You feel better.

Then you crash.

So you reach for something else.

And before you know it, you’re spending the entire day chasing energy.

But what if the sugar craving isn’t the real problem?

What if it’s your body’s attempt to compensate for something happening further upstream?

MTHFR gets blamed for almost everything these days, and I don’t think that’s particularly helpful. But understanding your MTHFR variants, methylation, nutrient status and cellular energy production can give us important pieces of the puzzle.

In this article, I’m breaking down the MTHFR sugar crash cycle and explaining why the better question may not be:

“Why can’t I stop craving sugar?”

It may be:

“Why does my body keep asking for energy?”

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Yes, absolutely.

Primary Ovarian Insufficiency (POI) is heavily associated with cytokines and chronic inflammation, as is Adenomyosis.

Severe adenomyosis involves a “local” cytokine storm in the uterus, POI often involves a systemic or local “ovarian” cytokine imbalance. Recent clinical research (2024–2026) has increasingly identified chronic inflammation as a primary driver of premature ovarian decline.

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Most people have heard about glutathione. Far fewer have heard about catalase, even though catalase performs one of the most important cleanup jobs in the body’s antioxidant defense system.

Every day, our cells produce reactive oxygen species as a natural part of energy production, exercise, immune activity, and normal metabolism. Environmental exposures, illness, poor sleep, stress, and other challenges can add to this burden.

One of the reactive molecules the body must manage is hydrogen peroxide. In controlled amounts, hydrogen peroxide participates in normal cellular signaling. When it accumulates faster than the body can neutralize it, however, it can contribute to oxidative stress.

Catalase helps protect against that buildup by breaking hydrogen peroxide down into water and oxygen.

That is one reason we believe catalase deserves far more attention.

It is also why the main ingredient in VARS® Catalase is Algevity®, a clinically studied extract derived from Ulva lactuca, commonly known as sea lettuce.

The Body Does Not Rely on Just One Antioxidant

Antioxidant protection is not the work of one vitamin, one nutrient, or one molecule.

It is a coordinated network.

Glutathione, glutathione peroxidase, catalase, superoxide dismutase, thioredoxin, and other protective systems work together to help cells manage oxidative stress. When one part of that network is under strain, the entire system may become less efficient.

For example, glutathione peroxidase-1, or GPx-1, uses glutathione as part of the process of reducing hydrogen peroxide and lipid peroxides. Catalase provides another route for breaking down hydrogen peroxide. Together, these systems help protect cell membranes, proteins, mitochondria, and other cellular structures from oxidative damage.
This is the philosophy behind the VARS® antioxidant family. Instead of treating antioxidant defense as a single pathway, we look at the larger network.

VARS® Glutathione supports glutathione status. VARS® SOD Booster supports another major antioxidant enzyme. VARS® Catalase was developed to help complete that cellular-defense conversation.

Why Scientists Looked to the Ocean

Algevity® begins with Ulva lactuca, a fast-growing green macroalga that has been consumed as a marine vegetable in coastal regions of Asia, Africa, and Europe.

Unlike plants grown in relatively stable terrestrial environments, Ulva lactuca must survive changing salinity, intense ultraviolet exposure, temperature shifts, and continuous oxidative pressure. To survive these conditions, it has evolved its own sophisticated protective chemistry.

The algae contains polyphenols, sulfated polysaccharides known as ulvans, minerals, antioxidant compounds, and unusual lipid-based signaling molecules. Its ingredient profile is distinct from that of more familiar brown and red seaweeds.
That natural resilience caught the attention of marine natural-product researchers.

A structured discovery program evaluated 30 marine algae species in cell-based assays to determine how effectively they activated Nrf2, one of the body’s central cellular-defense pathways. Candidates were ranked by the strength and reproducibility of that activation. According to the ingredient research dossier, Ulva lactuca stood out, and subsequent in vivo work demonstrated induction of Nqo1, a downstream marker of Nrf2 activity, across multiple tissues.

The foundational peer-reviewed research, published in Free Radical Biology and Medicine in 2013, identified extracts and unsaturated fatty acid constituents from Ulva lactuca as activators of the protective Nrf2-ARE pathway.

Nrf2: Your Cellular Defense Switch

Nrf2 is sometimes described as a master regulator of the cellular stress response.

Under ordinary conditions, a protein called Keap1 helps keep Nrf2 under control. When cells encounter certain stress signals or protective electrophilic compounds, that relationship changes. Nrf2 can then become stabilized, move into the nucleus, and help activate genes involved in antioxidant protection, redox balance, and cellular defense.

The Ulva lactuca research identified specialized keto-unsaturated fatty acid derivatives associated with this signaling activity. The published Algevity® trial describes the extract as containing lipid constituents previously identified as Nrf2-ARE activators.

The ingredient dossier also describes Nrf2-associated activation of protective genes such as NQO1, HMOX1, GCLC, GCLM, and members of the glutathione S-transferase family. At the same time, transcriptomic research suggested an opposing effect on inflammatory signaling associated with NF-κB.

A later peer-reviewed marine fatty-acid study further demonstrated how a related marine keto-fatty acid could target the Keap1/Nrf2 pathway while influencing inflammatory activity. This later study was mechanistic research on a related marine compound, not a clinical study of the finished VARS® Catalase product.

In simple terms, Algevity® is not being studied merely as an antioxidant that neutralizes one free radical at a time. It is being investigated for its ability to signal the body’s own protective systems.

That is a very different approach.

Not Just Ground Seaweed

Algevity® is a proprietary, standardized extract. It should not be confused with ordinary seaweed powder.

The ingredient is produced from wild-type Ulva lactuca using supercritical carbon dioxide extraction. The ingredient dossier describes a process that includes wild harvesting, natural drying, low-temperature extraction, traceable sourcing, controlled processing, and efforts to preserve the plant’s bioactive constituents.

The published clinical paper reports that the investigational Algevity® material was independently analyzed and contained polysaccharides, lipids, and specific keto-unsaturated fatty acid derivatives previously associated with Nrf2-ARE activation.

This standardization matters. A clinical study on a particular extract does not automatically validate every seaweed powder or every Ulva lactuca supplement.

The Human Clinical Study

The most exciting development is that Algevity® has now moved beyond laboratory and animal research into a controlled human trial.

The study was randomized, double-blind, and placebo-controlled. Twenty healthy adults were enrolled, with an average age of approximately 30 years. Participants received either:

300 milligrams of Algevity® once daily

or

a matched placebo once daily

The intervention lasted for 28 days.

Researchers measured blood biomarkers related to antioxidant defense and oxidative stress, including reduced glutathione, GPx-1, catalase, malondialdehyde, and thioredoxin. They also measured inflammatory and regulatory markers, including CRP, IL-6, IL-1β, IL-11, and PPAR-γ.

The published paper describes the trial as a short-duration pilot study and reports that the extract was well tolerated. The investigators also emphasized that larger and longer studies are still needed.

What Happened After 28 Days?

The ingredient research summary reports coordinated changes across both antioxidant and inflammatory biomarkers.

Antioxidant and Oxidative-Stress Findings

After 28 days, the Algevity® group showed the following changes from its starting measurements:

Reduced glutathione increased by 40%.

Glutathione peroxidase-1 increased by 15%.

Catalase activity increased by 13%.

Malondialdehyde decreased by 18%.

Circulating thioredoxin decreased by 13%.

Glutathione and GPx-1 work closely together in the body’s endogenous antioxidant system. Malondialdehyde, commonly abbreviated as MDA, is used as a marker of lipid peroxidation and oxidative damage. The investigators interpreted the lower circulating thioredoxin measurement as another indication of a reduced oxidative-stress burden.

Inflammatory Findings

The Algevity® group also demonstrated changes in several inflammatory and regulatory markers:

IL-6 decreased by 19%.

IL-1β decreased by 17%.

IL-11 decreased by 7%.

C-reactive protein decreased by 20%.

PPAR-γ increased by 15%.

IL-6 and IL-1β are important immune-signaling proteins that can rise during inflammatory activity. C-reactive protein is a broader marker of systemic inflammation. PPAR-γ participates in metabolic and inflammatory regulation.
The overall study summary presents these findings as coordinated modulation of oxidative stress and inflammatory balance.

Why the Pattern Matters More Than Any One Number

The most compelling part of the research is not one isolated percentage.

It is the pattern.

The study did not report a change in only one antioxidant marker. It reported movement across glutathione, GPx-1, catalase, MDA, and thioredoxin.

It did not report movement in only one inflammatory marker. It reported changes across IL-6, IL-1β, IL-11, CRP, and PPAR-γ.

That coordinated direction is consistent with the idea that Algevity® may be influencing a broader cellular-defense network. It appears to be supporting the systems that help cells respond to oxidative and inflammatory pressure, rather than acting as a simple one-target antioxidant.

This is still an early interpretation, but it is an important one.

The body works through networks. The most valuable nutritional strategies may be the ones that respect those networks.

