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Genes, Carbon Dioxide and Adaptation

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by Ray Peat, PhD

“Over the oxygen supply of the body carbon dioxide spreads its protecting wings.” Friedrich Miescher, Swiss physiologist, 1885

To reach useful simplicities, we usually have to sift through the accumulated rationalizations previous generations have produced to justify doing things their way. If we could start with an accurate understanding of what life is, and what we are doing here, science could be built up deductively as well as by the accumulation of evidence. But the fact that we have grown up amid false and unworkable models of what life is, means that we have to lean heavily on evidence, building up new models inductively, imaginatively, and scientifically. Textbooks and professional journals can be useful if they are seen as monuments to past beliefs, and not as authorities to be accepted. Examining the dogmatic models of life and the world in which life exists, we can better understand the nature of the existing barriers to constructive work.

The Central Dogma of the molecular geneticists, in their own words, was that information flows only from DNA to RNA, and from RNA to protein, never in the other direction. The Central Dogma was formulated to suppress forever the Lamarckian idea of the inheritance of acquired characters, that Weismann’s amputation of the tails of a multitude of mice had attempted to deal with earlier in the history of genetics.

The Central Dogma continues to be influential, even after a series of revisions. Until the 1990s, the only “practical” fruit of genetics had been genocide, but now it has become possible to insert genes into bacteria, and to use the bacteria to produce industrial quantities of specific proteins. In principle, that could be useful, although bovine growth hormone poses a threat to the health of both people and cows, human growth hormone poses a threat to athletes and old people, and human insulin could increase the number of treated diabetics. A deranged culture will put anything cheap to bad use. The ability to make organisms produce foreign proteins confirms that information can flow from DNA to protein, but as that technology was being developed, the discovery of retroviruses showed that the Central Dogma of molecular genetics was wrong, RNA is a very significant template for the production of DNA. And the scrapie prion shows that proteins can be infectious, passing along information without nucleic acids as the agent of transmission. The directed mutations demonstrated by John Cairns and others have thoroughly destroyed the Central Dogma of molecular genetics, even as it applied to the simplest organisms, but molecular genetics survives as an industrial and forensic technology.

Although evidence suggests that about 2% of human diseases involve the inheritance of an abnormal protein, the exact way the disease develops is never as clear as the geneticists would imply. And the major diseases, cancer, diabetes, heart disease, Alzheimer’s, epilepsy, depression, etc., that are so often blamed on “genes,” are so poorly understood that it is arbitrary and crazy to talk about the way genes “cause” them. People who had never had a problem with diabetes in their culture, very soon suffered from the same rate of diabetes as their neighbors when they immigrated into Israel and began eating the European style diet. The interesting thing about the genetic explanation for disease is how its proponents can believe what they are saying. If you read Konrad Lorenz’s writings on racial hygiene, you can imagine that he might have really come to believe what he was saying, even if it was an invention that earned him personal prestige and revenge against people who were reluctant to accept his ideas of cultural excellence and inferiority. When I listened to Gunther Stent praising the doctrine he had taken straight from Konrad Lorenz’s original genocide papers, I wondered how a German who had escaped the holocaust with his Jewish family when he was nine years old could talk about those doctrines without anger, and without pointing out the purpose for which they had been created. In the audience, a professor who had been a refugee from Hungary defended the doctrine, saying that a man and his work have nothing to do with each other, though the whole content of the doctrine was that a man and his work are identical, because his behavior is determined by his genes. These were mature, internationally known intellectuals, who made the most amazingly self-contradictory statements without embarrassment, because they were committed, for some deep, mysterious reason, to the doctrine of genetic determinism. If these refugees could espouse the rationale for “racial hygiene” as their own, I suppose it isn’t so hard to understand that people can devote their life to studying the genetics of diabetes, even though diabetes has appeared suddenly in one generation of immigrants when their diet was suddenly changed, a massive fact that bluntly contradicts the genetic doctrine. There is something very deep in our culture that loves genetics.

