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.

Nearly 75% of US adults are overweight or obese, and 40% have pre-diabetes or diabetes. This widespread issue has led to increased interest in medications like Ozempic (Semaglutide), a GLP-1 (glucagon-like peptide-1) receptor agonist.

Ozempic mimics the hormone GLP-1, which regulates blood sugar by stimulating insulin secretion and inhibiting glucagon release. It also slows digestion, increasing feelings of fullness and reducing caloric intake. This dual action helps improve glycemic control and can aid in weight loss. Efficacy varies among individuals; about 20% of users may not lose weight or may even gain weight. This is likely due to the fact that while for many people Ozempic reduces appetite, for some individuals Ozempic may lead to blood sugar that is too low, a condition known as hypoglycemia, which can increase cravings for carbohydrates and sugar.​

Ozempic has shown significant benefits for many, but it is not without risks. Known side effects include kidney damage, gastroparesis, gallbladder issues, muscle loss, nutrient deficiencies, thyroid cancer, and mental health concerns, including depression and increased suicidal ideation. Importantly, Ozempic is FDA-approved only for Type 2 Diabetes, not for weight loss.

​When discontinuing Ozempic, rapid weight gain, often termed "Ozempic rebound," is common. Studies show that within a year of stopping, two-thirds of users regain the lost weight, often ending up with a higher body fat percentage due to muscle loss (leads to lowered metabolic rate), poor dietary and lifestyle factors, and metabolic inhibition due to calorie restriction. ​

"With...[GLP-1]...treatments, there is a concomitant reduction in lean body mass, which seems to be in the range of 25%–40% of total weight loss." In other words, studies show that upwards of 40% of the weight lost on Ozempic isn’t the fat you’re hoping to bid adieu to – it’s muscle!

Additional Risks of Ozempic

• Pancreatitis (inflammation of pancreas): 9.09 times higher risk.
• Bowel Obstruction: 4.22 times higher risk.
• Gastroparesis (stomach paralysis): 3.67 times higher risk.
• Adipogenesis: Recent studies suggest that GLP-1 agonists can increase adipogenesis, the creation of new fat cells. While this might seem counterintuitive for weight loss, it emphasizes the importance of combining medication with lifestyle changes.
• Autoimmune Reactions: There have been reports of semaglutide-induced lupus erythematosus, which can involve multiple organs.
  
• Respiratory Risks: Some patients on semaglutide have experienced pulmonary aspiration of gastric contents.
  
• ​Appendicitis Risk: Emerging evidence suggests that GLP-1 receptor agonists, like Ozempic, may increase the risk of appendicitis.
  

Safety trial duration on Ozempic lasted only 30-68 weeks, so safety for use beyond this timeframe has not been evaluated.

For those seeking more advanced methods, peptides can be a powerful tool with fewer side effects than GLP-1 agonists. Some effective peptides include:

1. IGF-1 LR3: Increases muscle by stimulating hyperplasia.
2. Ipamorelin: Enhances muscle growth and suppresses hunger by increasing growth hormone secretion.
3. CJC-1295: Promotes fat loss and muscle protein synthesis by increasing IGF-1 and functioning as a growth hormone-releasing hormone.
4. Tesamorelin: Reduces visceral fat and stimulates muscle protein production.
5. 5-Amino-1MQ: Blocks NNMT, an enzyme linked to obesity, facilitating fat reduction and providing clean energy.

For injectable peptides, I recommend the companies Limitless Life or Peptide Sciences. If you're looking for quality oral peptide formulations, check out LVLUP Health.
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Also, it’s important to understand that the best effects from any of the peptides listed above come via pairing them with a consistent weight training routine, adequate protein intake, and a physically active lifestyle. 
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​While Ozempic has been demonstrated to mitigate blood sugar control and weight management, it's essential to weigh these against potential risks and side effects. Incorporating lifestyle changes and considering natural alternatives can help mitigate these risks and support long-term health. Natural alternatives and peptides can provide effective, safer options for achieving weight loss and muscle gain. Combining these with lifestyle changes is crucial for long-term success. Addressing the root causes of obesity through lifestyle changes is crucial for long-term health. Prioritizing physical activity, a balanced diet, reducing exposure to toxins, managing stress, and ensuring adequate sleep can significantly impact overall well-being and weight management.

Wadden, Thomas A. et al. “The Role of Lifestyle Modification with Second-Generation Anti-obesity Medications: Comparisons, Questions, and Clinical Opportunities.” Current Obesity Reports 12 (2023): 453 - 473. https://doi.org/10.1007/s13679-023-00534-z.
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Castellanos, Vanessa, et al. “Semaglutide-Induced Lupus Erythematosus with Multiorgan Involvement.” Cureus, vol. 16, no. 3, 1 Mar. 2024, p. e55324, pubmed.ncbi.nlm.nih.gov/38559525/, https://doi.org/10.7759/cureus.55324. 

Billings, Sabrina A., et al. “Rhabdomyolysis Associated with Semaglutide Therapy: A Case Report.” Cureus, vol. 15, no. 12, 1 Dec. 2023, p. e50227, pubmed.ncbi.nlm.nih.gov/38192938/, https://doi.org/10.7759/cureus.50227. 

Li, J, et al. “Case Report: Semaglutide-Associated Depression: A Report of Two Cases.” Frontiers in Psychiatry, vol. 14, 29 Aug. 2023, www.ncbi.nlm.nih.gov/pmc/articles/PMC10495976/#:~:text=At%20present%2C%20most%20reported%20adverse, https://doi.org/10.3389/fpsyt.2023.1238353.

Casella, Sarah, and Katelyn Galli. “Appendicitis: A Hidden Danger of GLP-1 Receptor Agonists?” ˜the œJournal of Pharmacy Technology, vol. 40, no. 2, 7 Dec. 2023, pp. 108–111, https://doi.org/10.1177/87551225231216638. 

