Melatonin and the Pineal Gland

Melatonin is a hormone with immune and antioxidant importance. It is produced in the pineal gland at nighttime when there is no light present. The pineal gland can be at risk of calcification. It needs iodine and may be more at risk of calcification when excess fluoride is present and/or limited magnesium. (See: Alzheimer’s Disease & Pineal Calcification, Carolyn Dean MD) (Magnesium sources) (Pineal Calcification, Melatonin Production, Aging, Associated Health Conditions and Rejuvenation of the Pineal Gland, PubMed)

Calcification of the pineal gland may also interfere with our sense of direction possibly due to disruption of internal magnetic fields. (Pineal Gland Calcification and Defective Sense of Direction, PubMed)

Complete darkness during sleep hours with blackout curtains and any nightlight/alarm clocks or other electronic equipment lights are covered. Having some full spectrum light during awake hours may also help. (See: Sleep and Health).

Lack of typical levels of melatonin is more common in patients with breast or prostate cancer or for people on the autism spectrum. See ~ 1:08:00 in the video: Quiet Wars: Frequencies of Death. 

There may be a protective effect by female hormones or increased risk for males- more severe calcification is associated with more severe prostate or pancreatic cancer and less severe with breast or cervical cancer. (Pineal Calcification Among Black Patients, PubMed).

Quiet Wars: Frequencies of Death.

/Disclaimer: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Autism may be able to be prevented prenatally with individualized perinatal education and nutrition therapy

This got long and complicated and I need to buy a couple of the articles and work on this more but in the meantime, I’m sorry for suggesting the food supply might have something to do with the increased rate of autism or that the health insurance companies don’t want a clear diagnostic procedure etc. but without a lab test that says someone is sick they can save money on paying claims — however costs in the long run may end up being a lot more than they might have been with an earlier diagnosis and preventative treatment. I’m sure the health insurance companies and government and FDA love us all and that autism must be a complete mystery – but leaving something a complete mystery still leaves it a worry for expectant parents and grandparents throughout the pregnancy and even into the early childhood years. The symptoms aren’t usually diagnosed until age two or older. But earlier diagnosis might help prevent more severe loss of function. The condition can cause a sudden or more gradual loss of social skills and development progress.  

Autism can leave a child unable to take care of themselves independently for the rest of their lives. At a rate of 1 child in 45, [Nov. 2015, CDC, http://health.usnews.com/health-news/articles/2015/11/13/cdc-child-autism-rate-now-1-in-45-after-survey-method-changes], there were 3,932,181 births in the USA in 2013, so roughly that would suggest that 87,381 of those children will go on to develop some symptoms of autism or pre-primary developmental delay — and that possibly 87,381 parents will no longer be able to work at their normal jobs because they will be needed as full time caregivers for their child with autism, possibly for the rest of their lives. So if that rate held steady for the decade then in ten years there could be 1,747,620 children with autism and parents who may not be able to work at a normal job. When will it be enough children and parents to do something about?

I closed with the following paragraph but I’m going to paste it here at the beginning too, as the best of the good news: a lab test has been developed that consistently predicted which infants would later go on to develop autism. This helps clear up the mystery of whether autism is a condition that a toddler can suddenly “get” like an infection or have suddenly develop as an acute reaction to something or whether it develops prentally — it develops prenatally and can get worse — which suggests that it might not also have to get worse if appropriate interventions can be provided. Autoimmune disease frequently can flair up, go into remission, flair up again, and go back into remission. Autism appears to be related to autoimmune conditions of the brain so dietary and lifestyle changes might be able to help keep the overactive white blood cells more in ‘remission’ and less busy doing brain damaging things — that would be my hope at least.

A method has been developed using samples of umbilical cord blood to identify which infants are likely to develop autism later in childhood. The method checks fifteen “biomarkers,’ — (various lab values or other physical signs, I haven’t read the full article yet, need to buy it) — infants whose values were more elevated or reduced compared to normal in a certain pattern were found to be predictive of which infants went on to develop autism. [6 ] This is early research but it would help identify which infants were at risk for autistic changes in a year or two, but at birth instead of having to wait — and worry — for a year or two.

I have some good news and some bad news. It looks plausible that autism could be caused prenatally by a combination of low vitamin D (or possibly a vitamin D system that is blocked by pathogens), and low folate availability (possibly due to a genetic methylation defect, [4], defects that may make the supplemental form, folic acid, not as helpful prenatally and possibly even harmful because the folic acid may inhibit the activity of whatever folate is available, [29] ), and increased formaldehyde either from dietary sources like Nutrasweet or from smoking or living in small enclosed rooms with poor ventilation. Other toxins might also be involved that add to an increased risk for there to be production of autoimmune antibodies in the vitamin D deficient mother and fetus. Malfunction in the vitamin D receptor immune functions could lead to malfunctions in the dendritic cell’s ability to inhibit autoimmune overactivity in the immune system. Autoimmune antibodies might cause problems during fetal brain development or later in the child’s life.

Low vitamin D in infants has been associated with autism – but not for all siblings with low vitamin D — so other factors must be involved. And not taking a prenatal vitamin during the three months prior to pregnancy and the first month of pregnancy has been associated with more risk for having a child with autism and certain genetic defects in the methylation cycle that helps make the B vitamin folate more bioactive have been associated with autism risk [4] – but not every mother who doesn’t take prenatal vitamins during the months prior to becoming pregnant has a child with autism — so other factors must be involved.

Not much information is available about Nutrasweet but during digestion the methanol portion of the larger molecule is released which then is broken down into formaldehyde – which is a known cause of birth defects and a known neurotoxin.

Formaldehyde is produced when something is burned so it could be a concern for any people who are around cigarette smoke or inhale other types of smoke regularly. Formaldehyde can also collect in the air in small enclosed spaces, and increased warmth may also increase volatility of the gas so warmer areas or overheated apartments may allow for more accumulation of the gas in poorly ventilated rooms.

Formaldehyde is also found in prepackaged juice products, particularly in older packages, as formaldehyde is produced as the fruit or vegetable juice ages. Formaldehyde is also produced during digestion from the methanol portion of the alternative sweetener Nutrasweet. Studies on the potential risk of the formaldehyde content that might be available to adults from dietary Nutrasweet found that it was a less significant risk than the amount an adult might receive as a cigarette smoker or from environmental exposures. However an adult has a fully mature liver while a fetus does not. Babies and children also have less mature livers and may be more at risk of having chemicals accumulate to toxic levels because they are not being broken down and excreted quickly enough. (Folate, a B vitamin, is necessary to break down formaldehyde, more on that later.)

Formaldehyde can cross the placenta to the fetus where it accumulates to a larger concentration than within the mother’s bloodstream. The fetal liver tissue is less able to detoxify formaldehyde than the mother’s.

