This documentary sheds light on the shocking truth behind the consumption of vegetable oils, revealing how they may be far more harmful to our health than previously thought. The film follows the history of these oils, their rise to ubiquity in our diets, and the serious implications for our long-term health. Let’s break down the key moments and insights covered in the documentary.

0:00 - The Switcheroo
The film opens by describing what the creators call "The Switcheroo"—a shift in public perception that occurred in the mid-20th century. Animal fats, which had been a dietary staple for centuries, were suddenly demonized, while vegetable oils were promoted as a heart-healthy alternative. This switch, the documentary argues, was based on questionable science and driven by powerful food and medical organizations.

1:52 - History of Vegetable Oils
The documentary delves into the origins of vegetable oils, originally introduced as cheap by-products of the industrial revolution. These oils, including canola, soybean, and corn oil, were never part of the human diet until modern processing techniques made them readily available. Despite their industrial beginnings, they quickly found their way into the food supply as replacements for butter and lard.

3:50 - Enter the American Heart Association
The American Heart Association (AHA) played a pivotal role in promoting vegetable oils as a healthier alternative to saturated fats. Backed by commercial interests, the AHA endorsed vegetable oils to help reduce cholesterol and prevent heart disease. The film points out, however, that this was based on flawed studies that failed to address the negative long-term effects of these oils.

5:27 - The Massive Increase in Vegetable Oil Consumption
Since the mid-20th century, the consumption of vegetable oils has skyrocketed. The documentary highlights data showing a dramatic increase in the use of vegetable oils in processed foods, leading to widespread exposure to their harmful effects.

6:06 - Is Vegetable Oil Bad or Benign?
While some argue that vegetable oils are neutral or even beneficial, the documentary challenges this notion. It raises questions about whether these oils are truly benign, pointing to emerging evidence of their links to chronic diseases and oxidative stress in the body.

6:55 - Why do some animals live longer than others?
In this segment, the film explores how the types of fats consumed by different animals affect their longevity. Animals that consume saturated fats tend to live longer, while those that rely on polyunsaturated fats—like those found in vegetable oils—show shorter lifespans. This raises concerns about how human health might be impacted by the widespread use of these oils.

7:51 - Vegetable Oil Stays in Your Body for Years
The documentary provides startling information about how vegetable oils accumulate in our tissues and remain in the body for years. These oils are stored in fat cells and can lead to inflammation and oxidative damage over time, contributing to the development of various diseases.

9:11 - Hidden Data
Throughout the documentary, the creators expose hidden data that was either ignored or suppressed by the food and medical industries. This includes studies that revealed the harmful effects of vegetable oils but were never given public attention due to commercial interests.

12:08 - Vegetable Oils are in EVERYTHING
One of the most alarming points is just how pervasive vegetable oils have become. They are found in nearly all processed foods, from snacks to salad dressings. The documentary emphasizes how difficult it is to avoid these oils, making it almost impossible for consumers to make informed choices about their health.

13:07 - Why Vegetable Oils are Bad for Health
The film explains that vegetable oils are high in omega-6 fatty acids, which promote inflammation in the body when consumed in excess. Chronic inflammation is a known contributor to heart disease, cancer, and autoimmune conditions. The imbalance between omega-6 and omega-3 fatty acids in modern diets is a key factor in the negative health outcomes associated with vegetable oil consumption.

15:04 - The Toxic Oxidation Products
When vegetable oils are heated, they produce toxic oxidation products, including aldehydes and other harmful compounds. These substances can damage cells, tissues, and DNA, increasing the risk of diseases such as cancer and neurodegenerative conditions. The film underscores the importance of avoiding fried foods cooked in vegetable oils.

16:28 - How Vegetable Oils are Made
The documentary offers a detailed look at the industrial process used to create vegetable oils, which involves high heat, chemical solvents, and deodorizers. This process strips the oils of any beneficial nutrients and creates harmful by-products. The film suggests that these oils are far from the "natural" products they are often marketed as.

18:33 - Are Vegetable Oils Linked to Alzheimer’s?
Emerging research is exploring the potential link between vegetable oils and Alzheimer’s disease. The documentary discusses how the inflammatory and oxidative properties of these oils may contribute to the development of neurodegenerative diseases by damaging brain cells over time.

20:06 - Mitochondria, The Powerhouse of the Cell
The film highlights the role of mitochondria—the cell’s energy producers—in relation to vegetable oil consumption. It argues that the toxic by-products of these oils can impair mitochondrial function, leading to reduced energy production, fatigue, and an increased risk of chronic illness.

24:35 - Most Studies on Vegetable Oils Aren’t Long Enough
Many studies that claim vegetable oils are safe are often too short to capture the long-term effects of consumption. The documentary argues that because these oils accumulate in the body over time, their health impacts may not become apparent until much later in life. Longer studies are needed to truly understand the risks.

26:04 - Why Aren’t More People Talking About This?
The documentary concludes by exploring why the dangers of vegetable oils are not more widely discussed. It points to conflicts of interest in the food and pharmaceutical industries, where financial incentives often overshadow public health concerns. Despite mounting evidence, the widespread promotion of vegetable oils continues, leaving consumers unaware of the potential harm.


The documentary presents a compelling case against the consumption of vegetable oils, revealing the hidden dangers of these seemingly harmless products. From their inflammatory effects to their role in chronic disease, the film makes a strong argument for rethinking the way we approach fats in our diet. With vegetable oils found in nearly every processed food, it’s important for consumers to be aware of the potential risks and seek healthier alternatives.

IgG4 differs from other subclasses due to its limited ability to activate the complement system, a key immune mechanism responsible for destroying infected cells. This characteristic has led to IgG4 being classified as an unusual antibody. One of its most intriguing features is Fab arm exchange, a process in which the two halves of an IgG4 antibody can dissociate and recombine with halves from other IgG4 antibodies. This creates bi-specific antibodies with two distinct Fab arms, reducing their ability to form immune complexes and stimulate immune responses.

IgG4 antibodies have low affinity for C1q and Fc receptors, which limits their capacity to initiate effector responses. However, this bi-specific structure enables IgG4 to potentially block the inflammatory effects of other antibody classes, such as IgG1 or IgE, by displacing their antigen-binding capabilities. This property contributes to IgG4's role as a "blocking antibody", known for its anti-inflammatory effects.​

The role of IgG4 in human health is complex, with evidence pointing to both protective and pathogenic effects. In allergy immunotherapy, for example, IgG4 is often viewed as a protective antibody due to its ability to reduce inflammation and prevent IgE-mediated allergic reactions. Elevated levels of antigen-specific IgG4 are associated with successful desensitization to allergens, allowing for the development of immune tolerance. During prolonged exposure to allergens, IgG4 competes with IgE for antigen binding, effectively neutralizing allergic responses without activating immune effector cells.
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However, IgG4 can also be involved in pathogenic processes. In some autoimmune diseases, such as pemphigus vulgaris (autoimmune disease that causes blistering of the skin and mucous membranes, such as the mouth, throat, and genitals), IgG4 plays a role in the disease’s progression by contributing to tissue damage. Additionally, IgG4 has been linked to the suppression of immune responses in certain types of cancer, where its blocking ability may inhibit the immune system's capacity to fight tumor cells.

In the context of allergy immunotherapy, IgG4’s lack of effector function and its capacity for half-antibody exchange raise questions about its role in modulating immune responses. Several studies have demonstrated that high levels of antigen-specific IgG4 are associated with successful outcomes in allergen-specific immunotherapy. This is because IgG4 can inhibit the effects of IgE, the antibody responsible for allergic reactions.
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Through allergen-specific memory T- and B-cell responses, the immune system adapts to tolerate allergens, reducing chronic inflammation and allergic responses. This process is crucial for building a more robust and balanced immune system.

In certain autoimmune diseases, IgG4 levels correlate with disease severity, and in experimental models, IgG4 has been shown to cause disease manifestations when injected into animals. This indicates the pathogenic role of IgG4 in these disorders.

IgG4 antibodies were found to interfere with anti-tumor immune responses, blocking the ability of other antibodies (such as IgG1) to target and destroy cancer cells. This was demonstrated in studies of cancers like malignant melanoma, where locally produced IgG4 antibodies hindered the immune system's response, allowing tumors to grow unchecked.

Studies using animal models confirmed that IgG4 promotes tumor growth by blocking local immune responses. For example, in a breast cancer model, the local administration of IgG4 significantly accelerated tumor growth compared to controls. These findings suggest that IgG4 antibodies assist cancer cells in escaping immune detection, facilitating tumor progression.

​Although immune checkpoint inhibitors targeting PD-1 are effective in some cancers, their IgG4 subclass raises concerns about potential side effects, including autoimmune reactions and rapid tumor progression. IgG4's role in blocking immune responses may explain the occurrence of hyper-progressive disease in some patients undergoing cancer immunotherapy.

Studies have shown that certain cancers, including malignant melanoma, extrahepatic cholangiocarcinoma, and pancreatic cancer, often have an abundance of IgG4-positive plasma cells in and around the tumor. 

A groundbreaking study by Karagiannis et al. revealed that cancer-specific IgG4 antibodies, unlike their IgG1 counterparts, do not activate the immune processes required to destroy cancer cells. Instead, IgG4 appears to interfere with IgG1's ability to promote tumor cell death, allowing the cancer to evade immune attack. This mechanism of immune escape enables the tumor to grow unchecked, making IgG4 a key player in cancer progression.

IgG4's Impact on Tumor Immune Evasion
Karagiannis and colleagues demonstrated that tumors producing IgG4 can actively inhibit the immune system’s ability to kill cancer cells. In their study, they found that IL-4 and IL-10, cytokines associated with immune regulation, were elevated in cancerous tissues, leading to increased IgG4 production. The research showed that IgG4 not only failed to fight tumors but also blocked other immune antibodies, like IgG1, from effectively doing so.

This was further supported by experiments using immunocompetent mice models, where the introduction of IgG4 antibodies sped up tumor growth. These findings suggest that IgG4 plays a direct role in helping cancers evade the immune system.

IgG4 and Cancer Immunotherapy
IgG4’s interference with the immune system extends to cancer immunotherapy. Specifically, nivolumab, a PD-1 blocking antibody used in cancer treatment, belongs to the IgG4 class. While effective in some cases, its IgG4 nature may also contribute to the rapid progression of cancer in others. In mouse studies, treatment with nivolumab led to faster tumor growth when compared to controls, suggesting that IgG4’s role in cancer therapy may have unintended negative effects.

The connection between IgG4 and cancer highlights the challenges of using ICIs. On the one hand, PD-1 inhibitors can stimulate the immune system to fight cancer, but on the other hand, they may inadvertently promote immune evasion and tumor growth when IgG4 is involved.

In light of these findings, Dr. Risch encourages individuals to be particularly attentive to any new or unusual symptoms in their bodies. Being proactive and aware of potential warning signs could help detect issues earlier.

Dr. Risch also discussed the way medical agencies track adverse events following vaccination. Officially, a person is not considered "vaccinated" until two weeks after their shot, meaning any negative reactions occurring before then are often counted as happening to unvaccinated individuals. However, Dr. Risch emphasized that a significant portion of adverse reactions, including serious health issues, can occur within the first few days of vaccination, yet they are being incorrectly attributed.

Dr. Risch criticized how public health policies were handled during the pandemic, saying key principles of public health were abandoned early on. He cited the denial of early treatments for COVID-19 and what he believes were unnecessary vaccinations, calling the approach a “colossal failure.” In his view, a lot of the current fear surrounding new COVID variants is being fueled by propaganda designed to promote more vaccinations, rather than genuine concern for public health.

While Dr. Risch acknowledges that the individual risk of a severe adverse reaction to the vaccine is relatively low, when millions of people are vaccinated, even small risks can translate to large numbers of individuals experiencing serious health consequences. According to him, these reactions can sometimes be worse than the virus itself, leaving hundreds of thousands of people with injuries or long-term health problems.

Given the mild nature of current COVID-19 variants, Dr. Risch strongly advises against receiving more mRNA vaccines. He believes that most people already have some immunity from previous infections and that the new variants are not life-threatening. For Dr. Risch, the focus should be on managing these illnesses as we do with other common infections, like the flu, without resorting to unnecessary vaccinations.
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In summary, Dr. Risch’s concerns reflect growing skepticism over the long-term effects of COVID-19 vaccines, particularly their potential link to an increase in cancer cases. His call for awareness, both from individuals and the medical community, underscores the need for further research into the vaccines’ impact on the immune system and overall health.

Antibody class switching is like your immune system changing the type of weapon it uses to fight an infection. When you get vaccinated, your immune system makes antibodies—proteins that help protect you by recognizing and neutralizing harmful invaders like viruses.
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At first, your body might make certain types of antibodies, like IgG1 and IgG3, which are really good at attacking and destroying a virus. But after repeated exposure to the same vaccine or virus (like with the repeated doses of the COVID-19 mRNA vaccines), your body may shift gears and start producing a different type of antibody, called IgG4.

IgG4 antibodies act more like peacekeepers than attackers. Instead of creating a strong inflammatory response to destroy invaders, IgG4 helps calm the immune system down. This happens after the immune system has been repeatedly exposed to the same thing over time, which is why it can occur after multiple mRNA vaccine doses.
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While this shift to IgG4 antibodies can help prevent excessive inflammation, it also means the immune response might be less aggressive, particularly in detecting and neutralizing immune threats. In the case of the COVID-19 mRNA vaccines, scientists have noticed that repeated doses can lead to higher levels of IgG4, and it appears to leading to higher rates of cancer and other IgG4-related diseases. The body might be learning to tolerate the spike protein (the part of the virus the vaccine targets), but the effects of this shift on long-term immunity are arguably worse than the disease itself.

Vaccines have long been claimed to be a cornerstone in disease prevention, but recent research has shown that certain vaccines can induce the production of IgG4 antibodies. While the mRNA COVID-19 "vaccines" have brought this response into focus, it's not unique to them—vaccines for diseases like HIV, malaria, pertussis, tetanus toxoid (TT) vaccine and the respiratory syncytial virus (RSV) have also been associated with IgG4 production. This antibody class switch is influenced by three key factors: antigen concentration, repeated vaccination, and the type of vaccine used.
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1. Excessive Antigen Concentration

The concentration of antigen in vaccines plays a crucial role in determining the body's immune response. Comparing the two prominent mRNA COVID-19 vaccines, mRNA-1273 (Moderna) and BNT162b2 (Pfizer), the higher dose of mRNA in the Moderna vaccine (100 µg vs. 30 µg in Pfizer) leads to a more prolonged IgG4 response. This is significant because the amount of antigen influences how long the spike protein is produced, potentially altering the body’s defense mechanisms. Notably, COVID-19-uninfected individuals who received Moderna’s vaccine showed elevated anti-S1 IgG4 concentrations, the long-term effects of which remain uncertain.

In contrast, adenovirus-based vaccines like AstraZeneca's did not elicit such a long-lasting IgG4 response (despite them being suspended in 18 countries for adverse events). The link between higher antigen doses and immune tolerance is well-documented: too much antigen can lead to T-cell exhaustion and immune tolerance, weakening the immune system’s ability to fight infections.

