor. It is not a physical factor. It is a totality of you brought to the experience of healing.

So if it’s not just a broken body, why do we get sick?

Since the dawn of the microbiome, exosomes, and placebo research, no longer can we hold onto the cold comfort of our genes. We weren’t simply “born with” our illnesses and struggles. They have been co-created by us in our environment. But are they meaningful beyond that? Purposeful, even? Teleology is the study of purpose as a driving force of nature. It flies in the face of the mechanistic, reductionist perspective that life is random, nature is meaningless, and that force, effort, and exactitude dictate all outcomes.

The attunement of the organism to the world is reciprocated by the action of the world on us. The world or environment is not something inert, passive, something waiting to be acted upon. – Maurita Harney

Far from being new age woo, this field is supported by burgeoning disciplines such as quantum physics and biosemiotics, non-linear exploration of top-down informational exchange in web-like matrices. The one gene-one pill-one ill model of random bad luck is a skin this snake has shed.

The Meaning of Your Illness Matters

I firmly believe that there is a personal invitation in every diagnosis, and even every symptom. It is an invitation to examine everything and anything from diet to spiritual beliefs, but could illness carry personal symbolism and meaning? Broom et al, the authors of the previous paper, suggest that:

“Some persons will represent their meanings and “stories” clearly in language, some in behavior, some in the body, and some (maybe most) in multiple ways.”

To appreciate the relevance of symbolism, the whole person must be assessed in a global view with sensitivity to the meaning for a given individual of their symptoms. They pull cases from the literature including;

“A woman developed the precancerous condition oral leukoplakia (and, later, oral cancer requiring seven surgical interventions/reconstructions) at age 33. After 22 years of disease she entered therapy, and, in the first session, it emerged that her dentist father had died by suicide when the patient was age 6 and when he was 33. At age 12, the patient had been told by her alcoholic mother that she, the daughter, had caused the father’s death because she had refused to sit on his knee! There was a profound shame at having “caused” his death. Brief therapy led to a rapid and, thus far, 15-year remission.”

This made me wonder if my postpartum thyroiditis symptoms of cloudiness and fatigue so many years ago were representative of my feeling suppressed and oppressed by my unexpressed self. Perhaps I developed exactly what it is that I needed to become more myself in this life, and that healing it rather than fighting it was the integration that rendered me one with my very personal process.

Broom et al might say yes. They propose a co-emergent framework. This is one in which mind and body are not causing effects in one another but are a part of an unbroken continuity of internal body processes and external interpersonal meanings and influences. In other words, it is a model that takes into account the person, their story, and their environment as all a part of a web that includes the body and its systems.

More Than the Sum of Our Parts

How can we can enter on all of these levels at once – body, mind, and meaning? With the launch of my course, Vital Mind Reset, I have witnessed that self-healing is possible when we escape the reductionist magic pill/magic bullet model and honor our weblike complexity. Medical meditation, examination of beliefs, engagement in community, detox, and nutritional medicine all synergize to bring about results that might not have otherwise been possible. In fact, Bloom states:

“It appears that a co-emergent framework commonly allows recovery from chronic illnesses unresponsive to biomedical treatments.”

When we use this multi-signal, personalized (by you, for you) approach, participants marvel at the simplicity of the interventions yet the robustness of the shift:

FullSizeRender (2) (2)

In fact, we don’t even need to know why this multilevel approach to healing works, or how. We can move beyond the chemical theories, the complex analysis, and simply be in the process of sending the bodymind a signal of safety. Safety looks like ease. Trust. Curiosity. And even surrender. It’s not a fight. It’s not a battle. It’s a cooperative exchange and an exploration. It’s becoming more of our whole selves because we are becoming less fragmented and self-evasive. We stop hiding parts of our personhood from our awareness. We embrace it all in order to heal.

I now look for the story in any physical symptoms that arise in me, and in the physiologic specifics of my patient’s conditions. Exploring these stories often reveals the key to true wellness.

Read More At: KellyBroganMD.com

Depression Caused by Genetics? Most Likely Not


Source: KellyBroganmd.com
February 1, 2020

Since the discovery of DNA, the central dogma of genetic translation has lured us in with a simple path from genes to illness. With the completion of the Human Genome Project, however, we were forced to begin to explore the limitations of the mutation model of illness and our assumptions about the biology behind illness and health. Despite this sobering reality, and the history of genetic studies of depression coming up empty-handed, many of the 30 million people in the US taking medication still believe that genes play a role in their “disease.” Frustration with the field’s current approach has been seeping into the industry. In 2017, Dr. Thomas Insel, former director of the National Institutes of Mental Health, said “I spent 13 years at NIMH really pushing on the neuroscience and genetics of mental disorders, and when I look back on that I realize that while I think I succeeded at getting lots of really cool papers published by cool scientists at fairly large costs-I think $20 billion-I don’t think we moved the needle in reducing suicide, reducing hospitalizations, improving recovery for the tens of millions of people who have mental illness.”

