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Green vegetables, fresh fruit, lemon water, and a clock representing short-term fasting before chemotherapy.

Fasting Before Chemotherapy: Can a Short-Term Fast Help Support Treatment?

Fasting Before Chemotherapy: Can a Short-Term Fast Help Support Treatment?

Fasting Before Chemotherapy: Can a Short-Term Fast Help Support Treatment?

When preparing for chemotherapy, most people assume they should focus on eating as much as possible to “keep their strength up.” Maintaining adequate nutrition throughout cancer treatment is extremely important—but emerging research suggests that, for appropriately selected patients, short-term fasting or a fasting-mimicking diet (FMD) around chemotherapy may create metabolic changes that could help protect healthy cells while making cancer cells more vulnerable to treatment.

This is an evolving area of integrative oncology research, and fasting should always be individualized based on nutritional status, cancer type, medications, treatment regimen, and overall health.

What Happens to the Body During Fasting?

When we stop eating for an extended period, the body shifts away from a nutrient-rich, growth-promoting state and toward a state focused more heavily on maintenance, stress resistance, and cellular repair.

Among the changes that may occur are reductions in:

  • Blood glucose
  • Insulin
  • Insulin-like growth factor-1 (IGF-1)
  • Growth-promoting signaling pathways such as PI3K/AKT/mTOR

At the same time, the body begins using stored fat and producing ketones as an alternative fuel source.

These metabolic changes are particularly interesting in oncology because many cancer cells rely heavily on growth signaling and abundant nutrient availability.

Protecting Healthy Cells While Stressing Cancer Cells

One of the most intriguing concepts behind fasting during chemotherapy is called differential stress resistance.

Healthy cells are metabolically flexible. When nutrients become scarce, normal cells can reduce growth and proliferation and shift resources toward maintenance and cellular protection.

Cancer cells often have mutations that continuously signal them to grow—even when nutrients are limited.

In laboratory models, this creates an interesting contrast:

Healthy cells:
Nutrient scarcity → slow growth → increase cellular protection and repair.

Cancer cells:
Nutrient scarcity → continued growth signaling → increased metabolic stress.

Researchers have proposed that this difference may allow fasting to protect normal cells from some chemotherapy-related stress while simultaneously increasing the vulnerability of malignant cells.

A related concept, differential stress sensitization, describes the potential for fasting conditions to make cancer cells more sensitive to anticancer treatment.

Much of the strongest evidence for these mechanisms remains preclinical, but human trials are beginning to explore whether these effects translate into meaningful clinical benefits.

What Is a Fasting-Mimicking Diet?

A fasting-mimicking diet is different from a water-only fast.

Instead of completely eliminating food, an FMD provides a carefully controlled, very-low-calorie diet designed to reproduce many of the metabolic effects associated with fasting.

These diets are generally:

  • Low calorie
  • Low in protein and certain amino acids
  • Primarily plant based
  • Designed to lower glucose, insulin, and IGF-1 signaling
  • Used for a short period surrounding treatment

For some patients, an FMD may be more practical than prolonged water-only fasting while still encouraging the metabolic transition associated with fasting.

What Does the Human Research Show?

One of the most frequently discussed clinical studies is the DIRECT trial, a randomized phase II study involving 131 women with stage II–III HER2-negative breast cancer receiving neoadjuvant chemotherapy.

Patients were assigned either their usual diet or a fasting-mimicking diet for several days surrounding chemotherapy.

The study did not demonstrate a significant reduction in overall grade III/IV chemotherapy toxicity or an improvement in pathological complete response, its major clinical endpoints.

However, several secondary findings were interesting.

Patients assigned to the FMD experienced a higher likelihood of radiologic complete or partial tumor response. Among patients who adhered to the fasting protocol, a greater proportion also demonstrated 90–100% tumor-cell loss on pathological assessment. The researchers additionally found less chemotherapy-associated DNA damage in circulating T lymphocytes in the FMD group.

A more recent randomized trial involving 44 patients with HER2-negative breast cancer also reported encouraging findings. Patients following an FMD around chemotherapy had lower rates of severe vomiting and neutropenia, along with favorable changes in IGF-1, inflammatory markers, and treatment response. Because this was a relatively small study, these findings need confirmation in larger trials.

Importantly, when researchers have looked at the clinical literature as a whole, the results are not yet definitive. A systematic review and meta-analysis found insufficient evidence that fasting reliably reduces chemotherapy toxicity compared with conventional diets. Another systematic review similarly concluded that existing studies are small and heterogeneous and emphasized the potential danger of fasting in patients experiencing involuntary weight loss or malnutrition.

A 2024 review in Cell Metabolism summarized the broader picture: preclinical research strongly supports several potential anticancer mechanisms of fasting and FMD, while early human trials suggest that cyclic FMD can be feasible and can produce meaningful metabolic and immune changes. Larger clinical trials are still needed to determine exactly which patients, cancers, and treatments are most likely to benefit.

Benefits Being Studied

Current research is investigating appropriately timed fasting or an FMD around chemotherapy for:

  • Lowering glucose and insulin signaling
  • Reducing circulating IGF-1
  • Reducing growth signaling through pathways such as AKT/mTOR
  • Increasing metabolic stress within cancer cells
  • Increasing cancer-cell sensitivity to chemotherapy
  • Protecting healthy cells from treatment-related cellular stress
  • Reducing chemotherapy-associated DNA damage in healthy cells
  • Supporting metabolic flexibility and ketone production
  • Improving treatment response in selected cancers

Is Longer Fasting Better?

Not necessarily.

The goal is not prolonged caloric deprivation.

In integrative oncology, we are often interested in creating a temporary metabolic environment surrounding treatment, followed by intentional nutritional recovery.

The optimal duration has not been established, and clinical studies have used substantially different protocols. Some have begun fasting or an FMD several days before chemotherapy and continued through the day of treatment, while others have used shorter fasting windows.

The appropriate strategy should therefore be individualized rather than applying the same fasting protocol to every patient.

Who Should NOT Fast Without Medical Supervision?

Fasting is not appropriate for everyone.

Particular caution is warranted in people with:

  • Significant or unintentional weight loss
  • Cancer cachexia
  • Low BMI or inadequate muscle mass
  • Difficulty maintaining adequate caloric or protein intake
  • Diabetes or glucose-lowering medications
  • Significant kidney or liver disease
  • Pregnancy
  • Eating-disorder history
  • Frailty
  • Certain medications that require food
  • Other medical conditions in which fasting could create additional risk

Maintaining lean body mass and adequate nutrition during cancer treatment remains critically important.

For some patients, nutritional rebuilding between chemotherapy cycles may be just as important as the fasting window itself.

Our Approach at Elevate Health

At Elevate Health, fasting is not used as a stand-alone cancer treatment.

Metabolic strategies such as fasting, fasting-mimicking diets, therapeutic nutrition, glucose and ketone monitoring, exercise, and other supportive therapies are used alongside standard oncology care.

Our goal is to help create a healthier internal metabolic environment while simultaneously supporting the body’s resilience throughout treatment.

The question isn’t simply:

“Should I fast?”

A better question is:

“Given my cancer, treatment, metabolic health, nutritional status, medications, and goals, is there a safe and useful metabolic strategy surrounding my treatment?”

References

  1. de Groot S, Lugtenberg RT, Cohen D, et al. Fasting mimicking diet as an adjunct to neoadjuvant chemotherapy for breast cancer in the multicentre randomized phase 2 DIRECT trial. Nature Communications. 2020;11:3083. doi:10.1038/s41467-020-16138-3.
  2. Vernieri C, Ligorio F, Zattarin E, et al. Fasting-mimicking diet plus chemotherapy in breast cancer treatment. Nature Communications. 2020;11:4274. doi:10.1038/s41467-020-18194-1.
  3. Zorn S, Ehret J, Schäuble R, et al. Therapeutic fasting in reducing chemotherapy side effects in cancer patients: a systematic review and meta-analysis. Nutrients. 2023;15(12):2666. doi:10.3390/nu15122666.
  4. Drexler U, et al. Fasting during cancer treatment: a systematic review. Quality of Life Research. 2023. PMCID: PMC10123040.
  5. Vernieri C, et al. Cyclic fasting-mimicking diet in cancer treatment: preclinical and clinical evidence. Cell Metabolism. 2024. PMID: 39059383. doi:10.1016/j.cmet.2024.06.014.
  6. Fasting mimicking diet during neo-adjuvant chemotherapy in breast cancer patients: a randomized controlled trial study. Frontiers in Nutrition. 2024. PMID: 39703333; PMCID: PMC11656309.

Medical Disclaimer: This information is educational and is not intended to replace individualized medical advice. Fasting during cancer treatment should only be considered with appropriate medical supervision and coordination with the patient’s oncology team, particularly when weight loss, malnutrition, diabetes, or other medical conditions are present.

Fruits and vegetables with green joice

Well-Meaning, But Bad Advice For Cancer

Well-Meaning, But Bad Advice For Cancer

4 Common Cancer Myths Worth Rethinking

Well-Meaning, But Bad Advice For Cancer

4 Common Cancer Myths Worth Rethinking

When someone is diagnosed with cancer, advice pours in from every direction — family, friends, social media groups, well-intentioned strangers. Most of it comes from a good place. Some of it is even advice that used to be correct. But a few pieces of “common knowledge” turn out to work against you once you look at what the current evidence actually shows.

Here are four of the most common ones, and what to do instead.

1. “Eat whatever you want to gain weight before chemo”

The advice: Treatment might make it hard to eat, so pack on calories now as a buffer.

Why it’s outdated: Major oncology guidelines actually recommend the opposite. The American Society of Clinical Oncology’s guideline on diet and weight management during cancer treatment focuses on preventing weight gain, not encouraging it [1]. In breast, colon, and prostate cancer specifically, higher body fat and weight gain during treatment are linked to worse outcomes, not better tolerance of chemo [2][3].

Why it matters: Excess fat tissue isn’t inert — it’s metabolically active and drives chronic, low-grade inflammation, which feeds tumor growth (more on that below). What actually helps heading into treatment is preserving muscle mass and metabolic health, through adequate (but not too much!) protein, deep therapeutic nutrition and movement — not stacking on calories and sugar.

2. The bigger picture: how sugar and insulin feed cancer growth

This is the science behind why myth #1 — and the next two — matter.

