Refined Sugar & Seed Oils High in Deuterium, Glyphosate, Causing Metabolic Disorders, Obesity Metabolic Syndrome.

Emerging research suggest that glyphosate and deuterium may act synergistically to disrupt mitochondrial function, contributing to metabolic disorders such as obesity and metabolic syndrome.

Glyphosate is proposed to cause metabolic disorders by substituting for the amino acid glycine in protein synthesis, leading to misfolded proteins, mitochondrial dysfunction, and increased deuterium retention.

Deuterium Accumulation: Glyphosate interferes with the body's ability to exclude deuterium (heavy hydrogen) from mitochondria. High deuterium levels break down the "rotary engines" (ATP synthase) that produce cellular energy, contributing to cancer and metabolic disorders.

Metabolic Control: Taurine and sulfur donors support the body's natural ability to lower deuterium levels at the cellular level.

Antioxidant Support: These compounds enhance antioxidant defenses (glutathione, SOD, CAT) which are impaired by deuterium toxicity.

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The Role of Glyphosate and Deuterium

Glyphosate as a Disruptor: Glyphosate is theorized to substitute for the amino acid glycine in proteins. This can impair critical enzymes like Heme Oxygenase-1 (HO-1) and various flavoproteins that are essential for maintaining low deuterium levels in mitochondria.

TMAO
Deuterium Toxicity
Stephanie Seneff, MIT

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Signaling Deuterium Overload: High levels of TMAO in the blood are thought to signal that the body is experiencing a "deuterium overload" in its methylation pathways.

Gut microbes produce deuterium-depleted nutrients (acetate and butyrate) to support mitochondrial health.

Elevated TMAO directly inhibits S-adenosylhomocysteine hydrolase (AHCY), a key enzyme in the methylation cycle, leading to the accumulation of S-adenosylhomocysteine (SAH), a potent inhibitor of methylation reactions.

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Summary of Pathological Mechanisms:

TMAO Accumulation, Inhibition of AHCY (methylation cycle), Impaired methylation.

TMAO Accumulation, Elevated Mitochondrial Deuterium, ATPase damage/ROS, Mitochondrial failure.

Inflammatory Signaling, NLRP3 activation/AMPK suppression, Chronic Disease (Heart Failure/CVD).

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The problem with most supplements is the deuterium they deliver.

Stephanie Seneff, MIT researcher:

"People are loading up on supplements that are actually hurting them — they're not supplying the low deuterium resource that would have happened if it had been biological."

Most supplements are made in chemistry labs.

The molecules are chemically identical to their natural counterparts.

But they lack one critical property: deuterium depletion.

Deuterium is a heavy form of hydrogen that damages ATPase pumps in the mitochondria.

Melatonin is the clearest example.

Your gut produces 400x more melatonin than your pineal gland — most of it inside mitochondria.

Seneff: Melatonin is not primarily a sleep hormone. It is a deuterium depletion system.

Here's the mechanism:

Gut microbes produce hydrogen gas that is 80% deuterium depleted.

That gas feeds a chain of conversions — producing methyl and acetyl groups that are severely low in deuterium.

Those methyl and acetyl groups get attached to serotonin, converting it into melatonin.

Each melatonin molecule now carries depleted hydrogen — ready to be delivered to the mitochondria.

Inside gut cells (enterocytes), an enzyme called CYP2C19 strips the methyl group off melatonin.

Each time it does, it releases four molecules of deuterium-depleted water directly into the mitochondria — protecting the ATPase pumps that generate your cellular energy.

Four depleted water molecules. Per cycle. To the ATPase pumps that need them most.

When melatonin is made synthetically — which is virtually all commercial melatonin — the methyl and acetyl groups come from bulk chemicals made in a lab.

Random high deuterium content. The biological depletion step never happened.

Your body cannot tell the difference.

Sleep improves. Antioxidant effects occur.

But the deuterium depletion cycle doesn't run. The mitochondria don't get what they actually need.

The short-term benefit masks the long-term harm.

The TMAO (Trimethylamine N-oxide) evidence:

TMAO is a marker for deuterium toxicity — deuterium-loaded methyl groups accumulating systemically.

People who ate eggs — no TMAO increase.

People who took synthetic choline supplements — elevated TMAO.

The mechanism: enzymes that metabolize methyl groups can detect deuterium — and refuse to process it.

The trimethylamine survives in the gut. Gets oxidized in the liver. Becomes TMAO in the blood.

The same problem applies to:

N-acetylcysteine (NAC) — the acetyl group is low deuterium from gut microbes, unpredictable when synthetic.

Choline bitartrate — Seneff: "If you're taking choline bitartrate, you need to stop."

Methionine — methionine-deficient rats lived longer in one study.

Seneff's interpretation: methionine restriction extended lifespan not because methionine itself is harmful — but because the rats stopped receiving deuterium-loaded synthetic methionine.

Their gut microbes produced it naturally — low deuterium.

The rats getting synthetic methionine wrecked their mitochondria with deuterium-enriched methyl groups.

The deficient rats didn't.

Methylated B vitamins — likely synthetic, likely the same problem.

The studies testing these supplements never account for the fact that they're synthetic.

They have no idea that's even a variable worth measuring.

What to do instead:

• Get methionine from meat, fish and eggs — not synthetic amino acid supplements.

• Get choline from eggs and animal foods — not choline bitartrate.

• Get tryptophan from food — chicken, turkey, beef, pork, fish, eggs, hard cheeses (parmesan, cheddar). Your gut microbes convert it through the biological pathway naturally, producing depleted melatonin the way biology intended.

One study: tryptophan loading increases serum melatonin 4-fold — even in rats without a pineal gland, confirming the melatonin was gut-sourced not pineal-sourced.

• Animal fats — butter, tallow — are among the lowest deuterium foods available. Derived from acetate produced by gut microbes from deuterium-depleted hydrogen gas. The same pathway that makes biological methyl groups low in deuterium.

• Eat certified organic. Glyphosate disrupts the gut microbiome — which disrupts the entire deuterium management system upstream.

• Fermented foods support acetate production and the whole chain. Whenever the food is fermented, the microbes are making nutrients that are low in deuterium.

• Keep your gut microbiome healthy. It is your primary deuterium management system.

Seneff is 78 years old. Still writing papers. Mentally sharp. Doesn't take any supplements.

"I don't take any supplements. None of these organic molecules. None."

The supplement industry sells you the molecule.

They don't sell you the mechanism biology built into the production process.