Broken Hearts and MEDICAL MONEY
I have few heros, and typically the people admire do not desire admiration. Ivan Illich was an Austrian philosopher, social critic, and Catholic priest. He was born on September 4, 1926, in Vienna, Austria, and died on December 2, 2002, in Bremen, Germany.
Illich gained prominence in the 1970s for his critiques of modern institutions and his anti-establishment views on education, medicine, and technology. He believed that many institutions in society had become counterproductive and oppressive, and he called for their deinstitutionalisation.
One of Illich's notable works that I have mentioned in many of my own works is "Deschooling Society" (1971), in which he argued that compulsory schooling was detrimental to true learning and personal growth. He advocated for a more decentralised, learner-centred approach to education, emphasising the importance of self-directed learning and community-based education.
In "Medical Nemesis" (1975), Illich criticised the medical establishment and its over-reliance on technology, arguing that it often creates dependency and diminishes individual responsibility for one's health. He called for a shift towards more holistic and participatory models of healthcare. Illich also wrote extensively on other topics, such as transportation, economics, and the role of technology in society. He was a vocal critic of consumerism and the pursuit of unlimited economic growth, which he believed led to social and environmental problems.
Illich's central thesis in "Medical Nemesis" is that the medical establishment, driven by a belief in the limitless power of technology and professional expertise, has created a system of institutionalised medicine that ultimately undermines human health and autonomy. He coined the term "medical nemesis" to describe the harmful consequences of this system.
According to Illich, medicalisation occurs when normal human conditions and experiences, such as birth, aging, and death, are called pathologies and subjected to medical intervention. This over-reliance on medical intervention, he argues, leads to the devaluation of individual responsibility for one's own health and the erosion of self-care practices. Indeed, we sat and watched from 2020 as the world sat awaiting a magic bullet from Pharma and accepted that no other options could work as the industry sought emergency approval due to a lack of “cure”.
Illich criticises the industrialisation and bureaucratisation of medicine, which he believes have transformed healthcare into a profit-driven enterprise focused on disease management rather than genuine healing. He argues that medical professionals have become institutional agents who primarily serve the interests of the medical system, often at the expense of patients' well-being.
Furthermore, Illich suggests that the medicalisation of society creates a dependency on professional healthcare services and fosters a passive attitude towards one's own health. He contends that people have been conditioned to believe that they need medical experts and technology to maintain their health, rather than relying on their own abilities and resources.
In response to the problems he identifies, Illich calls for a reevaluation of the role of medicine and a shift towards a more participatory and empowering model of healthcare. He advocates for a greater emphasis on self-care, preventive measures, and community-based support systems. Illich argues that individuals should take back control of their health and be actively engaged in making informed decisions about their well-being.
While "Medical Nemesis" sparked significant debate and controversy when it was published, it contributed to the broader discussions about the social and ethical dimensions of healthcare. It encouraged critical examination of medical practices and prompted calls for more patient-centred approaches that focus on holistic well-being rather than just the treatment of disease.
Another I admire is Albert Imre Szent-Györgyi de Nagyrápolt, commonly known as Albert Szent-Györgyi, who was a Hungarian physiologist and biochemist. He was born on September 16, 1893, in Budapest, Hungary, and passed away on October 22, 1986, in Woods Hole, Massachusetts, United States.
Szent-Györgyi is best known for his work on vitamin C and the discovery of its chemical structure. In the late 1920s, he isolated a substance from adrenal glands that could prevent and cure scurvy in guinea pigs. He named this substance "hexuronic acid," which was later identified as vitamin C or ascorbic acid. His discovery played a crucial role in understanding the importance of vitamin C in human health.
For his significant contributions to the field of biochemistry, Szent-Györgyi was awarded the Nobel Prize in Physiology or Medicine in 1937. He also conducted extensive research on muscle contraction and the biochemistry of cellular respiration, making notable contributions in these areas as well.
