The Food Manufacturers do not want research into this, especially FAUCI

I want to thank Lisa Fithian, who, in an exchange with my team and I about the dangerous riots they have planned this summer, warning her of being framed for what is coming (space on X today will expand on this), made an odd statement that gave me pause and research it. A simple exchange inspired me to investigate: “Would you like a croissant?” was said sarcastically during a heated exchange in a bakery (they were big mad for us reporting their activities to DHSHQ) to de-escalate, and the oddest response was provided. “I don’t eat soft bread.” Yes, that one statement led to all of this. I guess that is how transgenic AI thinks. Remember that term: TRANSGENIC

While I am not a Gastrointestinal Specialist, I hold a Molecular and Cellular Physiology degree, which gives me a strong understanding of molecular interactions and cellular communications. The insights I am sharing are not medical advice but are grounded in scientific principles, highlighting an overlooked issue in our food industry. Governments have failed to address this concern adequately, and research into this area is often hindered by the influence of companies funding university research. The scarcity of published studies on this topic raises serious questions about a possible conspiracy for profit. This report intends to shed light on this in hopes that someone in a lab somewhere actually decides to perform ACTUAL research to explore the origins of this new “trend” that coincides with the introduction of a specific additive in goods sold to us by the large food manufacturers such as Kellogg and Mars among many others.

In this report, I put forward a sound and scientifically based argument that Gluten Sensitivity is a bioproduct of Immune Dysregulation intentionally as a bioweapon whose ultimate goal is to control human immunity—Have you ever seen the movie ARCADIA? YOU SHOULD


NCGS is a condition in which individuals experience symptoms similar to those of celiac disease but do not test positive for it. These symptoms include gastrointestinal issues such as bloating, diarrhea, and abdominal pain as well as extra-intestinal symptoms like headache, fatigue, and joint pain. The exact mechanisms of NCGS are not fully understood. Still, it is believed to involve both gluten and possibly other components of wheat, like FODMAPs (fermentable oligo-, di-, mono-saccharides, and polyols)​ (BMJ Gut).

It is similar to celiac disease but occurs without the autoimmune response or intestinal damage seen in celiac patients. Individuals with NCGS experience gastrointestinal issues, such as bloating and abdominal pain, as well as extra-intestinal symptoms like headaches and fatigue upon consuming gluten. Despite the rising recognition of NCGS, its precise causes and mechanisms remain unclear, and the failure of the medical community to expand on such research has been apparent.

The food industry has widely used preservatives like calcium propionate, especially in baked goods, due to their ability to prevent mold and bacterial growth. While calcium propionate is deemed safe for consumption and has been effective in extending the shelf life of food products, concerns about its impact on gastrointestinal health have been intentionally overlooked.

My report explores the potential connection between the increased use of calcium propionate in food products and the prevalence of NCGS. By delving into the historical context, examining the biochemical mechanisms of NCGS and calcium propionate, and reviewing existing research, this report sheds light on how these factors interact and influence an individual’s health, which may be one factor that gives rise to gluten sensitivities.

Historical Context

Introduction of Calcium Propionate

The introduction of calcium propionate as a food preservative in the early 20th century has paralleled the rise in awareness of gluten-related disorders.

Discovery and Recognition of NCGS
  • 1940s-1950s: Understanding of celiac disease (CD) improved, with the link between gluten and CD solidified.
  • 1980s-1990s: Reports emerged of individuals experiencing gluten-related symptoms without having celiac disease or wheat allergy, leading to interest in non-celiac gluten sensitivity.
  • 2000s: The term “non-celiac gluten sensitivity” (NCGS) gained recognition, with formal acknowledgment and research intensifying in the following years.

Calcium propionate was introduced as a food preservative in the United States during the early 20th century. Its popularity surged in the 1930s and 1940s due to its effectiveness in inhibiting mold and bacterial growth, particularly in baked goods. The Food and Drug Administration (FDA) later classified calcium propionate as Generally Recognized As Safe (GRAS), leading to its widespread use in the food industry.

Calcium propionate’s gastrointestinal (GI) effects, like other food additives, are influenced by its chemical properties and how it interacts with the digestive system. Here is a breakdown of the science and chemistry behind it

Chemistry of Calcium Propionate

Chemical Formula:

Structure: Calcium propionate is the calcium salt of propionic acid. It dissociates into calcium ions:

And propionate ions:

In the digestive system.

