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.

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.
​
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.
​
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.

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.

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.
​
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.
​
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.

Giorgio Baroldi. The Etiopathogenesis of Coronary Heart Disease. CRC Press EBooks, Informa, 20 Jan. 2004. Accessed 29 Mar. 2024.

Sroka K. On the genesis of myocardial ischemia. Z Kardiol. 2004 Oct;93(10):768-83. doi: 10.1007/s00392-004-0137-6. PMID: 15492892.

Helfant, R. H., et al. “Coronary Heart Disease. Differential Hemodynamic, Metabolic, and Electrocardiographic Effects in Subjects with and without Angina Pectoris during Atrial Pacing.” Circulation, vol. 42, no. 4, 1 Oct. 1970, pp. 601–610, www.ncbi.nlm.nih.gov/pubmed/11993303., https://doi.org/10.1161/01.cir.42.4.601. 

Takase, B., Kurita, A., Noritake, M., Uehata, A., Maruyama, T., Nagayoshi, H., ... & Nakamura, H. (1992). Heart rate variability in patients with diabetes mellitus, ischemic heart disease, and congestive heart failure. Journal of electrocardiology, 25(2), 79-88.

Sroka, K., Peimann, C. J., & Seevers, H. (1997). Heart rate variability in myocardial ischemia during daily life. Journal of electrocardiology, 30(1), 45-56.

Scheuer, J., & Brachfeld, N. (1966). Coronary insufficiency: relations between hemodynamic, electrical, and biochemical parameters. Circulation Research, 18(2), 178-189.

Schmid, P. G., Greif, B. J., Lund, D. D., & Roskoski Jr, R. O. B. E. R. T. (1978). Regional choline acetyltransferase activity in the guinea pig heart. Circulation Research, 42(5), 657-660.

​Katz, A. M. (1971). Effects of ischemia on the cardiac contractile proteins. Cardiology, 56(1-6), 276-283.

Manunta, Paolo, et al. “Endogenous Ouabain in Cardiovascular Function and Disease.” Journal of Hypertension, vol. 27, no. 1, 1 Jan. 2009, pp. 9–18, journals.lww.com/jhypertension/Abstract/2009/01000/Endogenous_ouabain_in_cardiovascular_function_and.3.aspx, https://doi.org/10.1097/HJH.0b013e32831cf2c6.

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.

​Thayer, J. F., Yamamoto, S. S., & Brosschot, J. F. (2010). The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors. International journal of cardiology, 141(2), 122-131.

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.

The leading cause of death in the United States is cardiovascular disease, and the risk of cardiovascular issues can be predicted by factors such as blood pressure, heart rate variability, blood pressure variability, and cardiac vagal baroreflex sensitivity. The interplay between the cardiovascular and respiratory systems is highlighted, with a particular emphasis on how respiration affects key prognostic cardiovascular variables.

This study explores the impact of nasal breathing compared to oral breathing on cardiovascular health in young adults. Nasal breathing is associated with humidification, warming, and filtration of inhaled air, potentially leading to bronchodilation and improved breathing efficiency. While past research has shown nasal breathing to have positive effects on resting metabolic demands, its influence on cardiovascular markers is not well-understood.

The primary hypothesis is that nasal breathing, as opposed to oral breathing, will result in decreased blood pressure, improved heart rate variability, reduced blood pressure variability, and increased cardiac vagal baroreflex sensitivity at rest. The study aims to contribute to the understanding of how breathing patterns influence prognostic cardiovascular variables, aligning with the broader interest in the impact of breathing pace and training on cardiovascular health.

The secondary hypothesis focuses on the effects of nasal breathing during submaximal exercise. The expectation is that nasal breathing, by attenuating the ventilatory response and metabolic demands, will lead to reduced blood pressure responses, improved heart rate variability, and decreased blood pressure variability during exercise. This aspect is particularly relevant due to the association between elevated exercise blood pressure and the risk of developing hypertension and cardiovascular disease.

The study findings are summarized, focusing on the impact of nasal vs. oral breathing on physiological and subjective variables at rest and during exercise. At rest, nasal breathing is associated with lower mean and diastolic blood pressure, improved heart rate variability metrics, reduced LF/HF ratio, and lower ratings of perceived exertion (RPE) and breathlessness (RPB). However, it increased systolic blood pressure average real variability. During submaximal exercise, differences between nasal and oral breathing were observed for RPB, suggesting a modest effect on reducing breathlessness during acute exercise.