Many gene candidate studies have been sifting through haystacks, trying to pinpoint the exact snippets of DNA sequence that might be causing you to feel lethargic, unmotivated, and generally terrible. Your depression, they say, is your own DNA betraying you.

A new study is helping us understand how the field’s previous genetically-inclined direction of study might have been nothing more than a distraction.

New Study Finds No Correlation Between Candidate Genetic Biomarker Genes and Depression

A recently published study in the American Journal of Psychiatry found no support for the association between genetic polymorphisms and the development of “Major Depressive Disorder.” 1 A team of Colorado researchers compiled data gathered from the UK Biobank (with over 502,682 individuals from 22 centers across the UK between 2006 and 2010) and closely examined 18 candidate genes hypothesized to be genetic underpinnings of depression and found that previous depression candidate gene findings were most likely Type 1 errors—or false positives.

Using the UK Biobank data, collected from online mental health questionnaires and DNA samples, the researchers were able to analyze the relationship between several depression phenotypes and moderators, and supposed genetic markers for the different manifestations of depression.

But more importantly, the researchers tried to replicate the results of studies that have implicated the top 16 candidate genetic loci for causing depression. Performing analyses with a much larger sample size than those of previous false-positive studies, their results debunked the idea that these loci were actually linked to depression. Out of these 16, only three attained statistical significance, but those results are consistent with the low power to detect small associations.

Led by Richard Border and Dr. Matthew Keller, the research team suggested that the field should abandon the idea that depression is genetic.

“Our results demonstrate that historical depression candidate gene polymorphisms do not have detectable effects on depression phenotypes. Furthermore, the candidate genes themselves (with the possible exception of DRD2) were no more associated with depression phenotypes than genes chosen at random.”

Their study is the most comprehensive and well-powered investigation of historical candidate polymorphism and candidate gene hypotheses in depression to date.

What Had We Misunderstood?

How is it that the multitudes of previous peer-reviewed studies were able to be published with false positive findings? There might be several reasons.

1. Most candidate gene research had small samples sizes.

Earlier candidate gene studies analyzed small sample sizes and were, simply, underpowered.2 Between 2000 and 2009, the median sample size of these studies was 345.

Without enough data points, though, results of these studies don’t really mean anything, especially when trying to generalize a complex disorder to an entire population. That’s just basic statistics.

Even though the results of those studies might have revealed associations between genetic variations and depression, studies that gathered more data points have revealed no correlation.3 That could explain why targeted, well-powered genetic association studies of depression and other with larger samples didn’t support the candidate gene hypothesis. Genome-wide association studies have found that individual single-nucleotide polymorphisms across large samples exert small effects on genetically complex traits like depression.4

2. Some of these studies used incorrect analytic methods and inadequate control designs.

Researchers have suggested that the majority of published candidate gene studies have actually used incorrect analytic methods and inadequate control for population stratification.5,6 Since genetic phenotypes can take lifetimes to manifest themselves, the multitudes of confounding factors make it difficult to properly design controls. Improper analytics and experimental designs would account for the inconsistent results that these types of studies have yielded over the years.7 8 9 10

3. Clinical utility of identifying individual gene mutations is unclear.

Even if we could pinpoint individual gene mutations that caused depression, there’s no real point in doing so. Clinical utility has always been one of the critical limitations in building gene-environment models in psychiatry.11 Looking for gene markers might even be counterproductive to people’s healing, focusing efforts on allopathic medicine that seeks to marginalize the role of lifestyle factors in lieu of the one pill for one ill approach to symptom management.

4. Publication bias

Over the past years, this body of literature has shown significant publication bias. For example, the top nine of the 18 identified genes in the American Journal of Psychiatry study accounted for 86.59% of the studies. When so much effort and time is going into chasing these biomarkers, it’s easy for an entire field to get tunnel vision.

So Now What?

As humans, we’re inclined to seek certainty and answers—but this study shows that the answers to questions about the origins of depression are not in our DNA.

Through the lens of root-cause resolution, depression can be seen as an invitation to explore imbalances that can range from nutritional to psychospiritual. Recent research has been helping us deconstruct our assumptions and explore new frameworks including depression as a form of evolutionary mismatch. Maybe we should be moving past a reductive and misleading interpretation of depression to understanding that our bodies create symptoms when things out of alignment. Depression is that symptom—indicating to us that our lifestyles are often a mismatch with our biology. We don’t need drugs to “fix” depression. The way out of depression doesn’t require new ancestry, it can be found through simple steps towards self-ownership and attending to lifestyle habits that are asking to be transformed.

