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Part 6 - Where Did All This Iron Come From?

  • Writer: Bowie Matteson
    Bowie Matteson
  • Nov 14, 2025
  • 20 min read

Updated: Nov 15, 2025

By now we've illustrated the volatile nature of iron in the body. In being the catalyst for cellular energy, iron has the unique ability to both enliven and eliminate a cell. This balance between go and stop, yes and no, upregulate or downregulate lies in the cell's ability to harness and funnel iron's innate reactivity into productive outcomes. For those of us with chronic inflammation and its resulting symptoms and disorders (of which iron has left fingerprints all over), our main concern now it tracing exactly how this situation came to be.


In Part 6 we aim to uncover where exactly all of this iron came from. We also consider whether this is a sheer iron volume issue. What cast of vitamins, minerals and nutrients go into regulating iron? Is this something directly tied to iron itself, or rather the systems designed to keep it in check? Perhaps some combination of both.


Story of enrichment and fortification. Why? Who? When?


In medieval Europe, white flour, or ground whole wheat with the outer bran and germ of the grain removed, was deemed “healthier” than its whole flour counterpart. It was more mold-resistant and was lauded as a sign of social status among the Middle Age noble-elite. (IE you could afford to have your wheat specially treated). As a result, white flour persisted as the primary food staple into the 20th century.



In the early 20th century, food science was beginning to become more mainstream. Benjamin Jacobs, a chemist studying food and nutrition, began noting the differences in nutrient profiles of unprocessed and processed wheat flour. Wheat bran, or the outer shell, is rich in insoluble fiber and some trace minerals, while the wheat germ is about 10% fat (thus contributing to its decreased shelf life) and rich in B-vitamins. The endosperm, or innermost part of wheat, is the budding seed’s reservoir of nutrients. Things like iron, carbohydrates, proteins and B-vitamins are found there.


Thus, the white flour Jacobs saw was missing much of the insoluble fiber and B-vitamins that the stripped layers offered. Additionally, the bleaching process of the white flour after it was ground stripped a significant portion of the original nutrients of the endosperm. Jacobs, working for the US Bureau of Chemistry (what would become the FDA), established standards for modifying flour to contain added vitamins and minerals that were lost in processing. This was fast-tracked by the increased demand on American crops during World War I, when Europe was experiencing a widespread crop failure.



In the 1930s, on the heels of World War II and reeling from the Great Depression, the health of the American public was of government concern. The enrichment of white flour, because of its ubiquity across multiple social classes, was beginning to become an international standard. This served to ease the food requirements and decrease nutrient deficiencies during war-time rationing.


*An important note here is the general sentiment behind society-wide programs like grain fortification. These programs were put in place to avoid catastrophic deficiencies like those seen in the Industrial Revolution and the Irish Potato Famine. It was a way of ensuring an able-bodied workforce (especially during wartime). "Health" as we've come to know it was not in the conversation around enrichments and fortification. The nuance and balance of the mineral web was something yet undiscovered and altogether secondary to keeping people alive. But in the wake of long-term exposure to these programs there is a clear difference between warding off catastrophe and promoting sustainable health.

Iron was one of those nutrients added to the processed flour. It has since made its way into every consumable grain including cereals, rice and maize.

Check the ingredient list for almost every bread, baked good or granola product in your home. Enriched wheat flour will be one of them. Included in that enrichment are niacin (B3), reduced iron, thiamin mononitrate (B1), riboflavin (B2) and folic acid (B9). Reduced iron is sometimes listed as ferrous sulfate or iron sulfate.



These selective additions in the enrichment process upheld the linear, mechanistic ideas of modern science that the body is a series of individual parts that complete the whole. Much like the engine of a car, missing or faulty parts could be isolated, repaired and/or replaced to return to function. But this isolated replacement strategy failed to recognize the greater web of nutrient interactions. Consider why these specific nutrients, IE iron and B vitamins, were selected above the rest of the lost nutrients. The answer probably probably lies behind their visible energetic roles. As in, their replacement in the diet had the most immediate impact on consumer energy levels.


Those trace minerals and fat solubles, while not immediately recognized for their outward health benefits, serviced the interconnected systems designed to optimize those more visible energetic pathways; Both sets of nutrients being important cofactors for antioxidants in the cell and ensuring proper iron management in the liver, blood and immune systems. The reasoning goes:

  1. Our people lack energy. When we supplement iron and B-vitamins, their energy is immediately restored. The other minerals lack the clear-cut roles in energy output.

  2. To repeat this short-term positive feedback (more energy) let's microdose the staple crops to ensure long-term results.