Industrial exposure to formaldehyde is associated with an increased risk of the presence of cancer causing human alpha fetoprotein antigens. Occupational exposure to formaldehyde has also been associated with increased levels of alpha fetoprotein in adult male and female subjects. The study subjects with occupational exposure to formaldehyde were also found to have significantly reduced levels of Total Protein, Albumin, and White blood cell count. Subjects with workplace exposure to formaldehyde reported allergic type symptoms including: “sneezing/airways-related symptoms, itching and watery eyes.” [3] Formaldehyde exposure may also be a cause of systemic allergic contact dermatitis, [15, 16] possibly even on the eyelids. [13] A diet designed to avoid formaldehyde intake may be helpful for alleviating the eczema like rash. [14]

Levels of alpha fetoprotein are normally only elevated in pregnant women and the expected infant.

Levels of maternal serum alpha fetoprotein are already being checked regularly as a prenatal screening test because low levels are associated with having a baby with the genetic condition Down’s Syndrome. Levels of maternal serum alpha fetoprotein have been found to be more elevated for the mothers of children with autism than in mothers whose child did not have autism. [1] Alpha fetoprotein (AFP) has immunomodulatory effects and a recombinant human alpha fetoprotein (rhAFP) version has been found to help alleviate autoimmune symptoms in clinical trials that used mice with “experimental autoimmune encephalomyelitis (EAE), the animal model used for the study of MS.” [2] Alpha fetoprotein is normally produced by the fetus and it does cross into the fetal brain where it seems to be involved with controlling estrogen and helping baby girls to be more feminine and less masculine.

/Speculation: So if alpha fetoprotein antigens are involved in causing autism maybe boys are more at risk for the condition because the estrogen connection somehow is protecting baby girls from developing the antigens. However if the basic problem is a malfunctioning dendritic cell system which is making it more difficult for the mother’s body and fetus’ body to accept the presence of each other’s foreign DNA then other proteins might also have antigen/autoimmune antibodies develop. Male infants may simply be more susceptible to autism because their Y chromosome is more foreign to the mother’s body than a female infant’s X chromosomes. / — Someone already figured this part out and explains it better than me, in a Medical Hypotheses journal – if you have the money for the journal article ($31.50, now added to my shopping list). An excerpt from the Abstract: “Prenatal/maternal factors linked to increased autism risk include valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism. It will be shown how each of these risk factors may initiate expression of genes which are sensitive to retinoic acid and/or estradiol – whether by direct promotion or by reducing production of alpha-fetoprotein. It is thus hypothesized here that autism is not a genetic disorder, but is rather an epigenetic disruption in brain development caused by gestational exposure to chemicals and/or conditions which either inhibit alpha-fetoprotein production or directly promote retinoic acid-sensitive or estradiol-sensitive gene expression. This causation model leads to potential chemical explanations for autistic brain morphology, the distinct symptomology of Asperger’s syndrome, and the differences between high-functioning and low-functioning autism with regard to mental retardation, physical malformation, and sex ratio.” – CR King [29]

So speculatively,

  • if formaldehyde can make it more likely for someone to make alpha fetoprotein antigens,
  • and maternal serum alpha fetoprotein levels are more elevated in the mother’s of children with autism,
  • and low vitamin D is more common in babies who have autism,
  • and vitamin D helps the dendritic cells of the mother and infant accept each other’s foreign DNA instead of making autoimmune antibodies against each other’s foreign proteins,
  • then low vitamin D might leave the dendritic cells unable to prevent autoimmune antibodies from developing
  • which then may cause changes in the developing fetal brain and may leave the child with autoimmune antibodies that may continue to cause changes in the child’s developing brain later in life.
  • The formaldehyde could be from Nutrasweet and bottled juice products and/or from cigarette smoke or other environmental sources or the combined total of all of the sources. The timing of the introduction of aspartame/Nutrasweet to the U.S. food supply in 1981 and the increase in rate of children with autism is very closely correlated. [5] Nutrasweet and Neotame were both inventions of the Monsanto Company and limited research about them is available. Neotame was invented as the patent for Nutrasweet was expiring and Monsanto was able to get FDA approval for it by 2002. The patent for Neotame was sold to a private equity firm, the J.W. Childs Equity Partners II. L.P.. [https://theredpillguide.wordpress.com/2012/02/23/the-red-pill-guide-neotame/]

So in summary the good news is autism may be preventable – but the bad news is that it will be difficult to prove and preventative education and treatment will likely need to be individualized as so many factors are involved.

A summary of the factors that may interact during the prenatal and/or perinatal  (three months prior to conception) time period in a way that may lead to the development of autism within the fetal brain.

Possible Vitamin D Issues – it might not just be a lack of vitamin D or sunshine:

  • Simple vitamin D deficiency
  • An underlying genetic defect in the Vitamin D Binding Protein causes a tendency to become vitamin D deficient more easily than normal. [10, 11, 12] (Might a simple protein deficiency then also add a risk to a simple deficiency of all important proteins?)
  • An underlying infection is present with a pathogen that is suppressing the vitamin D receptor system.

Possible Folate Issues:

  • Simple folate/folic acid deficiency/lack of prenatal vitamin during the perinatal time period. [4]
  • Genetic defect in mother affecting the methylation cycle makes her more susceptible for folate deficiency. [4]
  • Genetic defect in the fetus affecting the methylation cycle makes it more at risk for autism. [4]
  • A methylated form of the vitamin may be more effective for reducing risk of developing autism. The natural food form, folate, is more bioactive than the supplemental form, folic acid, that is used in prenatal vitamins. [29]

Formaldehyde might be accumulating from several sources [3, 5]:

  • Aseptically packaged juices
  • Nutrasweet
  • Neotame
  • Smoking
  • Badly ventilated air.
  • Workplace exposure

Other, other factors that may be involved in development of autism may include a variety of chemicals known to be toxic for brain development and which may be common in our modern environment.  From the Abstract of a review article by Dr. Philippe Grandjean, MD and Philip J. Landrigan, MD, Neurobehavioural effects of developmental toxicity., (The Lancet Neurology, 2014):  “In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy.” [30]

And other factors associated with autism that were mentioned in the other hypothesis about autism and folic acid included: “valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism.”  – CR King [29]