References

  • 1 Border, R., Johnson, E., Evans, L., Smolen, A., Berley, N., Sullivan, P., & Keller, M. (2019). No Support for Historical Candidate Gene or Candidate Gene-by-Interaction Hypotheses for Major Depression Across Multiple Large Samples. American Journal Of Psychiatry, 176(5), 376-387. doi: 10.1176/appi.ajp.2018.18070881
  • 2 Munafò MR: Reliability and replicability of genetic association studies. Addiction 2009; 104:1439–1440
  • 3 Bosker FJ, Hartman CA, Nolte IM, et al: Poor replication of candidate genes for major depressive disorder using genome-wide association data. Mol Psychiatry 2011; 16:516–532
  • 4 Burton PR, Hansell AL, Fortier I, et al: Size matters: just how big is BIG? Quantifying realistic sample size requirements for human genome epidemiology. Int J Epidemiol 2009; 38:263–273
  • 5 Keller MC: Gene 3 environment interaction studies have not properly controlled for potential confounders: the problem and the (simple) solution. Biol Psychiatry 2014; 75:18–24
  • 6 Border R, Keller MC: Commentary: Fundamental problems with candidate gene-by-environment interaction studies: reflections on Moore and Thoemmes (2016). J Child Psychol Psychiatry 2017; 58: 328–330
  • 7 Stoltenberg SF, Burmeister M: Recent progress in psychiatric genetics: some hope but no hype. Hum Mol Genet 2000; 9:927–935
  • 8 Buckland PR: Genetic association studies of alcoholism: problems with the candidate gene approach. Alcohol Alcohol 2001; 36:99–103
  • 9 Munafò MR: Candidate gene studies in the 21st century: a metaanalysis, mediation, moderation. Genes Brain Behav 2006; 5(suppl1):3–8
  • 10 Munafò MR, Gage SH: Improving the reliability and reporting of genetic association studies. Drug Alcohol Depend 2013; 132:411–413
  • 11 Munafò MR, Zammit S, Flint J: Limitations of gene 3 environment interaction models in psychiatry. J Child Psychol Psychiatry 2014; 55:1092–1101

    Read More At: KellyBroganMD.com

Mental Illness in Pregnancy | To Medicate or Not Medicate


KellyBroganMD.com
Dr. Kelly Brogan

When a woman has a history of severe and relapsing mental illness, but is stable on her current treatment, and is planning a pregnancy or is postpartum, what is the best course of action for her and her baby?

In my conventional training, I spent (and continue to spend) countless hours analyzing the available registry, cohort, retrospective, and prospective studies on the safety and efficacy of psychotropic medications in pregnancy and lactation. As one of approximately 300 reproductive psychiatrists in the world, I am privy to the defensive posture of clinicians who deign to help these women, often perceived by general psychiatrists to be too high liability to treat.  I understand the feeling that psychiatric medications are held to a standard of obstetrical scrutiny that anti-emetics, antibiotics, steroids, and painkillers are not.  I know that there are more than 25,000 cases of SSRIs in the perinatal literature and yet there still isn’t a clear signal of any reproducible, consistent teratogenicity or danger that is definitely not attributable to the underlying illness.

Miscarriage, preterm birth, and neonatal adaptation are all considerations, but are such common and multifactorial outcomes, that it will be some time before clear A-causes-B information surfaces. In many ways, the collective outcome of this data surprises me – we are applying medications (often prepared with unstudied preservatives, dyes, and metals) based on subjective diagnostic parameters, to women who bring other burdens to the table that are largely uncontrolled for in these studies (high glycemic diets, xenoestrogen/endocrine modulator exposure, baseline inflammation).  We are rarely certain that the medication, if taken, has treated their symptoms to remission, and study after study fails to show a signal of serious danger on the order of alcohol, Accutane, or even Depakote.

These studies are compromised, fundamentally, by the fact that they are not, and will never be, randomized, double-blind-placebo controlled trials.  Analyzing the methodology, reading beyond the abstract, and contextualizing findings for any given patient requires serious dedication of a practitioner’s intellectual resources.  How do we personalize these recommendations? After all, studies are studies, and individuals are individuals.  In my perspective, we assess for a better treatment path for the patient that addresses root cause hormonal and inflammatory contributors and applies interventions that are low risk and potentially high yield, preferably with some degree of evidence base. We start by looking at interventions that have benefits for mom, mood, and baby (diet, exercise, meditation, fatty acids, l-methylfolate, vitamin D, probiotics, etc).

