RE: malic acid conundrum: Dr McCandless? ?

[Guest guest]

After oxygen & silicon, aluminum is the most abundant element in the crust of

the earth, so exposure is ubiquitous via food, water, air & soil.  Some things

we use it for: beverage cans, cooking pots, siding, roofing, Al foil, airplanes

etc etc it is also found in antacids, buffered aspirin, food additives esp

grains & cheeses, astringents, vaccinations, cat litter, antiperspirants, infant

formula & baking soda, etc etc etc.  Common dietary acids such as citrate &

malate can increase Al absorption, and those with low calcium can have increased

Al absorption.

We all take in lots of aluminum, and I tell parents not to use aluminum pots or

let their kids drink anything out of those foil-lined fruit juice boxes or wrap

their sandwiches in aluminum-foil. Apparently it is not how much we take in, it

is how well the body can detoxify it.

From a fibromyalgia site: " The most potent aluminum detoxifier is malic acid.

Malic acid is especially effective at decreasing aluminum toxicity in the brain.

Alzheimer's Disease patients have been found to have unusually high levels of

aluminum in their brains. It was once assumed that these people had ingested

large amounts of aluminum during their lifetimes. However, while that may be

true, it is now thought that how much aluminum is consumed is not nearly as

important as how well our bodies can detoxify and eliminate the substance.

Treatment with malic acid has been shown to greatly increase the fecal and

urinary excretion of aluminum and reduce the concentration of aluminum found in

various organs and tissues. Clinical tests are proving malic acid to be a great

asset in the treatment of fibromyalgia and chronic pain. In one clinical study,

reported in " The Journal of Nutritional Medicine, " 15 patients (aged 32-60)

taking a dosage of 200-2400 mg. of maIic acid with 300-600 mg of magnesium for

four to eight weeks, reported significant pain relief within 48 hours. "

I have several fibromyalgia patients who absolutely require magnesium and malic

acid to function. Sorry, I was not able to find a paper on the mechanism of the

detox noted in many clinical observations of the benefit of malic acid to

detoxify aluminum; maybe can help us out here. I have not always found

it efficacious in getting the hair levels improved, but have found TTFD (I use

Ecological Formulas' Authia because it does not smell so terrible) to

consistently be helpful. Dr. JM

I may be reading this wrong, but one statement in the study below " brain

aluminum concentrations were also raised by the intake of lactic, gluconic,

malic, citric, and oxalic acids " has me confused. I thought that Malic Acid

was used to RID the body of aluminum. This appears to say that Malic Acid

raises the concentration of Aluminum in the brain.

I think many of the kids are taking Malic Acid to actually chelate

Aluminum. Am I misreading this?

1. Malic Acid Aluminum toxicity may play a role in symptoms experienced

by magnesium-deficient ... However, the most potent; aluminum detoxifier

is malic acid. ...

http://www.healingw ithnutrition. com/fdisease/ fibromyalgia/ magnesiumstudy.

htm

l

2. Malic Acid readily crosses the Blood-Brain- Barrier and has been shown

to bind to aluminum. It functions in the body by drawing aluminum away ...

http://www.vitaneto nline.com/ forums/1/ Thread/134

3. Malic acid has been found to help remove the toxic metals lead,

strontium, and especially aluminum, among others. Your body manufactures

malic acid along ...

http://www.life- enhancement. com/article_ template. asp?ID=509

4. Effect of various dietary constituents on gastrointestinal absorption

of aluminum from drinking water and diet.

Domingo JL, Gomez M, DJ, Llobet JM, Corbella J.

Res Commun Chem Pathol Pharmacol. 1993 Mar;79(3):377- 80.

The influence of some frequent dietary constituents on gastrointestinal

absorption of aluminum from drinking water and diet was investigated in

mice. Eight groups of male mice received lactic (57.6 mg/kg/day),

tartaric (96 mg/kg/day), gluconic (125.4 mg/kg/day), malic (85.8

mg/kg/day), succinic (75.6 mg/kg/day), ascorbic (112.6 mg/kg/day),

citric (124 mg/kg/day), and oxalic (80.6 mg/kg/day) acids in the

drinking water for one month. At the end of this period, animals were

killed and aluminum concentrations in liver, spleen, kidney, brain, and

bone were determined. All the dietary constituents significantly

increased the aluminum levels in bone, whereas brain aluminum

concentrations were also raised by the intake of lactic, gluconic,

malic, citric, and oxalic acids. The levels of aluminum found in spleen

were significantly increased by gluconic and ascorbic acids, whereas

gluconic and oxalic acids also raised the concentrations of aluminum

found in kidneys. Because of the wide presence and consumption of the

above dietary constituents, in order to prevent aluminum accumulation

and toxicity we suggest a drastic limitation of human exposure to aluminum.