Like gas to a flame, the fortifications are good for a burst of energy but neglect the body's inherent systems designed to self-regulate. Every time an enriched good is eaten there is a small hit of energy, but an overall loss in the stability of the system as a whole.

Over time the energy centers become scorched and we've underserved the materials necessary to maintain them.

🥖 The Wheat Example: More Than Just a Carb

As we began, refining wheat into white flour offers the perfect metaphor for what happened to the food supply: in the pursuit of shelf life, texture, and scalability, we filtered out the parts of food that made it whole.


  • What was removed?

    • The bran: rich in magnesium, zinc, fiber, and antioxidant compounds

    • The germ: a source of fat-soluble vitamins (like vitamin E), B-vitamins, and essential fatty acids

    • What remained: energy-dense carbohydrate and protein structures without the co-factors necessary to properly metabolize them

  • What was added back in?

    • Fortification programs reintroduced iron, folic acid, thiamine (B1), niacin (B3), riboflavin (B2)—but not in the ratios or forms found in nature

    • These enrichments focused on preventing catastrophic deficiencies (e.g., rickets, pellagra, beriberi), but didn’t consider long-term consequences of overloading reactive metals like iron in the absence of their buffering partners (e.g., copper, magnesium, vitamin A/E)


This set the precedent for how nearly all modern food processing operates: removal of complexity, replacement with simplification.


🧪 The Anatomy of a Processed Food

Here’s what goes into most industrially processed foods and how each component alters nutrient dynamics or health signaling:


1. Refinement & Extraction

  • Examples: White flour, white rice, cane sugar, seed oils

  • Result: Removes co-factors, antioxidants, and structural diversity

  • Impact: Drives insulin response, oxidative stress, mineral depletion


2. Shelf Stabilizers & Preservatives

  • Examples: BHA/BHT, sodium benzoate, EDTA, nitrates/nitrites

  • Function: Inhibit bacterial or oxidative degradation

  • Impact: Can disrupt gut bacteria, generate ROS, or create reactive byproducts under heat or pH changes


3. Fortification & Enrichment

  • Intent: Replace nutrients lost in processing (e.g., iron, folic acid)

  • Problem: Often in inorganic, highly reactive forms (e.g., ferrous sulfate), and added in isolation without cofactors (e.g., copper, molybdenum, B6)

  • Effect: Can overload redox pathways, especially in individuals with impaired detox, slow methylation, or iron retention tendencies


4. Emulsifiers & Binders

  • Examples: Polysorbate-80, carrageenan, xanthan gum, guar gum

  • Purpose: Texture, mouthfeel, homogenization

  • Impact: Linked to increased intestinal permeability, altered mucus barrier, and gut dysbiosis


5. Flavor Enhancers & Artificial Sweeteners

  • Examples: MSG, aspartame, sucralose

  • Role: Hijack dopamine and taste receptors

  • Impact: Disrupt metabolic feedback loops, blunt insulin and leptin sensitivity


6. Colorants & Visual Modifiers

  • Examples: Red 40, Yellow 5, titanium dioxide

  • Use: Visual appeal, consistency

  • Risk: Some are banned in Europe due to behavioral or toxicological concerns (e.g., hyperactivity, immune irritation)


7. Herbicide/Pesticide Residues

  • Glyphosate (Roundup): Patented as an antibiotic; chelates minerals like zinc, copper, manganese

  • Atrazine, 2,4-D, Paraquat: Linked to endocrine disruption, neurological decline, and oxidative stress

  • Impact on food: These chemicals can deplete soil nutrient quality, alter crop uptake, and act as xenoestrogens or pro-inflammatory triggers


8. Artificial Fertilizers (NPK)

  • Formulated to optimize plant growth, but not plant nutrition

  • Over time, these fertilizers degrade soil biodiversity and limit the uptake of trace minerals, including selenium, chromium, iodine, and zinc

  • Crops may look robust but are hollow in micronutrient complexity

🧬 The Hidden Cost: Rewired Metabolism

The outcome of this evolution? A food system that:


  • Overfeeds calories but underfeeds cells

  • Favors rapid energy (glucose, iron, synthetic B-vitamins) without systemic balance

  • Skews metabolism toward inflammation, insulin resistance, and iron retention

  • Gradually shifts us from adaptation to compensation—until disease manifests

🧲 Iron: The Poster Child of Misguided Fortification

A critical takeaway in this chapter: iron fortification exemplifies the mismatch between well-meaning public health policies and biochemical nuance.