  1. valproic acid, a medication commonly used to prevent seizures in epilepsy, may also be prescribed for bipolar disorder or to prevent migraine headaches. (Valporate (VPA), sodium valproate, and divalproex sodium, Depakote). It has been known to cause serious abnormalities in babies when used by pregnant women and is no longer typically prescribed to women of childbearing years. [Wikipedia]
  2. thalidomide,a medication that was prescribed to pregnant women for preventing nausea in the 1960s but it was discovered to cause serious birth defects. It is still used for the treatment of leprosy and still has been known to cause birth defects in the babies of women with leprosy who become pregnant. [http://toxsci.oxfordjournals.org/content/122/1/1.full]
  3. alcohol, – alcohol use by the mother during pregnancy or by the father during the days prior to conception can be a cause of Fetal Alcohol Syndrome in the infant. A zinc deficiency in the pregnant woman may increase the risk of the expected infant developing FAS. [search term alcohol FAS zinc deficiency]
  4. rubella, – also known as German measles, it is the R part of the MMR vaccine. It is rare in the U.S. now with less than ten cases per year but can cause defects in an expected infant if a pregnant woman gets sick with the infection prior to 20 weeks gestation. [http://www.whattoexpect.com/pregnancy/pregnancy-health/complications/rubella.aspx]
  5. cytomegalovirus, a viral disease that may affect vitamin D levels: “However, when outliers were removed, the association was not apparent. The effect of outliers could not be assessed when vitamin D was dichotomized because no patients with CMV antibodies had sufficient vitamin D levels after outliers were dropped.” [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134182/]
  6. depression, – can be a symptom of hypothyroidism and has been associated with vitamin D deficiency [webmd.com/depression/news/20120627/vitamin-d-deficiency-linked-to-depression] and with folate deficiency. And the methylated form was given as a supplemental treatment, L-Methylfolate, rather than the unmethylated form, folic acid, which is the form used in prenatal vitamins.   [psychologytoday.com/blog/the-integrationist/201310/depression-wont-go-away-folate-could-be-the-answer] Depressive disorders have been associated with impaired methylation: [http://www.ncbi.nlm.nih.gov/pubmed/16194269] And with zinc deficiency: [https://www.psychologytoday.com/blog/evolutionary-psychiatry/201309/zinc-antidepressant]
  7. schizophrenia, vitamin D deficiency is more common in people diagnosed with schizophrenia. [http://psychcentral.com/news/2014/07/23/vitamin-d-deficiency-common-in-schizophrenia/72813.html] And folate and B12 have both been found to help treat schizophrenia symptoms (or help treat those patient’s whose symptoms are actually due to an underlying deficiency of folate or B12 which may cause symptoms that resemble schizophrenia and providing the nutrients simply is helping the brain to function normally again.) [http://www.naturalnews.com/039453_vitamin_B12_folate_schizophrenia.html] And a zinc deficiency/copper excess is more common in schizophrenia: [http://www.academia.edu/1096257/The_Role_of_Zinc_Supplementation_in_the_Treatment_of_Schizophrenia] And a zinc deficiency prenatally may be involved in the causing schizophrenia later in life: [http://www.ncbi.nlm.nih.gov/pubmed/1491625] [http://www.bmj.com/rapid-response/2011/10/30/does-zinc-deficiency-early-foetal-life-cause-schizophrenia]
  8. obsessive-compulsive disorder, – can be early symptoms of a B12 deficiency. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271502/] Has been associated with folate deficiency, elevated homocysteine levels and impaired methylation function: [http://www.ncbi.nlm.nih.gov/pubmed/16194269]
  9. autoimmune disease, – associated with vitamin D deficiency and malfunction of the dendritic cells ability to promote self tolerance of the immune system. The dry cleaning chemical and degreaser tetrachloroethylene has been shown to cause autoimmune disease in lab animal studies on toxicity: [http://www.atsdr.cdc.gov/sites/lejeune/tce_pce.html]
  10. stress, – increases cortisol and inflammatory stress chemicals, a lack of antioxidant nutrients may make it more difficult for the body to recover from the stress response. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876613/] And may use up stores of folate and cause elevated levels of homocysteine. [http://www.nejm.org/doi/full/10.1056/NEJMc066569] Elevated levels of cortisol during pregnancy has been shown to cause reduced growth rate in the babies in animal studies. [https://en.wikipedia.org/wiki/Cortisol]
  11. allergic reaction, and the vitamin D receptor and the Dendritic cells are what control the immune system’s allergic reaction. Excerpt: “1α,25-dihydroxyvitamin D(3) (calcitriol), the biologically active form of vitamin D, is an immunomodulatory hormone, e.g. it inhibits IgE synthesis in B cells. As its clinical application is limited by hypercalcemia, synthetic vitamin D receptor (VDR) agonists that mediate immunomodulatory activities without adverse hypercalcemic effects are of great interest.“- [http://www.ncbi.nlm.nih.gov/pubmed/21121929]
  12. hypothyroidism. – may be associated with iodine deficiency which prenatally can cause mental retardation and thyroid defects in the expected infant. Hypothyroidism in female workers has been associated with the flame retardant, polybrominated diphenyl ethers,  [http://www.ncbi.nlm.nih.gov/pubmed/26606679], and the insecticide chlorpyrifos,  [http://www.iss.it/binary/inte/cont/CPF_ENG.pdf], and the pesticide known as DDT dichlorodiphenyltrichloroethane also  [https://preventdisease.com/news/10/022510_pesticide_exposure_underactive_thyroid.shtml], [http://www.ncbi.nlm.nih.gov/pubmed/24064777], and polychlorinated biphenyls [https://www.researchgate.net/publication/26873383_Hypothyroidism_Induced_by_Polychlorinated_Biphenyls_and_Up-Regulation_of_Transthyretinand fluoride are also associated with risk of hypothyroidism.

To help prevent autism from occurring prenatally we may need to work together to show that a combination of nutritional deficiencies or metabolic defects and environmental toxins may be causing autism to develop in infants prenatally. And we may need to work together as a group of concerned individuals rather than waiting for the government or a medical corporation to look further into a problem that might leave them at some risk of legal repercussions. Historically there have been several examples of government and corporate interests blocking the lawsuits of factory workers or townspeople whose health was damaged by industrial chemicals. The lawyers were able to show expert testimony demonstrating that the supposedly ‘harmful’ toxin really had some beneficial use and was really a safe and helpful ‘treatment.’ If we could make this about helping the babies stay healthier and more on track developmentally then insurance companies and governments would probably save a lot of money in the long run actually.

Pretending things are a mystery makes it harder to work on solving the underlying problems and preventing more cases from developing into future years or future decades. Thalidomide was a mystery that got solved. Only a few pregnant women with leprosy have to worry about whether their baby might be born with thalidomide birth defects. Before the cause was known every pregnant woman of that generation probably was scared. Now we do have a variety of information about autism and putting together the puzzle is a little complicated but the good news is that it is not a complete mystery and may be preventable with individualized health guidance that begins at least one to three months prior to conception – the prenatal vitamin research suggests that the pre-conception diet is important.

