OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000

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Offline phasma

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Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Oct;27(10):1380-404.

Dietary exposure to metals and other elements in the 2006 UK Total Diet Study and some trends over the last 30 years.
Rose M, Baxter M, Brereton N, Baskaran C.

The Food and Environment Research Agency, Sand Hutton, York YO41 1LZ, UK. martin.rose@fera.gsi.gov.uk

Abstract
Concentrations of 24 elements including metals in the 2006 UK Total Diet Study (TDS) were measured and dietary exposures estimated. Composite samples for the 20 TDS food groups (bread, fish, fruit, etc.) were collected from 24 UK towns and analysed for their levels of aluminium, antimony, arsenic, barium, bismuth, cadmium, chromium, copper, germanium, indium, lead, manganese, mercury, molybdenum, nickel, palladium, platinum, rhodium, ruthenium, selenium, strontium, thallium, tin, and zinc. Concentrations of each of the elements in the food groups were lower than or similar to those reported in the previous TDS survey, conducted in 2000, with the exception of aluminium, barium, and manganese.
Dietary exposures to the 24 elements were estimated for UK consumers and compared with previous estimates made over the last 30 years in order to examine any trends in exposure to these elements in the typical UK diet. Population exposures to the elements have generally declined over time, and exposures to most of these elements remain at low levels. The independent UK Government scientific Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment (COT) commented on the estimated dietary exposures, taking into account their previous evaluations (in 2003 and 2008), and identified no major concerns for the health of consumers, but did advise that there was a need for more information on aluminium and barium, and also commented that dietary exposure to inorganic arsenic and to lead should continue to be reduced.
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Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #1 on: November 26, 2010, 06:30:58 am »
is this not proof? the only elements to be on the rise are the ones we know to be associated with chemtrail spraying? Surely, this is some kinda evidence?

I just emailed the papers author and asked for a full copy of the paper and asked why they thought these two elements might be up, and offered to share some info with him, should he be interested.
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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #2 on: November 26, 2010, 06:36:30 am »
A Very important story !

Please re-post this story on the Backup forum Global Gulag a.s.a.p. ?

We few, we happy few, we band of brothers; For he today that sheds his blood with me, Shall be my brother;

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Offline feeditup

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #3 on: November 26, 2010, 06:36:38 am »
Keep us updated man.
Facebook is the Barn of the sheep, time to break in, Tare some f**king wool up

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #4 on: November 26, 2010, 06:38:02 am »
Massive implications
We few, we happy few, we band of brothers; For he today that sheds his blood with me, Shall be my brother;

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Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #5 on: November 26, 2010, 06:40:39 am »
Will do EG - IF it will let me on - would'nt last time.

Will post ANY response I get and i`ll keep digging throu pubmed to see what else I can unearth.
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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #6 on: November 26, 2010, 06:59:15 am »
COMMITTEE ON TOXICITY OF CHEMICALS IN FOOD, CONSUMER
PRODUCTS AND THE ENVIRONMENT
COT Statement on the 2006 UK Total Diet Study of Metals and Other
Elements

http://cot.food.gov.uk/pdfs/cotstatementtds200808.pdf

Issue
1. The Food Standards Agency (FSA) has completed a survey of aluminium,
antimony, arsenic, barium, bismuth, cadmium, chromium, copper, germanium,
indium, lead, manganese, mercury, molybdenum, nickel, palladium, platinum,
rhodium, ruthenium, selenium, strontium, thallium, tin and zinc in the 2006 Total Diet
Study (TDS). The results provide up to date information on the concentrations of
these elements in foods and were used to estimate dietary exposures for UK
consumers. The Committee was asked to comment on the survey results and assess
if the levels of any of the elements in the diet posed a risk to human health. The COT
last evaluated population and consumer exposures to twelve of these elements
(aluminium, arsenic, cadmium, chromium, copper, lead, manganese, mercury, nickel,
selenium, tin and zinc) in 2003, using data from the 2000 TDS1. Eleven other
elements (antimony, barium, bismuth, germanium, molybdenum, palladium, platinum,
rhodium, ruthenium, strontium and thallium) were last analysed in the 1994 TDS and
evaluated by the COT in 19982; and indium was included for the first time in the 2006
TDS.

