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Are invisible forces making you fat, sick and tired? Electropollution

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Introduction


This is a copy-paste of all sections concerning mitochondria in the highly recommended book called "The invisible rainbow: A history of electricity and life" by Arthur Firstenberg. It is in no way a substitute for reading the book and the huge amounts of references it contains on the impacts of electropollution! If you never heard of mitochondria before see the next section. Before you read this post I recommend to first contemplate the fascinating observation of Dr. Jack Kruse which clicked anew for me while reading this book:

Everything in our universe that loses energy gets bigger - from your twisted ankle to a dying star.

Mitochondria 101


What?

How?

More? Read:



The electromagnetic nervous system


Page 135:

Everyone knows that the brain consumes more oxygen than any other organ, and that if a person stops breathing, the brain is the first organ to die. What the Italian team confirmed in 2009 is that as much as ninety percent of that oxygen is consumed not by the brain’s nerve cells, but by the myelin sheaths that surround them. Traditional wisdom has it that the consumption of oxygen for energy takes place only in tiny bodies inside cells called mitochondria. That wisdom has now been turned on its head. In the nervous system, at least, most of the oxygen appears to be consumed in the multiple layers of fatty substance called myelin, which contain no mitochondria at all, but which forty-year-old research showed contains non-heme porphyrins and is semiconducting. Some scientists are even beginning to say that the myelin sheath is, in effect, itself a giant mitochondrion, without which the huge oxygen needs of our brain and nervous system could never be met. But to truly make sense of this collection of facts will also require the recognition that both the neurons, as Ling Wei proposed, and the myelin sheaths that envelop them, as Robert Becker proposed, work together to form a complex and elegant electrical transmission line system, subject to electrical interference just like transmission lines built by human engineers.


Page 136:

In our cells, the manufacture of heme from porphyrins can be inhibited by a large variety of toxic

chemicals, and not—so far as we know—by electricity. But we will see in the coming chapters that electromagnetic fields interfere with the most important job that this heme is supposed to do for us: enabling the combustion of our food by oxygen so that we can live and breathe. Like rain on a campfire, electromagnetic fields douse the flames of metabolism. They reduce the activity of the cytochromes, and there is evidence that they do so in the simplest of all possible ways: by exerting a force that alters the speed of the electrons being transported along the chain of cytochromes to oxygen.


Every person on the planet is affected by this invisible rain that penetrates into the fabric of our cells. Everyone has a slower metabolism, is less alive, than if those fields were not there. We will see how this slow asphyxiation causes the major diseases of civilization: cancer, diabetes, and heart disease. There is no escape. Regardless of diet, exercise, lifestyle, and genetics, the risk of developing these diseases is greater for every human being and every animal than it was a century and a half ago. People with a genetic predisposition simply have a greater risk than everyone else, because they have a bit less heme in their mitochondria to start with.



Neurasthenia and heart disease


Page 148:

Compared to healthy individuals, people with this disorder were able to extract less oxygen from the same amount of air, and their cells were able to extract less energy from the same amount of oxygen. The researchers concluded that these patients suffered from a defect of aerobic metabolism. In other words, something was wrong with their mitochondria—the powerhouses of their cells. The patients correctly complained that they could not get enough air. This was starving all of their organs of oxygen and causing both their heart symptoms and their other disabling complaints. Patients with neurocirculatory asthenia were consequently unable to hold their breath for anything like a normal period of time, even when breathing oxygen.