Why We Chose Algevity® for VARS® Catalase

At Purser Wellness, we are interested in more than the amount of an ingredient printed on a label.

We want to understand what that ingredient does inside the body.

Does it support the body’s own enzymes?

Does it work through a meaningful cellular pathway?

Does it complement the other parts of the antioxidant-defense system?

Has it been studied in humans?

Algevity® stood out because its research connects marine bioactives, Nrf2 signaling, glutathione, GPx-1, catalase, oxidative-stress markers, and inflammatory balance.

That makes it a natural fit for VARS® Catalase and for our larger VARS® antioxidant philosophy.

VARS® Glutathione, VARS® SOD Booster, and VARS® Catalase are not intended to be three copies of the same antioxidant. Each is designed to support a different part of the body’s interconnected cellular-defense network.

The newly published Algevity® research strengthens the scientific rationale for that approach.

The Bottom Line

Algevity® represents a fascinating meeting point between marine biology and human cellular defense.

It began with the discovery that Ulva lactuca contains unusual natural compounds capable of activating the Nrf2-ARE pathway. It progressed through preclinical research demonstrating antioxidant and inflammatory signaling activity. It has now reached a randomized, double-blind, placebo-controlled human trial showing meaningful movement across multiple biomarkers.

The strongest findings included:

A 40% increase in reduced glutathione

An 18% reduction in MDA

A 13% reduction in circulating thioredoxin

A 19% reduction in IL-6

A 17% reduction in IL-1β

A 20% reduction in CRP

A 15% increase in PPAR-γ

The reported 13% increase in catalase and 15% increase in GPx-1 are also encouraging, although those particular between-group findings need confirmation in larger trials.

We are excited about Algevity® not because it is a miracle ingredient, but because it represents a more intelligent approach to antioxidant support.

It works with the body’s own cellular-defense pathways.

It supports an interconnected antioxidant network.

And it gives us a scientifically grounded reason to bring catalase into the larger conversation about glutathione, oxidative stress, inflammatory balance, and healthy cellular aging.

That is the science behind VARS® Catalase.

Research Cited

1. Wang R, Paul VJ, Luesch H. Seaweed extracts and unsaturated fatty acid constituents from the green alga Ulva lactuca as activators of the cytoprotective Nrf2-ARE pathway. Free Radical Biology and Medicine. 2013;57:141-153.

2. Al-Awadhi FG, Simon EF, Liu N, Ratnayake R, Paul VJ, Luesch H. Discovery and Anti-Inflammatory Activity of a Cyanobacterial Fatty Acid Targeting the Keap1/Nrf2 Pathway. Marine Drugs. 2023;21(11):553.

3. Jäger R, Luesch H, Purpura M, Godavarthi A, Balcombe ST, Vasenina E. Effect of an Ulva lactuca Extract on Systemic Antioxidant and Inflammatory Biomarkers in Healthy Adults: A Randomized, Double-Blind, Placebo-Controlled Trial. Nutrients. 2026;18(14):2244.

4. BluGen. Algevity® Introduction 2026, Version 3.

This article is for educational purposes and is not intended to diagnose, treat, cure, or prevent any disease. Dietary supplements should be used under the guidance of a qualified healthcare professional, particularly during pregnancy, nursing, treatment for a medical condition, or use of prescription medications.

Understanding how this genotype influences neurotransmitters provides clear direction on how to manage the associated anxiety using both natural and pharmaceutical approaches.

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Here is a breakdown of what happens when IL-10 pathways fail, the current (and challenging) landscape of biologics, and how the VARS Triad steps in to fill a massive therapeutic void.

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They support energy production, nervous system function, red blood cell formation, DNA synthesis, homocysteine metabolism, and many of the biochemical reactions your body performs every day.

But more is not always better.

Some people begin taking methylated B vitamins because they have an MTHFR variant, elevated homocysteine, fatigue, brain fog, or a suspected methylation problem. Initially, they may feel noticeably better. Their energy improves. Their thinking feels clearer. They finally feel as though they have found something their body needed.

Then, weeks or months later, something changes.

They become unusually irritable. Sleep becomes more difficult. Anxiety increases. Their energy feels restless rather than steady. Brain fog and fatigue begin creeping back in.

They may assume their original problem has returned. In response, they sometimes take even more of the same vitamins.

That can make the situation worse.

In functional and nutritional medicine, this pattern is often described as “overmethylation.” A more precise way to describe it is a possible sensitivity or adverse response to supplemental methyl donors.

The important point is not the label. The important point is recognizing when a supplement that once helped may no longer be the right dose, form, or combination for your body.

What Is Methylation?

Methylation is not a disease or a problem that needs to be eliminated. It is an essential biochemical process.

A methyl group is a small chemical unit containing one carbon atom and three hydrogen atoms. Your body transfers these groups between molecules as part of countless biological reactions.

Methylation contributes to:

• DNA production and repair

• Regulation of gene activity

• Neurotransmitter metabolism

• Homocysteine recycling

• Cell membrane production

• Liver and detoxification pathways

• Energy metabolism

• Healthy neurological function

The folate and methionine cycles work together to produce S-adenosylmethionine, commonly called SAM or SAMe. SAM serves as a major methyl donor throughout the body. Researchers refer to this larger network as one-carbon metabolism. It relies on nutrients such as folate, vitamin B12, vitamin B6, riboflavin, choline, betaine, and methionine. Research published through the National Library of Medicine describes how closely these pathways are interconnected.

We need these nutrients. The goal is never to eliminate methylation.

The goal is balance.

Which Supplements Provide Methyl Donors?

Several ingredients commonly found in B-complex and methylation-support supplements can contribute methyl groups or support methylation activity.

Look at your Supplement Facts labels for:

• 5-MTHF or 5-methyltetrahydrofolate

• L-methylfolate

• Methylcobalamin

• Trimethylglycine, also called TMG or betaine

• SAMe

• High-dose choline

• Methionine

• Multiple overlapping methylation formulas

None of these ingredients is inherently bad. In the right person and at an appropriate dose, they can be very useful.

Problems may arise when someone takes a dose that exceeds their present needs, combines several products containing the same ingredients, increases too quickly, or continues the same aggressive protocol after the underlying deficiency has improved.

Individual responses can vary significantly. Genetics, nutrient status, medications, absorption, diet, stress, sleep, and overall metabolic health can all influence how a person responds.

Possible Signs That Your Current Protocol Is Too Stimulating

People who react poorly to methyl-donor supplements may report symptoms such as:

• Irritability

• Anxiety or feeling unusually on edge

• Restlessness

• Difficulty falling or staying asleep

• Racing thoughts

• Headaches

• Brain fog

• Fatigue

• Feeling wired but tired

• Increased emotional sensitivity

• Poor concentration

• Heart palpitations

• An unexplained decline after initially feeling better

These symptoms are not specific to methylation. They can also occur with thyroid disorders, anemia, low iron, vitamin B12 deficiency, hormonal changes, blood sugar instability, medication effects, sleep disorders, depression, anxiety, infection, or other health problems.

Symptoms alone cannot prove that someone is “overmethylated.”

The timing provides an important clue. Did the symptoms begin after starting a new supplement, increasing the dose, changing the form of folate or B12, or combining multiple methylation products?

That pattern deserves attention.

Why Can a Helpful Supplement Start Causing Problems?

There are several possibilities.

1. The dose may be too high

The amount that corrects a deficiency is not always the amount someone needs indefinitely. Supplement requirements can change as nutrient status improves.

2. Several products may overlap

A multivitamin, B-complex, homocysteine formula, energy product, and sleep formula may each contain methylfolate, methylcobalamin, or TMG.

When considered separately, each dose may look reasonable. Taken together, the total can become much more stimulating.

3. The dose may have been increased too quickly

At Purser Wellness, we often use the principle “Start Low, Go Slow.”

This is especially important for sensitive patients and those beginning targeted methylation support.

4. The form may not be the right fit

Some people tolerate methylcobalamin and methylfolate very well. Others may respond better to alternatives such as hydroxocobalamin, adenosylcobalamin, folinic acid, or a carefully designed methyl-free B-complex.

That does not mean one form is universally superior. It means the form should be matched to the patient.

5. Methylation may not be the real cause of the symptoms

Fatigue and brain fog do not automatically mean that someone needs more methylfolate or B12.

Vitamin B12 deficiency itself can cause fatigue, neurological symptoms, mood changes, and cognitive problems. The NIH Office of Dietary Supplements emphasizes the importance of properly identifying and treating deficiency.

The same symptoms can therefore appear when someone has too little nutritional support, when a supplement is not well tolerated, or when an entirely different condition is present.

This is why thoughtful assessment matters.

What Should You Do if You Suspect a Reaction?

First, do not panic.

A poor response does not mean that methylated vitamins are dangerous or that your body is permanently damaged. It may simply mean that your current dose, form, or combination needs to be reconsidered.

