DISCLAIMER - A Must Read For All Visitors
Iron Overload… The Many Implications For The Liver… The Pancreas…
And So Much More!
Given that infants required only .8 mg to 1 mg of iron a day and they could be having a daily intake of anywhere from 20 – 70 mg per day, there was no denying that within this information was great reason for concern!
Prenatal vitamins, baby formulas and baby foods appeared to be contributing to iron overload in very young children! Foods on store shelves and vitamins – in general - were also very much “fortified” with iron and that meant that everyone could certainly be susceptible to “iron overload”.
It was also important to remember that women did not have a menstrual flow during pregnancy – at least not normally – and as such, a normal means of “flushing iron” in a woman – the menstrual flow – was no longer available during pregnancy. I had stated “not normally” because it seemed to me that more and more woman today spoke of “bleeding” during pregnancy. I had, personally, known several women who bled during pregnancy. Had this been their body’s way of attempting to rid itself of “extra iron” as opposed to passing too much iron on to the unborn child? I wondered!
As I thought about all this, I could not help but wonder - would iron-overload not trigger an immune system response – jaundice - in either newborns or infants who developed iron overload either due to toxic exposure in the womb or after birth, possibly as a result of ingesting iron fortified baby formulas and baby foods? Note that mothers who breastfed were often also told to remain on prenatal vitamins after the child’s birth – as I had been told to do.
Jaundice resulted from the breakdown of red blood cells, specifically, of hemoglobin. The “heme” part of “hemoglobin” was made up of iron and unconjugated bilirubin. The liver processed bilirubin and iron – but at birth, the liver was immature – not fully functional. Bile, the substance containing lactoferrin, was not produced until at least six months of age!
So many issues now raced through my head. If an infant suffered from iron overload, what would be the system’s response? If iron in excessive amounts was considered toxic, would the body not release its most powerful antioxidant – bilirubin – in excessive amounts – leading to jaundice? In my opinion, that certainly did appear to be a very likely scenario. If the liver was not fully functioning in infants suffering from iron overload and the body had no good mechanism for riding itself of iron – what happened to all that iron – in an infant?
As the infant broke down excess red blood cells at birth, without lactoferrin from breast milk or bile, did excess iron not – potentially – become “dangerous free radicals”. In my opinion, this certainly could be a possibility.
An infant had little or no hair at birth, there was “no menstrual flow” in an infant… thus - how - would the body rid itself of excess iron, especially given excess not all children were breast fed and bile was not produced until at least six months of age?
The only option that appeared to remain was the sloughing (casting off or shedding) of cells – the breakdown of cells – the very thing that happened in the condition known as jaundice!
The breakdown of extra red blood cells was a normal process at birth – a process that provided for the release of iron and unconjugated bilirubin - which was fat soluble - into the blood. This necessary process provided iron for growth spurts and a powerful antioxidant to fight infection. But, what if there was too much iron in the blood already and that triggered an immune system response? Would the breakdown of more cells – red blood cells containing iron - in an attempt to rid the body of excess iron not simply result in even more iron entering the blood – even more “iron overload” – more toxicity? Red blood cells also carried oxygen – something that certainly would be needed to help cells in distress but could excess oxygen not lead to oxidative stress. Bilirubin was usually taken out of the system by the liver – but, again, the liver of an infant was not fully functional at birth – it produced no bile!
The blood brain barrier, the envelope surrounding the brain was also immature at birth – taking up to six months to develop. Bilirubin encephalopathy was a condition in which bilirubin entered the brain of infants and was believed to lead to brain damage. In the case of bilirubin encephalophathy, studies were starting to show that liver dysfunction was the problem – not the normal breakdown of cells at birth. Liver dysfunction – an immature liver – liver dysfunction – jaundice!
Jaundice was also associated with something known as blood group incompatibility. How did that fit into the picture? Blood group incompatibility resulted when a mother had a negative Rh factor and the unborn child had a positive Rh factor for specific antibodies. Rh factor was associated with – red blood cells! The Rh factor of blood was an antigen - a protein - that was found on the surface of the red blood cell. Although fetal and maternal blood did not usually mix, it was believed that blood passing via the placenta between the mother and unborn child could result in an immune system reaction in the mother as her body came to “attack” the fetus due to differences or incompatibilities in antigens.
During the delivery, the mother and the child’s blood could interact and as such, it was believed the mother developed antibodies that could then attack the unborn child in a second pregnancy.
Well, if that were really the problem, why would not all women with blood types different from that of their child not result in a problem for future pregnancies if “blood mixing” was really what triggered this problem during the birth process. Would not the mixing of “A” and “B” blood at birth for example, not also be a problem – irrespective of Rh factor issues? Again, this made no sense to me whatsoever.
Much like the “breastmilk jaundice” issue, I had a very difficult time with the fact that a woman’s body could “naturally” see her child as an intruder and have an immune system response that could destroy her child or any future child. A first pregnancy was usually less of a problem than a second pregnancy with regard to Rh factor issues due to the fact that more antigens would have been created during the first pregnancy to “attack” – more aggressively – a second child. I just had a very difficult time with the fact that so often, the medical community believed that “incompatibilities” between mother and child could lead to immune system problems or even the death of that child. It made no sense to me that only “some” breastfed children developed “breastmilk jaundice”. Why did all breastfed children not have this condition? And why did it last so long – up to several months! As in the case of “breastmilk jaundice”, I just had a very, very difficult time buying that whole “Rh factor incompatibility thing”!
I suspected “breastmilk jaundice” would turn out to be just another “inaccurate” label – like “the cold mother syndrome” for autism – a label that just put the “blame on the mother” – as was so often the case – instead of seeing the issue for what it truly was. Autism, breastmilk jaundice, Rh factor incompatibility and gestational diabetes were now, in my opinion, very much all sounding like “blame it on the mother” labels for issues science had failed to understand.
Given that the Rh factor was found in red blood cells, and so much seem to be tied to the breakdown of red blood cells – and jaundice was also associated with matters relating to “Rh factor incompatibility” – surely, there had to be more clues here!
When “Rh incompatibility” existed, an immune system response resulted. In Rh incompatibility, it appeared the baby’s blood cells could swell and rupture, possibly dangerously lowering the baby’s blood count. What exactly would that do to the unborn child from an iron metabolism perspective? If the infant’s blood count was low, did that mean that blood cells had been destroyed – possibly releasing “more iron” into the unborn child’s system?
The treatment of this “incompatibility”, according to the medical community, resided in suppressing the mother’s immune system during pregnancy or providing a blood transfusion for the infant – still in the womb. That was just one of those other things that just did not “sound right” to me – suppressing a mother’s immune system and the “blood transfusion” – and it especially did not sound right to me if that “shot” included thimerosal – the mercury preservative found in so many vaccines! I knew that thimerosal free Rhogam injections were now available, but the fact remained, that for many mothers and their unborn infants, in the past, there had been exposure to the neurotoxin – mercury – via Rhogam.
Hum… Rhogam… mercury… mercury known “to love sulfur” and attack the blood and immune system… could there possibly be a connection here?
Of course, my first concerns with all this “Rh incompatibility” stuff had to do with the mercury and also with the fact that if this treatment suppressed the mother’s immune system – what did it do to that of the child – before birth with that first shot of Rhogam – and after birth – with the second shot given to the mother during the time when collostrum would be flowing? I did not know the answer to that, but this certainly was a valid question given that Rhogam circulated in the mother’s blood for weeks, perhaps months. Could that, somehow be tied to also – for some – to that “breastmilk jaundice” that lasted for months? What exactly did Rhogam do to the immune system of the infant given the infant’s immune system was so dependent on that of the mother?
During a first pregnancy, Rh incompatibility was “less of a problem” than during the second preganancy. During delivery, the mother and child’s blood could intermingle – and as such, the mother was said to develop antibodies – antibodies that could destroy any future child. But, I wondered – could the danger for the second child not result in the fact that – just maybe – the mother suffered from iron overload – and as such, with a second pregnancy – if extra iron went to the unborn child – would the “attack on the second child” in the womb not be perhaps related to the fact that the child was becoming “toxic” to the mother from an iron overload perspective? I truly wondered about the role of iron in all this also. If the issue was only one of blood intermingling at delivery, why was Rhogam provided at twenty eight weeks – the very time that gestational diabetes – also an immune system issue – surfaced and the very time when the blood of the unborn child was in the process of “switching” to alpha+beta blood instead of alpha+gamma blood.
What I had read indicated that Rh factor incompatibility required the giving of Rhogam at around twenty-eight weeks of gestation as well as after birth. Well, that in and of itself raised a major red flag. Why was this not an “immune system issue” earlier on in the pregnancy? Why was the “shot” given around twenty-eight weeks of gestation and then again within seventy two hours of child delivery? So, the mother received two shots. It seemed to me that Rh factor incompatibility had a lot more to do perhaps with “the switch” to beta blood and the fact that iron overload appeared to be causing distress in both the unborn child and mother. Obviously, doctors would not just “wait around” until the problem became so huge it had serious implications for the child.
The organs of the fetus had started to be functional in the eleventh week of gestation. As such, they would have blood flowing through them. Interestingly, the blood of a fetus had approximately fifty percent more hemoglobin (those red blood cells containing iron and unconjugated bilirubin) than the blood of the mother. Also interesting was the fact that research into fetal blood flow indicated that about fifty percent of the blood carried via the umbilical vein passed directly through the fetal liver – that little, immature liver!
