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Return To Book 3 Table Of Contents More Pieces To The Puzzle… Iron, Mercury, Sulfur, Fetal Hemoglobin, Heme Deficiency, Aluminum, Insulin, Gestational Diabetes, and B6 Bilirubin was a by-product that resulted from the breakdown of hemoglobin – specifically – what was known as the “heme” part of the hemoglobin. Hemoglobin was the oxygen carrying protein found in red blood cells. Hemoglobin appeared to be made of two proteins – the heme and the globin. Heme was made of iron plus unconjugated bilirubin (lipid/fat soluble). The following website, called “Heavy Metal Toxicology” by Dr. Theodore B. Hoekman provided for families a great overview of the detrimental effects of mercury – as well as many other metals: http://www.luminet.net/~wenonah/hydro/heavmet.htm. According to this site, hemoglobin, the oxygen carrying protein in red blood cells, consisted of the following: (C738 H1,166 Fe N203 O208 S2)4. Also according to this very informative site were the following statements: “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, emphasis added: Dr. Theodore B. Hoekman, Heavy Metal Toxicology, http://www.luminet.net/~wenonah/hydro/heavmet.htm]. Thus, from this site I learned that mercury loved sulfur – something critical to the proper functioning of blood, proteins and enzymes and that it appeared to attack antibodies because they, too, contained sulfur! This told me that mercury specifically attacked the blood, the immune system and anything havind to do with enzymes or proteins having sulfur. From what I could see, many scientists were raising issues as they related to mercury and sulfur. Indeed, Kirkman Labs, a maker of supplements specifically for persons with autism, had products to help boost sulfur levels also. Mercury… sulfur… enzymes… proteins… antibodies… all terms I had now seen over and over again in my journey with “autism”. Globin was a protein that surrounded the heme and hence the combined name – hemoglobin. Although there were literally thousands of sites on hemoglobin synthesis/production, the following site, http://sickle.bwh.harvard.edu/hbsynthesis.html, provided a good overview of this process. According to this site, both proteins – heme and globin – had to be present for hemoglobin to properly pick up and carry oxygen to other cells. Heme… globin… both proteins… both parts to hemoglobin… both… potentially… very targeted my mercury! Very interesting, however, was a another comment that had captured my attention on this same site, http://sickle.bwh.harvard.edu/hbsynthesis.html, a comment stating that prior to birth, something known as “beta protein” was not expressed in embryonic or fetal hemoglobin. It appeared that proteins could be alpha, beta or gamma. Yet, in the fetus, the alpha combined with the gamma. In the adult, the alpha combined with the beta. Gamma was a fetal protein only that seemed to substitute for the “beta” protein prior to birth. “Beta not expressed in fetal hemoglobin” – I was not sure as to exactly what that meant because other studies seemed to indicate that in a normal fetus, 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. In an article entitled “Delay in the fetal globin switch in infants of diabetic mothers” by SP Perrine, MF Greene, and DV Faller in the New England Journal of Medicine, Volume 312:334-338, February 7, 1985, Number 6, http://content.nejm.org/cgi/content/short/312/6/334, indicated that “switch to normal hemoglobin”was tied to insulin levels. In fetal environments that had been considered hyperglycemic due to the fact that the mother was diabetic, the normal switch to increased beta-globin was delayed. The beginning of this article talked about the normal fetus switch from fetal hemoglobin to normal hemoglobin as occurring at twenty eight to thirty four weeks of gestation. Yet, the end of the article seemed to indicate an increase in beta-globin production should be occurring between thirty six to thirty nine weeks of gestation. Perhaps the “beta not expressed in fetal hemoglobin” referred to the fact that beta was only present in small amounts until that thirty six to thirty nine week of gestation period – at which time the levels seemed to increase. Perrine also found the switch to “beta” blood to be related to “specific globin DNA hypomethylation” according to information provided on the following website: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2449361&dopt=Abstract. Hypomethylation appeared to be a process tied to increased cell mutations as this process appeared to turn genes “on or off”. Hypomethylation was also something very much associated with Downs Syndrome, a disorder where an entire chromosome duplicated itself – although not in an “exact match”. So much appeared to tie back to the blood… as such, I looked for more answers in matters relating to the blood. An article entitled The Synthesis of Hemoglobin, by Jay Gardner, Jeri Kalogeras, Vish Raj at http://www.molbio.princeton.edu/courses/mb427/1999/projects/9908/Synthesis.html, also referencing http://sickle.bwh.harvard.edu/menu_sickle.html, studies appeared to indicate that fetal hemoglobin could persist in fairly significant levels in the body for seven to eight months after birth. Well, needless to say, given my son had been low on “glucose levels” at birth and had been given a “special little glucose or sugar bottle”, and given that most children with autism seemed to show signs right around one and a half years of age, and given that “fetal alpha-beta blood switch” could be delayed, I had found this all very, very interesting! Of course, there was still more to this wonderful puzzle I had once only known as - “autism”. In no time at all I had found what appeared to be yet another critical key – again – tied to insulin and week twenty-eight of life in the womb for the unborn child! At week twenty-eight, lung formation in the unborn child underwent major changes. I quote from but one of many sources I had found on lung development in the unborn child: “The Saccular Period… this begins at about 28 weeks of gestation and is associated with striking changes in the appearance of the lung. There is a marked decrease in the prominence of the interstitial tissue and the airspace walls become narrower and more compact. There is a sudden increase in lung volume and surface area. There is a prenatal phase of alveolar development in the human. Alveoli appear in some lungs as early as 32 weeks gestation and are present in all by 36 weeks. Starting as early as 30 weeks but nearly always before 36 weeks, the subsaccules become alveoli. At