5. At present there are no specific limits on the levels of trace elements, minerals
or other micronutrients that may be contained in supplements sold under food law,
although the EU is currently in the process of setting maximum permitted levels for
vitamins and minerals in dietary supplements. Industry guidance on upper levels of
vitamins and minerals is available for manufacturers of supplements to ensure levels
are not excessive. However, the supplements industry is not obliged to follow this
guidance and is only bound by the provisions of the Food Safety Act, which make it
an offence to offer for sale a food product that is injurious to health

8. Most of the food groups had aluminium concentrations lower than or similar to
those reported in the 2000 TDS, the exceptions being bread, meat products, and
other vegetables groups. The miscellaneous cereals group had the highest mean
concentration of aluminium (17.5 mg/kg), although this was lower than the
concentration in the 2000 TDS (19 mg/kg). The miscellaneous cereals group was the
main contributor to the population dietary exposure (42%) to aluminium. Possible
sources of aluminium in this food group include aluminium compounds present
naturally, aluminium-containing additives, and contamination from processing and
storage of food in aluminium-containing utensils.
9. Barium concentrations were similar to or lower than those reported in the 1994
TDS except for the nuts group, in which the mean concentration was 131 mg/kg
compared to 56 mg/kg in 1994.

school children, young people, institutionalised elderly and vegetarian groups; and
mean-level intake for pre-school children) exceeded the PTWI set by the JECFA and
the EFSA (equivalent to 143 μg/kg body weight/day) by up to 2.4-fold. The current
average population exposure to aluminium (5.4 mg/day) was increased compared to
that reported in the 2000 and 1997 total diet studies (4.7 mg/day and 3.4 mg/day,
respectively) but lower than previous estimates (10 mg/day and 11 mg/day in 1991
and 1994, respectively).

Barium
34. Barium occurs in nature as a divalent cation in combination with other
elements. The two most prevalent naturally occurring barium ores are barium
sulphate and barium carbonate36. Barium sulphate is present in soils but only a
limited amount accumulates in plants. The main route of exposure to barium
compounds for the general population is oral intake via drinking water and food, with
food being the primary source36. Where barium levels in water are high, associated
10
with groundwater of low pH, drinking water may contribute significantly to barium
intake27. No data are available on levels of barium in drinking water in the UK.
35. Case reports indicated that in humans, intentional or accidental ingestion of
barium can cause gastroenteritis, hypokalaemia and hypertension. The WHO
considered that the critical end-points for deriving a TDI for barium are hypertension
and impaired renal function36. Hypertensive effects have been observed in humans
who ingested acute high doses of barium compounds and in workers who inhaled
barium carbonate and dusts of barium ores. Hypertension has also been reported in
rats exposed to barium chloride in drinking-water for 1 month at an estimated daily
dose of 7.1 mg barium/kg body weight. Drinking water studies in rats and mice also
indicated the kidney to be a sensitive target organ, with a lowest identified NOAEL of
45 mg/kg body weight in female rats given barium chloride in drinking water for 2
years. The WHO identified a NOAEL of 0.21 mg barium/kg body weight/day from a
10-week experimental study in humans (barium chloride in drinking water up to 10
mg/L) and an epidemiological study in populations living in communities with mean
drinking water barium concentrations of 0.1 and 7.3 mg/L. Blood pressures were not
significantly affected by barium exposure in either study. Applying an uncertainty
factor of 10 to the NOAEL to allow for database deficiencies and differences between
adults and children resulted in derivation of a TDI of 20 μg/kg body weight36. The
WHO assigned medium confidence to this tolerable intake because neither study
identified a LOAEL, and noted that there were uncertainties about the most sensitive
toxic end-point in humans, and about whether there were differences in toxicity or
toxicokinetics between adults and children.

37. As with the results from 1994, the highest levels of barium in the 2006 survey
were reported in nuts (131 mg/kg) and bread (0.81 mg/kg). All other foodstuffs
contained lower levels than in bread. Levels of barium in nuts were double those
reported in 1994 (131 mg/kg and 56 mg/kg, respectively). Estimated average
population dietary exposures to barium have increased by approximately 46% since
the last TDS in 1994.

BARIUM UP 46% ! ALUMINIUM ABOVE SET EXPOSURE LEVELS !
Things are not what they appear to be: nor are they otherwise - Surangama Sutra

Offline citizenx

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #7 on: November 26, 2010, 07:00:53 am »
Now, do the PTB want these particular substances in our bodies, and if so, why?

Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #8 on: November 26, 2010, 07:02:41 am »
Well, given they are in chemtrails - i guess they do want them in there.

Maybe because of the illness and morbidity that results

More off the wall ideas are to do with making us receptive to EM / HF radio waves.
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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #9 on: November 26, 2010, 07:05:40 am »
OH SH!T ! This is way worse than I imagined:

SINGLE MOST IMPORTANT SENTENCE RIGHT HERE

Consumption of tap water has the potential to increase high-level exposure to barium by 60-130%, which could result in a total

dietary exposure for high-level intake in pre-school children of 980% of the WHO TDI.
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Offline citizenx

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #10 on: November 26, 2010, 07:09:01 am »
Maybe they keep dumping substances like Barium on us, is specifically becasue they do not usually bioaccumulate -- unless you are continually absorbing/ingensting them!

