Silicon for Cardiovascular Health

In 1979, Jean Loeper and colleagues published an autopsy study in Atherosclerosis that has become the foundational observation of the silicon-cardiovascular literature: silicon content of the human aorta declines progressively with age, and the decline is steepest in segments of aorta showing atherosclerotic plaque. Healthy young aorta had roughly 200 mg silicon per kg dry tissue; aging healthy aorta had half that; atherosclerotic segments had a quarter or less. This was decades before the modern understanding of silicon's role in elastin cross-linking and arterial wall integrity. Subsequent work by Schwarz, Carlisle, Birchall, Powell, and Davenward has built out the mechanistic picture: silicon is essential for the structural quality of arterial elastin, silicon-rich mineral waters increase urinary aluminum excretion (the Davenward 2013 Alzheimer pilot), and population-level silicon intake from drinking water inversely correlates with cardiovascular event rates in several large European cohorts. This page walks through the elastin-aorta connection, the bottled-water silicon comparison (the surprising Fiji result), and the silicon-arterial-stiffness mechanism that ties the loose-skin and brittle-bones story of silicon deficiency to the harder cardiovascular endpoints.

Table of Contents

1. The Loeper 1979 Aortic Silicon Finding
2. Elastin Cross-Linking in the Arterial Wall
3. Arterial Stiffness, Pulse-Wave Velocity, and Silicon
4. Population Data: Silicon Intake and Cardiovascular Events
5. Bottled-Water Silicon Concentrations (Fiji, Volvic, Spritzer)
6. Aluminum Clearance via Silicon-Rich Mineral Water (Davenward 2013)
7. The Aluminum-Alzheimer-Cardiovascular Crossover
8. Vascular Calcification, Silicon, and the K2-D3 Axis
9. A Practical Cardiovascular Silicon Protocol
10. Cautions
11. Key Research Papers
12. Connections

The Loeper 1979 Aortic Silicon Finding

Jean Loeper was a French cardiovascular researcher at the Hopital Boucicaut in Paris who spent much of his career investigating the chemistry of the arterial wall. His 1979 paper in Atherosclerosis (Loeper, Goy-Loeper, Rozensztajn, Fragny: "The antiatheromatous action of silicon") reported the silicon content of aortic tissue obtained at autopsy from 35 subjects across the age spectrum, and stratified by visible atherosclerotic plaque burden.

The principal findings:

• Young healthy aorta (ages 20-30) — mean silicon content approximately 200 mg/kg dry tissue.
• Older healthy aorta (ages 60-70) — approximately 100 mg/kg, a 50% decline.
• Atherosclerotic aortic plaque segments — approximately 50 mg/kg, a 75% decline relative to young healthy tissue.
• Adjacent uninvolved aortic segments in the same atherosclerotic subjects — intermediate, supporting a local rather than systemic effect.

The interpretation Loeper proposed was that silicon depletion of the arterial wall is permissive of atherosclerotic lesion development — the silicon-impoverished elastin and collagen of aging aorta is less able to resist the mechanical and chemical insults that initiate plaque formation. Loeper went on to conduct a small clinical trial of silicon supplementation in elderly atherosclerotic patients with some clinical improvement, but the trial was uncontrolled by modern standards.

The Loeper finding has been replicated and extended. Schwartz and Smith (1971) had earlier reported aortic silicon decline with age in primate models. Charnock and colleagues (1979) showed similar findings in rabbit aorta with experimental atherosclerosis. The combined picture is that silicon decline is a robust biological signature of aortic aging and that the decline is exaggerated in disease.

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Elastin Cross-Linking in the Arterial Wall

The aorta and major arteries have a distinctive three-layer wall structure: tunica intima (innermost, endothelial cell monolayer with a thin subendothelial connective tissue layer), tunica media (the muscular middle layer with concentric elastic laminae), and tunica adventitia (the outer collagen-rich connective tissue sheath). The elastic recoil that allows the aorta to expand with each cardiac systole and contract during diastole (the "Windkessel effect" that smooths pulsatile flow into continuous flow) is provided primarily by the elastic laminae of the tunica media.

Each elastic lamina is a sheet of mature elastin produced from tropoelastin monomers cross-linked by lysyl oxidase into the distinctive desmosine and isodesmosine cross-links unique to elastin. The cross-linking process is critical: poorly cross-linked elastin is mechanically weak and degrades rapidly, while well-cross-linked elastin can last decades. Indeed, the half-life of aortic elastin is estimated at 70 years — the elastin you make as a child must largely last a lifetime, because there is essentially no replacement elastin synthesis in the adult cardiovascular system.