One of the cultural trends that makes genetic determinism attractive is the theory of radical individualism, something that has grown up with protestant christianity, according to some historians. Roger Williams’ work in nutrition seemed to be powered by this idea of individual genetic uniqueness, and in his case, the idea led him to some useful insights–he suggested that the environment could be adjusted to suit the highly specific needs of the individual. This idea led to the widespread belief that nutritional supplements might be needed by a large part of the population. Extreme nurturing of the deviant individual is the opposite extreme from the Lorenzian-Hitlerian solution, of eliminating everyone who wasn’t a perfect Aryan specimen.

But Williams’ genetic doctrine assumed that our nutritional needs were primarily inborn, determined by our unique genes. However, there is a famous experiment in which rats were made deficient in riboflavin, and when their corneal tissue showed evidence of the vitamin deficiency, they were given a standard diet. However, the standard diet no longer met the needs of their eye tissue, and during the remainder of the observation period, only a dose of riboflavin several times higher than normal would prevent the signs of deficiency. A developmental change had taken place in the cornea, making its vitamin B2 requirement abnormally high. If we accept the epigenetic, developmental idea of metabolic requirements, our idea of nurturing environmental support would consider the long-range effects of environmental adequacy, and would consider that much disease could be prevented by prenatal support, and by avoiding extreme deficiencies at any time. Williams himself emphasized the importance of prenatal nutrition in disease prevention, so he wasn’t a genetic totalitarian; combining the idea of unique genetic individuality with the recognition that malnutrition causes disease, led him to believe in the necessity for nutitional adequacy, rather than to the extermination of the sick, weak, or different individuals.

The idea of “genetic determinism” says that our traits are the result of the specific proteins that are produced by our specific genes. The doctrine allows for some gradations, such as “half a dose” of a trait, but in practice it becomes a purely subjective accounting for everything in terms of mysterious degrees of “penetrance” of genes, and interactions with unknown factors. Proteins, that supposedly express our genetic constitution, include enzymes, structural proteins, antibodies, and a variety of protein hormones and peptide regulatory molecules. Every protein, including the smallest peptide (except certain cyclic peptides), contains at least one amine group, and usually several. Amine groups react spontaneously with carbon dioxide, to form carbamino groups, and they can also react, nonenzymically, with sugars, in the reaction called glycation or glycosylation. These chemical changes alter the functions of the proteins, so that hormones and their “receptors,” tubules and filaments, enzymes and synthetic systems, all behave differently under their influences. (The proteins’ electrical charge, relationship to water and fats, and shape, change quickly and reversibly as the concentration of carbon dioxide changes; in the absence of carbon dioxide, these properties tend to change irreversibly under the influence of metabolic stress.)

This is the clearest, and the most powerful, instance of metabolic influence on biological structure. That makes it very remarkable that it has been the subject of so few publications. I think the absence of discussion of this fundamental biological principle can be understood only in relation to the great importance it has for a new understanding of development and inheritance–it is an easily documented process that will invalidate some of the most deeply held beliefs of most of the people who are influential in science and politics.

I will continue discussing some of these implications in newsletters on imprinting, degenerative diseases, heart attacks, high blood pressure, and other special biological questions, but I think the most important work that remains to be done is to work out the exact mechanisms by which metabolic energy, expressed largely by factors such as the ratio of carbon dioxide to lactic acid, guides both development and evolution. These ideas will have to take into account the actual resources of the world, as well as the internal processes and resources of the organism. Each development in the organism, whether it leads to maturation or to degeneration, consists of responses to and interactions with specific environments.

Curiosity, esthetics, creativity, and stimulation are necessarily and deeply linked to metabolic efficiency and structural-anatomical development. For example, the known effects of stimulation and success (or isolation and depression) on brain anatomy and function should be linked meaningfully with metabolic, hormonal and dietary processes. There is a large amount of information available that could be put to practical use, but there are still important ideological barriers to be overcome. Marshalling the information needed to optimize our own development runs counter to the program of our technical-scientific culture, which prefers to believe that degeneration is programmed, while emergent evolution is unforeseeable. But, if an optimization project is presented as a way to forestall the “programmed degeneration,” it might succeed in becoming part of the culture.