Fetal Alcohol Syndrome has been shown to be related to the father’s alcohol intake around the time of conception as well as the mother’s alcohol intake during the pregnancy so the father’s diet on the days before conception may also be involved in autism development — zinc is very important for male fertility. A longevity type study could include information about both the mother and the father’s health prior to conception and then follow the pregnancy and infancy and hopefully the preventative diet and lifestyle changes would have prevented autism from occurring. 

Part of the bad news that didn’t make it into the earlier discussion of the digestion of menthol and formaldehyde is that humans have a genetic defect that makes menthol extremely more toxic to us than to all other animals — so lab research would demonstrate that menthol isn’t really that bad after all –(to lab animals, that is, but let’s keep that part a secret between corporate research scientist’s and their consciences). So in a global corporate NAFTA/TPP type world where a corporation can sue nations over lost profits, feasibly corporate research scientists and lawyers could force nations to either accept the products made with aspartame and Neotame whether it is a risk to their citizen’s health or not, or else pay the corporation for their estimated lost profits.

Aspartame and Neotame are so much sweeter than sugar that they are simply cheaper to use in food products than sugar, and since its introduction in 2002 Neotame has never even had to be listed with the ingredients, so sweet, delicious, calorie free and guilt free, no alternative sweetener was used in that product according to the label. Aspartame is the number one food additive for consumer complaints to the FDA about adverse side effects. With Neotame not ever being listed on the food label consumers have no idea if they consumed it or not even if they do have an adverse effect and we have no idea if the FDA would have received consumer complaints about the food additive because it was never required to be added to the ingredient label. People who avoid aspartame due to it causing migraines can’t look for Neotame on the ingredient list.

Avoiding all processed foods and all restaurant meals seems like a lot to ask of pregnant women but that might be necessary in order to avoid Neotame. And with Neotame as a possible source of formaldehyde for the developing fetus then as a prenatal nutrition counselor that would be the most cautious advice given the research that is already known about menthol and formaldehyde’s risks to fetal development. Avoiding all toxins and reducing stress and risk of infection would be the ideal goal for all pregnant women.

Working towards removing aspartame/Nutrasweet and Neotame from the food supply may be an impossible goal given the deep pockets of corporations but trying to get Neotame added to the ingredient list seems like a necessary compromise or first step if we are really going to be able to help prenatal and perinatal women avoid all sources of formaldehyde in the hopes of helping prevent autism from developing in the child later in life.

*This got long and complicated and there’s more: The other, other factors would include undiagnosed cases of hypothyroidism and undiagnosed iodine deficiency and BPA/pthalate exposure. Each individual mother/child with autism probably have a slightly different combination of genetic and nutritional susceptibilities and negative load of various environmental toxins and maybe even a sensitivity to the supplemental folic acid (supposedly helping prevent spina bifida but may be adding to autism risk for the babies of moms who have certain genetic defects in the methylation cycle).

So this is a preliminary draft of a preventative health education strategy for trying to prevent autism. A longevity study that started with women at least three months prior to conception and followed them and their children for years would be able to try a multi-factored prevention plan and wait and see if fewer of the children developed autism than compared to the rate of children developing autism in the average population. [rate at 1 in 45 births, Nov. 2015, CDC, http://health.usnews.com/health-news/articles/2015/11/13/cdc-child-autism-rate-now-1-in-45-after-survey-method-changes] Imprecise diagnostic criteria makes it easier for insurance companies to deny coverage.

A method has been developed using samples of umbilical cord blood to identify which infants are likely to develop autism later in childhood. The method checks fifteen “biomarkers,’ — various lab values — infants whose values were more elevated or reduced compared to normal in a certain pattern were found to be predictive of which infants went on to develop autism. [6 ] This is early research but it would help identify which infants were at risk for autistic changes in a year or two, but at birth instead of having to wait — and worry — for a year or two.

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

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  26. Route of antigen delivery impacts immunostim activity of dendritic cell-based vaccines for hepatocellular carcinoma. [ http://www.ncbi.nlm.nih.gov/pubmed/26199728 ]
  27. Nonsecreted cytoplasmic alpha-fetoprotein: a newly discovered role in intracellular signaling & regulation. /cancer [ http://www.ncbi.nlm.nih.gov/pubmed/26162540 ]
  28. Carcinoembryonic antigen, alpha-fetoprotein, & prostate-specific antigen…exposed to phenol, formaldehyde, urea,… [ http://www.ncbi.nlm.nih.gov/pubmed/16966304 ]
  29. King CR, A novel embryological theory of autism causation involving endogenous biochemicals capable of initiating cellular gene transcription: a possible link between twelve autism risk factors and the autism ‘epidemic’.,  Med Hypotheses. 2011 May;76(5):653-60 [http://www.ncbi.nlm.nih.gov/pubmed/21388746]
  30. Dr. Philippe Grandjean, MD and Philip J. Landrigan, MD, Neurobehavioural effects of developmental toxicity., The Lancet Neurology, Volume 13, No. 3, p330–338, March 2014,   [http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(13)70278-3/abstract]
  31. Physiology of alpha-fetoprotein as a biomarker for perinatal distress: relevance to adverse pregnancy outcome. [http://www.ncbi.nlm.nih.gov/pubmed/17720945 ]
  32. Maternal serum transformed alpha-fetoprotein levels in women with intrauterine growth retardation. [ http://www.ncbi.nlm.nih.gov/pubmed/17361083 ]
  33. Dyslipidemia in pregnancy may contribute to increased risk of neural tube defects -a pilot study, north Indian pop.[ http://www.ncbi.nlm.nih.gov/pubmed/23105824 ]
  34. Comparison of proteins in CSF of lateral and IVth ventricles during early development of fetal sheep. – PubMed NCBI [http://www.ncbi.nlm.nih.gov/pubmed/6199091 ]

Vitiligo, hypothyroidism, and melanin

Vitiligo is a lack of melanin production and causes areas of the skin to look white or bleached – kind of like becoming an albino slowly in patches. The lack of color patches – freckles in reverse – can start developing when young and can increase with time. The melanocytes, specialized pigment cells, are no longer producing melanin.

The problem doesn’t have a known cause or cure. It is listed as an autoimmune disorder and does seem to run in families. Vitiligo seems to show up after head trauma. [18] “Melanocytes are destroyed by autoimmune activity of unknown origin“, and yet a mother with the condition shared in a patient forum that her white spots move around and became smaller during her pregnancy. [19] That does not sound like permanently damaged melanocytes but more like melanocytes that are getting confused signals from the pituitary or some other controlling gland in the brain (head trauma).It is not “contagious” in the normal sense of the word but Helicobacter pyloris, the bacteria found to be the underlying cause to many cases of stomach ulcers (and successfully treated with antibiotics), was mentioned.[20] Following this thread to the 1945 physician, J. Richard Allison from South Carolina, brought me the sound advice to eat whole grains and don’t depend on new-fangled supplements instead of good diet and still expect to stay healthy [21]. Fixing the underlying problems of low stomach acid during meals and reduced B complex intake helped patients in this physician’s caseload cure their skin conditions. The skin conditions he studied included:

  1. Metabolic eczema,
  2. Avitaminosis (pellegra, beri beri, pernicious anemia may be what he means – B vit. deficiencies),
  3. Urticaria (hives),
  4. Staphylococcus infection,
  5. Seborrheic dermatitis,
  6. Acne rosacea,
  7. Psoriasis,
  8. Alopecia,
  9. Vitiligo,
  10. Lichen plants (?),
  11. Lupus erythematosus.