PMID: 8480083

<?>

[Guest guest]

Dr. McCandless,

I just exhaled! Thank you so much for the detailed explanation. I really

appreciate it. L

From: csb-autism-rx [mailto:csb-autism-rx ]

On Behalf Of JAQUELYN MCCANDLESS

Sent: Sunday, September 21, 2008 2:59 PM

To: csb-autism-rx

Subject: RE: malic acid conundrum: Dr McCandless? ?

After oxygen & silicon, aluminum is the most abundant element in the crust

of the earth, so exposure is ubiquitous via food, water, air & soil. Some

things we use it for: beverage cans, cooking pots, siding, roofing, Al foil,

airplanes etc etc it is also found in antacids, buffered aspirin, food

additives esp grains & cheeses, astringents, vaccinations, cat litter,

antiperspirants, infant formula & baking soda, etc etc etc. Common dietary

acids such as citrate & malate can increase Al absorption, and those with

low calcium can have increased Al absorption.

We all take in lots of aluminum, and I tell parents not to use aluminum pots

or let their kids drink anything out of those foil-lined fruit juice boxes

or wrap their sandwiches in aluminum-foil. Apparently it is not how much we

take in, it is how well the body can detoxify it.

From a fibromyalgia site: " The most potent aluminum detoxifier is malic

acid. Malic acid is especially effective at decreasing aluminum toxicity in

the brain. Alzheimer's Disease patients have been found to have unusually

high levels of aluminum in their brains. It was once assumed that these

people had ingested large amounts of aluminum during their lifetimes.

However, while that may be true, it is now thought that how much aluminum is

consumed is not nearly as important as how well our bodies can detoxify and

eliminate the substance.

Treatment with malic acid has been shown to greatly increase the fecal and

urinary excretion of aluminum and reduce the concentration of aluminum found

in various organs and tissues. Clinical tests are proving malic acid to be a

great asset in the treatment of fibromyalgia and chronic pain. In one

clinical study, reported in " The Journal of Nutritional Medicine, " 15

patients (aged 32-60) taking a dosage of 200-2400 mg. of maIic acid with

300-600 mg of magnesium for four to eight weeks, reported significant pain

relief within 48 hours. "

I have several fibromyalgia patients who absolutely require magnesium and

malic acid to function. Sorry, I was not able to find a paper on the

mechanism of the detox noted in many clinical observations of the benefit of

malic acid to detoxify aluminum; maybe can help us out here. I have

not always found it efficacious in getting the hair levels improved, but

have found TTFD (I use Ecological Formulas' Authia because it does not smell

so terrible) to consistently be helpful. Dr. JM

I may be reading this wrong, but one statement in the study below " brain

aluminum concentrations were also raised by the intake of lactic, gluconic,

malic, citric, and oxalic acids " has me confused. I thought that Malic Acid

was used to RID the body of aluminum. This appears to say that Malic Acid

raises the concentration of Aluminum in the brain.

I think many of the kids are taking Malic Acid to actually chelate

Aluminum. Am I misreading this?

1. Malic Acid Aluminum toxicity may play a role in symptoms experienced

by magnesium-deficient ... However, the most potent; aluminum detoxifier

is malic acid. ...

http://www.healingw ithnutrition. com/fdisease/ fibromyalgia/

magnesiumstudy. htm

l

2. Malic Acid readily crosses the Blood-Brain- Barrier and has been shown

to bind to aluminum. It functions in the body by drawing aluminum away ...

http://www.vitaneto nline.com/ forums/1/ Thread/134

3. Malic acid has been found to help remove the toxic metals lead,

strontium, and especially aluminum, among others. Your body manufactures

malic acid along ...

http://www.life- enhancement. com/article_ template. asp?ID=509

4. Effect of various dietary constituents on gastrointestinal absorption

of aluminum from drinking water and diet.

Domingo JL, Gomez M, DJ, Llobet JM, Corbella J.

Res Commun Chem Pathol Pharmacol. 1993 Mar;79(3):377- 80.

