That Key Word...
Beta... Beta... Beta...
If there was one word that stood out for me in everything I had researched, it had to be the word "BETA"... it seemed this word appeared almost everywhere I turned...
1. The University of Calgary video on neurodegeneration due to mercury exposure (i.e., dental amalgams and vaccines both contained mercury) clearly indicated that:
"the mercury attaches itself to the GTP site in the beta subset preventing tubulin proteins from binding together and hence this striped neurites of their supporting structure, thus resulting in the collapse of neurons. GTP provided the energy for molecules to bind together."
Refer to: Lorscheider, F.L., Syed, N.I., Leong, C.C.W., Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, Neuroreport, Vol. 12, Number 4, March 26, 2001, ISSN 0959-4965.
Note also that this article/video had the following statement in it - I quote:
"A similar in vivo molecular lesion was observed in brains of 80% of Alzheimer's disease (AD) patients, but was not seen in brains from age-matched control patients" [end of quote, reference provided by University of Calgary research team was: Pendergrass, JC, Haley, BE, Vimy, MJ, et al., NeuroToxicology 18, 315-324, 1997, this quote taken from Lorscheider, F.L., Syed, N.I., Leong, C.C.W., Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, Neuroreport, Vol. 12, Number 4, March 26, 2001, p. 733, ISSN 0959-4965].
Note: This same quote was provided on the short video that captured the effects of mercury on neurons. Although a viewer may need to "hit play" a few times to get through this video (depending on downloading capability), this short video was a "must see" for all... because as they say... a picture is worth a 1,000 words and there was simply no denying the effects of mercury on neurons... as captured... on video... for all to see!
This video could be viewed by going to:
2. What were "Beta Cells"... also known as "b cells"...
There were two types of "beta cells" from what I could find...
a. Beta cells in the pancreas that secreted insulin
b. Beta cells that were part of the white blood cells and thus had immune system functions
It certainly seemed "odd" that two types of cells had the same name. Obviously, there had to be some reason as to why these cells were given the same name but I did not know what that reason was... I suspected it had something to do with the cell structure or molecule structure, etc.
Note that in the unborn child, cells that went on to form the liver (where blood was first produced in the unborn child prior to that function migrating to the bone marrow) and cells of the pancreas developed from similar and adjacent cells.
Note that - and I quote:
"Amyloid clumps, or plaques, are also present in the brains of Alzheimer's patients and the pancreas of type 2 diabetics..." [end of quote, emphasis added, Malick, A., An Alzheimer's Advance? If Proven Effective In Clinical Trials, New Therapy could Help Millions, May 15, 2002, http://abcnews.go.com/sections/living/DailyNews/SAP_drug_alzheimers020515.html ]
My son, Zachary, a child with autism, was born "low on glucose" - a clear sign of a problem with insulin on day 1. Although I was never diagnosed with gestational diabetes, this was indicative of a problem with insulin certainly in my son... and most likely in myself as well.
Clearly, BETA cells of the pancreas certainly appeared to play a role in all this.
Also important to understand in terms of "beta cells" was the fact that insulin and iron modulated one another... and prenatal vitamins were loaded with iron.
Note the comment in this article at http://www.ironoverload.org/anemia.htm , entitled A New Perspective on Iron Deficiency, a presentation given by Roberta Crawford in June 2001 at NIH Workshop in Bethesda, MD, - I quote:
"So how much iron does the human body really need?
Iron is not excreted. The iron you absorb stays and
accumulates in storage except that you can lose one
milligram a day through hair, finger nails, skin cells and other detritus.
That is the amount needed every day to replace the loss. One milligram.
(Women in reproductive years, one and a half milligram). The RDAs or RDIs
recommended by the Food and Nutrition Board is out of date and incorrect. The
other way to lose iron, of course, is by blood loss.
... and this quote... from the research indicating that iron and insulin modulate one another... note here that iron overload can be a problem in spite of "normal saturation" levels - a condition known as insulin resistance-associated hepatic iron overload (IR-HIO)!
"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 inflammatory cytokines influence these relationships, amplifying and potentiating the initiated events. The clinical impact of these interactions depends on both the genetic predisposition and the time frame in which this network of closely related signals acts. In recent years, increased iron stores have been found to predict the development of type 2 diabetes while iron depletion was protective. Iron-induced damage might also modulate the development of chronic diabetes complications. Iron depletion has been demonstrated to be beneficial in coronary artery responses, endothelial dysfunction, insulin secretion, insulin action, and metabolic control in type 2 diabetes. Here, we show that iron modulates insulin action in healthy individuals and in patients with type 2 diabetes. The extent of this influence should be tested in large-scale clinical trials, searching for the usefulness and cost-effectiveness of therapeutic measures that decrease iron toxicity. The study of individual susceptibility and of the mechanisms that influence tissue iron deposition and damage are proposed to be valuable in anticipating and treating diabetes complications." [end of quote, emphasis added, Diabetes. 2002 Aug;51(8):2348-54.
and from the same article...