Challa, Tenagne Delessa, et al. “Regulation of Adipocyte Formation by GLP-1/GLP-1R Signaling.” Journal of Biological Chemistry, vol. 287, no. 9, Feb. 2012, pp. 6421–6430, https://doi.org/10.1074/jbc.m111.310342. 

Willoughby, Darryn, et al. “Body Composition Changes in Weight Loss: Strategies and Supplementation for Maintaining Lean Body Mass, a Brief Review.” Nutrients, vol. 10, no. 12, 3 Dec. 2018, p. 1876, www.ncbi.nlm.nih.gov/pmc/articles/PMC6315740/, https://doi.org/10.3390/nu10121876.

Wilding, John P. H., et al. “Weight Regain and Cardiometabolic Effects after Withdrawal of Semaglutide: The STEP 1 Trial Extension.” Diabetes, Obesity and Metabolism, vol. 24, no. 8, 19 May 2022, pp. 1553–1564, pubmed.ncbi.nlm.nih.gov/35441470/, https://doi.org/10.1111/dom.14725.

Leehey, David J., et al. “Acute Kidney Injury Associated with Semaglutide.” Kidney Medicine, vol. 3, no. 2, Mar. 2021, pp. 282–285, https://doi.org/10.1016/j.xkme.2020.10.008.

Bezin, Julien, et al. “GLP-1 Receptor Agonists and the Risk of Thyroid Cancer.” Diabetes Care, vol. 46, no. 2, 10 Nov. 2022, https://doi.org/10.2337/dc22-1148.

The potential mechanisms underlying these observations involve several pathways. One hypothesis is related to the interaction of the SARS-CoV-2 spike protein with heparin and heparin-binding proteins in the brain, which are prone to self-assembly, aggregation, and fibrillation. Research suggests that the S1 region of the spike protein binds to these proteins, potentially acting as functional amyloid and forming toxic aggregates. These aggregates could seed the aggregation of misfolded brain proteins, leading to neurodegeneration.

Jee Hoon Roh, et al. “A Potential Association between COVID-19 Vaccination and Development of Alzheimer’s Disease.” QJM, 28 May 2024, https://doi.org/10.1093/qjmed/hcae103. 

Grobbelaar, Lize M, et al. “SARS-CoV-2 Spike Protein S1 Induces Fibrin(Ogen) Resistant to Fibrinolysis: Implications for Microclot Formation in COVID-19.” MedRxiv (Cold Spring Harbor Laboratory), 8 Mar. 2021, https://doi.org/10.1101/2021.03.05.21252960. 

​Idrees, Danish, and Vijay Kumar. “SARS-CoV-2 Spike Protein Interactions with Amyloidogenic Proteins: Potential Clues to Neurodegeneration.” Biochemical and Biophysical Research Communications, vol. 554, May 2021, pp. 94–98, https://doi.org/10.1016/j.bbrc.2021.03.100.

The pervasive issue of prescription drug-related deaths necessitates a reevaluation of current medical practices and regulatory policies. With most of these deaths being preventable, a more cautious approach to prescribing and better awareness of the risks associated with these medications could save countless lives. It is crucial for healthcare providers, regulators, and patients to acknowledge the dangers and work towards safer, more effective treatment strategies.

Every day, millions of people in the U.S. take prescribed drugs in an effort to help them live their lives. As our understanding of medicine has evolved, we’ve developed drugs to aid with some of the most common medical conditions—from pain and blood pressure drugs to asthma medication, thyroid treatments, and antidepressants.

This analysis uses prescribed medicines data from the U.S. Agency for Healthcare Research and Quality, released in 2021 for the 2019 calendar year. It also uses supporting drug and health information from MedlinePlus.

​Top 10 Most Prescribed Drugs in America (2019)

Prevalent Conditions Treated
​Most of the top prescribed drugs are used to treat high blood pressure or symptoms of it. This is significant as 108 million, or nearly half of adults in the U.S., have hypertension or high blood pressure.

Combining the total patients for blood pressure and cholesterol medications covers 33% of the U.S. population. Pain and inflammation medications were the most frequent on the top 30 list, prescribed to 13.6% of people.

A drug’s total number of patients doesn’t necessarily reflect its importance or cost. For example, levothyroxine, the fourth-most prescribed drug by total patients, was the second-most prescribed by total prescriptions with 102.6 million in 2019 at an average cost of $25.10 per prescription.
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More specialized medications like fluticasone had fewer total prescriptions (27.9 million) but a higher average cost of $97.68 per prescription. Prices are influenced by factors like demand, patent status, and healthcare system variations.

The study underscores ongoing concerns about financial conflicts of interest in the medical field. Researchers noted that such payments might influence physician prescribing behavior and potentially undermine patient trust in medical professionals. Despite these concerns, the practice of accepting industry payments remains widespread.

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Gøtzsche PC. Long-term use of antipsychotics and antidepressants is not evidence-based. Int J Risk Saf Med 2020;31:37-42.

Gøtzsche PC. Long-Term Use of Benzodiazepines, Stimulants and Lithium is Not Evidence-Based. Clin Neuropsychiatry 2020;17:281-3.

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Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005;294:1934–43.

FDA package insert for Risperdal (risperidone). Accessed 30 May 2022.

Koponen M, Taipale H, Lavikainen P, et al. Risk of Mortality Associated with Antipsychotic Monotherapy and Polypharmacy Among Community-Dwelling Persons with Alzheimer’s Disease. J Alzheimers Dis 2017;56:107-18.

Whitaker R. Lure of Riches Fuels Testing. Boston Globe 1998; Nov 17.

Whitaker R. Mad in America: Bad science, Bad medicine, and the Enduring Mistreatment of the Mentally Ill. Cambridge: Perseus Books Group; 2002:page 269.

Vanderburg DG, Batzar E, Fogel I, et al. A pooled analysis of suicidality in double-blind, placebo-controlled studies of sertraline in adults. J Clin Psychiatry 2009;70:674-83.