From researching the Rh factor incompatibility issue I had learned that about eighty five percent of the population was Rh positive. So, what had caused the Rh negative factor in that other fifteen percent? It seemed to me that if Rh positive was considered “normal”, and Rh negative was “the exception”, and Rh negative resulted in a woman’s body attacking her own child, that there had to be something to all of this Rh negative factor stuff that simply was not “normal”. Had it been caused by a gene mutation? What caused certain people to actually be Rh negative? The answer to that, I did not know.
What I did know was that Rh incompatibility factors were associated with jaundice in infants as well as with hemoglobin! Rh incompatibility led to the swelling and rupture of the baby’s blood cells and that could lead to dangerously low blood counts – Hum… could that not be the same as “heme deficiency”? Very interesting indeed!
Ruptured blood cells… jaundice… iron… bilirubin… lactoferrin… the breakdown of blood cells… hemoglobin…an immature liver – all these things kept going through my mind.
Hemoglobin… hemoglobin had two components – heme and globin. The heme part was that part that consisted of iron and unconjugated bilirubin. The globin part was that part that had to do with the alpha, beta and gamma proteins found in blood. In the fetus, there was only alpha and gamma. As mentioned earlier, the beta protein in blood was “not expressed” in embryonic or fetal hemoglobin.
Gamma was a fetal protein only that seemed to substitute for the “beta” protein prior to birth. The switch from the production of fetal hemoglobin (alpha 2 gamma 2) to the “normal” hemoglobin that did not have gamma in it or non-fetal hemoglobin (alpha 2 beta 2) occurred at twenty-eight to thirty-four weeks of gestation. How very interesting – that was exactly the time at which Rh factor seemed to become “an issue”!
How did all this relate to the research done by SP Perrine, MF Greene, and DV Faller in an article entitled “Delay in the fetal globin switch in infants of diabetic mothers” by in the New England Journal of Medicine, Volume 312:334-338, February 7, 1985, Number 6? This research had indicated that the “switch” to normal hemoglobin – the “beta” kind – was dependent on insulin levels. Obviously, given that “beta” part to the blood was in the “globin” part of hemoglobin, and as such that part associated with “antibodies”, certainly it appeared very likely that – just somehow – this could all be related. How interesting – again.
Rh factor incompatibility was considered an immune system dysfunction – and so was diabetes! Interestingly, gestational diabetes – an immune system response - affected mothers late in pregnancy, too!
I wondered… could the “delay in the switch from gamma to beta hemoglobin” in infants impact the processing of iron in newborns and “heme” levels? It certainly would make sense given that the “other part” of hemoglobin, the heme, was made of iron and unconjugated bilirubin. How did any “delay in the switch to beta” impact iron processing in the child? I did not have the answer to that, but I suspected the child would not be properly processing iron. Articles I had read on iron absorption seemed to indicate that excess iron would not be stored as heme. Iron could bind to so many things… and that - I now saw - could be either good or bad!
But, there was much more science now appeared to be finding out – including the “unsuspected” relationship that appeared to exist between iron and insulin! In an article entitled: “Cross Talk Between Iron Metabolism and Diabetes”, by Jose Manuel Fernandez-Real, Abel Lopez-Bermejo and Wifred Ricart, published in Diabetes 51(8):2348-2354, the unexpected relationship between iron and insulin appeared to be coming a little more into focus.
In this article, it was stated and I quote:
“Emerging scientific evidence has disclosed unsuspected influences between iron metabolism and type 2 diabetes. The relationship is bi-directional – iron affects glucose metabolism, and glucose metabolism impinges on several iron metabolic pathways. Oxidative stress and inflamamatory cytokines influence these relationships, amplifying and potentiating the initiated events… in recent years, increased iron stores have been found to predict the development of type 2 diabetes while iron depletion was protective… Here, we show that iron modulates insulin action in healthy individuals and in patients with type 2 diabetes… It is increasingly recognized that iron influences glucose metabolism, even in the absence of significant iron overload…all of these observations suggest that iron is more intimately linked to human pathophysiology than previously thought. In fact, iron metabolism is closely associated with the clinical presentation of numerous systemic diseases. Tissue iron excess contributes to produce and amplify the injury caused by free radicals as well as to modulate various steps involved in the inflammatory lesion… [end of quote – emphasis added - Fernandez-Real, et al., Cross Talk Between Iron Metabolism and Diabetes, Diabetes 51(8):2348-2354].
This article had several very interesting points. But, in just the above citation, there were several key things. The relationship being “bi-directional” was one. Did that mean that if iron modulated insulin - that insulin then – in turn - modulated iron?
Very interesting also, however, was the comment on “oxidative stress”. “Oxidative stress” – a phrase that seemed to appear almost everywhere I looked – a phrase having to do with “oxygen”. To “oxidate” something meant to combine it with “oxygen”.
As I read more and more about fetal development and especially, fetal blood – what in my opinion – was absolutely key to all this – something else “stuck out”. Fetal blood was said to have a tremendous affinity for oxygen. Given the infant in the womb had lungs that did not yet breathe in air, I wondered how it was that oxygen was processed in the unborn child given that I had seen this “oxidative stress” phrase in so many places. Well, not surprisingly, I soon discovered that fifty percent of fetal blood flowing through the umbilical vein went straight to the unborn child’s liver and that fetal blood could carry twenty to thirty percent more oxygen than maternal hemoglobin. Others appeared to place the “oxygen carrying ability” of fetal blood at close to fifty precent greater than that of the mother.
Well – twenty percent or fifty percent - kind of a “wide range” in my opinion in terms of scientific “accuracy” but the fact remained that clearly, fetal blood had a tremendous affinity for oxygen.
Fetal blood, I also soon discovered, was manufactured not in the bone marrow – as was the blood of adults – but in the liver! How very interesting – again!
So, given all this, if the unborn child had “elevated levels of iron” due to things like prenatal vitamins, and fetal blood was processed in the liver – not the bone marrow – and fetal blood had a tremendous affinity for oxygen would the interaction of iron and oxygen in the unborn child’s liver – just perhaps – not lead to – oxidative stress. It was a well-known fact that elevated iron levels in the liver was associated with liver cancer!
Could this be why so many children were now developing leukemia – cancer of the blood! Were cancer cells originating in the liver and then moving to the bone marrow as the child developed and blood formation functions went from the liver to the bone marrow? It certainly did appear to be a possibility, especially given that those in science were now suggesting that anemia was due to cancer cells infiltrating the bone marrow. Interestingly, anemia in children with autism suffering from iron overload was not due to “iron deficiency” – but to “iron overload”.
Anemia was also very much associated with oxygen levels. In anemia, the cells were not getting enough oxygen. Would that not provide an indication of an unborn child “in distress”, say, right around “twenty eight” weeks of gestation? Let us not forget also that iron accumulated especially in both the liver and the heart, and as such, certainly, fetal heartbeat could be impacted!
Depending on the test performed, one could get “different readings” relating to iron content in a person’s body. Were so many suffering from “anemia” – believed to be “iron deficiency” by the general population – and I suspected by most doctors, too – being given iron supplements when the problem was not deficiency – but overload – and thus, would iron supplementation not make the matter – only worse! Again, it certainly appeared to be a possibility!
According to a link I had found, anemia was caused by – and I quote:
“1.Blood loss: excessive bleeding such as hemorrhages or abnormal menstrual bleeding, 2.Chronic Illness: inflammatory diseases, arthritis, kidney or liver failure, chronic infections, 3.Cancer therapy: Surgery, radiotherapy, chemotherapy, and/or immunotherapy, 4.Infiltration (replacement) of bone marrow with cancer , 5.Breakdown or destruction of red blood cells, 6.Decreased red cell production due to low levels of erythropoietin (a hormone produced by the liver and kidney which promotes red blood cell proliferation).” [end of quote – emphasis added - Anemia Causes and Treatment, by Ernest H. Rosenbaum, MD, http://www.cancersupportivecare.com/anemia.html].
The following article explained how iron overload could be a problem in spite of an "anemia diagnosis":
How very interesting indeed!
Red blood cells… heme… heme deficiency…iron… unconjugated bilirubin… jaundice…the liver… fetal blood flow… fetal hemoglobin levels… the switch to “beta” blood… at twenty- eight to thirty-four weeks… Rh incompatibility… Rh factor… a protein located in red blood cells…Rhogam at twenty-eight weeks… gestational diabetes… occurring in late pregnancy between twenty-four and twenty-eight weeks of gestation… and an immune system disorder and indication of future type 2 diabetes…lactoferrin…can enhance iron availability…known to bind to iron…heme had iron… extra red blood cells broken down at birth releasing iron and bilirubin… breastmilk… lactoferrin known to bind to dna…breastmilk known to prevent diabetes…prenatal vitamins… extra iron… iron known to accumulate in the liver, causing cancer or liver failure, in the heart, causing heart failure, and in the pancreas and causing diabetes… beta… in the blood…insulin produced by the beta cells of the islets of Langerhans in the pancreas, beta-amyloid found in the pancreas of type 2 diabetics… beta amyloid altered by heme deficiency and coded by chromosome 21… heme deficiency known to result from low B6 levels… heme deficiency… also tied to aluminum… beta amyloid and aluminum… both clearly associated with Alzheimer’s…. iron… known to accumulate in the liver… fetal blood… fifty percent flowing to the liver first… fetal blood… having an affinity for oxygen… anemia… known to exist in children with autism who suffer from iron overlaod… anemia… a disorder involving oxygen levels and iron… oxidative stress… the liver… cancer of the liver associated with iron… fetal blood.. first produced – in the liver… anemia… oxygen… anemia… associated with the breakdown of red blood cells… excess red blood cells… broken down in the infant at birth… jaundice… found in newborns…a liver dysfunction indicator…jaundice… an immune system response in a child with something going horribly wrong – something that now very much seemed to implicate issues of hemoglobin production and breakdown, insulin, iron, oxygen, the liver, the pancreas - and that key word – “beta”!
