Restorative Massage & Lymphedema Therapy

Restorative Massage & Lymphedema Therapy Restorative Massage & Lymphedema Therapy offers registered massage therapy, lymphedema therapy, and

Yep!
10/31/2025

Yep!

Knowledge is power!Just in time for cold and flu season, learn the tools to strengthen your immune system and your resil...
10/25/2025

Knowledge is power!

Just in time for cold and flu season, learn the tools to strengthen your immune system and your resiliency.







10/24/2025

Cancer accounts for one in seven deaths worldwide and is the second leading cause of death in the United States, after heart disease. One of the standard cancer treatments is chemotherapy which sometimes can lead to chemoresistance and treatment failure. Therefore, there is a great need for novel th...

Pink ribbon will do nothing.  Addressing your body and mind will do everything.
10/23/2025

Pink ribbon will do nothing. Addressing your body and mind will do everything.





















In light of October being breast cancer awareness month, here is what happens when you play an ACTIVE role in your cance...
10/18/2025

In light of October being breast cancer awareness month, here is what happens when you play an ACTIVE role in your cancer journey.




Stubborn belly fat?  Low energy?  High blood pressure?  High cholesterol?  Joint pain?  Diabetes? Heart disease? Cancer?...
10/02/2025

Stubborn belly fat? Low energy? High blood pressure? High cholesterol? Joint pain? Diabetes? Heart disease? Cancer?

Lunch & Learn: Therapeutic Fasting & How To Do It Right

🏫Muskoka Market & Eatery - Food Cooperative
đź•™Saturday, October 4th 11am
đź’˛Free

09/28/2025

The Cell Danger Response: A Critical Conversation for Cancer Patients and Their Families



Understanding an Overlooked Factor in Cancer Treatment Success



For decades, cancer treatment has focused primarily on eliminating cancer cells through increasingly sophisticated methods. However, emerging research reveals a fundamental biological process called the Cell Danger Response (CDR) that may significantly influence both treatment outcomes and long-term cancer risk. This response, while essential for survival, can paradoxically work against patients when chronically activated by cancer therapies. Understanding CDR and discussing it with your oncology team represents a crucial step toward optimizing treatment outcomes and reducing the risk of future cancers.



What Is the Cell Danger Response?



The Cell Danger Response describes how cells react when they detect threats to their survival. Think of it as your body’s cellular alarm system. When cells encounter danger signals from infection, physical injury, toxins, or other stressors, they shift from their normal operations into a defensive state. This protective response involves changes in cellular metabolism, increased inflammation, altered communication between cells, and modifications to how genes are expressed.



In the short term, CDR helps cells survive threats and promote healing. However, when this alarm system remains activated for extended periods, it creates conditions within the body that can promote cancer development. The chronic inflammation, metabolic dysfunction, and cellular stress associated with prolonged CDR can damage DNA, disrupt normal cellular controls, and create an environment where cancer cells can thrive.



The Scientific Foundation: How CDR Was Discovered



The Cell Danger Response theory emerged from groundbreaking work by Dr. Robert Naviaux at the University of California, San Diego. In the early 2010s, Dr. Naviaux was investigating metabolic disorders and autism when he noticed striking patterns in how cells responded to various threats. His research revealed that whether cells faced viral infection, chemical toxins, or physical trauma, they activated remarkably similar defensive programs involving fundamental changes in cellular metabolism and communication.



Dr. Naviaux’s crucial insight was recognizing that these cellular responses, previously studied separately across different medical specialties, represented a unified, evolutionarily ancient survival mechanism. Published in 2014, his comprehensive theory connected seemingly disparate conditions ranging from chronic fatigue syndrome to cancer through this common cellular defense pathway. This work built upon decades of earlier research in cellular metabolism, immunology, and stress responses, synthesizing these findings into a coherent framework that explained how cells coordinate their defensive responses.



The CDR theory gained particular relevance to cancer when researchers recognized that tumor cells exploit these same ancient survival mechanisms. Further investigations revealed that cancer treatments themselves strongly activate CDR, creating conditions that could paradoxically promote cancer development and recurrence. This recognition has sparked a growing movement within oncology to develop treatment approaches that work with, rather than against, these fundamental cellular responses.