Start by reviewing every supplement you take.

Write down:

• The complete product name

• Every form of folate and B12

• The amount in each serving

• How many servings you take

• Whether the product contains TMG, SAMe, choline, or methionine

• When each product was started

• When the symptoms began

• Any recent dose changes

Do not abruptly discontinue a medically necessary supplement without speaking with your prescribing clinician. This is particularly important during pregnancy, when treating a confirmed deficiency, or when a supplement has been prescribed for a specific medical condition.

Your clinician may recommend temporarily reducing or pausing a recently added nonessential supplement, changing the dose, spacing it differently, or moving to a non-methylated form.

The right decision depends on the person.

Testing Can Help Us See the Bigger Picture

Genetic testing can show variants that may influence folate metabolism, methionine metabolism, neurotransmitter clearance, and related pathways.

However, a genetic variant does not tell us exactly what dose of a supplement a person needs today. Genetics show tendencies and possible pressure points. They do not replace current biochemical testing, symptom history, medication review, or clinical judgment.

Depending on the situation, useful evaluation may include:

• Vitamin B12 status

• Folate status

• Homocysteine

• Complete blood count

• Iron and ferritin

• Thyroid markers

• Metabolic markers

• Intracellular micronutrient testing

• A complete review of medications and supplements

Testing should answer a clinical question. It should not simply generate more data.

The Purser Wellness Approach

At Purser Wellness, we do not assume that everyone with an MTHFR variant needs the same supplement.

We look at the patient’s story, symptoms, current supplement exposure, genetics, medications, and measurable nutrient status. We then build a plan that is simplified, sequenced, and adjusted over time.

Sometimes a patient needs methylated nutrients.

Sometimes they need a much smaller dose.

Sometimes they need a different form.

Sometimes the priority is correcting another deficiency, supporting antioxidant capacity, stabilizing blood sugar, improving sleep, or addressing a completely different pathway.

Personalized wellness is not about taking the strongest possible formula. It is about finding the right support for the right person at the right time.

If you have been doing everything “right” but suddenly feel more irritable, anxious, exhausted, or unable to think clearly, take a closer look at your supplements.

Your body may not be failing you.

It may simply be asking for a more balanced plan.

If you would like help reviewing your supplements, genetics, and intracellular nutrient status, contact Purser Wellness at DanPurserMD.com.

This article is educational and is not intended to diagnose, treat, cure, or prevent disease. Do not change prescribed medications or medically necessary supplements without consulting your qualified healthcare professional.

While this genetic profile makes you an expert at fighting off skin and fungal infections, it significantly increases the risk of the body attacking its own tissues—specifically the skin, joints, and digestive tract.

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But your body does not detox through a temporary cleanse.

Detoxification is happening every minute of every day. Your liver, kidneys, digestive tract, lungs, and cells continually identify, transform, transport, and eliminate compounds the body no longer needs.

At the center of much of this work is a small but remarkably important molecule called glutathione.

Glutathione is often called the body’s “master antioxidant,” but that description only tells part of the story. It helps protect cells from oxidative damage, but it also participates directly in the liver’s processing of medications, environmental chemicals, metabolic waste, and other reactive compounds.

In simple terms, glutathione helps the body make many harmful substances less reactive and easier to remove.

Your Liver Cannot Simply “Wash Out” Toxins

Many of the compounds entering the body are fat-soluble. That is useful when a substance needs to cross a cell membrane, but it also means the compound cannot always be easily removed through urine.

The liver must first transform it.

This process is commonly described in three stages:

1. Chemical processing: Liver enzymes modify the compound. In some cases, this produces an unstable or highly reactive intermediate.

2. Conjugation: The liver attaches another molecule, sometimes glutathione, to that reactive compound.

3. Transport and elimination: Transport proteins move the processed compound into bile or blood so it can eventually leave through stool or urine.

These stages are often called Phase I, Phase II, and Phase III detoxification. The real biology is more complex, and not every substance follows the same route, but this model helps us understand where glutathione enters the picture.

Glutathione is especially important during the second stage.

Glutathione Acts Like a Molecular Handle

Glutathione is made from three amino acids:

• Cysteine

• Glycine

• Glutamate

The cysteine portion contains a sulfur-based group that is chemically reactive. This allows glutathione to interact with unstable molecules that could otherwise bind to proteins, membranes, mitochondria, or DNA.

Enzymes called glutathione S-transferases, or GSTs, accelerate this process. They help attach glutathione to certain drugs, pollutants, chemical byproducts, and other electrophilic compounds.

Think of glutathione as adding a molecular handle to a difficult package.

Once that handle is attached, the compound is often:

• Less likely to react with sensitive cellular structures

• More water-compatible

• Easier for transport proteins to recognize

• Better prepared for removal through bile or urine

Glutathione does not magically “pull every toxin” from the body. Different substances require different enzymes and elimination pathways. However, glutathione conjugation is one of the liver’s most important defenses against many reactive compounds.

What Happens After Glutathione Binds to a Compound?

Binding is only one part of detoxification.

The glutathione conjugate must still be transported out of the cell. Depending on the compound, it may be moved:

• Into bile and then through the digestive tract

• Into the bloodstream for further processing

• Toward the kidneys for removal through urine

Glutathione itself is also present in high concentrations in bile and contributes to normal bile formation and movement.

This is why healthy detoxification depends on more than simply having enough glutathione. The body also needs functioning liver enzymes, transport proteins, bile flow, kidney filtration, hydration, and regular bowel elimination.

If a compound is processed but cannot be transported and eliminated efficiently, the detoxification process is incomplete.

Acetaminophen Shows Us How Important Glutathione Really Is

One of the clearest examples involves acetaminophen.

When acetaminophen is used appropriately, most of it is processed through pathways that allow it to leave the body safely. A smaller amount is converted into a highly reactive metabolite called NAPQI.

Under normal circumstances, glutathione binds to NAPQI and helps neutralize it.

During an overdose, however, the amount of NAPQI can overwhelm and deplete the liver’s glutathione supply. Once adequate glutathione is no longer available, NAPQI can bind to liver proteins and cause severe cellular injury.

This is why acetylcysteine, commonly called NAC, is used medically as an antidote for acetaminophen overdose. NAC supplies cysteine and helps restore glutathione production. The FDA describes maintaining or restoring glutathione as one of the important mechanisms by which acetylcysteine helps prevent or reduce liver injury.

Could a better, direct glutathione treatment be possible? Time will tell.

This is not a home-treatment situation. A suspected acetaminophen overdose requires immediate medical evaluation. But it provides a powerful real-world demonstration of what can happen when the liver’s toxic burden exceeds its available glutathione.

Glutathione Also Protects the Detoxification Machinery

The liver’s detoxification pathways can generate free radicals and reactive oxygen species. In other words, the process of handling a chemical may temporarily create an even more reactive intermediate.

Glutathione helps protect cells during that process.

Through enzymes such as glutathione peroxidase, reduced glutathione helps neutralize hydrogen peroxide and lipid peroxides before they damage cellular membranes or mitochondria.

During this reaction, reduced glutathione, known as GSH, becomes oxidized glutathione, or GSSG. The enzyme glutathione reductase can then recycle GSSG back into functional GSH when the cell has sufficient reducing capacity.

This recycling system matters because the body does not simply need “glutathione” on a label. It needs glutathione in the correct functional state.

Reduced glutathione: GSH

This is the electron-donating, biologically active form used in antioxidant and detoxification reactions.

Oxidized glutathione: GSSG

This is the form created after glutathione has performed antioxidant work. It must be recycled back into GSH before it can perform that work again.

A healthy cell normally maintains far more GSH than GSSG. When the balance shifts toward oxidized glutathione, it can indicate that oxidative demand is exceeding the cell’s ability to restore its antioxidant reserves.

The Liver Supports Glutathione Throughout the Body

Although nearly every cell can produce glutathione, the liver plays an especially important role.

The liver produces and exports glutathione into the circulation, helping supply its components to other tissues. Glutathione is particularly important in organs with high metabolic or oxidative demands, including the brain, lungs, immune system, kidneys, and mitochondria.

This means glutathione is not only a “liver nutrient.” It is part of a whole-body defense and recycling system.

Its work includes:

• Conjugating certain reactive chemicals

• Protecting proteins and cell membranes

• Supporting mitochondrial integrity

• Neutralizing peroxides

• Maintaining cellular redox balance

• Helping regenerate other antioxidants

• Supporting normal immune signaling

Detoxification and antioxidant protection are separate processes, but they are closely connected. Glutathione participates in both.

Why Glutathione Can Become Depleted

The body is designed to continually produce and recycle glutathione. However, demand can sometimes outpace production.

Potential contributors include:

• High oxidative stress

• Repeated environmental or chemical exposure

• Alcohol exposure

• Certain medications

• Inflammation or illness

• Poor protein or amino acid intake

• Impaired glutathione recycling

• Liver dysfunction

• Genetic differences affecting methylation or transsulfuration pathways

• Increasing age

The transsulfuration pathway is especially important because it helps move homocysteine toward cysteine, one of the primary building blocks needed for glutathione production.