While the traditional view has supported the idea that “more is better” when it comes to antigen doses for vaccines, especially in cases like HIV or tuberculosis where there are no clear immune predictors of protection, this approach is not without drawbacks. The following key concerns arise from excessive antigen dosing:

• Clonal deletion: High antigen doses can lead to T-cell death, reducing the immune system's capacity to respond effectively.
• Immune tolerance: Prolonged exposure to large amounts of antigen can cause T-cell desensitization, where the immune system no longer reacts to infections, potentially leading to persistent infections or autoimmune disorders, including cancer.
• Terminal differentiation: Excessive antigen exposure can cause T cells to become highly specialized and lose their ability to proliferate, leading to immune exhaustion and reducing future immune responses.
• Avidity reduction: High antigen doses can lower the strength of the immune response by reducing the avidity (binding strength) between antigens and immune cells, making it harder for the body to mount an effective defense.

Studies have also shown that in some cases, lower vaccine doses can result in better T-cell responses. This has led experts to reconsider vaccine dosing strategies, suggesting that smaller doses may sometimes be more effective, especially in boosting immunity.

      2. Repeated Vaccination
Repeated exposure to vaccines, especially mRNA-based vaccines, can significantly influence the type of antibodies produced. After the initial two doses of COVID-19 mRNA vaccines, most individuals develop IgG1 and IgG3 antibodies, which are typically pro-inflammatory and play a key role in fighting infections. However, as more doses are administered, a shift occurs, with IgG4 levels increasing significantly, particularly after a third dose or subsequent infection with a SARS-CoV-2 variant.

Uversky, Vladimir N, et al. “IgG4 Antibodies Induced by Repeated Vaccination May Generate Immune Tolerance to the SARS-CoV-2 Spike Protein.” Vaccines, vol. 11, no. 5, 17 May 2023, pp. 991–991, www.ncbi.nlm.nih.gov/pmc/articles/PMC10222767/, https://doi.org/10.3390/vaccines11050991.

Koneczny, Inga. “Update on IgG4-Mediated Autoimmune Diseases: New Insights and New Family Members.” Autoimmunity Reviews, vol. 19, no. 10, Oct. 2020, p. 102646, https://doi.org/10.1016/j.autrev.2020.102646. 

Boretti, Alberto. “MRNA Vaccine Boosters and Impaired Immune System Response in Immune Compromised Individuals: A Narrative Review.” Clinical and Experimental Medicine, vol. 24, no. 1, 27 Jan. 2024, www.ncbi.nlm.nih.gov/pmc/articles/PMC10821957/#:~:text=Immunocompromised%20individuals%20may%20not%20mount, https://doi.org/10.1007/s10238-023-01264-1.

Perugino, Cory. “IgG4-Related Disease - Musculoskeletal and Connective Tissue Disorders.” Merck Manuals Professional Edition, Aug. 2023, www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/igg4-related-disease/igg4-related-disease.

​Rispens, Theo, and Maartje G Huijbers. “The Unique Properties of IgG4 and Its Roles in Health and Disease.” Nature Reviews Immunology, 24 Apr. 2023, https://doi.org/10.1038/s41577-023-00871-z.
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​Brogna, Carlo, et al. “Detection of Recombinant Spike Protein in the Blood of Individuals Vaccinated against SARS‐CoV‐2: Possible Molecular Mechanisms.” PROTEOMICS - Clinical Applications, 31 Aug. 2023, https://doi.org/10.1002/prca.202300048.

​Irrgang, Pascal, et al. “Class Switch toward Noninflammatory, Spike-Specific IgG4 Antibodies after Repeated SARS-CoV-2 MRNA Vaccination.” Science Immunology, vol. 8, no. 79, 27 Jan. 2023, https://doi.org/10.1126/sciimmunol.ade2798.

Efthymis Oraiopoulos, and Jan Jekielek. “Cancers Appearing in Ways Never before Seen after COVID Vaccinations: Dr. Harvey Risch.” The Epoch Times, 20 Sept. 2023, web.archive.org/web/20230923113807/www.theepochtimes.com/health/cancers-appearing-in-ways-never-before-seen-after-covid-vaccinations-dr-harvey-risch-5495364. Accessed 4 Oct. 2024.

​Goldman, Serge, et al. “Rapid Progression of Angioimmunoblastic T Cell Lymphoma Following BNT162b2 MRNA Vaccine Booster Shot: A Case Report.” Frontiers in Medicine, vol. 8, 25 Nov. 2021, www.ncbi.nlm.nih.gov/pmc/articles/PMC8656165/, https://doi.org/10.3389/fmed.2021.798095. Accessed 15 May 2024.

Microplastics and nanoplastics are small plastic particles that have significant environmental and health impacts, but they differ in size and behavior.

• Microplastics: There is no officially published definition of microplastics, but in general they are plastic particles that range in size from 1 micrometer (µm) to 5 millimeters (mm). They can be primary microplastics, like microbeads used in cosmetics, or secondary microplastics, which result from the breakdown of larger plastic items. Microplastics are large enough to be seen with the naked eye and can accumulate in various ecosystems, leading to potential ingestion by marine life and humans.
• Nanoplastics: Nanoplastics are much smaller, typically less than 1 µm in size, often in the nanometer scale (1 nm = 0.001 µm). Due to their tiny size, they can penetrate biological membranes more easily, potentially causing more significant health effects. Nanoplastics are challenging to detect and study, making their impact less understood but potentially more hazardous than microplastics.

Microplastics and nanoplastics are pervasive in the environment, originating from a variety of sources that are broadly categorized as primary or secondary.

• Primary Sources: These are plastics intentionally manufactured at a small size. Common examples include microbeads used in cosmetics and personal care products, microfibers from synthetic clothing, and plastic pellets or "nurdles" used in industrial manufacturing. These particles are released directly into the environment through product use or industrial processes.
• Secondary Sources: These originate from the breakdown of larger plastic items such as bottles, bags, and fishing nets. Over time, exposure to sunlight, wind, and water causes these larger plastics to fragment into smaller particles. Secondary microplastics are not intentionally manufactured at their small size but result from the degradation of larger plastic debris.

Mechanisms of Harm to Aquatic Wildlife

1. Physical Impacts:
   • Ingestion and Blockage: Marine animals often mistake microplastics for food, leading to ingestion. Once ingested, these plastics can cause physical blockages in the digestive systems of animals, reducing their ability to absorb nutrients and leading to starvation or malnutrition. For example, sea turtles, fish, and seabirds have been found with stomachs full of plastic, unable to process actual food.
   • Bioaccumulation: Microplastics can accumulate within the bodies of aquatic organisms over time. As these plastics move up the food chain, from prey to predator, they can reach concentrations that are harmful to larger species, including humans who consume seafood.
2. Biological Impacts:
   • Genotoxicity and Cytotoxicity: Microplastics have been shown to cause genetic damage (genotoxicity) and cellular toxicity (cytotoxicity) in aquatic organisms. The physical presence of these particles can disrupt normal cell functions, leading to mutations, cancer, or cell death. Studies have documented DNA damage in fish and invertebrates exposed to microplastics.
   • Oxidative Damage: Microplastics can induce oxidative stress by generating reactive oxygen species (ROS) within cells. This oxidative damage can lead to inflammation, impaired cellular functions, and even apoptosis (programmed cell death). Oxidative stress is a common pathway for toxicity in aquatic organisms exposed to environmental pollutants, including microplastics.
3. Chemical Impacts:
   • Toxicity Pathways: Microplastics often carry harmful chemical additives, such as plasticizers, flame retardants, and heavy metals, which can leach out and enter the tissues of marine animals. These chemicals can disrupt lipid metabolism, leading to energy imbalances and affecting growth and reproduction.
   • Neurotoxicity: The chemicals associated with microplastics can have neurotoxic effects, impairing the nervous system functions of marine animals. This can lead to behavioral changes, such as altered feeding habits, impaired predator-prey responses, and disorientation.

Specific Effects on Aquatic Wildlife

• Reduction of Feeding Activity: Ingestion of microplastics can reduce the feeding activity of marine animals, as their digestive systems become clogged with indigestible particles. This can lead to a decline in energy levels, growth rates, and reproductive success.
• Intestinal Damage: The sharp edges of microplastics can cause physical damage to the intestinal linings of marine organisms, leading to internal injuries, infections, and impaired nutrient absorption.
• Growth Delay: The energy required to process and expel ingested microplastics can detract from the energy available for growth. This results in stunted growth and developmental delays in juvenile marine species.
• Embryotoxicity: Microplastics have been found to impact the development of embryos in marine animals, leading to deformities, reduced hatching success, and impaired survival rates. Embryotoxicity is a critical concern for species with vulnerable early life stages.
• Behavioral Changes: Exposure to microplastics can lead to behavioral changes in marine animals, such as reduced feeding efficiency, altered swimming behavior, and impaired predator avoidance. These changes can have cascading effects on survival and reproductive success.
• Diseases in Marine Animals: Microplastics can serve as vectors for pathogens, carrying harmful bacteria, viruses, and parasites into marine organisms. This can lead to increased incidences of disease, further compromising the health of affected species.

The ecotoxicological effects of microplastics and nanoplastics on aquatic wildlife are not limited to individual organisms. The accumulation of these particles in marine environments can lead to broader ecological disruptions. For example, reduced feeding activity and growth delays in key species can affect the entire food web, leading to declines in predator populations and altering ecosystem dynamics.

Moreover, the persistence of microplastics in the environment means that these impacts can accumulate and intensify over time, potentially leading to long-term declines in biodiversity and the health of marine ecosystems.

The Great Pacific Garbage Patch is a glaring example of how our discarded plastic waste has come to dominate the world's oceans, creating a cycle of pollution that impacts both the environment and human health. As this floating mass of debris continues to grow, so does the urgency to find solutions to the plastic pollution crisis.
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Microplastics and nanoplastics are not just passive pollutants; they actively harm aquatic wildlife through a variety of mechanisms, including genotoxicity, cytotoxicity, oxidative damage, and neurotoxicity. These impacts, coupled with the physical presence of microplastics in the digestive systems of marine animals, can lead to significant ecological and biological disruptions, underscoring the urgent need for action to reduce plastic pollution in our oceans.

Mason's research, conducted in collaboration with the University of Minnesota, analyzed plastics found in various consumer products including beer, tap water, and salt. They discovered that sea salt is particularly susceptible to plastic contamination due to its production process, which involves evaporating saltwater and leaving behind the solid salt—along with any microplastics present in the water.

Mason emphasized that this contamination is not unique to any one region, stating, "It's not that sea salt in China is worse than sea salt in America, it's that all sea salt—because it's coming from the same origins—is going to have a consistent problem." She urged consumers to reconsider their plastic usage and its pervasive role in our society, suggesting that addressing the flow of plastic into the environment is essential to curbing this widespread contamination.
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As consumers become more aware of the hidden dangers in everyday products, the need for alternative materials and reduced plastic consumption becomes increasingly critical for both environmental and public health.

A Word on the Benefits of Consuming Salt
Contrary to popular belief, consuming high amounts of salt does not necessarily lead to increased thirst or elevated blood pressure. In fact, studies have consistently failed to support these common assumptions. Instead, elevated insulin levels are the real culprit behind salt retention, which can lead to increased blood pressure. What drives up insulin? Refined sugars and carbohydrates. So, rather than blaming salt, it's more accurate to point the finger at sugar for these issues. Your body requires both sodium and chloride ions, the main components of salt, and it cannot produce them on its own. Therefore, it's essential to obtain these ions through your diet.

If you decide to follow a low-carb diet or engage in fasting, your insulin levels will naturally drop, leading to increased salt excretion through urine. This can cause dizziness, a common symptom when your body lacks adequate salt. The solution? Increase your salt intake. Feeling low on energy? Take salt. Experiencing headaches, brain fog, or difficulty focusing? Salt could be the answer.

Salt is an essential hydration mineral, and not getting enough can negatively impact your quality of life. Unlike some other nutrients, if you consume too much salt, your body simply excretes it through urine. In fact, drinking salt water has been associated with anti-aging properties. Maintaining healthy salt levels can boost your energy, improve sleep quality, reduce muscle cramps, and enhance exercise performance.
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Starting your day with 16 ounces of water mixed with salt can set you on the right path for maintaining optimal hydration and overall well-being. So, rather than avoiding salt, recognize its vital role in your health and use it wisely to improve your quality of life.

​However, it's important to note that not all salt is created equal. Refined table salt is almost entirely sodium chloride, often with added man-made chemicals. In contrast, unprocessed salts, like pink Himalayan salt, offer a more balanced mix of sodium and chloride, along with other essential minerals such as calcium, potassium, and magnesium. These minerals not only contribute to the pink hue of Himalayan salt but also provide additional health benefits.

Oral Ingestion: Microplastics and nanoplastics enter our bodies predominantly through the food and water we consume. Experimental sampling, such as Fourier-transform infrared spectroscopy (FTIR) on tap, bottled, and spring waters, has confirmed the presence of microplastics in all these sources, highlighting the pervasive nature of this pollution. Studies have detected these particles in everyday items like honey, beer, salt, seafood, and even mineral water. Recent research has shown that a single bottle of water (1L) can contain as many as 240,000 nanoplastic particles. These particles are introduced into the food chain as animals ingest them in their natural environments or as food is contaminated during production processes. Alarmingly, microplastics have also been found in human feces, underscoring their presence in our diet. While the evidence of their presence in food is growing, comprehensive quantitative data on human exposure through diet remains scarce, and no specific legislation currently exists to regulate micro- and nanoscale plastics in foodstuffs.

Inhalation: Airborne microplastics are another significant source of exposure. These particles originate from urban dust, synthetic textiles, rubber tires, and other sources. Due to their small size and lightweight nature, microplastics can remain suspended in the air and be easily inhaled, leading to their deposition in the respiratory system. Research has shown that microplastics can accumulate in the lungs, potentially leading to respiratory issues. More of this down below...

Skin Contact: Although less studied, skin contact represents another potential route of microplastic entry into the body. Microplastics are found in various personal care products, such as exfoliants and cleansers, which can penetrate the skin or be absorbed through wounds. The potential for microplastics to penetrate the skin barrier is an area of active research, with implications for chronic exposure and cumulative health effects.

Recent research has revealed the alarming extent to which humans are exposed to microplastics, with estimates suggesting that we might inhale around 16.2 bits of plastic every hour—equivalent to 5 grams of plastic every week, which is about the weight of a credit card's worth of plastic in just one week. For the first time in history, microplastic particles have been tracked in the lower airways, raising serious concerns about the potential health impacts.
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Microplastics have been detected in various environments, including the air, water, oceans, lakes, snowfall, and rainfall, according to NOAA researchers. These tiny particles are produced from a wide range of sources, including:

• synthetic materials washed off clothes during laundry cycles, such as polyester and polypropylene
  
• abrasions to vehicle tires or brake components during transportation on the road that cause tiny tire shreds or brake wear particles to fly off
  
• abrasions to everyday plastic or synthetic objects, like the soles of shoes and cooking utensils
  
• runoff from plastic components used to develop and mark roads
  
• coatings used on marine equipment and infrastructure, such as container ships
  
• plastic components used in personal care products, such as plastic microdermabrasion beads in face wash
  
• plastic pellets used in manufacturing

Additionally, microplastics are a byproduct of sewage treatment, where wastewater containing these particles is released into the ocean and then evaporates into the atmosphere in large volumes.

The presence of microplastics in the air is particularly concerning. Microplastics may be present in 4-77% of the air you breathe on a regular basis. Studies have found that microplastics, especially synthetic fibers from textiles, can range in size from 1 to 5 microns—small enough to enter the respiratory system, pass through the lungs, and potentially enter the bloodstream. These particles can damage the air sacs in the lungs, increasing the risk of conditions like emphysema and lung cancer.