Well hello, bifocals, I hadn’t looked so closely at that list when I first read the article . . . B vitamin complex and whole grains for the whole group of diagnoses and have pickles or vinegar with each meal. Maybe there is a slight metabolic hitch in stomach acid production that normalizing B vitamin intake would restore. Or maybe these patients have a slight fault in their production of stomach acid since birth that will leave them more at risk for developing B vitamin deficiencies throughout life due to the reduced stomach absorption and digestion.

Ninety percent of the vitiligo patients had low hydrochloric stomach acid levels which would leave them digesting things poorly and absorbing B12 poorly (pernicious anemia link). (and maybe growing skin abnormally.)

My grandma had pickles on the table at every meal (because they were left out with the salt, pepper and butter dish). Her dilly beans and bread and butter zucchini pickles were wonderful and would both have good membrane building phospholipids as well as B vitamins. Serving vegetables as pickles turns them into salt and vinegar delivery units. Plain green beans or zucchini would still give the super nutrients of the bean or seed and a larger serving might be eaten. Serving them as a pickle would make the appetite satisfied sooner, triggered by the salt and vinegar signals to the tongue. A small pickle or serving spoon of bread-n-butter slices would probably satisfy the appetite and provide a good amount of the salt and vinegar without being too much.

Equivalent salt and vinegar delivery units in other cultures would be the chutney in Indian cuisine or the salsa in Mexican dishes. The milder creamy cucumber salad of German/European meals is served in larger amounts because the salt and vinegar content is similar to salad dressing rather than the bread-n-butter pickles. The texture is similar though. The advantage of a pickle to my grandma was root cellar storage for winter. Those jars had to last the family until spring. The creamy salad is a fresh cucumber dish which would probably work well with zucchini too.

The current treatment approach for people with vitiligo does not discuss vinegar, pickles, B vitamins or iodine. Steroid cream was mentioned and it is routine to eventually de-pigment the rest of the skin so the whitish patches aren’t standing out from the surrounding darker skin. I don’t know if that process has anything to do with “bleaching” of the skin but the pictures of people with the condition make it obvious to me at least why someone might prefer the more even skin tone that the de-pigmentation would produce. [1, dermnet Vitiligo pictures, some x rated].

I suffered from large patches of eczema off and on since childhood. Ugly, disfiguring and painful; at least the whitish vitiligo patches aren’t reported as painful (physically). I loved pickles as a child and would get scolded for drinking the juice from the (homemade) pickle bottle. I didn’t drink it regularly it is very acidic but I remember craving it occasionally and being scolded if caught by my mother. I don’t crave pickles now because I get too much acidity from my coffee habit. I learned over the years that a smidge of baking soda buffers the coffee. I believe when I used pH strips and checked the coffee was a 4.5 and the baking soda dusting on the end of a spoon handle brought it to 6.5, too much baking soda brought it to a 8 and it was very odd taste of coffee flavor with no tangy zip.

Vitiligo is a condition that I wasn’t familiar with that was listed as having been treated with the herb, gingko biloba. I looked it up and noticed that having vitiligo is also associated with having hypothyroidism. [4]

If you have vitiligo than you may also have hypothyroidism. Why wouldn’t someone be told that he might need iodine or thyroid hormone?

–because few people with the condition pass the lab tests is why and go on to win the synthetic hormone prize.

Hypothyroidism treatment history

Hypothyroidism only exists in the current medical/insurance industry minds if your lab scores match expected values.

I am familiar with hypothyroidism because I had all the symptoms but never got the diagnosis because my TSH was normal. Thyroid Stimulating Hormone levels increase to signal the thyroid gland to grow and gather more iodine in a case of scarcity. Goiters were lumps in the neck from bulging thyroid glands. They were so common in the Middle Ages that they were considered beauty marks if small and well placed. They can be seen in oil paintings from the time.

The current lab tests that the diagnosis is based on don’t recognize that the thyroid hormone might be present but may be malfunctioning. Goiter in the neck is the body’s last resort effort to gather more iodine from the diet. The thyroid gland expands in size in an attempt to gather iodine. Goiter is no longer as prevalent as it was in the 1800’s and earlier. The lab tests that are used currently include the thyroid stimulating hormone level, TSH. A low number is good and an elevated number suggests that the body is trying to stimulate more production of the hormone and would indicate hypothyroidism. Sometimes the actual hormone levels of thyroxine, T3 or T4, are also checked. Those lab tests do not detect whether the hormone is functional, simply whether it is present.

The current medical world doesn’t recognize the fact that if iodine isn’t available then the body makes the hormone with fluoride, bromide or perchlorate, a form of chloride. Iodine is chemically similar to those minerals but they are smaller so if a lab test could be developed that also measured the average molecular weight of the T3 or T4 hormone then we would be able to tell if that sample of thyroid hormone was lighter then it should be. Iodine is the heaviest and fluoride is the lightest of the four elements. Of course we could also simply look at the outward physical signs and symptoms and check the resting body temperature – but that might be inexpensive and slightly less “accurate” (black/white, right/wrong lab tests are nice because they are numerical compared to having to work through a variety of symptom checklists).

Congenital hypthyroidism

Congenital (born with it) hypothyroidism or cretinism is becoming more prevalent and iodine deficiency is not being recognized. A pregnancy can only provide what the woman is eating or has stored. The fetus can not build a body out of it’s mother’s small supply of synthetic thyroid hormone.

Hypothyroidism in a newborn is more common if the newborn is one of the last children of a large family or in pregnancies of multiples (twins, triplets) and when the mother has been diagnosed with hypothyroidism herself. Women are treated with replacement thyroid hormone if they are diagnosed but extra iodine is infrequently recommended. All of the glands of the body need some iodine. The thyroid needs the most and the pituitary gland needs a lot as well as the ovaries and testicles. My fibrocystic breast disease went away when I did the loading dose of Iodine for one month back in 2005. I’ve never had the symptoms return (painful hard breasts – no known cause or cure – just live with it is the typical treatment plan.)

Hypothyroidism in newborns is associated with small size in the children, a short and slim growth pattern leading to cute little pixie children. Infertility and incomplete sexual development is possible with childhood hypothyroidism. Actual genetic problems causing congenital hypothyroidism is rare.

