Fetal Alcohol Spectrum Disorder & its Legality

Fetal Alcohol Spectrum Disorder (FASD), previously denoted FAS, fetal alcohol syndrome, did not debut in medical literature until 1973. At that time, it seemed impossible that alcohol could be a teratogen (a chemical that can disrupt fetal development), as how would it not have been noted earlier? People assumed it must rather have been the immoral or unhealthy lifestyle accompanying some alcohol-consuming mothers that caused FAS. But in 1977, experiments in animal models showed that alcohol alone was responsible for the effects of FAS. By this time, the evidence was strong enough that the FDA published an advisory warning against heavy drinking during pregnancy and recommended a somewhat refrained limit of 2 drinks per day. By 1989, alcohol was required to have a label warning against drinking while pregnant. FAS, therefore is not as well understood as we would wish solely based on the fact that it was just discovered around 50 years ago.

FAS was renamed FASD upon the discovery that there is an incredibly variable spectrum of disease manifestations. This was precipitated by the discovery that some patients suffered from physical, neurological, and behavioral deficits due to FAS, yet lacked the facial disfigurement. In classic FAS, the symptoms are numerous: dysmorphology (facial: thin upper lip with a smooth philtrum, small palpebra fissures and epicanthal folds of the eyes, an upturned nose with a flat nasal bridge, and “railroad track” ears; organ and limb abnormalities), growth deficiencies, both pre- and post- natal (microcephaly, small brain, especially with diminished basal ganglia and anterior vermis of the cerebellum; low birth rate and possible continued growth retardation), and central nervous dysfunction (nerve cells that have migrated to inappropriate areas, neuroglial heterotopias and abnormal development of the cerebellum and corpus callosum or abnormalities in cerebral blood flow, neurotransmitters, and neuronal activity in the absence of true neuroglial heterotopias). Though these symptoms are all present in extreme cases, leading to low IQ and severe disabilities, mainly “deficits in attention, learning and memory, emotional dysregulation, and executive functioning are core deficits, likely reflecting the dysfunction of the frontal lobe”, there is great variety in FAS manifestation, hence the current nomenclature of FASD.

The symptoms of FASD often lead to the comorbidities of psychiatric illness (i.e. ADHD, expressive language disorder) and predisposition to addiction. In addition, FASD impairs immune function and may contribute to susceptibility to other disorders that are not neurologically relevant, such as sudden infant death syndrome (SIDS) due to the brain structure itself. Despite the burden of such encumbering disabilities associated with FASD, the strife often worsens: As FASD victims grow up and begin to be treated as adults, yet lack the frontal lobe abilities to reason with adult forethought, they often end up in jail. Streisseguth et al found that 50% of FASD individuals will be confined in jail at some point in their life. They also identified incredibly heightened risk for lowered life span, disrupted school experiences, inappropriate sexual behaviors, and alcohol/drug use. It is absolutely insane that this devastating and debilitating disorder is 100% preventable (by abstaining from alcohol consumption during pregnancy: no safe amount has been established) and one of the most common causes of birth defects, with full spectrum FASD affecting 1% of births in the population and up to 3% of FASD cases on the spectrum. FASD, though, is often misdiagnosed or undiagnosed when facial dysmorphology is not apparent.

There is currently a search for clear genetic markers that can be identified later in life, such that diagnoses may be improved and it can be ensured that FASD sufferers receive adequate treatment through resources (behavioral (therapy/communal living/environmental enrichment/establishment of routine) and medical (cognitive supplements, choline to improve neuronal plasticity, )). Currently, there are identifiable markers, fatty acid ethyl esters, found in newborn meconium (their first waste excretion) yet they can only detect maternal alcohol consumption up to about a month prior, though there is some speculation that it can be found in hair and used to date alcohol consumption back further. It is necessary that markers that indicate timing and levels of alcohol exposure are discovered, such that a greater understanding of such factors effect on the disease outcomes can be obtained. Screening through questionnaires is the greatest source of information regarding fetal alcohol consumption currently, yet they are vulnerable to lack of memory and mainly deceit by mothers (fearing legal repercussions or judgement). The greatest hope for an impending breakthrough in FASD diagnosis is the use of epigenetics. Specific changes (i.e. of histones) have not been identified as of yet, but there is great promise, as research has identified such changes by showing that alcohol imposes teratogenic effects even when its exposure is prior to conception: it alters the genetic composition, epigenetically, of the gametes (up to 244 quantifiable gene changes when both parents had binge drank prior to conception) resulting in cognitive and emotional effects on the offspring.

Given the seriousness and life-long burden of FASD, one would think that there would be laws in place to prevent its occurrence i.e. that it would be illegal to drink while pregnant… this is mostly not the case. First of all, there are issues of the definition of the fetus as a person with rights. In a court case in the UK, where a mother was sued for damages inflicted upon her daughter, who suffered from severe and crippling FASD, yet the “court wouldn’t award damages to a child with fetal alcohol syndrome because, they said, the damage was done in utero…  The unborn are not considered “persons” separate from their mothers in a legal sense; legal persons are accorded rights and protections by the state… It is well established that a fetus is not a ‘person’; rather it is a sui generis organism.” In the U.S. as well there are no federal laws that prohibit a mother from consuming alcohol while pregnant; purposely inflicting FASD upon your child is not a federal crime. It is left up to the state legislative level to impose restrictions on maternal alcohol consumption. This isn’t to say that they do, in fact New York has a law in place which requires bartenders to serve a drink to pregnant women requesting a drink, as a protection of human rights.

However, in 15 states substance abuse is classified as child abuse, in 3 states it is legal to confine a pregnant woman who consumes alcohol to a treatment facility (for mental health or substance abuse, and in 21 states it is either required or encouraged that physicians report suspected alcohol use during pregnancy to child protective services! Interestingly enough, though, the American Congress of Obstetricians and Gynecologists as well as NOFAS (an anti-FASD group) both strictly and strongly oppose any such laws that criminalize pregnant mothers who drink. This is due to the fact that there is some research showing that, “neither a state’s number of punitive laws nor its number of supportive laws are associated with a greater efficacy of its alcohol policies as measured by policy experts’ estimates,” as well as the idea that many such punitive measures cannot take effect until the baby is born and tested, thus they often lack any emphasis on preventative measures and often leave the child in state custody. In addition, research has shown that the threat of going to jail for illegal drug use deters pregnant mothers from seeking treatment, and supposedly this principle would apply equally to alcohol use during pregnancy, were it announced illegal.

To further complicate matters, some of the most devastating damage of alcohol consumption whilst pregnant take place in the very early weeks of development, before a mother may even realize she is pregnant. An interview of such mother by daily mail found that 2 such mothers indeed did not realize they were pregnant until 8 weeks into their pregnancy, at which point they completely stopped all alcohol consumption. They weren’t concerned at all about the health of their children, as they didn’t realize how far along they were when they found out they were pregnant until later. Upon diagnosis of their children with FASD (they were equally devastated and surprised. When people ask them about their children’s FASD they often pretend they had adopted the children, as the stigma of FASD mothers being low-life alcoholics is so prominent and few people realize that there are exceptional cases such as these mothers, where they never intentionally drank while pregnant. Due to this possibility, the CDC recommends that all women of reproductive age who are not on birth control abstain from alcohol.