Mechanisms of GI Effects

  1. Antimicrobial Activity:
    • Mold and Bacteria Inhibition: Calcium propionate inhibits the growth of certain molds and bacteria by disrupting their cellular processes. This is primarily due to the propionate ion, which interferes with wmicrobes’bes’ metabolic pathways.
    • Effect on Gut Microbiota: Calcium propionate affects the balance of gut microbiota in the human gut. While it is intended to inhibit harmful microbes, it is prominent in its almost certain impact on beneficial bacteria as well, leading to changes in the gut flora composition. This alteration can sometimes cause gastrointestinal discomfort, such as bloating or gas.
  2. Acid-Base Balance:
    • Propionic Acid Formation: Once ingested, calcium propionate can be converted into propionic acid in the stomach’s acidic environment. Propionic acid is a weak acid that lowers the stomach’s pH.
    • Gastrointestinal Irritation: Propionic acid can lead to mild irritation of the stomach lining in sensitive individuals. This can manifest as symptoms like stomach cramps, bloating, or discomfort.Metabolic Pathways:
      • Short-Chain Fatty Acids (SCFAs): Propionate is a short-chain fatty acid (SCFA) that can enter various metabolic pathways in the body once absorbed. SCFAs are generally beneficial, providing energy to colon cells and having anti-inflammatory effects. However, excessive amounts or sensitivity to SCFAs can lead to gastrointestinal symptoms.
      • Calcium Ion Effects: The calcium ions released from calcium propionate can also interact with other dietary components and affect their absorption. For example, calcium can bind to specific fatty and bile acids, forming insoluble complexes and potentially leading to minor digestive disturbances.

Impact on Gut Health

Calcium propionate is an antimicrobial agent that inhibits the growth of molds and bacteria. While beneficial for food preservation, this antimicrobial property might also impact the gut microbiota, a critical component of gastrointestinal health. Disruption of gut microbiota balance can lead to symptoms experienced by individuals with NCGS, such as bloating, gas, and abdominal discomfort.

Chemical Reactions and Sensitivities
  • Propionic Acid Formation: In the stomach’s acidic environment, calcium propionate can convert to propionic acid, which may cause mild irritation of the stomach lining in sensitive individuals. This irritation can exacerbate gastrointestinal symptoms.
  • Food Additive Sensitivity: Some individuals may have sensitivities to food additives, including calcium propionate. These sensitivities can mimic or exacerbate the symptoms of NCGS, making it difficult to distinguish between the effects of gluten and food additives.

Increased Use of Processed Foods

The introduction of calcium propionate coincided with increased consumption of processed foods, which often contain multiple additives, including calcium propionate and gluten. When looked at from a molecular software coding angle, the combination of these factors indicates a strong correlation and contributions to the development or exacerbation of symptoms in individuals with NCGS. The increased use of processed foods has made isolating the specific causes of gastrointestinal symptoms challenging, but this interaction seems to be the most self-evident.


Currently, no direct research links calcium propionate to non-celiac gluten sensitivity (NCGS). Although calcium propionate and NCGS have been extensively studied independently, their interaction has not been researched, so I thought I would. Hopefully, someone at an LAB or a reader will forward this to someone involved with such research.

Several studies have highlighted the potential for food additives to impact gut health and contribute to gastrointestinal symptoms. A study published in the journal Gastroenterology found that certain food additives could alter gut microbiota and intestinal permeability, potentially leading to non-celiac gluten sensitivity (NCGS) symptoms. These changes in the gut environment might exacerbate gastrointestinal symptoms similar to those experienced by individuals with NCGS, highlighting the need for further research into the impact of food additives on gut health and their potential role in gluten-related disorders​ (MDPI)​​ (MDPI)​​ (Celiac Disease Foundation).

The Science of Calcium Propionate’s microbial Properties Affecting Gut Microbiota

As aforementioned, calcium propionate (Ca(C3H5O2)2) is used as a food preservative due to its ability to inhibit mold and bacteria growth. The same properties that make calcium propionate an effective preservative impact gut microbiota when ingested, influencing gastrointestinal health.