During World War II, Szent-Györgyi was involved in medical research and served as a member of the Hungarian resistance against the Nazis. However, due to political turmoil in Hungary, he left the country in 1947 and settled in the United States, where he continued his scientific work.
Szent-Györgyi was a distinguished scientist who made significant contributions to our understanding of biochemistry and the role of vitamin C in human health. His work has had a lasting impact on the fields of nutrition and medicine.
Szent-Györgyi's research interests primarily focused on muscle physiology, cellular respiration, and the biochemistry of various compounds. He made significant contributions my early interest in the field of medicine, and specifically estrogen and progesterone due to the death of my own grandma from what I understand was a medical blunder that had profound consequences and left me questioning the requirement to be patient and consenting when advised by a medical practitioner.
In 1952-1953 Albert Szent-Györgyi conducted research on the "staircase effect" in heart muscle and the action of drugs on it. The staircase effect, also known as the treppe phenomenon or Bowditch staircase, refers to a phenomenon in which the strength of contraction of cardiac muscle increases stepwise with increasing frequency of stimulation.
Szent-Györgyi's study aimed to investigate the staircase effect in heart muscle and the influence of various drugs on this phenomenon. By studying the effects of different substances on the contraction of cardiac muscle, he aimed to gain a better understanding of the underlying mechanisms involved in the regulation of heart function.
Szent-Györgyi observed that estrogen treatment decreased the staircase effect, meaning that the strength of contractions did not increase significantly with an increase in the rate of stimulation. On the other hand, progesterone treatment increased the staircase effect, resulting in a more pronounced rise in the strength of contractions with higher rates of stimulation.
Szent-Györgyi's interpretation of the staircase effect as a process where function (rate of contraction) builds structure (size of the contraction) is an intriguing concept. In this context, it seems that progesterone facilitated the building of "structure" through contractions, while estrogen hindered this process.
Comparing these effects of hormones to the broader concepts of anabolic and catabolic hormones, which affect more permanent structures in cells, does provide an interesting perspective. Anabolic hormones generally promote growth, tissue repair, and the synthesis of complex molecules, contributing to structural development. In contrast, catabolic hormones facilitate the breakdown of complex molecules and energy release, often associated with a more dynamic state.
Szent-Györgyi's observations on the effects of estrogen and progesterone on the staircase effect in heart muscle contribute to our understanding of how hormones can influence cardiac function and potentially affect cardiovascular conditions such as heart failure. (1)
He noted the effects of progesterone, testosterone, and estrogen on heart function, as well as their relationship to chronotropy and the influence of hormones on shock and stress responses.
It is interesting to note that both progesterone and testosterone exhibit positive inotropic and lusitropic effects, meaning they enhance both contraction and relaxation of the heart muscle. This can contribute to improved overall cardiac function. In contrast, estrogen has been found to have negative lusitropic and inotropic effects, impairing both relaxation and contraction of the heart.
The distinction between inotropic and chronotropic effects is important in understanding how drugs or hormones impact heart rate. Inotropic effects refer to changes in the force of contraction, while chronotropic effects refer to changes in heart rate or the frequency of contractions.
The interaction between frequency and force in the staircase effect can lead to some confusion when classifying drugs based on chronotropism. In certain conditions like shock or estrogen dominance, an inotropic drug can actually slow down the heart rate by increasing the amount of blood pumped per contraction. This relationship may have contributed to the initial belief that drugs like digitalis primarily slowed the rate of contraction, despite their main effect being positive inotropy. Digitalis was traditionally used to treat edema, primarily through its inotropic action and resulting diuretic effect.
Hans Selye discovered that a large dose of estrogen could create a shock-like state. It's worth noting that shock and stress can lead to an increase in estrogen levels while simultaneously decreasing progesterone and testosterone levels. It was never tracked or even considered but I would hypothesis that given we know isolation increases estradiol in isolated rats, that similar happens in locked down humans and or humans injected with a large and often multiple dose of a pathogen (rather than the standard airways pathway of a respiratory pathogen) that may have caused a shock when hitting the bloodstream.