A political issue with the legality of alcohol consumption while pregnant is that it is often not a stand-alone topic; A study has recently found that, “states with a greater number of punitive pregnancy and alcohol laws are more likely to have greater restrictions on women’s reproductive rights. This finding suggests that a primary goal of pursuing such policies appears to be restricting women’s reproductive rights rather than improving public health.” In addition, these states with the greatest number of punitive pregnancy and alcohol laws (i.e. restrictions on maternal drinking or abortions) were found to have fewer policies that support women’s health and had higher maternal mortality rates.

Chris Hackler explores the complicated issues surrounding FASD prevention in his paper, Ethical, Legal and Policy Issues in Management of Fetal Alcohol Spectrum Disorder. He explains that the main balancing act is protecting the fetus’s life and life quality while protecting the mother’s privacy and trust in the physician. He cites that while education about FASD is generally quite effective, in the case of addiction or mental instability it would be necessary that an outside party is involved to enforce alcohol deprivation, whether it be a spouse, relative, mental health facility, or law enforcement individual, yet it is unethical for a physician to divulge patient information according to the Hippocratic oath and the very basis of what medicine believes in. In addition to the ethics, it is not wise to break patient-physician trust on an individual or large-scale level because in this case the mother may not ever even seek basic medical treatment, for fear of “tattling”. What does complicate this matter, though, is the fact that there are indeed exceptions to patients’ confidentiality, where the physician is actually required to report incidences, such as those of gunshot wounds or communicable diseases, where the main feature is that not reporting such cases could directly endanger (through bodily harm) an identifiable individual. The ambiguity here, then, is that it is currently legally ambiguous whether a fetus is an individual.

South Carolina, however, has taken legal measures to define a fetus as a person and therefore prosecutes pregnant women (on the basis of child endangerment) ‘risk harm to viable fetuses”, even attempting legalization of randomized cocaine testing in pregnant mothers for such penalization, though this was deemed unconstitutional by the supreme court. In Wisconsin, as well, mothers found of consuming alcohol during pregnancy can be “found guilty of ‘unborn child abuse’ and committed to involuntarily inpatient care; About a third of the states require that medical and other professionals report positive drug tests in pregnant women and newborns to an appropriate state agency.” However, in addition to the American Congress of Obstetricians and Gynecologists,  the American Academy of Pediatrics, the American Medical Association, the American Nurses Association, and the American Public Health Association all recommend against punitive measures in reaction to drinking alcohol during pregnancy, as they believe, “treats medical problems such as addiction and psychiatric illness as if they were moral failings, criminalizes otherwise legal maternal behavior, and unjustly affects the most vulnerable women. The ultimate effect of punitive policies may be to discourage prenatal care and undermine the physician-patient relationship.”

Based on the overall difficulties in dealing with FASD prevention, it seems that since it is imperative that it be prevented, yet punitive measures are greatly recommended against, there must be great, positive efforts to prevent maternal alcohol consumption, such as providing free counseling, supportive agencies, etc. Even so, I don’t foresee an end, as mothers will still be ashamed to admit maternal drinking once punitive measures are removed in places they are currently implicated due to the social stigma around drinking while pregnant. It seems the most effective measure we are able to currently take is to improve access to free birth control, such as to prevent accidental pregnancies, and make this service extremely visible—make a campaign of it. There certainly needs to be philosophical, scientific, and political collaboration to approach an issue as complicated as FASD.



















Hashimoto’s thyroiditis and Celiac Disease

There is a great comorbidity of autoimmune thyroid disease and Celiac Disease (CD), which is also an autoimmune disease (against gliadin (from gluten) or transglutaminase (a human enzyme). Basically, proposed mechanisms of comorbidity are that CD causes malabsorption of selenium and iodine, causing HT, that gluten (with or without the diagnosis of CD) causes leaky gut and invading bacterial antigens resemble epitopes on the thyroid such that it is attacked in conjunction with the bacteria (mainly Yersinia) through molecular mimicry, or that one class of antibodies is targeted against both the thyroid and gliadin or transglutaminase.

It is recommended that a gluten free (GF) diet imposed early on in the development of HT such as to change the trajectory of the autoimmune disease into one that is less severe and perhaps deteriorates into hypothyroidism later. In the absence of CD in HT patients implicating a GF diet, they may benefit from preventing the aforementioned leaky gut, which inadvertently creates anti-thyroid antibodies but they also may benefit because they have an undiagnosed gluten intolerance, which is much more common than many realize (see blog post 21), causing unnecessary inflammation and immune system activation that contributes to HT. Gluten sensitivity in the absence of CD is referred to as non-celiac wheat sensitivity. Along these lines, some physicians recommend going dairy-free to minimize such effects and alleviate HT severity. Many people also have a slight intolerance to dairy. Gluten not only causes leaky gut but also has been associated with the upregulation of Toll-like Receptor 2, an innate immune mechanism triggered by lipopolysaccharide that has been noted to play a role in HT. Microbiota may also be affected by gluten, furthering the autoimmune response as the imbalanced microbiome of the gut leads to “transcriptomic, proteinomic and the metabolomics” changes which induce auto-immunity by breaking tolerance to self-antigens (and non-pathogenic gut bacteria antigens).

HT patients who indeed suffer from CD certainly will benefit from a GF diet. CD is known to be causative of many glandular endocrinopathies, not just HT, due to the break in the gut wall barrier. Direct correlation to HT, though, is possibly through the shared embryonic origins of the thyroid and gut, with the thyroid developing from the pharyngeal gut on the 17th day of gestation, explaining the (still in investigation) cross-reaction of HT and CD antibodies. Other, more physical relations are the malabsorption of thyroid regulating vitamins selenium, iodine, iron, vitamin D, and B12. More advanced HT, resulting in hypothyroidism, may mask CD symptoms and also increase chances for gluten reactivity by decreasing diarrhea and weight loss due to lowered levels of circulating thyroid hormone (which regulate homeostatic activities, such as bowel movememnts). In addition, the treatment of HT and hypothyroidism may be quite hindered by the malabsorption characterized by CD, with reduced surface area in the small intestine impeding the absorption of thyroid replacement drugs and supplemental vitamins.

The statistics in support of the comorbidity of CD and HT are consistent, yet the results of a GF diet have not yet concurred.

  • Comorbidity
    • Freeman found that 17% of biopsy-confirmed CD adults to be suffering from autoimmune thyroiditis.
      • Of these comorbid patients, HT was diagnosed first in 13 of the 16 (81%)
    • Merhdad et al found that 2.9% of HT patients also suffer from serologically determined CD.
      • Of these comorbid patients, half suffered from HT and half suffered from non-autoimmune hypothyroidism
    • Larizza et al found that 7.7% of HT patients also suffer from biopsy-confirmed CD.
    • Collin et al found that 4.8% of Finnish HT patients also suffer from CD, compared to a 0.4% natural occurrence rate of CD in the Finnish population.
    • Hakanen et al found that 13.9% of CD patients also suffer from HT, compared to a 2.1% rate of HT in the controls group.
    • Ch’ng et al found that 11-30% of CD patients possess HT antibodies.
    • Kalyoncu and Urganci found that 26-41% of CD patients possess HT antibodies.
    • Hadithi et al found that 21% of CD patients also suffer from HT.
    • Lerner et al’s metaanalysis found that, “The prevalence of [HT] in patients with CD was suggested to be four times higher than that in the general population, though the range is very wide, spanning 1.2–30%. The range for HT in CD is narrower: 1.25–19%.”
    • “In the adult populations with CD the rate of hypothyroidism and/or HT is much higher than that in children, ranging between 12.9 and 30.5%.”