The influence of some frequent dietary constituents on gastrointestinal

absorption of aluminum from drinking water and diet was investigated in

mice. Eight groups of male mice received lactic (57.6 mg/kg/day),

tartaric (96 mg/kg/day), gluconic (125.4 mg/kg/day), malic (85.8

mg/kg/day), succinic (75.6 mg/kg/day), ascorbic (112.6 mg/kg/day),

citric (124 mg/kg/day), and oxalic (80.6 mg/kg/day) acids in the

drinking water for one month. At the end of this period, animals were

killed and aluminum concentrations in liver, spleen, kidney, brain, and

bone were determined. All the dietary constituents significantly

increased the aluminum levels in bone, whereas brain aluminum

concentrations were also raised by the intake of lactic, gluconic,

malic, citric, and oxalic acids. The levels of aluminum found in spleen

were significantly increased by gluconic and ascorbic acids, whereas

gluconic and oxalic acids also raised the concentrations of aluminum

found in kidneys. Because of the wide presence and consumption of the

above dietary constituents, in order to prevent aluminum accumulation

and toxicity we suggest a drastic limitation of human exposure to aluminum.

PMID: 8480083

<?>

[Guest guest]

Dr. JM,

Do you remember what study found that taking malic acid protected from

aluminum accumulation in tissues? I've put two studies below that show

quite the opposite. Another study measured fecal and urinary excretion and

found that citric acid caused more excretion of aluminum than malic acid.

Most of the studies talking about malic acid protecting from aluminum were

talking about plants, but it looks like in animals, malic acid (and its

close kin oxalate and ascorbic and citric acid) will increase the brain

uptake of aluminum if given at the same time.

It may be that benefits of malic acid are happening because of a different

mechanism and it might be related to a proneness to vitamin D deficiency in

fibromyalgia.

This might involve the glyoxlylate cycle which is a rather abbreviated or

" short-cut " citric acid cycle that origninally was thought not to occur in

creatures like us. Now we know after a lot of studies that we also have

this alternative energy cycle that converts fat to glucose.

Here is a picture of

it: http://www.udel.edu/chem/white/C643/GlyoxylateCycle.gif lor

http://www.chembio.uoguelph.ca/educmat/chm452/gif/glycycle.gif

You can see that in this cycle isocitrate is converted into glyoxylate and

then very favorably, glyoxylate is converted into malic acid, which is then

the precursor to oxaloacetate. At this point, the citric acid cycle takes

another spin. When oxalate is high, a lot of glyoxylate is formed, but

people with sulfur chemistry issues or deficiencies of pantothenic acic may

not be able to keep up the supply of acetyl CoA for that step to make malic

acid. I've never seen this addressed directly. It didn't seem important

to figure this out when humans were not supposed to have this pathway. One

group of scientists suggested the use of this pathway by an infectious

microbe could be involved with metabolic syndrome. Another study proposes

that cancer cells use this pathway, producing the wasting that is called

cachexia. Vitamin D3 seems to get involved with this cycle,, so it may be

this cycle cannot be used effectively in vitamin D deficiency, and taking

malate would subsititute. The loss of this cycle might define a reason why

D3 deficiency can lead to obesity.

..

I've put some articles below reviewing some of the new research..

Res Commun Chem Pathol Pharmacol. 1993 Mar;79(3):377-80.

Related Articles, Links

Effect of various dietary constituents on gastrointestinal absorption of

aluminum from drinking water and diet.

Domingo JL, Gomez M, DJ, Llobet JM, Corbella J.

Laboratory of Toxicology and Biochemistry, School of Medicine, University

of Barcelona, Reus, Spain.

The influence of some frequent dietary constituents on gastrointestinal

absorption of aluminum from drinking water and diet was investigated in

mice. Eight groups of male mice received lactic (57.6 mg/kg/day), tartaric

(96 mg/kg/day), gluconic (125.4 mg/kg/day), malic (85.8 mg/kg/day),

succinic (75.6 mg/kg/day), ascorbic (112.6 mg/kg/day), citric (124

mg/kg/day), and oxalic (80.6 mg/kg/day) acids in the drinking water for one

month. At the end of this period, animals were killed and aluminum

concentrations in liver, spleen, kidney, brain, and bone were determined.