The discovery of heart-stimulating molecules as metabolites of progesterone and the role of thyroid hormone in regulating cardiac function. Additionally, you mentioned the effects of water retention, the role of mitochondria in energy production, and the significance of calcium binding in muscle relaxation and heart failure.
Digoxin and other heart-stimulating molecules can be derived from progesterone and possibly DHEA metabolites adds to our understanding of the endogenous regulatory mechanisms within the body. These discoveries suggest that the body has its own mechanisms for modulating heart function. Furthermore, the positive lusitropic and inotropic actions of thyroid hormone have been recognised for over 20 years. Thyroid hormone plays a crucial role in regulating the synthesis of proteins, such as phospholamban and calcisequestrin, which control the binding of calcium in the cardiac cells. By promoting efficient energy production in the mitochondria and regulating calcium binding, thyroid hormone helps the cells maintain proper relaxation and contraction cycles.
When a muscle or nerve is fatigued, water retention can occur, limiting its ability to contract fully. This waterlogged state, with increased levels of sodium and calcium in the cytoplasm, can disrupt cellular function. Thyroid hormone, in conjunction with oxygen, sugar, and mitochondrial energy production, helps eliminate excess water and bind calcium efficiently. This allows the cells to relax fully, preparing them for the next contraction.
In heart failure, particularly in diastolic failure, the muscle is unable to relax adequately. Initially, this may be a result of water-logging and fatigue. However, over time, metabolic changes can lead to fibrosis and calcification of the heart muscle, further impairing its function.
During puberty, as estrogen levels increase and potentially interfere with thyroid function, some children may experience "growing pains" characterised by tense and sore muscles after prolonged activity. This suggests a potential interplay between hormonal changes and muscle discomfort during this developmental stage.
In cases of severe hypothyroidism, myopathy can occur, which involves painful swelling and the leakage of muscle proteins, particularly myoglobin, into the bloodstream. This condition can be diagnosed through a blood test. Furthermore, the combination of hypothyroidism, fatigue, and stress can lead to muscle cell breakdown and death, a condition known as rhabdomyolysis.
The use of certain blood lipid-lowering drugs, such as statins and fibrates, has been associated with impairments in mitochondrial respiration, as well as an increased incidence of rhabdomyolysis. While interference with coenzyme Q10 is one mechanism through which these drugs can cause myopathy, it is not the only one. Studies have indicated the harmful effects of lowering cholesterol levels, and the use of statins or lipid-lowering therapy in heart failure remains a topic of debate and controversy.
Both heart muscle and skeletal muscle exhibit similar structural responses when mitochondrial function is compromised, including swelling, reduced contractile ability, and dissolution. While the presence of myoglobin in the blood and urine has traditionally been attributed to skeletal muscle breakdown, there have been observations of depleted myoglobin in the heart of a patient with myoglobinuria. Additionally, in cases of known heart failure, similar changes can be observed in skeletal muscles.
Stress, in various forms such as pressure overload, overactivity of the renin-angiotensin system, sympathetic nervous system activation, or energy failure caused by conditions like diabetes, insulin deficiency, or hypothyroidism, can lead to a shift in energy production from the oxidation of glucose to the oxidation of fatty acids. This shift may result in the release of lactic acid produced from glucose instead of its complete oxidation. This sequence, from reduced energy production efficiency to heart failure, can be counteracted by agents that reduce the availability of fatty acids and promote the oxidation of glucose.
Niacinamide, for example, inhibits the release of free fatty acids from tissues, while thyroid hormone sustains the oxidation of glucose. This principle has gained recognition, and there are drugs approved by the FDA, such as raloxifene (approved in 2006), that inhibit fatty acid oxidation. However, it is important to note that such drugs may come with serious side effects. Glucose oxidation appears to be crucial in preventing the intracellular accumulation of free calcium and fatty acids. The calcium binding protein, activated by thyroid hormone and inhibited by estrogen, seems to be activated by glucose and inhibited by fatty acids.