Vernadsky’s idea of the Noosphere differs from the Gaia hypothesis (that the world is a self-regulating organism-like system) in the intrinsic directionality of Vernadsky’s Noosphere, which makes the course of human society crucial for the fate of the planet. It proposes that planets, like organisms, are going somewhere. The Gaia hypothesis is increasingly being interpreted as a justification for feeling no responsibility for the effects of technology on the environment, and some people are expressing that view of the world as essentially a justification for any vandalism that may come along. Kary Mullis, for example, says that mass extinctions of organisms have occurred in the past, and so it’s just natural for species to become extinct, and it isn’t appropriate to be concerned about the extinctions that are being caused by civilization’s technological depredations.

In the Noosphere, global warming and increased carbon dioxide would represent an advance toward a higher state of “metabolism” of the world, and this would support the emergence of new biological forms from those existing. But if whole systems of life are destroyed before that happens, the biological achievements of the past could be lost irretrievably; there is no guarantee that the system will continue to work, if major sectors are deleted from the interacting systems. Even in terms of the Gaia conception, that the earth is like an organism, consider what the loss of genetic complexity means for an organism. Sometimes, for example, things that happen to an individual lead to sterility several generations later, although the procedure didn’t seem lethal for the individual or its immediate descendants.

The whole idea of “evolution” is that the past is preserved within the present, or that the present is built upon the accomplishments of the past. The idea that evolution has been “random,” and that the world is simply self-regulating, might seem liberating to those who hate the idea that they might be intrinsically responsible for anything outside of themselves, but it is liberating only in the way that a vandal’s manifesto might be, declaring the world to be their playground.

The problem with such a manifesto of irresponsibilty is simply that it is built upon the same system of cultural assumptions that produced Nazi eugenics, and that those assumptions are false. The political assumptions of the people who controlled scientific institutions were built into a set of pseudo-scientific doctrines, which continue to be valued for their political and philosophical implications.

For hundreds or thousands of years, the therapeutic value of carbonated mineral springs has been known. The belief that it was the water’s lively gas content that made it therapeutic led Joseph Priestley to investigate ways to make artificially carbonated water, and in the process he discovered oxygen. Carbonated water had its medical vogue in the 19th century, but the modern medical establisment has chosen to define itself in a way that glorifies “dangerous,” “powerful” treatments, and ridicules “natural” and mild approaches. The motivation is obvious–to maintain a monopoly, there must be some reason to exclude the general public from “the practice of medicine.” Witch doctors maintained their monopoly by working with frightening ghost-powers, and modern medicine uses its technical mystifications to the same purpose.

Although the medical profession hasn’t lost its legal monopoly on health care, corporate interests have come to control the way medicine is practiced, and the way research is done in all the fields related to medicine.

The fact that carbon dioxide therapy is extremely safe has led to the official doctrine that it can’t be effective. The results reviewed by Yandell Henderson in the Cyclopedia of Medicine in 1940 were so impressive that carbon dioxide therapy would have been as commonly used and as well known as oxygen therapy, radiation treatments, sulfa drugs, barbiturates, and digitalis, but it was completely lacking in the thrilling mystique of those dangerous treatments.

Henderson assumed that carbon dioxide use was becoming a permanent part of medicine, to be used with anesthesia to prevent cessation of spontaneous breathing, during recovery from surgery to prevent shock and pneumonia, for stimulating respiration in newborns, and for resuscitating drowning or suffocation victims, as well as for treatment of heart disease and some neurological conditions (see below). However, its use in surgery and resuscitation has probably decreased since he wrote, despite occasional publications pointing out the dangers involved in the use of oxygen without carbon dioxide.

REFERENCES

O. Rahn, “Protozoa need carbon dioxide for growth,” Growth 5, 197-199, 1941. “

On page 113 of this volume, the statement of Valley and Rettger that all bacteria need carbon dioxide for growth had been shown to apply to young as well as old cells.” “…it is possible…to remove it as rapidly as it is produced, and under these circumstances, bacteria cannot multiply.”