Therefore, as far as comorbidity is concerned, figures for HT found in CD patients range from 11%-41% while figures for CD found in HT patients range from 2.9%-7.7% in the cited studies.

  • Treatment of HT with a GF diet results
    • Sategna Guidetti et al found that a 1 year GF diet reversed 71% of sub-clinical hypothyroidism, while of those suffering from euthyroid autoimmune disease (HT patients who still have a normally functioning thyroid), 25% shifted towards subclinical hyper- or hypo- thyroidism (this is a progression of HT, which most likely would have happened naturally and the study does note that there was poor GF diet compliance among these subjects, and 5.5% of subjects whose thyroid function was normal upon induction of the diet developed thyroid issues by the end of the year.
    • “Cooper et al considered that a gluten-free diet did not prevent development of autoimmune disorders and had little ameliorating effect on their course, apart from an occasional improvement in atopy.” (over-reactive allergic responses i.e. asthma)
    • “Sategna-Guidetti et al, however, noted that a gluten-free diet may reverse the abnormality in those with subclinical hypothyroidism although, like Viljamaa et al,found no correlation between duration of gluten exposure in adult CD and risk of autoimmune disorders.”
    • “Ventura et alfound that… thyroid-related antibodies tended to disappear following a gluten-free diet (14.4% [at diagnosis], 11.1% [at 6 months], 6.6% [at 12 months] and 2.2% [at 12 months] [of patients possessed high titers of] thyroid related antibodies)”
    • “Mainardi et al found no correlation between thyroid antibodies and the introduction of a gluten-free diet.”

Therefore, treatment of HT with a GF diet has been reported, in these cited studies, to be 0%-12.2% successful, though the literature is much more limited than studies concerning the comorbidity of CD and HT.

Ultimately, the research done is not consistent on the true prevalence of CD and HT comorbidity nor the treatment of HT with a GF diet. The quantity and expansiveness of clinical trials must be increased and thereafter meta-analyses will be much more conclusive about such topics. As these endeavors are underway, before anything can be stated with confidence, it seems that a proper recommendation would be for physicians to be cognizant of the possible comorbidities of HT and CD, as to test their patients when proper and for a GF diet to be considered in the case of HT not responsive to medicine or in the case of any HT were the patient feels the low possibility of reward is worth the lifestyle impact that adhering to a strict GF diet may make.

















Hashimoto’s Disease & nutritional factors

Selenium is certainly not the only nutritional factor that plays a role in Hashimoto’s Thyroiditis (HT) (see previous blog post,). Other known dietary factors that affect the disease are iodine, vitamin D, iron, and debatably gluten (see next blog post).


Iodine is a complicated factor in the disease, as too little as well as too much can exacerbate the progression and symptoms of thyroid disease. It has been known that iodine deficiency causes hypothyroidism, and it often did, worldwide, before the implementation of iodized salt (in developed countries) because iodine is necessary to produce thyroid hormones (T3 and T4), and cannot be produced by the body. Excess iodine, though, exacerbates HT and even hypothyroidism in some individuals.

In a normal thyroid gland, tyrosine molecules are iodinated by thyroid peroxidase (TPO) in the presence of hydrogen peroxide (H2O2). These mono- or di- iodotyrosines combine in different combinations to create T3 (with three iodine molecules attached) or T4 (with 4 iodine molecules attached) thyroid hormones which are released into the bloodstream after processing in the thyrocyte to release the thyroglobulin attached in their production.

High iodine intake inhibits the synthesis of thyroid hormone synthesis and antioxidant capacities of the thyroid gland by inducing apoptosis of thyrocytes and generating reactive oxygen species (which may be part of the reason that Se is decreased in HT patients). Reactive oxygen species are generated by the organification of iodine, which occurs in the thyroid. Apoptosis is more complicated. Iodine excess causes thyrocytes to upregulate ICAM-1, an adhesion molecule, which changes the immunogenicity of the cells. This upregulation is synergistically stimulated by H2O2, generated by iodine organification, which activates ICAM transcription. When a subset of CD4+ T-cells, Th1 cells, encounter ICAM-1 they bind to it and are stimulated to release the cytokine IL-6, as well as interferon gamma (IFN- γ) and tumor necrosis factor (TNF-α), which signify that there is a foreign pathogen that must be eliminated (ICAM binding allows the leukocytes to migrate into the thyroid, where they recognize foreign antigens present due to high iodine, such as highly iodinated thyroglobulin). IL-6, IFN- γ, and TNF-α lead to the downregulation or inactivation of T-reg cells, which dampen the immune response and help to anergize (de-activate) leukocytes which recognize foreign antigen in the absence of inflammation. Therefore, this combination of reactive oxygen species, production of cytokines via ICAM-1 upregulation, and dampening of T-regulatory t cells eventually leads to activation of the adaptive immune system without it being checked. This eventually leads to the production of antibodies against the thyroid and therefore its destruction.

The previously described processes will occur in any individual with excessive and chronic iodine intake. In particularly susceptible individuals, however, the iodine excess does all of the above as well as inducing Th17 (a type of CD4+, cytokine producing T-cell) production, which enters the thyroid and secretes pro-inflammatory cytokines and induces CD8+ cytotoxic T-cell activation. These individuals also produce TRAIL in response to high iodine, which is a TNF-related apoptosis-inducing ligand. Both of these phenomenon lead to the attack and destruction of the parenchyma cells of the thyroid.

It is now firm knowledge that iodine intake levels slightly below or above normal levels (about 150 mcg/L) are associated with disease risk. Iodine levels should be tested in all individuals, not just those suffering from thyroid disease, since iodine not only affects the disease progression and symptoms, but can also induce hypothyroidism or autoimmune thyroid disease (HT). Duntas, L. H. states that, “excessive iodine intake ([median urinary iodine excretion]>300 μg/l) could well become a serious public health concern because of its ability to substantially increase subclinical hypothyroidism and [Autoimmune Thyroiditis] rates.” Therefore, the threat is not necessarily an increase in overt cases of thyroid disease, but rather the rise of subclinical thyroid issues, lowering the quality of life for numerous patients nd persisting by not being easily identifiable.

Vitamin D

Vitamin D had been considered merely a fat-soluble vitamin, but recently has been acknowledged as a steroid hormone. It is responsible for regulating many immune processes. It is known without doubt that vitamin D is found lowered in HT patients, as a result of auto-immune processes. Some studies have also shown that vitamin D supplementation lowered TPO and Tg antibodies, though more trials must be done before this relationship is confirmed. Calcitriol (1a ,25(OH)2 D, the active form of vitamin D used by the body), mainly strengthens the innate immune response via antimicrobial peptide (defensin, etc) regulation. In addition, it dampens the adaptive immune response (the B and T cell response that triggers HT) by “inhibiting the pro-inflammatory effects of Th1 and Th17 cells and enhancing the anti-inflammatory activities of Th2 and Treg cells.” This alone would protect against HT progression, but vitamin D also helps protect against autoimmunity by inhibiting certain dendritic cell subsets from maturing or presenting antigen.