  • Reactive iron compounds like ferrous sulfate or reduced iron are often poorly absorbed and can oxidize lipids, proteins, and DNA in the gut

  • Without balancing nutrients like copper, vitamin A, B2, molybdenum, and magnesium, this extra iron accumulates

  • In those predisposed to iron retention or chronic inflammation, it sets the stage for oxidative stress, microbial imbalance, and beta cell damage



🧭 How Processed Foods Promote Iron Dysregulation


  1. 🥖 Refinement & Extraction  (e.g., white flour, sugar, seed oils)


Mechanism of Iron Disruption

Impact on Metabolic Health

Removes key cofactors for iron metabolism:


- Magnesium, copper, zinc, molybdenum, B2, B6 


 → Strips the very nutrients needed for safe iron transport, usage, and storage.

Promotes unbuffered iron absorption, destabilizes redox balance, sets stage for free radical damage.


  1. 🧂 Fortification & Enrichment  (e.g., ferrous sulfate, folic acid, B vitamins)


Mechanism of Iron Disruption

Impact on Metabolic Health

Iron is reintroduced in reactive, non-heme forms (e.g., reduced iron, electrolytic iron)


– Often without cofactors


– Tends to oxidize before being absorbed


– Triggers gut inflammation

Leads to subclinical overload, especially in those with poor detox capacity or low ceruloplasmin/copper stores. Over decades, accumulates in liver, pancreas, brain.


  1. 🧪 Shelf Stabilizers & Preservatives  (e.g., BHA, BHT, EDTA)


Mechanism of Iron Disruption

Impact on Metabolic Health

EDTA and others act as metal chelators but may mobilize iron in unpredictable ways


– Some create pro-oxidant byproducts when exposed to heat or acid


– Inhibit glutathione recycling

Can confuse intracellular iron signaling, impair detox, or worsen ROS conditions that call for the iron-hiding response.


  1. 🍦 Emulsifiers & Binders  (e.g., polysorbate 80, carrageenan)


Mechanism of Iron Disruption

Impact on Metabolic Health

Shown to erode the gut mucus barrier and increase permeability


– This exposes immune cells to dietary iron and pathogens, triggering inflammation

Stimulates hepcidin production, locks away iron in tissues, inhibits erythropoiesis, and disrupts iron–copper ratio.


  1. 🧁 Flavor Enhancers & Sweeteners  (e.g., MSG, aspartame)


Mechanism of Iron Disruption

Impact on Metabolic Health

Can overstimulate glutamate pathways, increasing metabolic demand and ROS


– Also impair GABA production, which normally slows sympathetic stress signaling

Chronically elevated stress increases iron retention, worsens oxidative tone, and may push beta cells toward burnout.


  1. 🎨 Colorants & Visual Modifiers  (e.g., Red 40, Yellow 5)


Mechanism of Iron Disruption

Impact on Metabolic Health

Often contain metal-based pigments (aluminum, titanium)


– These compete with zinc and iron transporters in the gut

Indirectly lead to micronutrient imbalance, disturb metallothionein function (which governs zinc/copper/iron equilibrium).


  1. 🌿 Pesticide/Herbicide Residues  (e.g., glyphosate)


Mechanism of Iron Disruption

Impact on Metabolic Health

Glyphosate chelates minerals like manganese, iron, and copper 


– Damages cytochrome P450 enzymes in the liver


– Reduces bile flow, key for fat-soluble nutrient uptake

Reduces ability to clear iron safely, increases intestinal permeability, and promotes dysbiosis that favors iron-hungry pathogens.


  1. 🧫 Artificial Fertilizers (NPK)


Mechanism of Iron Disruption

Impact on Metabolic Health

NPK reduces soil biodiversity, resulting in crops that are mineral-poor and imbalanced in iron–copper–zinc ratio 


– Especially low in selenium, boron, molybdenum for fat-soluble nutrient uptake

Consuming these plants contributes to low-grade iron retention paired with trace mineral depletion, compromising the redox buffering system.

🔁 The Result: A Metabolic Feedback Loop


  1. Processed foods = more iron in, less support out

  2. Imbalanced absorption → tissue storage

  3. Storage → oxidative stress, gut disruption, inflammation

  4. Inflammation → hepcidin upregulation, further sequestration

  5. Over time, this inflamed terrain undermines liver, gut, and immune systems — the very systems designed to protect the beta cell

  6. Beta cell dysfunction → diabetes, metabolic syndrome, accelerated aging

Indirect Iron Influencers

Part of what leads to iron's over-inflated influence doesn't necessarily have anything to do with iron itself. Yes, there may be too much coming in, but we've also become poorly equipped to safely manage what's already here.