A 2020 study in Environment International conducted in London found that the air samples collected from the top of a 9-story building contained between 575 to 1008 microplastics per square meter. The study also suggested that microplastics could travel great distances through wind and weather patterns, potentially reaching remote areas like the North Atlantic and the Arctic during certain seasonal conditions like the North Atlantic Oscillation (NAO).

This growing body of research underscores the pervasive nature of microplastic pollution and the urgent need for further studies to understand the full extent of their impact on human health and the environment.

Over time, the exposure to plastic really adds up. According to the World Wildlife Federation’s calculations, each month, you consume about 21 grams, or the equivalent of one Lego brick. In a year’s time, you’ve consumed 250 grams, or the size of a full dinner plate’s-worth of plastic.

In 10 years, you’ve ingested some 5.5 pounds, and in the average lifetime, a person will consume about 40 pounds. While much of this will pass through and be eliminated through your stool, some will remain and accumulate in your organs.

Recent research has uncovered alarming insights into the effects of weathered microplastics on human health, particularly concerning brain cells. Unlike newly manufactured plastics, weathered microplastics—those degraded by environmental factors such as heat and light—have been shown to trigger a more severe inflammatory response in human brain cells.

In an experiment led by Hee-Yeon Kim and colleagues at the Daegu Gyeongbuk Institute of Science and Technology (DGIST), researchers exposed microglia, the brain's immune cells, to weathered polystyrene microplastics. These plastics, which had undergone environmental degradation, caused a dramatic increase in inflammatory particles in the blood of mice. Additionally, there was a marked increase in brain cell death compared to those exposed to "virgin" or new microplastics.

The study found that weathered microplastics altered the expression (by a factor of 10-15) of proteins involved in energy metabolism and significantly increased proteins associated with brain cell death by a factor of five. The team suggests that these effects might be due to changes microplastics undergo when exposed to sunlight and UV radiation, such as increased brittleness and fragmentation, leading to a larger surface area and altered chemical bonds that heighten their reactivity.

This all amounts to an increased inflammatory response by brain cells — far more severe than what was produced by unweathered microplastics tested at equivalent doses.

This discovery has significant implications for human health, especially considering that much of the microplastic we consume comes from food sources. As plastic waste in the oceans breaks down into microplastics through exposure to sunlight, these particles are ingested by marine life, which then enters the human food chain. The increased neurotoxic potential of weathered microplastics emphasizes the urgent need for further research and potential policy interventions to mitigate the impact of microplastics on human health.

Recent research has highlighted the alarming effects of polystyrene nanoplastics (PS NPs) on cardiovascular health, specifically in the context of lipid accumulation and atherosclerosis. The study demonstrated that exposure to PS NPs, especially when combined with oxidized low-density lipoprotein (ox-LDL), led to significant lipid buildup in RAW264.7 macrophages. This lipid accumulation is a key marker in the development of atherosclerosis, a condition characterized by the hardening and narrowing of arteries due to plaque formation.

Using ultrasound biomicroscopy (UBM), researchers observed the development of atherosclerotic plaques in the aortic arch of ApoE-/- mice after three months of PS NPs exposure. This was further confirmed by Oil-red O and hematoxylin-eosin (H&E) staining, which revealed lipid deposition and plaque formation in the aortic root of these mice.

The study also linked the development of atherosclerosis in these mice to disturbances in lipid metabolism and oxidative stress damage in the liver. This suggests that PS NPs exposure not only affects local cardiovascular structures but also has systemic implications, disrupting lipid regulation and promoting inflammation.
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These findings underscore the potential cardiovascular risks posed by nanoplastic exposure. Atherosclerosis, closely associated with abnormal lipid metabolism and oxidative stress, is a significant contributor to heart disease. The study indicates that PS NPs might exacerbate these processes, raising concerns about their long-term impact on cardiovascular health.

In a study published in the International Journal of Molecular Sciences, researchers uncovered the cytotoxic effects of microplastics on human cells. The study demonstrated that microplastic particles are capable of entering cells within just 24 hours of exposure, where they predominantly accumulate around the cell nucleus. This rapid infiltration is concerning, as it directly impacts cell health. The study showed that as the concentration of microplastics and the duration of exposure increased, cell viability—meaning the ability of cells to survive—significantly decreased.

Additionally, the study observed alarming changes in immune response markers. Notably, the expression of tumor necrosis factor (TNF-a), a cytokine involved in inflammation, was found to be twice as high in the livers of mice exposed to microplastics compared to those that were not exposed. This suggests that microplastics not only harm individual cells but can also trigger broader immune responses, potentially leading to inflammation and other related health issues.

These findings add to the growing body of evidence that microplastics pose serious health risks, emphasizing the need for further research and public awareness regarding their pervasive presence in our environment and food supply.

Micro- and nanoplastics have been shown to cause liver inflammation, a critical concern as the liver is essential for detoxifying the body. These plastics disrupt mitochondrial membrane potential, which is stronger with 5 μm particles, inhibiting ATP production—a crucial energy source for cells. Additionally, MNPs negatively affect food absorption and digestion, leading to altered hepatic lipid metabolism. This can result in changes in cholesterol and triglyceride (serum and total cholesterol, serum and total triglycerides, HDL and LDL) levels, which are risk factors for cardiovascular diseases.

MNPs can severely affect the gastrointestinal system. They negatively affect food absorption, inhibit food digestion, decrease mucus secretion in the intestine and impair gut microbiota composition, essential for a healthy digestive system. The dysfunction of the intestinal barrier caused by MNPs can lead to gut dysbiosis and impaired bile acid metabolism, further contributing to digestive issues and metabolic disorders.

Nanoplastics, due to their tiny size (the smaller the more harmful), pose a significant threat to the brain. These particles can cross the blood-brain barrier (BBB) within just two hours, a crucial defense that protects the brain from harmful substances. Once they breach the BBB, they can lead to cognitive impairment, neurological disorders, and neurotoxicity. This neurotoxic effect is thought to be due to the inhibition of acetylcholinesterase activity and altered neurotransmitter levels, which can contribute to behavioral changes. The high surface area to volume ratio of these particles makes them particularly reactive and potentially more harmful than larger microplastics.

​Experimental studies have shown that MNPs absorbed into cholesterol molecules on the brain membrane surface can cross the BBB and increase the risk of inflammation and neurological disorders. This could potentially contribute to neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The plastic microparticles in the brain could induce neuroinflammation, leading to long-term damage and chronic neurological conditions.

​In a study published in the August 2023 issue of the International Journal of Molecular Sciences, researchers uncovered alarming evidence that microplastics extensively infiltrate the body, including the brain, and can induce behavioral changes reminiscent of dementia in as little as three weeks. This research involved exposing both young (4-month-old) and old (21-month-old) mice to varying levels of microplastics in their drinking water over a three-week period.

Behavioral testing at the conclusion of the study revealed that many of the mice exhibited dementia-like symptoms, with older animals showing more pronounced changes. The researchers theorized that age-related dysfunction might exacerbate the effects of polystyrene microplastics (PS-MPs) on behavioral performance. Lead researcher Jaime Ross described the findings as "striking" because the doses of microplastics administered were relatively low.

Upon dissecting the animals, the researchers discovered that microplastics had accumulated in every organ, including the brain, which was an unexpected and shocking finding. Although the presence of microplastics in the gastrointestinal tract, liver, and kidneys was anticipated, their expansion to other tissues, such as the heart and lungs, suggests that microplastics are capable of undergoing systemic circulation.

Of particular concern was the detection of microplastics in the brain, which should be protected by the blood-brain barrier, a mechanism designed to prevent harmful substances, including bacteria and viruses, from entering the brain. The presence of microplastics in brain tissue raises significant concerns, as it may lead to a decrease in glial fibrillary acidic protein (GFAP), a protein that supports cell processes in the brain. A reduction in GFAP has been associated with the early stages of neurodegenerative diseases, such as Alzheimer's disease, and even depression.

The study further explained that GFAP is commonly used as a marker for neuroinflammation and is typically found in mature astrocytes, which are cells located in the brain and spinal cord, and is involved in cellular processes such as autophagy, neurotransmitter uptake and astrocyte development. Although inflammation is usually linked to increased GFAP levels, the researchers observed a slight decrease in GFAP expression in the microplastic-exposed mice. This finding aligns with previous studies suggesting that early stages of certain diseases might be characterized by astrocyte atrophy, leading to decreased GFAP expression.
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These findings underscore the potential for microplastics to contribute to neurological damage and cognitive decline, emphasizing the need for further research to fully understand the implications for human health.

Microplastics, increasingly recognized as endocrine disruptors, are now believed to be present in the majority of people. These tiny particles can cause structural changes and physical damage in the body, potentially long before their long-term endocrine effects have a chance to accumulate and cause harm on their own. One of the most concerning impacts of microplastics is their potential role in male infertility.
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Many products, particularly canned and plastic goods, are high in synthetic forms of estrogen, such as bisphenol A (BPA). BPA, a well-known xenoestrogen, is notorious for leaching from polycarbonate plastics into food and drinks, especially when exposed to heat. This exposure can lead to various health issues, including alterations in liver function, insulin resistance, damage to developing fetuses, and modifications in reproductive and neurological functions.

Environmental toxins, including microplastics, are capable of penetrating the testicle and semen, potentially leading to deleterious effects on testicular function. This includes impairing testosterone production and sperm production, both of which are critical for male and female fertility. Research indicates that male factor infertility contributes to 50% of all infertility cases and is the sole cause in 20-30% of cases. The presence of microplastics and other endocrine-disrupting chemicals in the environment is increasingly seen as a significant factor in this rising trend.

Moreover, BPA and similar chemicals act as agonists for estrogen receptors, inhibiting thyroid hormone-mediated transcription, altering pancreatic beta cell function, and increasing the likelihood of obesity, cardiovascular diseases, and reproductive issues. The pervasive nature of these toxins in Western civilization underscores the urgent need to address their impact on human health, particularly concerning male fertility and overall endocrine function.
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This segment highlights the pressing concern that environmental pollutants like microplastics pose to human health, particularly through their role as endocrine disruptors and their potential contribution to the growing issue of male infertility.

Research has increasingly shown that these tiny plastic particles can induce severe biological effects that span multiple generations and trigger various health conditions, including cancer.

In vitro studies have demonstrated that polystyrene nanoparticles (PS NPs) can induce oxidative stress, which leads to cellular damage in a context-dependent manner. This oxidative stress can result in apoptosis (programmed cell death) and autophagic cell death, processes that can significantly impact the health of exposed organisms.

Research using zebrafish models has provided alarming insights into the long-term effects of PS exposure. Zebrafish injected with 20 nm-sized PS particles during their embryonic stage and later grown in a plastic-free environment still passed on significant health issues to their offspring. The affected offspring exhibited malformations, decreased survival rates, increased heart and blood flow rates, and impaired growth, including smaller eye size and reduced locomotor activity. These effects were linked to increased cell death, elevated reactive oxygen species, and decreased lipid accumulation in the larvae. This study highlights the potential for PS exposure to disrupt biological processes across generations and contribute to disease development, including cancer.

BPA, an endocrine-disrupting chemical widely used in plastic manufacturing, has been identified as a possible risk factor for developing breast cancer. BPA has a strong affinity for non-classical membrane estrogen receptors, such as G protein-coupled receptors (GPER), and can alter multiple molecular pathways within cells (estrogen-related receptor gamma (ERRγ) pathway, HOXB9 (homeobox-containing gene) pathway, bone morphogenetic protein 2 (BMP2) and (BMP4), immunoregulatory cytokine disturbance in the mammary gland). These changes include disruptions in the EGFR-STAT3 pathway, FOXA1 in estrogen receptor-negative breast cancer cells, and epigenetic modifications through the enhancer of zeste homolog 2 (EZH2). These molecular alterations can lead to the undesired stimulation or repression of genes, increasing the risk of developing breast cancer.

The evidence linking MNP exposure to significant health risks is growing. From inducing oxidative stress and cell death to potentially triggering transgenerational effects and increasing the risk of breast cancer, the implications of MNP exposure are profound. Limiting exposure to these harmful particles, especially BPA, is crucial in reducing the risk of developing serious health conditions, including cancer.

In a groundbreaking study published in IJIR: Your Sexual Medicine Journal, microplastics have been discovered for the first time in human penile tissue. This discovery raises concerns about a potential link between microplastics and erectile dysfunction (ED), opening up new avenues of research into the impact of environmental pollutants on male sexual health.

The study, highlighted by CNN Health, analyzed tissue samples from five men undergoing penile implant surgery for ED at the University of Miami. Astonishingly, four out of the five samples contained microplastics, with polyethylene terephthalate (PET) and polypropylene (PP) being the most common types found.

Ranjith Ramasamy, the study’s lead author and a reproductive urology expert, explained, "The presence of microplastics in the penis is unsurprising. The penis, like the heart, is a highly vascular organ." This observation underscores the potential risk that microplastics pose to vascular-rich organs, but the connection between these particles and ED remains uncertain.

Male infertility remains a global issue, with its causes often not well understood. Given the growing evidence of microplastics infiltrating various biological systems, such as blood and lungs, researchers are now exploring their potential effects on reproductive systems. Previous research has investigated the presence of microplastics in male reproductive organs. For example, in one study, researchers discovered 12 different types of microplastics in the testicles of dogs and humans. In dogs, they found that higher levels of certain microplastics correlated with lower sperm counts and reduced testis weight.

Further research is essential to determine whether microplastics contribute to ED or other health issues. According to Ramasamy, "We need to identify if microplastics are linked to ED and if there are specific types or quantities that cause harm." The discovery marks the beginning of what could be a critical exploration into how microplastics may affect male sexual function and overall health.
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As the scientific community continues to investigate, this study highlights the growing concern over the pervasive presence of microplastics in the human body and their potential implications for health, particularly in sensitive and vital tissues such as those involved in sexual function.

The study of microplastics and nanoplastics is fraught with challenges and complexities that make it difficult to fully understand their impact on the environment and human health. One of the main obstacles is the sheer diversity and complexity of these plastic particles. Micro- and nanoplastics are not a single type of material but rather a complex mixture of various polymers, additives, and contaminants. This diversity complicates efforts to develop standardized methods for detecting and analyzing these particles.

