Tag: autoimmune disease

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Calciphylaxis, molecular mimicry and egg white albumin; an experiment, n = 1

Calciphylaxis is a rare type of wound that is associated with hyperparathyroidism and is most commonly seen in patients who are receiving kidney dialysis due to end stage renal disease. The condition is also associated with an eight times increased risk of morbidity (death) compared to patients who don’t have calciphylaxis.

The term calciphylaxis came to my attention this year when I found out that I had an elevated parathyroid hormone level. See the following posts for more information about calciphylaxis and about other symptoms associated with elevated parathyroid hormone:

  1. Secondary hyperparathyroidism, calcium deficiency and irritability, 
  2. Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis, ‘Calciphylaxis is more of a risk with end stage renal disease but it has also been found in people who had normal vitamin D levels and normal kidney health. And “high dose vitamin D administration is capable of inducing STC (soft tissue calcification) and calciphylaxis in murine models. [56, 57] In an attempt to reestablish normal calcium-phosphate homeostasis, ESRD patients receive vitamin D analogs that could theoretically increase their risk of calciphylaxis if hyperphosphatemia and hypercalcemia ensued. [58, 59]” [3]

    “Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.4  – from a 1962 study, abstract is free. [4.5]’

  3. Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values, 
  4. Calciphylaxis may be caused by several different nutrient issues, 

Antibodies against chemicals that are a normal part of the human body can develop in autoimmune disease. The term molecular mimicry refers to the autoimmune antibodies that may be manufactured by overactive white blood cells in response to a large foreign protein allergens that may have made it through ‘leaky’ intestinal walls into the blood stream.  See: Robert S. Fujinami, et. al., Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease, Clin Microbiol Rev. 2006 Jan; 19(1): 80–94.

To skip to the point, egg white albumin is very similar to the albumin found in human blood. It is an essential protein within plasma and it helps maintain fluid balance between the blood plasma and extracellular fluid (too much extracellular fluid would be noticeable as edema – puffy ankles from excess fluid collecting outside of the cells and blood vessels.

After finding the research about egg white albumin on September 24, I eliminated egg white from my diet. My symptoms did get better fairly rapidly but I had tried a few strategies at the same time so it wasn’t clear whether stopping egg white had been necessary for the symptoms to improve or whether the other strategies I had tried may have been adequate on their own — so after feeling better for a couple weeks I decided to retry egg white to see if eliminating them had been an unnecessary strategy. Sadly I found that the day after trying egg white albumin again (in the form of baked chocolate chip cookies) my skin sores returned. I stopped eating egg white again. The sores aren’t as bad as they had been in September but calciphylaxis sores are termed necrotic wounds and necrosis means death and dead tissue in wounds can lead to gangrene and septic bloodsteam infections.

Open sores with oozing plasma that sticks to fabric is unpleasant and painful as well as being associated with an eight times increased risk of morbidity (which means death of the patient).

So I don’t have proof that my body set up autoimmune antibodies to albumin but I would rather stop eating egg white than continue having oozing sores – that is my choice, it is my body and I should have a right to take care of it to the best of my own ability rather than having to follow mainstream medical advice about a condition that is not well understood but is associated with an increased risk of death.

For more information about albumin antibodies and autoimmune disease see:

  • Rodríguez-Juan C, et. al., Increased levels of bovine serum albumin antibodies in patients with type 1 diabetes and celiac disease-related antibodies., J Pediatr Gastroenterol Nutr. 2003 Aug;37(2):132-5.
  • Excerpt from Abstract: “Although 46% of patients with autoimmune thyroiditis had positive results, the level detected (22.1 +/- 8.7 AU) was significantly lower than that recorded in patients with type 1 diabetes who had celiac disease antibodies (P = 0.04) and celiac patients (P = 0.04). Healthy volunteers showed no antibodies against bovine serum albumin.”  “Thirty-one percent of patients with diabetes yielded a positive result…” End stage renal disease is actually a significant risk for people with autoimmune Type 1 Diabetes because diabetes can cause an increased load on the kidneys from excess blood sugar and increased leaking of protein into the urine. Thirty-one percent of them might benefit from avoiding beef (bovine) or egg white albumin – but more research would probably be necessary before an ‘evidence-based’ recommendation could be made – except Rodriquez- Juan C, et al, did get a nice start on the project.

 

/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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Neuraminic acid was known first as sialic acid

Neuraminic acid, or sialic acid as it was first called, is a monosaccharide with nine carbons. It has a negative electric charge which gives compounds containing it a negative charge. This is useful for keeping molecules like red blood cells from getting too near to each other. The negative charge on the surface glycoproteins repels the red blood cells from each other or from the walls of blood vessels which also have compounds containing sialic acid.