All the dietary constituents significantly increased the aluminum levels in

bone, whereas brain aluminum concentrations were also raised by the intake

of lactic, gluconic, malic, citric, and oxalic acids. The levels of

aluminum found in spleen were significantly increased by gluconic and

ascorbic acids, whereas gluconic and oxalic acids also raised the

concentrations of aluminum found in kidneys. Because of the wide presence

and consumption of the above dietary constituents, in order to prevent

aluminum accumulation and toxicity we suggest a drastic limitation of human

exposure to aluminum.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 8480083 [PubMed - indexed for MEDLINE]

Kidney Int. 1991 Apr;39(4):598-601.

Related Articles, Links

Influence of some dietary constituents on aluminum absorption and retention

in rats.

Domingo JL, Gomez M, Llobet JM, Corbella J.

Laboratory of Toxicology and Biochemistry, School of Medicine, University

of Barcelona, Reus, Spain.

Eight groups of female Sprague-Dawley rats were treated with 281 mg

Al(OH)3/kg/day by gastric intubation five times a week for five weeks.

Concurrently, animals in seven groups received ascorbic acid (56.3

mg/kg/day), citric acid (62 mg/kg/day), gluconic acid (62.7 mg/kg/day),

lactic acid (28.8 mg/kg/day), malic acid (42.9 mg/kg/day), oxalic acid

(28.8 mg/kg/day), and tartaric acid (48 mg/kg/day) in the drinking water.

The eighth group did not receive any dietary constituent in the water and

was designated as the control group. Animals were placed in plastic

metabolic cages and urine was collected during the treatment period. The

liver, spleen, kidney, brain and bone aluminum levels of each rat were

measured, as well as the total amount of aluminum excreted into urine. All

the dietary constituents significantly increased the aluminum

concentrations in most of the tissues, with ascorbic and citric acids

showing the highest rate of aluminum accumulation. In contrast, no

significant differences between control and treated rats were observed in

the concentrations of aluminum excreted into urine. In view of these

results, we suggest that the effects of the simultaneous ingestion of

aluminum hydroxide and those dietary constituents in uremic animals should

be evaluated. Meanwhile, the diet of uremic patients should be carefully

monitored.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 2051716 [PubMed - indexed for MEDLINE]

Hum Toxicol. 1988 May;7(3):259-62.

Related Articles, Links

Comparative effects of several chelating agents on the toxicity,

distribution and excretion of aluminium.

Domingo JL, Gómez M, Llobet JM, Corbella J.

Laboratory of Toxicology and Biochemistry, School of Medicine, Reus, Spain.

The relative efficacy of citric, malic, malonic, oxalic and succinic acids,

and deferoxamine mesylate (DFOA) on the toxicity, distribution and

excretion in mice exposed to aluminum were compared. Chelating agents were

administered intraperitoneally at a dose equal to one-fourth of their

respective LD50. To determine the effect of the various chelators on the

toxicity of aluminum, various doses of aluminum nitrate (938-3188 mg/kg)

were administered intraperitoneally, followed by one of the chelators.

Survival was recorded at the end of 14 days. Malic and succinic acids were

the most effective. Malic acid and DFOA were the most effective in

increasing the urinary excretion of aluminum. Citric acid was the most

effective in increasing the faecal excretion of aluminum. Malonic, oxalic

and succinic acids had no overall beneficial effects. Citric acid would

appear to be the most effective agent of those tested in the prevention of

acute aluminium intoxication. However, before the use of these compounds in

human aluminium intoxication is possible, further investigations including

the effects of these chelators after chronic aluminium intoxication are

required.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 3391623 [PubMed - indexed for MEDLINE]

Med Hypotheses. 2008 Aug;71(2):222-8. Epub 2008 Apr 29.[] Links

Visceral adipose tissue specific persistence of Mycobacterium tuberculosis

may be reason for the metabolic syndrome.

Erol A.

Namik Kemal University, Faculty of Medicine, Department of Internal

Medicine, Namik Kemal Caddesi 14, Tekirdag, Turkey. adnanerol@...

Mycobacterium tuberculosis (Mtb) is highly successful intracellular

pathogen. Infection is maintained in spite of acquired immunity and resists

eradication by antimicrobials. Following bacillaemia, small numbers of

bacteria are disseminated to the extrapulmonary organs most likely

including visceral adipose tissue by a mechanism that may involve the

migration of M. tuberculosis within dendritic cells. In this lipid rich

environment, Mtb can metabolize the fatty acids in a glyoxylate cycle

dependent manner, and a state of chronic persistence may ensue. The

persistent bacilli primarily use fatty acids as their carbon source.