term gestation about 50 million alveoli are present. At birth there is a comparative slowing in the development of alveoli during the first 3 months. But later, there is a rapid increase in alveolar number during the first year of life, reaching approximately the adult number of 300 million by 3 years of age. Female infants have a lower incidence of RDS than males, suggesting that the lungs of female infants are functionally and structurally more mature. However, these differences between male and female infants are not significant. During childhood, these differences between male and female infants do become significant. After 2 years of age, males have larger lung volumes than females”. [end of quote, emphasis added, Pulmonary Function In Newborn, Division of Neonatology, Cedars-Sinai Medical Center, LA, CA, http://www.neonatology.org/syllabus/pulmonary.html]. Well… was this not all very fascinating? Again, this sure seemed to be putting a lot of pieces into place. If indeed insulin levels were tied to the development of the lungs in the unborn child, and the mother’s insulin levels – as in the case of gestational diabetes – could delay the switchover to “beta blood” – a switch that happened at exactly the same time in gestation as did this surge in lung development, would it not stand to reason that insulin levels would also impact or delay the unborn child’s lung development? Interestingly, I was obviously not the only one that suspected insulin levels had something to do with lung development. I quote: “…term infants of women with gestational diabetes tend to have delayed lung development and an increased incidence of RDS. It has been hypothesized that the fetal hyperinsulinemia frequently observed in these infants delays fetal lung development in utero. Surfactant is comprised of both lipid and protein components. The surfactant proteins (SP-A, SP-B, and SP-C) are required for the proper surface tension-lowering properties of pulmonary surfactant. The most abundant surfactant protein, SP-A, also serves a role in regulating surfactant homeostasis in the alveolus and in local immune function. We have shown that insulin decreases SP-A protein and mRNA levels…it is known that several hormones, in particular glucocorticoids and insulin, regulate fetal lung development… The results of our studies have elucidated pathophysiologic and molecular mechanisms by which hyperinsulinemia in the fetus of the gestational diabetic may inhibit fetal lung maturation.” [end of quote, emphasis added, Jeanne M. Snyder, Ph.D. Insulin Regulation of Gene Expression in Fetal Lung Tissue, University of Iowa, http://uiderc.icva.gov/Abstracts/snyder_j.htm]. If a child was not producing enough beta-globin, would that mean that the child’s hemoglobin, after birth, would not be providing enough oxygen to the cells in the body, thus leading to cell death? Normal hemoglobin required 2 alpha and 2 beta after birth, but, what if beta levels were too low? Would this not generate an immune system response of some kind? What was the impact of all this on the immune system and on the proper production and functioning of blood? What if the lungs were not properly developed? Would that not result in “oxidative stress”? Given that the lungs and blood were very closely related when it came to providing oxygen to the rest of the body, if the “switch” to alpha-beta blood was delayed, would lung development be delayed in a similar way or length of time in order to “match up” lung and blood development? I was starting to believe that indeed, this may be the case and that although children could be “full term”, their lungs could very well be “under-developed” at birth. When it came to oxygenation of the newborn, there was another area of concern that was now being raised by both parents and doctors – premature cord clamping. Cord clamping protocols appeared to have changed over time. It used to be that the cord of the infant was not clamped for a couple of minutes after birth, allowing the newborn child to continue to receive oxygen via the umbilical cord. Current practices appeared to reveal that doctors could be clamping the umbilical cord too early after delivery. Persons looking into this issue stated that past practices allowed for approximately two minutes prior to the clamping of the cord, but that now, the cord was clamped almost immediately. Researchers were not sure as to what actually caused a child to take his first breath. There were many theories on this subject. Many appeared to indicate or hypothesize that “air hunger” caused a “gasping reflex” in the child. Other “shock factors” were believed to include sudden exposure to the cold air, light, noise, gravity, etc. The startle/Moro reflex" could perhaps also play a role as it appeared to be “the perfect motion for expanding the lungs . . . the arms flung wide and then retracted” as described in this easy to read article at http://www.geocities.com/virtualbirth/archives/fetalcrc2.html on cord clamping issues and the importance of the umbilical cord in the newborn. This site same site provided some rather interesting comments when it came to understanding the many issues behind cord clamping. Some of these comments included the following: 1. “Again, there is no evidence to support the belief that it is safe to sever the umbilical cord within seconds or even minutes after birth. It would be nice if medical science could explore this key question, but until research provides answers, we need to err on the side of caution. Some things that research can tell us about premature cord cutting - it deprives the baby of valuable blood volume, and it deprives the baby of long-term iron stores. Here are some references: Cord Closure: Can Hasty Clamping Injure the Newborn? George M. Morley, MB., CH. B, C July 1998 OBG Management.”[ Excerpts from this article were available at: http://www.gentlebirth.org/archives/pulmperfusion.html] 2. “Nature assumes that babies are born vaginally, which involves a rather tight squeeze on the baby's chest. This helps to remove fluid from the lungs so they can expand more easily at birth. However, the role of the vaginal birth itself is minor compared to the role that labor plays. Even women planning a surgical birth should be informed that their baby will breathe more easily if some labor is experienced.” It is also important to provide accurate information about the effect that drugs have on the baby's respiration. "Shallow, ineffective respirations may occur in infants who are depressed as a result of maternal drugs or anesthesia. These gasping, irregular respirations may be insufficient to properly expand the lungs." This is such a serious problem that Narcan (stands for Narcotic Antagonist) is routinely used at births where mothers have received narcotics during labor.” 