This process is not for the impatient. It can take upwards of a year to truly rebalance a patient’s system, and to properly taper medication.  It is no wonder that data suggests a high risk of relapse. Abrupt discontinuation of antidepressants (and mood stabilizers/benzos/stimulants) places a demand for reequilibration that often overwhelms a system’s ability to achieve that without support, or return to medication. The process of medication weaning is a complex and time-consuming one that, in my experience, requires cell membrane, amino acid, and micronutrient support in the setting of painstakingly slow taper of dosage. I always tell my patients that the ultimate goal is to gently usher the medication out the back door, not push it off the balcony.

When I meet a patient who is already pregnant on medication, wondering what is best for her and her fetus, it is not a black or white decision-making process. We have to consider the central nervous system stimulation of medication withdrawal, potential relapse (often hard to distinguish from the former), safety of supplements in pregnancy, and then the flipside, which is the known and unknown risks of medications, assuming that it is helping her. This web is brilliantly illuminated in this paper, which I would imagine leaves most readers feeling a sense of sky-is-falling nihilism about treating pregnant patients. Oberlander holds all of our assumptions about the interplay between medications, genes, and the epigenome under a microscope, revealing all of the pores and wrinkles we were hoping to obscure with a professional distance. The number of “if, then…” clauses becomes overwhelming.

An example:  If the mother carries a short/short copy of the serotonin transporter gene (which we understand to confer “environmental sensitivity” or lack of resilience, and poor response to SSRIs), and she experienced childhood trauma herself, her serotonin trafficking may look very much like that of a woman with long alleles and SSRI exposure.  He references an animal study which suggests normalization of the stress response after SSRI exposure in utero, alluding to the potential effects of SSRIs that span well beyond the serotonin modulation and may even be protective in some cases.

Then, once the serotonergic imprinting has occurred in utero, the effects are further modulated by postnatal exposures such as nurturing care and breastfeeding so that cortisol levels may be normalized even if there was alteration of serotonin signaling in pregnancy that messed with the hypothalamic pituitary axis. It appears that genetic variants “matter” only in settings of environmental stress, and maybe only if that stress represents a “mismatch” to the in utero level of stress. After all, epigenetics is a means of preparing the baby for the world it appears to be entering.

The summary of this article reads like a “well, maybe, uhh, we’re not sure” conclusion to the examination of just one proposed system of influence – serotonergic tone in utero as regulated by SRIs, genetic variants, and mood disorders. It renders the reductionist model of depression as a serotonin-deficit disease cured by a reuptake inhibitor, embarrassingly simplistic.In light of this, it is important to feel comfortable sitting with uncertainty, giving wellness and healing a cautious and humble best effort while respecting the vast swaths of knowledge that have yet to be achieved. I don’t waste my patient’s time with hand waving about biochemical imbalances as an explanation for their state (I have been known to gesticulate wildly when talking about gluten, though).

Adding to this complexity, we suspect, based on a study by the same author that maternal antenatal depression may increase methylation of the glucocorticoid receptor (shutting down its on switch), leading to elevated stress response in the child at three months. He discusses some 15% of childhood behavioral problems being attributed to antenatal stress/anxiety.  This is a sign of a toxic, inflamed system, and it is no surprise that this maternal inflammation has a negative effect on the fetus.

What else can cause maternal inflammation?  Here’s the short list:

  • Processed foods/trans fats
  • Lack of sleep
  • Sugar and associated insulin resistance
  • Obesity
  • Environmental toxins/industrial chemicals
  • Vaccines
  • Chronic infection

I don’t know of many safety studies controlling for these individual variables, yet there are several that examine the deleterious effects on birth outcomes when a woman has evidence of inflammatory markers.

We are operating in a system of medication-driven treatment, and the only real time that medication risks are taken seriously is when a woman has seen that little plus sign on the stick in her bathroom.  Then they are often violently tossed out the window, and deemed contraindicated for the coming 1+ years of gestation and lactation.  We need to be thoughtfully examining how to best support a woman’s system from the time that she gets her first period (and even more so if that is before she is 13!), because engaging this line of rhetoric once she is pregnant is often too little to late, and a ones or zeros, meds or no meds approach does not do justice to the complexity of a system that is hard at work building another system.

Read More @ KellyBroganMD.com

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If you want to delve into more of Dr. Brogan’s work, please consider taking a look at the review of her absolutely stellar book, “A Mind Of Your Own” & The Truth Of How Women Can Heal Their Bodies

This post originally appeared on Mad in America as To Medicate or Not Medicate: That is Not the Question

New Insights on Gut Permeability and Depression


Source: KellyBroganMD.com
Kelly Brogan MD Team

If you know what depression feels like – the brain clouding, the flat moods, the tiredness – you’re not alone. Over 300 million people around the world have depression, and yet there’s a lot that we still don’t quite understand.1

Thankfully, the medical field is developing some new insights that just might help us understand depression better. In a new 2019 study, researchers decided to examine the potential mechanisms of major depressive disorder in teenage girls and found some evidence that could help us better understand exactly how gut permeability (leaky gut) can lead to inflammation, which in turn, leads to depression.