Hengartner MP, Plöderl M. Newer-Generation Antidepressants and Suicide Risk in Randomized Controlled Trials: a Re-Analysis of the FDA Database. Psychother Psychosom 2019;88:247-8.

Hengartner MP, Plöderl M. Reply to the Letter to the Editor: “Newer-Generation Antidepressants and Suicide Risk: Thoughts on Hengartner and Plöderl’s ReAnalysis.” Psychother Psychosom 2019;88:373-4.

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Coupland C, Dhiman P, Morriss R, et al. Antidepressant use and risk of adverse outcomes in older people: population based cohort study. BMJ 2011;343:d4551.

Smoller JW, Allison M, Cochrane BB, et al. Antidepressant use and risk of incident cardiovascular morbidity and mortality among postmenopausal women in the Women’s Health Initiative study. Arch Intern Med 2009;169:2128-39.

O’Neill A. Age distribution in the United States from 2012 to 2022. Statista 2024;Jan 25.

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​Brody DJ, Gu Q. Antidepressant Use Among Adults: United States, 2015-2018. CDC 2020; Sept. 

Centers for Disease Control and Prevention. Leading Causes of Death. 2024; Jan 17.

Drug Overdose Deaths. Centers for Disease Control and Prevention 2023; Aug 22. 

Davis JS, Lee HY, Kim J, et al. Use of non-steroidal anti-inflammatory drugs in US adults: changes over time and by demographic. Open Heart 2017;4:e000550.

Conaghan PG. A turbulent decade for NSAIDs: update on current concepts of classification, epidemiology, comparative efficacy, and toxicity. Rheumatol Int 2012;32:1491-502.

Bally M, Dendukuri N, Rich B, et al. Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data. BMJ 2017;357:j1909.

Bresalier RS, Sandler RS, Quan H, et al. Cardiovascular Events Associated with Rofecoxib in a Colorectal Adenoma Chemoprevention Trial. N Engl J Med 2005;352:1092-102.

Blower AL, Brooks A, Fenn GC, et al. Emergency admissions for upper gastrointestinal disease and their relation to NSAID use. Aliment Pharmacol Ther 1997;11:283–91.

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van der Hooft CS, Sturkenboom MC, van Grootheest K, et al. Adverse drug reaction-related hospitalisations: a nationwide study in The Netherlands. Drug Saf 2006;29:161-8.

Gøtzsche PC. Big marketing hoax: Non-steroidal, anti-inflammatory drugs (NSAIDs) are not anti-inflammatory. Copenhagen: Institute for Scientific Freedom 2022;Nov 10.

Perlis R. The time has come for over-the-counter antidepressants. Stat News 2024;April 8.

Gøtzsche PC. Critical Psychiatry Textbook. Copenhagen: Institute for Scientific Freedom; 2022. Freely available.

Tilley, Caitlin. “Corruption Fears as Report Finds US Doctors Received Record $12bn.” Mail Online, 3 Apr. 2024, www.dailymail.co.uk/health/article-13268371/Corruption-doctors-received-pharma-payments.html. 

Tanne, Janice Hopkins. “US Doctors Received More than $12bn in Industry Payments between 2013 and 2022, Study Shows.” BMJ, vol. 385, 2 Apr. 2024, p. q781, www.bmj.com/content/385/bmj.q781.full, https://doi.org/10.1136/bmj.q781. 

Since the declaration of the COVID-19 pandemic by the World Health Organization (WHO) on March 11, 2020, over 13.5 billion doses of COVID-19 vaccines have been administered worldwide. This remarkable achievement in vaccine distribution highlights the urgent need for comprehensive vaccine safety monitoring, as very rare adverse events associated with COVID-19 vaccines may only become apparent after widespread administration.

To address this need, the Safety Platform for Emergency Vaccines (SPEAC) initiative formulated a list of potential COVID-19 vaccine adverse events of special interest (AESI) in 2020. These AESI were selected based on various factors, including their associations with immunization, vaccine platforms, or adjuvants, as well as theoretical concerns related to immunopathogenesis.

One flexible approach for assessing AESI is the comparison of observed AESI rates following vaccine introduction with expected rates based on historical periods pre-vaccine rollout. This method, known as observed vs. expected (OE) analysis, can rapidly detect potential vaccine safety signals. For example, OE analysis played a crucial role in identifying thrombosis with thrombocytopenia syndrome (TTS) as a safety signal, prompting the suspension of the AstraZeneca COVID-19 vaccine in certain countries.

To further enhance vaccine safety monitoring, a global cohort study was conducted as part of the Global COVID Vaccine Safety (GCoVS) Project. This project, funded by the Centers for Disease Control and Prevention (CDC), involves multiple nations and aims to monitor COVID-19 vaccine safety on a global scale.

Thirteen AESI were selected for evaluation, including neurological, hematologic, and cardiovascular conditions, which are as follows:

1. Guillain-Barré syndrome (GBS),
2. Transverse myelitis (TM),
3. Facial (Bell’s) palsy,
4. Acute disseminated encephalomyelitis (ADEM), 
5. Convulsions (generalized seizures (GS), 
6. Febrile seizures (FS),
7. Cerebral venous sinus thrombosis (CVST),
8. Splanchnic vein thrombosis (SVT),
9. Pulmonary embolism (PE),
10. Thrombocytopenia,
11. Immune thrombocytopenia (ITP),
12. Myocarditis
13. Pericarditis

These conditions were chosen based on their relevance to real-world vaccine pharmacovigilance and the availability of background rates generated by GCoVS sites.

The study analyzed data from 10 sites across eight countries, comprising a total vaccinated population of 99,068,901 individuals. Notable findings include a statistically significant increase in Guillain-Barré syndrome (GBS) cases following the administration of the ChAdOx1 (India) vaccine and an increased risk of acute disseminated encephalomyelitis (ADEM) after the mRNA-1273 vaccine (Moderna).