3. “Summarizing current research on the timing of cutting the cord, Enkin et al. in _A Guide to Effective Care in Pregnancy & Childbirth, (2nd ed)_ write on p. 239: "Active management of the third stage of labour usually entails clamping and dividing the umbilical cord relatively early, before beginning controlled cord traction. Pre-emptying physiological equilibration of the blood volume within the fetoplacental unit in this way may predispose to retained placenta, postpartum haemorrhage, fetomaternal transfusion, and a variety of unwanted effects in the neonate, respiratory distress in particular. Delayed cord clamping results in a placental transfusion to the baby varying between 20 and 50 per cent of neonatal blood volume, depending on when the cord is clamped, at what level the baby is held before clamping, and whether oxytocics have been administered." 4. “Research tells us that immediate clamping of the umbilical cord is actively harmful to the baby, and responsible practitioners everywhere must work to change their own practices and educate their peers.” 5. “I think the following statement can stand on its own merit, without benefit of research: "Newborns in respiratory distress are most in need of continuing oxygen supply from the umbilical cord." Yet these are the newborns whose cords are likely to be cut most quickly. Why is this so? It is simply because the newborn resuscitation equipment is across the room rather than immediately accessible at the bedside.” 6. “There is not much research about the effects of epidurals on newborn breathing, but we do have numerous studies showing that epidurals interfere with the hormonal parade of normal labor and birth. In particular, we know that epidural anesthesia blocks the production of endorphins and adrenaline in the mother's system, which also prevents them from being passed through to the baby. This hormone deficit may explain the latching and nursing problems that nurses and lactation consultants are reporting in babies born to mothers with epidurals. It seems logical to assume that babies who are having trouble nursing probably had trouble with the once-in-a-lifetime challenge of jumpstarting respiration.” 7. “I have heard rumors that cutting the cord represents a legal cutting of the obstetrician's responsibility for the newborn's treatment. This is the best explanation for why distressed newborns have the umbilical cord cut most quickly, but I truly do not want to believe that an entire medical system is built on the premise that limiting legal liability is more important than providing the best possible care to newborns” End of quotes [1 –7] taken from Midwife Archives, compiled and maintained by Ronnie Falcao, http://www.geocities.com/virtualbirth/archives/fetalcrc2.html. More on the issue of the detrimental effects of cord clamping and the implications for the newborn infant could be read at: http://www.cordclamping.com/. I often spoke with my husband about those things I was researching. When I spoke to him about the issue of premature cord clamping, my husband, a man who had attended agricultural college, told me the following. In animals, such as cows, during the birth process, when the animal being born passes over the pelvic area of the mother, the umbilical cord was immediately severed. This created an automatic “gasping” reflex in the calf. As such, if the birth was a “breach”, farmers had to “pull the calf” quickly in order to prevent fluid from entering its lungs. Usually, a “breach” calf had to be “held upside down” in order to remove the fluid from the lungs. As we discussed this issue, and my husband began to walk away with his cup of coffee in hand, as he reminisced about those days on the farm, he laughed as he stated: “That’s one of the basics you are taught in agricultural college… I’ve had to hang a lot of calves in my life… all farmers know that… it’s interesting that animals have a very thin cord that severs rather easily but that the cord of humans is actually quite thick and hard to sever off…” There could be no denying that the “put the baby upside down” position certainly was also considered normal protocol in humans as well. Yet, more interesting than the hanging of calves upside down to empty the fluid from their lungs was the comment as it related to the “gasping reflex” that occurred immediately upon the severing of the cord. That certainly was interesting. In my entire life, I could honestly say I had never seen an umbilical cord still attached to the mother when kittens or dogs were born, for example. Animals, by nature, did not have the luxury of having someone there to assist in the birthing process and as such, it made sense that there had to be some mechanism in place to sever mother and baby in the animal kingdom. Of course it made perfect sense that the cord of a human child would be harder to sever off in order to better protect the child (normal or breach birth) and provide a mechanism for receiving valuable oxygen in the first few minutes after birth until the lungs were functioning properly. As such, in the first few minutes of life, I supposed one could think of the umbilical cord as a most valuable “backup system” for oxygenation of the child, a mechanism that provided several minutes of oxygen – allowing enough time to get the lungs going in a normal child. There was a tremendous amount of blood in the umbilical cord during the birth process – by some estimates, anywhere from 20% to 40% of the infant’s blood could be in the umbilical cord during the birth process and this blood was very “oxygen rich”. This too, of course, made perfect sense given that the delivery process could take several hours. The “gasping reflex” in calves upon the severing of the cord was rather interesting. Although science still did not agree as to what exactly “caused” an infant to take his first breath, a “gasping reflex” of some kind when the cord was cut certainly would make sense. Well, again, this certainly was all very, very interesting, as was an article entitled Pulmonary Function In Newborn, Division of Neonatology on the website for Cedars-Sinai Medical Center in LA, http://www.neonatology.org/syllabus/pulmonary.html, an article that provided another little bit of information that was of particular interest to me – regarding something that had to do with - “nasal flaring and grunting”. Recently, “grunting” was a behavior I had come