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Autism and Alzheimer’s: Matching bookends?

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by Sandy Gottstein

Timing is everything.

On the very same day that Vaccination News posted Dr. Yazbak's latest excellent piece, Heightened Awareness Lives On, The New York Times ran an article Dementia Care Cost Is Projected to Double by 2040. Between the lifetime care needs of the growing numbers (1 in 50?) of autistic individuals, and end of life needs of those with various forms of dementia, including Alzheimer's it's hard to imagine how our society will be able to function in the not too distant future. Not only will there be growing costs associated with the care at both ends of the age scale, but fewer and fewer people able to contribute to the financing of those costs, provide the free care currently contributed, and/or able to carry on without considerable help

Unfortunately, just as with the autism issue, there seems to be little official interest in legitimately pursuing avenues that might result in liability or a decrease in profits for those potentially responsible for this looming catastrophe.

Guess that leaves those of us with only a stake in understanding the truth to ferret it out.  So, just what DO we know, not know, need to know or simply wonder about?

1)      The incidence and/or prevalence of Alzheimer’s is increasing.

2)      The incidence and/or prevalence of Autism is increasing.

3)      While acknowledging the appearance of a surge in autism numbers, many “experts”, including the CDC and NIMH apparently still believe these increases may be a result of better diagnosis and increased awareness. 

4)      While there may be some small number of inclusions of mild autism cases causing some minor increases in its incidence, you can no more miss most cases of autism than you can miss Alzheimer’s.  And those small numbers simply cannot account for the enormous increase from 1 in 10,000 to 1 in 50 in the case of autism.  As for Alzheimer’s, it never went particularly unnoticed.  It just wasn’t always counted.

5)      In both cases, exposure to neurotoxins in vaccines are at best mostly ignored as a possible source of the conditions, and at worst disdained.  Note that the CDC doesn’t even mention toxins, neuro or otherwise, or vaccines, in its list of possible causes or proposals for future study.

6)      Many studies which allegedly look at any possible connection to vaccines are apparently designed to specifically disprove a connection rather than find one.  For instance, they usually do not include those who have experienced zero of a purportedly questioned substance.  In other words, they do not have an actual control, i.e., non-intervention, group, which ultimately, in the cases of vaccines, would be those who have never been vaccinated.  (And even when they do, there are design errors [or deliberated design flaws?], that predispose to finding no differences, as in the case of this study, in which the zero vaccines group was too small.)

7)      We don’t know much about the historical incidence of Alzheimer’s. (1, 2

8)      We don’t know the historical incidence of Alzheimer’s prior to introduction of flu vaccines containing thimerosal and what we know about the incidence of autism prior to DPT shots containing it should give us pause.  (Hint:  Autism was virtually unknown and in fact was first described and diagnosed in the 1940s.   The DPT shot was also introduced and first administered in the 1940s.  The first pertussis vaccine was licensed in 1915, although the first vaccine did not contain thimerosal.)

9)       Thimerosal was introduced in the 30s. The flu vaccine was introduced in the 1940s.  It would appear to be the case that the early flu vaccine contained thimerosal, as did the DPT shot. 

10)   From what I can tell, we don’t know much about the history of flu vaccine administration or coverage.

11)   Any person who receives a flu vaccine every year receives 25 micrograms of mercury each year. 

12)   After the “ban” on thimerosal in children’s vaccines, flu vaccines containing thimerosal began to be recommended for children.  Little to no effort has been made to inform parents that thimerosal free versions are available.

13)   Before the removal of thimerosal in most children’s vaccines, children received in some cases an amount that “could have exceeded Environmental Protection Agency (EPA) standards for the first six months of life”.

14)   Unless a child gets the little-known thimerosal-free flu vaccine, they will receive 25 microgram doses, plus the “trace” amounts included in some of the other childhood vaccines every year.  As noted by former NIH head Dr. Bernadine Healy, we do not know the amount, trace or otherwise, of thimerosal or any other vaccine ingredient or combination of ingredients that may cause neurological problems in a susceptible child.

15)   One has to wonder why, when thimerosal was removed from vaccines in the recommended “schedule”, it was then put back in. 