Expression of isocitrate lyase (ICL), gating enzyme of glyoxylate cycle, is

upregulated during infection. ICL is important for survival during the

persistent phase of infection. Expression of adipokines, particularly

monocyte chemoattractant protein-1 (MCP-1), which is a potent

proinflammatory cytokine, may be increased. MCP-1 contributes both to the

recruitment of macrophages to adipose tissue and to the development of

insulin resistance in humans. In addition, prolonged low level immune

stimulation induces local adipolipogenesis, increasing visceral fat.

Increased delivery of free fatty acid to the liver may stimulate the

glyoxylate cycle-induced gluconeogenesis, raising hepatic glucose output.

Hence, inhibition of the triggering enzyme ICL, which initiates all the

pathologies related to persistent Mtb infection, may block the growth of

the bacteria and may resolve the systemic metabolic complications.

PMID: 18448263 [PubMed - indexed for MEDLINE]

Med Hypotheses. 2005;65(3):525-9.[] Links

Retrograde regulation due to mitochondrial dysfunction may be an important

mechanism for carcinogenesis.

Erol A.

Silivri City Hospital, Department of Internal Medicine, Ali Cetinkaya Cad,

34930 Silivri, Istanbul, Turkey. eroladnan@...

Mitochondrial dysfunction has crucial importance in carcinogenesis. Due to

several reasons, it may lead to insufficiency in the electron transport

chain, which activates a series of cytosolic proteins. These proteins are

transported to the nucleus and promote the activation of genes leading to

intracellular diverse metabolic, regulatory, signalization and

stress-related pathways. Retrograde regulation is the general term for

mitochondrial signaling, and is broadly defined as cellular responses to

alterations in functional state of mitochondria. This signaling pathway is

triggered by mitochondrial dysfunction. The retrograde response is not a

simple On-Off switch, but rather it responds in a continuous manner to the

changing metabolic needs of the cell. Communication between mitochondria

and the nucleus is important for a variety of cellular processes such as

carbohydrate and nitrogen metabolism, cell cycle and proliferation, and

cell growth and morphogenesis. As a result of retrograde regulation, the

cell, actually a component of the multicellular organism, transforms to a

unicellular lifestyle and initiates a developing course, independent of the

systemic structure. This transformed cell runs metabolic regulations

effectively in order to utilize all energy depots, mainly the adipose

tissue of the multicellular organism. The most important one is the active

utilization of glyoxylate cycle, through which the malign cells supply

glucose from fats. Continuously acting glycolysis and gluconeogenesis,

fatty acid oxidation and de novo lipogenesis constitute futile cycles. This

in turn causes cachexia by maintaining the organism in constant negative

energy balance. Mitochondria-to-nucleus stress signaling activates some of

the genes implicated in tumor progression and tumor cell metastasis.

Retrograde regulation also renders the cell more resistant to apoptosis. It

is becoming clearer which genes control the retrograde response in human

cells. Most probably, MYC is one of the transcription factors necessary for

this response.

PMID: 15905043 [PubMed - indexed for MEDLINE]

Anat Rec. 1992 Dec;234(4):461-8.Links

Evidence for the glyoxylate cycle in human liver.

WL, Goodman DB.

Department of Biology, College of Natural and Applied Sciences, Abilene

Christian University, Texas 79699.

The enzymatic activities unique to the glyoxylate cycle of higher plants

and certain lower invertebrates, isocitrate lyase and malate synthase, have

been demonstrated in homogenates prepared from human liver. Human liver can

also carry out cyanide-insensitive fatty acid oxidation from palmitate.

Utilizing light microscopic immunocytochemistry with an antibody produced

against Euglena malate synthase, this enzyme localizes in numerous ovoid

granules in human hepatocytes. Also, immunocytochemistry using antibodies

produced against rat fatty acyl-CoA oxidase showed that this enzyme was

localized in similar structures. With routine cytochemistry, catalase was

seen in identical granular bodies. Both catalase and fatty acyl-CoA oxidase

are peroxisomal enzymes. The presence of malate synthase in liver

homogenates was further confirmed by Western blot analysis. These data

suggest that the human liver may be capable of utilizing the carbon

backbone of fatty acids for carbohydrate synthesis since the glyoxylate

cycle in lower organisms subserves this anabolic function.