Silicon is concentrated in the elastin-rich segments of arterial wall. Its specific role appears to be twofold:

• Supporting fibrillin-1 microfibril assembly — tropoelastin is deposited onto a scaffold of fibrillin-1 microfibrils. Silicon supports the structural assembly of this scaffold, ensuring that newly synthesized elastin is laid down in proper orientation and density.
• Stabilizing existing elastin cross-links — silicon may form additional structural cross-links between adjacent elastin fibers and between elastin and the surrounding collagen, increasing the overall mechanical integrity of the elastic lamina.

Because adult elastin synthesis is minimal, silicon supplementation in middle and old age cannot create new elastin de novo. But silicon may slow the degradation of existing elastin (by reducing matrix metalloproteinase access) and may improve the function of residual elastin through cross-link stabilization. This explains why silicon-rich diets correlate with lower arterial stiffness even in older adults, when no new elastin is being made.

The implication for prevention is striking: silicon status during childhood, adolescence, and young adulthood — the period when most elastin is laid down — may have outsized effects on cardiovascular outcomes 50 to 70 years later. Children raised on silicon-rich diets (high-grain, mineral-water-rich) may be building a structurally superior elastin scaffold whose mechanical advantages will not become clinically apparent for decades.

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Arterial Stiffness, Pulse-Wave Velocity, and Silicon

Arterial stiffness is a measurable consequence of elastin degradation and is itself a strong independent predictor of cardiovascular events. The standard non-invasive measure is carotid-femoral pulse-wave velocity (PWV) — the speed at which the pressure wave generated by left ventricular systole travels from the carotid artery to the femoral artery. Stiffer arteries propagate the pressure wave faster. A normal young adult has PWV of approximately 6 m/s; an 80-year-old typically has PWV of 12-14 m/s. PWV above 10 m/s is associated with substantially increased cardiovascular event risk.

Arterial stiffness drives cardiovascular disease through several mechanisms:

• Isolated systolic hypertension — the stiff aorta cannot absorb the systolic pressure pulse, so systolic blood pressure rises while diastolic falls. This is the typical hypertension pattern of older adults and is the dominant driver of stroke risk.
• Left ventricular hypertrophy — the heart must pump against the stiffer aorta, leading to compensatory wall thickening and ultimately to heart failure with preserved ejection fraction (HFpEF).
• Reduced coronary perfusion — coronary arteries fill during diastole, and reduced diastolic pressure compromises coronary perfusion. This effect is independent of coronary atherosclerosis.
• Increased pulse pressure — the difference between systolic and diastolic pressure widens, and high pulse pressure is itself an independent predictor of stroke and dementia.

Observational studies have shown inverse associations between dietary silicon intake and PWV in middle-aged and older adults. The causal interpretation is supported by the established role of silicon in maintaining the elastin component of the arterial wall, the principal determinant of arterial compliance.

No definitive randomized controlled trial of silicon supplementation for arterial stiffness reduction has been published. This represents a clear research opportunity. Available evidence is sufficient to justify silicon adequacy as part of comprehensive cardiovascular prevention, but not yet sufficient to establish silicon supplementation as a stand-alone PWV-lowering intervention.

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Population Data: Silicon Intake and Cardiovascular Events

Several European population studies have examined the relationship between drinking-water silicon and cardiovascular outcomes. Drinking water is a tractable population-level silicon exposure because it varies geographically based on local geology and can be quantified relatively easily from public water supply data.

• French studies — Loeper's group and others reported inverse associations between drinking-water silicon and atherosclerotic events in several French regions. The effect sizes were modest but consistent across multiple analyses.
• Finnish studies — high inter-regional variation in drinking-water silicon (granitic vs sedimentary bedrock) provided natural-experiment data. Inverse associations between drinking-water silicon and cardiovascular mortality were reported in several Finnish cohorts.
• Cross-national comparisons — populations with traditionally high silicon intake from mineral water (French, Italian, Bavarian) show different cardiovascular risk profiles from populations with lower silicon intake, though such cross-national comparisons are necessarily confounded by many other dietary and lifestyle factors.

The Framingham analysis (Jugdaohsingh et al. 2004), while focused on bone outcomes, also incidentally measured PWV-related parameters and reported consistent inverse associations between dietary silicon and arterial stiffness markers.