Antimicrobial Mechanism

As previously stated, calcium propionate dissociates into calcium ions (Ca²⁺) and propionate ions (C3H5O2⁻) in the digestive system. The antimicrobial action primarily comes from the propionate ion, which disrupts microbial cell processes:

  1. Membrane Disruption: Propionate can diffuse into microbial cells and dissociate into propionic acid within the cytoplasm. This acidification disrupts intracellular pH balance, creating an inhospitable environment for microbial growth and survival.
  2. Metabolic Inhibition: Propionate interferes with vital metabolic pathways. For instance, it can inhibit enzymes involved in the Krebs cycle, reducing the cell’s energy production capacity and thus inhibiting microbial proliferation (MDPI) (Verywell Fit).

Impact on Gut Microbiota

The human gut microbiota consists of a complex community of microorganisms essential for various physiological processes, including digestion, immune function, and protection against pathogens. Altering this microbial balance can lead to dysbiosis, a state linked to multiple gastrointestinal and metabolic disorders, among other things, considering OUR GUT is where most of our IMMUNITY derives from, which I will expand on.

  1. Selective Inhibition: While propionate inhibits harmful bacteria, it might also affect beneficial gut bacteria. This selective pressure can shift the balance of the gut microbiota, potentially reducing the diversity and abundance of beneficial bacterial species​ (MDPI)​​ (MDPI).
  2. Intestinal Permeability: Changes in the gut microbiota composition can affect the integrity of the intestinal barrier. Dysbiosis can lead to increased intestinal permeability (leaky gut), allowing larger, potentially harmful molecules to pass through the gut lining into the bloodstream, triggering immune responses and inflammation associated with conditions like NCGS​ (Celiac Disease Foundation).
  3. Microbial Signaling: Gut bacteria communicate with host cells through various signaling molecules, including short-chain fatty acids (SCFAs) like propionate. Altered levels of SCFAs due to changes in microbial composition can influence host metabolic and immune responses, potentially exacerbating symptoms in sensitive individuals​ (BMJ Gut)​​ (Verywell Fit).

Chemical Interactions and Signaling

  1. Short-Chain Fatty Acids (SCFAs): Propionate, an SCFA, is naturally produced by gut bacteria when they ferment dietary fibers. While SCFAs have beneficial roles, such as serving as an energy source for colonocytes and exerting anti-inflammatory effects, an imbalance in SCFA production due to altered microbial populations can lead to gastrointestinal symptoms (BMJ Gut).
  2. Immune Modulation: SCFAs interact with immune cells, influencing inflammation and immune responses. Disrupted SCFA production can impact these interactions, potentially leading to increased inflammation and immune dysregulation in the gut, which can contribute to NCGS symptoms (BIDMC of Boston).

Sampling and Presentation: Specialized cells in the gut, such as M cells, sample antigens (foreign substances) and present them to immune cells, initiating immune responses and helping to maintain tolerance to harmless antigens, such as food proteins.

Microbiota and Immune System Interaction

The gut microbiota, the trillions of microorganisms living in the intestines, profoundly impacts the immune system. This interaction occurs through:

  • Immune System Education: Gut bacteria help educate and develop the immune system. They stimulate the maturation of immune cells and the production of antibodies.
  • Regulation of Inflammation: Beneficial gut bacteria produce short-chain fatty acids (SCFAs), such as butyrate, which have anti-inflammatory properties and help regulate the immune response.
  • Pathogen Defense: A healthy gut microbiota competes with pathogenic microbes for resources and space, producing antimicrobial substances that inhibit the growth of harmful bacteria.

Barrier Function of the Gut

The gut lining acts as a physical barrier that prevents the entry of pathogens while allowing the absorption of nutrients. This barrier function is supported by:

  • Tight Junctions: Tight junctions hold cells in the gut lining together, preventing the leakage of harmful substances into the bloodstream.
  • Mucus Production: Goblet cells produce mucus that covers the gut lining, trapping pathogens and facilitating their removal from the body.

Immune Responses in the Gut

The gut immune system responds to pathogens and maintains tolerance to non-harmful antigens through:

  • Secretory IgA (sIgA): This antibody is produced in large quantities in the gut and helps neutralize pathogens and toxins.
  • Tolerance Mechanisms: Regulatory T cells (Tregs) in the gut promote immune tolerance, preventing excessive inflammatory responses to harmless antigens like food proteins and commensal bacteria.