The discussion delves into the potential clinical significance of these findings, particularly the reduction in diastolic blood pressure during nasal breathing at rest. The study suggests a greater parasympathetic to sympathetic dominance during nasal breathing, indicated by changes in frequency-domain metrics of heart rate variability. Although nasal breathing did not significantly affect beat-to-beat blood pressure variability, there is speculation about potential connections between respiratory variables and blood pressure changes, emphasizing the need for further investigation.

The study notes that the impact of nasal breathing on cardiovascular variables may have implications for various populations and suggests avenues for future research, including examining nasal breathing's effects on blood pressure over longer durations, both at rest and during activities like exercise. The discussion also touches on the potential benefits of interventions like mouth-taping overnight, emphasizing the importance of considering nasal breathing in the context of broader health outcomes.

Watso, Joseph C., et al. “Acute Nasal Breathing Lowers Diastolic Blood Pressure and Increases Parasympathetic Contributions to Heart Rate Variability in Young Adults.” American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 325, no. 6, 1 Dec. 2023, pp. R797–R808, pubmed.ncbi.nlm.nih.gov/37867476/, https://doi.org/10.1152/ajpregu.00148.2023.

The study utilized linear mixed-effects models to analyze data gathered during a weight loss and weight loss maintenance intervention. The results revealed 17 significant associations between various air pollutants and 10 distinct cardiometabolic outcomes. The focus was primarily on blood lipids, hormones, and glucose regulation, providing a comprehensive understanding of the multifaceted effects of air pollution.
​
Interestingly, the Baltic Sea Diet score did not appear to mediate the association between air pollution and cardiometabolic outcomes. However, the diet quality factor emerged as a key player in modifying the impact of particulate matter (PM2.5) on total cholesterol. Furthermore, it influenced the associations of nitrogen dioxide (NO) and ozone (O3) with ghrelin, a hormone associated with appetite regulation.

Healy, Darren R., et al. “Associations of Low Levels of Air Pollution with Cardiometabolic Outcomes and the Role of Diet Quality in Individuals with Obesity.” Environmental Research, vol. 242, 1 Feb. 2024, p. 117637, www.sciencedirect.com/science/article/pii/S0013935123024416, https://doi.org/10.1016/j.envres.2023.117637.

How many hugs have you had today? Neuroeconomist Paul Zak, also known as "Dr. Love," recommends at least eight hugs a day to feel happier and more connected, as well as nurture relationships. As psychotherapist Virginia Satir said:

"We need 4 hugs a day for survival. We need 8 hugs a day for maintenance. We need 12 hugs a day for growth."

There may very well be a "hug threshold" that allows your body to produce ample amounts of oxytocin, which is released in response to physical touch such as breast-feeding, orgasm, hugs, snuggling, holding hands, partner dance, massage, bodywork, and prayer. The neuropeptide oxytocin, released by your pituitary gland, is a naturally occurring hormone in the body with incredibly powerful, health-giving properties.

This "love hormone" is also a key reason why the simple act of hugging is such an incredible way to enhance bonding with others but also boost your physical, and emotional, health.

Hugging increases levels of oxytocin, a neurotransmitter that acts as a hormone. This, in turn, has been observed to have beneficial physiological effects on your cardiovascular health and emotional happiness. One group of researchers observed, for example, a reduction in blood pressure among adults following a brief episode of warm contact with their partner. A 20-second hug, along with 10 minutes of hand-holding, reduces the harmful physical effects of stress, including its impact on your blood pressure and heart rate (Grewen, Anderson, Girdler & Light, 2003). This makes sense, since positive physical contact as hugging and  reduces cortisol, increases oxytocin, and lowers systolic blood pressure in stressful situations (Holt-Lunstad, Birmingham & Light, 2008). But researchers suggest there is even more to it than that.

The skin contains a network of tiny, egg-shaped rapidly adapting mechanoreceptors called Pacinian corpuscles with a large receptive field that can sense pressure and vibration and which are in contact with the brain through the vagus nerve. The vagus nerve winds its way through the body and provides input and receives sensation from the heart, liver, and digestive tract. (Freberg, 2006). The vagus nerve is also connected to oxytocin receptors. One theory is that stimulation of the vagus triggers an increase in oxytocin, which in turn leads to the cascade of health benefits.