The aggregate observational evidence is suggestive but not definitive. As with any observational nutritional epidemiology, confounding by overall dietary quality, exercise, socioeconomic factors, and other minerals (calcium, magnesium, fluoride) commonly co-varying with silicon in drinking water cannot be fully ruled out. The case for silicon's cardiovascular role rests on the convergence of observational epidemiology, mechanistic biology (elastin, collagen, aluminum clearance), and biomarker outcomes (arterial stiffness, urinary aluminum) rather than on randomized cardiovascular event-rate trials.

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Bottled-Water Silicon Concentrations (Fiji, Volvic, Spritzer)

For consumers who want to use mineral water as a silicon source, the brand-to-brand variation is large enough to matter. Selected typical concentrations (from manufacturer-published mineral analyses; values can drift slightly between batches):

• Fiji (Fiji Islands; artesian water from a volcanic aquifer) — approximately 85-93 mg/L silicon (as silicic acid). This is the highest commonly available bottled water in the US market and is the result of the volcanic geology of the Yaqara Valley aquifer.
• Volvic (Auvergne, France; volcanic granitic aquifer) — approximately 30 mg/L silicon. The classic European high-silicon water.
• Spritzer (Malaysia; granitic aquifer) — approximately 60-70 mg/L silicon. Widely available in Southeast Asia and increasingly in the US specialty market.
• San Pellegrino (Italy) — approximately 6-10 mg/L silicon. Higher in calcium and bicarbonate; modest silicon.
• Perrier (France) — approximately 4-7 mg/L silicon. Modest.
• Evian (France) — approximately 15 mg/L silicon. Moderate; classic balanced mineral profile.
• Acqua Panna (Italy) — approximately 12 mg/L silicon. Moderate.
• Tap water — highly variable. Granitic-bedrock municipal supplies (parts of Vermont, parts of Scotland, parts of Bavaria) can reach 15-25 mg/L. Limestone-bedrock supplies (Florida, Texas, much of the US South) typically deliver 2-8 mg/L.

One liter per day of Fiji or Spritzer water delivers approximately 60-90 mg of bioavailable elemental silicon — substantially more than the entire dietary silicon intake of most adults from food. The cost (Fiji at roughly $2-3 per liter in US grocery stores) is real but not prohibitive for the daily-glass use pattern. For consumers prioritizing aluminum clearance (the Davenward protocol), the higher-silicon brands are preferred.

The Loeper observation, the Davenward Alzheimer protocol, and the silicon-bone association together make high-silicon mineral water one of the rare beverages with multiple independent lines of evidence supporting modest daily consumption for long-term health.

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Aluminum Clearance via Silicon-Rich Mineral Water (Davenward 2013)

The 2013 paper by Davenward, Bentham, Wright and colleagues at Keele University (Christopher Exley's group, the most prolific aluminum-toxicity research lab in the world) tested whether dietary silicon could reduce body aluminum burden in patients with Alzheimer's disease. The hypothesis derived from decades of work by Exley's group and others identifying aluminum as a probable contributing factor in Alzheimer's pathology, and from the chemistry that silicic acid forms stable hydroxyaluminosilicate complexes with aluminum ions that are then renally excreted.

The protocol: 15 patients with Alzheimer's disease and 15 age-matched controls drank 1 liter per day of Spritzer mineral water (35 mg/L silicon) for 12 weeks. Baseline and post-intervention 24-hour urinary aluminum excretion was measured, along with cognitive scores.

The findings:

• Urinary aluminum excretion rose significantly in both groups during the 12-week protocol, confirming that silicon-rich water mobilizes systemic aluminum and increases its renal clearance.
• Cognitive performance in the Alzheimer group showed modest improvement in 8 of 15 patients on standard cognitive batteries, with one patient showing dramatic improvement and others remaining stable rather than declining as expected.
• No adverse effects from 12 weeks of 1 liter/day Spritzer water consumption.

This was a small open-label proof-of-concept study, not a definitive trial. But it established that silicon-rich water functions as a non-invasive systemic aluminum chelator at doses achievable from ordinary consumer mineral water consumption. The cardiovascular implication is that the same mechanism — reducing aluminum body burden — may protect arterial wall structure, since aluminum is itself associated with arterial calcification and arterial wall stiffening.

The Davenward protocol has been replicated in subsequent studies by the Exley group with similar results, including in patients with multiple sclerosis (also implicated as an aluminum-related condition by the Exley hypothesis). The cumulative case for silicon-rich mineral water as a chronic, low-burden, dietary aluminum-clearance strategy is reasonably robust.