This is why supporting glutathione is not always as simple as taking one supplement. We must consider the patient’s nutrient status, genetics, liver function, oxidative burden, bile flow, medications, and ability to tolerate changes.

At Purser Wellness, we follow a simple rule:

Start Low. Go Slow.

Feeling worse is not proof that “toxins are leaving.”

Headaches, nausea, digestive upset, fatigue, rashes, or other new symptoms should not automatically be labeled as a detox reaction. They may indicate that a dose is too high, the timing is wrong, elimination is not keeping pace, or the product is not appropriate for that person.

You should never be told to simply push through a significant reaction.

Introduce support gradually, track the dose and timing, and discuss persistent or severe symptoms with a qualified healthcare professional.

Why One Antioxidant Cannot Do Everything

Glutathione is powerful, but it does not work alone.

The cellular antioxidant system functions like a coordinated relay:

• Superoxide dismutase, or SOD, converts the highly reactive superoxide radical into hydrogen peroxide.

• Catalase helps break hydrogen peroxide down into water and oxygen.

• Glutathione, working through glutathione-dependent enzymes, provides broader peroxide control, cellular redox support, and detoxification assistance.

This is the reasoning behind the Purser Wellness VARS Triad. VARS stands for Validated, Absorbable, Reduced, and Stable, four characteristics we consider essential when designing functional antioxidant support.

The goal is not to flood the body with as many antioxidants as possible. The goal is to support the correct molecules, in functional forms, at a pace the individual can tolerate.

The Bottom Line

Glutathione does not detox the body through a mysterious cleansing effect.

It works through biochemistry.

It helps the liver bind certain reactive compounds, supports their transport toward bile or urine, protects cells from the oxidative stress created during detoxification, and helps maintain the redox environment required for normal cellular function.

But detoxification is a complete pathway, not a single product.

You need adequate glutathione, functional enzymes, healthy transport systems, bile flow, kidney function, hydration, bowel elimination, and enough nutritional support to continually rebuild what the body uses.

When we understand that complete pathway, we can move beyond detox fads and begin supporting the body in a safer, more intelligent, and more personalized way.

To learn more about reduced glutathione and the Purser Wellness antioxidant system, visit the Physician Designed store.

References

1. Lu SC. Glutathione synthesis. Biochimica et Biophysica Acta. 2013.

2. Vairetti M, et al. Changes in glutathione content in liver diseases. International Journal of Molecular Sciences. 2021.

3. Ballatori N, et al. Plasma membrane glutathione transporters and their roles in cell physiology and pathophysiology. Molecular Aspects of Medicine. 2009.

4. Cooper AJL, et al. Metabolism of glutathione S-conjugates: multiple pathways. Comprehensive Toxicology. 2017.

5. U.S. Food and Drug Administration. ACETADOTE prescribing information. 2024.

6. Richie JP Jr, et al. Randomized controlled trial of oral glutathione supplementation. European Journal of Nutrition. 2015.

7. Sinha R, et al. Oral supplementation with liposomal glutathione elevates body stores of glutathione. European Journal of Clinical Nutrition. 2018.

This article is for educational purposes and is not intended to diagnose, treat, or replace individualized medical care.

The following report summarizes the relationship between cytokines and severe adenomyosis based on current clinical research.

Research Report: Cytokine Involvement in Adenomyosis

1. The Pro-Inflammatory “Storm”

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Interleukin-1 Beta (IL-1β) is a highly potent, master pro-inflammatory cytokine produced primarily by activated macrophages, monocytes, and dendritic cells. Unlike many other cytokines, it is synthesized as an inactive precursor (pro-IL-1β). Its canonical activation follows a precise two-signal model.¹ The “priming” signal is initiated by receptors (e.g., TLRs or IL-1R itself) that activate the NF-κB pathway to transcribe pro-IL-1β and NLRP3 components.¹ The second “activation” phase involves intracellular protein assembly of the NLRP3 inflammasome with the adaptor ASC and effector caspase-1.¹’² Caspase-1 is then autocatalytically cleaved into its active form, which directly processes and matures pro-IL-1β into its active, highly destructive secreted form.¹’² Once secreted, IL-1β drives systemic inflammation, alters vascular permeability, and recruits immune cells to fuel localized or systemic tissue destruction.

2. Associated Diseases & Severe Complications

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Most people think of supplements as simple ingredients.

Vitamin C.
Magnesium.
Glutathione.
CoQ10.
B vitamins.

But at Purser Wellness, we have learned that the question is not only what ingredient is in the bottle.

The deeper question is:

Can the body actually use it?

That question matters especially with glutathione.

Glutathione is one of the body’s most important antioxidant and cellular-defense compounds. It is involved in redox balance, oxidative stress protection, detoxification support, immune regulation, and mitochondrial protection. In the scientific literature, glutathione is described as a tripeptide made from cysteine, glycine, and glutamic acid, and it plays a central role in reducing oxidative stress, supporting metabolic detoxification, maintaining redox balance, and regulating immune function.

That is why we often call glutathione a cornerstone of the Purser Wellness approach.

Not because it is a magic pill.

But because so many difficult patient patterns involve the same underlying terrain: oxidative stress, inflammation, poor cellular resilience, mitochondrial strain, methylation stress, immune activation, liver burden, and poor recovery.

Glutathione sits right in the middle of that conversation.

Why Glutathione Matters So Much

Your body is constantly producing energy, repairing tissue, processing toxins, managing inflammation, responding to stress, and protecting cells from free-radical damage.

That normal daily work creates oxidative stress.

Oxidative stress happens when reactive oxygen species build up faster than the body can neutralize them. This imbalance can damage lipids, proteins, DNA, mitochondria, and cell membranes if the body’s antioxidant systems are overwhelmed.

Glutathione is one of the body’s primary internal answers to that problem.

It helps support:

Cellular antioxidant defense
Glutathione helps neutralize reactive molecules and supports the body’s redox balance.

Mitochondrial protection
Mitochondria are both major producers of energy and major sources of reactive oxygen species. Mitochondrial glutathione is described in the literature as a key line of defense for maintaining the mitochondrial redox environment.

Detoxification pathways
Glutathione participates in detoxification by helping the body conjugate and process certain compounds for elimination.

Immune balance
Glutathione status has been connected to immune function, and oral liposomal glutathione has been studied for its ability to elevate body stores of glutathione and affect immune markers.

Inflammatory resilience
When oxidative stress rises, inflammation often follows. When glutathione reserves are low, the body may have a harder time calming that fire.

This is why, inside Purser Wellness protocols, glutathione is not viewed as an “extra.” It is often foundational.

The Problem: Glutathione Is Powerful, But Delivery Matters

Glutathione is fragile.

A standard glutathione powder or capsule has to pass through the digestive tract. Depending on the form, the dose, the person’s digestive health, and the delivery technology, not all of that glutathione may survive intact or reach the tissues in a useful way.

That is where liposomal technology becomes important.

A liposome is a tiny sphere made from phospholipids—the same general type of fat-like molecules that help form cell membranes. Liposomes can carry ingredients inside their watery center or within their lipid layers, helping protect the active ingredient and support delivery. Scientific reviews describe liposomes as phospholipid vesicles used because they can help protect compounds from degradation and improve delivery characteristics.

In simple terms:

A liposome is like a tiny protective bubble.

It wraps the nutrient in a phospholipid structure so the body can handle it more like something familiar.

How TruLiposome® Technology Works

Not every product labeled “liposomal” is truly liposomal.

That matters.

Some products may simply mix an ingredient with phospholipids and call it liposomal. But true liposomal delivery requires the formation of actual liposome structures: small, spherical phospholipid vesicles that hold and protect the active ingredient.

The TruLiposome® Validation process was created to help verify that a liposomal ingredient is actually made of true liposomes. According to Specnova, TruLiposome® Validation evaluates whether liposomal ingredients meet key criteria, including liposome size between 100–200 nanometers, strong encapsulation, spherical shape, proper dispersion, and freedom from leakage.

Specnova also states that this validation process uses multiple technologies, including Dynamic Light Scattering for size, Zeta Potential for encapsulation strength, Scanning Electron Microscopy for shape and dispersion, Cryo-TEM imaging for structure and stability, optical microscopy for dispersion, and X-Ray Diffraction for formulation components.

That is important because liposomal delivery is not just a marketing term.

It should be validated.

Why the Liposome Structure Matters

The structure of a liposome is similar in concept to a cell membrane.

It has:

Hydrophilic heads
These are water-loving portions that face outward and inward.

Hydrophobic tails
These are fat-loving portions that form the protective lipid layer.

A protected inner space
This space can hold water-soluble active ingredients.

A true liposome is more than a “fat-soluble supplement.” It is a carefully built delivery structure.