Cancer cells run on glucose differently than healthy cells do. Even when oxygen is available, they preferentially ferment glucose for fuel, a phenomenon called the Warburg effect. Glucose and insulin spikes don’t just supply that fuel — insulin and related growth signaling can directly switch on the same cellular pathways tumors use to grow and spread.

Two researchers have spent their careers studying this:

Dr. Thomas Seyfried (Boston College) studies cancer as a metabolic disease and researches ketogenic metabolic therapy as a way to reduce the fuel — glucose and glutamine — that tumors depend on [4]. This is a genuinely active, still-evolving research area, considered an overlooked but important treatment avenue to leverage versus replacement for standard treatment.

Dr. Valter Longo (USC) has clinical trial data — including a randomized trial in breast cancer patients — showing that short fasting-mimicking diet cycles around chemotherapy improved treatment response and reduced fatigue, likely by protecting healthy cells while leaving cancer cells more vulnerable [5][6].

This same mechanism is also why we don’t recommend insulin potentiated therapy (IPT) — using injected insulin to drop blood sugar dramatically, then giving a much smaller dose of chemotherapy timed to that drop, on the theory that glucose-hungry cancer cells will preferentially take up the chemo and let you lower the overall toxic load. It’s an appealing idea, and it isn’t new — it dates back nearly a century — and initial results often look genuinely good: tumor shrinkage, far fewer side effects [7]. But insulin itself is a growth signal, switching on many of the same pathways described above, and in practice we tend to see a dramatic resurgence of the cancer within a short period of time afterward. Tellingly, the physicians who originally developed and popularized this low-dose IPT approach no longer use it themselves, having watched this same pattern play out [8].

The takeaway: lowering glucose and insulin load appears to work with treatment, not against it — but only when it doesn’t involve adding more insulin into the system. That’s why timing and method matter, and why the best time to start building a metabolic strategy is at diagnosis, with a properly trained practitioner, before chemo begins, not after.

3. Juicing

The advice: Juicing is a healthy way to load up on nutrients.

Why it’s outdated: In the late 1800s and early 1900s, juicing was genuinely useful — it concentrated nutrients from produce that was otherwise hard to eat in volume, in a food environment very different from today’s.

Two things have changed. First, even organic produce today can carry glyphosate residue, since it’s one of the most widely used herbicides in modern agriculture [9][10]. Juicing means drinking the extract of many servings of produce at once, so whatever residue is present is consumed in a concentrated dose rather than spread across whole servings and somewhat bound up in fiber. Second, and more directly supported by the evidence: juicing strips out the fiber that normally slows sugar absorption. The result is a fast, high-glycemic hit of fruit and vegetable sugar with none of the fiber that would blunt it — exactly the kind of glucose and insulin spike described above.

What helps instead: consume whole fruits and vegetables with the fiber intact, or blending (keeping the pulp) rather than juicing.

4. Getting repurposed drugs off social media, without medical oversight

The advice: Cancer support groups on Facebook and elsewhere often circulate “protocols” using repurposed drugs — ivermectin, fenbendazole, and others — as miracle treatments.

Why it’s dangerous: Fenbendazole is a veterinary dewormer. The FDA has never approved it for human use, in any form or dose. ASCO issued a clinical notice specifically recommending against using fenbendazole for cancer treatment outside of a formal clinical trial [11][12]. Documented harms include liver injury from self-administered fenbendazole, and the deeper danger is that nobody is monitoring for drug interactions, toxicity, or proper dosing alongside actual cancer treatment [13].

This isn’t hypothetical. About four years ago, I lost a patient who had obtained fenbendazole through a Facebook group with no medical oversight at all. That loss has stayed with me.

The flip side: Repurposed drugs and metabolic strategies can have a real, legitimate place in a treatment plan. The difference is doing it with a properly trained integrative or metabolic-oncology practitioner who monitors dosing, combinations, and timing alongside your oncology team — not a Facebook group.

The bottom line

A lot of “common knowledge” in cancer care was either never quite right or hasn’t caught up with what we now understand about metabolism, inflammation, and cancer growth. If you or someone you love is newly diagnosed, the best time to build a thoughtful, supervised metabolic strategy is now — before treatment starts, not scrambling afterward.

This is educational content, not medical advice. Always talk to your oncology team before changing your treatment, diet, or supplement plan.

References

1. Ligibel, J. et al. “Exercise, Diet, and Weight Management During Cancer Treatment: ASCO Guideline.” Journal of Clinical Oncology (2022). ascopubs.org/doi/10.1200/JCO.22.00687

2. “Pre-to-post diagnosis weight trajectories in colorectal cancer patients with non-metastatic disease.” PMC. ncbi.nlm.nih.gov/pmc/articles/PMC6394719

3. “Is weight gain preventable in women with early breast cancer undergoing chemotherapy?” PMC. ncbi.nlm.nih.gov/pmc/articles/PMC10564810

4. Thomas N. Seyfried faculty profile, Boston College Biology Department. bc.edu/…/thomas-seyfried.html

5. “Fasting mimicking diet as an adjunct to neoadjuvant chemotherapy for breast cancer in the multicentre randomized phase 2 DIRECT trial.” Nature Communications (2020). nature.com/articles/s41467-020-16138-3

6. “A Better Quality of Life and Less Fatigue: New Evidence of the Benefits of Fasting During Chemotherapy.” Fondazione Valter Longo. valterlongo.com/…fasting-during-chemotherapy

7. “Low-Dose Chemotherapy with Insulin (Insulin Potentiation Therapy) in Combination with Hormone Therapy for Treatment of Castration-Resistant Prostate Cancer.” PMC. pmc.ncbi.nlm.nih.gov/articles/PMC3357525

8. “Insulin Potentiation Therapy” overview — history, safety, and outcomes data. CAM-Cancer / CancerChoices. cam-cancer.org/insulin-potentiation-therapy and cancerchoices.org/therapy/insulin-potentiation-therapy

9. Vicini, J. et al. “Residues of glyphosate in food and dietary exposure.” Comprehensive Reviews in Food Science and Food Safety (2021). ift.onlinelibrary.wiley.com/doi/10.1111/1541-4337.12822

10. “Analysis of Glyphosate Residues in Foods from the Canadian Retail Markets between 2015 and 2017.” Journal of Agricultural and Food Chemistry. pubs.acs.org/doi/10.1021/acs.jafc.9b07819

11. American Cancer Society. “What to Know About Fenbendazole.” cancer.org/cancer/latest-news/what-to-know-about-fenbendazole.html

12. ASCO Clinical Notice: “Recommending Against Ivermectin and Fenbendazole for Cancer Treatment, Outside of Clinical Trials.” connection.asco.org/…fenbendazole-cancer-treatment

13. “Severe Drug-Induced Liver Injury Due to Self-administration of the Veterinary Anthelmintic Medication, Fenbendazole.” PMC. pmc.ncbi.nlm.nih.gov/articles/PMC11068125

Breast biopsy markers, ultrasound images, and breast cancer awareness symbols arranged in a calm medical setting

Breast Biopsy Markers: What Do We Know About the Local Tissue Response?

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Breast Biopsy Markers: What Do We Know About the Local Tissue Response?

Breast Biopsy Markers: What Do We Know About the Local Tissue Response?

Breast biopsy markers—often called breast clips—have become a routine part of breast imaging and biopsy procedures. These very small markers made of metal and polymers or other bioabsorbable materials are placed into the breast after a biopsy with the intent to identify the location of a sampled abnormality so that it can be found again on future mammograms, ultrasound, MRI, or during surgery.

If an abnormality becomes difficult to see after biopsy, responds to treatment, or needs to be surgically removed later, the metal marker provides a reference point for the original area of concern. Radiologists overall prefer use of breast biopsy markers as it helps them for follow-up imaging and surgical localization.

However, an important question remains that has not received appropriate attention :

What happens to the breast tissue surrounding a biopsy site and retained marker over time?

Breast Tissue Does React After Biopsy and Marker Placement

It is sometimes assumed that after the initial biopsy heals, the surrounding breast tissue simply returns to its previous state. Histologic studies—studies in which the actual tissue is examined under a microscope—show that this is not the case.

Researchers have documented changes around breast biopsy sites that include:

  • Local inflammation
  • Foreign-body reactions
  • Macrophage and multinucleated giant-cell accumulation
  • Granulation tissue
  • Fibrosis and scar formation
  • Fat necrosis
  • Hemorrhage and hemosiderin deposition
  • Fibrovascular tissue and new blood vessel formation
  • Persistent foreign material associated with some biopsy-marker carriers

These findings do not automatically mean that the marker itself is dangerous, nor do they establish that the marker is responsible for all of these changes. A needle biopsy itself creates tissue injury and initiates a wound-healing response. But the findings raise worthwhile questions about how long these changes persist and how much of the response may be related to the biopsy versus the retained marker and its surrounding materials.

A Study Looking Directly at Breast Tissue After Needle Biopsy

One particularly interesting study, published in Pathobiology and indexed in PubMed, examined surgically removed breast tumors from 73 women who had previously undergone image-guided needle biopsy.

Researchers specifically examined tissue surrounding the visible biopsy tract.

Their findings were striking.

Foreign-body giant-cell reactions with macrophage accumulation were identified in 53.4% of cases.

Organized granulation tissue containing fibroblasts along with chronic inflammation was present in 20.5%.

Another 20.5% demonstrated vascular-rich granulation tissue with extensive angiogenesis—the development of new blood vessels.

Fat necrosis occurred in 18% of specimens, and hemosiderin deposition was identified in 2.7%.

Perhaps particularly relevant to the discussion of breast markers, material believed to represent residual carrier material from the biopsy marker was visible in 60.2% of cases.

The researchers also found an association between visible biopsy-marker carrier material and inflammatory cells including neutrophils, eosinophils, and plasma cells. They proposed that this could represent a foreign-body response to the marker material.

It Isn’t Necessarily Just the Metal Clip

When we talk about a “breast clip,” it is easy to imagine that a tiny piece of titanium or stainless steel is the only material being introduced.

That isn’t the case.

Modern biopsy markers vary considerably in composition and design. Some incorporate materials intended to improve ultrasound visibility or help stabilize the marker at the biopsy site. Published reviews describe markers and carriers incorporating materials such as titanium, stainless steel, nitinol and various polymers, hydrogels, collagen and other bioabsorbable materials.