Mature red blood cells have an active life for about seven days.  White blood cells remove older red blood cells and de-sialylation of the surface proteins is one way the older cells are identified. Cancer cells with the ability to produce excess surface sialyation may have an increased chance to metastasize and turn up somewhere else in the body. [1, 3]

Our bodies need to be healthy and well enough nourished overall to keep the whole system working. The neuraminic acid is produced within our cells from other chemicals in a series of membranous channels called the endoplasmic reticulum and the golgi apparatus. The channels have embedded enzymes along the way somewhat like an assembly line in a factory. We can not just eat more sialic acid in our diet and have it show up on our cell surfaces – we have to be healthy enough and well enough nourished over all in order to be able to manufacture our own supply of sialic acid. All of the different enzymes within the assembly line like system of the endoplasmic reticulum and Golgi apparatus would have to be present and working which would mean trace minerals such as zinc might be essential for producing neuraminic acid/sialic acid.

Therapeutic glycoproteins are being developed and the problem of just the right amount of sialylation is one of the hurdles being studied. [2] In addition to the negative charge sialic acid tends to stabilize and stiffen the protein portion of the glyco-compound.  The proteins that line vessels were described to be somewhat like bottle-brushes; the protein being somewhat like the sturdy wire handle of the brush and with the negatively charged sialic acid acting as bristles that electrically repel other molecules of sialic acid. [1]

/This article was originally posted on 8/21/2013./ /Disclaimer: Information presented on this site is not intended as a substitute for medical care and should not be considered as a substitute for medical advice, diagnosis or treatment by your physician./

More recent research from the scientists at the University of Zurich, regarding sialic acid, found an association between the presence of autoimmune disease and reduced levels of sialic acid on the individual’s antibodies, which are important for the body’s immune cells to be able to recognize and remove infected or foreign or decaying cells: “Specific Sugar in Antibodies Structure Determines the Risk of Autoimmune Diseases,” Oct. 7, 2015, [molecularbiologynews.org]

References:

  1. S.A. Brooks, M. V. Dwek, U. Schumacher, Functional and Molecular Glycobiology, (BIOS Scientific Publishers, Ltd., 2002), Amazon.
  2. Bork K, Horstkorte R, Weidemann W., “Increasing the sialylation of therapeutic glycoproteins: the potential of the sialic acid biosynthetic pathway.” J Pharm Sci. 2009 Oct;98(10):3499-508. doi: 10.1002/jps.21684.  [ncbi.nlm.nih.gov]
  3. R. T. Almaraz, et. al., “Metabolic Flux Increases Glycoprotein Sialylation: Implications for Cell Adhesion and Cancer Metastasis.” Mol Cell Proteomics. 2012 July; 11(7): M112.017558. Published online 2012 March 28. doi:  10.1074/mcp.M112.017558 [ncbi.nlm.nih.gov]

 

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Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis

I’m feeling so much better after only two days of calcium supplements that I feel like throwing a party. Fatigue is tiring. Replenishing supplies of a trace nutrient deficiency can help resolve symptoms so quickly that it feels like a miracle. I’ve experienced rapid resolution of symptoms in the past when I had a problem with low B1 intake [2] that was due to a low intake of everything – I had an anorexic appetite at the time which I later found may have been due to an underlying zinc deficiency.

The anorexic appetite symptom resolved when I added zinc and B6 supplements after reading about pyroluria. Pyroluria is not yet treated or accepted by most main stream health practitioners but it is believed to be due to a genetic defect affecting an enzyme that helps break down old hemoglobin for reuse and recycling. Molecules of B6 and zinc are involved in the process and in normal health would be recycled but if the person has the genetic modification than the B6 and zinc is released in urine rather than being retained for reuse. [1]

Calciphylaxis is a symptom that is not well understood but is associated with severe hyperparathyroidism. It is a rare symptom in the general population but is seen more frequently in people with end stage renal disease. When the kidneys are no longer able to make normal amounts of 1, 25 dihydroxy D the plasma calcium levels can drop. And to try to maintain normal calcium levels the body responds by having the parathyroid glands increase production of parathyroid hormone which in normal health would tell the kidneys to activate more 1, 25 dihydroxy D which would then tell the intestines to absorb more calcium and would tell the bones to release more calcium from storage. [3] But in end stage renal disease there aren’t functional kidneys and the elevated levels of parathyroid hormone can cause other symptoms like irregular or rapid heart rate or in severe cases calciphylaxis may occur.