The Hidden Danger: How CDR Creates Cancer Stem Cells



One of the most concerning aspects of chronic CDR activation involves its effect on the body’s stem cells. These special cells serve as the body’s repair system, capable of regenerating damaged tissues throughout our lifetime. However, when exposed to persistent danger signals, these normally beneficial cells can undergo a sinister transformation into cancer stem cells.



This transformation process occurs gradually as healthy stem cells experience chronic inflammation and metabolic stress from ongoing CDR activation. The continuous exposure to danger signals causes these cells to accumulate genetic damage while simultaneously developing enhanced survival capabilities. Over time, they acquire the ability to resist normal growth controls, survive in hostile environments, and regenerate entire tumors from just a single cell.



Cancer stem cells represent perhaps the greatest challenge in cancer treatment. Unlike regular cancer cells that divide rapidly and respond to conventional therapies, cancer stem cells can enter dormant states that allow them to survive chemotherapy and radiation. They possess enhanced repair mechanisms, can actively pump out chemotherapy drugs, and maintain the flexibility to adapt their metabolism to survive in different environments. Most critically, these cells can remain hidden in the body for years or even decades after treatment, only to reactivate and cause cancer recurrence when conditions become favorable.



The presence of cancer stem cells explains why some cancers return after seemingly successful treatment. Even if therapy eliminates 99.9% of cancer cells, a small population of cancer stem cells can survive, remain dormant, and eventually regenerate the entire tumor. This makes addressing the CDR processes that create and maintain cancer stem cells essential for achieving lasting cancer cures rather than temporary remissions.



The Treatment Paradox: How Cancer Therapies Activate CDR



Every major form of cancer treatment can trigger the Cell Danger Response, though through different mechanisms and to varying degrees. This creates a fundamental paradox in cancer care: the very treatments designed to eliminate cancer can activate biological responses that may increase future cancer risk if not properly managed. More concerning still, these treatments can accelerate the transformation of healthy stem cells into cancer stem cells while failing to eliminate existing cancer stem cells.



Surgery, while often essential for tumor removal, creates immediate physical trauma that releases danger signals throughout the body. The healing process following surgery involves weeks to months of CDR activation as tissues repair themselves. During this time, growth factors and inflammatory signals intended to promote healing may inadvertently support the growth of any remaining cancer cells, activate dormant cancer stem cells, or promote the transformation of healthy stem cells in the surgical area.



Chemotherapy and radiation therapy work by damaging cancer cell DNA, but they also affect healthy cells throughout the body. This widespread cellular damage releases massive quantities of danger signals, including DNA fragments, cellular debris, and inflammatory molecules. These treatments can damage mitochondria, the energy-producing structures within cells, creating metabolic dysfunction that persists long after treatment ends. This sustained metabolic stress maintains CDR activation and creates conditions favorable for both cancer stem cell survival and the transformation of healthy stem cells into new cancer stem cells.



The damage to healthy stem cells during treatment proves particularly problematic. While regular cells that suffer severe damage typically die, stem cells often survive with accumulated mutations, entering protective dormant states. Years later, when called upon to repair tissues, these damaged stem cells may have transformed into cancer stem cells, explaining why treatment-related secondary cancers can appear decades after initial therapy.



Targeted therapies, despite being more precise than traditional chemotherapy, still induce CDR by disrupting cellular metabolism and causing cancer cell death. The sudden loss of specific cellular signals can create metabolic crises in both cancer and normal cells, triggering danger responses that spread throughout tissues. These metabolic disruptions can push healthy stem cells toward cancer stem cell transformation while potentially missing dormant cancer stem cells that have adapted alternative survival pathways.



Hormone blockade therapies create systemic metabolic stress as the body struggles to adapt to the sudden absence of hormonal signals, activating CDR through metabolic rather than directly cytotoxic mechanisms. This prolonged metabolic dysfunction particularly affects hormone-sensitive stem cells throughout the body, potentially initiating transformation processes that manifest as hormone-independent cancers years later.