This matters because the tissue response may depend not only upon the metallic marker but also upon the material surrounding it.

The Nature/Modern Pathology Findings

Another fascinating study published in Modern Pathology, a Nature journal, specifically examined tissue surrounding hygroscopic, ultrasound-visible biopsy markers.

The authors noted that biopsy tracts, wires and clips can produce histologic findings including:

local inflammation, foreign-body reaction, fat necrosis, fibrosis and hemosiderin deposition.

They also described inflammation, fibrosis, giant-cell reactions and accumulation of fibrinous material associated with certain marker materials.

Most interestingly, the researchers identified a distinctive response surrounding the hygroscopic markers: formation of pseudocyst-like structures lined by epithelioid histiocytes, a type of immune cell involved in foreign-body and inflammatory responses.

The authors pointed out that tissue responses to breast biopsy marking devices can vary depending upon the type of device being used.

That is an important distinction.

There isn’t one universal “breast clip.” There are numerous commercially available markers with different metals, shapes, coatings and carrier materials. A review from Memorial Sloan Kettering identified 38 different marker shapes from six manufacturers and documented considerable variation in marker composition and carrier properties.

Is It the Biopsy or the Marker?

This is probably the most important unanswered question.

A core or vacuum-assisted breast biopsy is itself a physical injury. Tissue is removed with a relatively large needle, bleeding occurs, and the body initiates normal wound healing.

Inflammation, macrophage recruitment, fibroblast activity, new blood vessel formation and eventually scar tissue can all be components of normal wound repair.

Therefore, finding inflammation or fibrosis around a clipped biopsy site does not prove that the clip caused it.

At the same time, the presence of foreign-body giant-cell reactions and inflammatory cells associated with visible marker carrier material suggests that the marker system itself may contribute to the local response.

Separating those two effects would require studies comparing similar biopsy procedures with versus without retained markers, ideally with longitudinal imaging and, where available, pathology.

Unfortunately, this specific question has not been studied nearly as thoroughly as other aspects of breast-marker safety.

“Safe” Can Mean Different Things

There are many studies involving breast markers, but they only study migration, visibility, localization accuracy, deployment, MRI artifact, surgical retrieval, or feasibility.  These ARE NOT SAFETY STUDIES for women. There is only one published “long term safety study”  of breast biopsy markers placed in women, and this study was conducted by authors affiliated with the medical device manufacturer, representing an important conflict of interest.  This retrospective study (retrospective means they went back and reviewed medical charts) evaluating 768 breast and axillary biopsy markers reported only three device-related events and no serious adverse events, concluding that the markers demonstrated favorable long-term safety. This is another important limitation: what did the researchers actually define as an adverse event?   Studies, like this one, meant to  evaluate the “safety” of biopsy markers commonly focus on outcomes such as serious adverse events, device malfunction, deployment problems, migration, inability to locate the marker, or complications affecting subsequent surgery.

Those endpoints do not answer a different and important question all women deserve to know:

Does the breast tissue surrounding a retained biopsy marker remain structurally and biologically unchanged over time?

The limited pathology literature demonstrates that it does not remain unchanged. Researchers have documented local inflammation, foreign-body giant-cell reactions, fibrosis, fat necrosis, granulation tissue and hemosiderin deposition at breast biopsy and marker sites.

This does not establish that the marker itself caused every one of these findings—the biopsy procedure is an important confounding factor—but it highlights a significant distinction between “no serious device-related adverse event was reported” and “the implanted material produces no persistent local tissue response.”

Both questions matter, and they should not be treated as though they are the same question.

Why More Research Is Needed

In clinical practice, I have personally observed tissue changes surrounding breast biopsy-marker sites repeatedly over many years and in well over 100 women.

Clinical observation alone cannot establish causation. There are several potential explanations for what we observe—including the original abnormality, biopsy trauma, hematoma formation, subsequent fibrosis, the body’s response to retained material, and even imaging artifact.

But repeated clinical observations can—and historically often do—generate important research questions.

The published pathology findings make this particular observation worth investigating rather than dismissing.

A valuable study would follow women prospectively before biopsy and after biopsy-marker placement, documenting the tissue at baseline and at defined intervals afterward. Ideally, researchers would compare biopsy sites with and without retained markers and evaluate different marker compositions.

Such a study could examine ultrasound architecture, mammographic changes, MRI findings, fibrosis, vascularity, elastography, symptoms and—when tissue is eventually removed—histopathology.

It could also determine whether particular marker materials produce greater or lesser tissue responses.

What Should Women Do With This Information?

This information is not a recommendation to refuse a breast biopsy.

Breast biopsy can provide critically important diagnostic information, and marker placement may be useful when an abnormality needs to be located again.

Rather, we should be avidly researching and working to make them as safe as possible. Women should be able to participate in an informed discussion about what is being placed in their bodies and not dismissed when questioning the safety of a procedure that clearly deserves more research and true, unbiased safety standards.  In my observation, this simply does not currently exist.

The Bottom Line

Breast biopsy markers have become an established norm in modern standard of care breast imaging. Available clinical safety studies focus on major adverse effects and migration, but are lacking in the realm of local tissue changes and potential harm to surrounding tissue and malignant processes.

Published pathology demonstrates that breast biopsy sites can exhibit persistent inflammation, foreign-body giant-cell reactions, granulation tissue, fibrosis, fat necrosis and hemosiderin deposition, and some studies have directly identified residual marker carrier material within these areas.

What we do not yet know well enough is how much of that response is caused by the biopsy itself versus the retained marker, how frequently clinically meaningful changes persist long term, whether certain marker materials produce greater reactions than others, and whether those changes have any implications beyond making the tissue look or feel different, especially important in the realm of cancer. 

These are reasonable questions and in my opinion, they should have been answered properly before this practice became widely accepted standard of care.

More than one million American women undergo breast biopsy every year, and biopsy-marker placement has become a routine component of image-guided breast biopsy. Despite this very large population potentially exposed to retained breast markers, surprisingly little to no research has specifically examined their long-term biological effects on surrounding breast tissue. Women deserve better.

References

Sustained Inflammation of Breast Tumors after Needle Biopsy. Pathobiology. Histologic evaluation of 73 breast cancer cases demonstrated persistent inflammatory and wound-healing changes adjacent to biopsy tracts, including foreign-body giant-cell reactions, granulation tissue, angiogenesis, fat necrosis, hemosiderin and residual biopsy-marker carrier material.

Hygroscopic sonographically detectable clips form characteristic breast and lymph node pseudocysts. Modern Pathology. This study describes histologic responses surrounding breast biopsy markers, including local inflammation, foreign-body reaction, fat necrosis, fibrosis, hemosiderin deposition and distinctive pseudocyst formation associated with hygroscopic markers.

Current status of biopsy markers for the breast in clinical settings. Expert Review of Medical Devices. Review of breast-marker composition, properties, applications and limitations.

Advantages and Challenges of Using Breast Biopsy Markers. Journal of Breast Imaging. Review of the clinical indications, advantages and challenges associated with breast biopsy markers.

lotus graphic with healing natural elements

Supporting the Body Through Biopsy and Cancer Surgery: An Integrative Approach to the Perioperative Window

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Supporting the Body Through Biopsy & Cancer Surgery:

An Integrative Approach to the Perioperative Window

Supporting the Body Through Biopsy and Cancer Surgery:

An Integrative Approach to the Perioperative Window

Biopsy and surgery are among the most important tools we have in cancer care. A biopsy can provide the diagnosis and molecular information needed to choose appropriate treatment. Surgery can remove a primary tumor, reduce tumor burden, prevent complications, and, for many localized cancers, offer the possibility of cure.

The goal of integrative care is not to avoid medically necessary biopsy or surgery.

Instead, we ask another question:

Can we support the body’s physiology before and after a procedure in ways that promote healing, preserve immune function, and potentially make the perioperative environment less favorable to residual cancer cells?

There are compelling biological reasons to have that conversation.

Surgery Is More Than a Local Event

When tissue is injured, the body immediately launches a sophisticated wound-healing program. Stress hormones rise. Inflammatory pathways activate. Blood vessels and connective tissue begin remodeling. Growth factors are released. Immune activity changes.

These responses are essential—we could not heal without them.

But cancer biology can sometimes take advantage of the same signals.

Research on the perioperative period has shown that surgical stress can increase catecholamines, prostaglandins, inflammatory cytokines, vascular growth signals, and other mediators while temporarily suppressing aspects of antitumor immunity, including natural killer (NK) cell function.

Many of these pathways—including inflammatory signaling, angiogenesis, tissue remodeling, migration, and stem/progenitor-cell programs—also participate in tumor progression. This overlap is one reason cancer has historically been described as behaving in some ways like a “wound that does not heal.”

This does not mean we should avoid biopsy and surgery. For many cancers, surgery is lifesaving and remains the cornerstone of curative treatment.

It means that the days surrounding biopsy or surgery represent a biologically active window that deserves attention.

What About Biopsy?

Needle-tract seeding has been reported with certain tumors and procedures, but it is uncommon for most cancers, and human studies have not established that routine biopsy increases distant metastasis.

At the same time, a biopsy is still a tissue injury and produces a localized wound-healing response. For that reason, we believe it is reasonable to think about supporting healthy inflammatory regulation and tissue repair around a biopsy.

The Perioperative Stress Response and Cancer Biology

Cancer surgery creates several overlapping physiological responses.

Inflammation: Tissue injury activates inflammatory mediators necessary for wound repair. In the cancer setting, some of these same pathways can also influence angiogenesis, invasion, epithelial-to-mesenchymal transition (EMT), and survival of residual tumor cells.

Stress hormones: Surgery and the psychological stress surrounding a cancer diagnosis can increase sympathetic nervous system activity and catecholamines such as epinephrine and norepinephrine.

Prostaglandins: Surgical inflammation increases prostaglandin signaling, including pathways involving COX-2 and PGE2.

Temporary immune suppression: NK cells and cytotoxic T cells are important components of immune surveillance against malignant cells. Their function may decline temporarily following major surgery.

The biological objective is therefore not to eliminate inflammation—we need inflammation to heal—but to support an appropriate, well-regulated inflammatory response while preserving immune resilience.

An Intriguing Area of Research: Beta Blockers and Anti-Inflammatory Medications

One of the most interesting areas of perioperative oncology research involves simultaneously targeting the stress and inflammatory responses.