Hematologic conditions such as cerebral venous sinus thrombosis (CVST) and immune thrombocytopenia (ITP) also showed elevated risk ratios following certain vaccine doses. Similarly, cardiovascular conditions like myocarditis and pericarditis demonstrated increased risk ratios, particularly after mRNA vaccine doses (Pfizer, Moderna, AstraZeneca).

Here is the raw data collected from the study:

Here is a chart summarizing the raw data collected in the study:

K. Faksova, et al. “COVID-19 Vaccines and Adverse Events of Special Interest: A Multinational Global Vaccine Data Network (GVDN) Cohort Study of 99 Million Vaccinated Individuals.” Vaccine, 1 Feb. 2024, https://doi.org/10.1016/j.vaccine.2024.01.100.

Technologies like cellular phones and wireless devices are ubiquitous in our daily lives, serving as essential tools for communication, entertainment, and productivity. In recent years, the proliferation of these wireless internet technologies has led to the mainstream become more aware of these devices emitting significant amounts of electromagnetic radiation (EMR)/electromagnetic frequencies (EMF). These devices, which operate as radio devices transmitting and receiving radio EMF within a large band of radio frequencies (RF), come with significant health concerns, particularly in the realm of reproductive health.

​The radiation emitted by mobile phones can have both thermal and non-thermal impacts on biological materials, with potential long-term effects on cellular functions and the hormonal balance in the human body. Emerging research points to a troubling link between mobile phone usage and male infertility, a condition that already affects nearly half of the 15% of couples worldwide struggling with reproductive issues.

For years the cell phone companies have assured people that cell phones are perfectly safe. Currently there are over 700 million cell phone users in the world. Analog phones operate at 450–900 MHz, digital phones (Global System for Mobile Communications [GSM]) at 850–1900 MHz, and third-generation phones at approximately 2000 MHz. ​The radiation emitted by Wi-Fi and all generations of mobile phones is classified as non-ionizing radiation, which falls within the microwave range (3–300 GHz).

• First generation (1G) and second-generation (2G) mobile phones operate at a frequency range of 850–1900 MHz
• Third-generation (3G) mobile phones can reach up to 2,500 MHz
• The most recent fourth-generation (4G) and fifth-generation (5G) mobile technologies operate at a wider and higher frequency range of 2–8 GHz and 3–300 GHz, respectively 
• Unlicensed spectrum bands of 2.4 and 5 GHz are used by Wi-Fi devices

​5G routers and modems, operating on higher frequencies, emit more powerful electromagnetic fields, potentially amplifying the risks. The introduction of 5G technology, which involves more frequent data transmissions at higher power levels, has raised concerns about whether this could intensify the reproductive risks posed by EMF radiation.

Keep in mind, the EMFs emitted by cell phones are a form of microwave energy. Specifically, cell phones emit RF radiation, which falls within the microwave portion of the electromagnetic spectrum. Microwaves, including the frequencies used by cell phones, are non-ionizing radiation, meaning they don't carry enough energy to ionize atoms or molecules.

Cell phones typically operate at frequencies between 800 MHz and 2.6 GHz, which are in the lower part of the microwave frequency range. This type of radiation is also used in other wireless technologies, such as Wi-Fi and Bluetooth.
​
While the power levels of cell phones are much lower than those of devices like microwave ovens, the concern over potential health effects has led to ongoing research on the long-term exposure to RF radiation emitted by mobile devices.

Impact on Semen
Studies examining the association between mobile phone use and semen parameters have yielded significant results. Men who stored mobile phones in their trouser pockets exhibited a decrease in the percentage of normal sperm morphology and luteinizing hormone levels. Additionally, exposure to mobile phone EMR was associated with:

• reduced sperm motility (sperm movement): For sperm to fertilize an egg, they need to be able to swim through the female reproductive tract to reach the egg. Sperm that move actively and in a straight line are considered to have good motility.
• reduced linear velocity (sperm speed): sperm with higher linear velocity are more likely to reach the egg, improving chances of conception. If sperm swim too slowly or in a disorganized way, they may not get there in time.
• reduced linearity index (how straight the sperm’s path is when it swims): A high linearity index means sperm are moving directly toward their target (the egg), which makes fertilization more likely. Sperm with a low linearity index may swim in random directions, wasting energy and reducing the chance of fertilization.
• reduced acrosin activity (ability to penetrate egg): Acrosin is an enzyme found in sperm that helps it penetrate the outer layer of the egg. Think of it like a key that helps sperm unlock the egg. Acrosin activity refers to how well this enzyme is working. Healthy acrosin activity ensures that sperm can do their job once they reach the egg.
• increased sperm DNA fragmentation (DNA damage): DNA fragmentation means that the sperm’s genetic material (DNA) is damaged or broken into pieces. The DNA inside sperm is critical because it carries the genetic information that gets passed on to the baby. Sperm with high levels of DNA fragmentation have damaged genetic material. High DNA fragmentation can lead to problems in fertilization, miscarriage, or developmental issues in the baby. Even if sperm are able to fertilize an egg, if the DNA is damaged, the embryo may not develop properly. This can reduce the chances of a successful pregnancy.

The frequency and duration of mobile phone use have been linked to declines in semen volume, sperm concentration, and total sperm count, indicating a detrimental effect on sperm quality and male fertility. Notably, carrying cell phones in hip pockets and on belts has been associated with lower sperm motility compared to other storage methods.
​
Moreover, prolonged exposure to EMF from mobile phones and routers has been linked to a higher rate of childlessness among certain professions, such as military personnel in the Royal Norwegian Navy. These findings suggest that frequent exposure to mobile phone radiation may impair reproductive health over time.

​Numerous studies have shown that radiation emitted by Wi-Fi and 5G routers, especially when used for prolonged periods, can negatively affect sperm quality, including sperm count, motility, and DNA integrity.

A laboratory study found that exposing sperm samples to a laptop connected to Wi-Fi for just four hours significantly reduced sperm motility and increased DNA fragmentation. This indicates that not only direct phone use but also proximity to routers and modems could affect sperm health.