To minimize your contribution to global microplastics pollution, it's essential to make conscious decisions about the plastic products you buy and how you dispose of them. The pervasive issue of microplastics begins with the widespread use of cheap, disposable plastic items that are used once and immediately discarded. With nearly 8 billion people on the planet, this behavior results in an immense amount of plastic waste being generated every day. 
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One of the most effective steps you can take is to choose recyclable plastic goods and recycle them correctly. Look for the universal recycling logo, often marked with a number inside the symbol. With approximately 299 million tons of plastic produced annually, these codes help identify how safe the plastic is, its environmental impact, and its recyclability. This number, known as the resin identification code, identifies the type of plastic and its recyclability. Here's a breakdown of common plastics and how to handle them:

• Polyethylene Terephthalate (PET, Plastic #1): Found in clear beverage bottles, synthetic fibers, and food packaging. PET is recyclable but should not be reused, especially if exposed to heat, as it can leach harmful chemicals, like antimony trioxide and DEHA, to leach into your liquids. Avoid reusing these containers as their porous nature can harbor bacteria.
• High-Density Polyethylene (HDPE, Plastic #2): Used in milk jugs, detergent bottles, and piping. HDPE is opaque, widely recyclable and considered one of the safer plastics. It has a low risk of leaching harmful substances and is widely accepted by recycling programs.
• Polyvinyl Chloride (PVC, Plastic #3): Common in plumbing pipes, cable insulation, medical tubing, and window frames, PVC is not recyclable and should be avoided, particularly for food-related use due to its harmful chemical (phthalates, dioxins, etc.) content which interfere with hormonal development.
• Low-Density Polyethylene (LDPE, Plastic #4): Found in grocery bags, containers, squeezable bottles and some food wraps, LDPE is difficult to recycle. It's better to reuse these items or switch to alternatives like reusable bags. Significant environmental impact.
• Polypropylene (PP, Plastic #5): Used in food containers, automotive parts, textiles, and medical devices, and yogurt cups, PP is generally safe and recyclable in many areas.
• Polystyrene (PS, Plastic #6): Used for disposable cutlery, food containers (foam plates/cups), foam packaging (Styrofoam, packing peanuts), and insulation materials, PS is notoriously difficult to recycle and can leach carcinogenic chemicals (styrene), especially when heated. It's best to avoid using PS altogether. It can take hundreds of years to decompose. 
• Other (Plastic #7): This category includes a variety of plastics (new/mixed plastics, LEXAN, etc.) that are often difficult to recycle and may contain harmful chemicals like BPA. Use products in this category with caution. Some are recyclable and some are not.
  • Polycarbonate (PC): Used in eyewear lenses, DVDs, automotive parts, and reusable water bottles. Should generally be avoided, especially in food and drink containers due to their potential to leach harmful chemicals. 
  • Acrylonitrile Butadiene Styrene (ABS): Found in LEGO bricks, automotive parts, and consumer electronics. It's environmental impact due to poor recyclability is concerning.
  • Polyamide (Nylon): Used in textiles, automotive parts, and industrial components.
  • Polytetrafluoroethylene (PTFE): Known as Teflon, used in non-stick cookware, plumbing tape, and industrial applications.
  • Polylactic Acid (PLA): A biodegradable plastic made from renewable resources like corn starch, used in disposable cups, packaging, and 3D printing. It’s still not perfect for high-temperature environments, as it can deform or release lactic acid under heat.

A 2020 review in Earth-Science Reviews identified microplastics in air pollution as potentially the largest contributor to microplastic contamination worldwide, affecting even remote regions like the Arctic and the vast expanses of our oceans. The pervasive nature of microplastics in the atmosphere is alarming, as these particles are not only inhaled but also deposited on land and water surfaces through precipitation, leading to widespread environmental and health impacts.
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However, there are steps individuals can take to mitigate their exposure to microplastics and reduce their environmental footprint:

1. Opt for Compostable or Biodegradable Products: Traditional plastics are made from synthetic materials that can take thousands of years to degrade. Products labeled as compostable or biodegradable are designed to break down more quickly, either by decomposing in the soil or being consumed by microorganisms. Examples of rapidly degrading materials include starch-based polymers, plant-based silvergrass, wood fiber, and coconut fiber.
2. Avoid Harmful Plastic Substitutes: While it's beneficial to reduce single-use plastics, not all alternatives are created equal. For instance, "biodegradable" plastic bottles or bags may still take years to break down and could release harmful chemicals during degradation. Similarly, bamboo products (straws and silverware), though sustainable in small quantities, could become problematic if demand leads to over-harvesting of bamboo forests. Re-used plastic (clothes or shoes made of “recovered” plastic) still keeps plastic in the manufacturing and consumption cycle, leading to further environmental pollution by microplastics
3. Consider Durable, Eco-Friendly Alternatives: Many companies now offer long-lasting alternatives to plastic, such as glass or stainless steel products. Though initially more expensive, these materials do not generate microplastics and can endure years of use. For example, using stainless steel or glass containers instead of plastic can significantly reduce microplastic exposure, especially when heating food or beverages.

Reducing plastic consumption and waste generation is an effective strategy. Simple steps like using reusable shopping bags, using your own coffee mug when getting coffee to go, avoiding plastic-wrapped dry cleaning, ​bringing drinking water from home in glass water bottles instead of buying bottled water, and store foods in glassware or mason jars instead of plastic bags. You can also take your own leftover container to restaurants, which can significantly cut down the amount of plastic that ends up in landfills and oceans, thereby decreasing the microplastic contamination in our food and water. 

​Strategies such as these will help to reduce the amount of plastic that can migrate into your food.  Plastic is all around us and can be extremely difficult to avoid. But if you start looking around, you may find many areas of your life where you can eliminate the use of plastic and replace the it with something inert that won’t harm the environment and your health.

Given that adults may ingest thousands of microplastics annually through water consumption alone, it is advisable to minimize the use of plastic water bottles. Opting for a non-plastic water container, like one made from stainless steel or copper, can significantly reduce this exposure. Additionally, experts recommend avoiding microwaving food in plastic containers or placing them in the dishwasher, as heat can cause more plastic to leach into food, and release into the environment.

These changes, while seemingly small, can collectively make a significant difference in reducing microplastic pollution and protecting both human health and the environment.

In the battle against plastic pollution, both businesses and individuals play crucial roles. One initiative that stands out is the B Corporation movement. B Corporations are businesses committed to reducing global waste and promoting fair hiring and manufacturing practices across their supply chains. These companies actively work to minimize the use of materials that generate microplastics, making them leaders in sustainability. When shopping, look for the B Corporation logo—a "B" encircled—to support companies that adhere to these eco-friendly standards.

On an individual level, protecting yourself from airborne microplastics is becoming increasingly important. Microplastic particles in the air, though often larger than typical pollutants like PM10 and PM2.5, still pose significant health risks. Thankfully, these larger particles are easier to capture with a high-performance air purifier.

​While many air purifiers can only trap smaller pollutants, high-performance models with centrifugal fans are specifically designed to capture even large and heavy microplastics. These purifiers filter out particles as small as 0.003 microns, which is far smaller than the tiniest microplastics.

Consider using a personal air purifier in spaces where microplastics are likely to accumulate, such as bedrooms or workspaces, where they can be emitted from clothing, appliances, and containers. Additionally, a car air purifier can help filter out microplastics from tire and brake wear, which can infiltrate your vehicle's interior, especially in high-traffic areas.

​Emerging research suggests that sweating, whether through exercise or sauna use, may play a role in detoxifying the body from accrued microplastics. A 2022 study detected microplastic particles such as polyethylene, PET, and polymers from sportswear in sweat collected after exercise, indicating that perspiration could aid in the elimination of these particles alongside other toxins like pesticides, flame retardants, and bisphenol-A. This adds to a growing body of evidence showing that sweating can facilitate the excretion of heavy metals, petrochemicals, and other pollutants.
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As with other toxins, microparticle content in sweat could indicate efficacy of interventions promoting clearance. Given the increasing prevalence of microplastics in our environment, inducing sweat through regular sauna use or exercise could offer a simple and accessible detoxification method to help reduce the body's burden of microplastics. However, more research is needed to understand the full impact of repeated sweating on microplastic levels in the body. Additionally, regulatory limits specific to nanoplastics in food and drinks could help safeguard public health given the unprecedented exposure uncovered by advanced microscopy techniques. After all, "seeing" the risk is the first step toward safety.

Notice this "U" shape in the curve when examining the relationship between RT and morbidity and mortality. This curve suggests that some RT is clearly beneficial, but has the volume of RT increases past a certain point the benefits drop and it becomes harmful. The concept of a "biphasic response" is fundamental to understanding hormesis. It describes the characteristic dose-response relationship observed in hormetic processes, where a substance or stressor elicits opposite effects at low and high doses. The response can be visualized as a U-shaped or J-shaped curve, illustrating the beneficial effects at low doses and potential harm at higher doses. ​

Paluch, Amanda E, et al. “Resistance Exercise Training in Individuals with and without Cardiovascular Disease: 2023 Update: A Scientific Statement from the American Heart Association.” Circulation, 7 Dec. 2023, https://doi.org/10.1161/cir.0000000000001189. Accessed 11 Dec. 2023.

Momma H, Kawakami R, Honda T, Sawada SS. Muscle-strengthening activities are associated with lower risk and mortality in major non-communicable diseases: a systematic review and meta-analysis of cohort studies. Br J Sports Med. 2022 Jul;56(13):755-763. doi: 10.1136/bjsports-2021-105061. Epub 2022 Feb 28. PMID: 35228201; PMCID: PMC9209691.

We’ve built an entire economy, not just in the United States but the entire Western civilization, on healthcare. For thousands of years, real control over populations has been around their food. Today, with billions of souls on the planet, controlling food has become a massive business and a means of ultimate political control. Between 1982 and 2000, something changed in our environment, overwhelming the immune system of the population. Diseases in different organ systems started going epidemic simultaneously, challenging the notion of a thousand different diseases.

In the late 1800s, we changed the way we farmed, leading to a disrespect for crop rotation and soil health. This disrespect for soil health resulted in the Dust Bowl of the 1920s and 30s, pushing us to outsource our food production and rely on imported food. After World War II, with a surplus of petroleum, we started producing chemical-based fertilizers, leading to the Green Revolution. While plants turned green due to nitrogen and phosphorus, they lacked essential nutrients and medicine.

This deficiency weakened plants, making them susceptible to diseases and pests. The chemical industry introduced pesticides and herbicides (including #Glyphosate), creating a co-dependent relationship between farmers and chemical solutions. Similarly, in healthcare, we’ve become dependent on drugs to manage symptoms, creating a cycle of side effects and more medications. The epidemic rise in diseases like autism, Alzheimer’s, Parkinson’s, and autoimmune disorders signals a deeper problem, challenging our understanding of the root cause of diseases.

It’s time to reconsider our approach to health, starting with understanding the importance of soil health and nutrition. Just as respecting soil is crucial for healthy crops, prioritizing our body’s nutritional needs is fundamental for overall well-being. Let’s shift our focus from symptom management to addressing the root cause, promoting a holistic approach to health.

Zach Bush, MD is triple board-certified physician specializing in internal medicine, endocrinology and hospice care. He is the founder of Seraphic Group, an organization devoted to developing root-cause solutions for human and ecological health in the sectors of big farming, big pharma, and Western Medicine at large. And he is also the founder of Farmers Footprint https://farmersfootprint.us/, a non-profit coalition of farmers, educators, doctors, scientists, and business leaders aiming to expose the deleterious human and environmental impacts of chemical farming and pesticide reliance - while simultaneously offering a path forward through regenerative agricultural practices.

Zach Bush MD is a physician specializing in internal medicine, endocrinology and hospice care. He is an internationally recognized educator and thought leader on the microbiome as it relates to health, disease, and food systems. Dr Zach founded Seraphic Group and the nonprofit Farmer’s Footprint to develop root-cause solutions for human and ecological health. His passion for education reaches across many disciplines, including topics such as the role of soil and water ecosystems in human genomics, immunity, and gut/brain health. His education has highlighted the need for a radical departure from chemical farming and pharmacy, and his ongoing efforts are providing a path for consumers, farmers, and mega-industries to work together for a healthy future for people and planet.

Show Notes

• A trip to the Philippines changed Zack’s life mission and how he viewed allopathic medicine afterward. (10:07)
• “The scientific method is nothing more than a technique for exploring truth, but at no point is science a body of knowledge or truth…” (28:16)
• Zach’s bedrock spiritual philosophy: I am. (41:06)
• Homo sapiens is an adaptive species and not a stagnant one. (55:09)
• What’s the difference between a rishi and a reishi mushroom? (1:14:00)
• A quantum physics fellowship. (1:23:20)
• Healing relationships at death’s door. (1:36:32)
• Random event generators and the death of George Floyd. (1:40:15)
• Do humans have the raw potential to co-create something magnificent? (1:50:21)

Resources

• Zack’s articles co-written with Deepak Chopra on June 1 and June 8 in the SF Gate
• Antoine Béchamp vs. Louis Pasteur
• The work of J.R.R. Tolkien and John Archibald Wheeler
• Mycorrhiza
• Superstring theory
• The Abdominal and Pelvic Brain by Byron Robinson
• Intestinal Gardening for the Prolongation of Youth by James Empringham
• Universal Sufism by H.J. Witteveen and Scott Sattler
• Streams of Wisdom by Dustin DiPerna and Ken Wilbur

From RT:

​Now, we have a thing called a messenger RNA vaccine (mRNA). RNA is, effectively, a single strand of DNA – the double helix that sits within our cells and makes up our genetic code. Many viruses are made up of a single strand of RNA, surrounded by a protein sphere.
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They enter the cell, take over the replication systems, make thousands of copies of themselves, then exit the cell. Sometimes killing the cell as they do so, sometimes exiting more gently. Covid19 (Sars-Cov2) is an RNA virus.

Knowing this, rather than attempting to create a weakened virus, which can take years, or break the virus into bits, the vaccine researchers decided to use Sars-Cov2’s RNA against itself. To do this, they isolated the section of RNA which codes for the ‘spike’ protein – which is the thing the virus uses as a ‘key’ to enter cells. 

They then worked out how to insert this small section of RNA, messenger RNA, into the cell, where it takes over a part of the protein replication mechanisms that sit inside all cells. They turn the mechanism into a 3D printer, churning out copies of the spike protein.

These spike proteins then leave the cell – somehow or other, this bit is unclear. The immune system comes across them, recognises them as ‘alien’ and attacks. In doing so, antibodies are created, and the immune memory system kicks into action. If, later on, a Sars-Cov2 virus gets into the body, the immune system fires up and attacks the remembered spike protein. Hopefully killing the entire virus.

This is all, certainly very clever stuff. What, as they say, could possibly go wrong?

The first thing to say is that, with something this new, we don’t really know. It could be that it is absolutely 100 percent safe. We are told that none of the mRNA can get into the nucleus of the cell, where it could become incorporated into the DNA. I hope so. Could it trigger an immune cascade? I hope not.
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I know that the researchers will be looking very, very, closely at the novel safety issues that could emerge. If they are not, they damned well should be. However, the timelines here are very short. It normally takes many years to create safe and effective vaccines. Here is it happening in, effectively, weeks.

Hydrogen comes in two “flavors”: regular hydrogen, which is actually called protium, and deuterium. Deuterium has all of the same properties as hydrogen, except that it's twice as big and heavy. This is due to an added neutron paired with the proton in the nucleus. Because of this, deuterium is also referred to as "heavy hydrogen," and it actually behaves quite differently from regular hydrogen in chemical reactions and in our bodies.

In nature, deuterium helps things grow. For example, deuterium is biologically necessary for growth in babies, teenagers, and developing plants and animals. But once you stop growing, having too much deuterium in your cells can result in mitochondrial dysfunction and lead to premature aging, metabolic problems, and disease.

Deuterium is like thick, gluggy oil  - when you put thick oil into an engine, the engine sputters, makes strange noises, and eventually breaks.


Nature has put systems in place to deplete deuterium and protect the nanomotors, or "little engines," in our cells’ mitochondria from coming into contact with this thick oil.


However, the side effects of a modern life - pollution, global warming, processed foods, less healthy lifestyles, etc. - have resulted in many people having way too much deuterium inside their cells. This results in an inability to effectively deplete deuterium and the destruction of our nanomotors.


This starts a vicious cycle of deuterium building up and breaking more of our nanomotors. Fewer nanomotors means less energy and more sickness and disease.

While deuterium is a natural and essential element, its presence has increased in the modernized environment within the food, atmosphere, and water. Deuterium levels is food will vary based o where that food is grown - deuterium is highest in the equator and in low elevations. Foods high in fat, as well as green plants, including algae and spirulina, which contain high amounts of chlorophyll, are lower in deuterium than fruits, roots, and underground vegetables. As it turns out, GMO foods tainted with glyphosate, as well as processed, synthetically made foods, possess high amounts of deuterium.