In a randomized phase II study of 38 women undergoing breast cancer surgery, patients received the beta blocker propranolol together with the COX-2–inhibiting anti-inflammatory medication etodolac, beginning five days before surgery and continuing through the perioperative period.

Compared with placebo, treated tumors showed favorable changes in several biomarkers associated with metastatic biology, including reductions in epithelial-to-mesenchymal transition and pro-inflammatory/pro-metastatic transcriptional activity.

Another randomized phase II trial studied propranolol alone for seven days before breast cancer surgery. Researchers observed reduced expression of mesenchymal and inflammatory programs—including changes involving NF-κB and AP-1—and changes suggesting greater immune-cell infiltration into the tumor.

These are fascinating findings, but there is an important distinction:

These trials demonstrated changes in biological markers. They have not yet established that perioperative beta blockers or anti-inflammatory medications reduce cancer recurrence or improve overall survival.

These medications also have real contraindications and risks. Beta blockers can affect heart rate, blood pressure, and airway function, while anti-inflammatory medications may affect bleeding, kidney function, gastrointestinal health, and surgical planning.

They should therefore only be considered in collaboration with the patient’s oncology, surgical, anesthesia, and prescribing teams.

Nutritional and Botanical Support

At Elevate Health, perioperative planning may also include nutritional and botanical compounds selected for their potential effects on inflammatory signaling, oxidative stress, tissue repair, and cancer-related pathways.

Depending upon the individual, compounds we may consider include:

  • Boswellia: approximately 1,000 mg twice daily
  • Curcumin phytosome: 500–1,000 mg twice daily
  • Quercetin: up to 1,000 mg twice daily
  • Grape seed extract: 250–500 mg once to twice daily
  • Berberine: 500 mg twice daily with meals
  • Black seed/thymoquinone: dosing individualized to the product; in some protocols approximately 200 mg twice daily

These doses are examples from our clinical protocols, not universal recommendations.

Evidence for these compounds ranges from mechanistic and preclinical research to limited human data; they should not be represented as proven methods of preventing perioperative cancer spread or recurrence.

Just as importantly, “natural” does not mean appropriate immediately before surgery. Supplements can affect platelet function, glucose, blood pressure, drug metabolism, anesthesia, or other aspects of perioperative care. Your surgeon and anesthesiologist should have a complete list of everything you take, and their instructions about what to stop before surgery take priority.

Modified Citrus Pectin and Galectin-3

Another compound we consider is modified citrus pectin (MCP).

MCP has been studied as an antagonist of galectin-3, a carbohydrate-binding protein involved in cellular adhesion, inflammation, fibrosis, angiogenesis, and several aspects of cancer biology.

Preclinical studies demonstrate effects of MCP on galectin-3–related tumor adhesion, angiogenesis, invasion, and growth. Human research remains preliminary, although a phase II study in men with biochemically recurrent prostate cancer found potentially favorable changes in PSA kinetics during MCP treatment.

Our clinical protocol commonly uses:

Modified citrus pectin: 15 grams daily, beginning approximately two weeks before biopsy or surgery and continuing for at least one month afterward.

In patients with confirmed cancer, we may also follow galectin-3 and individualize continued MCP use, with a clinical target of less than 10 ng/mL.

It is important to emphasize that using a galectin-3 target of <10 in this setting is an integrative clinical strategy rather than an established oncology guideline, and evidence has not established that MCP around surgery prevents metastasis or recurrence.

For benign biopsy findings, we generally do not continue cancer-directed MCP monitoring solely for this purpose.

Our Basic Pre- and Post-Biopsy/Surgical Support Protocol

Every patient is different, and surgical instructions always take priority. Depending on the procedure, medical history, medications, laboratory findings, and cancer type, our foundational protocol may include the following.

Vitamin C

1,000 mg two to three times daily for at least two weeks after surgery.

Vitamin C plays an important role in collagen synthesis and connective-tissue repair and supports antioxidant defenses during recovery.

Modified Citrus Pectin

15 grams daily, generally beginning two weeks before the procedure and continuing for at least one month afterward.

In selected cancer patients, galectin-3 may be monitored to help individualize longer-term use.

Zinc

25 mg twice daily or 50mg once daily with food, generally for two weeks before and two weeks after surgery.

Zinc is essential for immune function, protein synthesis, and wound healing. Higher-dose zinc should generally be used for limited periods unless zinc and copper status are being monitored.

Vitamin A

Our protocol may use 20,000 IU daily of emulsified vitamin A for approximately two weeks before and two weeks after surgery, when appropriate.

Vitamin A participates in epithelial integrity, immune function, and wound healing. This dose is not appropriate for everyone—particularly during pregnancy or when liver disease, retinoid medications, or other contraindications are present.

Probiotic Support

A mixed probiotic may be started approximately two weeks before surgery and continued for at least two weeks afterward, or continued longer when otherwise indicated.

One example used in our practice is RestorFlora, one capsule in the evening.

Fish Oil

We commonly have patients discontinue supplemental fish oil approximately 72 hours before major surgery, unless the surgical team advises otherwise.

This is generally not necessary for a routine fine-needle biopsy.

Restart timing should be confirmed with the surgeon, particularly when anticoagulants or antiplatelet medications are being used.

After Surgery: Supporting Recovery

Once the procedure is complete and the surgeon has confirmed that bleeding risk is controlled, our attention shifts toward recovery, mobility, connective-tissue repair, bowel function, pain management, and restoration of normal physiology.

Proteolytic Enzymes

Selected patients may use systemic proteolytic enzyme formulas such as Wobenzym or similar products, often taken away from food.

Because some enzyme products can affect bleeding or interact with medications, they should not be started immediately after surgery without clearance from the surgical team.

Gentle Lymphatic and Recovery Support

Depending on the surgery and stage of healing, supportive strategies can include:

  • Gentle walking and progressive movement
  • Hydration and adequate protein intake
  • Constipation prevention
  • Breathing exercises
  • Gentle lymphatic support when appropriate
  • Acupuncture for postoperative pain, nausea, and recovery
  • Castor oil packs later in recovery when appropriate and never over a fresh incision
  • Sauna only after adequate healing, hydration, and medical clearance

Rather than thinking of these interventions as “detoxing anesthesia,” we prefer to think about them as supporting circulation, bowel function, mobility, lymphatic flow, relaxation, and recovery while the liver and kidneys perform the body’s normal clearance processes.

What About IV Vitamin C?

For appropriate patients, we may consider intravenous vitamin C as part of an individualized postoperative oncology plan.

Our clinical protocol may include 25–50 grams of IV vitamin C within approximately 48 hours after surgery, once the patient is medically stable, followed by several treatments during the subsequent two weeks.

IV vitamin C has pharmacologic properties very different from oral vitamin C and is being actively investigated in oncology.

High-dose IV vitamin C also requires appropriate screening and medical supervision, including consideration of G6PD status, kidney function, hydration, iron overload disorders, and medication/treatment interactions. Timing must be coordinated with the oncology and surgical teams.

Homeopathic Support

Some patients in our practice also choose homeopathic preparations around major surgery, including Arnica, Staphysagria, Phosphorus, and Hypericum. These are optional complementary therapies which have long term historical use in healing and recovery and are well regarded as safe.  

The Bigger Picture: Don’t Fear the Procedure—Prepare for It

A cancer diagnosis can make every decision feel loaded with risk. 

Biopsies provide information that can be essential for choosing the right treatment. Surgery cures or controls many cancers. We should not delay a medically necessary procedure out of fear of the body’s wound-healing response.

At the same time, modern tumor biology gives us an increasingly sophisticated understanding of the perioperative period.

Surgery is not merely an event that happens to a tumor. It is an event experienced by the whole person—their nervous system, immune system, inflammatory pathways, metabolism, vasculature, and healing tissues.

That creates an opportunity.

Before a biopsy or surgery, we can ask:

How can we improve nutritional status?

How can we support wound healing?

How can we maintain muscle and metabolic health?

Can we improve sleep and reduce excessive sympathetic stress?

Are there deficiencies that should be corrected?

Which supplements should be stopped for surgical safety?

And, for patients with cancer, are there evidence-informed strategies worth discussing with the medical team to support the unique biology of the perioperative window?

This is what integrative oncology can do well: not replace necessary cancer treatment, but prepare the terrain around it.

The goal is to help patients enter surgery as physiologically resilient as possible—and come out with the support they need to heal, recover, and move confidently into the next phase of treatment.

Important Safety Note

This article is educational and is not a universal pre- or postoperative prescription. Supplements and medications can interact with anesthesia, anticoagulants, chemotherapy, targeted therapies, immunotherapy, blood-pressure medications, diabetes medications, and other treatments. Some supplements may need to be stopped considerably earlier than 72 hours before surgery.

Always provide your surgeon, anesthesiologist, oncologist, and integrative clinician with a complete medication and supplement list before a procedure. Do not start or stop prescription medications—including beta blockers or anti-inflammatory medications—without the prescribing and surgical teams.

References

Hiller JG, et al. Preoperative β-Blockade with Propranolol Reduces Biomarkers of Metastasis in Breast Cancer: A Phase II Randomized Trial. Clinical Cancer Research. 2020.

Shaashua L, et al. Perioperative COX-2 and β-Adrenergic Blockade Improves Metastatic Biomarkers in Breast Cancer Patients in a Phase-II Randomized Trial. Clinical Cancer Research. 2017.

Angka L, et al. Dysfunctional Natural Killer Cells in the Aftermath of Cancer Surgery. International Journal of Molecular Sciences. 2017.

Ben-Eliyahu S. et al. Research examining catecholamines, prostaglandins, perioperative immune suppression, and metastatic biology.

Keizman D, et al. Modified Citrus Pectin Treatment in Non-Metastatic Biochemically Relapsed Prostate Cancer: Results of a Prospective Phase II Study. Nutrients. 2021.

Jiang J, et al. Synergistic and additive effects of modified citrus pectin with two polybotanical compounds in the suppression of invasive behavior of human breast and prostate cancer cells. Integrative Cancer Therapies. 2013.

Shakhar G, Ben-Eliyahu S, and subsequent investigators. Reviews of perioperative stress, immune function, and metastatic mechanisms.