In addition, it has been postulated that chronic infection may actually cause autoimmunity. For example, Epstein-barr virus (a whole-body herpes virus that causes mononucleosis, EBV), may be a causal agent of auto-immune disease and vitamin-d regulated immune responses increase CD8+ T-cells, which clear cells infected with EBV to eliminate the virus.


Thyroid peroxidase (TPO) is a heme (iron) containing enzyme. Iron deficiency causes TPO to be inactive, leading to less T3 and T4 hormone being produced, causing the symptoms of thyroid disease, “In rodent studies, iron deficiency, with or without anemia, decreased serum T4 and T3 concentrations, lowered 5¢ -deiodinase activity, and reduced the ability to thermoregulate in response to a cold environment.” Furthermore, it has been proposed that iron deficiency also decreases the ability of T3 to bind to its receptors at extra-thyroid locations.

Meloni et al found that out of 14 hashimotos patients 6 had iron deficiency. The cause of iron deficiency in HT patients is often not the actual pathogenesis of HT, but the often comorbidity of auto-immune gastritis, which inhibits the absorption of nutrients. This gastritis is often related to celiac disease, found in many HT patients. This will be explored in the next post.










Thyroid autoimmunity & its link to glutathione peroxidase/selenium


Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis) is one of the most common autoimmune disorders of the thyroid and has complex factors which result in an autoimmune reaction resulting in the destruction of thyroid gland and constant inflammation via antibodies mainly against thyroperoxidase (TPO-AB). Accompanying clinical symptoms are elevated thyroid stimulating hormone (TSH) accompanied by paradoxically low free thyroid (T3 and T4) levels. It initially may lack symptoms other than elevated TPO-AB, then progress to hypothyroidism as the synthesis of thyroid hormone becomes increasingly impaired, which can essentially only be treated with synthetic thyroid hormone as a replacement measure. It is thus quintessential to investigate avenues of preventing progressive thyroid gland destruction via preventing autoimmunity to thyroid antigens by simple balance of vitamin co-factors involved in thyroid synthesis and autoimmunity.

Recent studies have investigated the effects of glutathione on Hashimoto’s thyroiditis. These speculations were fueled with anecdotal and case-study type evidence that glutathione (GSH) supplementation via intravenous supplementation of synthetic glutathione or oral supplementation with precursors to glutathione, such as cysteine, improved the conditions of cancer. There has also been preliminary evidence that glutathione plays an important role in the improvement of diabetes, neurodegenerative disorders, and other inflammatory and autoimmune diseases (via providing the redox potential of glutathione peroxidase). These speculations originated from the antioxidant function of glutathione, as the most abundant antioxidant in mammalian cells, as well as its involvement in immune system function (where it helps reduce reactive oxygen species after respiratory burst in phagocytes and also acts as a thiol regulator of the immune system, aiding in the shift from innate to adaptive immunity, therefore dampening inflammatory responses). Oxidation via free radicals generated by metabolic processes can damage organelles as well as DNA, resulting in serious disease. Damage caused by the presence of many reactive oxygen species or reduced cellular reduction potential also triggers inflammation. Hydrogen peroxide, H2O2, is produced and necessary for thyroperoxidase to fix iodine to tyrosyl residues of thyrocytes, thus glutathione peroxidase is necessary in the thyroid gland to neutralize excess H2O2. Studies investigating the role of glutathione in Hashimoto’s thyroiditis, though, have been less than conclusive.

It is important to understand that active, reduced, glutathione peroxidase requires a co-factor of selenium to function. It has been known for a long time, with substantial evidence, that selenium deficiency can exacerbate Hashimoto’s symptoms. Selenium supplementation has been shown to reduce TPO-AB and improve mood in some studies, though definitive knowledge has yet to have been obtained about its efficacy. It is being speculated that the positive effects are due to selenium’s role in glutathione peroxidase’s function. It is known that selenoproteins (using a selenocysteine form of selenium) include glutathione peroxidase and thioredoxin reductase, yet they also function as the iodothyronine deiodinase enzymes which convert T4 to the active, T3 form (and vice versa, depending on the isoform). In addition, selenium is involved in the upregulation of T-reg cells and CD4+ T cells, dampening inflammation (reducing cytokine production) via a SELENOS selenoprotein (which decreases cytokine production of TNF-a and IL-1b, known factors in Hashimoto’s thyroiditis), and the suppression of a certain MHCII expression on thyrocytes, reducing chances for antibody formation. Selenium aids these processes, including reduction (anti-oxidation) in adequate quantities, but is actually cytotoxic, producing opposite effects, at high levels (within about a 200 mcg range!).

The investigation of glutathione peroxidase as a main factor in the pathogenesis of Hashimoto’s thyroiditis is due to the known importance of selenium (which I necessary for glutathione peroxidase’s function) as well as the postulation that in the absence of adequate antioxidant activity, the damage thyroid gland and associated enzyme materials are what provide the antigens to which an autoimmune response is mounted, in the presence of “foreign” antigen and stresses cells due to reactive hydrogen peroxide. In addition, the thyroid gland contains more grams of selenium per tissue than any other organ in the body. Some studies have confirmed this hypothesis, reporting that, “mean [glutathione] levels in [Hashimoto’s thyroiditis] patients is markedly lower compared to healthy controls. The fall in [glutathione] levels coincided with a marked elevation of [glutathione peroxidase] activities in [H Hashimoto’s thyroiditis] patients; [glutathione] levels were inversely and significantly correlated with TPO-AB titers,” which presents clear and logical support for glutathione being a major to main factor in the etiology of Hashimoto’s thyroiditis. This, sadly, has not been replicated as it should be if it were strictly true. One study found that glutathione peroxidase levels and selenium levels were not correlated, nor were the levels altered in patients who were currently under treatment with levothyroxine for hypothyroidism (late Hashimoto’s). In addition, a meta-analytical study found that there was a high bias risk in many studies supporting selenium and glutathione’s role in Hashimoto’s thyroiditis, claiming that. “evidence to support or refute the efficacy of selenium supplementation in people with Hashimoto’s thyroiditis is incomplete and not reliable to help inform clinical decision making.”

It is imperative that larger scale studies investigating selenium and glutathione peroxidases’ role in the etiology of Hashimoto’s thyroiditis as well as certain aspects of their mechanisms in the pathogenesis are performed. Prior to such information, it would be unscientific and biased to make any claims about the involvement of such things in the disease. With the current information, it is sound to claim that selenium levels ought to be checked and supplemented if low, due solely to their implications in the immune response and the regulation of conversion between T3 and T4. As for the glutathione aspect, prior to knowing whether it is implicated in the disease, it would be completely risk free and perhaps beneficial to consume foods rich in glutamate, cysteine, and glycine, glutathione’s precursors (as supplementation done in excess may be detrimental).









The myth of Gluten Intolerance?