Twenty-eight weeks… twenty eight weeks… twenty eight weeks… was all this – again – “just coincidence”? Given gestational diabetes was now considered by science one of the strongest predictors of type 2 diabetes, and persons afflicted with type 2 diabetes were known to have “beta-amyloid” in their pancreas… let’s just say that, in my opinion, this was all much more than simply “coincidence”!
I had a prediction for those in science – I predicted that iron metabolism dysfunction disorders such as, in my opinion, diabetes could be, would be the best predictor for Alzheimer’s in the future… and if correct… that prediction was rather frightening given we had over one hundred and fifty million with diabetes worldwide and an explosion in diabetes not only in older persons but in children as well. I would have “predicted” hemochromatosis as well – the disorder ten percent of us were said to “carry the gene for”, however, when iron overload got to the point of it actually being recognized as “hemochromatosis”, you were – potentially – so close to death that the likelihood of surviving to go on to develop Alzheimer’s in “old age” [when more complications such lower heme production occurred] – in my opinion, was rather unlikely. Note that “hemochromatosis” was often misdiagnosed as “diabetes”.
And then, I found this statement on a website discussing mercury toxicity issues - http://www.ephca.com/metals.htm#merc_tox:
“Mercury compounds are immunomodulatory and the decrease in B-cell function indicates toxicity”!
and then, another statement from another website that appeared to be key – a government site – on the immune system:
“IgD is almost exclusively found inserted into the membranes of B cells, where it somehow regulates the cell's activation”.
What were “b” cells? These were white blood cells that made antibodies and as such, were an important part of the immune system. B cells came from bone marrow and were also called B lymphocytes. From what I could find, fetal b cells seemed to be somehow different than adult b cells and changes seemed to occur until the age of about one and a half to two years of age. Well, this was certainly very, very interesting to say the least – given this was right around the time that children often seemed to show those first signs of autism! What was the role of “b cells” in all this – and did that role somehow have anything to do with iron or insulin?
Well, not to my surprise, b cells in the unborn child developed in the liver!
Could RhoGAM, the treatment for Rh factor incompatibility have something to do with this IgD stuff and if IgD was found almost exclusively in the membrane of b cells and mothers who were Rh negative appeared to have no “D” immunoglobulin, was that an indication of possible mercury toxicity in mothers? And how did the fact that blood in an unborn child was produced – not in the bone marrow – but in the liver – fit into this?
RhoGAM was an Rh o(D) immune globulin. Apparently, this globulin was made with proteins from human blood plasma.
Blood plasma was known as the “liquid part” of blood. Plasma cells came from B cells and were anti-body producing cells. An anti-body was produced and secreted by B cells.
Antibodies were considered soluble proteins and were produced in response to the detection of an antigen. Antibodies were further capable of binding to the specific antigen that had been detected – thereby “marking” it for destruction. Antigens were things that produced an immune system response. Antibodies were also known as “immunoglobulins”. These included the following: IgG - believed to comprise about eighty to eighty-five percent of total antibody serum and believed to enhance something called phagocytosis to neutralize toxins. Phagocytosis appeared to be some process whereby particles were injested by cells. Then, there was IgA. IgA comprised about fifteen percent of antibody serum and was involved in the protection of mucosal surfaces. IgM, another immunoglobulin, comprised five to ten percent of antibody serum and also enhanced phagocytosis – especially for micro-organisms. IgE, yet another immunoglobulin, was associated with allergic reactions and comprised about two thousandths of a percent of the antibody serum. Note that allergic reactions were also considered immune system responses. But, the very interesting one in all this, was IgD, something that stimulated B cells to produce antibodies and comprised about two tenths of a percent of antibody serum.
An antigen was something that stimulated an immune system response. These could be proteins, carbohydrates or toxins that had been introduced into the body. The interesting thing about RhoGAM was that it was made with “anti-D” – what was considered the “working agent” found in Rh o(D). This “anti-D” was what was supposed to stop an Rh negative mother from reacting to the antigens protein in her unborn Rh positive child’s blood. There were supposedly no “blood cells” in the RhoGAM treatment.
Proteins… sulfur… mercury… carbohydrates… toxins… iron… heme deficiency… fetal hemoglobin produced in the liver… blood… the immune system…
So, if IgD was almost exclusively found in b cells… and b cell dysfunction was indicative of mercury toxicity… and human blood plasma cells came from b cells and plasma cells were anti-body producing cells, and antibodies were produced and secreted by b cells… it stood to reason that RhoGAM – made from human blood plasma, definitely had something to do with these “b cells” and that this Rh o(D) immune globulin was something very much related to IgD….
I was no scientist – this was true - but, there certainly appeared to be a connection here! Could iron, insulin or mercury decrease normal b cell functioning and hence possibly impair IgD functions. This IgD stuff was tied to Rh factor incompatibility between mother and child, and I very much suspected it was tied to a great deal more as well.
Rh factor incompatibility… an immune system response… an immune system response… iron overload… and for an infant or child in the womb, no options available to get rid of excess iron…
Heme deficiency… known to activate nitric oxide synthase… nitric oxide synthase… found it seemed – in highest concentration – in the cerebellum… that very part of the brain impacted most in autism.
Nitric oxide synthase was associated with the production of nitric oxide – something known to bind to iron… nitric oxide – in excess – was also known to lead to cell death!
In the immature infant, and especially in a child less than six months of age, there would be no bile to help process any excess iron. If a child were not breastfed, neither would there be lactoferrin to bind to the iron. Children with autism, in general, were known to have low levels of lactoferrin – very much indicating a malfunctioning liver.
Liver dysfunction… iron overload… vaccines…
One could lose eighty to ninety percent of liver function before going into liver failure and yet, children with autism appeared to have such dysfunctional livers – that could only have resulted from a major assault to the liver – iron overload and vaccines were definitely possibilities.
The liver, in addition to processing iron, had functions that included detoxification, hormone functions, the production of bilirubin, functions associated with ammonia (also known to be high in autism) and purines. It was also involved in maintaining blood glucose levels. All these things seemed so dysfunctional in children with autism. The liver was also involved in the breakdown of fats and proteins and was involved in the synthesis of blood proteins. If immune system option after immune system option failed, how would the child possibly rid himself of excess iron? The only option available to the immature infant, especially if not breastfed, would be the sloughing of cells – could this be diarrhea? Jaundice?
Even if the sloughing of cells, say perhaps, diarrhea, were an option, it appeared that iron very much was “recycled” within the body. As such, I wondered, even via the casting off of cells, how much iron could really leave the body if an infant, child or adult was suffering from iron overload?
Persons with Alzheimer’s would have had a fully functioning liver – at least earlier in life - and thus, they would have had bile production. Lactoferrin did bind to iron. It now looked to me as if lactoferrin acted as nothing more than a “transport mechanism” to move iron somewhere else… to perhaps have it bind somewhere else. Iron overload certainly could explain high lactoferrin levels found in the brains of persons with Alzheimer’s. But, if iron was moving or accumulating in the brain, what happened to it then? How would the iron be processed from there?
I knew iron was normally processed by the liver and then recycled to the bone marrow. Blood cells, both red and white were made via bone marrow processes.
Red blood cells… hemoglobin… iron…white blood cells… immune system functions…
As I thought about all these issues and iron overload, I wondered about testing for iron levels. Obviously, if iron were accumulating in organs and brain, hair tests would perhaps not capture total iron levels in the body. And what about the testing of blood levels? Would those be more accurate? Would that accurately indicate how much iron could now be stored in the organs? I simply did not know.
Iron… the blood… iron…
I searched for more answers and thought - iron… blood… it was then that I recalled a story my mother had told me of her youngest brother who had died from – leukemia – cancer of the blood.
Although my uncle had died well before I had even been born, he was only two at the time of his death. My mother had lost three brothers at very early ages – to illness or accident – and although they had long ago died, she had spoken of her brothers to her children, I suppose just so that we knew they had once been there and been important in her life. In speaking of her youngest brother, the strongest memory my mother seemed to have of him was one that had involved the drawing of a blood sample from her two-year-old brother. She recalled for me how she knew he was very sick just from - the color of his blood. She had told me that her brother’s blood was not red – but “rust” in color.
Rust… iron… leukemia… blood first produced in liver - then in the bone marrow… iron overload… oxidative stress… oxidation… to combine with oxygen… iron… fetal blood able to attract more oxygen than normal blood… anemia… resulting from cancer cells moving to bone marrow … iron… associated with cancer of the liver… the liver…where unborn children produce blood…leukemia… white blood cells… the immune system… T cells…so critical to the immune system…
T cells were known to first appear in the unborn child at about fourteen weeks gestation, but reached normal levels only at thirty to thirty two weeks gestation according to the Merck Manual [http://www.merck.com/pubs/mmanual/section19/chapter256/256a.htm]. Thus, until thirty to thirty two weeks gestation, the unborn child’s immune system, certainly could have a difficult time reacting to any problems that occurred prior to thirty to thirty-two weeks gestation – and that certainly would include not being able to properly react to the presence of any cancer cells that may have already begun to form within the immature liver – could it not?
An immune system response… an immune system response… the liver… leukemia… an explosion in leukemia in children…was leukemia also an immune system response – possibly – again, due to iron overload in the liver?
Leukemia usually resulted in an increase in the count of white blood cells - and white blood cells were involved in immune system functions. Indeed, if there were more “white” blood cells in the blood, did it not stand to reason that the very color of the blood would be changed too! Could that not produce “rust” colored blood? Again, I wondered!