The following quote sums up the treatment approach. Congenital hypothyroidism (CHT) has to do with iodine deficiency – first sentence – but it is usually treated with a daily dose of thyroid hormone . . . for the rest of the child’s life – last sentence.

“The most common cause of this defect is iodine deficiency. CHT is a condition of thyroid hormone  deficiency present at birth. Approximately 1 in 4000 newborn infants has a severe deficiency of thyroid function, while even more have mild or partial degrees. If untreated for several months after birth, severe congenital hypothyroidism can lead to growth failure and permanent mental retardation. Treatment consists of a daily dose of thyroid hormone by mouth.” [3]

If lack of iodine was the problem, then why isn’t it ever thought of as the solution? Iodine in addition to some external thyroid hormone would help the baby to have the immediate metabolic support to grow a normal size with normal glandular development throughout the body.

Prostate and breast cancer and hypothyroidism is less common in the Japanese population (I should look up rates of vitiligo—pdf). The average three year intake of sea vegetables in Japan (rich source of iodine) was 4 grams per day per capita (2005-2007 www.faostat.org). The average sea weed intake has been estimated to provide about 13.3 mg of iodine per day. Our national recommended intake for iodine has never changed or been retested since the initial work done in the 30’s and 40’s. The guideline of 150 micrograms (0.15 mg) is 88 times less than the average Japanese intake of iodine from sea vegetables. (Sea weed is also a good supplier of super fibers for strong membranes and glycocalyx).

Iodine therapy was found ineffective and somewhat dangerous because it isn’t a magic bullet medication. It takes many nutrients and some time to promote normal function. Tyrosine is an amino acid that may need to be converted from other amino acids and problems might exist in that pathway. Selenium is crucial to prevent hyperthyroidism – the body can go into overproduction of the hormone when a sudden supply of iodine becomes available. The selenium is essential to the enzyme that breaks down excess thyroid hormone. Life is a constant cycle of building, break down, and rebuilding.

Vitiligo and melanin production.

Vitiligo is a lack of normal melanin production in the skin. A dietitian type question on a mutli-disciplinary team of research scientists might be – well what is melanin made out of – what do we need to eat more of if we aren’t producing enough?

And how is melanin made?

I discovered that melanin is a pigment that is made out of the amino acid tyrosine with an intermediate chemical step, dihydroxyphenylalanine, also known as dopa, by the enzyme, tyrosinase. Copper is essential and known chemical binders of copper inhibit melanin production [2]. Iron and zinc are also mentioned more in discussion of variations of the chemical. Many different shades are produces throughout the animal kingdom and the melanin chemical is not always exactly the same, so some may have more iron or zinc than copper involved possibly [10 – very interesting but gets very not nutrition science related the farther done the page but I think melanin and iodine and the electromagnetic EPR signal may be involved in protecting us from cosmic ray activity as well as the daily electromagnetic forces that are in our gadgets and telephone pole wires.]

Cysteine is listed as a possible inhibitor of melanin formation as a compound that binds copper – an individual who is no longer able to convert cysteine into taurine very well might end up with increased levels of cysteine. Fluorotyrosine is on the list as a competitive inhibitor. [2] So the iodine connection might be that we have too much fluoride in our water and diet and it fills spots that iodine would have filled if available. Fluoride is used in patent medications because it increase binding affinities – lengthens the time the medication stays in the receptor. Good if you want a non-ending reaction but usually we want what went up to come back down again – that is what homeostasis and life is about.

The iodine connection may also be the tyrosine itself which is part of the thyroid hormone. Radioactive fluoridated dopa (dihydroxyphenylalanine, the intermediate step between the amino acid tyrosine and the pigment melanin) has been successfully used to locate tumors in the thyroid gland [9]. The fact that a radioactive fluoridated version of chemical metabolite of melanin can successfully be used to locate cancerous tumors in the thyroid gland suggests to me that it is involved with thyroid health and iodine as well as melanin and pigmentation or lack of pigmentation in the skin.

Melanin is stored within the membranous folds of the Endoplasmic reticulum and/or Golgi apparatus within the melanocytes. The melanin producing cells seem to have complex paper thin folded layers of membrane and the melanin is part of the membrane folds. [11] The melanocytes in individuals with albinoism do not produce melanin.

Melanin and other color pigments are reactive to light. The black of the melanin pigment absorbs radiation and helps protect us. Pigments also give off a weak magnetic signature of their own.[10, 12] So maybe we do occasionally react to each others’ “animal magnetism”.

Take home point – in order for our bodies to be able to assemble melanin we need the building blocks which include the amino acid tyrosine (and for it to not be fluoridated), copper and adequate supplies of cyclic AMP (energy source and rich in phosphorus).

Low iodine levels may simply be effecting the cyclic AMP energy supply. Fatigue and poor growth of cells that have a rapid growth/death turnover rate is characteristic of hypothyroidism. The outer third of the eyebrow tends to be absent. Brittle fingernails and thinning hair or hair loss is common also. Feeling cold and slow digestion with constipation problems is common, easy weight gain and depression also.

Skin pigmentation in a dark complexion may be simply such a large reservoir of resources that the chronically undernourished body can’t keep up with supplying the tyrosine/dopa. The membranous folds contain a lot of the individual molecules of melanin embedded within the membranes so I also suspect involvement of the phosphorus rich endogenous cannabinoids. Chances are that my membrane building diet will help return pigmentation to skin as long as the problem is one of nutrient supply rather than a defect in a chemical pathway or in the melanocyte.

I added the chemical structures of tyrosine, L-Dopa, and thyroxine at the bottom [15, 16, 17]. Fluoridated thyroxine increases risk of cancer to the thyroid and may be increasing risk of damage to the melanocytes. If the vilitigo blotches have actual structural changes in the melanocytes (like scar tissue is whiter than the surrounding skin) then restoring melanin production may not be possible but improving iodine intake and the other chemicals involved could slow down the progression of the disease. Beans and fruit and tuber/root vegetables are good sources of tyrosine and Dopa [10]. Copper is essential to melanin production but caution with any supplementation is a good idea because zinc balance can be effected by large amounts of copper and we frequently are low in zinc too (Especially good for men, zinc is needed for testosterone –  pumpkin seeds are a good source of zinc. Cashews are a good source of copper.)