Calciphylaxis “is a poorly understood and highly morbid syndrome of vascular calcification and skin necrosis.” [4] The word calciphylaxis may refer to the syndrome or to the patches of necrotic (decaying) tissue which may occur internally on the surface of bones or externally in patches on the surface of the skin. The decaying areas occur more commonly on the lower legs. The areas can first appear as reddish or purplish bruised areas that may feel like they have small hardened nodules under the skin. The skin surface may be itchy and eventually may break down to be an open wound that doesn’t heal easily. There is a risk of skin infections developing in the open wound which can become severe enough to cause sepsis and death as the patches of decaying skin or bone areas do not heal well.

Calciphylaxis is more of a risk with end stage renal disease but it has also been found in people who had normal vitamin D levels and normal kidney health. And “high dose vitamin D administration is capable of inducing STC (soft tissue calcification) and calciphylaxis in murine models. [56, 57] In an attempt to reestablish normal calcium-phosphate homeostasis, ESRD patients receive vitamin D analogs that could theoretically increase their risk of calciphylaxis if hyperphosphatemia and hypercalcemia ensued. [58, 59]” [3]

“Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.4  – from a 1962 study, abstract is free. [4.5]

Eczema is something I’ve had to cope with since infancy along with severe congestion problems. The images of calciphylaxis do not look quite like the itchy patches that I’ve been dealing with for a few months but they resemble the images of calciphylaxis more than they look like the patches of eczema that I’ve had off and on since infancy.

The fun thing about autoimmune disease is all the nifty weird symptoms that you get to experience – and which are so rare that many physicians don’t want to see you or the symptoms in their office –  because those unusual symptoms must be covered by some other specialist’s field. This quote said it well:  Calciphylaxis “is a poorly understood and highly morbid syndrome”. [4]  Maybe I wouldn’t want that syndrome to be my professional responsibility either, and maybe it is just too bad for me that it might be my personal responsibility whether I like it or not. However maybe I’m lucky that my professional and personal experiences have left me more informed about odd symptoms than other health professionals, and therefore I may possibly be better equipped to cope with the odd symptoms.

Thankfully just two days of calcium supplements (while continuing to avoid excess vitamin D and sunshine) have left me feeling less itchy and my open wound areas are beginning to form scabs instead of remaining open wounds with seeping plasma.

In normal physiology the activated hormone form, 1, 25 dihydroxy D, is typically found in elevated amounts only in areas of rapid growth or membrane breakdown, such as in scab formation by white blood cells, [6], and within the placenta during pregnancy. [5] – Maybe elevated 1, 25 dihydroxy D can also be an underlying problem causing calciphylaxis rather than it being due only to deficiency of the inactive vitamin 25-D or the active hormone 1, 25-D.

Yes, my vitamin 25-D level was low at 10.9 ng/mL and anything below 20-30 is considered deficient and I was recommended by my endocrinologist to take vitamin D and calcium. However my hormone 1, 25-D level was 55 pg/mL which is considered within the normal range by mainstream medicine (range: 18-72 pg/mL). Specialists in vitamin D/hormone D metabolism would consider levels of 1, 25-D above 42 pg/mL to be elevated enough to be an osteoporosis risk because above that level the bone cells start releasing calcium, phosphorus, and magnesium into the blood supply instead of absorbing the minerals from circulating plasma and storing them for increased bone strength or for later use. [7]

Calcium and magnesium are so important as electrically active ions that the body has a variety of ways to maintain the blood levels of the two minerals within a narrow range. Blood tests for calcium and magnesium levels may be normal even though there is inadequate dietary intake because the bones can act like a savings account at the bank. In normal health if the blood plasma dips a little low for calcium or magnesium, more minerals are released from the bone, and if levels are getting too elevated than more would be excreted by the kidneys, less would be absorbed by the intestines, and more would be absorbed into the bones for long term storage.

However if 1, 25-D levels are elevated above 42 pg/mL than even if calcium levels were elevated in the blood the abnormally elevated 1, 25-D level would still be telling the bones to release more calcium and for the intestines to absorb more calcium which would lead to way too much calcium for the kidneys to be able to excrete during good health let alone during renal disease (elevated blood calcium would normally signal the body to make more of the enzyme that de-activates 1, 25-D but some microbial pathogens seem to bypass our immune system by disabling our body’s ability to make that enzyme). Adequate magnesium is necessary for the kidneys to be able to excrete calcium and elevated 1, 25-D causes the intestines to preferentially absorb calcium rather than magnesium.