A 10-second hug a day can lead to biochemical and physiological reactions in your body that can significantly improve your health. Hugging has been observed to stimulates your nervous system while decreasing feelings of loneliness, combating fear, increasing self-esteem, defusing tension, and showing appreciation. According to researchers, hugging has been observed to (Forsell & Åström, 2012):

• Lower the risk of heart disease
  
• Reduce stress
  
• Fight fatigue
• Boost your immune system
• Fight infections
• Ease depression

There's no doubt that physical touch of all kinds feels good. Whether it is a hug or a handshake, physical touch has a powerful effect on the human psyche resulting in us feeling happy, regardless if you are the toucher or touchee; connection, big or small, results in happiness.

Yet, many people are touch-deprived. One poll found that one-third of people receive no hugs on a daily basis while 75 percent said they wanted more hugs. Findings such as these, coupled with the emotional and health benefits of human touch, have led to the emergence of cuddle therapy centers, where people can pay for a lunchtime cuddle.

However, some have questioned whether or not physical contact from strangers has the same impact as those from someone you know and trust. While cuddling with a spouse or partner has been shown to boost satisfaction in relationships, some researchers have observed that hugs are only beneficial if trust is involved.

Neurophysiologist Jürgen Sandkühler, Head of the Centre for Brain Research at the Medical University of Vienna actually cautioned against worldwide "free hugs" campaigns (where strangers offer hugs to others), saying that this may be perceived as threatening and actually increase emotional burden and stress. However, significant benefits have been found from cuddling with a pet, which shows hugs don't have to only be between humans to be beneficial to your heart and overall health.

On average, people spend on hour a month hugging. That doesn't seem like much, but when you consider that the average hug is 3 seconds long, that adds up to be a lot of hugs.

And if you had any doubt about the importance of touch, consider that children who lack physical connection have delays in walking, talking, and reading. The act of hugging has a near-immediate impact on health, lowering your heart rate and inducing a calming effect while also leading to a more upbeat mood.

Touch is described as a universal language that can communicate distinct emotions with startling accuracy. Researchers observed that touch alone can reveal emotions including anger, fear, disgust, love, gratitude, and sympathy, with accuracy rates of up to 83 percent (Hertenstein, Holmes, McCullough & Keltner, 2009).

Hugging is a way to encourage your body to release oxytocin, and the more oxytocin your pituitary gland releases, the better able you are to handle life's stressors.

Moreover, oxytocin quite likely plays a role in why pet owners heal more quickly from illness, why couples live longer than singles, and why support groups work for people with addictions and chronic diseases.

Oxytocin has also been found to reduce the cravings of drug and alcohol addiction, as well as for sweets. It even has a positive influence on inflammation and wound healing. Even beyond this, regular hugs have the added benefit of:

• Cultivating patience and showing appreciation
• Activating the Solar Plexus Chakra, which stimulates your thymus gland (this may help balance your production of white blood cells)
• Stimulating dopamine, the pleasure hormone, and serotonin, for elevated mood
  
• Balancing out your nervous system for better parasympathetic balance

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.

It's that time: time to test your blood. Most blood tests include a fasting lipid panel to assess one's risk of cardiovascular disease. A lipid panel is a test that measures fats and fatty substances used as a source of energy in the body. Lipids include cholesterol, triglycerides, high-density lipoprotein (HDL) and low-density lipoprotein (LDL).

Triglycerides are a powerful cardiovascular risk marker. Elevated triglyceride levels are a hallmark of too many carbohydrates in the diet.

60 percent of fructose is shunted toward the liver, where it is converted to triglycerides (which causes heart disease) (Gundry, 2017). In fact, fructose, which is the sugar found in most processed foods (often in the form of high-fructose corn syrup) can only be metabolized by your liver. If you eat a typical Western-style diet, you consume high amounts of it. The overload of fructose ends up damaging your liver in the same way alcohol and other toxins do (Mercola, 2017).

Our culture is obsessed with cholesterol levels, to the point that one in four adults in the U.S. take a statin drug to lower cholesterol levels. Nevertheless, elevated cholesterol levels are rarely a risk factor for heart disease, although elevated triglycerides clearly are. Fortunately, elevated triglycerides can easily be corrected and lowered to an ideal level of below 75 with the proper lifestyle interventions. The following tests can give you a far better assessment of your heart disease risk than your total cholesterol alone:

• HDL/Cholesterol ratio: HDL percentage is a very potent heart disease risk factor. Just divide your HDL level by your total cholesterol. That percentage should ideally be above 24 percent.
• Triglyceride/HDL ratios: You can also do the same thing with your triglycerides and HDL ratio. That percentage should be below 2.
• HS-CRP: This test measures the amount of a protein called C-reactive protein (CRP) in your blood. CRP measures general levels of inflammation in your body. There are two types, the regular test and the high sensitivity test (HS). It is best to get the more sensitive HS test done to measure CRP levels, which ideally should be below 0.7 mg/L.
• Your fasting insulin level: Any meal or snack high in carbohydrates like fructose and refined grains generates a rapid rise in blood glucose and then insulin to compensate for the rise in blood sugar.
• Your fasting blood sugar level:  Studies have shown that people with a fasting blood sugar level of 100 to 125 mg/dL had a nearly 300 percent higher risk of having coronary heart disease than people with a level below 79 mg/dL. This is easily monitored at home using a blood glucose meter.
• Your iron level: Iron can be a very potent driver of oxidative stress, so if you have excess iron levels you can damage your blood vessels and increase your risk of heart disease. Iron levels can be monitored by testing blood levels of ferritin; ideally, your level should be between 60 and 80 ng/nl.
  

High triglyceride levels (over 100 mg/dL) is known to cause leptin resistance. Leptin is a hormone located in fat cells, and like most hormones, it's function is complex. Leptin is tied to the coordination of our metabolic, hormonal, and behavioral response to starvation. Leptin essentially controls mammalian metabolism. Leptin decides whether to make us hungry and store more fat or burn fat. In other words, when your stomach is full, fat cells release leptin to tell your brain to stop eating. This is why people with low levels of leptin are prone to overeating.

One study observed participants with a 20 percent drop in leptin experienced a 24 percent increase in hunger and appetite, influencing their cravings for calorie-dense, high-carbohydrate foods, especially sweets, salty snacks, and starchy foods. The researchers discovered the drop in leptin was caused by sleep deprivation.

Leptin is also a pro-inflammatory molecule - it controls the creation of other inflammatory moleciles in your fat tissue throughout your body. This explains why overweight individuals are susceptible to inflammatory problems. Leptin is ranked highly on the body's chain of command, so imbalances tend to spiral downward and wreak havoc on virtually every system of the body beyond those directly controlled by leptin. Leptin, like insulin, is negatively influenced by carbohydrates. The more refined and processed the carbohydrate, the more imbalanced leptin levels become. When the body is overloaded and overwhelmed by substances that cause continuous surges in leptin, leptin receptors begin to turn off and you become leptin resistant. So even though leptin is now elevated, it doesn't work - it won't signal to your brain that you're full so you can stop eating.

Not a single drug or supplement can balance leptin levels. But better sleep, as well as better dietary choices will (Perlmutter, 2013).

Preventing cardiovascular disease involves reducing chronic inflammation in your body, and a proper diet is an absolute cornerstone. Although saturated fat has taken the blame for causing heart disease for the last several decades, the primary culprit in heart disease is sugar consumption.

A 2015 study published in the Journal of the American Medical Association concluded that there is " a significant relationship between added sugar consumption and increased risk for cardiovascular mortality." the 15-year study, which included data for 31,000 Americans, found that those who consumed 25 percent or more of their daily calories as added sugars were more than twice as likely to die form heart disease as those who got less than 10 percent of their calories from sugar. On the whole, the odds of dying from heart disease rose in tandem with the percentage of added sugar in the diet regardless of the age, sex, physical activity level, and body mass index (Dhurandhar & Thomas, 2014).

A 2014 study came to very similar conclusions. Here, those who consumed the most sugar - about 25 percent of their daily calories - were twice as likely to die form heart disease as those who limited their sugar intake to 7 percent of their total calories (Yang et al., 2013).

A 2013 study, published in the Journal of the Academy of Nutrition and Dietetics, looked at the differing effects of high-fat diets versus low-fat diets on blood lipid levels. The study included 32 studies and found that high-fat diets resulted in significantly greater improvements in reductions of total cholesterol, LDL cholesterol, and triglycerides and benificial increases in HDL cholesterol (Schwingshackl et al., 2013).

Of course, the choice to take medications, if referred by your physician is, and should, always be your choice. However, you have the right to be fully informed of the side effects of consuming anything. With this in mind, it is important to be aware of the unintended side effects of taking statins.

A study published in Clinical Cardiology concluded that "Statin therapy is associated with decreased myocardial [heart muscle] function," which often leads to heart failure. The  study did not address causes, but it's widely known that statins lower your CoQ10 levels by blocking the pathway involved in cholesterol production -- the same pathway by which Q10 is produced. Statins also reduce the blood cholesterol that transports CoQ10 and other fat-soluble antioxidants. The loss of CoQ10 leads to loss of cell energy and increased free radicals which, in turn, can further damage your mitochondrial DNA, effectively setting into motion an evil circle of increasing free radicals and mitochondrial damage (Mercola, 2011).