Competitive inhibitors, like aluminum, push iron out into circulation where it can exert its volatility. Additives like citrate, in excess, can down-regulate ceruloplasmin, decreasing the body's ability to safely mobilize iron stores. Glyphosate blocks iron balancers like zinc and copper and primes cell membranes for ROS vulnerability.


Let's explore how.


🧪 Aluminum and Iron: A Competitive & Disruptive Relationship


⚖️ 1. Absorption Competition at the Gut Level

  • Aluminum and iron share similar transport mechanisms, particularly through DMT1 (divalent metal transporter 1) in the small intestine.

  • When dietary aluminum is present (from cookware, food additives, pharmaceuticals like antacids), it competes with iron for uptake, effectively acting as a competitive inhibitor.

  • This may initially reduce serum iron absorption, but paradoxically, raises unbound iron in the gut, which can:

    • Fuel gut dysbiosis (especially iron-loving pathogens)

    • Generate hydroxyl radicals via Fenton-like reactions in gut tissue

    • Damage enterocytes and worsen permeability


*Result: Gut-level iron regulation is disrupted, favoring inflammation and poor systemic balance.


🩸 2. Displacement and Iron Misplacement

  • Aluminum can displace iron from its native binding sites, especially in ferritin, transferrin, and mitochondrial enzymes.

  • This results in:

    • Unbound free iron, which becomes redox-active

    • Poorly structured heme and iron–sulfur clusters, impairing oxygen transport and ATP production

    • Loss of iron buffering capacity → greater risk of ROS propagation


Clinical implication: This is especially dangerous in high-metabolic zones like beta cells, neurons, and hepatocytes, where misplaced iron accelerates mitochondrial damage and ferroptosis.


🔥 3. Exacerbation of Oxidative Stress

  • Aluminum indirectly amplifies oxidative stress by:

    • Blocking enzymes like catalase and glutathione peroxidase

    • Promoting lipid peroxidation in membranes

    • Increasing hydroxyl radical formation when iron is present (Fenton reaction)


Iron + aluminum = synergistic oxidative stress, especially in the brain, liver, pancreas, and bone marrow.


🧠 4. Neurotoxicity & Brain Iron Accumulation

  • Aluminum and iron together have been strongly implicated in neurodegenerative conditions, including:

    • Alzheimer’s disease, where both metals are found in plaques and tangles

    • Parkinson’s disease, with iron accumulation in the substantia nigra and aluminum-linked mitochondrial dysfunction


Mechanism:

  • Aluminum inhibits ceruloplasmin, the copper-based protein responsible for safe iron export, worsening brain iron retention.

  • Aluminum also disrupts calcium and glutamate signaling, increasing excitotoxicity and metabolic demand.


🦠 5. Immune Activation & Autoimmunity

  • Aluminum is immunostimulatory (used in vaccines as an adjuvant).

  • When aluminum is present in a chronically iron-inflamed terrain, it can:

    • Aggravate cytokine production

    • Confuse the immune system into reacting to iron-damaged or inflamed tissues, possibly promoting autoimmune mislabeling

    • Impair macrophage-mediated iron recycling


🧬 6. Aluminum, Iron, and Epigenetics

  • Both aluminum and iron can alter histone acetylation, DNA methylation, and gene expression.

  • Aluminum is known to impact iron-regulatory proteins and enzymes like iron-responsive element binding proteins (IRPs), leading to dysregulation of:

    • Ferritin synthesis

    • Transferrin receptor expression

    • Hepcidin activity


This may explain the long-latency effects of aluminum exposure — especially in combination with poor iron metabolism and mineral depletion.

🧩 Putting It All Together: Why This Matters to Our Iron Metabolism

  • Aluminum may appear to lower iron absorption but ultimately causes greater unbound iron damage by:

    • Displacing iron from its functional roles

    • Blocking iron excretion and buffering mechanisms

    • Amplifying the oxidative damage iron initiates

  • The beta cell, with its redox-naïve environment, is especially vulnerable to aluminum–iron synergy, due to:

    • Low catalase/GPx activity

    • High mitochondrial density

    • Poor antioxidant reserves

  • In a terrain already lacking copper, magnesium, selenium, and zinc, aluminum exposure becomes the match that lights the inflammatory fuse, accelerating iron-induced metabolic collapse.