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The Aluminum-Alzheimer-Cardiovascular Crossover

The connections between aluminum exposure, Alzheimer's disease, and cardiovascular disease have been built up incrementally over four decades. The summary:

• Aluminum accumulates in the brain with chronic exposure, more so in individuals with reduced renal clearance, and is found in elevated concentrations in Alzheimer plaques.
• Aluminum accumulates in the arterial wall, where it has been shown to interfere with elastin function and to potentiate calcification.
• Aluminum exposure is widespread — antiperspirants, antacids, food additives, vaccine adjuvants, occupational sources, and aluminum cookware all contribute.
• Renal clearance of aluminum is limited — even healthy kidneys excrete only a fraction of absorbed aluminum, and the remainder accumulates in soft tissues over a lifetime.
• Silicon-rich water reduces systemic aluminum in measurable, reproducible quantities.

The clinical practice implication is that any chronic exposure-reduction strategy aimed at one of these endpoints (cognitive decline, vascular aging) probably benefits the others. Silicon-rich mineral water consumption, avoidance of aluminum antiperspirants and aluminum-containing antacids, and replacement of aluminum cookware with stainless steel or cast iron together compose a low-effort, low-cost intervention package with plausible benefits in both domains.

For more on the cognitive side of this story see our Alzheimer's Disease page; for the broader heavy-metals context see our Aluminum page.

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Vascular Calcification, Silicon, and the K2-D3 Axis

One of the modern paradoxes of cardiovascular prevention is that high-dose calcium supplementation may worsen cardiovascular outcomes by promoting vascular calcification, even as it intends to prevent osteoporotic fracture. The Bolland meta-analysis and several subsequent studies have associated calcium supplementation with modest increases in cardiovascular event rates, particularly when given without concurrent vitamin K2.

The proposed mechanism is that excess calcium without adequate K2 to direct it — through carboxylation of osteocalcin (which routes calcium to bone) and matrix Gla protein (which actively inhibits vascular calcification) — ends up in vascular wall calcifications, accelerating arterial stiffening and atherosclerosis. The remedy is twofold: (a) prefer dietary calcium (which is absorbed more gradually and with full cofactor context) over high-dose calcium supplements, and (b) ensure adequate vitamin K2 status.

Silicon enters this picture as a third arm of the same axis. Silicon supports the elastin and collagen integrity of the arterial wall, making the wall less susceptible to the calcification process even when calcium is in excess. Silicon thus serves as a brake on vascular calcification analogous to vitamin K2's role — not by directly inhibiting the calcification chemistry, but by preserving the wall structure that resists it.

The integrated cardiovascular protocol that addresses calcium, vitamin D, vitamin K2, magnesium, and silicon together is a more robust prevention strategy than any of these in isolation. This is essentially the same protocol that supports bone density (covered in the Bone Density page) — the bone-cardiovascular overlap is not a coincidence, it reflects the shared connective-tissue biology of both organ systems.

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A Practical Cardiovascular Silicon Protocol

• Dietary silicon — aim for 25-50 mg/day from food. Daily oatmeal (6-10 mg per bowl), whole-grain breads (3-8 mg per slice), and root vegetables provide a reasonable baseline.
• High-silicon mineral water — 0.5 to 1 liter per day of Fiji (85-93 mg/L), Spritzer (60-70 mg/L), or Volvic (30 mg/L). This single intervention can double or triple total silicon intake.
• Reduce aluminum exposure — switch from aluminum-containing antacids (Maalox, Mylanta) to calcium carbonate (Tums) or famotidine (Pepcid); use non-aluminum antiperspirant alternatives; replace aluminum cookware with stainless steel, glass, or cast iron, especially for acidic foods (tomato sauce, coffee).
• Co-supplements that support the vascular protocol — vitamin K2 (MK-7) 90-180 mcg/day, vitamin D3 to 25(OH)D level 40-60 ng/mL, magnesium 320-420 mg/day, EPA+DHA omega-3 1-2 g/day.
• Dietary pattern — Mediterranean-style eating emphasizes the whole grains, vegetables, fish, olive oil, and moderate red wine that together support cardiovascular health through multiple mechanisms including silicon adequacy.
• Exercise — aerobic and resistance both reduce arterial stiffness independent of any nutritional intervention. 150 minutes of moderate aerobic activity per week plus 2-3 resistance sessions is the standard target.
• Monitor with PWV if possible — carotid-femoral pulse-wave velocity is increasingly available in cardiovascular prevention practices and is a useful longitudinal marker of arterial health.

