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Can Silicon Prevent Alzheimer’s Disease?
By Alan R. Gaby, MD
Healthnotes Newswire (May 5, 2005)—A high intake of the trace mineral silicon may reduce the risk of developing dementia or Alzheimer’s disease, reports a study in the American Journal of Clinical Nutrition (2005;81:897–902). While most nutritionists do not consider silicon an essential nutrient for humans, this study adds to the growing list of its reported benefits.
Although silicon has no known direct effect on brain function, it inhibits the absorption and increases the urinary excretion of aluminum, a toxic metal thought to play a role in the development of Alzheimer’s disease and other forms of dementia. Consequently, silicon might help preserve brain function by preventing the accumulation of aluminum.
Some 7,598 French women aged 75 years or older participated in the new study. At the beginning, an estimate was made of the amount of silica (silicon dioxide; one of the main forms of silicon in the diet) each participant consumed per day in their drinking water. Women with lower intakes of silica were found to perform worse on cognitive function tests, compared with women whose silica intake from drinking water was higher. A subset of approximately 20% of the participants was then followed for up to 7 years. During the follow-up period, women with lower intake of silica were at increased risk of developing Alzheimer’s disease; those who developed Alzheimer’s disease were nearly three times as likely to have a low silica intake from drinking water (4 mg per day or less).
While controlled trials are needed to confirm these preliminary results, the study suggests that increasing silicon intake may help prevent age-related mental decline and Alzheimer’s disease. Animal research and preliminary studies in humans suggest that silicon may also help prevent hardening of the arteries (atherosclerosis) and osteoporosis. In animals, silicon plays a role in promoting healthy connective tissue, including cartilage and bone, and inadequate silicon intake leads to osteoporosis. In humans, silicon appears to improve bone health by increasing bone formation and by enhancing the structural integrity of bone.
The richest dietary sources of silicon are the bran portions of grains such as wheat, oats, and rice. In contrast, refined grains contain little silicon. Unrefined soy products also contain relatively large amount of silicon. Silicon is also available as a nutritional supplement and as a component of some multivitamin-mineral products. Silicon is generally considered safe, although respiratory problems have occurred in industrial workers exposed to large amounts of silicon dust in the air.
Alan R. Gaby, MD, an expert in nutritional therapies, testified to the White House Commission on CAM upon request in December 2001. Dr. Gaby served as a member of the Ad-Hoc Advisory Panel of the National Institutes of Health Office of Alternative Medicine. He is the author of Preventing and Reversing Osteoporosis (Prima, 1994), and co-author of The Natural Pharmacy, 2nd Edition (Healthnotes, Three Rivers Press, 1999), the A–Z Guide to Drug-Herb-Vitamin Interactions (Healthnotes, Three Rivers Press, 1999), Clinical Essentials Volume 1 and 2 (Healthnotes, 2000), and The Patient’s Book of Natural Healing (Prima, 1999). A former professor at Bastyr University of Natural Health Sciences, in Kenmore, WA, where he served as the Endowed Professor of Nutrition, Dr. Gaby is the Chief Medical Editor for Healthnotes, Inc.
Copyright © 2005 Healthnotes, Inc. All rights reserved. Republication or redistribution of the Healthnotes® content is expressly prohibited without the prior written consent of Healthnotes, Inc. Healthnotes Newswire is for educational or informational purposes only, and is not intended to diagnose or provide treatment for any condition. If you have any concerns about your own health, you should always consult with a healthcare professional. Healthnotes, Inc. shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. HEALTHNOTES and the Healthnotes logo are registered trademarks of Healthnotes, Inc.