Gluten intolerance is emerging in research as a truly systemic allergy with some possibly catastrophic symptoms. There has been a lot of stigma associated with gluten allergy, as there seemed to be a sudden rise in people identifying themselves as gluten intolerant (presumably) since the from 2009 to 2013 gluten-free diet popularity tripled, while diagnosis of celiac disease remained constant, affecting about 0.7% of the population. This trend faced a lot of backlash, mostly on Facebook with people becoming avid anti-gluten-free proponents, bashing those who claimed to have brilliant results from going gluten free. They cited the fact that only about 1% of the population has Celiac Disease yet it seemed as if all their Facebook friends suddenly claimed to have it!

The main issue here, which is just beginning to come into clear vision in the medical research community and not even necessarily into the sights of practicing physicians, is that celiac disease is distinctly different from gluten sensitivity, which is indeed a condition. The reason why gluten sensitivity has been flying under the radar is that it doesn’t produce the gastrointestinal symptoms (villous atrophy) that Celiac Disease does nor does it produce the characteristic antibodies found in celiac disease; Gluten sensitivity can be directed at a variety of epitopes found on the wheat (or other grain), mainly gliadin, and is therefore harder to diagnose. These facts do not in any way discredit it as a genuine issue. The reason why gluten sensitivity is such a serious issue is because it shares the symptoms of Celiac Disease which are extra-intestinal. These symptoms have received little acknowledgment even within the Celiac community, and certain not in terms of gluten sensitivity, where the whole disease is often overlooked and the symptoms are not well categorized.

Estimates find that gluten sensitivity is six times as common as celiac disease: that’s about 6% of the population (almost 20 million individuals in the United States)! This means there are countless individuals that may be suffering from severe symptoms without any knowledge to the fact that they may be alleviated by a diet change which is quite simple nowadays. The issue in identification and numerical data supporting the prevalence of extra-intestinal symptoms of gluten sensitivity stems from the fact that all previous research has failed to separate Celiac disease from Gluten sensitivity, therefore there is no existing data on the prevalence of symptom’s distribution between the two. This gap will, thankfully, begin to be filled with the current rising knowledge of gluten sensitivity prevalence and significance. Another reason that there may be an under diagnosis of gluten sensitivity is the production of morphine-like gluten exorphins in gluten metabolism, which have opiate effects which may “mask” the symptoms of the intolerance, as proposed by Pruimboom and Punder. There has been insight to gravity of the situation, “as 57% of people with neurological dysfunction of unknown origin test positive for anti-gliadin antibodies.” And the neurological and psychiatric symptoms are absolutely devastating. It’s a shame that social media may have hindered the procession of research regarding gluten sensitivity and is living proof that you should always do your own research on anything claimed to be scientific found in a social media setting, especially when it concerns your own health.

The neurological symptoms of Gluten sensitivity and Celiac disease include gluten ataxia, epilepsy, peripheral neuropathy, inflammatory myopathies, myelopathies, headache, gluten encephalopathy, and white matter abnormalities. Gluten ataxia is the most thoroughly studied symptom, caused by anti-gliadin antibodies. Cerebellar dysfunction and disfigurement manifest as issues walking and involuntary movements (ataxia). The inflammation caused by the anti-gliadin antibodies is postulated to create an inflammatory environment in which antibodies to Purkinge cells, cortical neurons, and deep cerebellar nuclei brainstem and cortical neurons are generated. Studies have found that using a gluten free diet to treat gluten ataxia, as well as epilepsy, were largely successful. This carries huge implications for a condition such as epilepsy, where there are large numbers of patients that are resistant to medical treatment (physiologically) who may have not been screened for anti-gliadin bodies just based off the assumption that they couldn’t be the culprit in the patient isn’t experiencing the gastrointestinal symptoms associated with Celiac Disease.

The psychological complications carry such weight as do the neurological, with schizophrenia being an incredibly hard mental disease to treat, often due to drug resistance. Schizophrenia also carries and incredibly strong correlation to gluten sensitivity and Celiac Disease, which was identified as early as 1953. One study found that] reported 19% of a schizophrenia group and 0% of a control group were found to possess anti-gliadin antibodies. If a gluten-free diet (or ketogenic: see https://scienceandrhetoric.wordpress.com/2017/08/11/the-mystery-of-schizophrenia-lipodimics-and-the-possibility-of-treatment-via-a-ketogenic-diet/) is the key to end someone’s persistent schizophrenic symptoms, it is absolutely critical that physicians be more aware of the possible implications gluten sensitivity brings. Another major area of psychiatric disorders that may have a huge impact by awareness of its relation to gluten sensitivity is the prevalence of anxiety and depression (18.1 and 6.7 percent of the U.S. population suffers from these, respectively). Distinct biological links, of L-tryptophan and serotonin, have been identified as the etiological connection between gluten sensitivity and depression. Attention deficit hyperactive disorder and autism spectrum disorders have been proven in research to be related to gluten sensitivity, yet more research needs to be conducted before a strong case is made for an etiological relationship.

It’s clear that much research is left wanting to produce more data and to investigate the exact mechanisms which cause the correlation between gluten sensitivity and extra-intestinal symptoms. The fact that the medical community is becoming aware of the huge gap in care cause by dismissal of gluten sensitivity (which may be greatly influenced by social media and popular opinion inciting fear of ridicule amongst the medical community) is promising, as hopefully this elucidates the devastating effects of misdiagnosis, lack of diagnosis, and unidentified comorbidities have on unknowing and suffering patients. There is a need for greater awareness of how the entire body interacts and its systems interdigitate to produce symptoms that are not always clearly indicative of their origin.












The truth about immunization: Part 2

Now that I have debunked myths and presented basic facts to support what I stand by: vaccinations are necessary and good! Every parent should immunize their child except for in rare cases, such as SCID patients. We can now go one to criticize the current vaccination infrastructure and propose solutions to gain social trust back and boost vaccination rates. This critique is largely derived (so much so that one may call it a summarization) from the nonpartisan scientific paper, Vaccine risks: real, perceived and unknown, by Robert Chen. I chose an “outside” source as to steer clear of research and claims made solely by the companies who benefit monetarily from vaccinations.

Why have anti-vaccine attitudes been gaining strength?

  • As vaccination increases, vaccine-preventable diseases decrease. Though this is wonderful and means the vaccines are effective, it also means that adverse reactions to vaccination have outnumbered the occurrence of vaccine-preventable disease in “‘Mature’ immunization programs.” While from a logical standpoint this makes perfect sense, it may seem concerning at first glance. What truly compounds fears about adverse events are media claims about them that are not always well researched. If someone hears just a snippet of negativity about a vaccine from a reputable new source they may be quite impacted, even if the news source is solely reporting that other have those negative sentiments, making no claim to there being a solid reason for those attitudes. One must remember that news channels are much more comparable to a politician than a scientist and I certainly would prefer a scientist to influence my healthcare decisions.
    • About 11,000 reports per year are made to the United States Vaccine Adverse Event Reporting System (VAERS). This high number is in some proportion attributed to reports of events that may or may not be directly related to the administration of vaccination, but rather solely temporally related.
  • Chen cites the medical mantra of “first do no harm” as explanation for the low threshold of risk tolerance accepted for vaccine adverse reactions. If the same chance for adverse effects for vaccines applied to a treatment for a pre-existing disease, it would be deemed a miracle drug! It is unfortunate but true that vaccines will always be subject to much more rigorous criticism than treatments for existing disease, even though they themselves are indeed a treatment for disease (or even cancer i.e. Gardisil 9) much more powerful than those used for existing disease, they just work pre-emptively.
  • Once the anti-vaccine trend began, it seemed to compound itself and run away, turning real concerns into runaway, blatantly slanderous or unscientific claims. Anti-vaccine proponents have made claims that various vaccines are linked to chronic illness such as autism, multiple sclerosis, Guillain-Barré syndrome, diabetes, and asthma. No scientific experiments have found any solid evidence for such claims and those that supposedly do have been attempted to be repeated by other organizations and no such results were found. A scientific theory may not be deemed truthful if it may not be repeated by anyone using the same methods.