In human studies, semen analysis in the four cell phone user groups showed a decrease in sperm count, motility, viability, and normal morphology with the increase in daily use of cell phone - in a dose dependent manner (the more EMF radiation exposure, the greater the effects to semen). Other researchers suggested in their study on mice that Leydig cells are among the most susceptible cells to EMW, and injury to Leydig cells may affect spermatogenesis. Additionally, mobile phone EMR induced genotoxic effects on epididymal spermatozoa, which is critical for fertility.

Research indicates that prolonged RF-EMR exposure, such as frequent use of mobile phones over several years, can lower testosterone levels in men. Testosterone is a critical hormone for sperm production and general male health. Over time, men using mobile phones emitting 950 MHz RF-EMR experienced a gradual reduction in testosterone levels. ​

Additionally, RF-EMR negatively affects the anterior pituitary gland, which regulates several hormones, including cortisol, thyroid hormones, and adrenocorticotrophic hormone (ACTH). This interference with hormonal balance may result in decreased reproductive function.

Some studies have suggested that mobile phone radiation could lead to Leydig cell hyperplasia, a condition where these testicular cells overgrow and produce elevated testosterone levels. However, this increase is misleading, as reproductive functions, such as sperm quality, are still impaired despite the rise in testosterone. Decreased sperm count, motility, and quality have been consistently linked to mobile phone use, validating the harmful impact of mobile phone radiation on male fertility.

Animal Studies on RF-EMR Exposure
Animal studies have further validated these concerns. Exposure to RF-EMR, particularly at 900 MHz, has been shown to increase the levels of reproductive hormones such as FSH (Follicle Stimulating Hormone), LH (Luteinizing Hormone), and prolactin in animals. While these hormones are typically involved in regulating male reproductive functions, prolonged exposure to RF-EMR disrupts this balance. For example, increased LH levels in animals exposed to mobile phone radiation were accompanied by damage to Leydig cells via changes in protein kinase C, which led to reduced testosterone production.

Additionally, RF-EMR exposure increases oxidative stress in Leydig cells, leading to cellular damage and apoptosis (cell death). This oxidative stress, combined with thermal effects from radiation, can impair the function of the hypothalamus and pituitary gland, which are essential for regulating reproductive hormones like LH and FSH. When these hormones are out of balance, the entire reproductive system can be negatively impacted.

Human Studies on RF-EMR Exposure
In studies of men, the group exposed to EMFs had a considerable decrease in LH levels. Additionally, RF-EMR appears to have a negative relationship with the anterior pituitary gland
and the downstream effects of hormones released via the actions of the pituitary. Studies of men with long-term use of 950 MHz mobile phones (6 years) have revealed reduced testosterone levels, which is dependent on time, likely due to damage to Leydig cells and insufficient LH, as LH stimulates the secretion of testosterone by testicular Leydig cells.

These hormonal regulations by the hypothalamus and anterior pituitary are essential for male reproductive functions. RF-EMR emitted from mobile phones can cause thermal effects as manifested by the elevation of temperature and EMF strength value on the hypothalamus and pituitary gland after mobile phone exposure. The penetration of RF-EMR on the hypothalamus and pituitary gland is deeper in lower frequency bands (700 and 900 MHz).

Meo, Sultan, et al. Effects of Mobile Phone Radiation on Serum Testosterone in Wistar Albino Rats. 2010.

Maluin, Sofwatul Mokhtarah, et al. “Effect of Radiation Emitted by Wireless Devices on Male Reproductive Hormones: A Systematic Review.” Frontiers in Physiology, vol. 12, 24 Sept. 2021, p. 732420, www.ncbi.nlm.nih.gov/pmc/articles/PMC8497974/, https://doi.org/10.3389/fphys.2021.732420. Accessed 22 Oct. 2021.
​
Okechukwu, Chidiebere Emmanuel. “Does the Use of Mobile Phone Affect Male Fertility? A Mini-Review.” Journal of Human Reproductive Sciences, vol. 13, no. 3, 2020, p. 174, https://doi.org/10.4103/jhrs.jhrs_126_19.

​Agarwal, Ashok, et al. “Effect of Cell Phone Usage on Semen Analysis in Men Attending Infertility Clinic: An Observational Study.” Fertility and Sterility, vol. 89, no. 1, Jan. 2008, pp. 124–128, https://doi.org/10.1016/j.fertnstert.2007.01.166.

The human gut is teeming with a diverse array of bacteria collectively known as the gut microbiota. Among its many functions, one of the most vital is colonization resistance—the ability to prevent harmful pathogens from taking up residence in the gut and causing disease. However, understanding which microbiota communities are protective and which allow pathogens to thrive has long been a challenge.
​
In a groundbreaking study led by Spragge et al., researchers shed light on the complex dynamics of gut microbiota and their role in colonization resistance against two significant bacterial pathogens: Klebsiella pneumoniae and Salmonella enterica serovar Typhimurium. Their findings, published in Science, unveil the critical importance of microbiome diversity in safeguarding against pathogenic invasion.

Traditionally, it was believed that certain individual bacterial species might confer colonization resistance. However, Spragge et al. discovered that the true protective power lies in the collective diversity of the microbiota. They conducted meticulous experiments both in vitro and in gnotobiotic mice (mice that have been raised in a controlled environment where the microbial composition of their gut is precisely known and controlled), evaluating the ability of single bacterial species and increasingly diverse microbiota communities to resist pathogen colonization.

Surprisingly, the researchers found that single species alone provided limited protection against the pathogens. It was only when these species were combined into diverse communities consisting of up to 50 different species that colonization resistance was significantly enhanced. This underscores the importance of ecological diversity in promoting gut health.
​
Moreover, the study identified certain key species within these diverse communities that played a pivotal role in bolstering colonization resistance, even though they offered little protection on their own. These key species acted by consuming nutrients required by the pathogens, thereby depriving them of essential resources for growth and establishment in the host.