🍋 Citrate and Iron Metabolism: A Breakdown


🔹 1. Citrate: A Biological Primer

Citrate is a key intermediate in the citric acid (Krebs) cycle, naturally present in all living cells and used in energy metabolism. It’s also widely used in processed foods and pharmaceuticals as:


  • A flavor enhancer or preservative

  • A chelating agent (binding minerals to alter taste, solubility, or reactivity)

  • A pH regulator (especially in canned/bottled goods)

  • A “bioavailable” mineral form (e.g. magnesium citrate, zinc citrate)


But outside of its tightly regulated endogenous use, exogenous citrate (dietary or supplemental) can disturb mineral balance — especially in high, chronic, or isolated concentrations.


🔹 2. Citrate Chelates Iron — and Copper

Citrate is a well-known iron chelator. While this can theoretically reduce iron absorption in iron-rich diets (similar to polyphenols), it also has more complex effects downstream:


🧲 Chelation Effects:

  • Binds Fe³⁺ (ferric iron) preferentially, keeping it soluble and increasing its reactivity.

  • Unlike polyphenols (which typically reduce and trap iron in non-bioavailable forms), citrate may increase free iron reactivity under certain pH and oxidative conditions.

Result: More labile iron pool (LIP) formation = higher risk for ROS generation (especially with H₂O₂ present).

🔹 3. Citrate and Ceruloplasmin Suppression

There is evidence that citrate downregulates ceruloplasmin expression and secretion.


📉 What We Know:

  • Ceruloplasmin (CP) is a copper-containing ferroxidase that:

    • Converts Fe²⁺ → Fe³⁺ for proper loading onto transferrin

    • Mobilizes stored iron from tissues

    • Has powerful antioxidant properties (IE Prevents iron from reacting)

  • Exogenous citrate has been shown in some studies to:

    • Inhibit hepatic CP expression

    • Impair copper incorporation into CP

    • Disrupt the copper-dependent enzymatic activity of CP


Mechanism: Likely involves citrate interfering with copper transport and availability, which prevents proper assembly of ceruloplasmin in hepatocytes.

🔹 4. Citrate’s Broader Mineral Web Disruptions

🛑 Copper:

  • Chelates copper similarly to iron

  • Impairs hepatic delivery of copper to enzymes like:

    • Ceruloplasmin

    • Cytochrome c oxidase

    • Superoxide dismutase (Cu/Zn SOD)


🛑 Zinc & Magnesium:

  • Excess citrate intake (especially in supplements) has been shown to alter zinc and magnesium homeostasis, particularly in patients with kidney issues or metabolic imbalances.


🛑 Calcium:

  • Competes with calcium at absorption sites

  • Can also increase urinary calcium excretion, especially in citric acid-rich beverages (e.g., soda, flavored water)

🧬 Terrain Implications

Let’s tie this back to iron dysregulation and chronic illness patterns:

Citrate Effect

Resulting Risk or Impact

Chelates iron and copper

Raises circulating free radical-prone iron

Suppresses ceruloplasmin

Disrupts iron export from tissues and antioxidant defense

Impairs copper enzyme formation

Weakens ROS detoxification, mitochondrial respiration, and immune modulation

Imbalances zinc, magnesium, calcium

Further destabilizes metabolic signaling and inflammation resolution

In a terrain already struggling with iron overload or low ceruloplasmin, excess citrate acts like a saboteur. It may appear harmless — even helpful — but it silently unravels the mineral alliances responsible for redox balance, immune discernment, and metabolic resilience.

This makes citrate an underappreciated contributor to chronic inflammation, especially in processed food-heavy diets where:

  • Fortified iron is rampant

  • Copper is low or antagonized

  • Ceruloplasmin is already impaired

🔬 Glyphosate & Iron Metabolism: Direct and Indirect Impacts


1. 🧲 Chelation of Essential Minerals (Including Iron)

Glyphosate is a broad-spectrum chelating agent, originally patented not just as an herbicide, but also as a metal chelator. It binds divalent cations such as:


  • Fe²⁺ (Iron)

  • Mn²⁺ (Manganese)

  • Zn²⁺ (Zinc)

  • Cu²⁺ (Copper)

  • Ca²⁺ (Calcium)

  • Mg²⁺ (Magnesium)


→ Iron Absorption Impairment


Glyphosate chelates iron in the soil and plants, but this binding doesn't stop at the farm. In the gut, it:


  • Binds free iron, making it less bioavailable

  • Inhibits ferric reductase enzymes that convert Fe³⁺ to Fe²⁺, the absorbable form

  • Disrupts intestinal pH, affecting the iron transport gradient

  • Competes with and displaces other mineral cofactors (e.g., copper for ceruloplasmin, zinc for the antioxidant Superoxide Dismutase)


➡️ Result: Lower iron absorption, especially of bioavailable forms. This forces the body to retain circulating iron, increasing risk of unbound reactive iron.