Healthy food and graphic of stomach and intestines

Leaky Gut: Why Gut Barrier Health Matters More Than You Think

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Leaky Gut: Why Gut Barrier Health Matters More Than You Think

Leaky Gut: Why Gut Barrier Health Matters More Than You Think

“All disease begins in the gut.” While Hippocrates may not have understood the microbiome, modern research continues to reinforce how critical the intestinal barrier is for immune health, inflammation, metabolism, and even brain function.

At Elevate Health, we frequently evaluate patients with digestive complaints, autoimmune conditions, chronic inflammation, food sensitivities, fatigue, and even cancer support for evidence of impaired gut barrier function—commonly referred to as “leaky gut.”

What is “Leaky Gut”?

Your intestinal lining is designed to perform two very important jobs:

  • Absorb nutrients your body needs.
  • Keep harmful substances out of your bloodstream.

The cells lining your intestines are connected by structures called tight junctions. When these tight junctions are healthy, they selectively allow nutrients through while keeping bacteria, toxins, and partially digested food particles where they belong—inside the gut.

When the barrier becomes damaged, these junctions loosen. This increased intestinal permeability allows substances that normally stay inside the digestive tract to cross into circulation, where they can activate the immune system and contribute to chronic inflammation.

Our educational graphic illustrates the difference between a healthy gut—with abundant microbial diversity, a strong mucus barrier, healthy tight junctions, and low inflammation—versus a dysbiotic gut characterized by reduced microbial diversity, mucus degradation, weakened tight junctions, increased inflammatory cytokines, and toxin-producing organisms.

What Causes Leaky Gut?

One of the biggest misconceptions is that leaky gut simply happens randomly.

In reality, something is usually driving the damage. If we don’t identify and remove those triggers, simply taking supplements is often not enough.

Some of the most common contributors include:

Processed Foods and Gluten

For susceptible individuals, gliadin, a protein found in gluten, can stimulate the release of zonulin, a protein involved in regulating intestinal tight junctions. Increased zonulin activity may temporarily increase intestinal permeability.

Not everyone reacts the same way, but for many patients—especially those with autoimmune disease, digestive symptoms, or chronic inflammation—we often recommend minimizing or eliminating gluten while healing the gut.

Glyphosate and Environmental Chemicals

Modern agriculture exposes us to increasing amounts of:

  • Glyphosate
  • Pesticides
  • Herbicides
  • Food additives
  • Plastic chemicals (such as BPA)
  • Heavy metals

While research is ongoing, these environmental exposures may contribute to alterations in the gut microbiome, increased oxidative stress, and impairment of the intestinal barrier.

Whenever possible we recommend:

  • Choosing organic produce (especially the Environmental Working Group’s “Dirty Dozen”)
  • Filtering drinking water
  • Limiting ultra-processed foods
  • Reducing unnecessary chemical exposures

Gut Infections and Dysbiosis

One of the most overlooked causes of ongoing leaky gut is microbial imbalance.

Common offenders include:

  • SIBO (Small Intestinal Bacterial Overgrowth)
  • Candida overgrowth
  • Klebsiella
  • Clostridium species
  • H. pylori
  • Parasites
  • Chronic gastrointestinal infections

These organisms can produce toxins, degrade the protective mucus layer, and promote ongoing inflammation.

Whenever possible, we prefer testing rather than guessing, using comprehensive stool analysis, SIBO breath testing, or other functional testing when clinically appropriate.

Our Philosophy: Remove the Cause, Then Rebuild

Many “gut repair” programs jump straight to supplements.

Our approach is different.

We typically focus on three priorities:

1. Remove What Is Damaging the Gut

This may include:

  • Identifying food triggers
  • Eliminating gluten (when appropriate)
  • Reducing processed foods
  • Limiting glyphosate and environmental toxins
  • Addressing bacterial, fungal, or parasitic overgrowth
  • Improving digestive function

Without removing the ongoing injury, healing becomes much more difficult.

2. Restore a Healthy Microbiome

Not all probiotics are the same.

We often use MegaSporeBiotic®, a spore-based probiotic that helps support microbial diversity while creating an environment that favors beneficial organisms over opportunistic pathogens. Spore-forming probiotics are particularly resilient and survive stomach acid well, making them useful in many patients with dysbiosis.

The goal isn’t simply adding bacteria—it’s encouraging a healthier microbial ecosystem.

3. Repair the Gut Barrier

Once damaging factors are being addressed, we focus on rebuilding the intestinal lining.

One of our preferred products is MegaMucosa®, which provides:

  • Immunoglobulins (IgG) that help bind microbial antigens within the gut lumen
  • Amino acids that support intestinal cells
  • Bioflavonoids that provide antioxidant support
  • Nutrients that help nourish the protective mucosal layer

Rather than masking symptoms, these ingredients are designed to support restoration of the gut’s natural protective barrier.

Food Is Still the Foundation

Supplements work best when combined with an anti-inflammatory dietary pattern.

We commonly recommend emphasizing:

  • Colorful vegetables
  • High-quality protein
  • Healthy fats
  • Fermented foods (when tolerated)
  • Fiber-rich foods that nourish beneficial bacteria
  • Polyphenol-rich foods like berries, herbs, spices, green tea, and olive oil

At the same time, reducing refined sugars and highly processed foods helps decrease inflammation and limits the fuel available to many undesirable microbes.

Healing Takes Time

The gut lining has an impressive ability to regenerate—but only when ongoing damage is reduced.

Many patients notice gradual improvements in:

  • Bloating
  • Food sensitivities
  • Digestive symptoms
  • Energy
  • Brain fog
  • Skin health
  • Immune resilience

Because every patient’s underlying causes are different, there is no one-size-fits-all protocol.

Our Recommended Gut Support Protocol

For many patients working on intestinal barrier repair, our foundational protocol includes:

  • MegaSporeBiotic® – to support a healthier microbiome and microbial balance.
  • MegaMucosa® – to help nourish and restore the intestinal mucosal barrier while providing IgG immune support.

You can view and order our recommended gut health protocol through our Fullscript dispensary here:

https://us.fullscript.com/s/agandre/shop/plans/TXVsdGlQYXRpZW50UGxhbi0xNzU1MDA=

Ready to Get to the Root Cause?

If you’ve been struggling with chronic bloating, digestive symptoms, food sensitivities, autoimmune conditions, or unexplained inflammation, simply treating symptoms may not be enough. Identifying and addressing the underlying drivers of gut dysfunction can make a meaningful difference in long-term health.

At Elevate Health, we take a personalized, root-cause approach using advanced testing, evidence-informed nutrition, targeted supplementation, and individualized treatment plans to help restore optimal gut health.

Asian woman hand on chin thinking

Can Psilocybin Repair Nerve Damage from Chemotherapy?

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Can Psilocybin Repair Nerve Damage from Chemotherapy?

Can Psilocybin Repair Nerve Damage from Chemotherapy?

Here’s What the Research Actually Shows

Chemotherapy-induced peripheral neuropathy, or CIPN, is one of the most common and stubborn side effects of cancer treatment. It affects up to 70% of patients who receive neurotoxic drugs like taxanes and platinum-based chemotherapies, producing tingling, numbness, burning pain, and muscle weakness in the hands and feet. For many survivors, it lingers for years after treatment ends, and there is still no approved drug that reliably prevents or reverses it.

That gap is why a new psilocybin trial at MD Anderson Cancer Center has drawn attention. But it’s worth being precise about what this research is actually testing, because the popular framing of “psilocybin repairs nerve damage” runs ahead of the evidence. Here’s what’s real, what’s hypothesized, and what’s still unknown.

The MD Anderson trial: NeuroGuard

The study in question is a Phase 2 trial called NeuroGuard (ClinicalTrials.gov identifier NCT07227909), sponsored by MD Anderson Cancer Center with the Usona Institute as a collaborator, and led by principal investigator Dr. Moran Amit. It is designed to test whether psilocybin can prevent or reduce the severity of CIPN in patients about to start neurotoxic chemotherapy for breast, colorectal, or head and neck cancer.

The trial has three arms. In Arm A, participants receive two supervised oral doses of psilocybin a week apart before their first chemotherapy cycle, followed by two more supervised doses before cycles two and three. Arm B tests a “subperceptual” microdosing regimen, with low 1 mg doses taken every other day for two weeks before chemotherapy starts. Arm C is standard of care with no study drug, serving as the comparison group. The primary outcome is the proportion of participants whose CIPN symptoms worsen by 12 weeks, measured using the EORTC QLQ-CIPN20 sensory subscale, a validated patient-reported symptom questionnaire.

Two things are important to flag. First, this trial is aimed at prevention and symptom mitigation, not at reversing or “repairing” nerves that are already damaged. Second, as of this writing the trial has not yet reported results. It is a prospective study designed to generate evidence, not a completed study that has already shown psilocybin works for this purpose.

Why researchers think psilocybin might help

The rationale behind NeuroGuard draws on a few separate lines of research, none of which directly show peripheral nerve regeneration in humans, but which together make a plausible case for testing it.

The first line is preclinical work on psilocybin and pain. A 2025 study in Nature Neuroscience found that a single dose of psilocybin produced a rapid and long-lasting reduction in pain-like behavior in mice with nerve injury and inflammatory pain, an effect the researchers linked to activity in specific brain circuits rather than to any local effect at the injured nerve itself. A related study in the British Journal of Pharmacology reported similar findings: a single psilocybin dose led to prolonged reductions in pain behavior in a mouse model of neuropathy. Other preclinical work, summarized in an IUPHAR-affiliated review, ties these effects to activation of the serotonin 5-HT2A receptor, the same receptor responsible for psilocybin’s psychoactive effects. Penn Medicine’s research communications team summarized this body of work as psilocybin “targeting brain circuits” involved in pain processing, which is a meaningfully different mechanism than repairing damaged axons or myelin.

The second line is broader neuroplasticity research. A widely cited 2018 paper by David Olson and colleagues coined the term “psychoplastogen” to describe how psychedelics like psilocybin promote dendritic growth and new synaptic connections, initially observed in rodent cortical neurons. More recent work, including a 2025 eLife study using human iPSC-derived cortical neurons, extends this to human brain cells in a dish. This research supports the idea that psilocybin can promote structural plasticity in the central nervous system. It does not show that psilocybin regenerates injured peripheral sensory nerves in the hands and feet, which is a distinct biological process governed by different cell types (Schwann cells, dorsal root ganglion neurons) than the cortical plasticity these studies examine.