What real issues are these anti-vaccine attitudes fueled by?

  • According to Chen, “increasingly well organized consumer groups, the popularity of alternative health care, increasing competition in the news media and new rapid communication technologies have all contributed [to the rise of anti-vaccine milieu].” These are just realities of the world we live in today. Other factors, following, are much easier addressed.
  • Since extreme adverse reactions are so rare, they are difficult in respect to both scheme and funding to study. Most research done on adverse reactions has been in the form of case studies, from which is infinitely more difficult to draw a solid conclusion from than from a formal, controlled experiment. Therefore, we know little about the nature of the occurrence of rare adverse events (which may or may not be attribute to the vaccine).
  • Pre-licensure trials of new vaccines are not designed to solely assess safety, but rather efficacy. While they do accomplish the job of providing the rate and nature of typical adverse events, they fail to provide solid information on rare adverse events, delayed adverse events, or adverse events specific to sub-populations of peoples.
  • Case definitions of specific adverse events, such as fever, have not been standardized on any large scale so it is difficult to compile different studies’ findings to provide valuable meta-analytical statistics.
  • Sufficient resources have not been allocated to investigate reports to the VAERS. We do not know how many adverse reports are veritable (caused by the vaccine) versus how many happened to occur after vaccination, carrying no relationship.
  • In 1991 The World Health Organization recommended that all of its Expanded Programs on Immunizations implement surveillance of adverse events to vaccination yet by 1997 only 14% had instated such an infrastructure. Since this is our only true source of information about the frequency with which adverse events occur it should be universal and well attended to, but that is not the case.
  • In the 1990’s the Institute of Medicine (U.S.A.) reviewed existing literature concerning adverse events and found the data so incomplete in 76% of the research that there could not be a for or against conclusion drawn. They identified the following inadequacies, which agree with the previous statements in this article, “inadequate understanding of biologic mechanisms underlying adverse events; insufficient or inconsistent information from case reports and case series; inadequate size or length of follow-up of many population-based epidemiologic studies; limitations of existing surveillance systems to provide persuasive evidence of causation; few experimental studies published relative to the total number of epidemiologic studies published.”
  • There is indeed a lot of risk in vaccines since a lot of new research and technology is being implemented. For example, we narrowly escaped infecting everyone vaccinated with polio vaccine from 1955-1963 with a virus. The vaccination virus was grown in monkey cells such that it became adapted to them and was no longer infections to humans. No one was aware that SV40, a virus was present in many of the cell lines. By nothing other than luck it so happened to be that the particular virus found in those cells is not able to infect humans. Thank goodness, because SV40 causes disease which turns into cancer in the simians which it affects. That being said, yes! There are indeed huge risks involved with new vaccinations that are scary but I regret to say necessary to the world. Even if those vaccinations had been infectious with SV40, they still would have saved many lives and had the potential to change the world’s infection with polio forever.

What problems do these anti-vaccine attitudes create?

  • Since poliomyelitis is the only vaccine-preventable disease soon to be eradicated worldwide, all other vaccines currently being administered will certainly need to continue to be administered for unknown periods of time until either adherence to vaccination and the efficacy of certain vaccines (and the ability to administer them in third-world conditions) is elevated such that more vaccine-preventable diseases are on the verge of being eradicated. In the face of anti-vaccine actions there has actually been a decline in progress towards eradicating certain vaccine-preventable diseases such as measles even just in the United States (though it is slightly irrelevant to categorize eradication by location since travel and emigration is so extensive nowadays). The anti-vaccine attitudes certainly put not only the unvaccinated children at risk, but much more importantly the entire population of the world is being robbed of their shot at eradicated diseases that have claimed millions of lives in third world countries for centuries.
    • I must digress and note that there is current research investigating why occurrence of pertussis (whooping cough) outbreaks have not been as exactly related to a decline in vaccination rates. It is currently being hypothesized and tested whether the vaccination is effective at fighting the disease but not the infection.

What can we do to solve this?

  • Recent improvements have been made in the programs available for surveillance of adverse reactions, yet lack of funding (and therefore interest) has kept them from being globally implemented. While time will fix this, with increasing awareness in the medical community of the need to combat anti-vaccination fuel but this can be accelerated through spread awareness and petitioning. Finding more funding for the support of adverse reaction surveillance may need to be diverted from injury compensation, provided by the U.S. vaccine excise tax.
  • In the case of a reported severe adverse reaction, there ought to be a follow-up procedure including care and interviews such that it may be confirmed whether the reaction was truly due to vaccination as well as to assure the patient is taken care of. Again, the issue here is funding so there must be a policy change to divert funding towards adverse reaction compilation and care.
  • Another great area such resources should be allocated towards is study of un-immunized individuals. Data of the rates at which they contract vaccine-preventable diseases and what role they play in transmitting such diseases to the community would certainly be fresh and intriguing data to present in defense of vaccination.
  • Chen makes an indispensable suggestion (indispensable because it solely necessitates a shift in primary care and is therefore not restricted by funding), “a shift from traditional paternalistic to a shared decision making model can help produce more informed consumers.” He prescribes a two-tier model for implementing this doctor-patient information, one general vaccine education for the majority of patients, and a more detailed, scientifically involved argument (with sources) for medically informed populations of patients.
  • A National (or more ambitiously, Global) Immunization Review Safety Board ought to be instituted to quell society’s distrust in scientific data provided by the CDC, etc due to suspicions of bias.









The truth about immunization: Part 1

I intend to present the clearest picture of health risks associated with vaccination and to defend the importance and necessity of vaccines whilst not blindly advocating them; I want to fully consider the pros and cons. I must begin by stating some basic facts about why vaccines are necessary/good and show an example of the faulty rhetoric anti-vaccination proponents have polluted the web with before I can go on to be truly objective, through criticism, in my next post. This is the bottom line for any curious parent:


Why should you vaccinate your children?