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

_____________________________________________________________________

  1. Pictures of individual’s with vitiligo, includes some x rated areas of the body. The condition can occur in people of any skin color, it is just more obvious on the darker skin. [dermnet.com/Vitiligo]
  2. Biochemistry of Melanin Formation [physrev.physiology.org/content/30/1/91.full.pdf] (page 17, Table 1: Inhibitors of Melanin Formation In Vitro)
  3. Common and Rare Birth Defects or Congenital Disorders and Their Causes,  [healthmad.com/conditions-and-diseases/common-and-rare-birth-defects-or-congenital-disorders-and-their-causes/2/]
  4.  [medicinalplants.us/hypothyroidism ]
  5.  [chemicalelements.com/] “Iodine, Atomic Number 53 (# of protons), Atomic Mass, 126.90447 amu   (total weight) Bromide,  Atomic Number 35,                      Atomic Mass, 79.904 amu; Chloride,  Atomic Number 17, Atomic Mass, 35.4527 amu; Fluoride,  Atomic Number  9, Atomic Mass, 18.998404 amu”
  6.  [medicinalplants.us/ginkgo-biloba-uses-dosage-adverse-reactions*lists some dosage levels of ginkgo used in peer reviewed studies for a few different conditions. Vitiligo: 120 mg standardised extract daily
  7.  [ncbi.nlm.nih.gov/pubmed/1287627?dopt=AbstractPigment Cell Res. 1992 Nov;5(5 Pt 1):240-6., Melanin standard method: empirical formulaChedekel MR, Ahene AB, Zeise L
  8.  [physrev.physiology.org/content/30/1/91.full.pdfLerner, A. B. and Fitzpatrick, T. B., Biochemistry of Melanin Formation (Jan, 1950) 
  9. [jnm.snmjournals.org/content/49/4/524.long   F-Dihydroxyphenylalanine PET in Patients with Biochemical Evidence of Medullary Thyroid Cancer: Relation to Tumor Differentiation, (Koopmans, Klaas P.,  et al) doi: 10.2967/jnumed.107.047720 J Nucl Med April 2008 vol. 49 no. 4 524-531 
  10.  [tightrope.it/nicolaus/melanin95.htm] “Link 4-Melanin 95-97,In memory of Giovanna Misuraca, Melanins in Plants: “From legumes and from fruit it is possible to isolate tyrosine, DOPA, tyramine, DOPAamine, epinine (N-methyldopamine). The blackening which is seen in the course of maturation and conservation of bananas seems to be due to the neurologic melanogene DOPAamine. The typical blackening of slices of tubers (potatoes) and fruit (apples, pears, etc.) and plants (in the Vicia faba one finds large quantities of DOPA) seems to be a process of melanogenesis from tyrosinase or DOPA.” Melanins in Animals: “The melanins of vertebrates and invertebrates can be observed in the skin, in fur, in hair, in feathers, in scales, in the choroid, in the peritoneum, in the pia mater, in the brain, and in melanomas (malign tumours of an intense black colour). One cannot yet confirm that the various melanins coming from different sources are the same, even though they have the presence of a free radical and the potential capacity to conduct electrical current in common. Sometimes animal melanin has the function of protecting the skin from radiation (short wavelengths), of controlling temperature, of mimetisation. Little or nothing is known of the structure and the functions of neuromelanins (eg. substantia nigra) expecially with respect to the elecrical properties of this pigment (Link 22). Obviously the melanin associated with tumours has been studied more, by biologists.”Melanin as stable free radical. “Studies have been carried out on all the melanins in acqueous suspensions and almost always give an EPR signal at about 4-6 G. The spin concentration is around the value 4-10 x 1017spin/g. In the “polymer” there would be one free radical every 200-1,000 “monomers”. It would seem that there are two radicalic centres in the black products that originate from the o.phenols: one being essential (intrinsic), highly stable, generated in the course of melanogenesis and “trapped” in the product and the another being extrinsic, transient and reactive which can form in the melanin by the action of the different chemico-physical agents. Passing from black melanins to brown and red-brown products (pheomelanins) it is possible to observe radicals with better defined structures, at different pH, like those of semiquinonamine and semiquinone. EPR studies carried out on the hair and skin of several bovine races and on albinoes have mainly been used by geneticists and pathologists. Albino subjects, with the same phenotype character, have hair with differing electronic characteristics. In some albino subjects there is a weak EPR signal which is completely absent in others. There are, that is, true albinoes and false albinoes (6, l). ” 
  11.  [ncbi.nlm.nih.gov/pmc/articles/PMC2591998/?page=4Ultrastructure and cell biology of pigment cells. Intracellular dynamics and the fine structure of melanocytes with special reference to the effects of MSH and cyclic AMP on microtubules and 10-nm filamentsG. Moellmann, J. McGuire, and A. B. Lerner. 
  12.  [spectroscopy.lbl.gov/EPR-Robblee/EPR-Robblee.pdfElectron Paramagnetic Resonance (EPR),  John Robblee, Berkeley Spectroscopy Club, (18 April 2001) 
  13.  [books.google.com/booksWalter Sneader, Drug Discovery: a history. *I didn’t discover the iodine content of testicular tissue but sheep thyroid had 2.9% iodine content when Eugen Baumann started trying to isolate the active principle of the thyroid gland. In 1896 he got a 10% iodine concentration. Goitre was treated with iodine after this discovery but results were mixed especially with more advanced cases. Adequate selenium is essential to not become hyperthyroid when trying to replenish your body’s iodine level. Selenium is in the enzyme that breaks down the active thyroid hormones. Another researcher, Edward Kendall, isolated a 23% iodine containing chemical in 1910 and had the formula for the thyroid hormone worked out by 1914. “Kendall studiously avoided giving the hormone any name suggestive of the discredited idea that iodine was responsible for thyroid activity.” I don’t see how any molecule that contains 23% by volume iodine couldn’t also be considered to require iodine for proper function. T4 is so called because it has four atoms of iodine  (or bromides/fluorides/chlorides) and T3 has three of them. 
  14. Chemical formula for melanin: [natscience.com/Uwe/Forum.aspx/chem/3992/Chemical-Formula-for-Melanin ]
  15. [chemistry.about.com/od/imagesclipartstructures/ig/Amino-Acid-Structures/Tyrosine.htm]
Chemical structure of Tyrosine, (C-9-H-11-N-O-3)
Chemical structure of L-Dopa,

 

16: L-DOPA (L-3,4-dihydroxyphenylalanine) is a chemical that is made and used as part of the normal biology of some animals and plants. Some animals including humans make it via biosynthesis from the amino acid L-tyrosine. L-DOPA is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline) collectively known as catecholamines

17.  [chemistry.about.com/od/factsstructures/ig/Chemical-Structures—T/Thyroxine.htm]
***This is the thyroid hormone, T4. It has an extra 6 Carbon ring (size of a glucose sugar molecule) but otherwise is similar to tyrosine and L-Dopa. If fluoridated tyrosine could inhibit the production of melanin then it seems plausible that fluoridated thyroid hormone could also. Over the course of time fluoridated chemicals have a cancer promoting effect on the organs. It is well researched in thyroid cancer but the breasts, prostate, pancreas, and other glands contain iodine. Maybe the fluoridated thyroxine is not only not helping cause hypothyroid symptoms while confusing lab tests but is also collecting in melanocytes and occasionally leading to their malfunction. If the melanin is no longer being produced because of cell damage than the function may not be able to be restored but adding iodine to the diet might slow down the progression of the vilitigo blotches (iodine and tyrosine and selenium and adequate copper/zinc balance and phospholipids).