Hemochromatosis – that certainly did seem to indicate that too much iron in the body could result in “rust”. This disorder – hemochromatosis – was exactly that – a disorder resulting from the accumulation of too much iron in the body!
The following link provided a good general overview of hemochromatosis – the disorder known for “rusting out organs”: http://www.post-gazette.com/healthscience/19981110hemo1.asp.
This article had been written by Deborah Weisberg, and appeared in Post-Gazette.com, Tuesday, November 10, 1998. I quote key phrases from this article below:
“…hemochromatosis, a condition with no cure…. while the average person eventually excretes most of the iron he consumes through the bowels, the kidneys, the skin and the hair, [cell sloughing] those with hemochromatosis absorb iron, storing it in their organs…over time, it accumulates in toxic amounts, causing organs to fail because they literally rust… iron overload is the most common genetic [this I question] disorder in the United States… while it is easily treated, it also is among the most under-diagnosed conditions, often with deadly consequences. Because it can take years for overloading to occur, symptoms may not appear until middle age and, by then, the damage is done. "The hemochromatosis itself may have no symptoms, yet it can be the underlying cause of many other diseases, primarily hepatitis, cirrhosis of the liver, heart disease, diabetes, arthritis, and reproductive failure, including impotence ," says Dr. Geoffrey Block, a liver and genetic disease specialist… "Hemochromatosis is a kind of medical orphan," Block says, “because it has never really belonged anywhere [why not if so common and deadly?]… “early screening is important in catching the condition before much damage is done. " A person may be in end-stage organ failure before their hemochromatosis is discovered. With early screening, they might have been helped... A simple treatment… for hemochromatosis is phlebotomy, or letting of blood, since iron is transported to the organs through the blood… A doctor might remove a pint of blood weekly for the first year or so of treatment, but a patient's condition eventually can be maintained with less frequent treatments [emphasis added – end of quote, Deborah Weisberg, http://www.post-gazette.com/healthscience/19981110hemo1.asp ].
The story also included the statements of a woman who stated that her brother - a man, diagnosed with hemochromatosis at age 41 - had been treated for diabetes for years, with no one ever suspecting iron overload! He died six weeks after being diagnosed with hemochromatosis!
Thus, the key words here were… iron… overload… rust… medical orphan… hepatitis… cirrhosis of the liver… diabetes…etc.
Indeed, according to the CDC, hemochromatosis, was now one of the most common “genetic disorders” with as many as one in ten “carrying the gene” and as many as one in two hundred to one in four hundred actually having the disorder. That certainly sounded like another “scientifically impossible genetic epidemic”! Had “genetics” really gotten that bad in one generation? Hum…another “epidemic”… another “genetic disorder” arising almost “out of nowhere”. Very interesting indeed!
Let me once again ask the “obvious question”: If this was indeed a “genetic disorder” how could it be that “less frequent treatments” would eventually be needed to maintain the patient’s iron levels at acceptable levels?
This sounded a lot more like the result of having simply taken out “the excess” and that now, given organs had been damaged by the disorder and were in all likelihood less able to perform their functions on their own, fewer “treatments” were needed.
I suppose there was “some hope” here in that the “letting of blood” could perhaps also be helpful to others who suffered from iron overload – such as my son with autism. My concern with “the letting of blood”, however, was that with the release of blood, obviously, more would be made – and would that not put an excessive burden on the bone marrow and perhaps lead to failure in that functioning?
The Chinese in the past used leeches to help treat disorders - looks like they were perhaps a little ahead of modern medicine. If indeed hemochromatosis was “genetic”, a simple comparison study looking at “how many” persons around say iron docks where iron was shipped by boat, or persons working in iron mines had disorders like diabetes, liver problems, etc. compared to the average population. I suspected that these disorders would be more prevalent in such areas.
A “genetic” disorder - parents of children with autism had once blindly accepted that “label”, too. The more I studied iron overload, the more it was clearly evident that in attempting to “fortify” ourselves with iron, we had perhaps forgotten that iron could be toxic and as such we had not fortified our bodies – but rather led to their literal “rusting out” and breakdown, and that breakdown – also in my opinion – was now manifesting itself in disorders such as autism, schizophrenia, Alzheimer’s, diabetes, kidney failure, liver failure, cancer, and countless others.
The same words… popping up… over and over again… yet, this time, there was a new “condition” also associated with “iron overload” – reproductive failure! That, again, had particularly “stood out” for me. I had suffered two miscarriages and both had been so heartbreaking for me… both had been right around ten or eleven weeks of gestation – why? I know very much suspected that these “reproductive failures” had also been the result of iron overload and/or mercury poisoning because I now knew that blood began to flow through fetal organs right around this time during gestation – and half the fetal blood passed through the liver – a very, very immature liver indeed!
When I considered these facts and put that together with the information that had been provided stating that hemoglobin, the oxygen carrying protein in red blood cells, consisted of the (C738 H1,166 Fe N203 O208 S2)4 and that:
“Mercury simply loves sulfur…Sulfur is part of our blood cells as well as many other proteins and enzymes…Antibodies* contain sulfur and are therefore attacked by mercury — thereby destroying the body's natural disease defense system”[ end of quote, emphais added: Dr. Theodore B. Hoekman, Heavy Metal Toxicology, http://www.luminet.net/~wenonah/hydro/heavmet.htm].
I was finally beginning to see how all this fit together. “Mercury simply loves sulfur”. In my opinion, this had to be associated with low sulfur levels found in children with autism and explained why Epsom salt bath or creams were found to be so helpful. The fact that sulfur was found in the blood could also possibly help explain some issues as they related to mercury and blood dysfunction – and, also in my opinion – many forms of cancer given that clearly, both mercury and aluminum – a known gene mutant tied to heme deficiency – were known to affect the blood – and blood flowed through absolutely all parts of the body!
By this time, there was no doubt in my mind that iron, mercury and aluminum were all potentially huge problems for everyone – whether in the womb or not! The underlying cause of “genetic link” – to so many of these disorders – “genetic links” – for the most part, still very much unproven - was something I now questioned more than ever.
I had no doubt that, in some disorders, genetics could definitely play a role – the question now became, were the “genetics” playing the primary role – or were they perhaps secondary – perhaps only a “symptom” rather than “a cause”.
In looking at disorders such as hemochromatosis, and so many others, the “genetic link” simply made no sense. For the most part, disorders seemed to only “get worse” once diagnosed. Indeed, rare were “remissions” in any medical condition.
If hemochromatosis were indeed “genetic” for example, did it not stand to reason that as the disorder progressed, it would only get worse? Yet, in hemochromatosis, after the removal of several pints of blood, “things got better” and fewer treatments were necessary. That, to me, was very much indicative of an “environmental” implication to this rather than a “genetic”.
If simply removing excess iron resulted in “less of a problem”, less of a “disorder”, how could that disorder be “genetic”? Would a “genetic” disorder not continue on its path of destruction and continue to be just as bad – if not worse? The simple fact was that the “letting of blood” was completely an “environmental intervention”. There was no alteration to the “genetic code” itself. If a “genetic disorder”, would the genetics not continue “on their merry way” – continue to create havoc in the system and continue to cause the body to have “as much” an issue with “iron overload” as ever? How could an “environmental intervention” – something done by a doctor that had nothing to do with the “genetics” of the situation, alleviate a “genetic disorder” so that “fewer treatments” were necessary? This, again, made absolutely no sense to me.
Only human intervention seemed to make so many of these “genetic” disorders “better”… if “genetic”, how could that be? How could an “environmental intervention” change “genetics”? How could “environmental intervention” result in a reversal of a “genetic disorder” – in remission – for example? What was a “remission”?
If there was one disorder associated with the word “remission”, it certainly had to be cancer! But, again, what exactly was a remission? When someone experienced “remission” in a disorder, the signs and symptoms simply – disappeared! When that happened, a person was said to be “in remission”. Some “remissions” were temporary – others were permanent!
Thus, if all these disorders were indeed “genetic”, would the “genetic mutation” or “genetic code” not somehow have to be altered and returned to “normal” for one to go “into remission” and if the genetic code had been altered in a cancer patient, now in remission, would science, by now, not have figured out a lot more in terms of “preventing” cancer.
Clearly, a genetic mutation that had been present at the time of diagnosis would in all likelihood still be present during remission. Would that not indicate that perhaps – just perhaps – “genetics” had a lot less to do with the disorder in the first place and that remission, was more likely, at least in my opinion, a successful immune system response – either temporary or permanent – to an environmental variable?
Was an immune system response not more a function of the “environment” within the body than “genetics”? The immune system looked for problems in the body - its environment – and attempted to “do away with them”. Mutations were usually seen as “errors” in the genetic code and they had impacts in terms of cell reproduction or function. Chemicals and viruses were known to cause mutations. Clearly, both of these were “environmental” – not “genetic”. It seemed that once the “mutation” occurred and “was passed down to the following generation”, that the mutation became considered “genetic” – and hence – perhaps the explanation for the many “genetic disorders” we now have! But, again, the key was – what had caused the “mutation” in the first place – “genetics” themselves – or an environmental factor – such as a chemical or virus?
The simple fact remained, that in my opinion, we simply had too many “genetic epidemics” with “cause unknown”. If the “cause was unknown”, were we basing the “genetic” classification on a mutation here and there – mutations, that when looked at – as a whole – still failed to explain the great majority of what was seen in the disorder! That appeared to be a possibility. Even in looking at what we knew of the “genetic” factors, they failed to even come close to really explaining “the disorder” – and more importantly perhaps – the cause!
Autism, schizophrenia, Alzheimer’s, epilepsy, diabetes, hemochromatosis, cancer, and on and on and on… cause “unknown”!