In fact, these researchers virtually disproved the theory that the disease was caused by “stress” or “anxiety.” It was not caused by hyperventilation.30 Their patients did not have elevated levels of stress hormones—17-ketosteroids—in their urine. A twenty-year follow-up study of civilians with neurocirculatory asthenia revealed that these people typically did not develop any of the diseases that are supposed to be caused by anxiety, such as high blood pressure, peptic ulcer, asthma, or ulcerative colitis.31 However, they did have abnormal electrocardiograms that indicated that the heart muscle was being starved of oxygen, and that were sometimes indistinguishable from the EKGs of people who had actual coronary artery disease or actual structural damage to the heart.32


The connection to electricity was provided by the Soviets. Soviet researchers, during the 1950s, 1960s, and 1970s, described physical signs and symptoms and EKG changes, caused by radio waves, that were identical to those that White and others had first reported in the 1930s and 1940s. The EKG changes indicated both conduction blocks and oxygen deprivation to the heart.33 The Soviet scientists—in agreement with Cohen and White’s team—concluded that these patients were suffering from a defect of aerobic metabolism. Something was wrong with the mitochondria in their cells. And they discovered what that defect was. Scientists that included Yury Dumanskiy, Mikhail Shandala, and Lyudmila Tomashevskaya, working in Kiev, and F. A. Kolodub, N. P. Zalyubovskaya and R. I. Kiselev, working in Kharkov, proved that the activity of the electron transport chain—the mitochondrial enzymes that extract energy from our food—is diminished not only in animals that are exposed to radio waves,34 but in animals exposed to magnetic fields from ordinary electric power lines.


Page 151-152:

According to published literature, all of these diseases—neurocirculatory asthenia, radio wave sickness, anxiety disorder, chronic fatigue syndrome, and myalgic encephalomyelitis—predispose to elevated levels of blood cholesterol, and all carry an increased risk of death from heart disease.57 So do porphyria58 and oxygen deprivation.59 The fundamental defect in this disease of many names is that although enough oxygen and nutrients reach the cells, the mitochondria—the powerhouses of the cells—cannot efficiently use that oxygen and those nutrients, and not enough energy is produced to satisfy the requirements of heart, brain, muscles, and organs. This effectively starves the entire body, including the heart, of oxygen, and can eventually damage the heart. In addition, neither sugars nor fats are efficiently utilized by the cells, causing unutilized sugar to build up in the blood—leading to diabetes—as well as unutilized fats to be deposited in arteries.


And we have a good idea of precisely where the defect is located. People with this disease have reduced activity of a porphyrin-containing enzyme called cytochrome oxidase, which resides within the mitochondria, and delivers electrons from the food we eat to the oxygen we breathe. Its activity is impaired in all the incarnations of this disease. Mitochondrial dysfunction has been reported in chronic fatigue syndrome60 and in anxiety disorder.61 Muscle biopsies in these patients show reduced cytochrome oxidase activity. Impaired glucose metabolism is well known in radio wave sickness, as is an impairment of cytochrome oxidase activity in animals exposed to even extremely low levels of radio waves.62 And the neurological and cardiac symptoms of porphyria are widely blamed on a deficiency of cytochrome oxidase and cytochrome c, the heme-containing enzymes of respiration.63


Recently zoologist Neelima Kumar at Panjab University in India proved elegantly that cellular respiration can be brought to a standstill in honey bees merely by exposing them to a cell phone for ten minutes. The concentration of total carbohydrates in their hemolymph, which is what bees’ blood is called, rose from 1.29 to 1.5 milligrams per milliliter. After twenty minutes it rose to 1.73 milligrams per milliliter. The glucose content rose from 0.218 to 0.231 to 0.277 milligrams per milliliter. Total lipids rose from 2.06 to 3.03 to 4.50 milligrams per milliliter. Cholesterol rose from 0.230 to 1.381 to 2.565 milligrams per milliliter. Total protein rose from 0.475 to 0.525 to 0.825 milligrams per milliliter. In other words, after just ten minutes of exposure to a cell phone, the bees practically could not metabolize sugars, proteins, or fats. Mitochondria are essentially the same in bees and in humans, but since their metabolism is so much faster, electric fields affect bees much more quickly.

...