16)   There is enough evidence that mercury in general, and the mercury in vaccines specifically, accumulates in the brain to at least be concerned.  What follows are some relevant quotes:

  1. In general, mercury in tissues and blood following TM (thimerosal) treatment was predominantly found as Ino-Hg, but a considerable amount of Et-Hg was also found in the liver and brain.
  2. The results showed that the level of mercury was higher in the liver and kidney of the inorganic mercury group than in the thiomersal exposed group. However, the brain and blood concentrations of mercury were higher in the thiomersal exposed group.
  3. In sum, both the findings from epidemiological and demographical studies, the frequency of amalgam application in industrialized countries, clinical studies, experimental studies and the dental state of AD patients in comparison to controls suggest a decisive role for inorganic mercury in the etiology of AD.
  4. Brain concentrations of total mercury were approximately 3–4 times lower in the thimerosal group than in the methylmercury group, and total mercury cleared more rapidly in the thimerosal group (with a half-life of 24.2 days versus 59.5 days). However, the proportion of inorganic mercury in the brain was much higher in the thimerosal group (21–86% of total mercury) compared to the methylmercury group (6–10%). Brain concentrations of inorganic mercury were approximately twice as high in the thimerosal group compared to the methylmercury group. Inorganic mercury remains in the brain much longer than organic mercury, with an estimated half-life of more than a year. It’s not currently known whether inorganic mercury presents any risk to the developing brain.
  5. Mercury is one of the most toxic substances known to humans. It has been introduced into the human environment and has also been widely used in medicine. Since circumstantial evidence exists that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury, we conducted a systematic review using a comprehensive search strategy. Studies were screened according to a pre-defined protocol…Thirty-two studies, out of 40 testing memory in individuals exposed to inorganic mercury, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro models showed that inorganic mercury reproduces all pathological changes seen in AD, and in animal models inorganic mercury produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that inorganic mercury may promote neurodegenerative disorders via disruption of redox regulation. Inorganic mercury may play a role as a co-factor in the development of AD. It may also increase the pathological influence of other metals. Our mechanistic model describes potential causal pathways. As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as soon as possible.
  6. Higher mercury concentrations were found in brain regions and blood of some patients with Alzheimer's disease (AD). Low levels of inorganic mercury were able to cause AD- typical nerve cell deteriorations in vitro and in animal experiments. Other metals like zinc, aluminum, copper, cadmium, manganese, iron, and chrome are not able to elicit all of these deteriorations in low levels, yet they aggravate the toxic effects of mercury (Hg)…In sum, the findings from epidemiological and demographical studies, the frequency of amalgam application in industrialized countries, clinical studies, experimental studies and the dental state of Alzheimer patients in comparison to controls suggest a decisive role for inorganic mercury in the etiology of Alzheimer's disease. Other factors currently discussed as causes (e. g. other metals, inflammations, dietetic factors, vitamin deficiency, oxidative distress, and metabolic impairments) may act as co-factors.
  7. Blood mercury levels were more than two-fold higher in AD patients as compared to both control groups (p = 0.0005, and p = 0.0000, respectively). In early onset AD patients (n = 13), blood mercury levels were almost three-fold higher as compared to controls (p = 0.0002, and p = 0.0000, respectively). These increases were unrelated to the patients' dental status. Linear regression analysis of blood mercury concentrations and CSF levels of amyloid beta-peptide (A beta) revealed a significant correlation of these measures in AD patients (n = 15, r = 0.7440, p = 0.0015, Pearson type of correlation). These results demonstrate elevated blood levels of mercury in AD, and they suggest that this increase of mercury levels is associated with high CSF levels of A beta, whereas tau levels were unrelated. Possible explanations of increased blood mercury levels in AD include yet unidentified environmental sources or release from brain tissue with the advance in neuronal death.
  8. The incidence of neurodegenerative disease like Parkinson's disease and Alzheimer's disease (AD) increases dramatically with age; only a small percentage is directly related to familial forms. The etiology of the most abundant, sporadic forms is complex and multifactorial, involving both genetic and environmental factors. Several environmental pollutants have been associated with neurodegenerative disorders. The present article focuses on results obtained in experimental neurotoxicology studies that indicate a potential pathogenic role of lead and mercury in the development of neurodegenerative diseases. Both heavy metals have been shown to interfere with a multitude of intracellular targets, thereby contributing to several pathogenic processes typical of neurodegenerative disorders, including mitochondrial dysfunction, oxidative stress, deregulation of protein turnover, and brain inflammation. Exposure to heavy metals early in development can precondition the brain for developing a neurodegenerative disease later in life. Alternatively, heavy metals can exert their adverse effects through acute neurotoxicity or through slow accumulation during prolonged periods of life. The pro-oxidant effects of heavy metals can exacerbate the age-related increase in oxidative stress that is related to the decline of the antioxidant defense systems. Brain inflammatory reactions also generate oxidative stress. Chronic inflammation can contribute to the formation of the senile plaques that are typical for AD. In accord with this view, nonsteroidal anti-inflammatory drugs and antioxidants suppress early pathogenic processes leading to Alzheimer's disease, thus decreasing the risk of developing the disease. The effects of lead and mercury were also tested in aggregating brain-cell cultures of fetal rat telencephalon, a three-dimensional brain-cell culture system. The continuous application for 10 to 50 days of non-cytotoxic concentrations of heavy metals resulted in their accumulation in brain cells and the occurrence of delayed toxic effects. When applied at non-toxic concentrations, methylmercury, the most common environmental form of mercury, becomes neurotoxic under pro-oxidant conditions. Furthermore, lead and mercury induce glial cell reactivity, a hallmark of brain inflammation. Both mercury and lead increase the expression of the amyloid precursor protein; mercury also stimulates the formation of insoluble beta-amyloid, which plays a crucial role in the pathogenesis of AD and causes oxidative stress and neurotoxicity in vitro. Taken together, a considerable body of evidence suggests that the heavy metals lead and mercury contribute to the etiology of neurodegenerative diseases and emphasizes the importance of taking preventive measures in this regard.  