I hate to say, but Barium (atomic weight 56) is a "heavy metal" and toxic, though some people are affected by it and not others.  It is selective.  I think the most logical purppose is depopulation.

From Wikipedia:

Precautions
Soluble barium compounds are poisonous. At low doses, barium acts as a muscle stimulant, whereas higher doses affect the nervous system, causing cardiac irregularities, tremors, weakness, anxiety, dyspnea and paralysis. This may be due to its ability to block potassium ion channels which are critical to the proper function of the nervous system.[11] However, individual responses to barium salts vary widely, with some being able to handle barium nitrate casually without problems, and others becoming ill from working with it in small quantities. Barium acetate was used by Marie Robards to poison her father in Texas in 1993. She was tried and convicted in 1996.[
12]

[edit] Non-toxicity of barium sulfate
Because it is highly insoluble in water as well as stomach acids, barium sulfate can be taken orally. It is eliminated completely from the digestive tract. Unlike other heavy metals, barium does not bioaccumulate.

http://en.wikipedia.org/wiki/Barium

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Bottom line:  they can kill off only a percent of the population with Barium, as opposed to the whole human race, and when they stop dumping it, the effects will be completely stopped.

Strategic depopulation is the most logical reason for releasing these substances in he environment.

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Re. aluminum

From wikipedia again:

Health concerns
Despite its natural abundance, aluminium has no known function in living cells and presents some toxic effects in elevated concentrations. Its toxicity can be traced to deposition in bone and the central nervous system, which is particularly increased in patients with reduced renal function. Because aluminium competes with calcium for absorption, increased amounts of dietary aluminium may contribute to the reduced skeletal mineralization (osteopenia) observed in preterm infants and infants with growth retardation. In very high doses, aluminium can cause neurotoxicity, and is associated with altered function of the blood-brain barrier.[61] A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium, such as deodorants or antacids. In those without allergies, aluminium is not as toxic as heavy metals, but there is evidence of some toxicity if it is consumed in excessive amounts.[62] Although the use of aluminium cookware has not been shown to lead to aluminium toxicity in general, excessive consumption of antacids containing aluminium compounds and excessive use of aluminium-containing antiperspirants provide more significant exposure levels. Studies have shown that consumption of acidic foods or liquids with aluminium significantly increases aluminium absorption,[63] and maltol has been shown to increase the accumulation of aluminium in nervous and osseus tissue.[64] Furthermore, aluminium increases estrogen-related gene expression in human breast cancer cells cultured in the laboratory.[65] The estrogen-like effects of these salts have led to their classification as a metalloestrogen.

Because of its potentially toxic effects, aluminium's use in some antiperspirants, dyes (such as aluminium lake), and food additives is controversial. Although there is little evidence that normal exposure to aluminium presents a risk to healthy adults,[66] several studies point to risks associated with increased exposure to the metal.[67] Aluminium in food may be absorbed more than aluminium from water.[68] Some researchers have expressed concerns that the aluminium in antiperspirants may increase the risk of breast cancer,[69] and aluminium has controversially been implicated as a factor in Alzheimer's disease.[70] The Camelford water pollution incident involved a number of people consuming aluminium sulfate. Investigations of the long-term health effects are still ongoing, but elevated brain aluminium concentrations have been found in post-mortem examinations of victims who have later died, and further research to determine if there is a link with cerebral amyloid angiopathy has been commissioned.

According to The Alzheimer's Society, the overwhelming medical and scientific opinion is that studies have not convincingly demonstrated a causal relationship between aluminium and Alzheimer's disease.[72] Nevertheless, some studies, such as those on the PAQUID cohort,[73] cite aluminium exposure as a risk factor for Alzheimer's disease. Some brain plaques have been found to contain increased levels of the metal.[74] Research in this area has been inconclusive; aluminium accumulation may be a consequence of the disease rather than a causal agent. In any event, if there is any toxicity of aluminium, it must be via a very specific mechanism, since total human exposure to the element in the form of naturally occurring clay in soil and dust is enormously large over a lifetime.[75][76] Scientific consensus does not yet exist about whether aluminium exposure could directly increase the risk of Alzheimer's disease.[72]

Effect on plants
Aluminium is primary among the factors that reduce plant growth on acid soils. Although it is generally harmless to plant growth in pH-neutral soils, the concentration in acid soils of toxic Al3+ cations increases and disturbs root growth and function
.[77][78][79]