It was the English physiologist John Scott Haldane who first suggested, in his classic book,

Respiration, that “soldier’s heart” was caused not by anxiety but by a chronic lack of oxygen.65

Mandel Cohen later proved that the defect was not in the lungs, but in the cells. These patients

continually gulped air not because they were neurotic, but because they really could not get enough of it. You might as well have put them in an atmosphere that contained only 15 percent oxygen instead of 21 percent, or transported them to an altitude of 15,000 feet. Their chests hurt, and their hearts beat fast, not because of panic, but because they craved air. And their hearts craved oxygen, not because their coronary arteries were blocked, but because their cells could not fully utilize the air they were breathing.


These patients were not psychiatric cases; they were warnings for the world. For the same thing was also happening to the civilian population: they too were being slowly asphyxiated, and the pandemic of heart disease that was well underway in the 1950s was one result. Even in people who did not have a porphyrin enzyme deficiency, the mitochondria in their cells were still struggling, to some smaller degree, to metabolize carbohydrates, fats, and proteins. Unburned fats, together with the cholesterol that transported those fats in the blood, were being deposited on the walls of arteries. Humans and animals were not able to push their hearts quite as far as before without showing signs of stress and disease. This takes its clearest toll on the body when it is pushed to its limits, for example in athletes, and in soldiers during war.


The real story is told by the astonishing statistics.



The transformation of diabetes


Page 162-164:

The linked failure of both carbohydrate and fat metabolism is a sign of disordered respiration in the mitochondria, and the mitochondria, we have seen, are disturbed by electromagnetic fields.

Under the influence of such fields, respiratory enzyme activity is slower. After a meal, the cells

cannot oxidize the breakdown products of the proteins, fats, and sugars that we eat as quickly as they are being supplied by the blood. Supply outstrips demand. Recent research has shown

exactly how this happens.


Glucose and fatty acids, proposed University of Cambridge biochemist Philip J. Randle in 1963, compete with each other for energy production. This mutual competition, he said, operates independently of insulin to regulate glucose levels in the blood. In other words, high fatty acid levels in the blood inhibit glucose metabolism, and vice versa. Evidence in support appeared almost immediately. Jean-Pierre Felber and Alfredo Vannotti at the University of Lausanne gave a glucose tolerance test to five healthy volunteers, and then another one a few days later to the same individuals while they were receiving an intravenous infusion of lipids. Every person responded to the second test as though they were insulin resistant. Although their insulin levels remained the same, they were unable to metabolize the glucose as quickly in the presence of high levels of fatty acids in their blood, competing for the same respiratory enzymes. These experiments were easy to repeat, and overwhelming evidence confirmed the concept of the “glucose-fatty acid cycle.” Some evidence also supported the idea that not only fats, but amino acids as well, competed with glucose for respiration.


Randle had not been thinking in terms of mitochondria, much less what could happen if an

environmental factor restricted the ability of the respiratory enzymes to work at all. But during the last decade and a half, finally some diabetes researchers have begun focusing specifically on mitochondrial function.


Remember that our food contains three main types of nutrients—proteins, fats, and

carbohydrates—that are broken down into simpler substances before being absorbed into our

blood. Proteins become amino acids. Fats become triglycerides and free fatty acids. Carbohydrates become glucose. Some portion of these is used for growth and repair and becomes part of the structure of our body. The rest is burned by our cells for energy.


Within our cells, inside tiny bodies called mitochondria, amino acids, fatty acids, and glucose

are all further transformed into even simpler chemicals that feed into a common cellular

laboratory called the Krebs cycle, which breaks them down the rest of the way so that they can

combine with the oxygen we breathe to produce carbon dioxide, water, and energy. The last

component in this process of combustion, the electron transport chain, receives electrons from the Krebs cycle and delivers them, one at a time, to molecules of oxygen. If the speed of those

electrons is modified by external electromagnetic fields, as suggested by Blank and Goodman, or if the functioning of any of the elements of the electron transport chain is otherwise altered, the final combustion of our food is impaired. Proteins, fats, and carbohydrates begin to compete with each other and back up into the bloodstream. Fats are deposited in arteries. Glucose is excreted in urine. The brain, heart, muscles, and organs become oxygen-deprived. Life slows down and breaks down.