New Insight into Leaky Gut and Depression

In this 2019 study, Baylor College of Medicine researchers are directly looking at gut permeability and major depressive disorder, a study that is the first of its kind.2

With a sample of forty-one 12–17 year-old teenage girls who were medically healthy, the study measured the severity of the girls’ depressive symptoms, the activity of the autonomic nervous system, intestinal permeability, or gut leakiness, and the number of inflammatory cytokines.

To measure whether the girls were depressed, an interviewer performed the Children’s Depression Rating Scale-Revised (CDRS-R) and a clinical interview.  The CDRS-R is a rating scale that requires interviews of both child and parent to understand the severity of a child’s depression. Over the past few decades, the CDRS-R has become the most widely used rating scale for assessing severity and change in depression for clinical trials involving children and adolescents.3 In order to collect data on the autonomic nervous system activity, researchers measured pre-ejection period (PEP) and respiratory sinus arrhythmia (RSA) data, which are indicators for the activity levels of the sympathetic nervous system and parasympathetic nervous system respectively. They measured the leakiness of the gut using the lactulose-mannitol ratio (LMR), which involves having the teens first fast overnight and then ingesting a premeasured amount of lactulose and mannitol. The researchers then collected the urine for four hours after ingestion. By looking at the ratio of lactulose and mannitol that passed through the gut lining, researchers could calculate the permeability of the gut lining, or how “leaky” it was. To measure inflammation, the researchers took blood samples and measured inflammatory cytokines.

They found that in unmedicated teenage girls between the ages of 14-17, depression severity was associated with increased intestinal permeability, as measured by the lactulose to mannitol ratio. The leakier the gut, they found, the more severe the depression and depressive symptoms. They saw that the higher the concentration of the cytokine IL-1β, the more severe the depression. They also found that increased intestinal permeability may be the path between sympathetic nervous system activation and depression severity. Additionally, their evidence suggested that increased intestinal permeability may activate the innate immune system and push the development of depression.

The result of this study also helps clarify the mechanisms through which activating the sympathetic nervous system can increase gut permeability and activate the innate immune system—two things that are likely contributing to depression symptoms.

The Brain, The Gut, and the Immune System

If you’re wondering why intestinal permeability is related to depression, let’s back up and walk through the whole pipeline.

We start with the immune system. Throughout the last century, psychiatry has been exploring the role of the immune system in certain presentations of depression. Importantly, the gut houses over 70% of our immune system, which makes sense given that the lining of your gut is the barrier between your insides and the outside world. The gastrointestinal epithelium usually forms a single-cell-thick barrier that prevents the free movement of toxicants, microbes, and microbial antigens from entering into the rest of your body. This lining usually does a good job absorbing things we need (like food) and interfacing with foreign things that might wreak havoc—which is probably why most of our immune cells are located in the gut.4 The relationship between the gut and the brain is both complex and important. We’ve all felt the butterflies in our stomachs when we’re nervous or anxious, but it turns out that the relationship between the brain and the gut is actually bidirectional. Not only can our brains affect how our guts feel, but our gut can relay its state of calm or alarm to the nervous system and send those immune reactions up the vagus nerve to the brain.

To understand how the gut and depression are related, we should first better comprehend the triggers for inflammation, what inflammation is, and how it happens.

Stress Drives Inflammation

So what IS inflammation in the first place? Inflammation is the body’s defensive response to stresses, like injury or the ingestion of bodily-incompatible chemicals. Upon approaching a stressor, the immune system kicks into a higher gear to heal the body.

Stress is a catch-all term, a trigger that links hormones to inflammation. Essentially, when the body thinks something is wrong, the body releases hormones that tell the body to be on the lookout and get on defense, and inflammation occurs. These triggers can come in all forms, many of which are actually staples of modern American life, from sugar to stress to pesticides and pollution to anxiety to beyond. Whether psychological or physiological, stress drives the inflammation response by telling the brain to release cortisol, the steroid hormone that acts as nature’s built-in alarm system and makes it for our bodies to use blood sugar for energy so that we can flee from whatever is causing the stress.5

Once inflammation is started, not only does inflammation cause more inflammation, but recent studies have linked low-grade inflammation to depression. When inflammation reaches the brain, cells begin to take their limited supply of tryptophan to produce more anxiety-provoking chemicals like quinolinate.6 Medical literature has found that inflammation seems to be a consistent marker of depressive symptoms, like flat mood, slowed thinking, avoidance, alterations in perception, and metabolic changes.

How does inflammation get provoked in the gut?