2. 🧬 Disruption of the Shikimate Pathway and Microbiome Balance

While humans don’t use the shikimate pathway, gut bacteria do — and glyphosate inhibits it.


This leads to:

  • Loss of beneficial bacteria that assist in mineral metabolism (e.g., Lactobacillus, Bifidobacteria)

  • Overgrowth of iron-loving opportunistic species (e.g., Clostridium, E. coli, Salmonella)

  • Increased production of lipopolysaccharides (LPS) and endotoxins that drive inflammation


➡️ Result: Increased gut permeability (leaky gut) → iron leaks into places it shouldn't be → fuels systemic inflammation and oxidative stress.


3. 🧱 Impact on Cellular Membranes and Barrier Integrity

Glyphosate disrupts:

  • Tight junction proteins (e.g., zonulin, occludin)

  • Phospholipid membrane stability

  • Mitochondrial respiration and redox balance


➡️ This degradation of membrane integrity allows:

  • Intracellular iron to leak

  • More unbound iron to catalyze ROS

  • Greater likelihood of ferroptosis (iron-induced cell death)


This dynamic mirrors what we see in:

  • Beta cell failure

  • Neurodegenerative disease

  • Liver fibrosis


4. 🧪 Increased Risk of Cancer (Non-Hodgkin's Lymphoma and More)

Glyphosate has been classified as a “probable human carcinogen” by the IARC (International Agency for Research on Cancer). A key area of concern is its link to:

  • Non-Hodgkin’s lymphoma

  • Multiple myeloma

  • Leukemia


🔗 Potential Iron Link:

  • Lymphoid tissues are rich in macrophages, which recycle iron.

  • Chronic exposure to glyphosate → immune dysregulation + iron retention in lymph tissue.

  • Resulting oxidative stress (via Fenton chemistry) can lead to DNA damage, mutation, and malignant transformation of immune cells.


Additionally:

  • Cancer cells have altered iron metabolism and tend to hoard iron to support rapid proliferation.

  • Glyphosate may indirectly support tumor growth by enabling iron dysregulation, chronic inflammation, and immune suppression.


⚠️ Nutrient Web Disruption

Glyphosate weakens the entire mineral matrix that balances iron:

Nutrient

Glyphosate Effect

Iron Implication

Manganese

Chelated, depleted

Loss of MnSOD → ↑ ROS

Copper

Chelated

↓ Ceruloplasmin → iron trapped, ↑ unbound Fe

Zinc

Chelated

↓ SOD activity → ↓ ROS clearance

Magnesium

Disrupted transport

Compromised ATP production and gut barrier

Sulfur

Inhibited metabolism

Disrupted detox, bile → poor iron export


🔚 Conclusion – Part 6: A Terrain Built for Iron’s Downfall

It’s tempting to pin chronic disease on a single villain: iron, sugar, gluten, glyphosate, inflammation. But as we’ve uncovered across this series, pathology isn’t born from a single nutrient or trigger — it’s the terrain that makes the threat.


In Part 1, we learned how exceptionally valuable iron is — treasured by the body and conserved at nearly every step because of its central role in oxygen transport, redox metabolism, and energy creation. In Part 2, we saw how iron’s interaction with reactive oxygen species (ROS) is a double-edged sword: a vital spark for cellular activity, but also a wildfire if uncontained. Part 3 showed how iron’s presence accelerates the inflammatory cascade, especially in redox-naïve organs like the pancreas. Part 4 demonstrated how iron overload destabilizes multiple systems—liver, brain, gut, endocrine, immune—removing the scaffolding that normally protects the metabolically vulnerable beta cell. And in Part 5, we brought our focus to the beta cell itself: the sensitive sensor of metabolic chaos, and the final straw in a system flooded with iron and devoid of balance.


Now, in Part 6, we’ve asked the natural follow-up:

❓Where did all this iron come from? ❓Why is it no longer staying where it belongs?

The answer isn’t just more iron. It’s that the iron we’ve introduced through fortification, supplementation, and environmental additives has been divorced from its biological co-factors, its balancing nutrients, and its natural hierarchy.

🧂 Processing Removes the Brakes

Each stage of food processing — from refining flour to stripping oils to isolating sugars — removes more than just fiber or taste. It removes:


  • Fat-soluble vitamins (A, D, E, K) that support liver, gut, and membrane integrity

  • Trace minerals (copper, zinc, magnesium, manganese, selenium) that guide iron placement and prevent oxidation

  • Antioxidants that counterbalance oxidative metabolites

  • Hormone-regulating phytonutrients and bitter compounds that regulate bile, GSH, and immune tone


Fortification tried to “correct” this by adding iron back in, along with a few energy nutrients like B vitamins — but the subtle cofactors were never replaced. Iron is now concentrated, unbuffered, and bioavailable in the worst way: entering the bloodstream without guidance, saturating tissues without ceremony, and overwhelming systems without regulation.