Chemical structure of Thyroxine, (C-15-H-11-I-4-N-O-4)

18. [leucoderma.com/app/causes.asp]
Vitiligo – Causes

19. [medhelp.org/posts/Autoimmune-Disorders-/vitiligo-and-hypothyroidism/show/409731]

“My white spots move around and change, last year I had one looked like a heart on my tummy, this year I have twin spots about the size of hands on my shoulders, my friend says “it where my angel wings were” I also have a white patch of hair, and a few white eyelashes.

The only time I ever had any of the white spots fill in color, was when I was pregnant with my son, my knees completely filled in, after I had him, they went back to white.”. – Carla

20. [medhelp.org/posts/Autoimmune-Disorders-/h-pylori–the-only-cause-of-vitiligo/show/1196718]

21. [journals.lww.com/smajournalonline/Citation/1945/04000/The_Relation_of_Hydrochloric_Acid_and_Vitamin_B.2.aspx]
The Relation of Hydrochloric Acid and Vitamin B Complex Deficiency in Certain Skin Diseases*, by ALLISON, J. RICHARD M.D.

Southern Medical Journal: April 1945 – Volume 38 – Issue 4 – ppg 235-240 Original Article: PDF Only22. [books.google.com/books?id=7JxEAAAAYAAJ&pg=PA974&lpg=PA974&dq=Vitiligo+iodine+pickles&source=bl&ots=tREK10AzXx&sig=LLSXnZCgG8r8erF0CeNYF_Zxw4A&hl=en&ei=DNmFTqDXAeOQsQLD0uWUDw&sa=X&oi=book_result&ct=result&resnum=9&sqi=2&ved=0CHgQ6AEwCA#v=onepage&q=Vitiligo%20iodine%20pickles&f=false]
The American Journal of Clinical Medicine, Vol 19,(Jan 1912) page 974, Query 5846 – Vitiligo
*** Vitiligo spots were treated with 1-2 minutes of phenol (?) until redness occurs or cupping to induce redness. Maybe increasing blood flow to the area had a bit of increased nutrient flow or maybe they felt they had to try something.23. [nature.com/jid/journal/v115/n6/full/5600897a.html] Yu-Ling Li, Chia-Li Yu* and Hsin-Su Yu, IgG Anti-Melanocyte Antibodies Purified from Patients with Active Vitiligo Induce HLA-DR and Intercellular Adhesion Molecule-1 Expression and an Increase in Interleukin-8 Release by Melanocytes, Journal of Investigative Dermatology (2000) 115, 969–973; doi:10.1046/j.1523-1747.2000.00130

” In conclusion, our results are consistent with the possibility that V-IgG play an important role in melanocytic cytotoxicity immune-mediated: (i) increased HLA-DR expression on melanocytes enhances the antigen-presenting activity of the cells; (ii) ICAM-1 expression on melanocytes stimulates leukocyte/monocyte attachment and immune-mediated cytotoxicity; and (iii) increased IL-8 production from melanocytes chemoattracts T lymphocytes to the sites of lesions to increase melanocyte destruction.”

*** T lymphocytes are what the Marshall Protocol has found to be an underlying root of autoimmune conditions. Some of them are our fighters that we need to try to find the infected overactive ones (not mysteriously turned against us self but infected self that needs a healthy white blood cell to identify it and give it the apoptosis enzyme blast of death (love that phrase – I think it takes having suffered through it to really love feeling like they can be found and killed – but not if they all the healthy ones are killed with immune suppressing drugs like methotrexate and TNF inhibitor.)11-21-11 (happy birthday, Nick)

[cdf.nejm.org/pdf/Clinical_Practice_Companion.pdf]
Page 43 excerpt:

Infection with H. pylori is a cofactor in the development of three important upper gastrointestinal diseases: duodenal or gastric ulcers (reported to develop in 1 to 10% of infected patients), gastric cancer (in 0.1 to 3%), and gastric mucosa-associated lymphoid-tissue (MALT) lymphoma (in <0.01%). The risk of these disease outcomes in infected patients varies widely among populations. The great majority of patients with H. pylori infection will not have any clinically significant complications.

***Page 44, discusses Helicobactor pyloris and the reduced stomach acidity that is associated with infection by the bacteria when infection is advanced enough for the stomach lining to have broken down (aka – atrophic gastritis). Page 43 assures us that there are few associated problems if outright ulceration isn’t also present (1-10% of people who test positive for the bacteria were reported to develop ulcers). Based on the information from reference link 21, the 1945 skin condition research by Dr. A. J. Richard, I would suggest an external glance at skin integrity and would consider whether of a dash of vinegar or an acidic side dish with each meal would benefit individual’s who test positive for Helicobactor pyloris – before they progress to the 1-10% or worse 0.1% statistic groups –  in order to enhance B vitamin absorption in the stomach and prevent skin problems and hair loss (aka – thinning hair / hair loss) and eventual cancer or atrophic gastritis.

page 44 Excerpt:

Gastric Cancer 

Extensive epidemiologic data suggest strong associations between H. pylori infection and noncardia gastric cancers (i.e., those distal to the gastro-esophageal junction).9 The infection is classified as a human carcinogen by the World Health Or-ganization.10 The risk of cancer is highest among patients in whom the infection induces inflammation of both the antral and fundic mucosa and causes mucosal atrophy and intestinal metapla-sia.11 Eradication of H. pylori infection reduces the progression of atrophic gastritis, but there is little evidence of reversal of atrophy or intestinal metaplasia,12 and it remains unclear whether eradication reduces the risk of gastric cancer.13

***in other words they gave the patient antibiotics and the bacterial infection was killed but the broken down membrane lining did not get better / stayed atrophied / – in other, other words they gave the person antibiotics and did not repair the malnourishment and continued to leave the membrane lining and the army of white blood cells in a weakened condition unable to protect against bacteria from growing in great numbers.

So the antibiotics plus no additional food or nutritional guidance will likely lead to a relapse of the infection or for the cancer that is so common to develop. The same army of well nourished white blood cells would be ready to prune out the old decaying , atrophied cells and swap back stem cells with the correct information to become stomach lining material or intestinal membrane cells (or heart cells or brain cells or pancreas cells etc – eat well and the smart army of white blood cells rebuild us daily – every single body part is eventually replaced.)