Aluminium, silicium en (drink)water

http://www.deptplanetearth.com/pub/jad3jansson_p3.html

E.T. Jansson / Aluminum exposure and Alzheimer’s disease

Drinking Water Epidemiology Studies Linking Aluminum And Related Water Constituents to Alzheimer’s and Elderly Cognitive Impairment

2.1.2. Drinking water exposures

While there has been considerable debate about the contribution of drinking water aluminum to AD, eighteen drinking water studies have linked aluminum level to elevated risks of AD and elderly cognitive impairment [42]. On the other hand, five epidemiology studies show no effect [31,48,73,81,82]. An additional study cannot be interpreted due to uncertainty about the water contamination measurements [56]. Most of the no-effect studies involved low exposures, small sample populations, and lack of inclusion of significant modifying factors, making a statistical resolution over background variability unlikely. For example, a study from Korea involved average aluminum levels of only 28 ug/liter [73]. A series of multi-factor water studies from Canada, France and Great Britain are of particular interest be- cause they specifically identify aluminum as a key variable in both AD and elderly cognitive impairment risk – not only through levels of the metal itself in the drinking water, but also through the interaction with other water constituents that reduce the absorption of aluminum. Figure 1 summarizes seven studies that have changed our ideas about how to design epidemiology studies relating to aluminum. These and other studies highlight some of the issues relating to drinking water aluminum and AD.

a. Importance of water pH and other factors in absorption. Forbes and McLachlan’s study of the influence of various drinking water components including aluminum on AD risks in 85 year or older Canadians underscores the potential importance of other water constituents that affect the absorption of aluminum [30]. In this study, aluminum in excess of 250 ug/liter was associated with a 10-fold increase in AD risk, after controlling for six other water factors. With regard to these water factors, water pH had a large statistically significant effect on AD rates. Residents of water districts consuming drinking water with a pH in excess of 7.85 experienced a 50 percent reduction of AD risk compared to the more acid water districts. This and other epidemiology studies, as well as several studies of the complex aluminum chemistry associated with pH variations suggest that around 7.9 pH, aluminum forms compounds that are more difficult to absorb and of reduced toxicity [7,8]. The study found a 30 percent protective effect for fluoride, in the 0.5–0.98 ppm range. The mechanism by which fluoride acts is not known, but it has been speculated that it reduces aluminum absorption from food or drink, much as is the case with silicon. Fluoride appears to be effective over a fairly wide pH range [26]. There was also a 42 percent reduction in AD risk in water districts with high water turbidity – evidence that the utility had not used alum as a coagulant and but also an indication of possible preventative effects of other constituents of turbid water.

b. Skin, lung and nose absorption. The substantial effect of a more alkaline water pH in reducing both AD and elderly cognitive impairment risks at any given aluminum level is consistent with the idea that absorption of aluminum from drinking water takes place primarily through the more alkaline skin, lung and nose surfaces, as in taking a shower or bath, rather than through the highly acid stomach and the remainder of the gut [29].
The significant correlations shown by seven studies between reduced AD and elderly cognitive impairment risk and higher water pH would not be possible if the gut was the primary surface of absorption, because stomach acid would instantly acidify the water. There is striking evidence from laboratory and worker studies that these more alkaline body surfaces can be relatively efficient in absorbing aluminum. For example, Anane found that aluminum applied to the skin of laboratory animals penetrated to the brain [4,5]. Likewise, Perl and Good found that aluminum injected into the nose of laboratory rabbits went directly into the brain through the olfactory bulb [66]. And Gitelman finds the presence of a sensitive uptake process for aluminum through airway exposure [32]. Davenport and Goodall point out one exception to the suggestion that drinking water aluminum may be primarily absorbed through skin, lung and nose exposure [16]. Reconstitution of orange juice using city water containing aluminum created an elevated aluminum level, and complexed with citrate could present a much greater uptake of aluminum than a similar volume of tap water.

c. Sensitive drinking water epidemiology requires multi-factor analysis. Forbes’ series of multi-factor studies from Ontario, indicate that water districts with drinking water aluminum below 100 ug/liter, with water pH close to 7.9 and with about 1 ppm of fluoride can achieve a 70 percent reduction of elderly mental impairment and large reduction of AD risks [26,28]. The failure of any epidemiology study to control for water pH, with its 50 percent effect, would sharply reduce its likelihood of discovering an effect of aluminum on AD or elderly cognitive impairment risk. That is also true of other active water variables like fluoride, silicon, turbidity and calcium. Two studies conclude that drinking water silicon in excess of 10 ppm completely neutralizes the effects of higher aluminum contamination on both AD and elderly cognitive impairment risk [41,70]. As Jacqmin- Gadda summarized:
“. . . The association between cognitive impairment and aluminum depended on the pH and concentration of silica: high levels of aluminum appeared to have a deleterious effect when silica concentration was low, but there was a protective effect when the pH and the silica level were high. The thresh- old for an aluminum effect, however, was very low (3.5 ug per liter) and did not support the hypothesis of a deleterious effect for only high levels of aluminum” [41].