Importantly, Spragge et al. demonstrated that microbiome diversity not only increases the probability of protection against pathogens but also enhances the overlap in nutrient utilization profiles between the microbiota community and the pathogen. This nutrient blocking mechanism serves as a potent defense strategy against pathogenic invasion.

The implications of these findings are profound. They provide compelling evidence for the health benefits of a diverse gut microbiome and offer insights into the rational design of pathogen-resistant microbiota communities. By harnessing the protective power of microbiome diversity, we may pave the way for innovative strategies to combat infectious diseases and promote overall gut health.
​
In conclusion, Spragge et al.'s study unveils the intricate interplay between microbiome diversity and colonization resistance, highlighting the collective strength of diverse bacterial communities in defending against pathogenic threats. This research not only expands our understanding of gut microbiota dynamics but also holds promise for the development of novel therapeutics aimed at fortifying the body's natural defenses against infections.

Spragge, Frances, et al. “Microbiome Diversity Protects against Pathogens by Nutrient Blocking.” Science, vol. 382, no. 6676, 15 Dec. 2023, https://doi.org/10.1126/science.adj3502.

In recent years, researchers have uncovered a surprising trend in human physiology: a decline in body temperature over the past two centuries. Contrary to the long-standing belief that the normal body temperature is 37°C (98.6°F), studies spanning multiple cohorts and time periods have revealed a consistent decrease in average body temperature, suggesting a real physiological change rather than a mere artifact of measurement bias.

A groundbreaking study analyzed data from three cohorts spanning 157 years (over 600,000 data inputs), including Union Army Veterans of the Civil War, the National Health and Nutrition Examination Survey I, and the Stanford Translational Research Integrated Database Environment. The findings revealed a monotonic decrease in body temperature, with men born in the early 19th century having temperatures 0.59°C higher than men today. A similar decline was observed in women, indicating a significant shift in human physiology over time.
​
While some may attribute these findings to changes in measurement methods or biases, the study's authors argue that the observed drop in temperature reflects real physiological differences. Human body temperature is a crude surrogate for basal metabolic rate. These findings of a decrease in body temperature indicate a decrease in metabolic rate, which is supported in the literature when comparing modern experimental data to those from 1919. 

Resting metabolic rate, a key component of daily energy expenditure, has been linked to body temperature and longevity. The observed decrease in body temperature suggests a corresponding decline in metabolic rate, independent of changes in body size. This likely has implications for human health and longevity, as metabolic health underlies all vital organ functions. 

Protsiv, Myroslava, et al. “Decreasing Human Body Temperature in the United States since the Industrial Revolution.” ELife, vol. 9, 7 Jan. 2020, p. e49555, elifesciences.org/articles/49555, https://doi.org/10.7554/eLife.49555.

Dai, Dao-Fu, et al. “Mitochondrial Oxidative Stress in Aging and Healthspan.” Longevity & Healthspan, vol. 3, no. 1, 2014, p. 6, https://doi.org/10.1186/2046-2395-3-6. 

Obesogens, through their pervasive presence in our environment, exert insidious effects on metabolic function, including the intricate workings of mitochondria – the cellular powerhouses responsible for energy production. By disrupting mitochondrial function, obesogens can contribute to metabolic dysregulation and, ultimately, weight gain.

Mitochondria play a central role in energy metabolism, converting nutrients into adenosine triphosphate (ATP), the primary source of cellular energy. However, exposure to obesogens can impair mitochondrial function through various mechanisms, including:

• Oxidative Stress: Obesogens can promote the generation of reactive oxygen species (ROS) within mitochondria, leading to oxidative damage and dysfunction.
• Mitochondrial Biogenesis: Some obesogens interfere with the process of mitochondrial biogenesis, the creation of new mitochondria, which is essential for maintaining optimal energy metabolism.
• Respiratory Chain Dysfunction: Obesogens may disrupt the electron transport chain, a series of protein complexes within mitochondria that generate ATP, impairing energy production.
• Mitochondrial Membrane Integrity: Obesogens can compromise the integrity of mitochondrial membranes, affecting the transport of ions and molecules critical for energy production.

​The disruption of mitochondrial function by obesogens can have profound implications for metabolic health and contribute to obesity through several pathways:

1. Impaired Energy Expenditure: Dysfunctional mitochondria are less efficient at generating ATP, leading to reduced energy expenditure and a propensity for weight gain.
2. Insulin Resistance: Mitochondrial dysfunction can impair insulin signaling pathways, contributing to insulin resistance, a hallmark of obesity and metabolic syndrome.
3. Altered Lipid Metabolism: Mitochondria play a crucial role in lipid metabolism, including the breakdown of fatty acids for energy. Disrupted mitochondrial function can lead to aberrant lipid accumulation and adipogenesis, contributing to obesity.

The impact of obesogens on human health extends beyond weight gain, with associations documented with various health conditions, including:

• Obesity: Obesogens have been implicated in the global obesity epidemic, contributing to excess weight gain and adiposity. This includes being overweight, abdominal obesity (midsection fat), childhood and adult obesity.
• Insulin Resistance and Diabetes: Disruption of metabolic pathways by obesogens can lead to insulin resistance, a precursor to type 2 diabetes.
• Fatty Liver Disease: Chemical exposures, including those to bisphenols and phthalates, have been linked to the development of non-alcoholic fatty liver disease (NAFLD).