So let’s understand how exactly a leaky gut can lead to inflammation – the body’s language of imbalance.

When the body is stressed, the junctions between cells in the stomach can be less effective than they should be.7 This allows bacteria and toxicants to enter the bloodstream that can continue to cause widespread inflammation and possibly trigger a far-reaching reaction from the immune system.8 Having leaky gut cause inflammation sets off a problematic chain of events because the gut has a direct link to the brain through the vagus nerve.9

The medical field has been slowly inching up on a fuller understanding of the link between intestinal permeability (“leaky gut”) and depression. Previous studies focusing on depression and have found the chemical hints of leaky gut. For example…

Continue Reading At: KellyBroganMD.com

Depression & Mental Health | #Life | #Death | #Depression | #Suicide | #MentalHealth | #Psychology


BreakawayIndividual.com
Zy Marquiez
June 26, 2019

As a preamble, this piece on mental health is prompted by two different significant circumstances, one of which is personal, one of which is not, that took place the last day.  The personal component will lead to set the foundation for what follows.

This piece will only touch lightly on the subject of mental health as equal parts vent and equal parts reminder for others to make sure that whether you happen to know someone, or simply think someone else might have mental health concerns, let them know that you are there, no matter whatNo matter how many times it takes, for there are not enough ways to tell people you care for them.    

When any single person takes their life because they thought nobody was there for them, which has happened way more often than it ever should have, it shows the possibility that (1) these individuals were not told they were cared for, or loved, (2) they were told, but didn’t really believe it, (3) they were told, but they were not shown, (4) they were told and shown, but it never registered anyways, (5) they went through one of the above circumstances, but their health issues didn’t allow them to have their mental faculties in full, preventing them from noticing, or appreciating the truth behind someone’s actions, or (6) another issue altogether that couples to the above in a different way.

As it happens, I have been writing quite a bit about mental health the last couple of days, and all of this stemmed from a poem that I helped co-write, which was thankfully a collaboration with a very talented acquaintance that I only met nigh a week and a half ago or so.  During a conversation, she brought up the idea of a collaboration before me, and after we jumped at the chance, she settled on the topic of depression, which I didn’t mind whatsoever.

To say the least, the poem was incredibly thought provoking, and quite inspiring in a few different ways, which I kind of didn’t expect to be honest.  On a subjectively deeper level, this piece made me think of lots of personal emotions and issues that I haven’t delved into for quite some time for various reasons, and even downright buried for many years.  Having said that, what we wrote resonated with me so much that I have written dozens of poems of myriad types, some of which I plan on sharing in the future hopefully, including some the topic of depression, or darker subjects that revolve around mental health.

In fact, today, while I was stretching and writing poetry on this and other subjects, I got a text from a friend that said someone that we followed on social media had unfortunately passed away, which is where the second component of this blog posts comes in.

Through my friend I come to find out that Desmond “Etika” Amofah passed away due unfortunately to suicide.  Whether someone is a youtuber or not, it’s extremely unfortunate when someone takes their life, especially when there were significant mental health issues that were known for months beforehand, but this is also how it happens at times.

How I ran into Etika’s work was simply by watching him over a decade ago on Youtube covering gaming, which is something that I am incredibly fond of.  He was one of the content creators that clawed his way from the bottom and rose all the way to the top, and was incredibly popular for what he accomplished, and even inspired many in his journey.  I won’t cover much more than that given that there’s literally countless articles out there covering the deeper aspects of his life.  I simply mention this because although I didn’t know him, I did watch him enough to find an incredible affinity and kinship towards him, as many others have, when he was doing his work and it made me incredibly gloomy after hearing of his passing, especially given the circumstances.

The keystone point is, don’t ever assume people know you care, or even love them, and even if they do, they might still have problems reconciling that fact.  Everyone thinks differently, so how someone expresses how they care is vastly different from how another individual does.  Likewise, different people see acts of caring and love in different ways.  Some people see small circumstances and find a lot of caring and love behind it, others do not; some people express themselves in ways they think are obvious forms of caring and love towards others, but others might not see it that way given countless reasons.

With all of that in mind, it is downright crucial to show others that you care and/or them, whether they have mental health issues or not, but especially if they do.

Consistent acts of kindness, whether small or not, can go a long way to help others come out of the catacombs of mental health issues, or prevent them from getting there in the first place.

Never underestimate the power that showing others you care can have.  It might be the smallest gift you can give, but it might be the best gift someone could ever receive, because it just might change the course of their life forever.