Immunotherapy presents a unique situation where CDR activation is both the mechanism of action and a potential source of complications. While these treatments can effectively target some cancer stem cells by overcoming their immune evasion mechanisms, the massive inflammation they generate can paradoxically create conditions that promote new cancer stem cell formation in other tissues.



The Long-Term Implications: Secondary Cancers and Treatment Resistance



The chronic activation of CDR by cancer treatments helps explain several troubling observations in oncology. Cancer survivors face significantly elevated risks of developing new cancers compared to the general population, with these secondary malignancies often appearing years or even decades after successful treatment. This increased risk stems not only from genetic predisposition but significantly from the pool of damaged stem cells created during treatment and the ongoing CDR that promotes their transformation into cancer stem cells.



Treatment resistance frequently develops through cancer stem cell populations that survive initial therapy. These cells, having been exposed to treatment-induced danger signals, develop enhanced survival mechanisms that make them even more difficult to eliminate with subsequent treatments. The metabolic flexibility and stress resistance gained through CDR activation enable these cancer stem cells to survive treatments that successfully eliminate regular cancer cells, leading to recurrences that prove increasingly difficult to treat.



Why This Conversation Matters Now



Despite growing scientific evidence about the importance of CDR and cancer stem cells in treatment outcomes, these concepts remain largely absent from routine cancer care discussions. Many oncologists, while experts in administering cancer treatments, may not be fully aware of the latest research on how CDR drives cancer stem cell formation and treatment resistance. This knowledge gap represents a missed opportunity to optimize treatment outcomes and reduce long-term risks.



The scientific literature now contains extensive documentation of CDR’s role in cancer stem cell biology. Researchers have identified specific mechanisms by which chronic danger responses transform healthy stem cells, documented how cancer stem cells survive treatment through CDR-related adaptations, and began developing strategies to target these processes. However, translation of this knowledge into clinical practice has been slow, partly because it requires thinking beyond immediate tumor response to consider long-term cellular health and stem cell integrity.



Bridging the Gap: Comprehensive CDR Management



Fortunately, researchers have identified numerous interventions that may help modulate CDR during cancer treatment, with specific benefits for preventing cancer stem cell formation and eliminating existing cancer stem cells. These approaches work by normalizing the cellular environment to remove the advantages that cancer stem cells depend upon for survival while protecting healthy stem cells from transformation.



During active treatment, CDR modulation can enhance the elimination of cancer stem cells by disrupting their dormancy and metabolic advantages. By reducing inflammatory signals and normalizing metabolism, these interventions can push dormant cancer stem cells back into active cell division where they become vulnerable to conventional therapies. Simultaneously, protecting healthy stem cells from excessive danger signals prevents the creation of new cancer stem cells that could cause future recurrences.



Long-term CDR management proves equally critical for preventing cancer recurrence. By maintaining a cellular environment unfavorable to cancer stem cell reactivation and preventing the transformation of healthy stem cells, ongoing CDR modulation addresses the root causes of late recurrence. This approach recognizes that cancer survivorship requires active management of cellular health, not just surveillance for tumor return.



Repurposed medications such as metformin show particular promise in targeting the metabolic adaptations of cancer stem cells while protecting healthy stem cells from transformation. Natural compounds including specialized forms of curcumin and omega-3 fatty acids can help resolve chronic inflammation that drives stem cell transformation. These interventions aim not to eliminate all danger responses but to prevent the excessive, prolonged activation that creates and maintains cancer stem cells.



Initiating the Conversation with Your Oncology Team



Bringing up CDR and cancer stem cells with your oncologist requires a balanced approach that respects their expertise while advocating for comprehensive care. Consider opening the discussion by expressing interest in understanding all factors that might influence both immediate treatment success and long-term recurrence risk. You might specifically ask about the cancer stem cell population in your type of cancer and how your treatment plan addresses these particularly resistant cells.