If “the cause” was an environmental one, as opposed to a “genetic link”, would that not imply that the “fix” should be somewhat easier? There did exist methods for chelation of mercury and iron. It almost appeared as though the biggest difficulty seemed to reside in the admission as to what the issues truly were.
The human body had within it the ability to repair itself. This, again, in my opinion, tended to argue against a “genetic link” to so many disorders. This normal process of mutation repair within the body involved enzymes – there was that word again – enzymes. Some enzymes appeared to go through the body in search of mutations on genes in an attempt to restore the gene to its proper “genetic code”. Genetic engineering was based on this principle – the finding of certain genes and the “cutting, splicing and replacing” of what was not desired.
Enzymes… mutation repair… occurring naturally within the body… an immune system response…
As I researched this whole area a little more – again, more pieces started to fall into place.
Enzymes… that word that had now become so key in my son’s life… appeared to now play a critical role in the system’s ability to repair mutations in the genetic code. The fact that aluminum – a known gene mutant – had been pumped into our children via vaccinations seemed a much more likely “cause” of genetic mutations in so many of these disorders. Call me crazy, but it just seemed to stand to reason that if you injected a known gene mutant into the human body – you should expect to see mutations! Whether or not those mutations, however, had actually caused a disorder was again – a huge leap of faith on the part of the scientific community!
I knew that my son could not properly digest casein (a dairy protein) and gluten (a milk protein)….
Dairy… milk… breastmilk… casein! Breastmilk was an infant’s perfect food… and yet, Zachary could not digest milk properly… why not? What was it about “casein” that was “a problem”? Again, I just had a very hard time with the whole issue that my son could not drink the milk that had been specifically designed for him. The answer had to be related to “casein” – somehow and the working of enzymes to break down that casein. I had put Zachary on digestive enzymes that could be purchased from Houston Nutraceuticals, Inc. at http://www.houstonni.com for the breakdown of casein and gluten and since on those enzymes, Zachary had indeed made some progress although I still very much kept him on a casein and gluten free diet. Trace amounts of these proteins, however, could still be found in many products and as such, given children with autism were believed to be impacted by these proteins at molecular level, I had wanted to take no chances since everything I had read seemed to indicate these proteins – casein and gluten – acted as natural hallucinogens on my son’s brain – a natural “drug high”!
Casein… enzymes…mercury… known to target enzymes and proteins… milk… man’s first food…
As I continued to look for answers, and in comparing autism, Alzheimer’s and schizophrenia, I could not help but notice something that had become very obvious to me as it related to Alzheimer’s. An enzyme known as “casein kinase 1” had been found at over thirty times the normal level in the brain of persons with Alzheimer’s…. casein kinase 1… that sounded very much like something that could have something to do with the breakdown of casein. Casein kinase 1 also had dna repair functions! Research appeared to also be indicating that casein may also cause amyloidosis in lab animals. There appeared to be different types or classifications of “amyloidosis”, but, obviously, they were probably “similar enough” to at least give them the “same name” of “amyloidosis”.
If there was one thing I had learned in all this, it certainly was not to take “known facts” or “labels” as “definites”. Science seemed to always be reversing itself in terms of understanding so many things. We had once been told that “you could do without” your appendix, spleen, tonsils, adnoids, and gallbladder. It now very much appeared that all of these had “immune system functions”. So, if we were “discarding” these organs so readily, would that not make us a lot more susceptible to immune system disorders?
Clearly, over and over, I had seen that when science failed to understand something, we were just told: “It has no use or it’s not critical and so, you could live without it”. Science, obviously, had yet to understand the full role of all these “extra parts” – parts that perhaps would turn out to be a lot more critical than we could ever have imagined. So many of us now had immune system issues and so many of us were “missing” some of these previously so easily discarded “parts”, perhaps – just perhaps – these “extra parts” actually did have a role in the human body and in looking at the prevalence of disorders among those with specific “missing parts”, perhaps we could find correlations to indicate what those “extra” parts were for in the first place!
The issue of “discarding the unknown” appeared to be a rather common practice. In my opinion, the quick discarding of these “extra parts” was very similar to the quick “discarding” of that which we did not understand in psychology and psychiatry – things like the language of children with autism – what had for so long been referred to as “nonsense language” by those who did not understand it. Clearly, it made perfect sense when you finally did understand what was going on – and in my opinion, when understood, things like “nonsense language” – what I preferred to call “reference communication” – held the very keys to unlocking so many mysteries. This issue of “reference communication” was discussed at length in my second book, Breaking The Code To Remove The Shackles Of Autism: When The Parts Are Not Understood And The Whole Is Lost! There would be a great deal more on this issue of “nonsense” language in the next book I planned on writing – upon the completion of this one – a book looking specifically at issues of language and communication in children with autism.
Truly, the more I looked at the title of that second book I had written, the more I found it so descriptive not only of the condition seen in the child with autism – but of what we saw in those studying these issues also. I knew science could be a very difficult field to be in and I appreciated everything that had been done thus far – tremendously – I just wished that we were not so quick at “dismissing” or labeling as “no known purpose/function/expendable/not critical/not important” - things that could be so key to our understanding of so much.
The unknown… the misunderstood… the discarded… casein…milk… man’s first food… casein kinase 1… dna repair functions…Alzheimer’s…amyloidosis… beta amyloid…beta…beta cells… the pancreas…amyloid plaques… breastmilk… immune system functions… all very interesting indeed!
Granted, a specific enzyme could be associated with many, many functions within the body… but the fact that this particular enzyme – casein kinase 1 - had been found in high levels in the brain of person’s with Alzheimer’s and that this particular enzyme appeared to be somehow involved in both the breakdown of milk and in dna repair, truly made me wonder – again!
There were hundreds of enzymes in the human body. The fact that this particular enzyme - an enzyme having to do with the “casein” – and “casein” being the particular milk protein I knew my son could not digest – was another “coincidence” I truly questioned. In no time at all, I had also found information indicating that casein kinase 1 also appeared to be somehow tied to liver functions and sleep patterns with the liver seemingly having “clock functions” of its own.
Again, this certainly was very interesting. Humans had been drinking milk [casein] and had eaten grains [gluten] for hundreds of years yet it was only recently that we had experienced explosions in disorders such as autism, schizophrenia and Alzheimer’s. Why?
Although there were studies that wanted to show milk as the “cause” of autism, I simply did not believe that. It made absolutely no sense that man’s first food would be the actual cause of such horrible disorders. Furthermore, the fact that casein kinase 1 appeared to be tied to dna repair functions within the body tended to indicate that casein had a very important and critical role – a good role – in the human body. In my opinion, it seemed to me that given casein kinase 1 was tied to man’s first food and the ability of the body to actually repair itself [i.e., repair mutations], as well as liver functions and sleep patterns, I just could not see how milk could actually be the cause of autism. It appeared much more likely that the body’s ability to process “casein” had been “knocked out” and as such, a critical protein was no longer working the way it had been intended.
Indeed, if casein kinase 1 was tied to liver functions and the liver had been damaged due to iron overload, mercury and/or aluminum, and/or viruses, then, it certainly stood to reason that problems with casein breakdown and liver functions would occur.
Could the fact that this particular enzyme appeared to be involved in the breakdown of milk proteins not have implications in terms of the formation of bile in an infant? Bile was involved in the breakdown of fats… yet it was not produced in infants until at least six months of age… why not? Breastmilk had some fat in it…
Could it be that bile was not produced in the infant in order to allow casein kinase 1 time “to do its thing” in the infant in order to try repair any potential problems with “genetics” in the infant? I truly wondered! Again, I was no biochemist or scientist but I had taken a few classes in statistics and the “probability” of all this simply being “just coincidence” was – in my opinion – dwindling rather quickly.
Mercury… aluminum (a known gene mutant)… viruses… iron overload… insulin levels…gestational diabetes…amyloid plaques in Alzheimer’s and type 2 diabetes…beta amyloid… beta cells found in the pancreas… fetal hemoglobin… the switch to “beta hemoglobin… a delay in that switch resulting tied to insulin levels…casein… casein kinase 1…dna repair… Alzheimer’s…high levels of lactoferrin in Alzheimer’s spinal fluid… low levels of lactoferrin in children with autism… iron… known to accumulate in the liver and heart… bilirubin… jaundice…an immune system response…
Lactoferrin had been found to be elevated in the spinal fluid of persons with Alzheimer’s and this, it was believed, was an immune system response. Could excess levels of casein kinase 1 in the brain of persons with Alzheimer’s not also be an immune system response?
An immune system response… an immune system response… an immune system response…
Secretin… a hormone found in the pancreas…the liver… the upper intestinal tract… and the brain….
Secretin… found in the pancreas and liver… diabetes… dysfunction in the pancreas… bile… dysfunction in the liver…
Secretin ... … necessary for the activation of the amygdale – that part of the brain responsible for emotions and involved in “social interactions”… a part of the brain known to synapse directly with the frontal lobe… that part of the brain so impacted in all these disorders… secretin appeared to be low in children with autism because they showed less activation in the amygdale than did normal counterparts. Could secretin production also have been “knocked out” in the liver and pancreas – possibly by viral or chemical assault from vaccinations or from excess iron? I simply did not have the background to know but I certainly suspected this could be the case.
Secretin had been promoted as a new therapy among children with autism to help with the production of language. This issue was discussed in my second book, Breaking The Code To Remove The Shackles of Autism: When The Parts Are Not Understood And The Whole Is Lost! In this second book, I had discussed why I thought something other than secretin could have made a non-verbal child talk – a child with autism who – after having been given secretin – started talking. In that book, I had suggested that “something else” had perhaps played a role in making that child talk – something other than secretin. That something was – anesthesia.