And it turns out that eczema is an autoimmune disease so I may have been trying to figure out how to feel healthier since I was a baby. [8]

My mother gave up trying to spoon feed me. She said I would spit food into my hand, look at it, then put it back into my mouth before swallowing. She put cookie sheets around my highchair to block the mess (and possibly the view) and left me to feed myself from a fairly early age. I still don’t like to be fed by others, whether it’s just a taste of something on a spoon, or whether it is a dietary supplement that might cause my underlying autoimmune condition to worsen.

I’m feeling less itchy and the open wound areas are beginning to heal. The tachycardia problem is better, (having a rapid heart rate with little exercise), and an internal jittery feeling is less. The problem with trying to medicate a nutrient deficiency with psychiatric drugs is that the psychiatric drug can’t take the place of a nutrient in metabolic pathways. For years now physicians, family members and friends have been encouraging me to just take the psychiatric medication as prescribed and stop complaining about psychosomatic symptoms and imaginary problems. But the psychiatric medications that were offered all had bad side effects and while some helped slow down whirling thoughts they didn’t make the thoughts less sad or negative and they didn’t take away the internal feeling of tension.

I felt like a coiled spring internally, very jittery all the time and unable to concentrate as well as normal. I knew something was wrong and I knew feeling like a coiled spring all the time wasn’t an imaginary delusion and the feeling didn’t go away with the three different anti-psychotic medications that physicians or psychiatrists had me try.

We can’t afford ineffective health care as individuals or as a global community. Harsh medications that cause side effects in humans are probably also causing side effects in the health of the environment once the chemicals become waste products. Expensive pharmaceuticals that cause side effects in patients without addressing the person’s underlying condition are primarily helping the pharmaceutical company and may be causing the person’s condition to worsen over the long term.

Low protein intake may be involved as hypoalbuminemia is a risk factor for calciphylaxis. [9 -includes images of calciphylaxis wounds.] I don’t know for sure that my weird skin patches are early stage calciphylaxis wounds but I hadn’t been eating much protein in the weeks before my bruise like symptoms became more like open painful sores and I have probably had a low calcium intake ever since I started limiting my use of dairy products. I did take calcium supplements in the past but my chronic muscle cramps became a problem and the calcium seemed to make it worse. More recently not eating much for a couple weeks would have further reduced my intake of calcium from the sources such as sesame seeds and tree nuts that I normally do eat. Just two days of calcium supplements have helped me feel calm internally instead of jittery (I’m using about 500 mg spread out through the day in low doses). I’m also eating a more adequate amount of protein and other foods and the odd skin patches have less of a burning itchy painful feeling and the areas are starting to heal rather than remain open seeping wounds.

Twenty three and a half to fifty million Americans may have one or more types of autoimmune diseases. [10] So I don’t think that I am the only one who has been regularly told that her symptoms must all be imaginary and to go see a talk therapist or to go get stronger and stronger psychiatric medications. We can’t afford ineffective health care because it doesn’t help the patient and the medications may be bad for the environment once they become waste products. Calcium is a natural mineral that is not harmful to the environment and it is inexpensive.

6/15/15 lab values:

  • Parathyroid hormone level – PTH Intact – 154.1 pg/mL — normal range: [15.0-75.0]
  • Calcium – 8.8 mg/dL — normal range: [8.4-10.2]
  • Phosphorus was not ordered but would probably be good to check.
  • Vitamin D, 25 – 10.9 ng/mL — normal is considered: [30.0-100.0]
  • Vitamin D 1, 25 – 55 pg/mL — normal is considered: [18-72]

I did schedule an appointment with a physician but it will be a few weeks and the tachycardia was not pleasant, the internal coiled spring feeling made it hard to concentrate and hard to not over react to outside events, and the open seeping sores were painful.

I don’t see why I should not try to take care of myself rather than having to follow the orders/recommendations of physicians or psychiatrists when they are working from the premise that “we don’t know what is causing your symptoms or how to cure them but we would really like you to take these harsh medications anyway because we guess that they might reduce some of your symptoms – and please just ignore the negative side effects that the medication is actually adding to your problems because we guess that the medication might help reduce some of the symptoms that you originally came to see us about.” That is an example of circular logic based on guesses and I’m not buying it anymore now than I did when I was sitting in a highchair covered with eczema, milk based formula, and baby food.

Medications can be life saving and certainly are a modern miracle but nutrients will always be our body’s building blocks. Providing medicines to reduce symptoms of nutrient deficiency will only prolong the time the body is left without adequate nutrients and some deficiencies can cause long term damage that is not reversible once the nutrient is added back to the diet. A long term deficiency of Vitamin B12 can cause irreversible nerve damage, [11], and it turns out that calcium or vitamin D deficiency can cause osteoporosis if the deficiency is chronic enough to lead to secondary hyperparathyroidism.