There are various lifestyle practices that have led to increased deuterium levels including a lack of sleep, particularly deep REM sleep. In addition, breathing shallow and fast via the mouth and chest also contributes to elevated levels of deuterium.

Researchers have demonstrated that elevated of deuterium can contribute to:

• Chronic fatigue
• Diminished deep and REM sleep
• Anxiety and depression
• Increased aging, leading to to diseases like diabetes, cardiovascular disease, and Alzheimer's
• Increased cancer cell growth
• Immune dysregulation

It is widely recognized that radiation exposures such as X-rays and gamma radiation can increase the risk of cancer in humans and animals. These types of radiation are referred to as ionizing radiation (Ionization energy is defined as the minimum amount of energy required to remove an electron from an atom or molecule in the gaseous state). This is different from nonionizing radiation, which includes ultraviolet (UV), visible light, extremely low frequency radiation (ELF), and radiofrequency or microwave (RF) radiation. Conventionally, researchers believed that nonionizing radiation is not harmful or carcinogenic, despite evidence surfacing regarding the relationship between UV radiation and skin cancer.

Research evaluating the exposure to RF radiation was conducted primarily by military agencies. Due to the advent and use of cellular telephone systems, which involve widespread public exposures, reevaluation of exposure risk has become urgent.

Four types of physiological effects has been observed by researched in multiple studies:

1. Increased spontaneous abortion,
2. Shifts in red blood cell and white blood cell count,
3. Increased somatic mutation rates in lymphocytes, and
4. Increased childhood, testicular, and other cancers.

These findings suggest that exposure to RF radiation, including from devices such as microwave ovens, are potentially carcinogenic and have other health effects. An important point to consider is that low dose radiation exposure over time has damaging effects, rather than one large exposure to radiation.

Rather than using a microwave, consider using a stove or convection oven. These methods take a bit more time, but it is well worth it! Consider using headphones to talk on cell phones rather than placing the device directly to your head. If possible, request to avoid airport scanners by opting for a pat-down. Lastly, try to reduce overall radiation exposure over time.

Goldsmith, J. (1997). Epidemiologic Evidence Relevant to Radar (Microwave) Effects. Environmental Health Perspectives, 105, 1579. https://doi.org/10.2307/3433674

Ayurveda offers insight into the earlier stages and enables those monitoring their health to take care of any small imbalances well before developing any serious illness. The length of the each stage may vary from weeks, to months, even years, depending on the person and the degree of aggravation.

The six stages of disease development are:

1. Accumulation
   
2. Aggravation
3. Dissemination
4. Localization
5. Manifestation
6. Complication
   

The first stage, accumulation, represents imbalance, a build up or collection of something in the body. Being exposed to and acquiring a pathogen via the external environment is an example of accumulation. This stage can also be caused by the internal environment, such as from eating an imbalanced diet leading to excess inflammation or mucous. Accumulation in the body leads to the the next stage, aggravation.

As the imbalanced elements continue to increase, the symptoms become more aggravated and will begin to be noticed throughout the body. This stage is a sign of continued accumulation. This stage can manifest, as seen in the Kapha state, as loss of appetite, indigestion, nausea, excess saliva, oversleeping, sluggishness; or as seen in the Pitta state, as increased acidity, burning sensations in the abdomen, lowered vitality, or insomnia; or as seen in the Vata state, as pain in the lower abdomen, excess flatulence, and light-headedness.

Once the site of origin is full with excess accumulation and is aggravated, it will begin to overflow into or disseminate throughout the rest of the body using different channels of transportation. Overflow typically begins in the GI tract, then spilling into the circulating plasma and blood, allowing the accumulation to spread systemically, and eventually seeping into the organs and tissues (dhātus). Simultaneously, the symptoms at the site of origin will grow worse.

The excess accumulation will then move to wherever a weak site exists in the body. This is where and when diseases begin to develop. This stage is also where genetics matter; the weak spots are determined by genetics - as the saying goes, genetics loads the gun, environment pulls the trigger. This stage can manifest, as seen in the Vata state, as arthritis. In a Pitta state, this can be seen as an ulcer, and in the Kapha state, manifestation may begin in the lungs. At this stage, healing is still regarded as simple.

This is the first state of the development of illness for which modern Western medicine can detect signs of disease. It is at this stage where diseases progress and become fully developed, showing signs of clinical features. Manifested imbalances are given names at this stage, such as arthrosclerosis, cancer, colitis, etc. It is at this stage where conventional medicine attempts to mask the symptoms by offering pharmaceutical drugs.

Complications of the dis-ease begin at this final stage. Often times, conventional medicine attempts to solve the problem by simply removing the affected tissue (e.g., small intenstine, colon, thyroid, etc.) from the body. The symptoms become clear enough so that the elemental cause (i.e., dosha constitution such as Vata, Kapha, Pitta) may be determined. Some medical professionals describe this stage as the chronic phase of development. For example, if one develops inflammation in the manifestation stage, in this stage, complications set in, and the inflammation may grow worse into a chronic problem.

Being aware of the stages of the dis-ease process is helpful because one can gain a better understanding in how prevent, and perhaps even reverse, it. To be clear, the information provided here is not claiming to treat, cure or diagnose disease.

Cabral, S. (2018). The 6 Stages of the Disease Process (Ayurvedic Principle). [podcast] The Cabral Concept. Available at: https://itunes.apple.com/us/podcast/cabral-concept-by-stephen/id1071469441?mt=2

Tirtha, S. (2007). The Āyuveda encyclopedia. Bayville, NY. Ayurveda Holistic Center Press.

The environment that we live in is toxic. It is worrisome to think that the status quo has occurred with the help of corporations knowingly dumping harmful chemicals into the environment.

The Environmental Working Group (EWG) has studied the current state of our world in great detail and has discovered that before a child is even born they already have approximately 287 toxins in their blood and tissues. These results came from 10 newborns whose parents gave permission to have their toxins measured at birth.

The results of this study indicate that an average of 200 chemicals was found in each newborn. Of the toxins tested, 47 were consumer ingredients such as cosmetics, 212 were industrial and pesticide byproducts. In this study, only around 400 total chemicals were actually tested for - thousands of others may have been found if larger parameters were used.

Many of the toxins measured in the newborns included plastics, flame retardants, and other chemicals that disrupt brain function, IQ, hormones, and the nervous system of the child. Some of the toxins observed like DDT, have actually been banned since 1972 (over 3 decades ago), but are still being measured in laboratory samples. Certain chemicals never fully degrade in the environment.

So, there is not question about it, the environment we live in is toxic. All of us have disease-creating toxins inside of our bodies, the question boils down to which ones and how much.

But there are some solutions: lab tests and detoxification.

Transcript:
"You hear all this talk about blue light being harmful, but do you know what blue light actually is?

Blue light is one of the types of light that form the white light we get from the Sun. Together with
red, orange, yellow, green, violet, and indigo. This is called the electromagnetic (EM) spectrum of visible light. At the end we have the UV light, which can't actually be seen by the human eye. The energy of these waves increases as we go towards the end, which makes blue lights one of the highest intensity types of visible light.

Light is made of EM waves that emit energy and it's this energy that we perceive as light. These waves come in different wavelengths, which means we get different colors of light. These are the different colors of light that we can perceive from the EM spectrum. So blue light is actually everywhere; it's in the light that travels from the Sun all the way to the Earth.

Because the wavelength of blue light is so small they collide with air molecules a lot more than any other color and they get scattered everywhere - that's actually what makes the sky blue. That's why your body uses this blue light from the Sun to make the difference between day and night and
regulate your sleep cycle. But our eyes natural filters barely provide us with enough protection from blue light on a particularly sunny day.

The blue light from your devices is even worse. LED devices emit much stronger blue light than we get from the Sun. Spending hours staring at a screen can cause eye damage and fatigue. This is due to most lower energy waves being absorbed by the cornea, the eyes outer membrane. Blue light goes straight through due to its high energy and slowly deteriorates the retina. And because our brains use blue light to differentiate between day and night and boost alertness, spending time on your phone tablet or laptop late at night fools your body into thinking it should keep you awake. It's all of them - phones, tablets, any gadget with an illuminated display. They all use blue LEDs because they are energy efficient and cheaper to produce, but your body disagrees.

Basically, what keeps you awake and alert during the day can severely affect the quality of your sleep at night. Blue light has also been shown to suppress secretion of melatonin, a hormone that is produced at night and helps your body prepare for sleep. Melatonin isn't just linked to poor
sleep, scientists have also managed to find a correlation between melatonin deprivation and conditions like cancer, diabetes and clinical depression. Do you still think your tablet is that harmless?

Well there is a way you can prevent it. Scientists have now designed special screen protectors that stop the blue light from reaching your eyes and causing damage to your retina at a microscopic level. This glass has tiny ridges that block blue waves and let the other less harmful light go through. These glasses can block up to 60% of blue light and 99% of UV rays. People have reported that their sleeping patterns were significantly improved after only a few days. There was also significant reduction in eye strain and headaches. Or you can go for full protection and buy eyewear that you can use for all blue light-emitting devices: computers, TV laptops, or your phone. These work in a slightly different way - the protectors as the yellow, absorbs rather than blocks blue and UV light, and lets other types of light go through.

No matter what you do, whether its buying a protective glass or reducing the time you spend on your device make sure you stay on the lookout for the unseen damage that your day-to-day gadgets can do to your health."

Key benefits of red light include:

1. Minimal Melatonin Suppression: Studies show that exposure to red light has little to no impact on melatonin levels, allowing the body to maintain its natural sleep-wake cycle.
2. Reduced Eye Strain: Red light is gentler on the eyes compared to the harsh glare of blue or white light, especially in low-light conditions.
3. Natural Ambiance: The warm glow of red incandescent bulbs mimics the light of a natural sunset, signaling the brain to prepare for rest.

Applications of Red Incandescent Lighting

• Evening Lighting: Replace bright white or blue-tinged LED or CFL bulbs with red incandescent bulbs in bedrooms, living rooms, and bathrooms.
• Nighttime Usage: For those who need to wake during the night, red light provides sufficient illumination without disrupting sleep.
• Technology Filters: Pair red lighting with blue-light filtering settings on electronic devices to further minimize blue light exposure.

​Several studies support the use of red light for circadian health:

• Melatonin Preservation: Research indicates that red light exposure does not suppress melatonin production, making it ideal for nighttime environments. 
• Minimized Disruption: Comparisons between red and blue light exposure highlight red light’s negligible impact on the SCN and circadian timing.

When selecting red incandescent light bulbs:

• Opt for bulbs labeled as "true red" to ensure they emit light solely in the red spectrum.
• Choose low-wattage bulbs (15-25 watts) to create a soothing ambiance without excessive brightness.
• Confirm the absence of blue or white light leakage by testing in a dark room.

Welcome to the first episode of our brand new docuseries - Remedy: Ancient Medicine for Modern Illness.

(If you are not registered for the full Remedy docuseries yet, click this link to join us for all 9 episodes - https://remedy.thesacredscience.com/r... )

Episode 1 is called “The Quest For Lost Medicine” and it lays the groundwork for the entire series - some of what you will witness may shock you… Over the 9-part Remedy series, we’ll be uncovering powerful herbal remedies for major diseases - but first, we need to understand why this vital healing information has been kept from us.

Here’s some of what we will reveal in this first episode…

• Why many effective green medicines are not finding their way to the people who are in critical need of them - and the powers who would like it to remain this way
  
• The unsung heroes (women) who have safe-guarded this healing information for centuries and who are now bringing it forward to heal a world in crisis
  
• Why 82% of the world uses herbal remedies as their primary medicine… BEFORE turning to modern approaches
  
• Why the U.S. is one of the ONLY countries in the world where it is illegal to practice herbalism
  
• How a belief about chemical “heroic medicine” took root in the public consciousness and why it is blocking many from accessing true medicines
  
• The overwhelming scientific proof that plants are perfectly designed to heal the illnesses and challenges we humans face - with very few side effects
  

This eye-opening episode sets the stage for everything else we cover in the Remedy docuseries. Again, if you are not registered for the full series, click here - https://remedy.thesacredscience.com/r...

The researcher, Dr. José Baselga, a towering figure in the cancer world, is the chief medical officer at Memorial Sloan Kettering Cancer Center in New York. He has held board memberships or advisory roles with Roche and Bristol-Myers Squibb, among other corporations, has had a stake in start-ups testing cancer therapies, and played a key role in the development of breakthrough drugs that have revolutionized treatments for breast cancer.

According to an analysis by The New York Times and ProPublica, Dr. Baselga did not follow financial disclosure rules set by the American Association for Cancer Research when he was president of the group. He also left out payments he received from companies connected to cancer research in his articles published in the group’s journal, Cancer Discovery. At the same time, he has been one of the journal’s two editors in chief.

At a conference this year and before analysts in 2017, he put a positive spin on the results of two Roche-sponsored clinical trials that many others considered disappointments, without disclosing his relationship to the company. Since 2014, he has received more than $3 million from Roche in consulting fees and for his stake in a company it acquired.

Dr. Baselga did not dispute his relationships with at least a dozen companies. In an interview, he said the disclosure lapses were unintentional.

He stressed that much of his industry work was publicly known although he declined to provide payment figures from his involvement with some biotech startups. “I acknowledge that there have been inconsistencies, but that’s what it is,” he said. “It’s not that I do not appreciate the importance.”

Dr. Baselga’s extensive corporate relationships — and his frequent failure to disclose them — illustrate how permeable the boundaries remain between academic research and industry, and how weakly reporting requirements are enforced by the medical journals and professional societies charged with policing them.

A decade ago, a series of scandals involving the secret influence of the pharmaceutical industry on drug research prompted the medical community to beef up its conflict-of-interest disclosure requirements. Ethicists worry that outside entanglements can shape the way studies are designed and medications are prescribed to patients, allowing bias to influence medical practice. Disclosing those connections allows the public, other scientists and doctors to evaluate the research and weigh potential conflicts.

“If leaders don’t follow the rules, then we don’t really have rules,” said Dr. Walid Gellad, director of the Center for Pharmaceutical Policy and Prescribing at the University of Pittsburgh. “It says that the rules don’t matter.”

The penalties for such ethical lapses are not severe. The cancer research group, the A.A.C.R., warns authors who fill out disclosure forms for its journals that they face a three-year ban on publishing if they are found to have financial relationships that they did not disclose. But the ban is not included in the conflict-of-interest policy posted on its website, and the group said no author had ever been barred.

Many journals and professional societies do not check conflicts and simply require authors to correct the record.

Officials at the A.A.C.R., the American Society of Clinical Oncology and The New England Journal of Medicine said they were looking into Dr. Baselga’s omissions after inquiries from The New York Times and ProPublica. The Lancet declined to say whether it would look into the matter.

Christine Hickey, a spokeswoman for Memorial Sloan Kettering, said that Dr. Baselga had properly informed the hospital of his outside industry work and that it was Dr. Baselga’s responsibility to disclose such relationships to entities like medical journals. The cancer center, she said, “has a rigorous and comprehensive compliance program in place to promote honesty and objectivity in scientific research.”

Asked if he planned to correct his disclosures, Dr. Baselga asked reporters what they would recommend. In a statement several days later, he said he would correct his conflict-of-interest reporting for 17 articles, including in The New England Journal of Medicine, The Lancet and the publication he edits, Cancer Discovery. He said that he did not believe disclosure was required for dozens of other articles detailing early stages of research.