Most acid soils are saturated with aluminium rather than hydrogen ions. The acidity of the soil is therefore a result of hydrolysis of aluminium compounds.[80] This concept of "corrected lime potential"[81] to define the degree of base saturation in soils became the basis for procedures now used in soil testing laboratories to determine the "lime requirement"[82] of soils.[83]

Wheat's adaptation to allow aluminium tolerance is such that the aluminium induces a release of organic compounds that bind to the harmful aluminium cations. Sorghum is believed to have the same tolerance mechanism. The first gene for aluminium tolerance has been identified in wheat. It was shown that sorghum's aluminium tolerance is controlled by a single gene, as for wheat.[84] This is not the case in all plants
.

http://en.wikipedia.org/wiki/Aluminium
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So, Al is also a toxin and neurotoxin as well as being an agent to acidify soil so as to destroy crops potentially, especially if those plants are particulary genetically susceptible.  (Think GMO food combined with chemtrail acidification...)



Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #11 on: November 26, 2010, 07:21:15 am »
The guy replied me! He kindly sent me the whole paper - anyone, am i able to copy / paste the entire thing in or not? its in pdf format - no url, so can`t put up a link
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Offline citizenx

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #12 on: November 26, 2010, 07:26:49 am »
http://emedicine.medscape.com/article/165315-overview

eMedicine Specialties > Emergency Medicine > Toxicology
Toxicity, Aluminum
Author: Jose F Bernardo, MD, MPH, FASN, Assistant Professor, Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh
Coauthor(s): Michael R Edwards, MD, Medical Director, Department of Emergency Services, Beebe Medical Center; Barbara Barnett, MD, Associate Program Director, Assistant Professor, Department of Emergency Medicine, Albert Einstein College of Medicine
Contributor Information and Disclosures

Updated: Aug 4, 2010

Print ThisEmail This
Overview
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Learn about an FDA approved treatment option.
Get the facts Introduction
Background
Aluminum is a trivalent cation found in its ionic form in most kinds of animal and plant tissues and in natural waters everywhere.1 It is the third most prevalent element and the most abundant metal in the earth's crust, representing approximately 8% of total mineral components.2 Due to its reactivity, aluminum in nature is found only in combination with other elements.

Dietary aluminum is ubiquitous but in such small quantities that it is not a significant source of concern in persons with normal elimination capacity. Urban water supplies may contain a greater concentration because water is usually treated with aluminum before becoming part of the supply. Subsequent purification processes that remove organic compounds take away many of the same compounds that bind the element in its free state, further increasing aluminum concentration.

All metals can cause disease through excess. In addition, essential metals can affect the human body in the case of deficiency or imbalance.3 Malabsorption through diarrheal states can result in essential metal and trace element deficiencies. Toxic effects are dependent upon the amount of metal ingested, entry rate, tissue distribution, concentration achieved, and excretion rate. Mechanisms of toxicity include inhibition of enzyme activity and protein synthesis, alterations in nucleic acid function, and changes in cell membrane permeability.
No known physiologic need exists for aluminum; however, because of its atomic size and electric charge (0.051 nm and 3+, respectively), it is sometimes a competitive inhibitor of several essential elements of similar characteristics, such as magnesium (0.066 nm, 2+), calcium (0.099 nm, 2+), and iron (0.064 nm, 3+). At physiological pH, aluminum forms a barely soluble Al(OH)3 that can be easily dissolved by minor changes in the acidity of the media.2

Approximately 95% of an aluminum load becomes bound to transferrin and albumin intravascularly and is then eliminated renally. In healthy subjects, only 0.3% of orally administered aluminum is absorbed via the GI tract and the kidneys effectively eliminate aluminum from the human body. It is only when the GI barrier is bypassed, such as intravenous infusion or in the presence of advanced renal dysfunction, that aluminum has the potential to accumulate. As an example, with intravenously infused aluminum, 40% is retained in adults and up to 75% is retained in neonates.4

Mayor et al suggested that parathyroid hormone may increase intestinal absorption of aluminum.5

Up to this time, no biological function has been attributed to this metal, and, more importantly, aluminum accumulation in tissues and organs results in their dysfunction and toxicity.2 Aluminum is absorbed from the GI tract in the form of oral phosphate-binding agents (aluminum hydroxide), parenterally via immunizations, via dialysate on patients on dialysis or total parenteral nutrition (TPN) contamination, via the urinary mucosa through bladder irrigation, and transdermally in antiperspirants. Lactate, citrate, and ascorbate all facilitate GI absorption. If a significant load exceeds the body's excretory capacity, the excess is deposited in various tissues, including bone, brain, liver, heart, spleen, and muscle. This accumulation causes morbidity and mortality through various mechanisms.