Although not everyone would agree, e.g.: “Since brain mercury concentrations from deceased subjects with either Alzheimer's disease or multiple sclerosis are not significantly higher than controls, the present study provides no scientific support that mercury plays a significant role in the pathogenesis of these neurologic disorders.“, most would concede that mercury is likely a problem.

17)   And then there is aluminum, an adjuvant also found in many vaccines: Aluminium is a trivalent cation that does not undergo redox changes. It has, nonetheless, been implicated in a variety of neurological disorders that have been associated with an increase in the formation of reactive oxygen species (ROS). The exact mechanism of aluminium toxicity is not known. However, accumulating evidence suggests that the metal can potentiate oxidative and inflammatory events, leading to tissue damage. A review of the epidemiological and clinical evidence linking aluminium to Alzheimer's disease (AD) is presented. The article discusses the role of aluminium in two mechanisms that have been linked to neurodegenerative disorders, including AD. Studies are summarized that describe how aluminium can potentiate iron-induced oxidative events. Involvement of aluminium in inflammatory responses, mediated by interleukins and other inflammatory cytokines, is also discussed. Although a direct relationship between aluminium and AD has not been clearly demonstrated, a detailed mechanistic basis for the hypothesis that aluminium may exacerbate events associated with AD is clearly emerging. The results discussed here have broad implications for the role played by aluminium and other metals in neurodegenerative diseases, and suggest that long-term exposure to supra-physiological amounts these metals should be avoided.

18)   The idea that there is no “evidence of harm” from thimerosal is false.  (See, for instance, the list of studies I once compiled that only goes to February 2011.)

19)   The idea that there is no connection between flu shots/mercury and Alzheimer’s is false.  (See, for instance, the previously quoted studies as well as Dr. Hugh Fudenberg.)

20)   Irony of ironies, the flu vaccine may not particularly work (1, 2) , especially in the elderly.  

The world is facing a crisis of epidemic proportions. Declarations of thimerosal and other vaccine ingredients’ innocence, based on industry-funded and/or otherwise influenced “research”, must be challenged.  Ad hominem platitudes, attacks and derision aimed at so-called “anti-vaccinationists” (who are in fact mostly heart-broken former pro-vaccinationists), must be scorned.  Outright rejection of anecdotal evidence (i.e., observation, a cornerstone of scientific enquiry), particularly in the face of the enormous amount of it, must stop.  The humiliation of those who dare to even mention temporal connections between vaccines and various adverse events must cease.

Efforts to disprove, rather than discover, connections, no matter how unpalatable they might be, must end.  Honest, no-holds-barred attempts to understand what causes Alzheimer’s and autism must begin in earnest. 

Properly designed studies which compare the vaccinated to the never-vaccinated must be conducted.

The time has come to stop believing the excuses, dissembling, and sleight of hand.  The time has come to open our eyes, our minds, and, no less our hearts. 

The time has come for the public to understand that when they are told the benefits of vaccines outweigh the risks, that they are the ones mostly taking the risks while the vaccine manufacturers are the ones mostly reaping the benefits. 

There are clues, it would seem, in these matching bookends, one young, one old.  We need to dust them off and look them straight in the eye.

Our future depends on it. 

Sandy Gottstein 

Date: 4-9-2013

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“Eternal vigilance is the price of liberty.” – Wendell Phillips (1811-1884), paraphrasing John Philpot Curran