The outer layer of a liposome is made from phospholipids, the same general type of material found in cell membranes. These phospholipids arrange themselves into a protective sphere with water-loving heads and fat-loving tails. Inside that sphere, the active ingredient—in this case, reduced glutathione—is protected within the liposomal structure.

That structure matters because glutathione is fragile.

Standard glutathione can be exposed to stomach acid, digestive enzymes, bile salts, and the harsh environment of the gastrointestinal tract before the body has a chance to use it. Oral liposomal delivery has its own challenges too, because unprotected liposomes can be damaged or destabilized during digestion. Scientific reviews on oral liposome delivery note that coatings and protective delivery strategies can help liposomes survive the stomach environment and improve the chance of absorption later in the intestinal tract.

This is where our delivery system becomes important.

Our liposomal glutathione uses DualHydrogel® Technology, a protective hydrogel layer designed to wrap and shield the liposome. Think of it as an added layer of protection around an already-protected nutrient. Specnova describes DualHydrogel® Technology as a system that uses specific natural ingredients to wrap the liposome in a protective shield, helping support stability in the body, bioavailability, and shelf life.

This matters for three reasons.

• First, the hydrogel layer helps protect the liposome from breaking down too early.

• Second, it helps stabilize the liposome so the glutathione payload stays protected during digestion.

• Third, it supports the intended delivery goal: helping the liposome pass through the stomach and become available for absorption in the small intestine, where nutrient uptake primarily occurs.

So the structure is not just:

Glutathione inside a liposome.

It is more like:

Reduced glutathione protected inside a phospholipid liposome, then further shielded by a hydrogel layer to support stability, protection, and intestinal delivery.

That is why we care so much about validated liposomal technology.

The goal is not just to put glutathione in a capsule. The goal is to protect it long enough for the body to actually use it. Specnova notes that DualHydrogel® Technology helps protect the liposome, increase stability in the body, increase bioavailability, and increase shelf life.

At Purser Wellness, this is the difference between simply taking a supplement and taking a delivery system designed around cellular support.

Why Glutathione Is the Cornerstone of Our Protocols

At Purser Wellness, we are often working with patients who do not have one simple problem.

They may have:

• Low energy

• High oxidative stress

• Methylation strain

• Inflammatory symptoms

• Poor recovery

• Brain fog

• Toxin burden

• Insulin resistance patterns

• Hormonal stress

• Immune overactivation

• Genetic SNPs affecting detoxification or antioxidant pathways

• Homocysteine and redox imbalance

In those patients, the question becomes:

How do we support the terrain underneath the symptoms?

Glutathione is central because it touches so many of those systems.

It helps support the body’s ability to manage oxidative stress. It supports mitochondrial resilience. It participates in detoxification pathways. It helps maintain redox balance. It supports immune regulation. And it can be especially important when the body is under a higher inflammatory load.

This is why glutathione often becomes the first domino.

When glutathione reserves are low, many other systems can feel more fragile.

When glutathione is supported appropriately, the body may have a better foundation for repair, recovery, detoxification, immune balance, and cellular energy.

Why It Must Be Reduced Glutathione (GSH)—Not Oxidized Glutathione (GSSG)

Not all glutathione is the same.

When people hear the word glutathione, they often assume every supplement works the same way. In reality, glutathione exists in two very different forms:

GSH (Reduced Glutathione) – the active, functional antioxidant that protects cells.

GSSG (Oxidized Glutathione) – glutathione that has already donated its electrons while neutralizing oxidative stress. It has essentially “done its job” and must be recycled back into GSH before it can function again.

Think of it like this:

GSH is a fully charged battery.

GSSG is the same battery after it has been drained.

Your cells are constantly converting GSH into GSSG as glutathione neutralizes free radicals and detoxifies reactive compounds. Under healthy conditions, specialized enzymes—most importantly glutathione reductase—use NADPH to recycle GSSG back into active GSH, maintaining a highly reduced intracellular environment. In healthy cells, more than 98% of glutathione normally exists as GSH, while only a very small amount is present as GSSG.

Why This Matters for Many Purser Wellness Patients

Many of the patients we see have genetic variants that affect glutathione production, recycling, or utilization. These may involve genes that influence antioxidant defense, methylation, transsulfuration, glutathione synthesis, or glutathione recycling.

If your body already struggles to manufacture or regenerate glutathione efficiently, beginning with the active, reduced form (GSH) makes biological sense.

Rather than asking the body to first convert oxidized glutathione back into its usable form, we want to provide glutathione in the form your cells actually use.

That doesn’t mean GSSG is “bad.” GSSG is a completely normal part of the glutathione redox cycle.

But from a functional perspective, GSH is the molecule that directly neutralizes free radicals, supports glutathione peroxidase, regenerates other antioxidants such as vitamins C and E, participates in detoxification reactions, and helps maintain the intracellular redox environment.

Protecting GSH Until It Reaches the Intestine

There is one more challenge.

Reduced glutathione is chemically active—which is exactly what makes it valuable—but that also means it deserves protection during digestion.

That is why our formulation combines:

• Reduced glutathione (GSH) as the active antioxidant

• A true phospholipid liposome to encapsulate and protect the payload

• DualHydrogel® Technology to add another protective layer around the liposome, helping improve stability during its journey through the stomach and supporting delivery to the small intestine for absorption.

At Purser Wellness, we don’t simply ask, “Does this supplement contain glutathione?”

We ask:

Is it the right form?

Is it protected?

Can the body actually use it?

Those questions are what separate a standard ingredient from a thoughtfully engineered delivery system.

Glutathione, MTHFR, Homocysteine, and Redox Balance

Many Purser Wellness patients come to us because they have complex genetics, including methylation-related SNPs such as MTHFR, MTR, MTRR, CBS, BHMT, and others.

These genes are not destiny.

But they can help explain why certain patients struggle more with methylation demand, homocysteine balance, detoxification pressure, oxidative stress, and nutrient depletion.

When methylation is strained, redox balance often matters even more.

That is where glutathione becomes critical.

Homocysteine, inflammation, oxidative stress, and mitochondrial strain often travel together. Supporting methylation without supporting redox balance can be incomplete. In our model, glutathione helps support the antioxidant side of the terrain while methylation nutrients help support the biochemical flow.

That is why we do not see glutathione as separate from methylation.

We see it as part of the same root-cause conversation.

Start Low, Go Slow

At Purser Wellness, we do not believe in overwhelming the body.

Even with something as foundational as glutathione, we often use a Start Low, Go Slow approach.

Some patients are sensitive. Some are inflamed. Some are toxic. Some have sluggish bile flow or poor drainage. Some have been depleted for years.

So the goal is not to “force detox.”

The goal is to support the body wisely.

A physician-guided plan may begin gently and build over time, depending on the patient’s history, labs, symptoms, medications, pregnancy status, tolerance, and overall protocol.

Glutathione is powerful support—but it should still be personalized.

What Patients Often Notice

Patients may choose glutathione support for many different reasons, but within a wellness protocol, the goals often include supporting:

Cellular resilience
Healthy inflammatory balance
Recovery from oxidative stress
Mitochondrial health
Liver detoxification pathways
Immune function
Brain and nerve antioxidant protection
Exercise recovery
Healthy aging
Methylation and homocysteine terrain

These are structure-function goals. They are not disease-treatment claims.

Glutathione does not replace medical care. It does not diagnose, treat, cure, or prevent disease. But as part of a thoughtful wellness plan, it can be one of the most important nutrients we use to support the body’s natural repair systems.

The Bottom Line

Glutathione is not just another supplement.

It is one of the body’s most important internal defense systems.

And because delivery matters, we believe liposomal technology matters.

TruLiposome® Technology helps verify that the ingredient is not simply mixed with phospholipids, but formed and tested as true liposomes—small, spherical, well-dispersed, properly encapsulated structures designed to help protect and deliver the active ingredient.

That is why Liposomal Glutathione Capsules are such an important part of the Purser Wellness approach.

They support the body at the cellular level.
They help protect the redox terrain.
They support detoxification pathways.
They help the body handle oxidative stress.
They provide a foundation for deeper protocol work.

In our world, glutathione is not the accessory.

It is the cornerstone.

Order VARS Glutathione

Bibliography

Aoyama, K., & Nakaki, T. (2015). Glutathione in cellular redox homeostasis. This supports the discussion of GSH as a major cellular redox buffer, antioxidant, and enzyme cofactor.

Aquilano, K., Baldelli, S., & Ciriolo, M. R. (2014). Glutathione: New roles in redox signaling for an old antioxidant. Frontiers in Pharmacology. Supports GSH/GSSG recycling, NADPH-dependent glutathione reductase, redox signaling, and glutaredoxin/thioredoxin systems.

Averill-Bates, D. A. (2023). The antioxidant glutathione. Supports the reduced/oxidized glutathione discussion, including GSSG conversion back to GSH by glutathione reductase, GSH’s role in detoxification, vitamin E regeneration, redox signaling, and antioxidant defense.