The information you provided underscores the importance of energy metabolism, particularly the balance between glucose and fatty acid oxidation, in maintaining proper cellular function and preventing heart failure. It also highlights the role of hormones such as thyroid hormone and estrogen in modulating these processes. Further research in these areas may help elucidate the underlying mechanisms and potentially lead to the development of therapeutic interventions for heart failure and related conditions.
In conditions such as diabetes or fasting, there is an increase in free fatty acids, which leads to a shift in cellular energy metabolism from glucose oxidation to fatty acid oxidation. This shift inhibits the binding of calcium, which can impact heart function. However, studies have shown that providing a small amount of sugar, such as 0.8% sucrose in drinking water, can restore calcium binding and heart function without increasing thyroid hormone or insulin levels. Lowering free fatty acids through the restoration of glucose oxidation improves the ability to oxidize sugar, lowers serum glucose levels, and increases overall cellular efficiency. This restoration of efficiency also leads to a decrease in sympathetic nervous system activity.
Digoxin, a medication used to treat certain heart conditions, has been found to stimulate mitochondrial energy production in both skeletal and heart muscle. This stimulation promotes the oxidation of glucose rather than fatty acids, supporting the beneficial effects of thyroid hormone. In contrast, statin medications have been shown to decrease the oxidation of glucose, which may have different effects on cellular energy metabolism.
Estrogen has been associated with chronic increases in the circulation of free fatty acids and a preference for long-chain polyunsaturated fatty acids, including EPA and DHA. These fatty acids have various effects on the heart, including slowing the heart rate, prolonging the excited state (action potential), and exhibiting negative inotropic properties. While they are bizarrely being investigated as potential heart-protective drugs. It is worth noting that EPA and alpha-linoleic acid have also been associated with the prolongation of the QT interval, a measurement of cardiac electrical activity and delayed relation and re-polorisation.
While estrogen has been traditionally considered by the industry as a cardioprotective hormone, there is an increasing recognition of its role in heart failure and sudden cardiac death. Prolonged excited states (action potentials) and delayed relaxation (QT interval) have been linked to an increased risk of arrhythmias and sudden death. Estrogen has been found to induce these changes in humans, and studies have shown that it can cause sudden cardiac death in susceptible rabbits. Furthermore, the administration of an adrenergic stimulant can increase arrhythmias, while progesterone and androgens have been found to prevent them. Progesterone's protective effect appears to be related to its ability to accelerate the recovery of the resting state.
Estrogen's interaction with adrenaline in promoting blood vessel constriction has been known for some time, and progesterone has been found to block this effect of estrogen. Environmental estrogens, such as bisphenol A (BPA), have been shown to exacerbate ventricular arrhythmias induced by estrogen. In animal studies, mice genetically engineered to lack aromatase, the enzyme responsible for synthesising estrogen, demonstrated increased resistance to damage when deprived of blood for a certain period of time. This led researchers to suggest that inhibiting aromatase might have potential benefits in the context of heart disease.
In the stressed and energy-depleted failing heart, the loss of muscle cells and their replacement by connective tissue cells contributes to stiffening and reduced functioning of the heart. However, under the influence of thyroid hormone, a high workload can lead to functional enlargement of the heart, which increases its pumping ability. Traditionally, it was believed that heart cells could not replicate, so this functional growth was thought to be solely due to cell enlargement. However, in recent years, the existence of stem cells capable of generating new heart muscle cells has been recognized. Thyroid hormone is likely one of the hormones responsible for facilitating the differentiation of stem cells into cardiomyocytes.
Considering cellular differentiation as an ongoing process throughout life, we can understand the changes observed in a failing heart as a form of differentiation that takes an inappropriate course. For instance, the calcification of blood vessels caused by excessive phosphate and vitamin K deficiency involves the expression of a protein that is normally found in the skeleton. The replacement of heart muscle with fibrous connective tissue and even bone represents a fundamental biological issue in differentiation. The factors involved in this process, such as stress, increased estrogen, deficient thyroid hormone, and suppression of glucose oxidation by fatty acids, are also implicated in differentiation problems observed in other degenerative conditions such as sarcopenia, dementia, and cancer.