“I have spent my career caring for cancer patients and bringing new therapies to the clinic with the goal of extending and saving lives,” Dr. Baselga said in the statement. “While I have been inconsistent with disclosures and acknowledge that fact, that is a far cry from compromising my responsibilities as a physician, as a scientist and as a clinical leader.”

Dr. Baselga, 59, supervises clinical operations at Memorial Sloan Kettering, one of the nation’s top cancer centers, and wields influence over the lives of patients and companies wishing to conduct trials there. He was paid more than $1.5 million in compensation by the cancer center in 2016, according to the hospital’s latest available tax disclosures, but that does not include his consulting or board fees from outside companies.

Many top medical researchers have ties to the for-profit health care industry, and some overlap is seen as a good thing — after all, these are the companies charged with developing the drugs, medical devices and diagnostic tests of the future.

Dr. Baselga’s relationship to industry is extensive. In addition to sitting on the board of Bristol-Myers Squibb, he is a director of Varian Medical Systems, which sells radiation equipment and for whom Memorial Sloan Kettering is a client.

In all, Dr. Baselga has served on the boards of at least six companies since 2013, positions that have required him to assume a fiduciary responsibility to protect the interests of those companies, even as he oversees the cancer center’s medical operations.

The hospital and Dr. Baselga said steps had been taken to prevent him from having a say in any business between the cancer center and the companies on whose boards he sits.

The chief executive of Memorial Sloan Kettering, Dr. Craig B. Thompson, settled lawsuits several years ago that were filed by the University of Pennsylvania and an affiliated research center. They contended that he hid research conducted while he was at Penn to start a new company, Agios Pharmaceuticals, and did not share the earnings. Dr. Thompson disputed the allegations. He now sits on the board of Merck, which manufactures Keytruda, a blockbuster cancer therapy.

Ms. Hickey said the cancer center cannot fulfill its charitable mission without working with industry. “We encourage collaboration and are proud that our work has led to the approval of novel, lifesaving cancer treatments for patients around the world,” she said.

Some disclosures are required; others aren’t. After the scandals a decade ago over lack of disclosure, the federal government began requiring drug and device manufacturers to publicly disclose payments to doctors in 2013.

From August 2013 through 2017, Dr. Baselga received nearly $3.5 million from nine companies, according to the federal Open Payments database, which compiles disclosures filed by drug and device companies.

Dr. Baselga has disclosed in other forums investments and advisory roles in biotech start-ups, but he declined to provide a tally of financial interests in those firms. Companies that have not received approval from the Food and Drug Administration for their products — projects still in the testing phases — do not have to report payments they make to doctors.

Serving on boards can be lucrative. In 2017, he received $260,000 in cash and stock awards to sit on Varian’s board of directors, according to the company’s corporate filings.

ProPublica and The Times analyzed Dr. Baselga’s publications in medical journals since 2013, the year he joined Memorial Sloan Kettering. He failed to disclose any industry relationships in more than 100, or about 60 percent of the time, a figure that has increased with each passing year. Last year, he did not list any potential conflicts in 87 percent of the articles that he wrote or co-wrote.

Dr. Baselga compiled a color-coded list of his articles and offered a different interpretation. Sixty-two of the papers for which he did not disclose any potential conflict represented “conceptual, basic laboratory or translational work,” and did not require one, he said. Questions could be raised about others, he said, but he added that most “had no clinical nor financial implications.” That left the 17 papers he plans to correct.

Early-stage research often carries financial weight because it helps companies decide whether to move ahead with a product. In about two-thirds of Dr. Balsega’s articles that lacked details of his industry ties, one or more of his co-authors listed theirs.

In 2015, Dr. Baselga published an article in the New England Journal about a Roche-sponsored trial of one of the company’s drugs, Zelboraf. Despite his financial ties to Roche, he declared that he had “nothing to disclose.” Fourteen of his co-authors reported ties to Roche.

Dr. Baselga defended the articles, saying that “these are high-quality manuscripts reporting on important clinical trials that led to a better understanding of cancer treatments.”

Industry ConnectionsSome of Dr. José Baselga’s known relationships with health care companies. He has failed to disclose any industry ties in dozens of research articles since 2013.

The guidelines enacted by most major medical journals and professional societies ask authors and presenters to list recent financial relationships that could pose a conflict.

But much of this reporting still relies on the honor system. A study in August in the journal JAMA Oncology found that one-third of authors in a sample of cancer trials did not report all payments from the studies’ sponsors.

“We don’t routinely check because we don’t have those kind of resources,” said Dr. Rita F. Redberg, the editor of JAMA Internal Medicine, who has been critical of the influence of industry on medical practice. “We rely on trust and integrity. It’s kind of an assumed part of the professional relationship.”

Jennifer Zeis, a spokeswoman for The New England Journal of Medicine, said in an email that it had now asked Dr. Baselga to amend his disclosures. She said the journal planned to overhaul its tracking of industry relationships.

The American Association for Cancer Research said it had begun an “extensive review” of the disclosure forms submitted by Dr. Baselga.

It said that it had never barred an author from publishing, and that “such an action would be necessary only in cases of egregious, consistent violations of the rules.”

Among the most prominent relationships that Dr. Baselga has often failed to disclose is with the Swiss pharmaceutical giant Roche and its United States subsidiary Genentech.

In June 2017, at the annual meeting of the American Society of Clinical Oncology in Chicago, Dr. Baselga spoke at a Roche-sponsored investor event about study results that the company had been counting on to persuade oncologists to move patients from Herceptin — which was facing competition from cheaper alternatives — to a combination treatment involving Herceptin and a newer, more expensive drug, Perjeta.

The results were so underwhelming that Roche’s stock fell 5 percent on the news. One analyst described the results as a “lead balloon,” and an editorial in The New England Journal called it a “disappointment.”

Dr. Baselga, however, told analysts that critiques were “weird” and “strange.”

This June, at the same cancer conference, Dr. Baselga struck an upbeat note about the results of a Roche trial of the drug taselisib, saying in a blog post published on the cancer center website that the results were “incredibly exciting” while conceding the side effects from the drug were high.

That same day, Roche announced it was scrapping plans to develop the drug. The news was another disappointment involving the class of drugs called PI3K inhibitors, which is a major focus of Dr. Baselga’s current research.

In neither case did Dr. Baselga reveal that his ties to Roche and Genentech went beyond serving as a trial investigator. In 2014, Roche acquired Seragon, a cancer research company in which Dr. Baselga had an ownership stake, for $725 million. Dr. Baselga received more than $3 million in 2014 and 2015 for his stake in the company, according to the federal Open Payments database.

From 2013 to 2017, Roche also paid Dr. Baselga more than $50,000 in consulting fees, according to the database.

These details were not included in the conflict-of-interest statements that are required of all presenters at the American Society of Clinical Oncology conference, although he did disclose ownership interests and consulting relationships with several other companies in the prior two years.

ASCO said it would conduct an internal review of Dr. Baselga’s disclosures and would refer the findings to a panel.

Dr. Baselga said that he played no role in the Seragon acquisition, and that he had cut ties with Roche since joining the board of a competitor, Bristol-Myers, in March. As for his presentations at the ASCO meetings in the last two years, he said he had also noted shortcomings in the studies.

The combination of Perjeta with Herceptin was later approved by the F.D.A. for certain high-risk patients. As for taselisib, Dr. Baselga stands by his belief that the PI3K class of drugs will be an important target for fighting cancer.

Ornstein, C & Thomas, K. (2018). Top Cancer Researcher Fails to Disclose Corporate Financial Ties in Major Research Journals. [online] Retrieved from: https://www.nytimes.com/2018/09/08/health/jose-baselga-cancer-memorial-sloan-kettering.html

The anti-cancer assertions made by medical cannabis advocates are no longer just based on anecdotal success stories. In the following video, Dr. Christina Sanchez, a molecular biologist at the Complutense University of Madrid, explains how her research supports the claim that cannabis kills cancer.

Through several human and animal experimental observations, researchers, such as Dr. Sanchez, have discovered that the application of the popular psychoactive compound found in cannabis, tetrahydrocannabinol (THC), has the potential to induce apoptosis in carcinogenic cells; in other words, THC kills cancer cells. This treatment significantly differs from other cancer treatments, such as chemotheraphy, because THC is able to distinguish between healthy and unhealthy cells, whereas chemotherapeutic agents cannot, resulting in a myriad of undesirable and deleterious side effects.

According to Dr. Sanchez, "One of the advantages of cannabinoids, or cannabinoid based medicines, would be that they target a specifically, tumor cells. They don’t have any toxic effect on normal, non-tumoral cells. This is an advantage with respect to standard chemotherapy that target basically everything."

Sanchez has further revealed that the cancer-killing effect of THC is potentiated by the presence of cannabidiol (CBD), a very potent antioxidant that protects the brain from stress and oxidative damage. These synergistic effects of both THC and CBD could make for a very safe and effective cancer concoction.

Sanchez states, "I cannot understand why in the states cannabis is under schedule I, because it is pretty obvious not only from our work but from work from many other researchers that the plant has very wide therapeutic potential."

The human body responds to the cannabinoids found in cannabis because it also makes its own endogenous cannabinoids. These endocannabinoids, which are lipid-based retrograde neurotransmitters that bind to cannabinoid receptors and proteins that are expressed throughout the mammalian central and peripheral nervous system, have been observed to mediate homeostasis via a variety of physiological and cognitive processes. This endocannabinoid system, named after the plant that led to its discovery, is a biological system of the body has many important regulatory functions affecting fertility, pregnancy, reproduction, appetite, pain-sensation, mood, locomotor behavior, exercise-induced euphoria, and memory.

The endogenous cannabinoid system is perhaps the most important physiologic system involved in establishing and maintaining human health. Endocannabinoids and their receptors are found throughout the body: in the brain, organs, connective tissues, glands, and immune cells. In each tissue, the cannabinoid system performs different tasks, but the goal is always the same: homeostasis, the maintenance of a stable internal environment despite fluctuations in the external environment.

A growing body of evidence continues to validate the miraculous healing capabilities of cannabinoids. Supporting the cultivation of cannabis and continued scientific research will lead to more availability of various cannabis strains specifically designed to have high doses and specific ratios of certain cannabinoids to serve as a safe and effective therapeutic treatment for a variety of disorders and diseases. The use of medical marijuana and cannabis-derived medicines in the treatment of diseases such as cancer, epilepsy, chronic pain, diabetes, multiple sclerosis, insomnia, depression, etc., will continue to grow. Cannabis may yet become one of the most useful natural remedies to some of the most crippling diseases of mankind.

Physiologically, fasting:

• Stabilizes blood sugar
• Reduces insulin levels and improves insulin resistance
• Recovers and regenerates the gastrointestinal and immune system
• Increases ketone production
• Increases metabolic rate
• Removes damaged cells
• Reduces hunger
• Reduces excess body fat
• Reduces level of hormones thought to promote cancer
• Reduces the rate of aging
• Sheds excess body fat
• Protects brain function

The only other strategy that has so many research-baked benefits for longevity is long-term calorie restriction, which requires a significant long-term reduction in the amount of food you eat so that you are essentially living on the brink of starvation. Compliance with calorie-restricted diets is abysmal. Fortunately, there are many ways to fast, and there is likely a form of fasting out there that you will be able to tolerate and incorporate into your life. It's important for you to remember that fasting can provide nearly identical benefits without the pain, suffering, and compliance challenges of calorie restriction.

Instead of regulating how much food you eat, as with long-term calorie restriction, you only need to modify when you eat - and of course wisely choose the foods you do eat.Simply cycling between periods of eating and fasting on a daily, weekly, or monthly schedule has been shown to provide many of the same benefits as long-term calorie restriction. Choosing when to eat and when to fast in this way is known as "intermittent fasting."

Intermittent fasting is rapidly growing in popularity for the simple reason that it works. It does so whether you're trying to loss excess body fat or improve biofeedback for optimal health. As a general rule, intermittent fasting involves cutting calories, in whole or in part, either a couple of days a month or a week, every other day, or even daily.
 
There are many ways to fast, from consuming nothing but water for two to three days each month to eating a normal amount of calories every day but during a restricted window of time so you still get a good long stretch without food intake during each 24-hour period.

Here's a brief overview of a couple of different options:

2- to 3-Day Water Fast
It is generally not recommended to go without food for any period longer than about 18 hours. However, if you are overweight and have serious health challenges, a medically supervised water fast may be appropriate.

A water fast consists of consuming nothing but water and some minerals for a finite period of time. This type of fast can give you a shorter transition into fat burning because the body will rapidly burn through glycogen stores and begin using fat for energy.

This fast may be appropriate if you have just received a very serious diagnosis, such as brain cancer. Although if you are limited by any of the following conditions, consult with your health care practitioner before embarking of this type of fast:

• Already underweight
• Nutritionally compromised
• Taking diuretics or blood pressure medications
• Have low blood pressure
• Have diabetes, thyroid disease, chronically low sodium levels, or cardiovascular disease

5-Day Fast
This fast consists of spending five consecutive days of each month on a modified fast. You do not abstain from food entirely during these days. On the first day, you eat about 1,000 to 1,100 calories, followed by 725 calories on the remaining four days. As with all fasting options, the foods you do eat should be low in net carbohydrates and protein, and high in healthy fats.

Researchers have observed when people who have fasted five consecutive days once a month for three consecutive months saw improvements in biomarkers for cell regeneration. Risk factors for diabetes, cancer, cardiovascular disease., and aging also declined (Brandhorst et al., 2015).

Beware that is can be quite challenging to go for a full five days with very little food, especially if you've never fasted before, so you may want to work your way up slowly to this type of fast. Remember, "low and slow."

1-Day Fast
With this fast, you skip eating for one day of every week, consuming only water on that day. Your fast should be broken with a regular-sized meal, and you can maintain your regular exercise program without any special diet recommendations for workout days.

Fasting for 24 hours can be rough for some people, but eating a high-fat low-carb diet can make a 24-hour fast easier, as a higher fat diet will tend to normalize your hunger hormones and provide improved satiety for longer periods of time. You can also fast from dinner to dinner, skipping a full 24 hours of eating while still eating each day.

Alternate-Day Fasting
This program consists of eating on one day, and not eating on the next. During fasting days you restrict your eating to one meal of about 500 calories. On nonfasting days, you can eat normally.

When you include sleeping time, your fast can end up being as long as 32 to 26 hours. According to Krista Varady, Ph.D., author of The Every-Other-Day Diet, alternate-day fasting can help you lose up to two pounds of body fat per week.

Another benefit to alternate-day fasting is that your body tends to adapt to the regularity of the program. In clinical trials, about 90% of participants were able to stick to alternate-day fasting, whereas the other 10% dropped out within the first two weeks.

Peak Fasting
This form of fasting is by far the easiest to maintain once your body has shifted over from burning sugar to burning fat as its primary fuel, and it also appears to support steady circadian rhythms.

Peak Fasting is done every day rather than a few days per week or month. However, you can certainly cycle in off days to suit your schedule or social commitments - this flexibility is another major benefit of Peak Fasting. If circumstances allow, it is recommended implementing this type of fasting about five days a week. The process is quite simple.

The crux of Peak Fasting is to restrict your eating each day to a 6- to 11-hour window. As a result you will avoid eating for 13 to 18 hours every day. The simplest way to implement this type of fasting is to stop eating at least three hours before bed and then delay your first meal of the following day until at least 13 hours have passed since you last ate.

This may seem like an awfully long time to go without eating on a daily basis, but once you have transitioned to burning fat as your primary fuel, you won't experience those frequent hunger pains. Another benefit of Peak Fasting is that you will be able to go hours without a dip in energy because fat provides a continuous source of fuel. This is in contrast to glucose, which triggers glucose/insulin spikes, frequent hunger pains, and energy crashes as cues to consume more high-carb foods.