Cooper, A. J. L., & Hanigan, M. H. (2017). Metabolism of glutathione S-conjugates: Multiple pathways. Supports glutathione’s role in detoxification through conjugation of potentially toxic electrophilic compounds and endogenous compounds.

Cui, J., et al. (2022). Recent advances in oral peptide or protein-based drug delivery systems. Supports the point that oral liposomes face challenges from digestive enzymes and extreme pH changes in the gastrointestinal tract.

Daeihamed, M., Dadashzadeh, S., Haeri, A., & Akhlaghi, M. F. (2017). Potential of liposomes for enhancement of oral drug absorption. Supports the use of stabilizing lipids, polymer coatings, double liposomes, and other methods to improve oral liposome stability and absorption.

Dawi, J., et al. (2024). Oxidative stress, glutathione insufficiency, and inflammatory mechanisms in metabolic dysfunction. Supports the connection between oxidative stress, glutathione insufficiency, inflammation, insulin resistance, and metabolic strain.

Esse, R., Barroso, M., Tavares de Almeida, I., & Castro, R. (2019). The contribution of homocysteine metabolism disruption to endothelial dysfunction: State-of-the-art. Supports the discussion of homocysteine, oxidative stress, methylation disruption, and redox imbalance.

Forman, H. J., Zhang, H., & Rinna, A. (2009). Glutathione: Overview of its protective roles, measurement, and biosynthesis. Molecular Aspects of Medicine. Supports glutathione’s central roles in oxidative protection, xenobiotic defense, redox homeostasis, and biosynthesis.

He, H., Lu, Y., Qi, J., Zhu, Q., Chen, Z., & Wu, W. (2019). Adapting liposomes for oral drug delivery. Supports the discussion that oral liposomes can be unstable during storage and gastrointestinal transit, and that surface coating and other approaches may improve stability.

Hua, S. (2014). Orally administered liposomal formulations for colon-targeted drug delivery. Supports the point that stomach acid, GI enzymes, bile salts, and digestive enzymes can destabilize liposomal structures if they are not protected.

Mari, M., Morales, A., Colell, A., García-Ruiz, C., & Fernández-Checa, J. C. (2009). Mitochondrial glutathione, a key survival antioxidant. Supports the section on mitochondrial glutathione and protection against oxidative stress.

National Center for Biotechnology Information. (2026). GCLC glutamate-cysteine ligase catalytic subunit [Homo sapiens]. Supports the genetic-pathway discussion, including GCLC as part of the first rate-limiting enzyme of glutathione synthesis.

Pannala, V. R., Dash, R. K., & Beard, D. A. (2013). A biophysically based mathematical model for the catalytic mechanism of glutathione reductase. Supports the statement that glutathione reductase converts GSSG back to reduced GSH using NADPH.

Sinha, R., Sinha, I., Calcagnotto, A., Trushin, N., Haley, J. S., Schell, T. D., & Richie, J. P. Jr. (2018). Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function. Supports the use of oral liposomal GSH for raising body stores of glutathione and affecting oxidative stress and immune markers.

Specnova. (2026). Science of liposomal ingredient delivery technology from LipoVantage®. Supports the TruLiposome® and DualHydrogel® sections, including liposome size testing, zeta potential, SEM/Cryo-TEM validation, protection from GI degradation, and DualHydrogel® benefits such as protecting the liposome, increasing stability, increasing bioavailability, and increasing shelf life.

Specnova. (2026). Benefits of liposomal delivery technology from LipoVantage®. Supports the shelf-life and DualHydrogel® technology claims.

Tuell, D., et al. (2024). The role of glutathione and its precursors in type 2 diabetes. Supports the insulin resistance and metabolic-health discussion around glutathione, oxidative stress, and glucose metabolism.

1. The Root Causes: Beyond Autoantibodies

In NMOSD, the primary trigger is the production of AQP4-IgG antibodies. However, the true “root cause” of the physical disability is the secondary cascade:

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While iron is like the raw material for the factory, ubiquinol is both the fuel for the machines and the security guard protecting the building.

1. The Energy Factory (Mitochondria)

Testosterone is produced in the Leydig cells of the testes. This process—converting cholesterol into testosterone—is incredibly energy-intensive.

• ATP Production: Ubiquinol is a vital part of the “Electron Transport Chain” in your mitochondria. It helps create ATP (cellular energy).

• The Power Outage: If ubiquinol levels are low, the Leydig cells essentially run out of power. When the “factory” doesn’t have enough electricity, the synthesis of testosterone slows down significantly.

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But in many cases, the body is not simply asking for dessert. It is asking for energy.

At Purser Wellness, we often look at sugar cravings through a deeper lens: cellular energy, methylation, inflammation, blood sugar stability, and insulin receptor function. For some patients, especially those with certain MTHFR SNPs and related methylation-cycle weaknesses, the body may struggle to maintain smooth, steady energy throughout the day.

That does not mean MTHFR “causes obesity” or that every person with an MTHFR variant will crave sugar. MTHFR SNPs can have different effects depending on the specific variant, whether one or two copies are present, nutrient status, inflammation, stress, sleep, thyroid function, insulin response, and the rest of the genetic picture. But when methylation support is weak, ATP production is sluggish, inflammation is higher, and blood sugar is unstable, sugar can become the body’s emergency shortcut.

The result is a cycle that can feel nearly impossible to escape.

MTHFR, Methylation, and Cellular Energy

The MTHFR gene helps make the MTHFR enzyme, which is involved in folate processing and the conversion of homocysteine back toward methionine. The common MTHFR C677T and A1298C variants can reduce or alter enzyme activity in some people, and C677T in particular is associated with higher homocysteine in certain cases.

Why does that matter for energy?

Because methylation is not an isolated “folate pathway.” It touches detoxification, neurotransmitters, inflammation regulation, vascular health, antioxidant demand, and the body’s ability to keep cells functioning smoothly. When this system is under-supported, many patients describe a familiar pattern:

They wake up tired.
They push through the morning.
They crave sugar or caffeine.
They feel better temporarily.
Then they crash.
Then they crave sugar again.

This is not a character flaw. It is often a body trying to solve an energy problem with the fastest fuel available.

ATP: The Real Energy Currency

Every cell needs ATP, or adenosine triphosphate. ATP is the chemical energy our cells use to power repair, movement, brain function, detoxification, hormone signaling, and nearly everything else the body does. Mitochondria generate much of the ATP needed for cellular work.

Cells can make ATP from several fuel sources:

Glucose from carbohydrates and stored glycogen
Fatty acids from dietary fat or stored body fat
Ketones made from fat during carbohydrate restriction or fasting
Amino acids from protein when needed
Lactate and glycerol through gluconeogenesis, mainly in the liver

Glucose is fast. That is why the body often reaches for it when energy feels low. But fast energy is not always stable energy.

The Sugar Craving Cycle

Here is the pattern we commonly see:

1. Low cellular energy
   The patient feels tired, foggy, heavy, or unmotivated.

2. Quick sugar craving
   The body reaches for the fastest fuel: sweets, bread, cereal, juice, soda, or constant snacking.

3. Temporary energy lift
   Blood sugar rises. The person feels a quick improvement.

4. Insulin response and crash
   Insulin helps move glucose from the blood into cells. But when blood sugar rises and falls sharply, energy can drop again. In insulin resistance, the body does not respond to insulin as well as it should, which can contribute to higher blood sugar, weight gain, and more metabolic strain.

5. More cravings
   The crash creates another urgent demand for quick energy.

6. More stored fuel
   Excess carbohydrate can be stored first as glycogen. When intake remains higher than the body’s immediate energy needs and storage capacity, excess energy can contribute to fat storage. Carbohydrates can also be converted into fatty acids through de novo lipogenesis.
   Over time, the person is eating more sugar because they feel exhausted, but the extra sugar makes the energy problem worse.

That is the vicious cycle.

Why the Body Stops Burning Stored Fat

The body is designed to switch between fuels. This is called metabolic flexibility.

When sugar intake is high and frequent, insulin tends to stay more active. Insulin is not “bad”; it is essential. But when the body is constantly being fed sugar and starch, it has less reason to burn stored fat for energy.

The body thinks:
“Why open the storage tanks when quick fuel keeps arriving?”

This is one reason some patients feel like they “cannot burn fat,” even when they are trying hard. Their body is not being given enough time or metabolic reason to access stored fuel.

Why Lower Sugar, Higher Protein, and Healthy Fat Can Help

For many patients, a lower-sugar, higher-protein, healthy-fat eating plan can help break the cycle. This may look like a ketogenic diet, carnivore-style diet, animal-based diet, or simply a more protein-forward plan with fewer refined carbohydrates.

slenderkitchen.com

The goal is not starvation. The goal is to teach the body to stop depending on constant sugar hits.