Stresses, including hypoxia, can induce dedifferentiation of cells, and hypoxia can activate the "estrogen receptor" even in the so-called absence of estrogen. Estrogen, in certain situations, acts as a hormone of dedifferentiation by promoting the formation of new cells in stressed tissues through the induction of aromatase. However, the presence of polyunsaturated fats, which tend to increase with age, can lead to exaggerated inflammation during the processes of cell renewal. Prostaglandins, which participate in development and differentiation, contribute to this inflammatory response. Estrogen, by increasing the concentration of free fatty acids, especially polyunsaturated fatty acids, can shift metabolism away from glucose oxidation and organ-specific differentiation towards the production of lactic acid.
This perspective highlights the common biological basis underlying heart failure, cancer, and other degenerative diseases, explaining why certain conditions and therapies may be applicable across these conditions.
When viewed through these mechanisms, seemingly trivial problems take on more significance. Some problems that become common in middle age include palpitations, orthostatic hypotension, orthostatic tachycardia, and varicose veins. The negative inotropic effect of estrogen on the heart has a parallel effect on the smooth muscles of veins. Insufficient opposition of estrogen by progesterone weakens the vein muscles and increases their distensibility. This abnormal distension of veins in the lower part of the body when standing reduces the amount of blood returning to the heart, resulting in a smaller volume of blood pumped with each stroke, necessitating a faster heart rate. The reduced blood volume reaching the brain can lead to fainting. Over time, this condition can cause progressive distortion of the veins. Excess estrogen has been associated with varicose veins in both men and women.
Understanding the interplay between estrogen, progesterone, fatty acids, and the biological mechanisms involved in cell differentiation and inflammation helps explain the connections between various health conditions and provides insights into potential therapeutic approaches.
Certain interventions such as supplementing thyroid, progesterone, and sugar, avoiding excess phosphate in relation to calcium, and limiting polyunsaturated fats can be implemented by individuals, it is important to approach self-care with caution and consult with healthcare professionals, especially when it comes to hormone supplementation.
The use of thyroid supplements, particularly the active T3 hormone, for heart-related conditions is still a matter of debate among physicians. While heart transplant surgeons have observed benefits of administering T3 to heart donors before transplantation, its widespread use as a "heart drug" remains controversial. Breathing into a paper bag to increase carbon dioxide levels in the blood can have a vasodilating effect and potentially help lower blood pressure and improve heart rhythm. Rhubarb and its component emodin have shown heart-protective properties. Vitamin K has been studied for its potential in treating hypertension, but its use is often cautioned against due to a poorly evidenced “association" with blood clotting. The value of warfarin, a vitamin K antagonist, has been questioned for individuals with heart failure.
The speed of relaxation of the Achilles tendon reflex twitch has been traditionally used as an indicator of thyroid function. Hypothyroidism can cause delayed relaxation, which can also be observed as a prolonged QT interval in an electrocardiogram. Defective relaxation can be associated with conditions such as insomnia, mania, and asthma, influenced by low thyroid function and an insufficiently opposed influence of estrogen.
While these observations and interventions are not those of a doctor, it is crucial to approach self-care in conjunction with professional medical advice (I fully encourage you to study and challenge their diagnostics skills, a good doctor should relish the chance to prove their findings) Always consider individual health circumstances and potential interactions with other medications or treatments, doctors often don’t do this as my grandma found out.
Little can be done to undo the many factors that seem to correlate with our damaged hearts, but we must step back and investigate our own health. Accepting doctors interpretations of bloods as “normal” does little to help us unpick our own mystery and we should own our health. Get the print out or get your own tests done and then start learning.
References:
Hajdu, S., & Szent-Gyorgyi, A. (1952). Action of DOC and serum on the frog heart. The American journal of physiology. 168(1): 159–170. https://doi.org/10.1152/ajplegacy.1951.168.1.159