Only recently was it proven that this actually happens in diabetes. For a century, scientists had assumed that because most diabetics were fat, obesity causes diabetes. But in 1994, David E. Kelley at the University of Pittsburgh School of Medicine, in collaboration with Jean-Aimé Simoneau at Laval University in Quebec, decided to find out exactly why diabetics have such high fatty acid levels in their blood. Seventy-two years after insulin was discovered, Kelley and Simoneau were among the first to measure cellular respiration in detail in this disease. To their surprise, the defect turned out not to be in the cells’ ability to absorb lipids but in their ability to burn them for energy. Large amounts of fatty acids were being absorbed by the muscles and not metabolized. This led to intensive research into all aspects of respiration at the cellular level in diabetes mellitus. Important work continues to be done at the University of Pittsburgh, as well as at the Joslin Diabetes Center, RMIT University in Victoria, Australia, and other research centers.15


What has been discovered is that cellular metabolism is reduced at all levels. The enzymes that break down fats and feed them into the Krebs cycle are impaired. The enzymes of the Krebs cycle itself, which receives the breakdown products of fats, sugars, and proteins, are impaired. The electron transport chain is impaired. The mitochondria are smaller and reduced in number. Consumption of oxygen by the patient during exercise is reduced. The more severe the insulin resistance—i.e., the more severe the diabetes—the greater the reductions in all these measures of cellular respiratory capacity.


In fact, Clinton Bruce and his colleagues in Australia found that the oxidative capacity of the muscles was a better indicator of insulin resistance than their fat content—which threw into question the traditional wisdom that obesity causes diabetes. Perhaps, they speculated, obesity is not a cause but an effect of the same defect in cellular respiration that causes diabetes. A study involving lean, active young African-American women in Pittsburgh, published in 2014, seemed to confirm this. Although the women were somewhat insulin resistant, they were not yet diabetic, and the medical team could find no other physiological abnormalities in the group except two: their oxygen consumption during exercise was reduced, and mitochondrial respiration in their muscle cells was reduced.16


In 2009, the Pittsburgh team made an extraordinary finding. If the electrons in the electron transport chain are being disturbed by an environmental factor, then one would expect that diet and exercise might improve all components of metabolism except the last, energy-producing step involving oxygen. That is exactly what the Pittsburgh team found. Placing diabetic patients on calorie restriction and a strict exercise regime was beneficial in many respects. It increased the activity of the Krebs cycle enzymes. It reduced the fat content of muscle cells. It increased the number of mitochondria in the cells. These benefits improved insulin sensitivity and helped control blood sugar. But although the number of mitochondria increased, their efficiency did not. The electron transport enzymes in dieted, exercised diabetic patients were still only half as active as the same enzymes in healthy individuals.17


In June 2010, Mary-Elizabeth Patti, a professor at Harvard Medical School and researcher at the Joslin Diabetes Center, and Silvia Corvera, a professor at the University of Massachusetts Medical School in Worcester, published a comprehensive review of existing research on the role of mitochondria in diabetes. They were forced to conclude that a defect of cellular respiration may be the basic problem behind the modern epidemic. Due to “failure of mitochondria to adapt to higher cellular oxidative demands,” they wrote, “a vicious cycle of insulin resistance and impaired insulin secretion can be initiated.”


But they were not willing to take the next step. No diabetes researchers today are looking for an environmental cause of this “failure to adapt” of so many people’s mitochondria. They are still, in the face of evidence refuting it, blaming this disease on faulty diet, lack of exercise, and genetics. This in spite of the fact that, as Dan Hurley noted in his 2011 book, Diabetes Rising, human genetics has not changed and neither diet, exercise, nor drugs has put a dent in the escalation of this disease during the ninety years since insulin was discovered.