Pathophysiology
Aluminum toxicity is usually found in patients with impaired renal function. Acute intoxication is extremely rare; however, in persons in whom aluminum clearance is impaired, it can be a significant source of pathology. Aluminum toxicity was originally described in the mid-to-late 1970s in a series of patients in Newcastle, England, through an associated osteomalacic dialysis osteodystrophy that appeared to reverse itself upon changing of the dialysate water to deionized water (ie, aluminum-depleted water).

Previously, the only known dialysis-associated bone disease was osteitis fibrosa cystica, which was the result of abnormalities in vitamin D production that resulted in a secondary hyperparathyroidism, increased bone turnover, and subsequent peritrabecular fibrosis. In aluminum-related bone disease, the predominant features are defective mineralization and osteomalacia that result from excessive deposits at the site of osteoid mineralization, where calcium would normally be placed.

Since the role of aluminum in disease has been identified, more attention has been paid to the element, leading to its recognition in several other processes. For example, among patients with osteomalacia, there has been a closely associated dialysis encephalopathy, which is thought to be caused by aluminum deposition in the brain. Aluminum brain concentrations should be lower than 2 μg/g.6 A 10-fold increase in aluminum concentrations was reported in patients with aluminum intoxication through the use of hemodialysis solutions with high levels of aluminum.7

Aluminum causes an oxidative stress within brain tissue.8 Since the elimination half-life of aluminum from the human brain is 7 years, this can result in cumulative damage via the element's interference with neurofilament axonal transport and neurofilament assembly. Some experts believe it plays a role in leading to the formation of Alzheimer-like neurofibrillary tangles. Blaylock et al suggest that the heterogeneous symptoms of autism spectrum disorders have a connection with dysregulation of glutamatergic neurotransmission in the brain along with enhancement of excitatory receptor function by proinflammatory immune cytokines as the underlying pathophysiological process.9
 
In this regard, dietary excitotoxins including aluminum can exacerbate the clinical presentation by worsening of excitotoxicity and by microglial priming. This opens the discussion to the use of nutritional factors that reduce excitotoxicity and brain inflammation as a maneuver to alleviate neurotoxic effects of aluminum.10,11 The central nervous system appears to be extremely sensitive to metal-induced oxidative stress. High aluminum concentrations have been found in postmortem brain specimens of patients with Parkinson's disease and on animals models where administration of aluminum caused a strong decrease in dopamine content of the striatum.12

Aluminum also has a direct effect on hematopoiesis. Excess aluminum has been shown to induce microcytic anemia. Daily injections of aluminum into rabbits produced severe anemia within 2-3 weeks. The findings were very similar to those found in patients suffering from lead poisoning.

Aluminum may cause anemia through decreased heme synthesis, decreased globulin synthesis, and increased hemolysis. Aluminum may also have a direct effect on iron metabolism: it influences absorption of iron via the intestine, it hinders iron's transport in the serum, and it displaces iron's binding to transferrin. Patients with anemia from aluminum toxicity often have increased reticulocyte counts, decreased mean corpuscular volume, and mean corpuscular hemoglobin.

Other organic manifestations of aluminum intoxication have been proposed, such as a slightly poorer immunologic response to infection, but the mechanism by which it exerts its effect is complex and multifactorial. It has also been linked to vaccine-associated macrophagic myofasciitis and chronic fatigue syndrome, thus highlighting the potential dangers associated with aluminum-containing adjuvants as described recently.13

Frequency
United States
The actual incidence of aluminum toxicity is unknown. The greatest incidence is observed in patients with any degree of renal insufficiency. A higher incidence is observed in populations who have aluminum-contaminated dialysate or who are taking daily oral phosphate-binding agents. Patients who require long-term TPN are at increased risk as well.

Brown et al determined the potential for aluminum toxicity caused by parenteral nutrition in patients (n=36; age 50.4±20.4 y, weight 90.2±32.8 kg) who have risk factors of both acute kidney injury and parenteral nutrition support.4 Aluminum exposure was determined for each patient by multiplying the volume of each parenteral nutrition component by its concentration of aluminum. The initial serum urea nitrogen and serum creatinine levels were 47±23 and 3.3 ± 1.4 mg/dL, respectively. Twelve patients received supportive dialysis. The mean aluminum exposure was 3.8±2 μg/kg/day in the 36 patients; the majority of patients, 29 out of 36, had safe calculated aluminum exposure (<5 μg/kg/d), and 7 had high calculated aluminum exposure (>5 μg/kg/d). Patients with high aluminum exposure received more aluminum from calcium gluconate compared with those who had safe aluminum exposure (357±182 vs 250±56 μg/d).