Silicon bonds with aluminum, and can protect fish from death in waters enriched with aluminum [9]. Similarly, a study of early onset AD in the UK found that when “soluble” silicon in the drinking water exceeded about 3.5 ppm, soluble aluminum fell to very low levels [75]. While the sample size was too small to al- low statistical significance, water districts where soluble silicon levels exceeded 3 ppm experienced a 20 percent reduction of early onset AD risk. Silicon is a safer alternative for high aluminum refractory waters than fluoride, which has been demonstrated to have worrisome biological effects [46,80].

d. Better definition of AD improves epidemiology results. Today, it is still difficult to identify all of the AD cases during life with existing testing methods, which will reduce the sensitivity of any epidemiology study. Unlike Canada, neither death certificates nor methods for measuring aluminum in drinking water are standardized in the United States. As a result, it would be difficult to replicate the Ontario epidemiol- ogy studies on drinking water aluminum in the United States. McLachlan’s study from Ontario confirmed the presence of AD in his drinking water study population based on the Canadian Brain Tissue Bank rather than from death certificates [53,54]. He found that drinking water in excess of 100 ug/liter of aluminum carries an AD risk equivalent to carrying the APOEe4 allele. The effects of aluminum were dose related. The odds ratio of having AD was 2.6 at 100 ug/liter of water aluminum and increased to 7.6 at 175 ug/liter. It should also be noted that an unpublished study by William Forbes found that these odds ratios were increased when fluoride was added as a second variable to McLachlan’s study. An accidental spillage of aluminum sulfate into the water supply of Camelford, UK produced damage to cerebral function that persisted three years among per- sons aged in their early 40’s, although the high exposure period took place over only a few weeks [2]. While the analysis of this spill is controversial because the sample was self-chosen as part of a court case, it employed a very sensitive neurological test method, and the results are similar to findings for dialysis patients, exposed to aluminum but without overt aluminum toxicity [3].

e. Iron coagulants can substitute for alum. Much of the biologically active aluminum exposure from the public water supply comes from alum, aluminum sul- fate, added by the water utility as a coagulant [18,57]. The replacement of alum with iron coagulants not only reduced aluminum contamination,but also reduced iron levels in the finished water which addresses concerns that iron coagulants might pose a risk of iron overload in elderly people [57]. Furthermore, the Framingham Study demonstrated that inorganic iron presented in food and drink is not a significant source of iron over- load to the elderly, suggesting that iron coagulants do not pose the health risk associated with heme iron and vitamin pills [24]. Further, iron coagulants are equally effective if not more so than alum in purifying drink- ing water [15,20,37,57,76] while presenting no additional cost [49,76]. As is the case with substitution of aluminum based baking powder or aluminum based antacids with alternatives constituted with calcium,cost is not the major basis of decision.

f. Control of drinking water pH is an inexpensive method to reduce aluminum toxicity: The Canadian studies by Forbes and McLachlan indicated that the maintenance of drinking water in a pH band close to 7.9 can reduce AD rates by 50 percent. This is an inexpensive program conferring other benefits for water utilities. More alkaline water does reduce corrosion, water main breaks, and leaching of lead and copper into the finished water [45].

McLachlan, 1995: Alzheimer’s Identified From the Canadian Brain Tissue Bank and Compared to Drinking Water Aluminum in Ontario [53][54] • 2.5 Odds Ratio: Drinking water aluminum in excess of 100 ug/liter carried an odds ratio for AD of 2.5, equivalent to the increased risk of developing AD among those with the APOEe4 allele. • 6.7-8.14 Odds Ratio: Depending on how the AD patients were grouped, drinking water containing 175 ug/liter of aluminum was associated with an odds ratio of developing AD of 6.7 to 8.14.