Prepare specific questions about how your treatment plan might be optimized to target cancer stem cells while protecting healthy stem cells from transformation. Ask whether any CDR-modulating interventions might enhance cancer stem cell elimination during treatment or reduce the risk of creating treatment-resistant cells. Inquire about biomarkers that could monitor cancer stem cell burden and CDR status throughout treatment and into survivorship.



If your oncologist is unfamiliar with CDR concepts or cancer stem cell biology in relation to danger responses, approach this as an opportunity for collaborative learning. Many physicians appreciate engaged patients who bring new scientific perspectives to their attention, particularly when these insights could improve long-term outcomes. Offer to share key research papers that provide evidence-based information about CDR, cancer stem cells, and treatment optimization.



Moving Forward: A New Paradigm in Cancer Care



The recognition of CDR’s role in cancer stem cell biology represents a fundamental shift in how we should approach cancer treatment. Rather than focusing solely on eliminating detectable tumors, we must consider how treatments affect the stem cell populations that drive recurrence and create new cancers. This perspective enhances our ability to achieve lasting cures rather than temporary remissions.



For patients currently undergoing treatment, understanding the cancer stem cell challenge emphasizes the importance of comprehensive approaches that go beyond tumor shrinkage. For survivors, it underscores why ongoing cellular health management remains crucial years after treatment completion. For those facing treatment decisions, it provides additional factors to consider when evaluating options and planning long-term strategies.



Conclusion: Empowerment Through Comprehensive Understanding



Knowledge of how the Cell Danger Response drives cancer stem cell formation empowers patients and families to engage more meaningfully in treatment planning. By understanding that cancer involves not just tumor cells but also the cellular conditions that create and maintain cancer stem cells, patients can work with their medical teams to develop truly comprehensive treatment strategies.



The science clearly demonstrates that addressing CDR and cancer stem cells requires attention during active treatment to enhance cancer elimination and throughout survivorship to prevent recurrence. This dual focus offers the potential for genuine cures rather than the current reality of indefinite cancer risk. Every patient deserves treatment approaches that consider not just immediate tumor response but also the cellular mechanisms that determine whether cancer returns.



As you navigate your cancer journey, remember that advocating for CDR-aware care that addresses cancer stem cells represents an investment in both immediate success and long-term health. By raising these issues with your oncology team and remaining engaged in treatment planning, you contribute to the evolution of cancer care toward more sophisticated approaches that target the root causes of treatment resistance and recurrence. The goal is not merely to survive cancer but to achieve lasting cellular health that prevents its return.



Dr. Daniel Thomas, DO, MS

Metabolic & Nutritional Medicine

Integrative Cancer Therapeutics

Mount Dora, Florida

drthomas@healthyandstrong.com



Disclaimer: The information in this article is for general educational purposes and is not a replacement for professional medical advice. If you have specific concerns about your health, please consult a qualified healthcare provider.


Reference: Naviaux RK. Metabolic features of the cell danger response. Mitochondrion. 2014 May;16

Artemisinin is an effective anti malarial TCM herb, that also has potent anti cancer properties. Artesunate (ART) is the...
09/27/2025

Artemisinin is an effective anti malarial TCM herb, that also has potent anti cancer properties. Artesunate (ART) is the semisynthetic derivative of artemisinin. ART has a better absorption than its natural counterpart artemisinin. This study demonstrates ART anti cancer effect on prostate cancer, but artemisinin and ART also effective for other cancers including breast, ovarian, gastric, and melanomas.

From the study:
"Recent studies have shown that ART acts on the electron transport chain (of cancer) and is directly involved in reactive oxygen species generation, which leads to mitochondrial membrane depolarization and an apoptosis response cascade.
In summary, our study is the first demonstration that lncRNA participates in the antitumor effect of ART. ART significantly inhibited the viability and mobility of PCa cell lines triggered by UCA1 down-regulation. All the described clinical data support the proposition that over-expression of UCA1 may play a key role in PCa progression and development."
https://www.oncotarget.com/article/15353/text/



https://doi.org/10.18632/oncotarget.15353 Yan Zhou, Xiuju Wang, Jianjun Zhang, Aina He, Ya Ling Wang, Kun Han, Yang Su, Junyi Yin, Xiaobin Lv, Haiyan Hu

The Power of Pepper! đź’Ş Spices make your food taste great AND give a tone of anti cancer nutrition!đź’šPiperlongumine (long ...
09/24/2025

The Power of Pepper! đź’Ş
Spices make your food taste great AND give a tone of anti cancer nutrition!đź’š

Piperlongumine (long pepper) is a very effective anti cancer spice, that helps induce cancer cell death.