to notice occurring a little more frequently in Zachary. In addition, Zachary had always been “a sniffer”. According to this article, Pulmonary Function In Newborn, under the section entitled: Clinical Assessment of Pulmonary Function, the following was stated – I quote: “Five common presenting physical signs relay indirect information regarding pulmonary function. These are respiratory rate, retractions, nasal flaring, grunting, and cyanosis… nasal flaring is another sign of respiratory distress frequently observed in infants… grunting… with normal breathing the vocal cords abduct during inspiration and adduct (without any sound) during expiration. When respiratory function is disrupted, the work of breathing is greatly increased, and neonates attempt to compensate by closing their vocal cords during expiration. Expiration through partially closed vocal cords produces the grunting sound. Grunting may either be intermittent or continuous depending on the severity of the lung disease. During the initial phase of expiration, the infant closes the glottis, holds air in the lungs, and produces an elevated transpulmonary pressure in the absence of airflow. During the last part of the expiratory phase, gas is expelled from the lungs against partially closed vocal cords, causing an audible grunt. It is not actually the grunt, then, that produces the elevated transpulmonary pressure, but the ability of the infant to partially close the vocal cords after end inspiration. During the expiratory phase, when the vocal cords are partially or completely closed, there is an improved ventilation/perfusion ratio because of increased airway pressure and increased lung volume. The end result of this airway closure may be an impairment in gas exchange”. [end of quote, emphasis added, Pulmonary Function In Newborn, Division of Neonatology, Cedars-Sinai Medical Center, Los Angeles, CA, http://www.neonatology.org/syllabus/pulmonary.html]. If the child was born with immature lungs, what would happen in terms of the flow of oxygen in that child? It appeared the above was stating that the child often compensated by “closing the vocal cords” in order to breathe better. If that was indeed the case, could this explain why so many children with autism were non-verbal? Could they be closing their vocal cords in order to breathe better? It certainly would be interesting to see how many children who were non-verbal showed signs of “grunting”! And if that child was given vaccines very early on, how did that play into all this given vaccines had toxins in them? Would vaccines not contribute to “additional” stress for the child when it came to providing oxygen to the brain and other key organs? Hemoglobin – or blood - was the body’s way of getting oxygen from the lungs to all cells. I did a little more research as it related specifically to hemoglobin… and soon discovered on the National Institute Of Environmental Health Sciences website a reference to an article by Bruce Ames entitled: Heme Deficiency In Neurons Causes Metabolic Disruptions Similar To Alzheimer’s Disease. The citation for the short reference on this website was as follows: Atamna, H, Killileas DW, Killilea AN, Ames, BN. Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23): 14807-12. Needless to say this was all – again - very interesting given that the young infant may have a delay in that switch from “gamma” to “beta” hemoglobin if the mother had gestational diabetes and mercury was known to target sulfur – found in blood, enzymes, proteins and antibodies. Gestational diabetes was – after all – an immune system response. Thus, surely this had some implications – especially for children with autism who had been born to mothers who had were known to have had gestational diabetes and anyone who had received mercury-laced vaccines or dental amalgams (“silver fillings). I now very much suspected that this had implications for many others as well since I suspected many could have suffered from iron overload due to prenatal vitamins, etc. and as such had a dysfunctional liver and pancreas from very early on. These three paragraph that followed were taken directly – and in full – from information provided on the website of the National Institute of Environmental Health Sciences at http://www.niehs.nih.gov/dert/profiles/hilites/2002/heme.htm, paragraphs that appeared to have been taken directly from the referenced research article cited below the quotation: “Background: Normal aging of the brain and neurodegenerative changes share certain pathological and physiological changes including mitochondrial dysfunction, oxidative stress, and loss of iron homeostasis. Heme synthesis also declines with age. Heme is the major intracellular functional form of iron. It is synthesized in the mitochondria and the decline in synthesis could explain the loss of iron homeostasis in aging. Heme functions in hemoglobin and in a variety of enzymes as well as promoting the growth of nervous tissue. Advance: To further investigate the role of heme in nerve cell function, these investigators induced heme deficiency in a nerve cell culture system. Heme deficiency was detrimental to normal mitochondrial function, stimulated oxidative stress by activating nitric oxide synthase, altered amyloid proteins, and inhibited zinc and iron homeostasis. The metabolic changes seen during the heme deficiency were similar to those in dysfunction neurons in patients with Alzheimer's disease. Implication: Common reasons for heme deficiency are iron and vitamin B6 deficiencies, aging, and exposure to toxic metals such as aluminum. In addition, degradation of heme by heme oxygenase, which increases with age and in the brains of Alzheimer's patients, may be a factor in changes in the metabolism of iron and heme with age. Therefore, heme deficiency may be an important and preventable part of the neurodegenerative process, which deserves more research and attention.” [end of quote, emphasis added: Atamna H, Killilea DW, Killilea AN, Ames BN. Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14807-12.” Note that in this article – aluminum – was also mentioned. Aluminum was a known gene mutant found in vaccinations. Thus, not only did it appear that children could be born with problems due to improper insulin levels (i.e., Zachary’s little glucose bottle at birth) and immature lungs (dependent on the proper balance of insulin levels for lung maturation), but, now, aluminum, found in vaccines, could also lead to heme deficiency – a problem with the proper production of blood – the very source of oxygen for all cells in the body! I now suspected that gestational diabetes or mothers with insulin regulation problems as well as infant glucose levels at birth could be among the best predictors of children “at risk for autism”… truly a frightening thought given approximately four percent of women now developed gestational diabetes in pregnancy! Thus, again, more pieces to this amazing puzzle of “autism” certainly were falling quickly into place! According to another website I had found, aluminum was also very much a concern since the FDA had never tested aluminum for safety and there apparently existed no limitation on the amount of aluminum that could be “used” in products. Again, I quote: “Aluminum has been exempted from tesitng for safety by the FDA under a convoluted logic wherein it is classified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety and there are NO restrictions whatever on the amount or use of aluminum.” [end of quote, emphasis added: Aluminum Toxicity information compiled and submitted by Frank Hartman and available at: http://www.luminet.net/~wenonah/hydro/al.htm#toxic, the website of Dr. Dr. Theodore B. Hoekman]. This research, referenced above, by Atamna H, Killilea DW, Killilea AN, Ames BN. Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14807-12, was showing heme deficiency could be having some major implications. Aluminum… B6, iron… zinc, oxidative stress, nitric oxide, altered amyloid proteins, mitochondria dysfunction, metabolic changes… all things that by now, had become all too familiar to me! Iron… part of the “heme” in hemoglobin… something also found in prenatal vitamins. In looking at iron issues, there was one thing I had definitely come to see - that determining whether or not was suffering from iron deficiency or iron overload was a rather confusing task. It appeared that in some tests, one could be shown as “iron deficient”, and that in others, one could be shown as having “iron overload”. Although iron, vitamin B6 and aluminum, could cause heme deficiency, clearly, in Alzheimer’s and autism, many studies indicated “iron overload” – not iron deficiency. In my opinion, that left vitamin B6 (known to be very deficient in children with autism) or aluminum as “potential culprits” for heme deficiency… or potentially, a delay in that “switch” to “normal blood” in infants due to improper insulin levels in the mother or unborn child. For me, the question now became, how did iron levels change over time… from fetal – through fetal development – to birth, and then from infant development through Alzheimer’s – and what impact did this have on system functions – brain and body? Vitamin B6 deficiency was also very, key. B group vitamin deficiencies were certainly known to exist in autism and Alzheimer’s. Also interesting, however, was the comment under the “Advance” paragraph – stating that heme deficiency somehow activated nitric oxide synthase (NOS) – implicated in the production of nitric oxide – a gas neurotransmitter found in the body. Nitric oxide synthase (NOS) was found in rather high concentration in the cerebellum – that very part of the brain so clearly found to be implicated in autism. Excessive nitric oxide levels were associated with cell death! Looking at iron metabolism and iron levels – in my opinion – these were indeed – key! But, how did iron levels relate to vitamin B6? I knew B6 therapy had been heavily promoted by Dr. Bernard Rimland who had for so long pioneered work in the understanding of autism. Well, again, it did not take much time, before I understood the B6 and iron connection! In an article written by Paul Holman M.A., M.B., B.Chir., M.R.C.Psych., on the subject of Vitamin B6, http://www.acnem.org/journal/14-1_july_1995/pyridoxine-vitamin_b6.htm, the following comment was made – and again – I quote: “Vitamin B6 promotes iron excretion and this has been used as a rationale for treatment in iron storage diseases”. [end of quote – emphasis added - Paul Holman Vitamin Pyridoxine – Vitamin B6, http://www.acnem.org/journal/14-1_july_1995/pyridoxine-vitamin_b6.htm]. Well, the pieces of the puzzle were certainly starting to fall into place… There were now so many issues to think about… gestational diabetes… heme deficiency… iron overload… B6… and on… and on… and on. No studies on aluminum… no studies on mercury… very short term studies on vaccines…
Where had been the studies on the safety of iron in pregnant women – in the general population? Call me “suspicious”, but I “suspected” that again, perhaps there had been – none!
If studies did exist for iron levels, had these only been studies lasting a few days or weeks also? Or worse, had daily iron requirements simply been “guesses” as to the amount of iron needed by a woman during pregnancy? The FDA had “guessed” that mercury and aluminum were safe – why not guess that “iron” was “safe too” – after all – all three substances were known toxins in the world of science. If the FDA saw one as “safe” – based on who knows what criteria – I had no doubt that in their “genius”, they could potentially see all as “safe”.
Iron, aluminum and mercury – all toxic substances that “built up” in the body given that the body had no good way of “flushing them”.
When it came to iron, this was especially true in men since they had no menstrual cycle as did women.
And, where were the studies on iron as it related to doses in prenatal vitamins for pregnant women? Was iron content the reason for which so many women seemed to have problems tolerating these vitamins? Was iron content the reason so many women now had miscarriages? Had studies taken into consideration the fact that the menstrual flow no longer occurred in a pregnant woman – and as such, she retained an additional fourteen to twenty eight mg of iron per month – the amount of iron thought to be released via the monthly menstrual flow. Prenatal vitamins were not “custom made”. What was the impact of retaining an extra fourteen mg of iron per month verses an extra twenty-eight mg of iron per month? The menstrual flow was not a particularly “hot topic” among men. Given the majority of scientists were men, especially as we went back further in time – when iron requirements would have been determined – could that all important source of extra iron – the menstrual flow cessation in gestation – have been overlooked? Given so much in so many areas had been “overlooked” by the FDA, I very much suspected there had been “negligence” in several areas. That certainly made me wonder – “what else” – the FDA had missed. My confidence in this organization in its role as “protector” for the public had gone completely out the window!