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Author Notes:

[1] I say perhaps, because I am uncertain of what these individuals have gone through, or go through, but subjectively speaking I have found this to be true for myself and some close to me)

[2] Honestly, I wouldn’t had written this blog post if I hadn’t collaborated with the person I co-wrote that depression poem with.  It’s not that I don’t have appreciation for mental health issues, it’s just hard for me to speak about these issues subjectively given some things that have happened in my past.  But having had to privilege not only to write something on this very topic, but have it be meaningful in a way, incredibly so in fact for me personally, has nudged me in a direction that I hadn’t contemplated in going toward, but one that I appreciate to the fullest extent. I definitely let the person know that I appreciated the opportunity and I sure hope we can work together again, not only because (I think) we worked well together, but also because of how well the poem came out, but that will ultimately be up to them.

Either way, this situation is just one of those seemingly little circumstances that can change your outlook on many things, and make you realize that there are people out there that will relate with what you have to say at the deepest levels, and I haven’t been able to do that with this topic, not like that.  Especially given that I often mask emotions with metaphors and I am not as blunt as I am in my personal journal or random accounts I often employ in various nooks across the internet just to let off steam.

My main point is that many times people think that there aren’t others out there that care, or care enough to listen to them, or to help them wade through the issues, when in fact the opposite is true.  There are people that would walk through oceans of fire for them to make sure that they are okay.  But as I’ve alluded to elsewhere, many people often don’t show others that they care because they see the acts that they themselves undertake as ‘obvious’ acts of kindness, even when others might not see it that way.  And if a person sees their own actions as an obvious act of kindness and love, why wouldn’t others?  Simple: because not everybody thinks likes you, feels like you, acts like you, or ultimately lives like you, why is why you should never underestimate the power of acting out of love, no matter who this action is towards, and whether you know that person or not.

You all have a great evening, and no matter what, always show others you care.

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If you find value in this information, please share it.  This article is free and open source.  All individuals have permission to republish this article under a Creative Commons license with attribution to Zy Marquiez and  BreakawayIndividual.com
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About The Author:

Zy Marquiez is an avid book reviewer, inquirer, an open-minded skeptic, yogi, and freelance writer who aims at empowering individuals while also studying and regularly mirroring subjects like Consciousness, Education, Creativity, The Individual, Ancient History & Ancient Civilizations, Forbidden Archaeology, Big Pharma, Alternative Health, Space, Geoengineering, Social Engineering, Propaganda, and much more.

Simplifying For The Sake Of Health | #Mindset | #Health | #Mindfulness | #SocialMedia

“Our life is always frittered away by detail.  Simplify, simplify.”
– Henry David Thoreau

“Simplify your thoughts, desires and life.  Complexities and confusion make a hell out of heaven.”
– Philip Arnold


BreakawayIndividual.com
Zy Marquiez
May 30, 2019

What follows is part vent, part blog post on simplicity, but it’s going to be a bit longer than my usual blog posts.  Although it might seem that I am meandering a bit, there’s a logical sequence to certain steps I (and others) took yesterday across various social media platform.  More on that in a moment though.

Yesterday, I wrote about meeting someone that just moved here that was a family member, and that was my uncle.  We got to talking about a variety of things, but one moment stood out most of all.

Sometimes in life, while you are talking to someone you get to a point where the conversation takes a very serious tone, the type of tone when you just have to shut the @#!$ up and let someone vent their heart out; this was one of those moments.  I let him vent about his health, life, and him not having too much time left, and then the conversation leveled out to less dismal topics.  This conversation left me incredibly emotional, though I masked it rather well (I hope) and I knew I just wanted to go home.  Why so?

Because it reminded me of a circumstance that took place when I was much younger, though both scenarios aren’t exactly alike, but you will understand why it reminded me in a second.

In the early 2000s, I visited Puerto Rico for the first time since we moved as a family to Arizona.  In a nutshell, at one point I wanted to take a picture with my grandma.  And anybody that knows me personally knows that I hate taking pictures.  I don’t mind it, but most of the time I don’t (usually) like taking pictures for reasons I will not get into here.  And a lot of the pictures that I have taken are always on my phone, mostly pictures with friends, family and so on.  This is because if I do end up taking a picture, it means a lot to me, which is why the pictures always with me.  That, or you have to be one of my conniving friends (bless their hearts) and sneak a picture when I least expect it.  Taking pictures of friends?  Sure, I love that; I love photography in general, and I love taking pictures of my friends.  But I’m not usually in a lot of the pictures.

The reason I say that is because even though I hate pictures where I’m in them, I wanted really bad to take a picture with my grandmother when we visited; so you know, I had to want to take a picture with my grandma really bad for me to even bring it up.  That last day, for hours, I hounded her about taking a picture with her and she wasn’t having it.  Her reasons were, because she didn’t look ‘good’ and so on.  I told her that I didn’t care, but she wasn’t having it.  In any respect, I gave up because she was getting annoyed and I didn’t want to bug her any longer.  Now when leaving, I just had this overwhelming feeling that I would never see her again.  I had never had a feeling like that before, and I thought it was stupid.  In reality, I didn’t know when we (or I) would be back to visit, but I just felt really overwhelmed.  It turned out that she passed away a couple of years later, all because a medical mistake in which the medical personnel didn’t read a damn chart.