🧪 Additives that Accelerate the Problem

Meanwhile, modern additives like:

  • Aluminum displace iron from protein carriers, freeing it up for oxidative damage

  • Citrate interferes with ceruloplasmin and mineral coordination

  • Glyphosate disrupts gut barrier function, microbiome integrity, tryptophan metabolism, and mineral absorption… all quietly weaken the body's containment systems — allowing iron to leak, accumulate, and inflame.


We didn’t just add too much iron — we removed the entire ecosystem that knew how to handle it.

🧬 The Outcome: A Terrain Unfamiliar with the Rules

Our terrain is now:

  • Iron-rich but copper-, zinc-, and magnesium-poor

  • Sugar- and starch-dense but fiber- and fat-deprived

  • Overstimulated by ROS, but under-prepared with enzymes like SOD and catalase

  • Inflamed, not because of pathogens or bad genes, but because our internal checks and balances have been stripped


We’re left with a body built to conserve, forced to handle excess iron without the raw materials, signaling molecules, or architecture it needs to do so gracefully. In that vacuum, inflammation thrives.


🔄 A Loop of Replacements, Not Restoration

The further we go down the rabbit hole of modern nutrition and industrial shortcuts, the more we see a pattern of substitution, not replenishment:

  • Refined sugar instead of nutrient-dense carbohydrates

  • Synthetic iron instead of food-bound mineral webs

  • Antacids instead of digestive repair

  • Stimulants instead of mitochondrial support

  • Sterility instead of symbiosis


In doing so, we’ve created a world where nutrients are added back in isolation, not in their original contextual matrix — and iron, the once-revered catalyst of life, becomes a slow-burning match left unmonitored in every cell it touches.


🔜 What Comes Next

If this is how we got here… how do we begin to clean the slate?

In Part 7, we’ll begin the restorative turn:

  • How can we safely offload excess iron?

  • What nutrients help rebalance the iron landscape?

  • Which practices help seal the gut, stabilize redox signals, and restore terrain balance — so the beta cell, and the rest of the body, can finally breathe?

This is no longer about chasing symptoms or “fixing iron.” It’s about building the kind of internal ecosystem where iron can return to its rightful role — not a villain, not a victim, but a vital part of a self-regulating whole.


📚 Suggested Reading & Key Scientific Citations:


⚖️ Absorption & Competition for DMT1

  • Chappell, H. F., et al. (2019).The uptake of iron and aluminium by human intestinal Caco-2 cells: competitive interactions and implications for iron homeostasis.Toxicology in Vitro, 58, 176–185.https://doi.org/10.1016/j.tiv.2019.03.004→ Demonstrates competition between Fe²⁺ and Al³⁺ at intestinal DMT1 transporters and how aluminum impairs iron uptake.

  • Thompson, K. J., et al. (2002).Iron transport proteins in enterocytes and their regulation.Annual Review of Nutrition, 22, 117–142.https://doi.org/10.1146/annurev.nutr.22.011602.092728→ Details the mechanisms of DMT1 and ferroportin and the role of hepcidin; shows vulnerability to disruption by other metals.

🔥 ROS Amplification & Fenton Chemistry

  • Exley, C. (2004).The pro-oxidant activity of aluminum.Free Radical Biology and Medicine, 36(3), 380–387.https://doi.org/10.1016/j.freeradbiomed.2003.11.018→ Highlights how aluminum catalyzes lipid peroxidation and amplifies oxidative stress in the presence of iron and ROS.

  • Gutteridge, J. M. C. (1995).Lipid peroxidation and antioxidants as biomarkers of tissue damage.Clinical Chemistry, 41(12), 1819–1828.→ Discusses how both iron and aluminum catalyze radical formation that damages cellular membranes.

🧠 Neurotoxicity & Iron–Aluminum Interactions in the Brain

  • Bondy, S. C. (2010).The neurotoxicity of environmental aluminum is still an issue.NeuroToxicology, 31(5), 575–581.https://doi.org/10.1016/j.neuro.2010.05.009→ Details aluminum’s interaction with iron and copper in the brain, and its contribution to Alzheimer’s pathology.

  • Lemire, J., et al. (2010).Aluminum disrupts mitochondrial function and induces oxidative stress in human astrocytes.Journal of Inorganic Biochemistry, 104(9), 1010–1015.https://doi.org/10.1016/j.jinorgbio.2010.04.018→ Mitochondrial dysfunction and ROS elevation from aluminum toxicity—exacerbated when iron is present.