Rondeau et al, 2000: Drinking Water Aluminum and Alzheimer’s in France – An Eight Year Follow-Up Study [70] • 2.14 Odds Ratio: The best fit model (\#5) found drinking water aluminum in excess of 0.10 mg/liter associated with a 2.14 odds ratio for AD. • Silica in excess of 11.25 mg/liter was associated with about a 27 percent reduction of risk. • Control factors included age, gender, education, place of residence and wine consumption.

Jacqmin-Gadda et al, 1996: Silica and Aluminum in Drinking Water and Elderly Cognitive Impairment [41] • The threshold for an effect of aluminum on elderly cognitive impairment was very low at 3.5 ug/liter. • 1.30 Odds Ratio: Water districts with high aluminum but low silica and low pH experienced a 1.30 odds ratio for elderly mental impairment. • 0.75 Odds Ratio: But high aluminum combined with high silica and high pH (in excess of 7.35) showed an odds ratio of only 0.75. French water silica levels range from 4.2 to 22.4 mg/liter, and the threshold for effects on elderly mental impairment was found to be 10.4 mg/liter.

Taylor et al, 1995: Early Onset Alzheimer’s and Drinking Water Aluminum and “Soluble” Silicon in Great Britain [75] • At about 3.5 mg/liter of “soluble” silicon, “soluble” aluminum fell to less than 25 ug/liter in all districts. • 0.8 Odds Ratio: For this population of less than 65 years of age, the odds ratio of having AD where drinking water soluble silicon exceeded 3 mg/liter was 0.8 – suggestive a 20 percent reduction of risk. But the sample size was very small, and the results not statistically significant

Ann Clin Lab Sci. 1996 May-Jun;26(3):227-33

The role of silicic acid in the renal excretion of aluminium.

Bellia JP, Birchall JD, Roberts NB.

Clinical Chemistry Department, Royal Liverpool University Hospital, United Kingdom.

The chemical affinity of silicic acid for aluminium (AI) has been shown to reduce the bioavailability of AI in studies of human gastrointestinal (GI) absorption. Investigations were carried out to ascertain whether or not similar interactions may also enhance the renal excretion of AI by assessing the urinary output of both elements. Healthy individuals given monosilicic acid as naturally found in beer, excreted the majority of the silicic acid content (mean 56 percent) within 8 hours, concomitant with a significant increase in AI excretion (P < 0.05). Ingestion of increasing doses of silicic acid resulted in dose related increases in excretion of Si. Excretion of AI reached a maximum and then declined, consistent with depletion of AI body stores. This was confirmed using the 26AI isotope. The low serum but high urine concentration of Si suggests that if AI and Si interact to form an excretable species they do so in the kidney lumen such that Si limits the reabsorption of AI. Silicic acid's effect on the depletion of aluminium stores and reduced GI absorption suggest its addition to municipal water supplies may be a low risk public health measure to reduce the AI burden in the general population.
Am J Epidemiol. 2000 Jul 1;152(1):59-66.

Relation between aluminum concentrations in drinking water and Alzheimer's disease: an 8-year follow-up study.

Rondeau V, Commenges D, Jacqmin-Gadda H, Dartigues JF.

INSERM Unite 330, Universite Victor Segalen Bordeaux II, France.

To investigate the effect of aluminum and silica in drinking water on the risk of dementia and Alzheimer's disease, the authors analyzed data from a large prospective cohort (Paquid), including 3,777 subjects aged 65 years and over living at home in 75 civil parishes in Gironde and Dordogne in southwestern France in 1988-1989. The subjects were followed for up for 8 years with an active search for incident cases of dementia or Alzheimer's disease. Mean exposure to aluminum and silica in drinking water was estimated in each area. The sample studied included 2,698 nondemented subjects at baseline, for whom components of drinking water and covariates were available. A total of 253 incident cases of dementia (with 17 exposed to high levels of aluminum), including 182 Alzheimer's disease (with 13 exposed to high aluminum levels), were identified. The relative risk of dementia adjusted for age, gender, educational level, place of residence, and wine consumption was 1.99 (95 percent CI: 1.20, 3.28) for subjects exposed to an aluminum concentration greater than 0.1 mg/liter. This result was confirmed for Alzheimer's disease (adjusted relative risk = 2.14, 95 percent CI: 1.21, 3.80). However, no dose-response relation was found. Inversely, the adjusted relative risk of dementia for subjects exposed to silica (> or = 11.25 mg/liter) was 0.74 (95 percent CI: 0.58, 0.96). These findings support the hypothesis that a high concentration of aluminum in drinking water may be a risk factor for Alzheimer's disease.