Brown et al concluded that, using their calculations, most patients with acute kidney injury who require parenteral nutrition do not receive excessive exposure to aluminum from the parenteral nutrition formulation. The limitation of the study was its retrospective design, which resulted in calculated versus direct measurement of aluminum.

Animal studies in rats and case reports have implicated the use of oral aluminum-containing antacids during pregnancy as a possible cause for abnormal fetal neurologic development.14,15

Potential additional sources of increased chances for contamination are as follows: (1) a role for fatty acids common in food as factors that lead to an increase of the paracellular absorption of aluminum16 ; (2) advances in nanotechnology have led to the exposure of humans to engineered aluminum nanomaterials (NMs) that could potentially induce genomic changes. (By using a rat model, Balasubramanyam et al17 found that Al(2)O(3) NMs were able to induce size- and dose-dependent genotoxicity in vivo.17 ); (3) intravesical irrigation with aluminum for hemorrhagic cystitis, a life-threatening complication that might occur in bone marrow transplantation, chemotherapy, and radiotherapy, as described in a pediatric patient.18

International
Some evidence suggests that, in developing countries where contaminated dialysis water is still used, aluminum-related disease is more prevalent. Also, as people still use over-the-counter aluminum-containing phosphate binders, aluminum deposition within the bone will continue and serve as a reservoir for continued exposure because of its long elimination half-life.

Mortality/Morbidity
The mortality rate may be as high as 100% in patients in whom the condition goes unrecognized. Today, however, recognition by nephrologists is the norm, and increased awareness by all practitioners has led to earlier detection and overall avoidance of the syndrome. Morbidity and mortality have been diminished significantly. Prior to this, bone pain, multiple fractures, proximal myopathy, and the sequelae of dementia have been the main sources of morbidity.

Race
Aluminum toxicity has no predilection for any race.

Sex
Aluminum toxicity has no predilection for either sex.

Age
Aluminum toxicity is observed in all age groups, but its end-organ effects are more prevalent in elderly persons, who may have diminished renal function.

Clinical
History
The signs and symptoms of aluminum toxicity are usually nonspecific.


In patients on long-term hemodialysis, osteomalacia is associated with the accumulation of aluminum in bone. Most evidence to support skeletal toxicity is from animal studies.

Studies have also shown that patients on hemodialysis who are exposed to dialysate containing high aluminum concentrations are at increased risk of osteomalacia.

Some of the clinical symptoms of the disease entity reflect the chief complaint. An emergency physician will rarely consider aluminum toxicity as a possible diagnosis in a patient on dialysis who presents with an acute mental status change; however, these patients are the specific group most closely associated with the syndrome.

Typical presentations may include proximal muscle weakness, bone pain, multiple nonhealing fractures, acute or subacute alteration in mental status, and premature osteoporosis. These patients almost always have some degree of renal disease. Most patients are on hemodialysis or peritoneal dialysis.

When obtaining the history, ask specifically about the supplemental use of oral aluminum hydroxide, particularly if the patient does not undergo dialysis.

In children, special awareness must be made in those who require parenteral nutrition so as not to give excessive amounts of aluminum in the TPN.

Physical
Unfortunately, physical findings are often noticeably lacking in patients with aluminum toxicity, and findings usually mimic other disease processes.


Patients can present with multiple fractures (particularly of the ribs and pelvis), proximal muscle weakness, mutism, seizures, and dementia.

Some studies have shown a direct correlation between aluminum levels and intensity of uremic pruritus.

In children, bony deformity is more commonly due to the increased rate of growth and remodeling. Children may also express varying degrees of growth retardation.

The areas of deformity in children usually involve the epiphyseal plates (ie, femur, wrist).

In adults, thoracic cage abnormalities, lumbar scoliosis, and kyphosis can be present.


Causes
Toxic effects are dependent upon the amount of metal ingested, entry rate, tissue distribution, concentration achieved, and excretion rate.19,20,21,22

Mechanisms of toxicity include inhibition of enzyme activity and protein synthesis, alterations in nucleic acid function, and changes in cell membrane permeability.

Aluminum toxicity is usually found in patients with renal impairment. Acute intoxication is extremely rare; however, in persons in whom aluminum clearance is impaired, it can be a source of significant toxicity.