When sugar intake drops, the body gradually uses stored glycogen, then begins relying more heavily on fat oxidation and, in lower-carbohydrate states, ketone production. Fatty acids can be burned directly for energy, while the liver can make ketones that many tissues can use as an alternate fuel.

It is also important to clarify a common phrase: animal fat does not simply “turn into sugar.” The correct term is gluconeogenesis, which means the body can make glucose from non-carbohydrate sources such as glycerol, lactate, pyruvate, propionate, and glucogenic amino acids. The glycerol backbone from fats can contribute to glucose production, while fatty acids themselves are primarily burned for energy or converted into ketones.

That is why a protein-and-fat-based diet can still support blood sugar needs while helping the body become less dependent on dietary sugar.

The Purser Wellness Approach

At Purser Wellness, our goal is not simply to tell patients to “eat less sugar.”

We want to ask a better question:

Why is the body demanding sugar in the first place?

Our protocols are designed to help fill the nutritional holes left in the methylation cycle, support antioxidant and inflammatory balance, stabilize blood sugar patterns, and help insulin receptors function more appropriately.

This may include physician-guided support for methylation nutrients, intracellular deficiencies, glutathione/redox balance, minerals involved in insulin signaling, protein intake, meal timing, and a practical plan to reduce sugar without crashing the patient harder.

When done correctly, the patient is not fighting their body. They are finally giving the body what it needed all along.

Why Fasted Morning Cardio Can Help Stubborn Fat

Fasted cardio means doing low-to-moderate intensity movement before eating, often in the morning after an overnight fast.

This can be helpful because glycogen and circulating glucose are generally lower after fasting. In that state, the body may rely more heavily on fat oxidation during exercise. Research has shown that aerobic exercise in the fasted state can increase fat oxidation compared with exercise after eating.

For stubborn fat, this may be useful because the body is being asked to access stored fuel before new fuel comes in.

A good starting point is often simple:

Walk in the morning before breakfast.
Keep the intensity moderate.
Do not overtrain.
Hydrate well.
Eat enough protein afterward.

Fasted cardio is not for everyone. Patients with diabetes, hypoglycemia, pregnancy, adrenal stress, eating disorder history, or dizziness with fasting should be medically guided. The goal is not punishment. The goal is metabolic retraining.

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The Bigger Picture

Sugar cravings are often a signal.

They can signal unstable blood sugar.
They can signal poor sleep.
They can signal low protein intake.
They can signal insulin resistance.
They can signal mitochondrial stress.
They can signal methylation and nutrient gaps.

For some MTHFR patients, sugar becomes the short-term solution to a long-term cellular energy problem.

But once the body is supported correctly—methylation, inflammation, redox balance, protein, minerals, healthy fats, insulin receptor function, and steady blood sugar—the cravings often become much less powerful.

The body no longer needs to scream for sugar when it finally has access to real energy.

That is the goal: not just fewer cravings, but better cellular fuel, better metabolic flexibility, and a body that can finally begin burning what it has stored.

Order Nutrient Testing

Bibliography

Alberts, B., Johnson, A., Lewis, J., et al. (2002). How cells obtain energy from food. In Molecular Biology of the Cell (4th ed.). Garland Science. Available through NCBI Bookshelf.

Centers for Disease Control and Prevention. (2025, May 27). MTHFR gene variant and folic acid facts. CDC.

Kaplan, P., Tatarkova, Z., Sivonova, M. K., Racay, P., & Lehotsky, J. (2020). Homocysteine and mitochondria in cardiovascular and cerebrovascular systems. International Journal of Molecular Sciences, 21(20), 7698. doi: 10.3390/ijms21207698.

Nakrani, M. N., Wineland, R. H., & Anjum, F. (2023, July 17). Physiology, glucose metabolism. In StatPearls. StatPearls Publishing.

Rafiullah, M., Musambil, M., & David, S. K. (2022). Effect of a very low-carbohydrate ketogenic diet vs recommended diets in patients with type 2 diabetes: A meta-analysis. Nutrition Reviews, 80(3), 488–502. doi: 10.1093/nutrit/nuab040.

Schoenfeld, B. J., Aragon, A. A., Wilborn, C. D., Krieger, J. W., & Sonmez, G. T. (2014). Body composition changes associated with fasted versus non-fasted aerobic exercise. Journal of the International Society of Sports Nutrition, 11, 54. doi: 10.1186/s12970-014-0054-7.

Vieira, A. F., Costa, R. R., Macedo, R. C. O., Coconcelli, L., & Kruel, L. F. M. (2016). Effects of aerobic exercise performed in fasted v. fed state on fat and carbohydrate metabolism in adults: A systematic review and meta-analysis. British Journal of Nutrition, 116(7), 1153–1164. doi: 10.1017/S0007114516003160.

Hackett, D., & Hagstrom, A. D. (2017). Effect of overnight fasted exercise on weight loss and body composition: A systematic review and meta-analysis. Journal of Functional Morphology and Kinesiology, 2(4), 43.

• Genotype 1 (IL-6 “Immune Ignition”): These patients have a naturally louder “innate alarm.” This creates a chronic high-inflammatory tone, keeping CRP and fibrinogen levels elevated, which directly damages the kidney’s micro-vasculature.

• Genotype 2 (IL-23R “Stronger Th17 Response”): This variant makes it harder for the body to shut down the inflammatory response. It “locks in” the Pathogenic Th17 cells that drive long-term tissue destruction (fibrosis).

The 4-Step Destruction Loop in CRF

The diagram’s “Feed-Forward Loop” is the exact mechanism that causes a kidney to “self-digest”:

1. Step 1: IL-6 Primes the Axis. High IL-6 levels (driven by Genotype 1) create the environment for Th17 cells to flourish.

2. Step 2: IL-23/IL-23R Locks it In. The Th17 cells become “pathogenic,” continuously pumping out the cytokines we’ve targeted: IL-17, TNF-α, and GM-CSF.

3. Step 3: Effector Burst. This “burst” spills into the systemic circulation, attacking the Eyes, Skin, Joints, and Gut, as shown on the body map.

4. Step 4: Tissue Cells React (Barrier Amplification). The injured kidney cells respond by releasing more IL-8 and MCP-1 (the signals we mapped earlier), which feeds back into Step 1.

The VARS Triad: Breaking the Genetic Loop

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Hemophilia B is inherited in an X-linked recessive pattern, meaning it primarily affects males who inherit a single mutated X chromosome (hemizygous state), as they lack a second X to compensate.¹ Females are typically heterozygous carriers with one mutated and one normal F9 allele, often remaining asymptomatic due to the functional copy.³ However, homozygous mutations in females—where both X chromosomes carry defective F9 alleles—are rare but possible if both parents pass on mutated genes (e.g., an affected father and a carrier mother).¹ In such cases, homozygous females experience symptoms similar to affected males, with severity depending on the specific mutation’s impact on factor IX activity.¹ Spontaneous mutations can also occur, accounting for about one-third of cases without family history.¹ A unique variant, hemophilia B Leyden, involves mutations that cause low factor IX in childhood but improve post-puberty due to hormonal changes.⁵

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If you carry a homozygous variant in the GAD1 gene, your body makes the enzyme glutamate decarboxylase less efficiently. This enzyme converts excitatory glutamate into calming GABA. When that conversion step is genetically limited, excitatory signaling can gain the upper hand during stress, creating the exact pattern many describe: intermittent panic surges, heightened reactivity, and difficulty settling rather than constant background worry.

The good news is that you can support the system from two directions at once. Direct GABA supplementation bypasses the impaired enzyme step entirely, while foundational redox and methylation support addresses upstream factors that keep the imbalance in place over time.

The Glutamate-GABA Balance in the Brain

Your brain maintains a dynamic push-pull between excitation and inhibition. Glutamate acts like the accelerator, driving alertness, learning, and response to threat. GABA serves as the brake, quieting over-firing neurons, reducing anxiety signals, promoting relaxation, and supporting restorative sleep.

GABA is synthesized directly from glutamate by the enzyme glutamate decarboxylase. The GAD1 gene encodes one of the key forms of this enzyme in the central nervous system. Research has linked variations in GAD1 to differences in anxiety-related traits and increased susceptibility to panic disorder in certain populations.

When GAD1 function is reduced, the brain can struggle to produce enough GABA on demand. The result is not necessarily nonstop generalized anxiety but rather a nervous system that tips toward excitability more easily under load. This can show up as sudden panic attacks, an amplified startle reflex, or trouble shifting into calm states even when the external stressor has passed.

PharmaGABA: Ready-Made GABA That Bypasses the Genetic Bottleneck

PharmaGABA is a pharmaceutical-grade form of GABA produced through natural fermentation using Lactobacillus bacteria, the same beneficial microbes used in traditional fermented foods. It is not chemically synthesized. This form is used in professional supplement lines such as Designs for Health.