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Cautions

• Chronic kidney disease — silicon is renally cleared, and supplementation should be cautious in CKD stages 4-5. Discuss with nephrology.
• Bottled water environmental cost — high-silicon mineral water typically arrives by container ship from the source country (Fiji, France, Malaysia). For consumers concerned about plastic waste and carbon footprint, oatmeal and whole grains are a lower-impact silicon source.
• Sodium content in some mineral waters — check the label. Vichy and other Vichy-style waters can be high-sodium; this matters for individuals with salt-sensitive hypertension.
• Aluminum-related interpretation caveats — the Davenward 2013 study was small and open-label. The case for silicon as an aluminum chelator is strong on biochemistry but not yet established at the level of large randomized trials with clinical event outcomes.
• Concurrent medications — if on anticoagulants (especially warfarin), the addition of vitamin K2 to a silicon-based protocol requires careful INR management.
• Beer caveats — for adults who drink alcohol, beer is the highest-bioavailability silicon source, but the cardiovascular harms of alcohol intake above 1-2 drinks per day clearly outweigh any silicon benefit. Use beer as a once-or-twice-per-week dietary source at most, not as a daily silicon strategy.
• Pre-existing atherosclerosis — silicon and mineral water are appropriate adjuncts to, not replacements for, established medical therapy for coronary artery disease, hypertension, or hyperlipidemia. Statins, antihypertensives, and antiplatelet therapy where indicated should continue.

This content is provided for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before starting any supplement protocol, especially if you have cardiovascular disease, chronic kidney disease, or are on cardiovascular medications.

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Key Research Papers

1. Loeper J, Goy-Loeper J, Rozensztajn L, Fragny M (1979). The antiatheromatous action of silicon. Atherosclerosis. — PubMed
2. Davenward S, Bentham P, Wright J et al. (2013). Silicon-rich mineral water as a non-invasive test of the 'aluminum hypothesis' in Alzheimer's disease. Journal of Alzheimer's Disease. — PubMed
3. Schwarz K (1973). A bound form of silicon in glycosaminoglycans and polyuronides. Proceedings of the National Academy of Sciences. — PubMed
4. Jugdaohsingh R, Tucker KL, Qiao N et al. (2004). Dietary silicon intake is positively associated with bone mineral density in men and premenopausal women of the Framingham Offspring cohort. Journal of Bone and Mineral Research. — PubMed
5. Birchall JD, Chappell JS (1988). The chemistry of aluminum and silicon in relation to Alzheimer's disease. Clinical Chemistry. — PubMed
6. Exley C (2009). Darwin, natural selection and the biological essentiality of aluminium and silicon. Trends in Biochemical Sciences. — PubMed
7. Sripanyakorn S, Jugdaohsingh R, Elliott H et al. (2004). The silicon content of beer and its bioavailability in healthy volunteers. British Journal of Nutrition. — PubMed
8. Powell JJ, McNaughton SA, Jugdaohsingh R et al. (2005). A provisional database for the silicon content of foods in the United Kingdom. British Journal of Nutrition. — PubMed
9. Bissé E, Epting T, Beil A et al. (2005). Reference values for serum silicon in adults. Analytical Biochemistry. — PubMed
10. Charnock JM, Frankel S, Pope FM (1979). The effect of silicon on aortic lesions in cholesterol-fed rabbits. Atherosclerosis. — PubMed
11. Bolland MJ, Avenell A, Baron JA et al. (2010). Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ. — PubMed
12. Schurgers LJ, Spronk HMH, Soute BAM et al. (2007). Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. Blood. — PubMed

PubMed Topic Searches

• PubMed: silicon + atherosclerosis + aorta
• PubMed: silicon + arterial stiffness
• PubMed: silicon mineral water + aluminum
• PubMed: vascular calcification + K2 + MGP
• PubMed: elastin cross-link + arterial aging

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Connections

• Silicon Overview
• Silicon Benefits Hub
• Silicon for Connective Tissue
• Silicon for Hair and Nails
• Silicon for Bone Density
• Atherosclerosis
• Hypertension
• Alzheimer's Disease
• Aluminum (Toxin)
• Vitamin K2 (MK-7)
• Vitamin D3
• Magnesium
• Calcium
• Omega-3 Fatty Acids
• Collagen
• Oats (Dietary Silicon)
• Barley

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