The production of language was located in the frontal lobe along with the sense of smell. Anesthesia involved the sense of smell. Secretin was found in the amygdale. The amygdale – responsible for matters of identification of emotion in others – was now known to synapse directly with the frontal lobe. The frontal lobe had both control of emotion and production of language within it. So, the question was, did secretin actually “trigger” language production in a non-verbal child with autism – or was the amygdale tied to the frontal lobe more for matters relating to “control of emotions” – also found in the frontal lobe!
In my opinion, secretin had not caused the production of language, although, certainly, given that I did believe all functions in the various parts of the brain were much more interrelated than previously thought, perhaps secretin had played “some role”, but I did not believe it had been the “primary” role in “language production”. If my theory were correct, secretin would perhaps be involved in the “control of emotions” in the frontal lobe and that function – control of emotions – would then be involved in the production of language. But it also appeared the “sense” located within a specific region of the brain appeared to have the most to do with the functions located within that lobe. In the frontal lobe – the only “sense” – of the five senses man had – was the sense of “smell”. Did secretin going from the amygdale to the frontal lobe or secretin possibly already in the frontal lobe involve “smelling”? It did not appear to me that the “nose” was involved in secretin here – perhaps I was wrong – but, I just did not see how secretin – between the frontal lobe and the amygdale – involved - the nose – something clearly needed to “smell”.
Yet, the sense of smell – olfactory processing – was also found in the temporal lobe – and a sign of right temporal lobe damage was – persistent speech. In my opinion, it appeared perhaps anesthesia had resulted in right temporal lobe damage in this child and as such – there had been “production of speech”. Of course, this was just “my theory” – nothing more. I had no way of knowing for sure either way. But, given that since the writing of my second book I had now come to do a great deal more research on brain structure and function and had now come to understand that the frontal lobe and the amygdale – known to have secretin – synapsed directly, yes, there was certainly a possibility that secretin had played some role in “language production” in this child. But, had it been the “primary” reason for it? I still suspected it had not – but, again, that was just “my opinion”. Perhaps the fact that the amygade and frontal lobe synapsed directly, however, could help explain why results had been “mixed” in secretin studies with children having autism.
Secretin… found in the amygdale, the liver and the pancreas… diabetes… dysfunction in the pancreas… bile… dysfunction in the liver…
The pancreas… the liver… the pancreas… the liver… - the brain…
Diabetes was considered… an immune system response too. Persons with type 2 diabetes had been found to have amyloid plaques in the pancreas – but beta amyloid plaques – long chains of beta amyloid proteins bound together - were usually associated with the brain of those with Alzheimer’s… what was the connection? It certainly seemed to me that the formation of these beta amyloid plaques had to be involved in some kind of immune system response too - but a response to what?
From the study previously discussed, I now knew that heme deficiency altered amyloid proteins. Heme was also known to degrade with age and thus, this too, certainly had to fit into the equation.
There was no doubt in my mind that viruses, mercury or aluminum would generate an immune system response… given that iron could be toxic, surely that could easily result in an immune system response too if iron overload did indeed exist.
Iron… iron overload… heme deficiency… heme degradation… iron…
In researching iron levels in the human body, I soon discovered that a normal adult man lost approximately one mg of iron per day – a normal adult woman, approximately two mg per day. It was also believed that a man should have an intake of approximately ten mg per day, a woman twenty mg per day – just to keep up with “normal functioning” due to the fact that iron from our foods were poorly absorbed – generally having only approximately a ten percent absorption rate. In addition, women could lose anywhere from fourteen mg to twenty-eight mg during the menstrual flow. Yet, menstrual flow was not present during pregnancy and hence, obviously, women should be retaining more iron while pregnant. In addition, pregnant women were usually on prenatal vitamins that provided “extra iron”.
Extra iron… extra iron… extra iron… this certainly appeared to be one of the possible “first triggers” to a number of problems in the unborn child, young infant and pregnant mother. But, was it the first domino – or did that honor belong to mercury? Mercury was known to impact hormones. Everything in science was measured in parts per billion. Yet, hormones were so sensitive that they were measured in parts per trillion. Insulin was a hormone. Insulin and iron had a bi-directional relationship – with insulin impacting iron and iron impacting insulin. Either iron or mercury – or both in combination - could be that first “domino”.
I had a mouthful of mercury… yet, Zachary had made some progress at birth before slipping so deeply into his world of “autism”. He had been able to go down the stairs “the right way” at one time… that I definitely remembered.
When I was in college, my dentist had commented on the fact that I had “so many fillings”. I told her I was French Canadian and that I had been raised with the typical “maple syrup, maple sugar, maple everything” French Canadians absolutely loved. Upon learning of my “sweet tooth” heritage, she had stated: “Well, that explains it… French Canadians have the worse tooth decay in the world”.
That certainly had been an interesting comment. As I looked back on that comment made by my dentist, I wondered. French Canadians ate a lot of sugar and they had a lot of fillings – at least those that I knew. Sugar certainly would have altered insulin levels and fillings certainly would have contributed to mercury overload in this population. Yet, autism was no more a problem in this culture than in any other. Why not? If dental fillings were the primary cause of mercury poisoning, would French Canadians or other populations with “lots of fillings” not have “more autism”? The same would hold true for insulin levels. That left mercury and aluminum in vaccines or iron overload as the primary culprits in all this. Vaccines had provided an “overdose” of mercury for many children. Dental amalgams would have only resulted in a “slow leak” situation. Certainly, that mercury could have also found its way to the unborn child. Indeed, in Zachary’s case, that could have been part of the problem. Yet, I had also very much taken prenatal vitamins while I was pregnant – and they were loaded with iron.
The body had no good mechanism for riding itself of extra iron. The only way for a pregnant woman to rid herself of “extra iron” would be via bleeding, the sloughing of cells (shedding or casting off of cells), or transfer to the developing fetus given that the menstrual flow was inhibited during pregnancy.
The sloughing of cells… the shedding off of cells… iron… another clue!
When cells were destroyed – iron, did not appear to be discarded by the body – it was processed in the liver and recycled in the bone marrow! But, in the unborn child, given blood was produced in the liver, would that “recycling” of iron not be to the unborn child’s liver – only further complicating matters for that immature liver!
Iron…. recycled to the bone marrow… leukemia… cancer of the blood… blood, produced in the liver in unborn children… and later produced in the bone marrow.
That “recycling of iron”, certainly had the potential for even greater “iron overload” in pregnant mothers and their unborn child. Iron had the ability to bind to many proteins and that certainly could result in harmful impacts to their structures. Thus, if a mother had “iron overload” while pregnant and she could not release that iron via the menstrual flow due to her state of pregnancy, the only options available to her immune system were either the “sloughing of cells” or the passing off of that extra iron to the unborn child.
Although the mother certainly could easily pass that iron to the unborn child, I suspected that somehow – before that option occurred – perhaps the “sloughing of cells” occurred in an attempt to prevent iron toxicity in the unborn child. Again, it just seemed to me that a woman’s body would not injure her unborn child unless this was a very “last resort”.
If a woman who was pregnant had to “cast off cells”, what cells would be “cast off” or “shed” if indeed an immune system response did occur in the mother in an attempt to inactivate the extra iron and save the unborn child by preventing excess iron from being passed to that unborn child?
Well, given the fact that the unborn child did not have “beta” in the blood hemoglobin, but rather, had “alpha and gamma” until the “switch to beta” occurred at approximately twenty- eight weeks – in normal gestation – and given the fact that “beta” was not “expressed” in fetal hemoglobin and seemed to truly increase in levels just prior to birth, and given the fact that beta cells were found in the pancreas and diabetes was an immune system response whereby beta cells in the pancreas either failed to produce insulin or produced inadequate amounts, and given gestational diabetes – an immune system response in the mother - occurred right around this same timeframe of twenty eight weeks and disappeared after the birth of the child, and given insulin was produced by the beta cells in the pancreas, and given insulin levels were known to impact the “switch” from gamma to “beta” hemoglobin and delay that “switch” – given all this – was it not possible that the immune system response in a pregnant woman suffering from iron overload – a substance known to accumulate in the pancreas and cause pancreatic dysfunction – given all this – was it not possible, that in an attempt to save her unborn child, the mother’s immune system response would be the sloughing of cells – of say, perhaps, “beta cells” – and hence, gestational diabetes! Furthermore, could this not also explain jaundice in a newborn – a newborn potentially suffering from iron overload, and/or low glucose levels due to insulin production issues in the mother.
In the normal newborn, extra red blood cells were supposed to get “cast off” or “shed” at birth. The breakdown of heme resulted in the release of iron and unconjugated bilirubin – iron necessary for growth spurts and bilirubin, now known to be perhaps the most powerful antioxidant known to man. But, what happened if the newborn child had experienced a delay in the “switch” to “beta” in hemoglobin? What happened if more iron was released into a child potentially already suffering from iron overload? Would a child already having high iron levels break down those “extra cells” anyway? What happened to all those extra red blood cells in the newborn suffering from iron overload? Was this why we saw jaundice associated with Rh factor incompatibility? Could this explain the “other jaundices”? In my opinion, there was no doubt that the potential was there!
Certainly, all this was “just my theory”, yet “this theory” certainly would explain a great deal – would it not – especially given that beta-amyloid was also found in the pancreas of persons with type 2 diabetes and in the brains of persons with Alzheimer’s and that beta-amyloid was considered a “by-product” or waste that accumulated in the brain. “Waste” sounded very much to me like that could be from the “sloughing of cells” also! The fact that Alzheimer’s patients were high in spinal fluid lactoferrin (indicating a possible immune system response to iron overload) and the fact that iron was also known to accumulate in the brain, also, very much made me suspect that this too, was somehow related to issues that now so much, all seemed to fit together.