The conclusion of this 2018 Indian research paper on colon cancer reads:

"Our study emphasizes that PL inhibits tumor growth by targeting multiple components of Ras/PI3K/Akt signaling axis and its downstream events such as activation of NF-ÎşB and evasion from apoptosis. Therefore, PL appears to be an attractive bioactive [phytochemical](https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/phytochemical) with future clinical application for colon cancer treatment."

https://www.sciencedirect.com/science/article/pii/S0753332218342999

Colorectal cancer (CRC) is the most common carcinoma of the digestive tract. The slow growing nature of CRC offers a great opportunity for prevention …

09/22/2025

NEW DISCOVERY SHOWS HOW CANCER CELLS DODGE CHEMOTHERAPY AND HOW WE MIGHT STOP THEM

When cancer patients receive chemotherapy, their treatment often works initially, only to have the cancer return later, resistant to the same drugs that once fought it effectively. Scientists have long known that cancer cells can develop resistance through genetic mutations, but these changes typically take months to evolve. Now, researchers at Northwestern University have uncovered a much faster escape route that cancer cells use within just hours of treatment. They have also found a potential way to block it.
The Speed of Survival
The research, published in the Proceedings of the National Academy of Sciences, reveals that cancer cells don’t need to wait for lucky mutations to survive chemotherapy. Instead, they rapidly reorganize their DNA packaging to activate survival genes, making life-or-death decisions within hours of encountering toxic drugs.
“Cancer cells exhibit a remarkable resilience to cytotoxic stress,” explains the research team led by Dr. Vadim Backman. Their study shows that this resilience comes from the cells’ ability to quickly change how tightly their DNA is packed inside the nucleus. This process determines which genes can be turned on or off.
Understanding DNA’s Filing System
To understand this discovery, imagine DNA as a massive instruction manual for the cell. This manual isn’t simply floating loose in the nucleus; instead, it’s carefully organized into structures called chromatin packing domains. These tiny compartments measure roughly 160 nanometers across, about 1,000 times smaller than the width of a human hair.
These packing domains work like a filing system. When DNA is packed tightly, genes in that region become difficult to access and remain silent. When the packing is looser, genes become more accessible and can be activated. The researchers discovered that cancer cells can rapidly reorganize these domains when threatened by chemotherapy, allowing them to activate genes that help them survive.
A Physics-Based Prediction Model
The Northwestern team developed a sophisticated model that uses principles from physics to predict which cancer cells will survive chemotherapy based on their chromatin organization. They found that cells with a specific type of chromatin structure were much more likely to survive treatment. The researchers measure this structure using a parameter they call “Dn.”
When the researchers tracked cancer cells over 48 hours during chemotherapy treatment, they observed a clear pattern: cells with higher Dn values before treatment were more likely to survive, and the average Dn of the surviving population increased over time. This pattern held true across six different cancer types, including ovarian, breast, colon, and uterine cancers, and with various chemotherapy drugs.
Finding the Achilles’ Heel
Armed with this understanding, the researchers asked a crucial question: Could they make cancer cells more vulnerable to chemotherapy by preventing them from reorganizing their chromatin?
They screened 50 compounds for their ability to reduce Dn values and identified several promising candidates they call Transcriptional Plasticity Regulators (TPRs). The most effective was celecoxib, a drug already FDA-approved as an anti-inflammatory medication.
When cancer cells were treated with both chemotherapy and celecoxib, the combination proved far more effective than either treatment alone. In laboratory experiments, the combination treatment increased cancer cell death across multiple cancer types. Importantly, celecoxib had minimal effects on normal, non-cancerous cells, suggesting it could selectively target cancer cells’ adaptive mechanisms.
From Lab to Living Systems
To test whether this approach could work in living organisms, the researchers used patient-derived xenograft models. These are tumors from ovarian cancer patients grown in mice. The results were striking: while tumors treated with chemotherapy alone doubled in size over 30 days, those treated with the chemotherapy-celecoxib combination grew by only 20%.
Remarkably, the enhanced effectiveness wasn’t due to celecoxib’s known anti-inflammatory properties. The researchers found no significant changes in immune cell infiltration or inflammatory markers in the tumors. Instead, the benefit appeared to come directly from celecoxib’s ability to prevent chromatin reorganization.
Implications for Cancer Treatment
This research offers a fundamentally new way to think about cancer treatment resistance. Rather than trying to kill every cancer cell outright or waiting for resistance mutations to develop, this approach targets the cells’ ability to adapt in real-time.
The discovery is particularly promising because it appears to represent a fundamental mechanism used by many different cancer types. The researchers observed similar chromatin changes in ovarian, breast, colon, and uterine cancers, suggesting this could be a broadly applicable therapeutic strategy.
Looking Forward
While these results are encouraging, more research is needed before this approach can be used in patients. The team plans to conduct broader screens to identify additional TPR compounds and to better understand exactly how these drugs disrupt chromatin organization. They also need to test whether this approach works in immune-competent models that more closely resemble human physiology.
Nevertheless, this work represents a significant advance in our understanding of how cancer cells evade treatment and offers a concrete strategy for making existing chemotherapies more effective. By targeting cancer cells’ ability to adapt rather than just trying to kill them, this approach could help prevent the development of resistance and improve outcomes for cancer patients.
As cancer treatment continues to evolve toward more precise and personalized approaches, understanding and targeting the physical properties of cancer cells, not just their genetics, may prove to be a crucial piece of the puzzle in our ongoing fight against this disease.
Dr. Daniel Thomas, DO, MS
Metabolic & Nutritional Medicine
Integrative Cancer Therapeutics
Mount Dora, Florida
drthomas@healthyandstrong.com
Reference: Frederick J, Virk RKA, Ye IC, Almassalha LM, Wodarcyk GM, VanDerway D, et al. Leveraging chromatin packing domains to target chemoevasion in vivo. Proc Natl Acad Sci U S A. 2025;122(30):e2425319122.
Disclaimer: The information in this article is for general educational purposes and is not a replacement for professional medical advice. If you have specific concerns about your health, please consult a qualified healthcare provider.

