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

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

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

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

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

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

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

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

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

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

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

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

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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.
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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.
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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.
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These vulnerable plaques are believed to be a blend of inflammatory buildup and low-density lipoprotein (LDL), the primary targets of statin drugs. Consequently, the widespread adoption of statin therapy is advocated as a preventive measure against heart attacks, fueled by angiogram studies purportedly showcasing the prevalence of unstable plaques as the leading cause of myocardial infarctions (MIs).

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

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

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

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

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

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

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

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

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

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

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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.

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

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