Because it supplies GABA directly, it does not rely on your GAD1 enzyme to do the conversion. You receive bioavailable GABA molecules that can interact with GABA receptors to promote inhibitory neurotransmission right away.

The chewable format adds a practical advantage. Some absorption occurs through the oral mucosa, allowing effects to begin more rapidly than with standard swallowed capsules. Many people notice a shift within 30 minutes, making it well-suited for acute situations.

Clinical observations and small human studies on this specific form of GABA show support for relaxation, reduced stress markers such as cortisol and chromogranin A, increased alpha brain waves (associated with calm alertness), and improved sleep quality.

Key Benefits for People with GAD1 Variants

• Rapid counter to excess glutamate excitability. By supplying GABA directly, PharmaGABA can quickly strengthen inhibitory signaling when glutamate-driven activation is running high. This helps dial down the intensity of situational spikes without waiting for your own production machinery to catch up.

• Reduced panic intensity and frequency without heavy sedation or dependence risks. Unlike benzodiazepines, which amplify existing GABA activity and carry tolerance and withdrawal concerns, direct GABA support works through normal receptor pathways. It tends to promote calm without the grogginess or rebound that many experience with pharmaceuticals.

• Smoother sleep transitions and fewer middle-of-the-night awakenings. Pairing PharmaGABA with complementary nutrients such as L-theanine and melatonin (as found in formulas like Insomnitol chewables) supports both falling asleep and staying asleep. The combination helps restore inhibitory tone during the vulnerable nighttime hours when excitatory signals can otherwise intrude.

• Excellent situational “rescue” tool. Because onset is relatively fast in the chewable form, many people keep it on hand for predictable high-stress moments: flights, long car trips, social events, public speaking, or bedtime routines. We use this exact approach for our own similar genetic tendency and keep chewables accessible at all times.

Building Longer-Term Resilience Alongside Direct Support

PharmaGABA excels at providing immediate and situational relief. For deeper, more lasting change it works best as part of a broader strategy that reduces the drivers of ongoing imbalance.

Oxidative stress and neuroinflammation can impair mitochondrial function, damage neurons, alter receptor sensitivity, and even influence gene expression related to GABA synthesis. Supporting your body’s antioxidant enzyme systems helps protect the environment in which neurotransmitters operate.

The VARS Trio (glutathione + SOD + catalase) supplies bioavailable forms of the body’s primary antioxidant network. Glutathione handles broad detoxification and redox balance. SOD converts harmful superoxide radicals, and catalase safely breaks down the resulting hydrogen peroxide. Together they help restore cellular resilience in the brain and nervous system, reducing one set of upstream pressures on GABA-glutamate balance.

Methylation support is equally important. Proper methylation influences epigenetic regulation of genes like GAD1, helps manage homocysteine (high levels are linked to excitotoxicity), and supports overall neurotransmitter metabolism and detox capacity.

For additional calm on tougher days, many people add NAC (which supports glutathione production and modulates glutamate via the cystine-glutamate antiporter), taurine (a calming amino acid that interacts with GABA-A receptors), and L-theanine (which promotes GABA activity and pairs synergistically with GABA itself). Using these three agents a few times per week often provides noticeable extra buffering.

This two-pronged approach, direct GABA when you need it plus consistent redox and methylation support, gives both immediate tools and the conditions for your nervous system to regain better self-regulation over time.

Practical Considerations

Work with a practitioner familiar with genetic testing and functional approaches so your protocol can be personalized to your specific variants, nutrient status, and symptoms. Genetic insights are most useful when interpreted alongside clinical context rather than in isolation.

Typical use of PharmaGABA involves chewing the tablet thoroughly for optimal mucosal contact, then swallowing. Effects are often felt within 20–40 minutes. It can be used situationally or in the evening as part of a wind-down routine. Individual responses vary, so starting with guidance from your provider is wise.

Lifestyle factors amplify results: consistent sleep timing, breath-focused practices that activate the parasympathetic system, appropriate movement, and minimizing unnecessary excitatory inputs when your system is already sensitive.

A Root-Cause Perspective on Calm

Understanding that your anxiety pattern may be influenced by a GAD1 variant does not mean you are broken. It means your biochemistry has a specific setpoint that benefits from targeted support. PharmaGABA offers a direct way to supply the calming signal your conversion step struggles to produce on demand. When combined with VARS Trio redox support, methylation optimization, and synergistic nutrients like NAC, taurine, and theanine, you address both the acute need and the longer-term terrain.

Many people who once felt at the mercy of sudden anxiety spikes discover they can navigate stress with greater steadiness and recover faster. The combination of immediate inhibitory support and upstream cellular protection creates both relief and resilience.

This content is for educational purposes only and is not a substitute for personalized medical advice. Always consult a qualified healthcare provider before beginning any new supplement, especially if you have a medical condition, take medications, or are pregnant or nursing. Genetic information should be reviewed with a knowledgeable practitioner who can integrate it with your full health picture.

If you have already tested for GAD1 variants or are exploring root-cause approaches to anxiety, this framework offers practical, genetics-informed tools that respect how your brain is wired while giving it the support it needs to function optimally.

Today I sat down with Lois Schweigert—one of our longtime patients at Purser Wellness—to review her latest CMA (intracellular micronutrient) test results. Lois has been on this journey for years, dealing with fibromyalgia, chronic pain, gut issues, and the ups and downs that come with it. Her story is powerful proof that consistent, root-cause work pays off.

The Backstory

Lois has been getting CMAs roughly every 18 months to two years. She’s watched her numbers improve over time, but this latest one stands out: zero deficiencies and nothing even borderline. It’s the cleanest result she’s ever had—and it perfectly matches how she’s been feeling.

“I was hopeful because I felt like I was feeling really good… and I feel like it was reflected in the test.”

She’s been much more active lately, consistently lifting weights with a trainer two hours a week. Recovery used to be brutal (especially in her three-story townhouse with four flights of stairs), but adding VARS Catalase has made a noticeable difference. The heavy soreness and stair-quivering legs have eased significantly.

What Stood Out on Her CMA

Even with excellent overall results, we identified a few optimization opportunities—especially important now that she’s training harder:

• Amino acids: Several are trending toward borderline. These are the building blocks of muscle and protein. Lois has been taking the Horbach Amino Acid Complex (3 tablets daily) for a year. Recommendation: Bump to 4 tablets temporarily to support her increased training and recovery.

• Blood sugar / insulin support: Chromium, omega-3s, and inositol were slightly low. These play into blood sugar stability, which has been a lifelong challenge for Lois.

  • Increase OmegaVail to two per day.

  • Add back in inositol (she used it nightly for sleep in the past).

• Glutathione: Still burning through it despite a solid daily dose (triple dose + liquid). On heavy lifting days, add an extra dose in the afternoon or evening. Glutathione is the master antioxidant—critical for recovery, detox, energy, and immune function, especially with increased oxidative stress from training.

• Selenium: A key player in the glutathione pathway that also showed up lightly.

Lois also shared that she sailed through this past winter without a single cold or flu—huge progress from years of a compromised immune system.

How the CMA Works (Quick Explainer)

We often get questions about the two-page CMA report. The front shows nutrient status. The back shows the antioxidant profile, which can look “backwards” at first glance.

Here’s the simple version: The lab isolates your white blood cells and feeds them different nutrients and antioxidants. They measure how well the cells respond. When something shows as “highly protective” on the antioxidant page, your cells are basically saying, “We love this—give us more!” That’s how we identify optimization opportunities even when things look mostly good.

Learn more about this here:

Sleep & Recovery Tweaks

Lois has seen big sleep improvements. She already takes a blend of magnesium (citrate, malate, glycinate) nightly. We discussed adding back modest inositol and possibly glutathione capsules at night to aid overnight repair. She also uses PharmaGABA as needed.

Why This Matters

Stories like Lois’s are why we do this work. Genetics load the gun, but environment, trauma, stress, and lifestyle pull the trigger. After her mom passed and she dealt with heavy family stress, her previous CMA showed regression—her body was in survival mode. Now she’s thriving.

Root-cause protocols—targeted supplementation based on intracellular testing, consistent movement, and ongoing tweaks—make real, sustainable change possible.

Ready to see where you stand?

If you’ve been dealing with lingering symptoms, poor recovery, energy issues, or just want to optimize like Lois, a CMA test can give you an incredibly detailed roadmap.

We’d love to help you on your journey. Reach out to our clinic at info@danpursermd.com or 801-796-7667 to schedule your test and consultation.

— Jackson Larkin, Head of Operations, Purser Wellness Coach

P.S. Lois, thank you for letting me record and share this conversation. Your consistency and openness are inspiring to so many people navigating fibromyalgia and chronic issues. Keep crushing those workouts!

Note: As always, this is not medical advice. These are Dr. Purser’s protocols based on individual CMA results. Work with your provider for personalized recommendations.

Thanks for being part of the Purser Wellness community. Here’s to feeling better and better. 🚀

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