If extra iron was no longer being “flushed” via the menstrual flow, was iron not accumulating in the pregnant woman – month after month after month? Did it not make sense that – just perhaps – this had been the body’s natural mechanism for providing iron to the unborn child and – just perhaps – not that much excess iron was needed in the form of supplements during gestation? Where were the studies looking at the effects of iron supplements in pregnant women in relation to calcium supplementation and the possible effects on the unborn child in terms of “iron metabolism” in various stages of gestation?
Estimates for iron intake, form what I had found, appeared to vary a little with recommended daily intake for pregnant women being anywhere from twenty two – thirty six mg of iron. A recent conversation with my sister – now pregnant – made me have even greater concerns. When I had discussed my suspicions of “too much iron” in prenatal vitamins with my sister, she naturally checked the iron content on her bottle and stated it provided sixty mg of iron! Granted, I had not seen the bottle myself, but, I did ask my sister to repeat the amount of iron in her prenatal vitamins and twice she stated it was a whopping sixty mg “per serving”!
One gram of iron was enough to cause severe poisoning in a child under two. Three grams were considered lethal. Over the course of pregnancy, it certainly appeared that via prenatal vitamins alone, women could be exposed to unsafe levels of iron!
Obviously, the amount of iron needed by a pregnant woman, it seemed logical, should depend on iron stores in the body for each individual woman. Yet, at no time in my particular pregnancy had I ever been told “how much iron I needed” – for me – personally. In addition, all women were pretty well given the same prescription and dosage for prenatal vitamins. Did that, not again, seem rather odd given that iron could be toxic and that women varied in “how much iron” they had stored up in their bodies?
Vitamin C was known to increase iron absorption. Red meat, fish, poultry… all these were now known to be sources of iron or to play a role in iron metabolism. But other foods were believed to interfere with iron absorption – these included vegetables (high in phenols), tea and coffee, soy and foods that were rich in - calcium! Bananas, apples, raisins and tomatoes - I also knew to be high in phenols – and Zachary had always very difficult time with these foods.
Iron… calcium… milk…vegetables… phenols…iron …heme iron…calcium…milk… - casein – the “milk protein” Zachary could not digest!
Women were told to drink lots of milk while pregnant or to take calcium supplements – that calcium was needed for proper bone health. Calcium and tea were both known to inhibit the absorption of iron.
During the third trimester, it was believed that the calcium in the mother was passed in greater amounts to the unborn child as it began to develop and strengthen its bone structure. Thus, it was believed that if the mother had inadequate stores of calcium, the unborn child would “draw the calcium” from the mother’s bones and that, was believed to be bad for the mother’s bone health in future years.
Iron… calcium… known to inhibit iron absorption… third trimester… gestational diabetes… switch to alpha-beta blood in the unborn child… twenty eight weeks…delayed by abnormal insulin levels… Zachary’s little glucose bottle… As I thought about that little glucose bottle my son had been given at birth, and the fact that insulin production was known to be abnormal in autism, Alzheimer’s and schizophrenia, I wondered how this all fit together. Glucose was considered one of the only sources of energy for the brain. In schizophrenia, insulin therapy had been done since the 1940s, giving persons suffering from schizophrenia more insulin. Insulin was a hormone secreted by the beta cells of the islets of Langerhans found in the pancreas and promoted the utilization of glucose. Pretty well every woman who became pregnant in the US was now tested for gestational diabetes. Gestational diabetes occurred when women with no prior history of diabetes developed high blood sugar levels during pregnancy. In the US, it was estimated that up to one hundred and thirty five thousand women developed gestational diabetes each year. In gestational diabetes, hormones blocked the mother’s ability to make use of her insulin leading to a condition known as insulin resistance. As such, mothers needed up to three times normal insulin levels. If the body could not produce enough insulin, this led to a build up of glucose levels in the blood – a condition known as hyperglycemia. Interestingly, gestational diabetes developed during pregnancy – usually between weeks twenty- four and twenty eight and generally subsided after the birth of the child. It was estimated that one in twenty pregnant women developed gestational diabetes. It was also estimated that up to fifty percent of women with gestational diabetes would go on to develop type 2 diabetes later in life – usually within the next ten to fifteen years! A mother with gestational diabetes had a pancreas working “overtime” to produce more insulin. Yet, that insulin did not lower blood sugar levels and although insulin did not cross the placenta, glucose, apparently did, resulting in elevated fetal glucose levels. As a result of high glucose levels in the fetus, the baby’s pancreas now went into “overdrive” too – making extra insulin to get rid of the high glucose now found in the fetus. Due to the fact that the unborn child of a mother with gestational diabetes had to produce excess insulin, these newborns could have low blood glucose levels at birth. These children were then at risk for obesity and type 2 diabetes. The condition known as hyperinsulinism resulted when there was an excessive amount of insulin, caused by overproduction of insulin by the beta cells of the islets of Langerhans in the pancreas or by an excessive dose of insulin. Hyperinsulinism could cause hypoglycemia - low blood-glucose levels. There was that word again – beta! Beta… beta… beta!!! Beta-amyloid was known to accumulate in the brain of persons with Alzheimer’s and in the pancreas of those with type 2 diabetes! Diabetes was an immune system problem. In type 1 diabetes, now known as “juvenile diabetes” because it occurred primarily in the younger population, the pancreas failed completely in the production of insulin. Insulin… glucose… Zachary’s little glucose bottle… glucose… the brain’s energy… gestational diabetes… switch to alpha-beta blood in the unborn child…at twenty eight weeks… known to be delayed