"Fourth, a novel syndrome of hepatic iron overload has been described that associates hyperferritinemia with normal transferrin saturation and is not linked to the HLA-A3 antigen, a common marker for hereditary hemochromatosis (39). This condition is known as insulin resistance-associated hepatic iron overload (IR-HIO) and combines abnormalities in iron metabolism (isolated hyperferritinemia with normal transferrin saturation), steatohepatitis, and the insulin resistance syndrome (obesity, hyperlipidemia, abnormal glucose metabolism, and hypertension) (39-41). In IR-HIO, iron overload occurs in both hepatocytes and sinusoid cells, being higher in the latter cells in 45% of cases, a finding seen in only 3% of subjects with hemochromatosis (42)." [end of quote, emphasis added, taken from an article by Jose Manuel Fernandez-Real, Abel Lopez-Bermejo, Wifredo Ricart, entitled Cross-talk between iron metabolism and diabetes (Perspectives in Diabetes), Diabetes, 51 (8): 2348-54, August, 2002, http://www.findarticles.com/cf_dls/m0922/8_51/90389345/p4/article.jhtml?term=].
Note also that according to this same article on the bi-directional relationship of iron and insulin, the following was stated:
"... iron deposition in islets, albeit variable, is restricted to [beta]-cells (28)"
[end of quote, taken from article by Jose Manuel Fernandez-Real, Abel Lopez-Bermejo, Wifredo Ricart, entitled Cross-talk between iron metabolism and diabetes (Perspectives in Diabetes), Diabetes, 51 (8): 2348-54, August, 2002, http://www.findarticles.com/cf_dls/m0922/8_51/90389345/p4/article.jhtml?term=, reference 28 was provided as follows: (28.) Rahier JR, Loozen S, Goebbels RM, Abrahem M: The hemochromatotic human pancreas: a quantitative immunohistochemical and ultrastructural study. Diabetologia 30:5-12, 1987]
Was it not also very interesting that "gestational diabetes" was diagnosed right around the same time that "Rh Factor incompatibility" was diagnosed given again the apparent implication of "BETA" cells in this "disorder", too!
" IgD is almost exclusively found inserted into the membranes of B cells, where it somehow regulates the cell's activation." [end of quote, emphasis added, B Cells and Antibodies, Understanding The Immune System, http://www.thyroid-info.com/immune/imm07.htm ]
Rh Factor incompatibility was "treated" by giving Rhogam or Rho (D) to the mother... http://www.rhogamfyi.com/rh_incompatibility.html occurred when the mother did not have IgD present (immunoglobulin D).
Note that Rhogam shots, given to the mother at week 28 of gestation and usually again within 72 hours of delivery contained MERCURY... mercury that certainly could find its way to the unborn child and to the newborn (via breastmilk).
For more on understanding Rh Factor incompatibility go to:
Note that both gestational diabetes and Rh Factor incompatibility were diagnosed right around week 28 of gestation! Just Coincidence? As clearly indicated in "book 3" (posted in full on this website), I had seen too many "coincidences" in all this! I once worked with a man who had majored in mathematics and as we once discussed "the obvious" in a work problem, he once told me that most people just "knew" that 2+2 = 4... but that he could "prove it". I would always laugh as I told him that all you need to know is that 2+2 = 4... you don't have to be able to prove it mathematically... and although I may not be a scientist, as I had stated before, neither did I need to be a fireman or a chemical engineer to know "Where There's Smoke... There's Fire".... and I now saw many "smokescreens" merging into one... with the underlying cause very much appearing to be metal toxicity (iron, aluminum, mercury, etc.)!
I could not help but wonder if iron from prenatal vitamins was somehow destroying beta cells... in both the pancreas and in the red blood cells... beta cells, it appeared to me, were very, very sensitive to metal toxicity... beta cells in the pancreas, in the blood, and in the brain (i.e., as shown in Univ. of Calgary video).