Y. Henderson, “Carbon Dioxide,” Cyclopedia of Medicine, 1940. “

Before considering these matters, it will be best that the mind be cleared of certain deep rootedmisconceptions that have long opposed the truth and impeded its applications. It will be seen that carbon dioxide is truly the breath of life.”

“The human mind is inherently inclined to take a moralistic view of nature. Prior to the modern scientific era, which only goes back a generation or two, if indeed it can be said as yet even to have begun in popular thought, nearly every problem was viewed as an alternative between good and evil, righteousness and sin, God and the Devil. This superstitious slant still distorts the conceptions of health and disease; indeed, it is mainly derived from the experience of physical suffering. Lavoisier contributed unintentionally to this conception when he defined the life supporting character of oxygen and the suffocating power of carbon dioxide. Accordingly, for more than a century after his death, and even now in the field of respiration and related functions, oxygen typifies the Good and carbon dioxide is still regarded as a spirit of Evil. There could scarcely be a greater misconception of the true biological relations of these gases.” “Carbon dioxide is the chief hormone of the entire body; it is the only one that is produced by every tissue and that probably acts on every organ. In the regulation of the functions of the body, carbon dioxide exerts at least 3 well defined influences: (1) It is one of the prime factors in the acid-base balance of the blood. (2) It is the principal control of respiration. (3) It exerts an essential tonic influence upon the heart and peripheral circulation.”

“A frog’s muscle will contract effectively and repeatedly under suitable stimulation in an atmosphere of pure nitrogen. In contraction, a muscle produces lactic acid, partly by reconversion into sugar. In other words, oxygen is not one of the primary factors in muscular work. The reserve store of oxygen in the body is small. Vigorous breathing does not take place before an exertion; the exertion is first made and then the oxygen needed to clear the system in preparation for another exertion is absorbed. The demand for oxygen for this scavenging of waste and restoration of power is termed by A.V. Hill the “oxygen deficit” of exercise.”

“On the other hand, present knowledge indicates that carbon dioxide is an absolutely essential component of protoplasm. It is one of the factors in the balance of alkali and acid for the maintenance of the normal pH of the tissues. Acapnia, that is diminution of the normal content of carbon dioxide, involves therefore, a disturbance of one of the fundamental conditions of life.”

“These observations upon the circulation showed also that in animals reduced to a state of shock the carbon dioxide of the blood, or as it now be generally termed, the “alkaline reserve,” is greatly reduced. This experimental result was later confirmed by the observations of Cannon upon wounded soldiers during the war.”

“Catatonia.—Finally, mention may be made of the extraordinary observations reported by the late A.S. Lovenhart, in which he found that inhalation of carbon dioxide to cases of catatonia induced a temporary restoration of intelligence and mental responsiveness. The simplest explanation of the results in these cases is attained by postulating an habitual contraction of blood-vessels in the brain of the catatonic patient, similar to that in the heart and limbs of the cases discussed in the previous section. If this view is correct, the beneficial effects of the inhalation are due to improvement in the circulation in the brain under the influence of carbon dioxide upon the finer blood vessels.”

Vojnosanit Pregl 1996 Jul-Aug;53(4):261-74. [Carbon dioxide inhibits the generation of active forms of oxygen in human and animal cells and the significance of the phenomenon in biology and medicine]. Boljevic S, Kogan AH, Gracev SV, Jelisejeva SV, Daniljak IG