Beta amyloid… beta… type 2 diabetes…jaundice… jaundice… jaundice – liver dysfunction…iron… beta cells… insulin… the pancreas… b cells... RhoGAM… an immune system response…Rh factor incompatibility – associated with jaundice… mercury… jaundice…iron overload… sloughing of cells… gestational diabetes…delayed “switch” to beta cells in fetal hemoglobin… parallels in apoptosis of Alzheimer’s disease and bilirubin encephalopathy… jaundice…jaundice… jaundice – a sign of something going very, very wrong!
A person with Alzheimer’s would have had a fully functioning liver initially, unlike the unborn child or immature infant and as such, I understood why lactoferrin was “in excess” in patients with Alzheimer’s – this, indeed, appeared to be a possible immune system response to iron overload – something persons with Alzheimer’s also suffered from. Persons with schizophrenia obviously also had insulin related issues since “insulin treatment” for schizophrenics dated back decades!
As I thought of my son, Zachary, and that “little glucose bottle” he had been given at birth, although I was not diagnosed with gestational diabetes, clearly, there were issues with his pancreatic function from day one – of that, I had no doubt. Yet, Zachary was not “diabetic”. He had never – to my knowledge – experienced serious insulin issues, such as diabetic shock or coma. Thus, although he had “issues” with insulin levels at birth, clearly, he was not “diabetic”. But, was he more “at risk” for diabetes later on? I very much suspected he could be and as such, now limited processed sugars – allowing sugars to come almost completely from “natural sources” such as apples, bananas, etc.
As I looked back and thought about Zachary’s autism, among the many things that stood out for me were the constant bouts of diarrhea – something so common in children with autism. And now, I could not help but ask the obvious. Could there be “good diarrhea”?
Could diarrhea, for children with autism, be somehow an immune system response – the sloughing of cells - in an attempt to get rid of excess iron? Bacteria and viruses were known to thrive on iron… but not all bacteria thrived on iron. There did exist “good bacteria” in the intestines and according to Kathy Blanco’s article on iron overload, these “good bacteria” - found in Kirkman Labs products for autism – were not iron dependent. Thus, given “good bacteria” or “probiotics” such as acidophilus, did not thrive on iron, could that not mean that “bad bacteria” could be a way for the body to rid itself of iron and as such, if “bad bacteria” did “eat up iron” that could make diarrhea a “good thing” – could it not – provided the child was very closely monitored for dehydration – a potentially lethal issue if not properly monitored?
Vitamin C was also known to increase iron absorption. Tea (i.e., green tea) and calcium were known to inhibit iron absorption. Perhaps that explained why so many parents of children with autism had found a product called “Ojibwa tea” helpful. Many, many parents on both the “mercury” and “enzyme” parent discussion boards in Yahoo Groups (in my opinion – among the best sources of information for parents of children with autism) had mentioned this. Parents wanting to discuss matters relating to enzyme therapy, mercury poisoning and “options” available could get a lot of information from other families living with autism via these discussion boards. These provided a great place to go to simply – as a question.
Persons on these boards realized that with the great explosions in autism – many were new to the “autism world” and as such – no question was a “dumb question”. Parents were very understanding of newcomers on these boards. Persons wanting to read “what other parents were saying” could do so by joining these groups via: http://groups.yahoo.com/ by simply doing a search on “autism mercury” or “autism enzymes” to get to the discussion boards. No subject was off limits or “too gross to discuss” when it came to trying to “break the code” in the parent world of autism! Discussions involved everything from behavioral issues, to rashes, to “poop talk”, to things that worked and things that did not, to chelation (procedure to remove metals from the body) to supplements, etc.
Parents actually went into what could be pretty extensive discussions into matters the average person would never even think of “bringing up” in a public forum. Certainly, if this was true of one area of discussion – it had to be “poops” or “stools” in children with autism. It had been in some of these discussions that I had read of parents discussing “undigested foods” in their children with autism.
I knew there were certain foods – like corn – that Zachary had trouble digesting. But, other parents appeared to have some “much bigger” issues than corn. For example, one discussion had involved the fact that a mother stated when her child ate meat – it went through the system – almost undigested and came out at the other end – clearly evident in “what it was”.
If there was one thing that parents of children with autism had been forced to be, it certainly had to be diaper and “poop analysis” investigators given so many children with autism had such a difficult time with digestion and “potty training”. To find twelve year olds – not potty trained – was not uncommon. So, “poop analysis” it was in an attempt to “break the code” as to what was going on in the digestive system of our children.
I certainly had done my share of “poop analysis” too. I usually gave Zachary about twenty raisins with corn flakes and either a sprinkling of rice milk or water – sometimes - orange juice (since he could not drink regular milk). Recently, I noticed something I had not seen before – a few undigested, whole raisins! Given everything I now knew of iron overload in autism, I had indeed found this very interesting. Could this other mother’s undigested meat and my son’s undigested raisins have anything to do with “iron overload”. Both meat and raisins were sources of iron. Was this the body’s way of saying: “no more”? Was this an indication only of a problem in the proper balance of enzymes necessary to food breakdown or was it perhaps also an indication of an actual immune system response – that if the body had “too much iron”, it would simply “know” not to digest certain foods that could release even more iron into the body?
The reason I said that had to do with more than “just food”. When I considered the fact that the acids in the human stomach were known to be very strong and able to break down many, many things, I wondered, how was it that the body “knew” what things “not to break down”. For example, a piece of plastic could “go right through” if accidently injested… and so could a penny – although, certainly, the pennies of today were more toxic than ever and they could have some serious impacts on the system. Yet, in spite of the fact that the acids of the stomach were very strong and anything going through the digestive track was certainly put through “the ringer”, there certainly were “some things” that were not processed and simply allowed to “go through” and come out “almost intact”. Why was that? And more importantly, was this what was happening with “undigested foods”? Was the issue only one - of say - enzyme imbalance or could it also be one of an actual immune system response?
According to a publication by Kirkman Labs – a company that specialized in autism research and the making of supplements for children with autism – a publication entitled: Guide To Intestinal Health In Autism Spectrum Disorder, up to two thirds of all immune system activity occurred in the intestinal tract. So, in addition to “processing food”, could the “lack of processing” be an indication of an immune system response – in and of itself? In my opinion, that certainly could be an explanation for “undigested food” – could it not? Again – as I had done on so many occasions, I truly wondered!
Kirkman Labs’ “Guide To Intestinal Health” was a valuable resource in terms of getting to understand many of the gastrointestinal issues in autism. In the past, Kirkman Labs had provided this reference, for free downloading, online, however, it had since been removed from their website – the reason for that – I did not know. I suspected the odds were pretty good of finding parents with this document/file on parent discussion boards.
Also very informative was Kirkman Labs’ actual product catalog – providing information as to why certain products were helpful for children with autism. For new parents, this was also another good place to at least “start” to understand some of the issues. The Kirkman Labs product catalog was available via Kirkman Labs by calling 800-245-8282 in the US, or 506-694-1600. Kirkman Labs could also be found online at www.kirkmanlabs.com.
I had learned a great deal from parent discussion boards and from materials provided by Kirkman Labs. Although I did not agree one hundred percent with their products, overall, I did find Kirkman Labs products had helped Zachary tremendously. The simple fact was that each child was different, and as such, not all products worked well or in the same way for all children. There had to be some “trial and error” there. Those problems I personally had encountered with certain products, I discussed in my second book. Kirkman Labs did offer “trial sizes” for parents also. In my opinion, there was simply no denying that this company had been instrumental and invaluable in helping with Zachary’s gastrointestinal issues – issues that impacted Zachary – overall – in more than just matters relating to “eating”!
It had been on discussion boards and information from resources such as Kirkman Labs and Houston Nutraceuticals, Inc. – a maker of enzymes to help children with autism in the digestion of casein, gluten and phenols – all problem areas in autism, that I had learned about so many helpful supplements via parent discussion groups.
Kirkman Labs – a company focused on autism research and supplements for children with autism – provided an excellent buffered vitamin C supplement. Vitamin C was believed to boost the immune system, inhibit Candida growth, help with detoxification, and heal the gut. These certainly were critical functions, yet, as I thought about matters relating to vitamin C and iron absorption, again, it seemed I now had more questions than answers for Zachary.
If vitamin C increased iron absorption – was that a good thing – or a bad thing? If that iron absorption was “in bacteria, etc.” that could then later be flushed via diarrhea, then that was a good thing. But, what about increasing overall iron absorption? Surely, in children already suffering from iron overload, would that not be a “bad” thing? Once again, I seemed trapped in that “catch 22” – seeing the critical need for a product – but then, also seeing a potential downside to its use.
Recently, I had read an article on another product – zinc – so critical to enzyme functioning and so much in the body, but, yet, this particular article indicated that excess zinc could lead to plaque formation. Everything certainly was a balancing act.
I knew that the pharmaceutical industry was already moving to have supplements become “prescription items” using the argument that supplements were “overused” by the public and that therefore, this could be dangerous. Well, given that iron had been so promoted – and so misunderstood by the FDA and those making iron supplements, I had little confidence that the FDA or many doctors or scientists would recognize “problems” any better than I could. Indeed it had been the lack of understanding at the FDA and in the science community and the heavy promotion of a controlled, prescription substance – prenatal vitamins - that had gotten us in the boat in the first place!
As such, to argue that “controlling” substances such as supplements that had – forever been non-prescription - by making them only available via prescription would make us all safer – was in my opinion – a totally invalid argument to be made on the part of the FDA and/or the pharmaceutical industry.