Regardless of the fasting program you choose, or even if you choose not to adapt any formal type of fasting, you should stop eating at least three hours before you go to bed. This simple change can help optimize your mitochondrial function and prevent cellular damage. Many factors influence why you will reap health benefits if you develop the habit of not eating within three hours of bedtime:

• When you are sleeping, your energy needs are at their lowest, and providing excess fuel at this time will result in the production of excessive amounts of damaging free radicals.
• Sleep is your body's time for detox and repair, and needing to digest a meal during sleep will impair these important processes.
• Nighttime is a common time for your body to use ketones for energy, since glycogen stores are typically depleted within 18 hours (13 hours if you are eating low quantities of carbohydrates), and eating too close to bedtime can replenish glycogen stores and prevent the body from burning fat for overnight fuel.
• Not eating for at least three hours before bed enables you to extend that period of time without eating food on a daily basis.

A compilation of scientific literature published in 2011 provides much of the experimental work supporting the advice from eating too close to bedtime. The message is clear: since the body uses the least amount of calories when sleeping, eating close to bedtime adds excess fuel which will generative excessive free radicals that will damage the tissues, accelerate aging, and contribute to chronic disease (Pamplona, 2011).

Although intermittent fasting, particularly Peak Fasting, is a powerful way to improve your physiological function all the way down to the mitochondrial level, it is not for everyone. Individuals taking medications, especially those with diabetes, need medical supervision; otherwise there is a risk of hypoglycemia.

If you have serious adrenal challenges or chronic renal disease, are living with chronic stress (adrenal fatigue), or have cortisol dysregulation, you would likely need to resolve these issues before implementing intermittent fasting. Also, if you have a disease called porphyria, you should not fast.

If you goal is to build large muscles or engage in competitive sports such as sprinting that require glucose for anaerobic fast twitch muscle fibers, intermittent fasting is not likely to be your best strategy.

Pregnant women and nursing mothers should not practice intermittent fasting, as the baby needs a wider range of nutrients during and after birth.

Children under 18 should also not fast for extended periods. Moreover, anyone of any age with concerns of malnutrition, or who is underweight (with a BMI less than 18.5), or who has an eating disorder such as anorexia nervosa should avoid fasting.

When implementing intermittent fasting, keep your eye on any signs of hypoglycemia, or low blood sugar, which include:

• Light-headedness
  
• Shakiness
  
• Confusion
  
• Fainting
  
• Excessive sweating
  
• Blurred vision
  
• Slurred speech
  
• Feelings of an atypical heartbeat
  
• Pins and needles sensation (neuropathy) in the fingertips
  

If you suspect that your blood sugar is low, make sure to eat something that will not impact your blood glucose levels, such as foods with a lower glycemic index quantity, including coconut oil in black coffee or tea.

The most challenging part of any intermittent fasting plan is getting through the initial transition, which can take anywhere from a week to two months. In some people this transition may take even longer, depending on how insulin resistant they are and other factors such as weight, blood pressure, and how consistent they are with their fasting regimen.

Roughly 10% of people report headaches as a side effect when they first begin fasting, but the biggest complaint is hunger. This is why it is so important to remain hydrated, especially while adding extra magnesium. It may be helpful to remember that one reason you're craving food is because your body has not yet made the switch from burning sugar to burning fat as its primary fuel. As long as you're running on sugar, frequent hunger pains will be the norm. Fat is far more satisfying, as it's a much slower-burning fuel.

Another factor that can cause disruption during the transition period is purely psychological. If you're used to grazing in the evenings, it may take some time to break the habit. One trick is to make it easier to go longer periods of time without eating is to drink more water. Oftentimes people mistake thirst for hunger.

It typically takes a few days to work up to 13 hours of fasting, but once you start activating your fat-burning system you will easily achieve this. The most effective way is to keep to your fat-burning plan by limiting your net carbs to under 40 grams per day and not exceeding more than 1 gram of protein per kilogram of lean body mass.

More than 2000 references on the biological responses to radio frequency (RF) and microwave radiation, published up to June 1971, have been well-documented by the U.S. Naval Medical Research Institute. Devices that emit RF and microwave radiation include, but is not limited to, cellphones, two-way radios, Wi-Fi routers, cellphone towers, smart watches, bluetooth devices, Smart meters, cordless cell phone base stations, wireless baby monitors, microwave ovens, and any WiFi-connected smart devices that receives and transmits data. Particular attention has been paid to the effects on man of non-ionizing radiation at these frequencies.

Reported Biological Phenomena (*Effects') and Some Clinical Manifestations Attributed to Microwave and Radio-Frequency Radiation

A. Heating of Organs*
(Applications: Diathermy, Electrosurgery, Electro-coagulation, Electrodesiccation, Electrotomy)

1. Whole Body (temperature regulation defects), Hyperpyrexia
2. Skin
3. Bone and Bone marrow
4. (a) Lens of Lye (cataractous lesions - due to the avascular nature of the lens which prevents adequate heat dissipation (b) Corneal damage also possible at extremely high frequencies
5. Cenitalia (tubular degeneration of testicles)
6. Brain
7. Sinuses
8. Metal Implants (burns near hip pins, etc.)

The effects are generally reversible except for 4a.

B.  Changes in physiologic function

1. Striated Muscle Contraction
2. Alteration of Diameter of Blood Vessels (increased Vascular elasticity, Dilation
3. Changes in Oxidative Processes in Tissues and Organs
4. Liver Enlargement
5. Altered Sensitivity to Drug Stimuli
6. Decreased Spermatogenesis (decreased fertility, to sterility)
7. Altered Sex Ratio of Births (more girls!)
8. Altered Menstrual Activity
9. Altered Fetal Development
10. Increased Lactation in Nursing Mothers
11. Reduction in Piuresis (Na+ excretion, via urine output)
12. Altered Renal function (decreased filtration in tubules)
13. Changes in Conditioned Reflexes
14. Increased Electrical Resistance of Skin
15. Changes in the Structure of Skin receptors of the (a) Digestive, and  (b) Blood Carrying Systems
16. Altered BIood Flow Rate
17. Alterations In the Biocurrents (EEG?) of the Cerebral Cortex (in animals)
18. Changes In the Rate of Clearance of Tagged Ions from Tissue
19. Reversible Structural Changes In the Cerebral Cortex and the Diencephalon
20. Electrocardiographic (EKG) Changes
21. Alterations In Sensitivity to Light, Sound, and Olfactory Stimuli
22. Functional (a) and Pathological (b) Changes in the Eyes: (a) decrease in size of blind spot, altered color recognition, changes in intraocular pressure, lacrimation, trembling of eye-lids; (b) less opacity and coagulation, altered tissue respiration, and altered reduction-oxidation processes
23. Myocardial Necrosis
24. Hemorrhage in Lungs, Liver, Gut, and Brain (At Fatal Levels of Radiation)
25. Generalized Degeneration of all Body Tissue of Radiation (At Fatal Levels of Radiation)
26. Loss of Anatomical Parts
27. Death
28. Dehydration
29. Altered Rate of Calcification of Certain Tissue

C.  Central Nervous System Effects

1. Headaches
2. Insomnia
3. Restlessness (Awake and During Sleep)
4. Electroencephalographic (EEG) Changes
5. Cranial Nerve Disorders
6. Pyramidal Tract Lesions
7. Conditioned Reflex Disorders
8. Vagomimetic Action of the Heart; Sympaticomimetic Action
9. Seizures, Convulsions

D.  Autonomic Nervous System Effects

1. Degenerative Disorders (e.g., alteration of heart rhythm)
2. Fatigue
3. Structural Alterations in the Synapses of the Vagus Nerve
4. Stimulation of Parasympathetic Nervous System (Bradycardia), and Inhibition of  the Sympathetic Nervous System

E.  Peripheral Nervous System Effects

1. Effects on Locomotor Nerves

F. Psychological Disorders ("Human Behavioral Studies") - the so-called "Psychophysiologic (and Psychosomatic) Responses"

1. Neurasthenia - (general "bad" feeling)
2. Depression
3. Impotence
4. Anxiety
5. Lack of Concentration
6. Hypochondria
7. Dizziness
8. Hallucinations
9. Sleepiness
10. Insomnia
11. Increased Irritability
12. Decreased Appetite
13. Loss of Memory
14. Scalp Sensations
15. Increased Fatigability
16. Chest pain
17. Tremor of the hand

G. Behavioral Changes (Animal)

1. Reflexive, Operant, Avoidance, and Discrimination Behaviors

H. Blood Disorders
changes in:

1. Blood and Bone Marrow
2. Phagocytic (polymorphs) and Bactericidal Functions
3. Hemolysis Rate (increase), (a shortened lifespan of cells)
4. Sedimentation Rate (increase), due to changes in serum concentration levels or amount of fibrinogen. (?))
5. Number of Erythrocytes (decrease), also number of lymphocytes
6. Blood Glucose Concentration (increase)
7. Blood Histamine Content
8. Cholesterol and Lipids
9. Gamma (also alpha and beta) Globulin, and Total Protein Concetration
10. Number of Eosinophils
11. Albumin/Globulin Ratio (decrease)
12. Hemopoiesis (rate of formation of blood corpuscles)
13. Leukopenia (increase in number of white cells), and Leukocytosis
14. Reticulocytosis

I. Vascular Disorders

1. Thrombosis
2. Hypertension

J. Enzyme and Other Biochemical Changes
Changes in activity of:

1. Cholinesterase
2. Phosphatase
3. Transaminase
4. Amylase
5. Carboxydismutase
6. Protein Denaturation
7. Toxin, Fungus, and Virus Inactivation (at high radiation dose levels), Bacteriostatic  Effect
8. Tissue Cultures Killed
9. Alteration In Rate of Cell Division
10. Increased Concentration of RNA in Lymphocytes, and Decreased Concentration in  Brain.  Liver,  and  Spleen
11. Changes in Pyruvic Acid, Lactic Acid, and Creatinine Excretions
12. Change in Concentration of Glycogen in Liver (Hlyperglycemia)
13. Alteration in Concentration of 17- Ketosteroids in Urine

K. Metabolic Disorders

1. Glycosuria (sugar in urine; related with blood sugar?)
2. Increase in Urinary Phenol (derivatives? DOPA?)
3. Alteration of rate of metabolic Enzymatic Processes
4. Altered Carbohydrate Metabolism

L. Gastro-Intestinal Disorders

1. Anorexia (loss of appetite)
2. Epigastric Pain
3. Constipation
4. Altered Secretion of Stomach "Digestive Juices"

M. Endocrine  Gland  Changes

1. Altered Pituitary Function
2. Hyperthyroidism
3. Thyroid Enlargement
4. Increased Uptake of Radioactive Iodine by Thyroid Gland
5. Altered Adrenal Cortex Activity
6. Decreased Corticosteroids in Blood
7. Decreased Glucocorticoidal Activity
8. Hypogonadism (usually decreased testosterone production)

N. Histological Changes

1. Changes in Tubular Epithelium of Testicles
2. Gross Changes

O. Genetic and Chromosomal Changes

1. Chromosome Aberrations (e.g., linear shortening, pseudochiasm, diploid structures, amitotic division, bridging, "sticky" chromosomes, irregularities in chromosomal envelope)
2. Mutations
3. Mongolism
4. Somatic Alterations (changes in cell not involving nucleus or chromosomes, cellular transformation)
5. Neoplastic Diseases (e.g*, tumors)

P. Pearl Chain Effect (Intracellular orientation of subcellular particles, and orientation of cellular and other (non-biologic) particles) Also, orientation of animals, birds, and fish in electromagnetic fields

Q. Miscellaneous Effects

1. Sparking between dental fillings
2. Peculiar metallic taste in mouth
3. Changes in Optical Activity of Colloidal Solutions
4. Treatment for Syphilis, Poliomyelitis, Skin Diseases
5. Loss of Hair
6. Brittleness of Hair
7. Sensations of Buzzing Vibrations, Pulsations, and Tickling About the Head and Ears
8. Copious Perspiration, Salivation, and Protrusion of Tongue
9. Changes in the Operation of Implanted Cardiac Pacemakers
10. Changes in Circadian Rhythms

Glaser, Z. (1971). Bibliography of reported biological phenomena ('effects') and clinical manifestations attributed to microwave and radio-frequency radiation. Navel Medical Research Institute. https://archive.org/details/DTIC_AD0750271/mode/2up?view=theater​

In 1965, researchers conducted an experiment on rats exploring the health effects of sugar and fat. The rats were divided into two groups: one group of rats was a fed diet containing 75% fat and no sugar, while the other group was fed a diet containing 15% fat and 60% sucrose. The results of this experiment led the researchers to believe that rats fed sucrose, a simple carbohydrate, developed thiamine deficiency, often leading to cardiovascular disease, while more complex carbohydrates helped create gut bacteria that synthesized thiamine (Nutritional Reviews, 1965). Based on internal documents, the Sugar Research Foundation (SRF) has discounted evidence linking sucrose consumption to cardiovascular disease.

This research prompted funding, among the SRF, to understand the relationship between sugar and any metabolic effects related to chronic disease beyond its caloric effects. The foundation (which has organizational ties to the Sugar Association, the International Sugar Research Foundation [ISRF], and ISRF's successor, and the World Sugar Research Organization) led a group of researchers, referred to as Project 259, to study the effect of sugar on gut bacteria in 1967. The researchers observed a positive association between rodent sugar-rich diets and triglyceride levels, which contributed to higher urinary concentrations of beta-glucoronidase, a well-established  marker of bladder cancer (Paigen, Peterson and Paigen, 2017). Albeit, the Sugar Association has consistently denied that sucrose has any metabolic effects related to chronic disease.

In 2016, the Sugar Association issued a press release criticizing findings from a study published in Cancer Research using multiple mouse models that suggested that dietary sugar induces increased tumor growth and metastasis when compared to a nonsugar starch diet. The Sugar Association stated that no credible link between ingested sugars and cancer has been established. In contrast, evidence suggests that that the sugar industry terminated funding of an animal study that was finding unfavorable results with respect to the association between dietary sugars and cancer, with possible translational importance to humans (Sugar Association, 2016).

Researchers have discovered internal documents that suggest the sugar industry muffled research indicating a significant relationship between sugar and adverse health effects including, heart disease and cancer (Kearns, Apollonio & Glantz, 2017). And this isn't the first time the sugar industry has been caught in the act. Researchers uncovered evidence suggesting the sugar industry systematically misrepresented research linking sugar to cancer, obesity, and heart disease (Kearns, Schmidt and Glantz, 2016).

In response to the study, the sugar industry released a statement, saying: “The article we are discussing is not actually a study, but a perspective: a collection of speculations and assumptions about events that happened nearly five decades ago, conducted by a group of researchers and funded by individuals and organizations that are known critics of the sugar industry” (Foley, 2017).

Ideally, you want your plate to look like a mosaic, painted with various colors from different foods. Create a rainbow of colors on your plate, with fruits and vegetables. Eating a variety of different foods offer more nutrients.

In this powerful TED talk, Dr. William Li discusses the powerful synergistic effects of combining food.

According to the National Cancer Institute, the rate of new melanoma cases among American adults has tripled since the 1970s, from 7.9 per 100,000 people in 1975 to 25.2 per 100,000 in 2014 (National Cancer Institute, 2017). A similar trend can be observed in regards to melanoma death rate for white American men, the highest risk group, which has escalated sharply, from 2.6 deaths per 100,000 in 1975 to 4.4 in 2014. From 2003 to 2012, the rates of new melanoma cases among both men and women have been increased by 1.7 and 1.4 percent per year (Centers for Disease Control and Prevention, 2016).