Moreover, for those at risk of heart disease taking statins who are unwilling or unable to bring down their cholesterol and/or triglyceride levels naturally with dietary changes, the potential for liver or muscle damage should be acknowledged. In addition, the potential for brain-related side effects, such as memory loss and confusion, as well as Parkinson’s-like symptoms is of concern. Statin drugs also appeared to increase the risk of stroke and developing diabetes. In 2013, a study of several thousand breast cancer patients reported that long-term use of statins may as much as double a woman's risk of invasive breast cancer.

There are 71 diseases that may be associated with these drugs, and this is only the tip of the iceberg. There are actually over 900 studies showing the risks of statin drugs, which include:

• Cognitive loss
• Neuropathy
• Anemia
• Acidosis
• Frequent fevers
• Cataracts
• Sexual dysfunction
• An increase in cancer risk
• Pancreatic dysfunction
• Immune system suppression
• Serious degenerative muscle tissue condition (rhabdomyolysis)
• Hepatic dysfunction

Plant-based diets have been shown to lower cholesterol just as effectively as first-line statin drugs, but without the risks. In fact, the "side effects" of healthy eating tend to be good - less cancer and diabetes risks and protection of the liver and brain (Gregor, 2015).

Baker, A. (2012). What's the real driver of elevated cholesterol? hint: it's not saturated fat! - Nourish Holistic Nutrition. [online] Nourish Holistic Nutrition. Available at: nourishholisticnutrition.com/whats-the-real-driver-of-elevated-cholesterol/ [Accessed 8 Feb. 2019].

Dhurandhar, N. and Thomas, D. (2015). The Link Between Dietary Sugar Intake and Cardiovascular Disease Mortality. JAMA, 313(9), p.959. https://doi.org/10.1001/jama.2014.18267 [Accessed 8 Feb. 2019].

Gregor, M. (2015) How Not to Die. London: Pan Books

Gundry, S. (2017). The Plant Paradox. New York, NY: Harper Wave

Hyman, M. (2016). 7 Ways to Optimize Cholesterol. [online] Dr. Mark Hyman. Available at: https://drhyman.com/blog/2016/01/14/7-ways-to-optimize-cholesterol/ [Accessed 8 Feb. 2019].

Mercola, J. (2017). Fat for Fuel. Carlsbad, CA: Hayhouse Inc.

Mercola, J. (2011). New Study Shows Using Statins Actually Harms Heart Function. [online] Mercola.com. Available at: https://articles.mercola.com/sites/articles/archive/2011/06/22/new-study-show-using-statins-actually-worsens-your-heart-function.aspx [Accessed 8 Feb. 2019].

Mercola, J. (2015). Conventional Heart Disease Advice May Make Matters Worse. [online] Mercola.com. Available at: https://articles.mercola.com/sites/articles/archive/2015/08/02/heart-disease-risk-factors.aspx [Accessed 8 Feb. 2019].

Perlmutter, D (2013). Grain Brain. New York, NY: Little Brown

Ray, K. et al. (2010). Statins and All-Cause Mortality in High-Risk Primary Prevention. Archives of Internal Medicine, 170(12), p.1024. Available at: https://doi.org/10.1001/archinternmed.2010.182 [Accessed 8 Feb. 2019].

Rubinstein, J., Aloka, F. and Abela, G. (2009). Statin Therapy Decreases Myocardial Function as Evaluated Via Strain Imaging. Clinical Cardiology, 32(12), pp.684-689. Available at: https://doi.org/10.1002/clc.20644 [Accessed 8 Feb. 2019].

Schwingshackl, S., et al. (2013). Comparison of Effects of Long-Term Low-Fat vs High-Fat Diets on Blood Lipid Levels in Overweight and Obese Patients: A Systematic Review and Meta-Analysis. Journal of the Academy of Nutrition and Dietetics, 113(12), pp. 1640-61. Available at: https://doi.org/10.1016/j.jand.2013.07.010 [Accessed 8 Feb. 2019].

Wallerwellness.com. (2019). Understanding Triglycerides. [online] Available at: https://www.wallerwellness.com/health-and-aging/understanding-triglycerides [Accessed 8 Feb. 2019].