I’ve searched everywhere, but I don’t think I ever took a picture with my grandma, at least not one that I can remember.  I’ve gone through family photos and so on, and all I’ve seen are her and I when I was much younger, a baby for instance.  Anyways, the point of this whole (lengthy) preamble is that, although I do have a feeling I will see my uncle again, he’s already on borrowed time.

This whole scenario with my grandma flashed in my mind, which made it hard for me to keep my composure because well, knowing that someone’s ticket with the reaper has already been punched will make anyone sad, if not downright depressed.

After we were done having dinner, we said our goodbyes, and I went home (and couldn’t get there fast enough) because I just wanted to lay down and not think, not that that’s possible but I just had to get home.  I get home, and after changing my mind, I write the blog post that I did, which involved my uncle because that was my way of sort of venting on the issue, but I held a lot back as is evident now.

From there, I end up deciding not to lie down, and instead opt to get on a variety of social media platforms to see if I can just talk to some friends and vent.  Lo and behold, it’s nothing but fire and brimstone everywhere, people arguing over the most inconsequential and trivial things that, in the grand scope of things, don’t really matter.  What’s worse is how everyone were treating each other (or me) in a few respects, so I was about to make a call and get some friends to do our usual Facebook mass purge of all of our accounts as well as on other social media, but someone beat me to the punch and was seeing if we wanted to start a group on Skype to do it all simultaneously while catching up.

Before going on, why would it be important for me to purge accounts on many social media platform?  This is because (1) I have already lost a few friends this year and it’s been the toughest year emotionally speaking yet that I can remember.  Moreover, as mentioned before, (2) my uncle is dealing with stage 3 cancer that can’t be handled and is already on borrowed time, (3) there’s a family member in a coma (not joking) that my lovely father just happens to tell part of the entire family weeks later because (you just can’t make this stuff up) he “didn’t think it was important”.

Predictably, I’m till downright furious about that.  ANY family member being in a coma, HELL, ANY HUMAN BEING, being in a coma, is as real as it gets.  Not only that, but there’s also (4) the issue of my Mom’s health where she doesn’t seem to be getting completely better even though the doctors say “everything is okay” and “the cancer is gone” (we’ve heard that one before).  Lastly, (5) I have been out of remission with my disease for months, and any stress affects it greatly, which is why I often seek a mindful approach, as well as employ yoga when I can at home or the gym.

My own personal reason for purging (or muting) accounts was due to stress and my goal to simplify where I can in my attempts to regain my health and get back into remission.  I can’t be the best me if I’m not healthy, and I can’t be healthy if I repeatedly expose myself to things that are stressful, no matter how mindful I am, and expect for significant progress to take place.  These were the vanguard reasons for me purging accounts of myriad types yesterday.

With this personally in mind, myself and others all started on Skype, but when the room got really crowded we moved to Discord, and we just began purging accounts for 6-7 hours or so.  It’s exhausting removing hundreds and hundreds of accounts from multiple Facebook accounts that I use for activism and the like, dozens on Instagram, WordPress, Twitter, you name it.

I just wasn’t having it any longer, my health’s too important for me to subject myself to things I don’t have too.  Some people, the ones I’ve known for a long time, I either told the straight up that I’m muting them because x,y,z, reason, and they understood.  Others, if we didn’t know them in any way shape or form, or had never even realized they were on our friends list, then they got removed, while also removing accounts that are constant negativity for the sake of negativity; that was the main approach for myself and my friends.  And people that I ‘kind of’, ‘sort of’, knew, it was fifty-fifty based on judgment calls for me personally.

It’s not like I don’t care about some of these people, I do.  But the bottom line is that, to a great extent, we are a product of our environments, History and Epigenetics have taught us this much.    If you end up subjecting yourself to stressful situations, negativity, and lots of things that you don’t have too, it’s just going to have detrimental effects on your being on an overarching basis.

Given that, at an emotional level, my plate is incredibly full and I’m already significantly stressed about many circumstances, I’m just going to be incredibly selective to what I expose myself too.  It’s not that I don’t care or simply won’t talk to people and debate, or that I will not at all read things that might seem dismal and so on; it’s just that repeatedly doing so when there’s no need to doesn’t make any sense.

This year has already been incredibly tough, and I know it’s going to get tougher with time given all the above and more.  I just don’t want to get to a point where I irrevocably shatter and can’t pull myself back together again is all.

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