While the exact cause of melanoma is unknown, researchers have established that risk factors for melanoma include family history, indoor tanning, the number of moles on a person’s skin, fair skin, freckles, blue or green eyes, blonde or red hair and a history of severe sunburns, among others (Centers for Disease Control and Prevention, 2017). People are able to modify only three of these risk factors: indoor tanning, exposure to UV radiation and severe sunburns.

In December 2012, the Food and Drug Administration began to enforce new laws designed to improve sunscreens and consumer protection. The new laws restrict certain bogus label claims, but they allow most sunscreens to advertise “broad spectrum” skin protection. Sunscreen manufacturers are permitted to tell consumers, that with proper use, their products can help reduce the risk of skin cancer. However, the FDA and the International Agency for Research on Cancer have concluded that the available data does not support the assertion that sunscreens alone reduce the rate of skin cancer (Food and Drug Administration, 2011; IARC 2001).

Recent research by the Center for Disease Control and Prevention found 96% of the U.S. population has oxybenzone in their bodies, a common chemical used in sunscreens; a chemical that is a known endocrine disruptor, linked to reduced sperm count in men and endometriosis in women (Environmental Working Group, 2017).

Researchers have observed that adults who put on sunscreen containing 4% oxybenzone (the US allows up to 6%) in the morning and evening—mimicking what they’d do while on vacation—continued to excrete the chemical in their urine for five days afterwards, suggesting that it was being stored in the body (Gustavsson Gonzalez, Farbrot & Larko, 2002).

Aside from oxybenzone — which is found in 70% of sunscreens — other commonly used chemicals that can enter your bloodstream and can cause toxic side effects, including hormone disruption, include but are not limited to:

Mechanical sunscreens, including zinc oxide and titanium dioxide, have proven over years of use to be safe and effective mechanisms for blocking both UVA and UVB light. According to the Environmental Working Group (EWG) - a non-profit environmental organization that specializes in research and advocacy in the areas of toxic chemicals, agricultural subsidies, public lands, and corporate accountability - sunscreens made with zinc oxide and titanium dioxide are better alternatives because they provide strong sun protection with few health concerns and they don’t break down in the sun. Zinc oxide is EWG’s first choice for sun protection. Most studies to date have shown that zinc oxide and titanium dioxide are safe and unlikely to penetrate your skin when applied topically, as long as they are not nanosized. However, in an attempt to meet the desire of their consumers for products that don't leave a thick film on the skin, some manufacturers have reduced the size of the molecules, creating nanoparticles (microscopic particles measuring less than 100 nanometers).

This nanotechnology has several different effects. Some are concerned that the particles have become so small that they may be absorbed directly into your skin. Although mixed, some studies have found significant negative health effects from the absorption of nanoparticles (European Union Public Health, 2006). While these nanoparticle technologies may make an excellent drug delivery system, it is questionable for use in sunscreen (De Jong & Borm, 2008).

Titanium dioxide is more effective in UVB range and zinc oxide in the UVA range, therefore the combination of these particles assures a broad-band UV protection (Smijs & Pavel, 2011). Zinc oxide is beneficial because it remains stable in heat, but as a nanoparticle, the problems with toxicity probably outweigh the benefits to sun protection. Upon systemic distribution, toxicity of zinc oxide nanoparticles may affect the lungs, liver, kidneys, stomach, pancreas, spleen, heart and brain (Tian et al., 2015). Findings have also demonstrated that aging has a synergistic effect with zinc oxide nanoparticles on systemic inflammation and neurotoxicity, affecting your brain and neurological system. In other words, the older you are, the higher your risk of neurotoxicity from zinc oxide nanoparticle absorption.

Spray-on sunscreens, containing zinc oxide and/or titanium dioxide, pose an additional hazard by releasing these toxic nanoparticles into the air. The FDA has previously expressed concern that inhaling these products may be risky, especially to children, and has warned parents to avoid spray-on sunscreens (Food and Drug Administration, 2006).
While these two minerals are the safest topical sunscreen agents around, inhaling them is a whole different story. When these minerals are inhaled, they have been shown to irritate lung tissues and potentially lead to serious health problems, and the finer the particles, the worse their effects appear to be (Grassian, O’Shaughnessy, Adamcakova-Dodd, Pettibone & Thorne, 2006). The lungs have difficulty clearing small particles, and the particles may pass from the lungs into the bloodstream. Insoluble nanoparticles that penetrate skin or lung tissue can cause extensive organ damage. Some researchers speculate that the toxic effects of nanoparticles relate to their size being in the range of a virus, which may trigger your body's immune response (Buzea, Pacheco Blandino & Robbie, 2007).

The International Agency for Research on Cancer (IARC) has classified titanium dioxide as a "possible carcinogen" when inhaled in high doses. According to IARC:

"Titanium dioxide causes varying degrees of inflammation and associated pulmonary effects including lung epithelial cell injury, cholesterol granulomas and fibrosis. Rodents experience stronger pulmonary effects after exposure to ultrafine titanium dioxide particles compared with fine particles on a mass basis (IARC, 2006).

The use of nanoparticles in cosmetics poses a regulatory challenge because the properties of nanoparticles may vary tremendously, depending on their size, shape, surface area and coatings. A number of manufacturers sell products advertised as containing “non-nano” zinc oxide and titanium dioxide - these claims are generally misleading. While particle sizes vary among manufacturers, nearly all would be considered nanomaterials under a broad definition of the term, including the definition proposed in 2011 by the Food and Drug Administration (Food and Drug Administration, 2011b). According to the available information, these mineral sunscreens must be delivered in nanoparticle form to render a layer that is reasonably transparent on the skin.

According to EWG, even with the existing uncertainties, zinc oxide and titanium dioxide lotions are among the best choices on the American market. Here’s why:

• The shape and size of the particles affect sun protection.

The smaller they are, the better the SPF protection and the worse the UVA protection. Manufacturers must then find a balance: small particles provide greater transparency but larger particles offer greater UVA protection. The form of zinc oxide most often used in sunscreens is larger and provides greater UVA protection than the titanium dioxide products that appear clear on the skin.

• Nanoparticles in sunscreen may not penetrate the skin.

Some studies indicate that nanoparticles can harm living cells and organs when administered in large doses. But a large number of studies have produced no evidence that zinc oxide nanoparticles can cross the skin in significant amounts. Researchers found that less than 0.01 percent of either form of zinc entered the bloodstream. The study could not determine if the zinc in the bloodstream was insoluble nanoparticles, therefore the European regulators concluded it was most likely zinc ions, which would not pose any health risk (Scientific Committee on Consumer Safety, 2012). However, more research should be conducted to reach definitive conclusions.

• It is unlikely that nanoparticles in sunscreen cause skin damage when energized by sunlight.

Titanium dioxide, and to a lesser extent zinc oxide, are photocatalysts, meaning that when they are exposed to UV radiation they can form free radicals that damage surrounding cells. Nanoparticle sizes of these minerals are more affected by UV rays than larger particles. Sunscreen manufacturers commonly employ surface coatings that can dramatically reduce the potential for photoactivity, with data suggesting that they reduce UV reactivity by as much as 99% (SCCNFP..., 2000). In sunscreens, problems may arise if particles are not treated with inert coatings, if the coatings are not stable, or if manufacturers use forms of zinc oxide or titanium dioxide that are not optimized for stability and sun protection. However, tests of living skin from human volunteers and animal testing suggest that these hazards are not a concern for human safety because the free radicals that are generated by nanoparticles on skin are quenched by the skin’s own antioxidant protections (Popov et al., 2009).

Currently, all available evidence suggests that zinc oxide and titanium dioxide can be safely used in sunscreen lotions applied to healthy skin and pose a lower hazard than most other approved sunscreen ingredients.

More human studies need to be conducted in regards to the health effects of inhaling of zinc oxide particles, especially at lower levels, such as from brief exposure to sunscreen spray. However, using these spray-on products are clearly an unnecessary risk since safer options are readily available. Your safest bet is to use topical zinc oxide or titanium dioxide that does not contain nanosized particles.

In theory, applying sunscreen with a sun protection factor (SPF) of 100 would allow sunbathers to be exposed to the sun 100 times longer before suffering a sunburn. For example, an individual who would normally redden after 30 minutes in the afternoon sun could theoretically stay out for 50 hours.

But for high-SPF sunscreens, theory and reality are two different things. Researchers have observed that people are misled by the claims on high-SPF sunscreen bottles. They are more likely to use high-SPF products improperly and as a result may expose themselves to more harmful ultraviolet radiation than people relying on products with lower SPF values. The FDA has long contended that SPF higher than 50 is “inherently misleading” (Food and Drug Administration, 2007).

Here are some reasons against applying sunscreens with SPF values greater than 50:

• Marginally better sunburn protection.

Sunbathers often assume that they get twice as much protection from SPF 100 sunscreen as from SPF 50. In reality, the extra protection is negligible. Properly applied SPF 50 sunscreen blocks 98% of UVB rays, while SPF 100 blocks 99%. When used correctly, sunscreen with SPF values in the range of 30 to 50 will offer adequate sunburn protection, even for people most sensitive to sunburn.

• Consumers misuse high-SPF products.

High-SPF products tend to deceive users into staying in the sun longer and overexposing themselves to both UVA and UVB rays. Saturated with a false sense of security, people extend their time in the sun well past the point when users of low-SPF products would head indoors. As a result, they get as many UVB-inflicted sunburns as unprotected sunbathers and are likely to absorb more damaging UVA radiation.

Researchers have conducted numerous studies on sunbathers and have observed that high-SPF products spur “profound changes in sun behavior” that may account for the increased melanoma risk found in some studies. The researchers confirmed that European vacationers spent more total time in the sun if they were given an SPF 30 sunscreen instead of an SPF 10 product (Autier et al., 2000). It is assumed the difference would also apply to products with SPF values greater than 50.

Here are some helpful tips to help protect yourself from the sun's harmful UV rays:

Your safest and best choice for sunscreen protection is zinc oxide. However, avoid nanoparticles, which are common in spray sunscreens, to circumvent potential toxicity. Unfortunately, it can be challenging to find a product without other chemical additives. To help you choose the safest product, EWG performs an annual sunscreen evaluation based on effectiveness and safety.

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Autier, P., Doré, J.-F., Reis, A. C., Grivegnée, A., Ollivaud, L., Truchetet, F., … Césarini, J.-P. (2000). Sunscreen use and intentional exposure to ultraviolet A and B radiation: a double blind randomized trial using personal dosimeters. British Journal of Cancer, 83(9), 1243–1248. http://doi.org/10.1054/bjoc.2000.1429

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Centers for Disease Control and Prevention. (2017). What Are the Risk Factors for Skin Cancer?. Cdc.gov. Retrieved 3 August 2017, from https://www.cdc.gov/cancer/skin/basic_info/risk_factors.htm

Centers for Disease Control and Prevention. (2016). Skin Cancer Trends. (2017). Cdc.gov. Retrieved 3 August 2017, from https://www.cdc.gov/cancer/skin/statistics/trends.htm

De Jong, W. H., & Borm, P. J. (2008). Drug delivery and nanoparticles: Applications and hazards. International Journal of Nanomedicine, 3(2), 133–149.

Environmental Working Group. (2017). EWG's 2017 Guide to Safer Sunscreens. Ewg.org. Retrieved 3 August 2017, from http://www.ewg.org/sunscreen/report/the-trouble-with-sunscreen-chemicals/#.WYKSS4UnHPp

European Union Public Health. (2006). What are potential harmful effects of nanoparticles?. Ec.europa.eu. Retrieved 3 August 2017, from http://ec.europa.eu/health/scientific_committees/opinions_layman/en/nanotechnologies/l-3/6-health-effects-nanoparticles.htm

Food and Drug Administration. (2011). Labeling and Effectiveness Testing: Sunscreen Drug Products for Over-the-Counter Human Use. Regulations.gov. Retrieved 3 August 2017, from https://www.regulations.gov/document?D=FDA-1978-N-0018-0698

Food and Drug Administration. (2011b). FDA Draft, Not for Implementation: Guidance for Industry. Enforcement Policy – OTC Sunscreen Drug Products Marketed Without an Approved Application. Available at www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/UCM259001.pdf

Food and Drug Administration. (2006). PETITION REQUESTING FDA AMEND ITS REGULATIONS FOR PRODUCTS COMPOSED OF ENGINEERED NANOPARTICLES GENERALLY AND SUNSCREEN DRUG PRODUCTS COMPOSED OF ENGINEERED NANOPARTICLES SPECIFICALLY. FDA.gov. Retrieved 3 August 2017, from https://www.fda.gov/ohrms/dockets/dockets/06p0210/06p-0210-cp00001-01-vol1.pdf

Food and Drug Administration. (2007). Sunscreen Drug Products for Over-the-Counter Human Use; Proposed Amendment of Final Monograph; Proposed Rule - FR Doc 07-4131. (2017). Fda.gov. Retrieved 3 August 2017, from https://www.fda.gov/OHRMS/DOCKETS/98fr/07-4131.htm

Grassian, V., O’Shaughnessy, P., Adamcakova-Dodd, A., Pettibone, J., & Thorne, P. (2006). Inhalation Exposure Study of Titanium Dioxide Nanoparticles with a Primary Particle Size of 2 to 5 nm. Environmental Health Perspectives, 115(3), 397-402. http://dx.doi.org/10.1289/ehp.9469

Gustavsson Gonzalez, H., Farbrot, A., & Larko, O. (2002). Percutaneous absorption of benzophenone-3, a common component of topical sunscreens. Clinical And Experimental Dermatology, 27(8), 691-694. http://dx.doi.org/10.1046/j.1365-2230.2002.01095.x

International Agency for Research on Cancer (IARC). (2006). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. IARC.fr. Retrieved 3 August 2017, from https://monographs.iarc.fr/ENG/Monographs/vol93/mono93.pdf

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Groups of cells, collectively known as tumor microenvironment of metastasis (TMEM), can serve as gateways for tumor cells entering the blood vessels. The researchers observed that several types of chemotherapy can increase the amounts of TMEM complexes and circulating tumor cells in the bloodstream (Karagiannis et al., 2017).

Dr. Karagiannis, the lead author of the study, found the number of doorways was increased in 20 patients receiving two common chemotherapy drugs. It should be noted such a small sample size constitutes a major limitation of this study, the results and implications of this research are very significant.

While prevention is by far the best cure for chronic disease, not everyone has this luxury. A number of modifiable risk factors are responsible for many premature or preventable diseases and deaths. Modifiable risk factors fall into three main groups (Danaei et al., 2011):

• Lifestyle risk factors, such as tobacco smoking, physical activity, and alcohol use.
• Dietary risk factors, such as a high salt intake or a low intake of fruits and vegetables.
• Metabolic risk factors, such having high blood pressure or blood cholesterol and being overweight or obese.

In regards to dietary interventions, numerous studies have substantiated the chemopreventative effect of increasing cruciferous vegetable intake against cancer. As a chemoprevention agent, sulforaphane, the active molecule in cruciferous vegetables, possesses many advantages, such as high bioavailability and low toxicity (Li et al., 2010).

Increasing the consumption of cruciferous vegetables is only one of the many preventive measures that can be taken when taking control of your health. Remember, the health of your environment reflects the health of your body; you are the product of your environment.