J Theor Biol. 1997 Nov 21;189(2):133-9.

Hydroxyaluminosilicates and acute aluminium toxicity in fish

Exley C, Pinnegar JK, Taylor H.

Birchall Centre for Inorganic Chemistry and Materials Science, Department of Chemistry, Keele University, Staffordshire, ST5 5BG, U. K.

The essentiality of silicon in biology might be explained in the terms of its chemistry with aluminium. In a previous study we demonstrated the elimination of acute aluminium toxicity in fish by silicon. We suggested that the reaction of silicic acid with aluminium to form hydroxyaluminosilicates reduced the biological availability, and hence toxicity, of aluminium. Though assumed in a burgeoning number of studies and contended in others this detoxification mechanism has remained unproven. Herein we have tested the toxicity of hydroxyaluminosilicates in fish and in doing so we have provided evidence which strongly supports a role for hydroxyaluminiosilicates in the elimination of acute aluminium toxicity in fish by silicon.

Literatuur van voor 2000:
1. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Science 1993;261:921–5.[ISI][Medline]
2. McLachlan DRC. Aluminum and the risk for Alzheimer's disease. Environmetrics 1995;6:233–75.[ISI]
3. Huang Y, Herman MM, Liu J, et al. Neurofibrillary lesions in experimental aluminum-induced encephalopathy and Alzheimer's disease share immunoreactivity for amyloid precursor protein, A beta, alpha 1-antichymotrypsin and ubiquity-protein conjugates. Brain Res 1997;771:213–20.[ISI][Medline]
4. Cucarella C, Montoliu C, Hermenegildo C, et al. Chronic exposure to aluminum impairs neuronal glutamate-nitric oxide-cyclic GMP pathway. J Neurochem 1998;70:1609–14.[ISI][Medline]
5. Roberts NB, Clough A, Bellia JP, et al. Increased absorption of aluminium from a normal dietary intake in dementia. J Inorg Biochem 1998;69:171–6.[ISI][Medline]
6. Alfrey AC, Legendre GR, Kaehny WD. The dialysis encephalopathy syndrome: possible aluminum intoxication. N Engl J Med 1976;294:184–8.[Abstract]
7. Martyn CN, Barker DJP, Osmond C, et al. Geographical relation between Alzheimer's disease and aluminum in drinking water. Lancet 1989;1:59–62.[Medline]
8. Flaten TP. Geographical associations between aluminium in drinking water and death rates with dementia (including Alzheimer's disease), Parkinson's disease and amyotrophic lateral sclerosis in Norway. Environ Geochem Health 1990;12:152–67.[ISI]
9. McLachlan DRC, Bergeron C, Smith JE, et al. Risk for neuropathologically confirmed Alzheimer's disease and residual aluminum in municipal drinking water employing weighted residential histories. Neurology 1996;46:401–5.[Abstract]
10. Forster DP, Newens AJ, Kay DWK, et al. Risk factors in clinically diagnosed presenile dementia of the Alzheimer type: a case-control study in northern England. J Epidemiol Community Health 1995;49:253–8.[Abstract]
11. Martyn CN, Coggon DN, Lacey RF, et al. Aluminum concentrations in drinking water and risk of Alzheimer's disease. Epidemiology 1997;8:281–6.[ISI][Medline]
12. Rifat SL, Eastwood MR, McLachlan DRC, et al. Effect of exposure of miners to aluminium powder. Lancet 1990;336:1162–5.[ISI][Medline]
13. Graves AB, Rosner D, Echeverria D, et al. Occupational exposures to solvents and aluminium and estimated risk of Alzheimer's disease. Occup Environ Med 1998;55:627–33.[Abstract]
14. Graves AB, White E, Koepsell TD, et al. The association between aluminum-containing products and Alzheimer's disease. J Clin Epidemiol 1990;43:35–44.[ISI][Medline]
15. Colin-Jones D, Langman MJS, Lawson DH, et al. Alzheimer's disease in antacid users. (Letter). Lancet 1989;1:1453.
