What is Alpha Lipoic Acid (ALA) and Can You Use as a Chelator for Mercury Detoxification?

By Rebecca Rust Lee, Certified Health Coach, November 11, 2025

Whether ALA (alpha lipoic acid) is or is not a mercury chelator is a controversial question. Is ALA just an agent that encourages the body to make glutathione, or is it an actual dithiol, fat, and water-soluble chelator of mercury? Andrew Cutler, PhD brought his expertise to the analysis of two important studies that address this question.

Who Was Andrew Cutler, PhD?

Andy Cutler, PhD, PE was a health care consultant in the Seattle area. He is the author of Amalgam Illness, Diagnosis and Treatment, Hair Test Interpretation, Finding Hidden Toxicities, and The Mercury Detoxification Manual. Andy had a PhD in chemistry from Princeton University and a BS in physics from the University of California. Because of extensive self-study, he brought an unique knowledge of chemical kinetics, inorganic chemistry, and biochemistry to his analysis of mercury toxicity and his development of the Andy Cutler chelation protocol. His approach was not theoretical as he developed his protocol to save his own health from the mercury poisoning he got from some bad dental work.

Is Alpha Lipoic Acid a Chelator or Just an Antioxidant?

Alpha lipoic acid (ALA) is a naturally occurring compound found in every cell of the body. It plays a critical role in mitochondrial energy production and is both fat and water-soluble - a rare feature that allows it to act in all the compartments of the body. Because ALA can cross the blood-brain barrier, it’s often considered as a potential chelator. A chelator is a substance that can bind to heavy metals and help remove them from tissues. A fat-soluble chelator can move metals across lipid barriers like cell membranes and the blood brain barrier..

Some people believe that ALA is an “NRF2 upregulator” and any detoxing ability it has is because it makes the body produce more glutathione which leads the body to detox in a “natural” way. In this case, you can take any form of it and as much of it as you want at any old time. But if it’s truly a dithiol chelator (meaning it binds directly to certain metals), then it must be taken on a precise schedule based on its half-life - otherwise, it can move mercury from safer tissues into more sensitive ones like the brain. This distinction is vital, especially for anyone with amalgam fillings or recent mercury exposure. If a person takes a fat soluble chelator while they have amalgams in their mouth the chelator will allow the lipid barriers to “open” and the body’s natural tendency to seek equilibrium across the formerly impermeable membranes will force the metals INTO the cells rather than out.

The Gregus Study: Evidence That ALA Acts as a Chelator

An important study that supports ALA being a chelator is the Gregus Z et al., 1992 study published in Toxicology and Applied Pharmacology 114,88-96 which discusses how ALA works.

Andy Cutler said about this study: “I spent a lot of time with it. It is really a good, interesting paper. My reading of it was that it was conclusive proof of the chelating ability of ALA, and also was very useful in establishing the pharmacokinetics especially as excretion rates from the paper matched those in the Leskova study to the extent they can be compared by appropriate calculations.”

To understand the Gregus paper, it is important to know about the various forms of mercury and how they exert their harmful effects.

  • Elemental Mercury Vapor (Hg0) is the form that off-gases from amalgam fillings into the oral cavity. Like the inorganic forms of mercury, it is fat-soluble.

  • Methylmercury (CH3Hg+ ( MM in the Gregus paper)) is a form of organic mercury commonly found in fish. It is readily absorbed into the body from the intestines where it will go to the blood stream and circulation.

  • Ethylmercury (C2H5 Hg) is the form of organic mercury that is found in the Thimerosal component of vaccines. When this is injected, it goes directly into blood circulation.

Ethylmercury (C2H5 Hg) is the form of organic mercury that is found in the Thimerosal component of vaccines. When this is injected, it goes directly into blood circulation.

Organic mercury, as well as elemental mercury vapor are all fat-soluble and can cross cellular membranes and readily get into the brain. All three of these forms will circulate in the blood and enter into cells, organs and the brain where the mercury will be attracted and attach itself to sulfhydryl (SH) groups. Inside the cells the body slowly converts the elemental mercury vapor and organic mercury to a non fat-soluble form.

These non fat-soluble forms or, inorganic mercury (Hg++) become stuck in the cells, organs and the brain and are not able to leave. While some natural processes may remove small quantities of inorganic mercury from organs over a very long time, whatever is in the brain basically remains there for life. Only a fat-soluble chelator is able to cross the blood/brain barrier and remove inorganic mercury from the brain. The Gregus study shows that alpha lipoic is such a fat-soluble chelator.

In the Gregus study, rats were injected with specific metals and alpha lipoic acid. Bile was collected for analysis every 30 min. At the end of the three hour experiments the rats were sacrificed and samples of blood and tissues were collected for analysis. The experiments showed that alpha lipoic acid dramatically increased the excretion of inorganic mercury into bile.

At the lowest lipoic acid dose there was a 12-fold increase of inorganic mercury excretion while at the largest dose, a 40-fold increase in inorganic mercury was found in bile. Gregus did a further series of experiments that treated rats with DEM (diethyl maleate), which depletes liver glutathione. The experiments showed that this pretreatment “did not significantly influence the biliary excretion of Hg++ during the first 2h after administration of mercuric chloride”.

Results showed:

  • A 12–40x increase in mercury excretion into bile, depending on dose.

  • The mercury/ALA treated rats had 1.72 nmol Hg++ per gram in the brain at the end of the experiment

  • This increase persisted even when glutathione was depleted, proving that ALA’s effect was not dependent on glutathione or NRF2 activation.