The third line is early clinical signal in adjacent conditions. A systematic review published in Regional Anesthesia & Pain Medicine found that across the studies it examined, 57% showed statistically significant reductions in chronic neuropathic pain symptoms after psilocybin therapy, though the review covered a small and heterogeneous set of studies. A separate trial has examined psilocybin-assisted therapy in patients with advanced cancer, finding improvements in quality of life, pain control, and anxiety, though this population was not selected for CIPN specifically. A preference-assessment study called PEACE-PAIN has also been conducted to gauge patient interest in psilocybin for chronic neuropathic pain ahead of a planned efficacy trial.

What this research does not show

It’s worth being explicit about the gap between the headlines and the data. No published human study has demonstrated that psilocybin repairs structural damage to peripheral nerves, such as regenerating axons or restoring myelin, in people with CIPN or any other form of peripheral neuropathy. The strongest mechanistic evidence so far points to central nervous system effects: altered pain processing in the brain and increased plasticity in cortical neurons. Whether those central effects translate into meaningful, durable relief of CIPN symptoms, let alone actual nerve repair, is precisely the question NeuroGuard and similar trials are designed to answer. It hasn’t been answered yet.

There’s also a regulatory backdrop worth noting. In early 2025, the FDA released draft guidance specifically addressing prevention and treatment of CIPN in drug development, reflecting how difficult this condition has been to target: symptoms are subjective and hard to standardize, the underlying biology involves multiple overlapping injury mechanisms, and because CIPN is a quality-of-life issue rather than immediately life-threatening, drug developers have historically been cautious about adding new agents that could interact with chemotherapy regimens.

The bottom line

MD Anderson’s NeuroGuard trial is a legitimate, actively-designed Phase 2 study testing whether psilocybin, given around the time of chemotherapy, can prevent or reduce CIPN symptoms. It’s grounded in real preclinical findings about psilocybin’s effects on pain circuits and neural plasticity. But it is testing a hypothesis, not confirming one, and the underlying science so far describes changes in brain pain processing and cortical plasticity, not regeneration of damaged peripheral nerves. Anyone encountering claims that psilocybin has been “shown” to repair chemo-induced nerve damage should treat that as a significant overstatement of where the evidence currently stands. The honest version of the story is that this is a promising, well-motivated line of inquiry with results still to come.

References

  1. NeuroGuard: Psilocybin Trial for Preventing Chemo-induced Neuropathy. ClinicalTrials.gov, Study NCT07227909. https://clinicaltrials.gov/study/NCT07227909
  2. Psilocybin for Neuropathy — Phase 2 Clinical Trial overview (MD Anderson Cancer Center, PI Moran Amit, MD). Power. https://www.withpower.com/trial/phase-2-psilocybin-4-2026-40959
  3. Single-dose psilocybin rapidly and sustainably relieves chronic pain-like behavior via brain circuit effects. Nature Neuroscience (2025). https://www.nature.com/articles/s41593-025-02068-0
  4. Askey, T. et al. Psilocybin as a novel treatment for chronic pain. British Journal of Pharmacology. https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.17420
  5. Psilocybin induces long-lasting effects via 5-HT2A receptor activation in mouse models of pain. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC12107474/
  6. Psilocybin targets brain circuits to relieve pain. Penn Medicine News. https://www.pennmedicine.org/news/psilocybin-targets-brain-circuits-to-relieve-pain
  7. Olson, D. E. Psychoplastogens: A Promising Class of Plasticity-Promoting Neurotherapeutics. ACS Pharmacology & Translational Science (2018), reviewed via SAGE Journals. https://journals.sagepub.com/doi/10.1177/1179069518800508
  8. Psilocin fosters neuroplasticity in iPSC-derived human cortical neurons. eLife (2025). https://elifesciences.org/articles/104006
  9. Investigating the therapeutic efficacy of psilocybin in advanced cancer. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC11271737/
  10. Prospective Preference Assessment for the Psilocybin for Enhanced Analgesia in Chronic nEuropathic PAIN (PEACE-PAIN) Trial. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11552286/
  11. Psilocybin and chronic neuropathic pain: a systematic review. Regional Anesthesia & Pain Medicine. https://rapm.bmj.com/content/50/11/845
  12. Chemotherapy induced peripheral neuropathy research is on the rise. The Foundation for Peripheral Neuropathy (Oct. 2025). https://www.foundationforpn.org/chemotherapy-induced-peripheral-neuropathy-research-is-on-the-rise/
  13. FDA draft guidance: Prevention and Treatment of Chemotherapy-Induced Peripheral Neuropathy — Developing Drug and Biological Products (2025). https://www.fda.gov/regulatory-information/search-fda-guidance-documents/prevention-and-treatment-chemotherapy-induced-peripheral-neuropathy-developing-drug-and-biological
Stethoscope and calendar

Why We Recheck Labs Every 4-6 Weeks for Our Cancer Patients

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Why We Recheck Labs Every 4-6 Weeks
for Our Cancer Patients

Why We Recheck Labs Every 4-6 Weeks for Our Cancer Patients

If you’re being actively followed by our clinic for a cancer diagnosis, you’ve probably noticed a pattern: we don’t just run labs once and call it done. Patients sometimes ask why we test so often, especially when they’re feeling well. Here’s the honest answer: a single lab draw is a snapshot. What we’re really after is the movie.

A snapshot only tells you so much

One set of labs tells us where things stand today. But the body is not static — it’s responding, in real time, to infections, stress, sleep, inflammation, treatment, food, and everything in between. A single “normal” or “abnormal” result can’t tell us whether something is a blip or a trend. Only a series of labs, drawn consistently under the same conditions, can do that.

That’s why we ask you to fast 12-16 hours, be well hydrated, skip the coffee and tea, and try to test at the same time of day and month each time. Consistency in how the labs are drawn is what makes the trend line trustworthy.

Two cadences, individualized to you

This kind of frequent monitoring is specific to our cancer patients — it isn’t a one-size-fits-all schedule, and it isn’t how we approach every patient in our practice.

A core panel — CBC with differential, CMP, hsCRP, LDH, and sedimentation rate (ESR) — is rechecked every 4-6 weeks. These five give us the fastest-moving read on immune status, organ function, and inflammation, which is exactly why they’re worth checking often.

Everything else — methylation and nutrient markers, thyroid studies, iron storage, angiogenesis markers, and cancer-specific markers — is generally tracked every 1-3 months. The exact frequency is individualized to your case, your treatment plan, and what we’re watching most closely for you.

What these labs are actually telling us

Each of these labs is a window into a different system that can be stressed long before you feel it:

Metabolic function — glucose, fasting insulin, HgA1c, and the comprehensive metabolic panel (kidney and liver markers, electrolytes, protein and albumin) tell us how your body is handling fuel, hydration, and organ workload. Rising glucose or insulin, for example, can flag dysglycemia or stress on the endocrine system well before it becomes a bigger problem.

Immune status and cell counts — your CBC with differential (white cells, red cells, platelets, and the ratios between them) is one of the most sensitive windows we have into immune function and bone marrow activity. A dropping white count, a shifting neutrophil-to-lymphocyte ratio, or rising platelets can all point to something worth investigating — whether that’s a lingering viral infection, an inflammatory flare, or something that needs closer attention.

Inflammation markers — LDH, hsCRP, and sedimentation rate (what we sometimes call “the trifecta”) give us a read on inflammation and mitochondrial stress throughout the body. Individually, each can be nonspecific. Together, and tracked over time, they become far more meaningful.

Methylation and nutrient status — markers like homocysteine, MCV/MCH/MCHC, and vitamin D help us see how well your body is processing B vitamins, folate, and detoxification pathways. Methylation issues rarely show up as a single dramatic number; they show up as a slow drift that only becomes obvious when you’re looking at several data points in a row.

No single one of these labs is a verdict. Together, and repeated on a consistent cadence, they become a much clearer picture of what’s actually stressing your body — so we can address it proactively, rather than waiting for it to become symptomatic.

Why the trend matters more than any one result

This is the piece that’s easy to underestimate: the same result can mean very different things depending on what came before and after it, and catching a shift early is what allows us to actually do something about it.

We’ve seen this play out in our own patients. In one case, a patient being followed on this kind of frequent cadence had several key moments during treatment flagged by his labs — moments that, had they gone unchecked and unaddressed, could have shifted his terrain toward one more amenable to cancer progression. Because we were watching on a 4-6 week cycle rather than waiting months between draws, we caught those shifts early enough to act on them, rather than discovering them only after the fact.

That’s the real value of testing this often instead of only when something feels wrong. It’s not just about telling noise from signal — it’s about having enough lead time to actually change course. Over the long run, that difference in cadence can be the difference in outcome.

The bottom line

Frequent, consistent lab testing isn’t about chasing numbers. It’s about giving us — and you — the clearest possible view of your body’s terrain over time, so we can catch what’s stressing it early, tell the difference between noise and signal, and adjust your care proactively rather than reactively.

If you have questions about your own lab schedule or what a particular result might mean for you, please bring them to your next visit — this article is general education and isn’t a substitute for a conversation with your care team about your specific results.

Long Covid cells connectors to people

Long COVID, Microclots, and Chronic Inflammation: Part 2

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Long COVID, Microclots,
and Chronic Inflammation: Part 2

Long COVID, Microclots, and Chronic Inflammation: Part 2

Many people who develop long COVID describe the same frightening experience:

You were functioning normally before infection, and afterward your body no longer feels predictable or resilient. Simple activities can wipe you out. Your brain feels inflamed or “offline.” Foods, supplements, smells, stress, heat, exercise, or even basic daily tasks can suddenly trigger symptoms that seem disproportionate or irrational.

And perhaps most frustrating of all — standard labs are often “normal,” while you still feel profoundly unwell.

What I want you to understand is this: there are real biologic reasons this can happen.

One of the most important — and most overlooked — pieces may involve damage to the membranes surrounding your cells and mitochondria.

Why Long COVID Can Feel Like Your Body “Lost Its Reserve”

After COVID, many patients develop a pattern involving:

  • profound fatigue
  • post-exertional crashes
  • mast cell activation symptoms (MCAS)
  • brain fog
  • dizziness or POTS-like symptoms
  • hypersensitivity to foods, chemicals, medications, or supplements
  • nervous system overactivation
  • poor stress tolerance

This pattern is not simply psychological or “just inflammation.”