  • Vaccination protects your child from preventable diseases, some of which are still prevalent in The United States of America nowadays, such as whooping cough.
    • States with policies that make it easy to exempt children from immunizations were associated with a 90 percent higher incidence of whooping cough in 2011.
    • Even diseases which are not endemic to the U.S.A may be brought over by travelers or immigrants and be encountered by your child
  • Vaccinating your child protects many others including:
    • Other children who have not yet been vaccinated due to being too young
    • Older people, such as your parents or grandparents, who no longer possess a functioning thymus with which to fight novel infections (70 years old+)
    • Immunocompromised people such as chemotherapy patients or organ transplant recipients
    • While there are indeed side-effects associated with vaccination, the most common side effects are mild such as swelling at the site of injection. These drawbacks are small compared to results of diseases against which we have vaccines, which can result in serious consequences including lifelong disability or death.
    • It is true that there can be serious side effects from vaccination, but in weighing risk vs reward these are not even a slight argument for not vaccinating due to their rarity: (AEFI= Adverse Events Following Immunization)


  • Vaccination has absolutely no link to autism. Claims about these links are made about thimerosal (which contains mercury) and the Measles, Mumps, Rubella vaccine, both of which have been studied multiple times and on large scales to be proven wrong. In addition, thimerosal is no longer in use in current vaccines due to better adjuvants having been discovered.
  • Gardisil 9, the HPV vaccine has no link to the deaths purportedly caused by it. Confusion arose from the general onset of diseases such as Guillain-Barré syndrome, complex regional pain syndrome, and postural orthostatic tachycardia syndrome being around the time of Gardisil vaccination (11 years old). Decisions regarding the vaccines risk made in Japan were largely by politicians, not scientists.

While the above facts are scientific and true in that they have been proven by replicable studies, many parents do not believe them. This is due to very persuasive propaganda on the web. I found one such site/book written by an actual chemist (MS in organic chemistry) who created a whole seemingly scientific rant about medicine in general such as to build up his business: book and supplement sales. One of his targets is vaccinations and I chose select points of his to prove him wrong and expose “scientific” rhetoric on the web which is making flat out lies and preying on concerned, yet naïve civilians. Here a few select idiotic claims, rebutted (I’d really like to rewrite the whole article: it’s pure rhetoric and the fact that it claims to be scientific is deeply wrong)



  • Like argumentative apes, pro-vaccine parents and their physicians start pounding their chest in favor of [herd immunity]. They use [it] to attack anti-vaccine parents, accusing them of “putting vaccinated kids at risk due to a breakdown in herd immunity.”
    • Anyone arguing this is just as dull as the person that wrote this article. Ask any supporter of the herd immunity hypothesis and they will kindly explain that the unvaccinated kids are actually posing a threat to infants who have not yet been vaccinated and those with compromised immune systems either from age (a deteriorated thymus and therefore inability to make new antibodies) or a compromised immune system i.e. cancer patients, NOT to other vaccinated children.
  • The World Health Organization (WHO)… wrote that, “Children under two years of age do not consistently develop immunity following vaccination.” Therefore, vaccines can fly “below the radar” of our immune system. Not only does this weaken the immune system, it renders many vaccines ineffective.
    • This is because vaccines err on the side of safety, and requiring multiple vaccines to ensure immunity, is certainly much more of a medical concern than creating a vaccine so strong that it is always effective yet prone to revert to a pathogenic state. The immune system is not weakened by mounting a response, in fact it is actually “trained” to use the correct antibody response and if it is not, according the hygiene hypothesis, you are at higher risk for hyper-IgE responses i.e. chronic allergies.
  • Polio is the most feared childhood illness. It has caused paralysis and death for much of human history. The world experienced a dramatic increase in polio around 1910. Epidemics became regular events. They were the driving force behind a great race toward the development of a polio vaccine. The vaccine was developed in 1953 and an oral version came soon after.

But the vaccines came too late. Thanks to better hygiene, sanitation and nutrition, the rates of polio infection had already plummeted as documented in my book, Over-The-Counter Natural Cures. And it’s a good thing, because both forms were a total failure. In fact, instead of preventing polio… they actually caused it!

Medical journals around the world have exposed this outcome. The Medical Journal of Australia discovered “the relation of prophylactic inoculations [polio vaccines] to the onset of poliomyelitis [polio]” as far back as 1951.

And the trend has continued…

In a 2007 article, entitled “Nigeria Fights Rare Vaccine-Derived Polio Outbreak,” Reuters showed how the vaccine itself ignited outbreaks of polio in Nigeria, Chad and Angola.

And according to The Indian Journal of Medical Ethics, the polio vaccine program launched by Bill Gates paralyzed 47,500 children in 2011 alone. And those injured by the vaccine died at twice the rate of those infected by “wild” polio!

  • Polio cases have decreased by over 99% since 1988, from an estimated 350 000 cases then, to 37 reported cases in 2016. As a result of the global effort to eradicate the disease, more than 16 million people have been saved from paralysis.  As long as a single child remains infected, children in all countries are at risk of contracting polio. Failure to eradicate polio from these last remaining strongholds could result in as many as 200 000 new cases every year, within 10 years, all over the world.
  • It’s comical that better hygiene is cited as a cause of polio decline prior to introduction of the vaccine because in actuality, greater sanitation throughout the U.S. in the 1900’s (industrial revolution) caused an outbreak of polio, as children were not getting infected as quickly and by the time they encountered the disease they no longer had maternal antibody protection. It is easy to become confused when looking at biased graphs such as:


But one must find a better representation of true virus nature: it is in constant motion and will always rise and fall until eradicated (or near eradication):



  •  Is it true that vaccine-derived polio has caused polio cases? YES! But it has only caused 21 cases in 2017 and is derived from an escaped vaccine virus, not contracted directly through immunization. Yes, this number was greater than the 6 wild polio cases in 2017 (worldwide) but when considering the fact that polio is nearly eradicated due to the vaccine 21 cases (worldwide) is a blessing compared to the near 60,000 cases in the united states alone in 1951.


If you are interested in further debunking of anti-vaccine myth I highly encourage you to check out: https://respectfulinsolence.com/2010/03/29/the-intellectual-dishonesty-of-the-vacci/ , where graphical manipulations are exposed.

Sources cited:

























Fight formula! Why you should breastfeed your baby #2

Non-immunological benefits for baby:

Health and mental benefits for breastfed babies reach beyond a strengthened immunity in many ways that last throughout lifetime as well as some that are protective throughout infancy. The major protection in infancy conferred through breastmilk in the form of tryptophan. Tryptophan is a major amino acid component in the synthesis of melatonin hormone, which regulates sleep/wake cycles (circadian rhythm). This not only increases sleep per night by an average of 45 minutes, but more importantly, studies have shown that breastfed infants are more easily aroused from sleep at ages 2-3 months compared to formula fed infants, who are therefore at a greater risk of sudden infant death syndrome (SIDS).

Erythropoietin and prolactin are two other protective molecules transferred through breast milk. Erythropoietin stimulates the production of blood cells, which is not only a survival factor in neonates but also serves as a neuroprotective measure. Prolactin is beneficial to full-term babies as well as neonates, being a factor in lung and gut development as well as aiding in the intestinal absorption of nutrients. In a study of neonates, high prolactin blood levels was associated with fewer days on the ventilator, quicker transition to enteral feedings, and greater growth in length.

Other benefits for the baby are not due to a single supplement, but rather the holistic nutrients and growth factors that breast milk provides as well as the psychological development from mother-baby intimate contact. These developmental benefits are not as easily quantifiable, but multiple studies have confirmed them. One study found that infants who were exclusively breastfed for 6 months (rather than being introduced to solid foods at 4 months of age) crawled sooner and had a higher probability of beginning to walk by the age of one year. Tests conducted between the ages of one and a half years and two and half years of age revealed higher scores on the Bayley Scale of psychomotor development for breastfed (rather than bottle-fed) babies.