16. Birchall JD, Chappell JS. Aluminium, water chemistry, and Alzheimer's disease (Letter). Lancet 1989;1:953.
17. Exley C, Pinnegar JK, Taylor H. Hydroxyaluminosilicates and acute aluminium toxicity in fish. J Theor Biol 1997;189:133–9.[ISI][Medline]
18. Jacqmin-Gadda H, Commenges D, Letenneur L, et al. Components of drinking water and risk of cognitive impairment in the elderly. Am J Epidemiol 1994;139:48–57.[Abstract]
19. Jacqmin-Gadda H, Commenges D, Letenneur L, et al. Silica and aluminum in drinking water and cognitive impairment in the elderly. Epidemiology 1996;7:281–5.[ISI][Medline]
20. Letenneur L, Commenges D, Dartigues JF, et al. Incidence of dementia and Alzheimer's disease in elderly community residents of south-western France. Int J Epidemiol 1994;23:1256–61.[Abstract]
21. Barberger-Gateau P, Commenges D, Gagnon M, et al. Instrumental activities of daily living as a screening tool for cognitive impairment in elderly community dwellers. J Am Geriatr Soc 1992;40:1229–34.
22. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Edition III revised (DSM-III-R). Washington DC: American Psychiatric Association, 1987.
23. Mc Khann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ARDA work group under the auspices of the department of health and human services task force on Alzheimer's disease. Neurology 1984;34:939–44.[Abstract]
24. Hachinski V, Lliff L, Zilhka F, et al. Cerebral blood flow in dementia. Arch Neurol 1975;32:632–7.[Abstract]
25. Commenges D, Letenneur L, Joly P. Re: "Serum transferrin saturation, stroke incidence, and mortality in women and men. The NHANES I Epidemiologic Followup Study." (Letter). Am J Epidemiol 1997;146:683–4.[ISI][Medline]
26. Commenges D, Letenneur L, Joly P, et al. Modelling age-specific risk: application to dementia. Stat Med 1998;17:1973–88.[ISI][Medline]
27. Klein JP, Moeschberger ML. Survival analysis: techniques for censored and truncated data. New York, NY: Springer-Verlag, 1997.
28. Letenneur L, Gilleron V, Commenges D, et al. Are sex and educational level independent predictors of dementia and Alzheimer's disease? Incidence data from the Paquid project. J Neurol Neurosurg Psychiat 1999;66:177–83.[Abstract/Free Full Text]
29. Orgogozo JM, Dartigues JF, Lafont S, et al. Wine consumption and dementia in the elderly: a prospective community study in the Bordeaux area. Rev Neurol 1997;153:185–92.[Medline]
30. Folstein MF, Folstein SE, McHugh PR. "Mini-Mental State": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975;12:189–90.[ISI][Medline]
31. Jacqmin-Gadda H, Fabrigoule C, Commenges D, et al. A 5-year longitudinal study of the Mini- Mental State Examination in normal aging. Am J Epidemiol 1997;145:498–506.[Abstract]
32. Aalen OO. Effects of frailty in survival analysis. Stat Methods Med Res 1994;3:227–43.[Medline]
33. Forbes WF, McAiney LM, Agwani N. Geochemical risk factors for mental functioning based on the Ontario Longitudinal Study of Aging (LSA) II. The role of pH. Can J Aging 1994;13:249–67.[ISI]
34. Taylor GA, Ferrier IN, McLoughlin IJ, et al. Gastrointestinal absorption of aluminium in Alzheimer's disease: response to aluminium citrate. Age Ageing 1992;21:81–90.[Abstract]
35. Birchall JD. The interrelationship between silicon and aluminium in the biological effects of aluminium. (Ciba Found Symp 169). Chichester, England: John Wiley & Sons, 1992;50–68.
36. Belles M, Sanchez DJ, Gomez M, et al. Silicon reduces aluminum accumulation in rats: relevance to the aluminium hypothesis of Alzheimer disease. Alzheimer Dis Assoc Disord 1998;12:83–7.[ISI][Medline]

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