In many patients, the infection appears to trigger a prolonged immune and oxidative stress response that affects the very structure of the cell itself — especially the membranes that surround mitochondria.

And this matters enormously because mitochondria are responsible for producing the energy your body needs to heal, detoxify, regulate inflammation, think clearly, and tolerate stress.

Your Mitochondria Are Not Just “Low Energy” — They May Be Structurally Injured

Many people think of mitochondria as tiny batteries. But mitochondria are actually highly sophisticated energy factories, and they depend on delicate membrane structures to function properly.

The inner mitochondrial membrane is where your cells produce ATP — the energy currency of the body.

When these membranes become damaged from inflammation and oxidative stress:

  • energy production becomes inefficient
  • cells leak energy
  • the nervous system becomes unstable
  • inflammation becomes amplified
  • recovery after exertion becomes impaired

This is why many patients with long COVID feel like:

“I can do something once, but then my body crashes afterward.”

The system is operating without reserve.

Why This Can Become a Barrier to Healing

This is one of the most important concepts to understand.

If mitochondrial membranes are damaged, your body may struggle to tolerate even treatments that are technically “good” for you.

This is why some patients:

  • react badly to supplements
  • flare with detox protocols
  • worsen with aggressive antimicrobial treatment
  • crash after exercise
  • become hypersensitive to medications or foods

The body may not have enough cellular resilience to process increased demands.

In these cases, the problem is not that the patient is “failing treatment.” The problem may be that the foundation has not yet been rebuilt.

This is especially common in patients with:

  • MCAS
  • post-exertional malaise
  • chronic infections or co-infections
  • mold exposure
  • persistent inflammation after COVID

The Connection Between MCAS and Membrane Damage

Mast cells are immune cells that become overly reactive in many long COVID patients.

Once activated, mast cells release inflammatory chemicals that can further damage phospholipid membranes.

This creates a vicious cycle:

  1. inflammation damages membranes
  2. damaged membranes lower mast cell thresholds
  3. mast cells become more reactive
  4. more inflammation and oxidative stress occur
  5. mitochondrial function worsens further

Over time, patients can become increasingly sensitive and debilitated.

This is why your symptoms may feel “multi-system”:

  • fatigue
  • GI symptoms
  • brain fog
  • dizziness
  • burning sensations
  • histamine reactions
  • sensory overload
  • anxiety-like surges
  • autonomic instability

They may all trace back to interconnected immune, mitochondrial, and membrane dysfunction.

Why We Are Looking at Cell Membrane Health

One of the reasons to assess more deeply is because there may still be a significant underlying mitochondrial membrane issue contributing to debilitating symptoms — even if you have made progress.

The persistence of:

  • fatigue
  • brain fog
  • hypersensitivity
  • limited resilience
  • post-exertional worsening
  • mast cell instability

suggests there may still be a deeper “structural” issue limiting recovery capacity.

This is where membrane health becomes extremely important.

What Is ProdromeScan?

ProdromeScan is a specialized lipid and membrane assessment that looks at the health of the fats and phospholipids that make up your cellular and mitochondrial membranes.

Instead of only asking:

“Are the mitochondria functioning?”

it asks:

“Do the mitochondria have the structural integrity needed to function and heal?”

The test evaluates things like:

  • phospholipid reserves
  • plasmalogens (protective membrane fats)
  • omega-3 and omega-6 distribution
  • sphingomyelin and ceramides (important for nerve and myelin health)
  • markers of oxidative membrane injury
  • patterns suggesting mitochondrial membrane stress

This can help us understand whether your body is stuck in a chronic “cell danger” or survival state where healing capacity remains impaired.

Why This Matters as a Root Cause Issue

If membranes are damaged, the body will struggle to:

  • produce energy
  • regulate inflammation
  • calm mast cells
  • repair the nervous system
  • detoxify properly
  • tolerate therapies
  • recover after activity

In other words:
you can address infections, inflammation, and triggers — but if the cell itself remains fragile, recovery will plateau.

This is why membrane repair can become a foundational step rather than just another supplement strategy.

How Membrane Repair Is Addressed

The goal is not to aggressively “stimulate” the body.

In fact, many patients worsen when treatment is pushed too quickly.

Instead, the approach is usually gradual and supportive:

  • stabilizing mast cells
  • lowering oxidative stress
  • improving bile flow and digestion
  • replenishing phospholipids
  • restoring omega balance
  • supporting plasmalogens
  • carefully rebuilding mitochondrial resilience
  • pacing treatment in a sequence the body can tolerate

**This is often why patients begin improving only after treatment is slowed down and layered more strategically.

There Is Hope

Many patients with long COVID feel hopeless because recovery is nonlinear and because they have often been told:

  • “your labs are normal”
  • “it’s anxiety”
  • “you just need exercise”
  • “nothing else can be done”

But emerging research and clinical experience increasingly show that long COVID can involve measurable disturbances in immune signaling, mitochondrial function, oxidative stress, and membrane biology.

When we identify and support these deeper layers carefully, patients often regain:

  • better energy
  • clearer thinking
  • less reactivity
  • improved tolerance
  • more stability
  • more resilience

Not overnight. Not all at once. But progressively.

And importantly — recovery often accelerates once the body finally has enough cellular reserve to heal safely.

Assessing your membrane and mitochondrial health may be an important next step in understanding what is still holding your system back.

Cells

Long COVID, Microclots, and Chronic Inflammation: Why Recovery Is Often More Complicated Than It Seems

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Long COVID, Microclots, and Chronic Inflammation: Why Recovery Is Often More Complicated Than It Seems

Long COVID, Microclots, and Chronic Inflammation: Why Recovery Is Often More Complicated Than It Seems

For many people, COVID-19 ends after a few days or weeks.

But for others, symptoms linger for months — sometimes years.

This condition, often called Long COVID, can affect nearly every system in the body and may include:

  • Severe fatigue
  • Brain fog
  • Shortness of breath
  • Dizziness or POTS symptoms
  • Joint and muscle pain
  • Sleep problems
  • Anxiety or depression
  • Digestive issues
  • Exercise intolerance
  • Heart palpitations

One of the most frustrating parts of Long COVID is that many patients are told their labs are “normal,” even while they continue to feel profoundly unwell.

Researchers are now uncovering why recovery can become so complex — and why Long COVID may involve far more than just lingering viral symptoms.

Long COVID Is Likely Not Just One Condition

One of the biggest shifts in understanding Long COVID is the realization that it is probably not a single disease.

Instead, it appears to be a multi-system chronic inflammatory condition that can affect the immune system, blood vessels, nervous system, gut, mitochondria, hormones, and even clotting pathways.

Different people may experience different combinations of dysfunction.

This helps explain why symptoms vary so widely from person to person.

What Researchers Think May Be Driving Long COVID

Scientists are currently investigating several overlapping mechanisms that may contribute to persistent symptoms.

1. Persistent Viral Fragments

Some studies suggest that pieces of the virus — particularly spike protein or viral RNA — may linger in the body long after the initial infection resolves.

These lingering viral fragments may continue stimulating the immune system and promoting inflammation.

2. Reactivation of Dormant Viruses

COVID may also reactivate viruses that were previously dormant in the body, including:

  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • Herpes viruses

This may contribute to fatigue, immune dysfunction, swollen lymph nodes, and nervous system symptoms.

Many people with Long COVID report symptoms similar to chronic viral illnesses.

3. Chronic Inflammation and Immune Dysregulation

In some people, the immune system appears to remain stuck in an activated state long after infection.

Instead of turning off appropriately, inflammatory signaling continues.

This may contribute to:

  • Ongoing fatigue
  • Body pain
  • Brain fog
  • Autoimmune symptoms
  • Mast cell activation
  • Nervous system hypersensitivity

4. Gut Dysfunction and “Leaky Gut”

The gut appears to play a major role in Long COVID.

Researchers have found evidence that COVID may disrupt the intestinal barrier, allowing inflammatory compounds and bacterial fragments to enter the bloodstream.

This may contribute to:

  • Digestive symptoms
  • Food sensitivities
  • Immune activation
  • Brain fog
  • Systemic inflammation

Changes in the gut microbiome may also reduce the production of anti-inflammatory compounds that normally help regulate immunity.

The Emerging Microclot Theory

One of the more talked-about theories in Long COVID research involves microclots.

These are extremely tiny abnormal clots that may form in the blood and interfere with oxygen delivery to tissues.

Researchers believe these microclots may contribute to symptoms such as:

  • Fatigue
  • Exercise intolerance
  • Muscle pain
  • Brain fog
  • Shortness of breath
  • Dizziness

The theory is that even though oxygen is entering the lungs normally, it may not be reaching tissues efficiently because blood flow at the microscopic level becomes impaired.

Why Standard Clotting Tests May Miss the Problem

One of the challenges is that many standard clotting tests can appear normal in people with Long COVID.

Researchers suspect this may happen because these microclots behave differently than traditional blood clots.

Some studies suggest the clots may resist normal breakdown mechanisms, making them harder to detect through routine testing.

This is still an evolving area of research, but it may help explain why patients can have severe symptoms despite reassuring standard lab work.

How Long COVID Can Affect Energy Production

Another major focus of current research is mitochondrial dysfunction.

Mitochondria are the tiny structures inside cells responsible for producing energy.

When inflammation, oxidative stress, or impaired blood flow affect mitochondria, the body may struggle to generate adequate energy.

This may lead to:

  • Post-exertional malaise
  • Severe exhaustion after activity
  • Muscle weakness
  • Cognitive fatigue
  • Poor recovery after exercise

This pattern is very similar to what has long been seen in ME/CFS (chronic fatigue syndrome).

Why Some People Become More Sensitive After COVID

Many people with Long COVID notice they become unusually sensitive to:

  • Foods
  • Supplements
  • Medications
  • Stress
  • Chemicals or fragrances
  • Environmental toxins

Researchers believe this may reflect nervous system and immune system dysregulation.

In some cases, COVID may trigger:

  • Mast cell activation
  • Autonomic dysfunction (POTS/dysautonomia)
  • Heightened inflammatory responses
  • Increased oxidative stress

The body essentially becomes “stuck” in a state of overactivation.

The Importance of Looking Beyond the Virus

One of the most important lessons emerging from Long COVID research is this:

Sometimes the lingering symptoms are not only about the virus itself.