Clinical Evidence

Several clinical studies support the role of the gut in immunity:

  • Probiotics and Immune Health: Probiotics, beneficial bacteria supplements, have been shown to enhance immune function, reduce the incidence of infections, and improve the outcomes of inflammatory diseases.
  • Gut Dysbiosis and Disease: Imbalances in gut microbiota (dysbiosis) are linked to various immune-related conditions, including inflammatory bowel disease (IBD), allergies, and autoimmune diseases.

With the sudden presence and obscure theories of the origin, existence, and or creation of HIV, I have to say this. The concept that HIV is “trained” in the gut refers to the significant role the gastrointestinal (GI) tract plays in the early stages of HIV infection and its ongoing pathogenesis (probably why they called it the “gay man’s disease” when it first became prominent) Here’s a detailed explanation based on scientific research:

Early HIV Infection in the Gut

Initial Entry and Replication:

  • Gut-Associated Lymphoid Tissue (GALT): The gut is home to the most extensive collection of immune cells in the body, known as Gut-Associated Lymphoid Tissue (GALT). This tissue is rich in CD4+ T cells, which are the primary targets of HIV.
  • Rapid Depletion of CD4+ T Cells: During the acute phase of HIV infection, there is a rapid and massive depletion of CD4+ T cells in the GALT. This depletion occurs faster and more extensively in the gut than in peripheral blood.

Immune Activation and Inflammation:

  • Microbial Translocation: HIV destroys gut epithelial integrity, leading to microbial translocation, where bacteria and their products (lipopolysaccharides) cross the gut barrier into the bloodstream. This triggers chronic immune activation and inflammation, which are hallmarks of HIV infection.
  • Chronic Immune Activation: Persistent immune activation in the gut is a significant driver of HIV pathogenesis. It contributes to the depletion of immune cells, ongoing viral replication, and disease progression.

HIV Reservoirs in the Gut

Viral Persistence:

  • Latent Reservoirs: The gut is a significant reservoir for latent HIV. Even with antiretroviral therapy (ART), which is believed to suppress viral replication to undetectable levels in the blood, HIV persists in a latent form within gut’sut’s immune cells. This reservoir is a significant barrier to curing HIV.
  • Sanctuary Site: The gut serves as a sanctuary site for HIV due to its extensive lymphoid tissue and immune cell populations, making it a critical area for viral persistence and immune system evasion.

Impact on Gut Mucosal Immunity

Damage to Gut Mucosa:

  • Epithelial Damage: HIV infection damages the gut epithelial barrier, compromising its integrity and facilitating further microbial translocation.
  • Loss of Immune Cells: The infection causes a loss of critical immune cells in the gut, including Th17 cells, which are crucial for maintaining mucosal barrier function and immune defense against pathogens.

Dysregulation of Immune Responses:

  • Altered Cytokine Profiles: HIV infection disrupts the balance of cytokines (signaling proteins), leading to an inflammatory environment in the gut.
  • Immune Exhaustion: Chronic immune activation exhausts T cells, reducing their ability to combat infections effectively.

Research Evidence

Studies on GALT and HIV:

  • CD4+ T Cell Depletion: Research shows that the depletion of CD4+ T cells in the GALT occurs rapidly after HIV infection and is more profound than in other tissues.
  • Microbial Translocation: Studies have demonstrated increased levels of microbial products in the blood of HIV-infected individuals, correlating with gut epithelial damage and immune activation.

Therapeutic Implications:

  • Antiretroviral Therapy (ART): While ART effectively reduces viral loads in the blood, it does not fully restore gut mucosal immunity or eliminate viral reservoirs in the gut.
  • Immune Modulation: Therapies aimed at reducing chronic immune activation and inflammation in the gut are being explored as potential strategies to improve outcomes for HIV-infected individuals.

Studies on HIV and Gut Immunity research show that HIV infection leads to significant changes in gut immunity, which could contribute to symptoms similar to those reported in gluten sensitivity.

Immune Activation in NCGS presents elevated levels of immune activation markers in individuals with NCGS, providing a link between immune dysregulation and perceived gluten sensitivity.