In the body, substances tend to move from areas of higher concentration to areas of lower concentration. In the case of Gregus’ rats, when they were injected with mercury chloride (Hg++) the blood contained a higher concentration of mercury than the brain. The only way that the Hg++ could move into the rats’ brains was if the ALA somehow “helped” or “chelated” the mercury and moved it in. The treatment with ALA allowed the inorganic mercury to cross the otherwise impermeable membrane of the blood/brain barrier and move into the brain. The direction (into the brain) followed a concentration gradient from higher to lower concentration.

In other words, ALA itself — or its metabolite, dihydrolipoic acid (DHLA) — acts as a true chelating agent.

The Gregus study shows that rats treated with ALA had higher mercury levels in the brain than untreated controls. Lipoic acid’s fat-solubility allowed it to carry mercury across the blood-brain barrier, confirming its chelation potential, but also its danger when used improperly.

The Leskova Study: Supporting Evidence from Russian Research

Another study that supports lipoic acid’s use as a chelator is [Leskova GE. Gig Tr Prof Zabol 1979 Protective effect of lipoic acid amide in experimental mercurialism]. Most people are not aware of this paper because it is written in Russian. In the Leskova study rats were treated with mercury vapor. Half of these rats were treated with lipoic acid (technically they used lipoic acid amide). The experiments went on for 5 months.

The lipoic acid treated rats excreted 59.6% more mercury in urine and feces as compared to the control rats with no treatment. The mercury concentration in the kidneys of the control rats was 1.5 X higher than the lipoic acid treated rats at the end of the experiment. The mercury concentration in the liver of the control rats was more than 2 X higher than the treated rats. The investigators concluded that: “The protective action of lipoic acid amide is based, on the one hand, on binding to mercury and excreting it from the organism and, on the other hand, on the protection of carbothiolic groups of some biologically active compounds.”

After five months of treatment, the ALA group showed:

  • 59.6% more mercury excretion through urine and feces,

  • Less mercury accumulation in kidneys and liver,

  • And evidence that ALA binds directly to mercury.

Leskova concluded that ALA’s protective effect comes both from binding mercury for excretion and protecting cellular thiol groups. The study showed direct proof of lipoic acid’s ability to chelate.

Dr. Andrew Cutler’s Expertise and the ALA Chelation Protocol

Andy Cutler developed a chelation protocol based on lipoic acid’s ability to chelate and his understanding of the pharmacokinetics of the situation. The chelators used in the protocol are dosed on their half-life which prevents mercury from being dropped in sensitive tissues and ensures that detoxification happens gently and directionally out of the body.

  • Chelators: Alpha lipoic acid (ALA), DMSA, or DMPS. DMPS and DMSA are considered “accessory chelators” and only chelate extra-cellular mercury. DMSA chelates lead.

  • Timing: Every 3 hours (ALA) around the clock for 3–4 days (a “round”).

  • Rest periods: Equal or longer than the on-round time.

  • Prerequisite: All amalgam fillings removed for at least 3 months.

Andy Cutler advised not to take ALA when there is any mercury amalgam in the mouth and also to avoid ALA in the first three months after the final removal of amalgam fillings. If patients take ALA when they still have amalgam fillings in their mouths the ALA will draw from the huge reservoir of mercury of the fillings and transport it INTO the brain and organs because the concentration gradient favors that direction. Three months after the last exposure to mercury, the concentration in blood will be lower than that of the brain. At that point, the concentration gradient will favor mercury moving out of the brain.

ALA vs. R-LA as a Mercury chelator

While both ALA and R-LA are marketed as the same compound, they behave differently. Andy Cutler warned against using R-lipoic acid even on a proper chelation schedule. All of the people who got better with the Andy Cutler Chelation protocol used ordinary ALA (RS - lipoic acid) and people who attempted chelation with the R-LA reported worsening. For chelation, use only standard ALA (RS form), never R-LA.

Real-World Experience and Anecdotal Evidence

Thousands of mercury-toxic individuals have shared similar experiences: taking ALA or R-LA incorrectly, in single or infrequent doses, can lead to neurological regression, depression, fatigue and other mercury symptoms. Conversely, many report gradual improvement after switching to the Cutler protocol with proper ALA dosing intervals. Observation is the foundation of the scientific method and when hundreds of people report the same pattern, it is more than coincidence.

  • ALA is a true chelator, capable of crossing the blood-brain barrier.

  • Improper use can redistribute mercury into the brain.

  • Never take ALA (or R-LA) while amalgam fillings remain, or within 3 months of removal.

  • Follow the half-life schedule to ensure mercury moves out - not into sensitive organs or the brain.

Few practitioners understand the chelating ability of alpha lipoic acid. It is often prescribed in high, infrequent doses because of its antioxidant ability. Apparently it works well for diabetic neuropathy. But overtime, because of its ability to chelate and because it is fat-soluble, it will drive mercury in the wrong direction and cause great harm. Andy Cutler summed things up well with this comment:

“The misuse of lipoic acid is the alternative medicine community’s contribution to the mercury holocaust.”

Recommended Reading:

  • Gregus Z et al. Toxicology and Applied Pharmacology, 1992.

  • Leskova GE. Gig Tr Prof Zabol, 1979.

  • Herbert B. Gerstner & James Edward Huff (1977) Clinical toxicology of mercury, Journal of Toxicology and Environmental Health, 2:3, 491-526, DOI:10.1080/15287397709529452

  • Bjørklund G et al. Journal of Inorganic Biochemistry, 2019.

maybeitsmercury

Privacy Policy | HIPAA | Disclaimer [Shop]

Developed and managed by Mobin

@ 2025 Maybeitsmercury.com