COVID may also expose or worsen underlying vulnerabilities such as:

  • Hormonal imbalances
  • Nutrient deficiencies
  • Hidden infections
  • Mold exposure
  • Autoimmune tendencies
  • Gut dysfunction
  • Nervous system dysregulation
  • Mitochondrial stress

This is why recovery often requires a broader, whole-body approach.

A More Comprehensive View of Recovery

Many clinicians now view Long COVID through a “systems biology” lens — meaning they look at how multiple systems interact rather than focusing on a single symptom.

Areas commonly addressed include:

Inflammation Reduction

Supporting the body’s ability to regulate chronic inflammatory signaling.

Mitochondrial Support

Improving cellular energy production and recovery capacity.

Gut Health

Repairing the gut lining and restoring microbiome balance.

Nervous System Regulation

Supporting autonomic balance and reducing chronic stress signaling.

Sleep and Recovery

Improving restorative sleep and circadian function.

Nutrient Repletion

Correcting deficiencies that may impair immune or mitochondrial function.

Circulation and Clotting Support

Addressing vascular health and blood flow when clinically appropriate.

The Emotional Side of Long COVID

Long COVID can be deeply isolating.

Many patients feel dismissed because they “look healthy” or because their testing fails to fully explain the severity of their symptoms.

But ongoing research continues to validate what patients have been experiencing:

Long COVID is real, biologically complex, and often multi-systemic.

Recovery is rarely linear, and healing often requires patience, individualized care, and addressing multiple layers of dysfunction at once.

The Bigger Picture

Long COVID is teaching medicine an important lesson:

Health is not simply the absence of disease on a lab test.

The body is an interconnected system involving the immune system, nervous system, circulation, mitochondria, hormones, gut, and brain.

When those systems become dysregulated together, symptoms can persist long after the initial infection ends.

Understanding these mechanisms offers hope — not because there is one magic cure, but because researchers are finally beginning to understand why so many people continue struggling after COVID.

And with better understanding comes the possibility of better treatment, better support, and ultimately, better recovery.

Woman thinking with her hand on her chin

Mast Cell Activation: Could an Overactive Immune Response Be Driving Your Symptoms?

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Mast Cell Activation: Could an Overactive Immune Response Be Driving Your Symptoms?

Mast Cell Activation: Could an Overactive Immune Response Be Driving Your Symptoms?

Do you struggle with symptoms that seem unrelated — yet somehow connected?

Maybe you experience:

  • Brain fog
  • Fatigue
  • Hives or itching
  • Food sensitivities
  • Anxiety or panic feelings
  • Flushing
  • Headaches or migraines
  • Digestive problems
  • Dizziness or POTS symptoms
  • Chemical sensitivities
  • Sleep issues
  • Chronic inflammation

If so, an increasingly recognized condition called Mast Cell Activation Syndrome (MCAS) may be part of the picture.

Although awareness of MCAS is growing, many people live with symptoms for years before realizing mast cells could be involved.

What Are Mast Cells?

Mast cells are specialized immune cells found throughout the body.

They are especially concentrated in areas that interact with the outside world, including:

  • The skin
  • Airways
  • Gut lining
  • Blood vessels
  • Nervous system

Their job is to help protect the body from threats such as infections, toxins, and allergens.

When mast cells detect danger, they release chemical messengers like:

  • Histamine
  • Cytokines
  • Leukotrienes
  • Prostaglandins

This process is called mast cell activation.

In healthy situations, mast cells help coordinate healing and immune defense.

But in MCAS, mast cells become overly reactive and begin releasing inflammatory chemicals too easily or too often.

Why MCAS Can Cause So Many Different Symptoms

Mast cells exist throughout the body, which is why MCAS can affect multiple systems at once.

Depending on where mast cells become activated, symptoms may appear in different ways.

Skin Symptoms

  • Hives
  • Itching
  • Flushing
  • Rashes
  • Eczema

Nervous System Symptoms

  • Brain fog
  • Anxiety
  • Panic sensations
  • Headaches or migraines
  • Sensitivity to light, sound, or smells

Digestive Symptoms

  • Bloating
  • Reflux
  • Nausea
  • Diarrhea
  • Food sensitivities

Cardiovascular Symptoms

  • Rapid heart rate
  • Dizziness
  • Low blood pressure
  • POTS or orthostatic intolerance

Respiratory Symptoms

  • Nasal congestion
  • Shortness of breath
  • Asthma-like symptoms

Because symptoms can affect nearly every system, many people with MCAS feel dismissed or misunderstood before receiving answers.

Conditions Commonly Associated with Mast Cell Activation

Researchers have found mast cell involvement in a surprisingly wide range of chronic conditions, including:

  • Allergies and asthma
  • Autoimmune disease
  • Long COVID
  • Mold illness
  • Lyme disease
  • Fibromyalgia
  • Migraines
  • IBS and gut dysbiosis
  • POTS/dysautonomia
  • Eczema and psoriasis
  • Anxiety and depression
  • Chronic fatigue syndromes

MCAS is also increasingly being studied in connection with neuroinflammation and chronic inflammatory illnesses.

Histamine: More Than Just Allergies

Many people think histamine only affects seasonal allergies.

But histamine is actually a powerful signaling chemical involved in:

  • Immune responses
  • Stomach acid production
  • Brain function
  • Blood vessel regulation
  • Sleep and wakefulness
  • Inflammation

When histamine levels become excessive, symptoms can become widespread.

This is why MCAS can feel so different from person to person.

Why Some People Become “Sensitive to Everything”

One hallmark of MCAS is increasing sensitivity over time.

People may suddenly react to:

  • Foods
  • Supplements
  • Medications
  • Alcohol
  • Fragrances
  • Mold or chemicals
  • Stress
  • Temperature changes

This happens because mast cells become hyper-reactive and begin overresponding to triggers that previously caused no issue.

The nervous system and immune system essentially become stuck in an exaggerated “threat response.”

MCAS and the Brain

One of the most fascinating areas of MCAS research involves the brain and nervous system.

Mast cells interact closely with immune cells in the brain called microglia.

When mast cells become overactive, they may contribute to:

  • Neuroinflammation
  • Anxiety
  • Mood changes
  • Cognitive dysfunction
  • Sleep disruption
  • Sensory hypersensitivity

This may help explain why many people with chronic inflammatory illnesses experience both physical and neurological symptoms at the same time.

Natural Compounds That May Help Stabilize Mast Cells

A growing body of research is exploring natural compounds that may help calm mast cell activity and reduce histamine release.

Many of these compounds belong to a group called flavonoids — plant compounds found in herbs, fruits, vegetables, and medicinal plants.

These compounds appear to have antioxidant, anti-inflammatory, and mast cell stabilizing effects.

Quercetin: One of the Most Studied Natural Mast Cell Stabilizers

Quercetin is a flavonoid found in foods such as onions, apples, and berries.

Research suggests quercetin may help:

  • Reduce histamine release
  • Lower inflammatory cytokines
  • Calm allergic responses
  • Support immune balance

Some studies have even suggested quercetin may inhibit mast cell activation more effectively than certain conventional mast cell stabilizers in laboratory settings.

Luteolin: A Powerful Neuro-Immune Flavonoid

Luteolin is another plant flavonoid receiving attention in MCAS research.

It appears to have several potential benefits:

  • Anti-inflammatory effects
  • Mast cell stabilization
  • Neuroprotective properties
  • Reduced microglial activation in the brain

Luteolin is found in herbs such as:

  • Lemon balm
  • Perilla
  • Stinging nettle

Because of its effects on both mast cells and neuroinflammation, it is being explored in conditions involving brain fog and nervous system symptoms.

The Role of Histamine Receptors

Histamine works through several different receptors in the body, which helps explain why MCAS symptoms can be so diverse.

H1 Receptors

Associated with:

  • Allergies
  • Itching
  • Nasal congestion
  • Skin symptoms
  • Wakefulness and anxiety

H2 Receptors

Associated with:

  • Stomach acid production
  • Reflux
  • GI symptoms
  • Some cardiovascular effects

H4 Receptors

Associated with:

  • Immune activation
  • Inflammation
  • Mast cell signaling

Some herbs and nutrients appear to influence these histamine pathways naturally.

Herbs Commonly Used in Mast Cell Support

Several herbs discussed in current mast cell research may offer supportive benefits.

Stinging Nettle

May help:

  • Block H1 histamine receptors
  • Reduce allergy symptoms
  • Calm histamine release

Lemon Balm

Traditionally used for:

  • Anxiety and stress support
  • Digestive symptoms
  • Nervous system calming

Black Cumin Seed

Studied for:

  • Anti-inflammatory effects
  • Gut support
  • Histamine modulation

Turmeric/Curcumin

Known for:

  • Broad anti-inflammatory activity
  • Immune modulation
  • Potential mast cell stabilizing effects

Baikal Skullcap

May support:

  • Neuroinflammation
  • Immune balance
  • Cognitive function

These compounds are not “magic cures,” but they may help support a calmer immune response in some individuals.

Diet and Lifestyle Matter Too

Many people with MCAS benefit from reducing the overall inflammatory burden on the body.

Common strategies may include:

  • Lower-histamine diets
  • Improving gut health
  • Stress reduction
  • Sleep support
  • Mold and environmental toxin reduction
  • Nervous system regulation
  • Identifying personal triggers

Because MCAS is highly individualized, what helps one person may not help another.

Why MCAS Often Overlaps with Long COVID and Chronic Illness

Researchers increasingly believe mast cell activation may be one piece of the puzzle in conditions like:

  • Long COVID
  • Mold illness
  • Lyme disease
  • Chronic fatigue syndrome
  • Fibromyalgia
  • Dysautonomia/POTS

In many of these illnesses, the immune system appears chronically activated and hypersensitive.

Mast cells may act as amplifiers — turning inflammation up and making symptoms feel more intense and widespread.

The Bigger Picture

Mast cells are not “bad.”

They are an essential part of the immune system.

The problem arises when they become chronically overactivated and begin responding inappropriately to everyday triggers.

Understanding mast cell activation helps explain why some people experience such a wide range of seemingly disconnected symptoms — from allergies and gut issues to anxiety, fatigue, and brain fog.

And perhaps most importantly, it reminds us that chronic illness is often not “all in your head.”

Sometimes the immune system is simply stuck in a state of overprotection.

With better understanding, targeted support, and individualized care, many people can begin calming that response and improving quality of life.

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