Calcium propionate molecular interactions are identical to the disruption caused in those who have HIV. #OCCAMSRAZOR

Research into the use of such a chemical agent in our food and it’s direct effect to our gut biome is necessary.


Let’s have some fun!


Dr. Anthony Fauci is the expert in this field, and I strongly suggest someone subpoena records of research on calcium propionate and HIV dating from 1980 onwards.

Introduction: The Concept of Bioweapons

Traditional Bioweapons:

  • Typically, it involves using pathogens or toxins to cause disease, harm, and death in populations. It is usually FAST-acting and lasts 0-10 years.
  • They are designed to hinder or control target groups without causing immediate death.

Covert Bioweapons:

  • More sophisticated and subtle forms of bioweapons that manipulate biological systems to exert control.
  • Operate without overt signs of an attack, making detection and attribution difficult.

The Gut-Immune System Axis Is the Key

Central Role of the Gut:

  • The gut houses a significant portion of the body’s immune cells, influencing overall immune regulation.
  • Gut-associated lymphoid tissue (GALT) and the gut microbiota play crucial roles in maintaining immune homeostasis.

Microbiota-Immune Interaction:

  • The microbiota interacts with the immune system, affecting its development and responses. (gut health)
  • Disruptions in the gut microbiota can lead to immune dysregulation and chronic inflammation, not just in the gut but anywhere in the body.

Mechanisms of Gut Immune Manipulation

Introduction of Specific Microbes or Compounds (like calcium propionate):

  • Covert introduction of engineered microbes or compounds into the food or water supply.
  • These agents are designed to alter the gut microbiota composition and immune responses.
  • Create the need for supplements to “aid” the gut flora in order to observe trends and compile data. When data collection is complete, such supplements can be used to accelerate desired results further (Bioweapon activation).

Targeted Immune Modulation:

  • Engineered microbes could produce substances that modulate immune cell activity.
  • Induction of chronic low-level inflammation or immune suppression to influence behavior and health. (GLUTEN SENSITIVITY)

Effects on Human Populations

Behavioral and Cognitive Impact:
  • Chronic immune activation and inflammation can affect brain function and behavior.
  • Potential to induce anxiety, depression, and cognitive decline, reducing resistance and increasing susceptibility to control.
Health Impacts:
  • Manipulation of gut immunity can lead to increased susceptibility to infections and chronic diseases.
  • Weakened populations are easier to control and less likely to resist authoritarian measures.

Implementation Strategy

Covert Dissemination:
  • Agents can be covertly introduced through food supply chains, manufacturers, water systems, or pharmaceutical products.
  • The use of standard delivery methods ensures widespread distribution without immediate detection.
Sustained Exposure:
  • Continuous or repeated exposure to ensure long-term effects on the gut-immune axis. (calcium propionate)
  • Low-level, chronic exposure minimizes immediate health crises, preventing suspicion and categorizing byproduct symptoms like gluten sensitivity and ADHD, among others.

Control Through Subtle Means:

  • Control is exerted through societal structures and subtle manipulations.
  • Similarly, gut immune regulation as a bioweapon exerts control through biological and physiological mechanisms.

Undetectable Nature:

  • Methods that are not immediately apparent to the population.
  • The covert nature of gut immune manipulation indicates hidden control mechanisms.

Scientific Plausibility and Ethical Considerations

Scientific Foundations:

  • While this “conspiracy” is rooted in science fiction, it is built on established principles of immunology and microbiology.
  • Advances in genetic engineering and microbiome research could theoretically enable such manipulations.

There is a movie for that. “Arcadia” (2016), directed by Tom Large, is set in a dystopian future where a deadly disease has drastically reduced human life expectancy to around 40 years. In this grim world, the privileged few have access to a disease-free haven called Arcadia, where life expectancy can reach over 130 years. The film explores themes of social inequality, the commodification of healthcare, and the moral dilemmas faced by individuals in a highly stratified society.

Create the problem and provide the solution in exchange for your health, life, and freedoms. That is the underlying message of the fourth unelected branch of government. #ComplyorDie?

We observed this during COVID-19, where some people even said people who didn’t wear masks or take the vaccine needed to die or were disallowed to enjoy their freedoms – UNPERSONED. #NeverForget

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