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http://emedicine.medscape.com/article/165315-treatment

eMedicine Specialties > Emergency Medicine > Toxicology
Toxicity, Aluminum: Treatment & Medication
Author: Jose F Bernardo, MD, MPH, FASN, Assistant Professor, Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh
Coauthor(s): Michael R Edwards, MD, Medical Director, Department of Emergency Services, Beebe Medical Center; Barbara Barnett, MD, Associate Program Director, Assistant Professor, Department of Emergency Medicine, Albert Einstein College of Medicine
Contributor Information and Disclosures

Updated: Aug 4, 2010

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Overview
Differential Diagnoses & Workup
Treatment & Medication
Follow-up
References
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Further Reading

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Postmenopausal osteoporosis treatment showed significant BMD increases.
Learn more Treatment
Medical Care
The most important part of emergency medical treatment is the recognition of possible aluminum toxicity based on risks (eg, renal insufficiency, aluminum exposure) and symptoms (eg, altered mental status, anemia, osteoporosis).
 
Treatment of aluminum toxicity includes elimination of aluminum from the diet, TPN, dialysate, medications, antiperspirants, and an attempt at the elimination and chelation of the element from the body's stores.


Avoidance of aluminum is easily achieved once the need to do so is recognized.

Elimination is accomplished through the administration of deferoxamine through any of several routes.

Serum aluminum level greater than 50-60 µg/L (mcg/dL) suggests aluminum overload, may correlate with toxicity, and can be used as an indication to start chelation therapy in symptomatic patients.
Symptomatic patients with lower serum aluminum levels (eg, greater than 20 mcg/dL) may require chelation therapy.
Kan et al suggested that a low dose of deferoxamine therapy (2.5 mg/kg/wk) is therapeutically effective as standard dose (5 mg/kg/wk) for the treatment of aluminum overload.23
Chelation therapy with deferoxamine should be initiated in consultation with a nephrologist and a medical toxicologist, and this can be performed upon admission.

Deferoxamine, the metal-free ligand of the iron-chelate isolated from the bacterium Streptomyces pilosus, is used for acute and chronic iron toxicity and aluminum toxicity.
It has a high affinity for ferric iron and does not affect iron in hemoglobin or cytochromes.

Surgical Care
No surgical care is applicable to this disorder. Hemodialysis is performed in conjunction with deferoxamine as therapy for whole-body chelation.

Consultations
Usually, a nephrologist is already a part of the patient's medical team. If not, one should be consulted early in the course.

A hematologist and a neurologist may be able to assist with the patient's care.

Diet
Since dietary aluminum is ubiquitous, no specific dietary guidelines are available for its avoidance. Special diets should be maintained for specific associated disease entities (eg, diabetes, renal failure).

Activity
Activity modification may not be necessary unless the patient is at risk for frequent falls. If this is the case, a home attendant or family member should assist the patient with daily living activities.

Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Metal chelators
These agents bind free metal and do not chelate other trace metals of nutritional importance. Metals are excreted in the urine and bile.



Deferoxamine mesylate (Desferal mesylate)
Metal-free ligand of the iron chelate isolated from the bacterium S pilosus. Used for acute and chronic iron toxicity as well as aluminum toxicity and has a high affinity for ferric iron. Does not affect iron in cytochromes or hemoglobin. PO/IM administration not established. Several case reports and cohorts using varying doses indicate effectiveness when administered IV.


Offline citizenx

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #13 on: November 26, 2010, 07:34:35 am »
Barium
Elevated levels of barium can induce a wide range of effects in mammals including gastrointestinal distress, muscular paralysis, and cardiovascular effects. Barium is does not bioaccumulate, and concentrations in higher species rarely exceed 10 mg/kg (Moore 1991).

http://www.epa.gov/region5superfund/ecology/html/toxprofiles.htm

Toxicological Profile for Barium and Barium Compounds. Agency for Toxic Substances and Disease Registry". CDC. 2007..

http://www.atsdr.cdc.gov/toxprofiles/tp24.pdf

Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #14 on: November 26, 2010, 07:41:22 am »
http://www.dtic.mil/cgi-bin/GetTRDoc?Location=U2&doc=GetTRDoc.pdf&AD=ADA413896

Military Paper on stratospheric aluminium

Not only is it bad for us it is some what responsible for ozone depletion! (see page 4 - end of intro)

Thanks Citizen X
The amount of crap they spray - it must be having an effect somewhere! Just a case of knowing where to look.

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Offline SongBird

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #15 on: November 26, 2010, 07:42:50 am »
The guy replied me! He kindly sent me the whole paper - anyone, am i able to copy / paste the entire thing in or not? its in pdf format - no url, so can`t put up a link

http://www.mediafire.com

Online uploader, let's you share your stuff.

Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #16 on: November 26, 2010, 07:49:33 am »
thanks Songbird - will have a play later so far it keeps saying failure when i try to upload it :S
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Offline SongBird

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #17 on: November 26, 2010, 07:51:29 am »
thanks Songbird - will have a play later so far it keeps saying failure when i try to upload it :S

Megaupload, that one may work, no worries. :)

Offline citizenx

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #18 on: November 26, 2010, 07:54:46 am »
[quote author=phasma link=topic=193323.msg1146629#msg1146629
37. As with the results from 1994, the highest levels of barium in the 2006 survey
were reported in nuts (131 mg/kg) and bread (0.81 mg/kg). All other foodstuffs
contained lower levels than in bread. Levels of barium in nuts were double those
reported in 1994 (131 mg/kg and 56 mg/kg, respectively). Estimated average
population dietary exposures to barium have increased by approximately 46% since
the last TDS in 1994.
[/quote]
Umm.. I would completely lay off the nuts in that case.  Can't possibly be good.

Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #19 on: November 26, 2010, 07:59:51 am »
Nope. Nuts (esp brazil nuts i believe) best avoided it seems.

ALSO filter your drinking water ppl ! A good filter should remove some of the barium, almost 1000% higher than W>H>O recommends daily? FFS!
Things are not what they appear to be: nor are they otherwise - Surangama Sutra

Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #20 on: November 26, 2010, 02:07:48 pm »
Bump Once for the late comers :)
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Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #21 on: November 26, 2010, 08:01:34 pm »
Does any one know what kind of filter would be needed to completely remove barium?
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Offline Weasel

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #22 on: November 26, 2010, 09:07:16 pm »
How about a Berkey with the black filters? According to the website they take out just about everything not good for you.

http://www.berkeywaterfilters.com/blbetesp.html

Seems there is some good news about growing in alkaline soil with alkaline water.   ;D
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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #23 on: November 26, 2010, 09:14:23 pm »
eat cilantro everyday  also you can take Source Naturals Potassium Iodide
to help remove the metals from the body

Offline DesertEagle602

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #24 on: December 02, 2010, 02:22:36 am »
eat cilantro everyday  also you can take Source Naturals Potassium Iodide
to help remove the metals from the body

I live in Phoenix,Az and there chemtrailing us all the time!  :'( Ill eat more cilantro its actually tasty to me lol. I'll point to the skys and my friends and my family dont belive me about the chemtrails.

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #25 on: December 02, 2010, 02:35:20 am »
Barium would accumulate in Soybeans

But you already avoid Soy products right ?
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Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #26 on: December 02, 2010, 02:32:29 pm »
I mostly avoid soy - i do eat some tofu. I have not seen anything about accumulation in soy beans though, do you have a link?

The most awesome thing happened to me today - I went to my local (veggie) cafe in liverpool, I got change of a tenner - a five pound note with "CHEMTRAILS KILL LOOK UP! The woman behind the til read it looked confused and asked if it was ok (with writing on) I told her hell yes it was the best thing i`d seen all day, then asked her if she knew what chemtrails were - then gave her and the other 5 staff my elevator pitch on chemtrails - jaws on the floor and alot of them askin where can they get more info - i sent  them this ways :)
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Offline planning4acrash

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #27 on: December 13, 2010, 05:29:55 pm »
Soy beans are processed with acid in huge aluminum vats. This gives them high levels of aluminum. Not the case with traditionally fermented soy in wooden barrels.

http://www.westonaprice.org/soy-alert/1623-soy-recovery-the-toxic-metal-component.html

Heavy Metals: Soy consumption can also lead directly and indirectly to heavy metal toxicity—directly, because soy products are often processed or packaged in aluminum or processed with fluoridated water, and indirectly, because soy foods contribute to low levels of cysteine, zinc, pantothenic acid and other factors needed for detoxification. This can result in a buildup of mercury, cadmium, arsenic, aluminum and other toxic metals in the body, ultimately affecting every metabolic process. (You wonder why its being promoted?! And all the GM soy multiply these and other issues)

Offline phasma

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #28 on: December 13, 2010, 05:40:01 pm »
Thanks for the info !!!
Things are not what they appear to be: nor are they otherwise - Surangama Sutra

Offline redeux

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #29 on: December 13, 2010, 08:16:10 pm »
Moreover if you're a male Soybeans should be avoided like the plague... unless you like to cry and desire breasts....
Protect your manhood, demand Testosterone..........

Offline planning4acrash

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Re: OMG THIS IS HUGE PPL !!! ALUMINIUM BARIUM LEVELS IN FOOD UP SINCE 2000
« Reply #30 on: December 14, 2010, 02:14:09 am »
Well. Moderate quantities of fermented, organic soy products are actually beneficial. Its the way we prepare and consume them in the west that is the problem.

For the full story, with all the links, including a brochure to print out and distribute, visit this website: http://www.westonaprice.org/soy-alert.html


Or, purchase the Whole Soy Story by Kaayla Daniel. She is speaking in London, March 26: westonaprice.org/london