to thirty six to thirty nine weeks in women with gestational diabetes having high insulin levels… heme… heme deficiency… heme iron… iron… calcium…calcium - known to inhibit iron absorption but needed in third trimester for bone development in the unborn child… gestational diabetes…iron overload… gestational diabetes… occurring between twenty four and twenty eight weeks of pregnancy… third trimester… forty weeks of gestation… divided by three trimesters… equals thirteen and one third weeks per trimester… equals twenty six and two thirds weeks for the completion of two trimesters… equals exactly the “midpoint” for the development of gestational diabetes… the “switch” to alpha-beta blood… at twenty eight weeks… insulin… known to impact “the switch”… B6… known to play a role in insulin production… B6… associated with heme deficiency… B6… known to promote iron excretion… calcium… known to inhibit iron absorption! As calcium left the mother and went to the unborn child, was iron overload in the mother triggering gestational diabetes? It certainly appeared to be a very good possibility! Was it possible that women suffered from iron overload… that the immune system response involved the pancreas and “beta cells” that were involved in the production of insulin… and that this helped the mother’s immune system to guard itself against iron overload… but that, at least in the first two trimesters, the unborn child could have potentially suffered from iron overload as excess iron passed from the mother to the child… and that then, at the time of the third trimester, as calcium intake increased in the unborn child for bone growth…that iron intake was “slowed” in the unborn child as calcium interfered with the absorption of iron during the last stages of development within the womb… but that iron absorption – at the same time – increased in the mother as calcium left her body. At birth, given the child had experienced a significant “calcium intake” in the third trimester, could iron levels have been seen as “normal” in the infant at birth? As the child then shed extra red blood cells – a process that naturally occurred after birth, were iron levels once again becoming excessive in the child as excess red blood cells were cast off releasing iron and bilirubin (a powerful antioxidant) into the blood for both growth spurts and the protection of the child’s immune system? If iron levels were indeed excessive, would that not result in “jaundice” – an immune system response? And, if that “switch” to beta blood in the infant was delayed – in any way - what were the implications from an iron metabolism, heme production, mitochondria dysfunction (where heme is synthesized) perspective as well as from an immune system perspective given that the “beta” part to blood was part of the “globin” part to blood – and that had to do with the immune system! And what about mercury’s role in attacking the blood, enzymes, proteins and immune system antibodies containing sulfur? Children with autism were known to have a “hypogammaglobulnemias”… what exactly that was, I did not know… but, it certainly sounded like something having to do with “gamma”… “globin”… and maybe iron (given that anemia was associated with both iron deficiency and iron overlaod) – although perhaps, in this term, it simply meant low in “gammaglobulins”. “Gamma globulins” and the fetal “2 alpha + 2 gamma” blood may be related somehow… but, it appeared that these “gammas” - “gamma globulins” and “fetal gamma blood” were different. Gamma globulins appeared to be “part” of normal blood. Most antibodies in the blood appeared to be “gamma globulins”. They became “more abundant” after infections. This site, by Kenneth R. Bridges, M.D., provided one of the best information sources I had seen on the subject of “beta blood”. It was written in a way that I could certainly at least grasp some key pieces to the puzzle… http://sickle.bwh.harvard.edu/hbsynthesis.html. The notation at the bottom of this link was as follows: “For more information, see "Hemoglobin: molecular, genetic, and clinical aspects", Bunn and Forget, Saunders, 1986.” If indeed the “switch” to “beta globin” blood was delayed in some of these children, what did that mean? How long would it take for that “switch” to happen in these children? How long was the “total switchover” supposed to take? How long was it taking in these children of diabetic mothers? What about mothers who had been “borderline diabetic” in pregnancy? What were the impacts of the delay in this “swith” on iron metabolism, oxygen transport, hemoglobin production, and most importantly, on immune system functions and immune system responses to things such as “iron overload”, mercury and - aluminum… known to lead to heme deficiency! The fact that a mother’s breastmilk only contained one half to one mg of iron per liter told me that an infant really did not need “that much” iron. Indeed, studies indicated that one gram of iron was enough to do damage in terms of iron poisoning in a child under the age of two – and three grams was considered a lethal dose! As I thought about matters relating to iron overload, I could not help but think of my young nephew, Andrew, diagnosed with PDD (Pervasive Developmental Disorder – a disorder on the autism spectrum). Excess iron was known to accumulate in the liver and the heart. Andrew had been born with heart problems. At age five, he had undergone open-heart surgery. At birth, he suffered from jaundice and had to be placed under those special lights for close to a week. I recalled how as a young child, he had showed me “his zipper” as he lifted his shirt, showing me his chest after he had returned home from surgery – “the zipper” - the markings left by stitches that went from the top of his chest down. My sister-in-law, Christine, and her husband had also gone through so much. The heart… the liver… jaundice… iron overload… had excess iron caused Andrew’s heart problems while he was still in the womb or shortly after birth? Again, I could not help but wonder! This was all very interesting to me. In my heart, in knew all of this was very much related. Certainly - “in my heart” - was rather “unscientific”… but, there were simply too many coincidences here! I knew I did not have the understanding I needed to have of all these issues – I would be the first to admit that – but I also knew that all this just had to be related… the metabolism of iron… the impact of calcium intake… gestational diabetes… the switch to “normal blood”… insulin delaying “that switch”… the timing of the switch… the timing of gestational diabetes… and of the “third trimester” bone