The snow fungus, more than skin deep.The royals of Tang Dynasty (618-907 BC) consumed and bathed in copious amounts of t...
09/21/2025

The snow fungus, more than skin deep.

The royals of Tang Dynasty (618-907 BC) consumed and bathed in copious amounts of the medicinal snow fungus, or silver ear ( tremella fuciformis) to support their health and perfect complexion. Today silver ear is still used in the skin care industry for its anti-aging and moisturizing properties

The benefits of silver ear go way beyond skin deep. Its ant cancer properties help to suppress tumour immune system evasion, tumour blood supply, and metastasis!

https://pmc.ncbi.nlm.nih.gov/articles/PMC10220659/




Anti-tumor activity of Tremella fuciformis polysaccharides (TFPS) has been widely reported, but its mechanism remains poorly understood. In this study, we established an in vitro co-culture system (B16 melanoma cells and RAW 264.7 macrophage-like ...

🔎 Beyond the Scale: What Obesity Really Means in CancerObesity doesn’t just affect body weight—it alters the immune syst...
07/04/2025

🔎 Beyond the Scale: What Obesity Really Means in Cancer

Obesity doesn’t just affect body weight—it alters the immune system, promotes inflammation, and reshapes the tumor microenvironment.

Obesity impacts cancer development, progression, and treatment response.

👉 Read it here:

In recent decades, obesity has ceased to be seen merely as a cosmetic issue or a cardiovascular risk factor. Today […]

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