🧬 Iron Regulation, Hepcidin, & Epigenetic Disruption

  • Reed, M. D., et al. (2014).Aluminum and iron disrupt protein and gene expression of iron metabolism in rats.Biological Trace Element Research, 160(1), 105–113.https://doi.org/10.1007/s12011-014-0029-7→ Evidence for aluminum’s impact on ferritin, transferrin, DMT1, and hepcidin expression levels.

  • Zhao, N., & Enns, C. A. (2012).Iron transport machinery of human cells: players and their interactions.Current Topics in Membranes, 69, 67–93.https://doi.org/10.1016/B978-0-12-394390-3.00003-2→ Mechanistic overview of iron transport, highlighting potential regulatory disruptions.

🩺 Immunotoxicity & Autoimmune Activation

  • Gherardi, R. K., et al. (2015).Macrophagic myofasciitis: characterization and pathophysiology.Lupus, 24(4–5), 424–437.https://doi.org/10.1177/0961203314560208→ Shows how aluminum-laden macrophages contribute to chronic inflammation and immune misdirection.

  • Flarend, R., et al. (1997).In vivo absorption of aluminum-containing vaccine adjuvants using 26Al.Vaccine, 15(12–13), 1314–1318.https://doi.org/10.1016/S0264-410X(97)00041-8→ Tracks aluminum migration through tissues and potential for accumulation.

📘 General Reference Texts

  • "Iron Metabolism: From Molecular Mechanisms to Clinical Consequences" – C. Andrews & R. Fleming (2018)→ A thorough reference on iron metabolism and interactions with other metals.

  • "Toxic Metal Chemistry in Marine Environments" – A. Tessier & D. R. Turner (1995)→ Offers insight into metal–metal interaction dynamics, including aluminum and iron in biological systems.


Citrate, Iron, and Mineral Disruption

🧪 Citrate and Ceruloplasmin Suppression

  • Prohaska, J. R., & Broderius, M. A. (1986).Citrate-fed rats exhibit decreased hepatic copper and ceruloplasmin activity.The Journal of Nutrition, 116(4), 641–648.https://doi.org/10.1093/jn/116.4.641→ Demonstrated that dietary citrate reduced liver copper content and ceruloplasmin activity in rats, even with adequate copper intake.

  • Hellwig, M., et al. (2018).Food processing and Maillard reaction products: Effect on bioavailability of essential trace elements.Molecular Nutrition & Food Research, 62(1).→ Covers how food additives and processing (including citric acid) affect trace mineral bioavailability and utilization.

🔬 Citrate as an Iron Chelator & Metal Transport Modifier

  • Lien, Y. H. (1991).Citrate and renal stone formation.Mineral and Electrolyte Metabolism, 17(5), 320–326.→ Explains how citrate binds calcium and other divalent cations, altering renal and systemic mineral handling.

  • Lönnerdal, B. (2000).Dietary factors influencing zinc absorption.The Journal of Nutrition, 130(5S Suppl), 1378S–1383S.→ Highlights how compounds like citrate can compete for transport and influence absorption efficiency of zinc and other minerals.

  • Bresgen, N., & Eckl, P. M. (2015).Oxidative stress and the homeodynamics of iron metabolism.Biomolecules, 5(2), 808–847.https://doi.org/10.3390/biom5020808→ Discusses the fine balance of iron homeostasis and how external compounds, such as chelators, affect oxidative stress.

⚖️ Copper, Iron & Ceruloplasmin Interdependence

  • Gitlin, J. D. (2003).Copper homeostasis: A network of interconnected pathways.Current Opinion in Chemical Biology, 7(2), 165–170.→ Gives a solid overview of how copper metabolism integrates with ceruloplasmin production and iron regulation.

  • Fox, P. L., et al. (2015).Ceruloplasmin and hephaestin: A review of their roles in iron metabolism and human health.Advances in Nutrition, 6(6), 640–650.https://doi.org/10.3945/an.115.009233→ Emphasizes the role of ceruloplasmin as a copper-dependent regulator of iron metabolism and oxidative stress.

🧠 Food Additives and Their Systemic Impact

  • Poti, J. M., et al. (2017).Ultra-processed food intake and chronic disease risk: A review of epidemiologic studies.Current Obesity Reports, 6(4), 413–428.→ Includes data on food additives like citric acid and their correlation with metabolic dysfunction and nutrient imbalance.


📚 Glyphosate


 
 
 

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