development needs of the unborn child…heme… iron plus unconjugated bilirubin… bilirubin - the most powerful antioxidant known to man… jaundice… an indication of something going wrong…and on and on and on… Heme was made up of iron and unconjugated bilirubin. Bilirubin was fat-soluble. Beta protein was absent in fetal hemoglobin. Beta production in the fetus was delayed if the mother had diabetes. Insulin was produced by beta cells in the pancreas. Beta protein… beta protein… beta protein… beta… beta… beta… could this “beta” have anything to do with the “beta-amyloid” found in Alzheimer’s? Did it explain my son’s low glucose levels at birth? Although I did not personally have diabetes there had been a lot of diabetes in my father’s family. My paternal grandmother and at least three of my uncles on my father’s side had suffered from diabetes. Given beta-amyloid was tied to both Alzheimer’s and type 2 diabetes, I had a strong suspicion that all this was indeed inter-related! An article entitled “An Alzheimer’s Advance? If Proven Effective In Clinical Trials, New Therapy Could Help Millions” by Dr. Amy Malick, PhD, the full text of which was available at at http://abcnews.go.com/sections/living/DailyNews/SAP_drug_alzheimers020515.html, stated the following: “The treatment, called CPHPC, is aimed at preventing and potentially reversing the abnormal deposits of amyloid proteins that are a hallmark of several rare diseases called “amyloidoses”, and which are present in the more common Alzheimer’s and diabetes. In the amyloidosis diseases, which affect approximately one of every 100,000 Americans, clumps of amyloid protein accumulate and clog up organs throughout the body, causing them to malfunction and become diseased. Areas of the body most severely affected by these deposits are the heart, kidneys, brain and digestive tract, leading to problems such as stroke, malnutrition, and heart and kidney failure. Amyloid clumps, or plaques, are also present in the brains of Alzheimer’s patients and the pancreases of type 2 diabetics, though it is not known if these protein deposits have a direct role in the cause of disease symptoms, or if they are simply by-products of an as yet unknown tissue destroying process” [end of quote, emphasis added: Dr. Amy Malick, If Proven Effective In Clinical Trials, New Therapy Could Help Millions” available at http://abcnews.go.com/sections/living/DailyNews/SAP_drug_alzheimers020515.html]. The article went on to state that four million Americans now had Alzheimer’s and more than fifteen million had type 2 diabetes! Interestingly, however, was “where” amyloid protein accumulates the most – the heart, kidneys, brain, pancreas and digestive track – definitely places in the body that were also impacted by excess iron! Other sources put the statistics a little higher, indicating that slightly over six percent of the US population has diabetes. One in every four hundred to five hundred children and adolescents had Type 1 diabetes – now known as “juvenile diabetes” because it occurred in children and young adults. Juvenile diabetes was considered an autoimmune system disorder. In juvenile diabetes, the beta cells in the pancreas were destroyed and thus, the person afflicted by this autoimmune system disorder was unable to produce insulin. As such, they became “insulin dependent” – requiring up to several injections of insulin per day. The company most known for producing insulin to diabetics – was also the company that had first put mercury in vaccines – Eli Lilly! My desire to understand the workings of human blood as it related to heme had led me down a path that now included issues of diabetes as I came to understand that the composition of fetal blood changed just prior to birth from gamma to beta proteins. Although this was, in my view, a critical piece to the puzzle, a puzzle that to me, seemed to have pieces that now broke into even smaller pieces, and thus made the puzzle harder to complete, I now saw that I had to “backtrack” and understand the infant immune system a little more. Although autism, schizophrenia and Alzheimer’s were generally thought of as “neurological” disorders – disorders of the brain, the more I researched, the more I truly came to see these as “immune system dysfunction” disorders. There was no denying that there were neurological impacts in all these disorders, but it now seemed that the root cause of the “neurological disorders” were truly rooted in problems with the immune system whereby the immune system either failed to accomplish a function it needed to accomplish and/or it resulted in the system almost “attacking itself”. The way a disorder was classified had tremendous impacts in terms of how it was studied. To classify disorders as “neurological” implied they were, primarily, disorders of the brain. As such, the focus of study would tend to be on the brain. To classify these as immune system disorders, however, would place the focus on the immune system and that was exactly where it belonged! Currently, these disorders were all considered “neurological” as opposed to disorders of the immune system. Yet, it was a known fact that in Alzheimer’s and autism, enzymes were not working properly and those enzymes were associated with the liver, pancreas and blood. When cells started to break down either in form (physical structures) or function (the way they worked), this was indicative of an immune system problem – and as such, once again, that put vaccines squarely in the middle of matters relating to these disorders because vaccines were given to generate an immune system response. With so many parents of children with autism pointing the finger to vaccines as the cause of autism in their injury, more than ever, there was no denying that the vaccine link to these disorders now had to be truly and seriously investigated. If autism, Alzheimer’s and schizophrenia were immune system disorders, then, what was going on in the immune system to cause such devastation? In autism and Alzheimer’s, I knew there were problems with enzymes not working. Children with autism could not properly digest casein (milk protein) and gluten (grain protein). The brain of persons with Alzheimer’s, I now knew, had excess levels of casein kinase 1. But, how did all this fit together? I had to go back to the basics. What were the basics of the immune system – the very basics? If I were a person who knew basically nothing about the immune system – where would I start? Autism – a problem with a milk protein – a problem with a milk protein – milk - breastmilk! |
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