/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./

Bibliography:

  1. Pyroluria: anxiety and deficiency of B6 and zinc, 
  2. Thiamin: people with anorexia or alcoholism are more at risk for vitamin B1 deficiency, 
  4. Julia R Nunley, MD, “Calciphylaxis,” Medscape, July 21, 2014, [4-Overview,  4.5-Pathophysiology]
  5. Liu NQ et al., “Vitamin D and the regulation of placental inflammation.” J Immunol. 2011 May 15;186(10):5968-74. doi: 10.4049/jimmunol.1003332. Epub 2011 Apr 11, [5]
  6. Eleftheriadis T., et al., “Vitamin D receptor activators and response to injury in kidney disease.” JNephrol 2010: 23(05): 514-524 [6]
  7. Meg Mangin, Rebecca Sinha, and Kelly Fincher, “Elevated 1,25(OH)2D appears to be evidence of a disabled immune system’s attempt to activate the VDR to combat infection.” Inflamm Res. 2014; 63(10): 803–819., 2014 Jul 22. [7]
  8. by Charlotte LoBuono, “For the First Time, Study Proves Eczema Is an Autoimmune Disease.” Jan. 5, 2015, [8]
  9. Dermnet NZ, “Calciphylaxis,” [9]
  10. AARDA, “Autoimmune Statistics,” [10]
  11. “Vitamin B12 deficiency can cause long term nerve degeneration.” August 21, 2013, [11]

Additional references about risk factors for calciphylaxis in dialysis patients:                   These articles are not mentioned in the text above and the research studies are not about secondary hyperparathyroidism but they do suggest that adequate protein intake may help reduce risk for calciphylaxis and that having elevated phosphorus or alkaline phosphatase levels may increase the risk.

  • Zacharias JM, Calcium use increases risk of calciphylaxis: a case-control study. Perit Dial Int. 1999 May-Jun;19(3):248-52.  [link] *This small research study is about calciphylaxis occurring in patients on kidney dialysis – calcium supplements were found to increase risk of calciphylaxis, while iron intake may have been protective, vitamin D intake made no difference between groups, (n=8 women). The study group’s parathyroid hormone and albumin levels were not found to be significantly different then the lab values of the control group of dialysis patients who did not have calciphylaxis. The conclusion includes the suggestion that “use of calcium salts as a phosphate binder” during dialysis might have something to do with the increased rate of calciphylaxis that was being seen at dialysis centers at the time.
  • A Rauf Mazhar, et. al., Risk factors and mortality associated with calciphylaxis in end-stage renal disease.  Kidney International (2001) 60, 324–332; doi:10.1046/j.1523-1755.2001.00803.x [link] *This study (n=19) found an increased risk for calciphylaxis in dialysis patients who were female, and when the patient had elevated phosphorus and/or alkaline phosphatase levels and/or low serum albumin levels. “Calciphylaxis independently increased the risk of death by eightfold.”
  • Doweiko JP, Nompleggi DJ. The role of albumin in human physiology and pathophysiology, Part III: Albumin and disease states. JPEN J Parenter Enteral Nutr. 1991 Jul-Aug;15(4):476-83. [link] *Albumin is the main protein found in blood plasma and having low albumin levels is also associated with poor wound healing and an increased risk of death.
  • Albumin levels can be low even when there is adequate protein intake in the presence of edema. Fluid imbalance can make the albumin values seem lower due to the change in concentration of the blood serum rather than due to changes in diet. However edema and low protein intake may both be problems. A low protein intake can increase the risk for edema.
  • Pickwell K, Predictors of lower-extremity amputation in patients with an infected diabetic foot ulcer. Diabetes Care. 2015 May;38(5):852-7. doi: 10.2337/dc14-1598. Epub 2015 Feb 9. [link] *Severe edema is also a sign of ill health. the presence of edema increased the risk of poor wound healing and the need for amputation for patients with a diabetic foot ulcer.

 

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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./

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  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=Abstract] Pigment Cell Res. 1992 Nov;5(5 Pt 1):240-6., Melanin standard method: empirical formula, Chedekel MR, Ahene AB, Zeise L. 
  8.  [physrev.physiology.org/content/30/1/91.full.pdf] Lerner, 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=4] Ultrastructure 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 filaments. G. Moellmann, J. McGuire, and A. B. Lerner. 
  12.  [spectroscopy.lbl.gov/EPR-Robblee/EPR-Robblee.pdf] Electron Paramagnetic Resonance (EPR),  John Robblee, Berkeley Spectroscopy Club, (18 April 2001) 
  13.  [books.google.com/books] Walter 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.)