Benefits for mom:

There are also many benefits for the mother that may be considered to promote breastfeeding. Decreased estrogen levels when breastfeeding are responsible for a variety of personal and societal benefits. Lowered estrogen leads to fewer and lighter menstrual periods, called lactational amenorrhea, which also confers a natural contraceptive to space out births. Estrogen levels are also a key factor in the development of breast, endometrial, ovarian, and uterine cancer as well as arthritis. This period of reduced estrogen levels decreases cancer risk for breastfeeding mothers, by as much as 4.3% per year of lactation for breast cancer.

Estrogen decrease is also accompanied by prolactin and oxytocin increase. Both have been proven to protect the mother against stress by decreasing cortisol levels. This may contribute to the reduced chances of developing postpartum depression as a breastfeeding mother (measured by the edinburgh postnatal depression scale) which conferred statistically significant protection for up to four months. The actual act of breastfeeding, especially when mother-child contact is established early and initiating breastfeeding within one hour of delivery decreased chances of child abandonment by 50%! This finding may hold great opportunity to improve children’s lives, especially in areas where orphans are abundant.

Mothers may also reap the benefits of a decreased chance of smoking relapse after breastfeeding as well as the loss of postpartum weight (exclusive breastfeeding for six months caused an average weight loss of 12 kg in nursing mothers).





















Fight formula! Why you should breastfeed your baby #1


I’d like to preliminarily state that medical advice is not always the best. It is always best t do your own research to confirm anything you hear even if it comes from a physician! Think and act scientifically! I say this because for most of the 20th century physicians supported formula feeding and had no idea that this led to extreme infant morbidity. By the 1940’s physicians regarded formula as “a well known, popular, and safe substitute for breastmilk.” And that as a result of this, “by 1946–1950, initial breast-feeding of first-born infants had decreased to 50% and only 20% were breast-fed for at least 6 months.”


Breastfeeding your baby provides it with its only source of IgA, a specific secretory antibody isotype that is necessary for protection of mucosal surfaces. Breastfeeding transfers 0.25-0.5 grams of IgA from mother to baby per day. This is critical in the time period of 3 months to a year, where the baby experiences diminishing maternally transmitted antibodies and has yet to produce significant amounts of their own antibody: this time period is where many infant deaths occur due to a vulnerable immune system (see chart). The main benefit provided directly by this is a greatly lowered rate of infection of the baby due to a strengthened immune response in the GALT and MALT (Gut and mucosal associated lymphoid tissue) to fight disease before it can breach the mucosal membranes and cause systemic infection. This IgA protection has been directly proven to reduce the prevalence and numbers of Clostridium difficile and Escherichia coli in the gut microbiota even in health, and the occurrence of infection by a wide range of dangerous pathogens such as Helicobacter pylori, Giardia lamblia, and Salmonella. This reduction accounts for less tonsillitis, sepsis and necrotizing enterocolitis (which is twenty times more common in formula fed babies) occurrence in breastfed babies for years.

All of these immune system responses are aided by other elements of the colostrum, such as lactoferrin and other immune-stimulatory and modulatory cytokines, peptides, and oligosaccharides. These, as well as growth factors such as PDGF and TGF a/b cause the thymus in breastfed babies to be larger than in formula-fed children, indicating higher levels of T-cell production. T cells are a lymphocyte (white-blood cell) absolutely central to the adaptive response, which is recruited when the innate immune response cannot clear a pathogen. The innate immune response is necessary, as mutants with abnormalities in T-cells, B-cells, or other lymphoid associated cells or signals typically are lethal.

Not only does the more advances immune system in breastfed babies protect against pathogens, but also cancers. One study found that as the duration of breastfeeding decreased, a child’s odds ratio for cancer development increased for all types of cancers. Another study considering 99 different childhood cancers found support for the hypothesis that breastfeeding reduces cancer risk and found especially high statistical support (p<0.001) for exclusive breastfeeding (not combined with formula feeding) being tied to childhood cancer risk (the control groups averaged 4.6 months while the cancer groups averaged 3.2 months of exclusive breastfeeding).

Immunological benefits of breastfeeding, since they affect the development of the immune system and therefore can cause prolonged immune system strength by increasing lymphocyte production, etc. This is proven in a study tracking the healthcare of breastfed vs purely formula fed babies, finding the babies that were 1,000 exclusively breastfed for at least 3 months required 2,033 less office visits, 212 less days of hospitalization, and 609 fewer prescriptions compared to 1,000 formula fed babies.













Top Ten Favorite Scientists: a homage to our foundations

I believe in the light of being in a position where we have the honor of being burdened with such scientific power that we are obligated to discern whether our actions which we are capable of are moral or immoral and be responsible for that decision, we must honor and respect our foundation: science and its pioneers. When we lose respect for science’s beginnings and base we will certainly be lost in the dark as we try to navigate the moral pathway being laid before us. To honor the source of our technology and what has shaped so much of current society I made a list of my top ten favorite scientists:

  • Hippocrates of Kos- Father of the Hippocratic Oath, he was eons ahead of science in anticipating that one day our scientific abilities would exceed our moral abilities to agree on what is ethical, creating relentless controversy.


  • James Watson and Francis Crick- Though it may be argued that they swiped the credit from Rosalind Franklin, they are great examples of how perhaps non-traditional methods need to be implemented in order to reach quicker and unexpected groundbreaking conclusions.


  • Gregor Mendel- Proof that some discoveries indeed require simple patience and hard work. Though Mendel’s observations weren’t accredited until generations after his death, he paved a crucial path, which allowed science to proceed towards genomic understanding.


  • Joseph J. Schildkraut- Published ‘The Catecholamine Hypothesis of Affective Disorders: A Review of Supporting Evidence,’ which spurred a whole new realm of quantifying mental disorders through the study of neurotransmitters, turning the study of mental disease into a science rather than a stigmatized voodoo.


  • Alfred Wallace- He came from extreme poverty and worked hard, also dabbling in social activism. He practically birthed all of the Darwinistic ideas, yet doesn’t receive as much credit, all for the lack of coining the phrase “natural selection”.


  • Ernest Rutherford- Not only the father of nuclear physics and the discoverer of the proton, but also a protector of the integrity of science-he refused to shake hands with Fritz Haber (who used science for evil, researching warfae technology such as poison gas).


  • John Forbes Nash Jr.- His paper on game theory delves into the risky science of chance and brings up the controversy of the relationship between religion and science-just how much of our lives can be explained by each? Above this, Nash is an example of the emotional struggles that the intellectually gifted often suffer as a tradeoff for their genius, which is often uncelebrated and unbeknownst to the public. (I would highly recommend watching A Beautiful Mind for a glimpse at this struggle)


  • Marie Curie- It is indispensible for scientific credibility as well as eligibility for the Nobel Prize to be extended to women and therefore judged on a basis of merit rather than gender (or any other bias)—this is something we strive for everyday in our current society.


  • Brahmagupta- Where would we be without ‘0’? Or basic algebraic functions?


  • Charles Lyell- How can we improve and understand our current selves without exploring and comprehending our past and origins?