Additionally, obesogens are highly related to the following health conditions and physiologic imbalances:

Relatively little is known about the extent to which obesogen exposure programs dysfunctional adipose tissue that may store but not mobilize fat. However, emerging evidence suggests that obesogens may contribute to adipocyte dysfunction, leading to altered fat storage and metabolism. One potential underlying factor is suboptimal liver detoxification pathways due to inadequate micronutrient cofactors.
​
Inadequate levels of essential micronutrients, such as vitamins and minerals, can impair liver detoxification pathways responsible for metabolizing and eliminating obesogens from the body. As a result, obesogens may accumulate in adipose tissue, disrupting metabolic function and contributing to weight gain. Additionally, micronutrient deficiencies can compromise mitochondrial function, further exacerbating metabolic dysfunction and obesity risk.​

In the quest for weight loss, many of us often find ourselves fixating on calorie counting, fad diets, or intense workout regimens. However, what if I told you that the key to achieving a healthy weight isn't solely about shedding pounds but rather fixing your metabolism? Enter obesogens – a lesser-known yet influential factor in the obesity epidemic.

As mentioned, obesogens are chemicals found in our environment, ranging from pesticides and plastics to food additives and personal care products. These substances have the uncanny ability to disrupt our body's natural weight-regulating mechanisms, leading to weight gain and metabolic dysfunction. Instead of solely blaming calories in versus calories out, it's essential to recognize the role obesogens play in shaping our metabolism.

2. Consume Micronutrients: Vital micronutrients, such as vitamins and minerals, serve as essential cofactors in metabolic pathways. Ensuring adequate intake of these micronutrients through a balanced diet rich in fruits, vegetables, whole grains, and lean proteins can support optimal metabolic function. Additionally, supplementation may be necessary to address any deficiencies and promote metabolic health.
​
The conventional approach to weight loss often overlooks the critical role obesogens play in metabolic dysfunction. Instead of solely focusing on calorie restriction or intense exercise, shifting our focus to fixing metabolism through toxin reduction and micronutrient consumption offers a more holistic and sustainable solution to achieving optimal health. By addressing the underlying factors contributing to metabolic disruption, we can pave the way for lasting weight management and overall well-being.

Online/In-Person Guidance
One of the standout features of the Integral Wellness Program is its flexibility, offering both online and in-person consultations tailored to individual preferences and needs. Whether you prefer the convenience of virtual sessions or the hands-on approach of in-person coaching, our team of experienced wellness professionals is dedicated to supporting you every step of the way.

This article challenges the conventional understanding of heart disease, particularly the widely accepted theory that attributes its cause primarily to events occurring in the coronary arteries. Instead, a paradigm shift is proposed, contending that a deeper understanding of heart disease, encompassing angina, unstable angina, and myocardial infarction (heart attack), necessitates a focus on events within the myocardium, the muscular tissue of the heart. Over the past decades, the prevailing belief in the coronary artery theory has led to costly surgical interventions, widespread medication use with questionable benefits, and dietary recommendations that may exacerbate rather than alleviate the problem. By delving into the precise pathophysiological events that underlie heart attacks, we can uncover alternative approaches to prevention and treatment, such as adopting a "Nourishing Traditions"-style diet and utilizing safe and affordable medicines like g-strophanthin. Furthermore, this shift in perspective prompts us to confront broader issues, including the impact of modern lifestyles on human health, the need for a new medical paradigm, and the importance of ecological consciousness. Ultimately, reexamining the root causes of heart disease offers a pathway to addressing this pervasive health challenge and forging a healthier future for all.

The information is summarized based on the work of Dr. Thomas Cowan, vice president of the Physicians Association for Anthroposophical Medicine and is a founding board member of the Weston A. Price Foundation. During his career he has studied and written about many subjects in medicine. These include nutrition, homeopathy, anthroposophical medicine, and herbal medicine.​

The traditional understanding of heart attacks, largely centered on arterial blockage due to plaque buildup, has faced challenges in recent years. Initially, it was believed that blockages in the major coronary arteries led to oxygen deficiency in the heart, causing chest pain (angina) and eventually progressing to a heart attack. This simplistic view prompted invasive procedures like angioplasty, stents, and coronary bypass surgery as standard treatments. However, clinical observations and research findings have cast doubts on this approach.
​
Anecdotal evidence (admittedly low quality evidence) from a trial in rural Alabama revealed surprising outcomes among individuals with single artery blockages. Contrary to expectations, less than 10% of those who experienced heart attacks did so in the region of the heart supplied by the blocked artery.

Similarly, a comprehensive study conducted by the Mayo Clinic highlighted the limited efficacy of bypass surgery in preventing future heart attacks. While the procedure offered relief from chest pain, it did not significantly reduce the risk of subsequent heart events, except in high-risk patients.

Contrary to popular belief, blockages exceeding 90% are often compensated for by collateral blood vessels, which develop over time to ensure uninterrupted blood flow to the heart. This extensive network of collateral vessels serves as a natural bypass system, mitigating the impact of arterial blockages on blood circulation.

However, diagnostic procedures like coronary angiograms, which rely on injecting heavy dye into the arteries, often fail to accurately assess the extent of blockages and the true blood flow in the heart. As a result, many patients undergo invasive treatments such as bypass surgery, stents, or angioplasty based on misleading information about the severity of their arterial blockages.

Moreover, studies have shown that these procedures provide minimal benefit, if any, to patients, particularly those with minimally symptomatic blockages exceeding 90%. Despite the widespread use of these interventions, their efficacy in restoring blood flow and preventing heart attacks remains questionable.
​
These revelations underscore the need for a reevaluation of conventional treatment strategies and a deeper exploration of the underlying mechanisms behind heart attacks. Rather than focusing solely on arterial blockages, a more holistic approach that considers factors beyond plaque buildup may offer greater insights into the prevention and management of heart disease.

The prevailing focus in cardiology has long been on the stable, progressing plaque within the coronary arteries, deemed responsible for heart attacks. However, recent insights challenge this notion, redirecting attention to the unpredictable nature of unstable plaques. Unlike their calcified counterparts, unstable plaques are soft and prone to rapid evolution, abruptly occluding arteries and triggering downstream oxygen deficits, angina, and ischemia.
​
These vulnerable plaques are believed to be a blend of inflammatory buildup and low-density lipoprotein (LDL), the primary targets of statin drugs. Consequently, the widespread adoption of statin therapy is advocated as a preventive measure against heart attacks, fueled by angiogram studies purportedly showcasing the prevalence of unstable plaques as the leading cause of myocardial infarctions (MIs).