PMID: 1456449 [PubMed - indexed for MEDLINE]

FASEB J. 1989 Mar;3(5):1651-5.[] Links

Glyoxylate cycle in the rat liver: effect of vitamin D3 treatment.

WL, s JL, Goodman DB.

Department of Anatomy, Baylor College of Dentistry, Dallas, Texas 77030.

Evidence for the glyoxylate cycle in the mammalian rat liver was sought.

Activity of two unique glyoxylate cycle enzymes, isocitrate lyase and

malate synthase, was found in rat liver homogenates. Vitamin D3 treatment

of rachitic animals produced a five- and fourfold increase, respectively,

in the activity of these enzymes. Vitamin D3 also increased the peroxisomal

fatty acid oxidation and the accumulation of glycogen in liver slices in

the presence of palmitate. These data suggest that the mammalian rat liver

can convert fatty acid carbon to carbohydrate carbon directly.

PMID: 2537775 [PubMed - indexed for MEDLINE

Bone. 1989;10(3):201-6.Links

The glyoxylate cycle in rat epiphyseal cartilage: the effect of vitamin-D3

on the activity of the enzymes isocitrate lyase and malate synthase.

WL, RG, Farmer GR, Cortinas E, s JL, Goodman DB.

Department of Anatomy, Baylor College of Dentistry, Dallas, Texas 75246.

The effect of vitamin-D deficiency and subsequent vitamin-D replacement on

the metabolism of rat epiphyseal growth plate cartilage was studied.

Biochemical analyses showed the presence of the two unique glyoxylate cycle

enzymes isocitrate lyase and malate synthase in cartilage. The activity of

these enzymes was markedly increased after treatment with the vitamin.

Additionally, rat cartilage showed the capacity to oxidize fatty acid in

the presence of cyanide. This cyanide-insensitive fatty acid oxidation is

characteristic of peroxisomal B-oxidation rather than mitochondrial

B-oxidation. Vitamin-D treatment also increased fatty acid oxidation.

Lastly, incubation of rat cartilage in the presence of a fatty acid

substrate such as palmitate, resulted in a higher tissue glycogen content.

Tissue glycogen was further elevated by vitamin-D. Such data indicate the

presence of glyoxylate cycle enzymes in a vertebrate tissue and raise the

possibility that mammalian cartilage has the capacity to convert lipid to

carbohydrate.

PMID: 2553083 [PubMed - indexed for MEDLINE]

Biochim Biophys Acta. 1990 Mar 9;1051(3):276-8.Links

Hibernation activates glyoxylate cycle and gluconeogenesis in black bear

brown adipose tissue.

WL, Goodman DB, Crawford LA, OJ, s JL.

Department of Anatomy, Baylor College of Dentistry, Dallas, TX.

Biochemical studies on brown adipose tissue removed from a hibernating

black bear and a non-hibernating control animal demonstrate that this

tissue: (1) can carry out cyanide-insensitive fatty acid oxidation, and (2)

possesses catalase activity and the enzyme activities unique to the

glyoxylate cycle, isocitrate lyase and malate synthase. These activities

are all markedly increased in brown fat obtained from the hibernating

animal. Additionally, hibernation enhances the ability of the tissue to

synthesize glycogen in the presence of a fatty acid substrate. The

glyoxylate cycle enzymes and the ability to convert fatty acid carbons to

glucose have been generally regarded as being absent from vertebrate cells

and tissues.

PMID: 2310778 [PubMed - indexed for MEDLINE

At 02:59 PM 9/21/2008, you wrote:

>...

>Treatment with malic acid has been shown to greatly increase the fecal and

>urinary excretion of aluminum and reduce the concentration of aluminum

>found in various organs and tissues. Clinical tests are proving malic acid

>to be a great asset in the treatment of fibromyalgia and chronic pain. In

>one clinical study, reported in " The Journal of Nutritional Medicine, " 15

>patients (aged 32-60) taking a dosage of 200-2400 mg. of maIic acid with

>300-600 mg of magnesium for four to eight weeks, reported significant pain

>relief within 48 hours. "

>

>I have several fibromyalgia patients who absolutely require magnesium and

>malic acid to function. Sorry, I was not able to find a paper on the

>mechanism of the detox noted in many clinical observations of the benefit

>of malic acid to detoxify aluminum; maybe can help us out here. I

>have not always found it efficacious in getting the hair levels improved,

>but have found TTFD (I use Ecological Formulas' Authia because it does not

>smell so terrible) to consistently be helpful. Dr. JM

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