Note that the cerebellum (one of areas most impacted in autism), the amygdale (also one of areas most impacted in autism) and the hippocampus (area most impacted in Alzheimer's) were all areas known to have secretin - a hormone that was also associated with secretions from the pancreas and liver. Note again that the pancreas was involved in the production of insulin and that the liver was involved in many, many functions, including metal detox and glucose metabolism functions. The liver was also where blood was produced in the unborn child prior to that function moving to the bone marrow later in gestation. I now suspected recent secretin trials for the treatment of autism may very well be "mixed" due to something known as "insulin resistance iron overload"... for more on this particular condition, refer to the article by Jose Manuel Fernandez-Real, Abel Lopez-Bermejo, Wifredo Ricart, entitled Cross-talk between iron metabolism and diabetes (Perspectives in Diabetes), Diabetes, 51 (8): 2348-54, August, 2002, http://www.findarticles.com/cf_dls/m0922/8_51/90389345/p4/article.jhtml?term= ]
"recent studies have shown secretin to be present in the amygdala, hippocampus and cerebellum--three areas of the brain that are known to be defective in autism" [end of quote, Edelson, SM., Secretin, Center for the Study of Autism, Salem, Oregon, http://www.autism.org/secretin.html ].
Note also that mercury was known to impact beta cell functioning...
“Mercury compounds are immunomodulatory and the decrease in B-cell function indicates toxicity”! [end of quote, http://www.ephca.com/metals.htm#merc_tox ]
.... and mercury was now known to bind with cell membranes, making them more permeable and as such more susceptible to toxins and interfering with proper cell functioning... for more on this, refer to: http://www.home.earthlink.net/~berniew1/damspr19.html
Note that studies also now indicated that mothers with gestational diabetes were also more likely to go on to develop type 2 diabetes later in life.
"Five additional pieces of scientific evidence favor the hypothesis that iron plays a role in type 2 diabetes"... [end of quote, emphasis added, taken from an article by Jose Manuel Fernandez-Real, Abel Lopez-Bermejo, Wifredo Ricart, entitled Cross-talk between iron metabolism and diabetes (Perspectives in Diabetes), Diabetes, August, 2002, http://www.findarticles.com/cf_dls/m0922/8_51/90389345/p4/article.jhtml?term=].
Note also that secretin was now being studied for the treatment of schizophrenia as well as for autism and that insulin therapy had been used since the 1940s for the treatment of schizophrenia, refer to: http://www.priory.com/homol/insulin.htm .
Having researched autism, schizophrenia and Alzheimer's, I was now truly convinced that these were all one and the same disorder over the life spectrum. For the medical community to argue that these were "different" based on age of onset required something very critical - that the brain be a constant - and clearly - the brain changed greatly over the life spectrum, undergoing tremendous changes through age 6, then again at puberty, with the cerebellum maturing only after 20+ years, and for forth. To compare the brain of a newborn to that of a teenager or person in their 20s or 80s was in my opinion simply not a valid comparison to make and given the many, many parallels among these disorders and their very common history, I could not help but conclude that these were indeed one and the same - disorders caused by metal toxicity (i.e., mercury, aluminum and iron toxicity) - impacting especially beta cell functioning!
Note: autism used to be called "childhood schizophrenia"
schizophrenia used to be called "dementia praecox"
Alzheimer's used to also be called "dementia praecox"
Indeed, Alois Alzheimer's... the man credited with discovering Alzheimer's... worked for Emil Kraepelin and was considered Kraepelin's protege. Kraepelin was the man who discovered "schizophrenia".
For more on this, please see my section entitled: A Critical Lesson In History!
Note: Although amyloid plaques and neurofibrillary tangles have been the "big area of study" in Alzheimer's, research based on autopsies of normal aging has shown that amyloid plaques and neurofibrillary tangles do naturally form in the brains of normal elderly throughout the neocortex, hippocampus, and amygdala (Reisberg, 1981).
Persons interested in researching this further could do so by referring to: Reisberg, Barry, MD. (1981). Brain Failure: An Introduction to Current Concepts of Senility. New York: The Free Press. pgs. 12-37. ISBN: 0-02-926260-7.
Neurofibrillary tangles were found in other disorders as well. In other words, they were not "unique" to Alzheimer's.
Of course, there was always another way of looking at this. Given over 50% of Americans over 85 now developed Alzheimer's, perhaps "the normal brain" was now one that went on to develop Alzheimer's and that this was why we were now seeing "plaques" in "normally aging brains" also. But, then again, why was that? So, what was causing even "normal brains" to develop these amyloid plaques? Certainly this had not always been the case. It was not the "ability to view this via technology such as MRIs" that I was alluding to but rather the fact that never had so many gone on to develop Alzheimer's... regardless of the ability to "actually see the damage" to the brain or not. In the past, people simply did not forget their entire lives as they got older the way they now did with Alzheimer's! :o(
Note that the basal ganglia of persons with Alzheimer's were also found to be high in iron.
For much, much more on all this, I strongly encourage you to read: Redefining The Role Of Insulin: Could It Play A Major Role In Metal Detoxification?
The autistic child - once the forgotten child - now the key to so much!