Cancer and the starvation of life


Page 174:

During the coming years—with a break during which he served in the World War—Warburg, using techniques that he developed, proved that respiration in a cell took place in tiny structures that he called “grana” and that we now call mitochondria. He experimented with the effects of alcohols, cyanide, and other chemicals on respiration and concluded that the enzymes in the “grana” must contain a heavy metal that he suspected, and later proved, was iron. He conducted landmark experiments using spectrophotometry that proved that the portion of the enzyme that reacts with oxygen in a cell is identical with the portion of hemoglobin that binds oxygen in the blood. That chemical, called heme, is a porphyrin bonded to iron, and the enzyme containing it, which exists in every cell and makes breathing possible, is known today as cytochrome oxidase. For this work Warburg was awarded the Nobel Prize in Physiology or Medicine in 1931.


Meanwhile, in 1923, Warburg resumed his research on cancer, picking up where he had left off fifteen years earlier. “The starting point,” he wrote, “has been the fact that the respiration of sea urchin eggs increases six-fold at the moment of fertilization,” i.e. at the moment that it changes from a state of rest to a state of growth. He expected to find a similar increase of respiration in cancer cells. But to his amazement, he found just the opposite. The rat tumor he was working with used considerably less oxygen than normal tissues from healthy rats.


“This result seemed so startling,” he wrote, “that the assumption seemed justified that the tumor lacked suitable material for combustion.” So Warburg added various nutrients to the culture medium, still expecting to see a dramatic rise in oxygen use. Instead, when he added glucose, the tumor’s respiration ceased completely! And in trying to discover why this happened, he found that tremendous amounts of lactic acid were accumulating in the culture medium. The tumor, in fact, was producing fully twelve percent of its weight in lactic acid per hour. Per unit time, it was producing 124 times as much lactic acid as blood, 200 times as much as a frog’s muscle at rest, and eight times as much as a frog’s muscle working to the limit of its capacity. The tumor was consuming the glucose, all right, but it was not making use of oxygen to do it.3


Page 176:

Cellular changes that indicate damaged respiration—including reductions in the number and size of mitochondria, abnormal structure of mitochondria, lessened activity of Krebs cycle enzymes, lessened activity of the electron transport chain, and mutations of mitochondrial genes—are being routinely found in most types of cancer. Even in tumors caused by viruses, one of the first signs of malignancy is an increase in the rate of anaerobic metabolism.


Experimentally inhibiting the respiration of cancer cells, or simply depriving them of oxygen, has been shown to alter the expression of hundreds of genes that are involved in malignant transformation and cancer growth. Damaging respiration makes cancer cells more invasive; restoring normal respiration makes them less invasive.10



Living longer while feeling like shit


As researchers into the aging process have emphasized, the engine of our lives is the electron transport system in the mitochondria of our cells.15 It is there that the oxygen we breathe and the food we eat combine, at a speed that determines our rate of living and our lifespan. That speed is in turn determined by our body temperature, and by the amount of food we digest.


But there is a third way to slow our rate of living: by poisoning the electron transport chain. One way to do this is to expose it to an electromagnetic field. And since the 1840s, at a gradual but accelerating rate, we have immersed our world, and all biology, in a thickening fog of such fields, that exert forces on the electrons in our mitochondria and slow them down. Unlike calorie restriction, this does not promote health. It starves our cells not of calories, but of oxygen. Resting metabolic rate does not change, but maximum metabolism does. No cell—no brain cell, no heart cell, no muscle cell—can work to its capacity. Where calorie restriction prevents cancer, diabetes, and heart disease, electromagnetic fields promote cancer, diabetes, and heart disease. Where calorie restriction promotes well-being, oxygen deprivation promotes headaches, fatigue, heart palpitation, “brain fog,” and muscular aches and pains. But both will slow overall metabolism and prolong life.


Industrial electricity in any of its forms always injures. If the injury is not too severe, it also prolongs life.



Solutions


From my current level of research, understanding and personal experience some solutions are:



And a paradigm shift as proposed by professor Doug Wallace (his slide below) and others.



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