Williams, J. (2017). How To Lower Dangerously High Triglyceride Levels. [online] Renegade Health. Available at: http://renegadehealth.com/blog/2017/03/31/how-to-lower-dangerously-high-triglycerides-levels [Accessed 8 Feb. 2019].

Yang, Q., et al. (2014). Added Sugar Intake and Cardiovascular Diseases Mortality Among US Adults. JAMA Internal Medicine, 174(4), pp.516-24. Available at: https://doi.org/10.1001/jamainternmed.2013.13563 [Accessed 8 Feb. 2019].

Despite food manufacturers claiming that refined vegetable oils were healthy, Americans experienced an up-rise in heart disease during the early 20th century. Like many new inventions, few questions were initially posited. Unfortunately, an alternate nutrient took the blame due to the research of a single scientist.

In 1951, American physiologist and professor Ancel Keys went to Europe in search of the cause of cardiovascular disease. In his quest, he went to observe the eating habits of individuals living Naples, Italy due to reports of a low prevalence of heart disease.

During this time, post-war conditions resulted in finite and unusual circumstances in regards to agriculture and infrastructure. Therefore what Keys perceived as a cultural tradition was dubbed the "Mediterranean diet".

Keys observed the residents in Naples consumed primarily pasta and plain pizza, with vegetables, olive oil, cheese, fruit for dessert, a moderate amount of wine, and very little meat (except among individuals belonging to a higher socioeconomic status).

Through an informal study measuring cholesterol serum levels among Rotary club members (those who could not afford meat, but could afford cheese) conducted by Keys's wife, whom at the time was a medical technologist, Keys deduced that avoiding meat resulted in a lower incidence of heart attacks.

Ancel Keys continued on his biased search for proof that a diet high in saturated fat is correlated with a higher risk of cardiovascular disease. He eventually compiled data from six more countries with high rates of heart disease and diets typically high in saturated fat. At first glance, Keys's research seemed logical and compelling. The evidence was based on the premise that individuals in America, who consumed high amounts of saturated fat, died from heart disease at a higher rate than individuals in Japan, who consumed low amounts of saturated fat.

Unfortunately, Keys had gained the interest of people in positions of power. Upon President Eisenhower's heart attack in 1955, Keys proposed his theory to the president's primary care physician, Paul Dudley White. Days following, White began to advise to the public to reduce the consumption of saturated fat and cholesterol in an effort to prevent cardiovascular disease.

Through his connections and influence, Keys soon joined the nutrition committee of the American Heart Association (AHA) which, based on Keys's research, released a report in 1961 that advised patients with a high risk of cardiovascular disease to reduce their consumption of saturated fat. (Interestingly enough, the AHA began its rise to prominence in 1948, the same year Proctor & Gamble donated over $1.7 million to the organization - resulting in the AHA indebted to Crisco.)

In 1961, Time magazine placed Ancel Keys on the front cover touting him as "the twenthiest century's most influential nutrition expert."

By 1970, Keys published the Seven Countries Study, which detailed his original research - this study has now been cited in over a million other scientific publications. While Keys associative observations between saturated fat and cardiovascular disease never proved causation, he had won the battle of public opinion.

With the help of Ancel Keys, the American medical community and mainstream media has advised consumers to stop eating the animal products that have been consumed for centuries, replacing them with bread, pasta, margarine, low-fat dairy, and vegetable oil. This was the dietary shift that was codified by the United States government in the late 1970s.

Central Committee for Medical And Community Program of the American Heart Association. (1961). Dietary Fat and Its Relation to Heart Attacks and Strokes. Circulation [online] 23, pp.133-36. Available at: https://circ.ahajournals.org/content/circulationaha/23/1/133.full.pdf [Accessed 26 Jan. 2019]

Keys, A. (1953). Atherosclerosis: A Problem in Newer Public Health. Journal of Mt. Sinai Hospital, [online] 20(2), pp.118-39.

Keys, A. (1970). Coronary Heart Disease in Seven Countries. Circulation. 41 (1), pp.1186-95.

Keys, A. (1995). Mediterranean Diet and Public Health: Personal Reflections. American Journal of Clinical Nutrition, [online] 61 (6), pp.1321S-1323S. Available at: https://dx.doi.org/10.1093/ajcn/61.6.1321s [Accessed 26 Jan. 2019]

Marvin, H. (1964). The 40 Year War on Heart Disease. New York: American Heart Association.

Mercola, J. (2017). Fat For Fuel. Carlsbad, California: Hay House.

Teichholz, N. (2014). The Big Fat Surprise. New York: Simon & Schuster, pp.32-33.