If the body had no good way of getting rid of excess iron, and infants did not have bile to help process it, or were not breastfed or only shortly breastfed and as such, had little or no lactoferrin, was it possible that in an attempt to rid the body of excess iron, the infant produced more bacteria, bacteria that thrived on iron, and that then, the sloughing (casting off or shedding) of cells was seen in the form of “diarrhea”, perhaps flushing both iron and excess bacteria from the infant’s system or that of the young child? I knew excess iron was absorbed in the intestinal walls… but, the question thus became – was iron actually being “flushed” during bouts of diarrhea – or was it simply being recycled through the body? I had no way of knowing but it certainly would seem to make sense that if “iron was needed for bacteria and viruses to grow” that it was somehow being “used up”!
If iron was not being “flushed” in meaningful amounts, but was simply being “recycled” through the body, then diarrhea could only be making matters worse as the lining of the intestinal walls could only be getting ever more “stressed”. This was a potentially very nasty situation indeed! I had no way of knowing if iron was being shed via diarrhea.
Zachary certainly did have a lot of diarrhea and it certainly did seem to increase after I stopped breastfeeding – and diarrhea – in general – was just something we learned to “live with”. This was just another “theory” – but certainly another “theory” that made a lot of sense.
It seemed society had always seen “diarrhea” as a “bad thing” – but could it actually be a good thing? Could this not simply be another immune system response to try to clear the body of whatever ailed it? I understood fully that dehydration was a serious and valid concern in matters relating to excessive diarrhea and that this was the reason it seemed society, in general, attempted to “snuff it out” as quickly as possible via things like the BRAT diet (bananas, rice, apples, toast) to “bind up” the system – but, again, I could not help but wonder, especially given the fact that the intestines were known to be critical to iron absorption in the body, if diarrhea could also be an immune system response in the form of the sloughing of cells – a reaction to iron overload.
Vitamin C was also supposed to help inhibit certain viruses. I found it very interesting, however, that whenever I drank a lot of orange juice, I always seemed to get cold sores – viral infections. Was this due to the fact that vitamin c increased iron absorption and viruses thrived on iron? There were so many issues… some small, some huge… that all seemed to tie back to iron!
Also critical to the processing of iron, however, was the liver. There was no doubt that the liver was immature at birth – with bile being produced at only six months of age. Yet, this was the main detoxifying organ in the body – and it was this very organ that was first assaulted via vaccinations!
Jaundice was also a sign or symptom associated with hepatitis. The hepatitis b vaccine – a thimerosal or mercury containing vaccine – could be given to a newborn as young as twelve hours of age if the mother was known to have hepatitis – but, even without the presence of hepatitis in the mother – the hepatitis b vaccine was given to newborns usually within the first days immediately following birth!
As I reviewed Zachary’s immunization schedule – sure enough – at three days, then again at six weeks, then again at nine months! Three “hits” to the liver by a vaccine for a disorder – hepatitis – known to be a liver dysfunction. Three “hits” to my son’s immature liver – two of them very much before bile was even being produced! This was only for the hepatitis b shot – obviously, before six months, before bile was even produced – there had also been many “other” hsots as well – many of them – laced with mercury and aluminum! By the time Zachary was two and a half, he had received his usual toxic doses from vaccines – many of them with mercury – shown to devastate neurons by the University of Calgary video of neural degeneration due to low level mercury exposure… vaccines containing viruses… viruses now suspected of lodging and weakening glial cells – cells that provided the brain’s scaffolding… vaccines containing aluminum – a known gene mutant – vaccines, vaccines, vaccines – vaccines that had potentially exposed my son to more than one hundred times safe levels of mercury as established by the EPA, vaccines with virtually no long term studies on the effects of either mercury or viruses in the body – vaccines that had “studies” lasting only a few days to a few weeks at best!
Also interesting was the fact that the DPT vaccine contained something called procine (pig) pancreatic hydrolsate of casein. There was another familiar word – casein. Zachary had received the DTP shot at two and a half months, four months, six months, and eighteen months. Like the MMR, many parents felt the DPT shot had “caused” autism in their children. So, what exactly was that “casein pig stuff” in the DPT vaccine and how would a child whose liver was not fully functional and/or a child who had difficulty processing casein react to this? Of course, I had no idea, but this certainly was another “interesting issue”.
Iron overload… and vaccines! A stressed, immature immune system, no long-term studies into the safety of vaccines and toxin overload from the first days of life!
It seemed to me that one did not need to have any background in science to know that if the liver was immature and not yet producing bile, and that meant that the body’s main detoxifying organ was not fully functional, that we should not be assaulting that very organ from the first few days of life. And yet, that had been exactly what had been done to my son – and indeed to all children who had been vaccinated prior to six months of age.
I had not known that bile did not form until six months of age… I had not known so, so many things. Like so many other parents of children with autism, I had learned everything – the hard way. My heart seemed to melt within me! How could I have so trusted “the system” with my son – my only son – my beautiful son!
Liver dysfunction… it now seemed so obvious to me… so much now appeared to fall into place. In researching so much in terms of so many issues, I had discovered that the liver was an organ believed to be able to “regenerate”. One could actually lose eighty to ninety percent of liver function before going into “liver failure”. Yet, clearly, children with autism and persons with schizophrenia and Alzheimer’ s appeared to have many “liver dysfunctions”. I wondered, if mercury or viruses had permanently “knocked out” certain liver function. I had no way of knowing – only time would tell. So much I had once “known” to be true because of my blind trust – had come crashing down all about me!
Everyday it seemed science was disproving what those in government agencies involved in vaccination program and those in doctor’s offices and in pharmaceutical labs had told us they “knew” to be true. Research was now also showing the “cork” or “plug” in the cervical opening of a pregnant woman was more than just a mechanical barrier. It now appeared to serve protective functions for the baby as well. The results of this study were published in the July 1st, 2002 issue of the American Journal of Obstetrics and Gynecology. Science had now discovered that this “plug” contained lactoferrin (there was that word again) and human lysozyme. Lysozyme was an antibacterial agent. Lactoferrin was known to improve immune system functioning and also acted as an antibacterial agent. Lactoferrin was also known to be an antiviral agent - believed to inhibit the reproduction of viruses. Could this “plug” protect the child from hepatitis or other disorders that could be passed from mother to child during childbirth? Could this “plug” prevent a reaction in the mother and child during delivery as the blood of the two, perhaps, mixed? The more I read, the more I realized that science actually knew so little about the workings of the human body.
I had had to “guess so much” – and quite obviously, “science” in many regards was “guessing, too”!
With all these “new discoveries” in science – again – I could not help but ask: Were vaccines doing more harm than good? Perhaps, in some cases, vaccines had helped control deadly diseases, however, as a parent and member of society, I did question the aggressive vaccination policies that were now in place – especially given so many mental illness explosions. The simple fact was also that many diseases were on the decline prior to the introduction of vaccines due simply to better hygiene practices (i.e., hand washing, clean water, etc.).
Truly, with no long-term vaccine studies, how could we possibly know if the autism, schizophrenia and Alzheimer’s explosions were not linked to vaccines! The CDC - without studies - was only “guessing” that the two were not related. There were many parents and families, however, who were now “guessing” these disorders, were tied to vaccinations – and their “guesses” were often backed by family videos taken just after vaccinations – videos often showing normal children who appeared to have changed – overnight!
Man had a saying: “Seeing is believing”! Was this why the administration had attempted – though unsuccessfully - to put forth legislation that would have sealed vaccine injury lawsuit records from the public – lawsuits that could have made public such overnight changes captured by parents on video?
And now, the strong pharmaceutical industry was quick to market its new five in one vaccine as a “fewer tears” vaccine since fewer shots/needles would be needed. As the parent of a child with autism who had shed countless tears, I feared oceans more would be cried worldwide! Certainly, no one could even begin to count how many tears parents of children with autism had already shed throughout the world!
It was time tax dollars and private dollars went to truly investigating these issues – and finding the truth! Mercury and aluminum were known to accumulate in the brain. Mercury was known to suppress one’s ability to get rid of iron. Iron was known to accumulate in the brain also. These metals were also known to accumulate in the liver, kidneys and pancreas possibly causing liver failure, kidneys failure and diabetes. It was a known fact that more and more patients on dialysis for kidney problems also suffered from diabetes. Over fifteen million Americans now suffered from diabetes – one hundred and fifty million worldwide. Four million in the US had Alzheimer’s – eighteen million worldwide. Millions more had autism or schizophrenia.
If there was an autism-vaccine link, as I very much believed there was, was it not time to investigate that issue honestly via independent study?
Mercury was the second-most toxic substance known to man. A report comparing autism and mercury poisoning, Autism: A Unique Type Of Mercury Poisoning by Sallie Bernard*, Albert Enayati, B.S., Ch.E., M.S.M.E.**, Teresa Binstock, Heidi Roger, Lyn Redwood, R.N., M.S.N., C.R.N.P., Woody McGinnis, M.D. (*Contact: email@example.com, **Contact: (201) 444-7306, firstname.lastname@example.org ) when combined with the University of Calgary video, left no doubt that mercury led to autism. This report was available at the following website address:
And what about aluminum – another metal found in vaccinations - believed to be the fourth most toxic metal. It was a well-known fact that the most common types of cancer in children were cancer tumors in the brain (where mercury and aluminum accumulated) and cancer of the blood, or leukemia. It was a known fact that brain cancer and leukemia were very much on the rise in children. Cancer was a “cell mutation”. The trend figures were sobering indeed! So many children – with cancer! How could things have gotten “so bad”? Genetics or environmental factors? In my opinion, the answer now seemed rather – obvious!