An accurate understanding of myocardial ischemia necessitates consideration of the primary risk factors associated with heart disease, including gender, diabetes, smoking, and chronic psychological stress. Curiously, none of these risk factors directly implicate coronary artery pathology; instead, they impact capillary health or exert indirect effects.

Over the past five decades, key medications in cardiology, such as beta-blockers, nitrates, aspirin, and statins, have demonstrated some benefits for heart patients. However, their mechanisms of action must be scrutinized within a comprehensive theory of myocardial ischemia.

A groundbreaking revelation in heart disease prevention and treatment stems from the autonomic nervous system's role in ischemia genesis, as illuminated by heart-rate variability monitoring. The autonomic nervous system comprises two branches—the sympathetic and parasympathetic—responsible for regulating physiological responses. Imbalance between these branches emerges as a significant contributor to heart disease.

Studies reveal a notable reduction in parasympathetic activity among patients with ischemic heart disease, particularly preceding ischemic events triggered by physical or emotional stressors. Conversely, abrupt increases in sympathetic activity rarely culminate in ischemia without antecedent parasympathetic decline. Notably, women exhibit stronger vagal activity than men, potentially influencing sex-based disparities in MI incidence.

Multiple risk factors, including hypertension, smoking, diabetes, and stress, diminish parasympathetic activity, underscoring the pivotal role of the regenerative nervous system in heart health. Conversely, pharmacological interventions like nitrates, aspirin, and statins stimulate parasympathetic mediators, promoting ANS balance.
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In essence, while traditional risk factors and interventions influence plaque and stenosis development, their paramount impact lies in restoring ANS equilibrium. Thus, understanding the sequence of events leading to myocardial infarction demands a deeper exploration of autonomic nervous system dynamics.

In the vast majority of cases, the pathology leading to myocardial infarction (MI) begins with a decreased tonic activity of the parasympathetic nervous system (rest and digest), often exacerbated by physical or emotional stressors. This reduction prompts an increase in sympathetic nervous system activity, triggering heightened adrenaline production and directing myocardial cells to break down glucose via aerobic glycolysis, rather than their preferred fuel source of ketones and fatty acids (often explaining why patients report feeling tired before a MI). Remarkably, despite these metabolic shifts, no change in blood flow, as measured by the myocardial cell oxygen level (pO2), occurs.

The shift towards glycolysis results in a surge of lactic acid production within myocardial cells, a phenomenon observed in nearly all MIs. This surge, coupled with localized tissue acidosis, impedes calcium entry into cells, compromising their contractility. Consequently, localized edema ensues, leading to hypokinesis—the hallmark of ischemic disease—and eventual tissue necrosis characteristic of an MI.
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Moreover, the ensuing tissue edema alters arterial hemodynamics, escalating sheer pressure and exacerbating plaque instability. This process elucidates the rupture of unstable plaques and their role in exacerbating arterial blockage during critical, acute scenarios. This explanation accounts for all the observable phenomena associated with heart disease.

Understanding the etiology of heart disease holds profound implications beyond academic curiosity. It informs therapeutic strategies aimed at preserving parasympathetic activity, fostering holistic approaches to heart health, and challenging prevailing "civilized" industrial lifestyles. Central to this paradigm shift is the recognition of the vital role played by g-strophanthin—a hormone derived from the strophanthus plant. G-strophanthin is an endogenous hormone made in the adrenal cortex from cholesterol, whose production is inhibited by statin drugs, that does two things that are crucial for heart health and are done by no other medicine. G-strophanthin uniquely stimulates the production of acetylcholine, the primary neurotransmitter of the parasympathetic nervous system, while also converting lactic acid—the metabolic poison implicated in ischemic processes—into pyruvate, a preferred myocardial cell fuel. Perhaps this “magic” is why Chinese medicine practitioners say that the kidneys (i.e., adrenals, where ouabain is made) nourish the heart.

Embracing this understanding not only guides therapeutic interventions but also underscores the imperative of dietary modifications. A diet abundant in healthful fats and fat-soluble nutrients, while low in processed carbohydrates and sugars, emerges as a cornerstone of heart health—a departure from the industrialized diets synonymous with modern civilization.

In essence, unraveling the metabolic symphony orchestrating myocardial ischemia offers a transformative lens through which to perceive heart disease, fostering a holistic approach that transcends conventional paradigms and embraces the profound interconnectedness of mind, body, and environment.

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Doepp, Manfred. “May Strophanthin Be a Valuable Cardiac Drug ? .” American Journal of Medical and Clinical Research & Reviews, vol. 2, no. 9, 15 Sept. 2023, pp. 1–6, ajmcrr.com/index.php/pub/article/view/75/74, https://doi.org/10.58372/2835-6276.1069. Accessed 29 Mar. 2024.

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Recent breakthrough studies have shone a light on the intriguing link between our microbiome – the diverse community of microorganisms residing in our gut and mouth – and the secret to a longer, healthier life. Scientists have long suspected that our genes, environment, and internal factors like the microbiome play a role in determining how long we live, but the specifics remained elusive. Now, thanks to cutting-edge research, we're getting closer to unraveling the mysteries of longevity.
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In this groundbreaking exploration, scientists employed a sophisticated approach called Mendelian randomization (MR) to delve into the intricate relationships between the human microbiome and longevity. By analyzing genetic data from large cohorts, they uncovered some compelling associations that shed light on the microbial players in the quest for a longer life.

Liu, Xiaomin, et al. “Mendelian Randomization Analyses Reveal Causal Relationships between the Human Microbiome and Longevity.” Scientific Reports, vol. 13, no. 1, 29 Mar. 2023, p. 5127, www.nature.com/articles/s41598-023-31115-8, https://doi.org/10.1038/s41598-023-31115-8. 

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.