Carbon dioxide (CO2) influence in generation of active oxygen forms (AOF) in human mononuclear cells (blood phagocytes and alveolar macrophages) and animal cells (tissue phagocytes, parenchymal and interstitial cells of liver, kidney, lung, brain and stomach) was investigated. The AOF generation was examined by the methods of chemiluminiscence (CL) using luminol, lucigenin and NBT (nitro blue tetrazolium) reaction. It was established that CO2 in concentrations similar to those in blood (5.1%, pCO2 37.5 mmHg) and at high concentrations (8.2%, pCO2 60 mmHg; 20%, pCO2 146 mmHg) showed pronounced inhibitory effect on the AOF generation in all the studied cells (usually reducing it 2 to 4 times). Those results were obtained not only after the direct contact of isolated cells with CO2, but also after the whole body exposure to CO2. Besides, it was established that venous blood gas mixture (CO2 – 45 mmHg, +O2 – 39 mmHg, + N2 – 646 mmHg) inhibited the AOF generation in cited cells more than the arterial blood gas mixture (CO2 – 40 mmHg, + O2 – 95 mmHg, + N2 – 595 mmHg). Carbon dioxide action mechanism was developed partially through the inhibition of the OAF generation in mitochondria and through deceleration of NADPH oxidative activity. Finally, it was established that CO2 led to the better coordination of oxidation and phosphorylation and increased the phosphorylation velocity in liver mitochondria. The results clearly confirmed the general property of CO2 to inhibit significantly the AOF generation in all the cell types. This favors the new explanation of the well-known evolutionary paradox: the Earth life and organisms preservation when the oxygen, that shows toxic effects on the cells through the AOF, occurs in the atmosphere. The results can also be used to explain in a new way the vasodilating effect of CO2 and the favorable hypercapnotherapy influence on the course of some bronchial asthma forms. The results are probably significant for the analysis of important bio-ecological problem, such as the increase of CO2 concentration in the atmosphere and its effect on the humans and animals.

Aviakosm Ekolog Med 1997;31(6):56-9. [Functional activity of peripheral blood neutrophils of rats during combined effects of hypoxia, hypercapnia and cooling]. Baev VI, Kuprava MV

Functional activity of neutrophilic leukocytes was studied in blood of rats immediately following single and repeated gradual increase in carbon dioxide and decrease in oxygen concentrations with the ambient temperature at 2 to 3 degrees C. Phagocytic activity was shown to alter as the number of phagocyticneutrophilic granulocytes, absorptivity or the phagocytic index, and the coefficient of phagocytosis completeness were elevated and levels of oxygen-dependent and oxygen-independent metabolism were reduced.

Izv Akad Nauk Ser Biol 1997 Mar-Apr;(2):204-17. [Carbon dioxide–a universal inhibitor of the generation of active oxygen forms by cells]. Kogan AKh, Grachev SV, Eliseeva SV, Bolevich S

Studies were carried out on blood phagocytes and alveolar macrophages of 96 humans, on the cells of the viscera and tissue phagocytes (liver, brain, myocardium, lungs, kidneys, stomach, and skeletal muscle), and liver mitochondria of 186 random bred white mice. Generation of the active oxygen forms was determined using different methods after direct effect of CO2 on the cells and biopsies and indirect effect of CO2 on the integral organism. The results obtained suggest that CO2 at a tension close to that observed in the blood (37.0 mm Hg) and high tensions (60 or 146 mm Hg) is a potent inhibitor of generation of the active oxygen forms by the cells and mitochondria of the human and tissues. The mechanism of CO2 effect appears to be realized, partially, through inhibition of the NADPH-oxidase activity. The results are important for deciphering of a paradox of evolution, life preservation upon appearance of oxygen in the atmosphere and succession of anaerobiosis by aerobiosis, and elucidation of some other problems of biology and medicine, as well as analysis of the global bioecological problem, such as ever increasing CO2 content in the atmosphere.

Ukr Biokhim Zh 1978 Mar-Apr;50(2):150-4.. [Content of adenine nucleotides and creatinephosphate in brain, myocardium, liver and skeletal muscle under combined action of hypercapnia, hypoxia and cooling]. Baev VI, Drukina MA

Cooling of rats under conditions of hypercapina and hypoxia induced no changes in the content of adenine nucleotides in the brain and skeletal muscles and decreased their concentration in the liver and myocardium. The content of creatine phosphate increased in the brain, but had no changes in the other tissues. 48 hours after cooling the amount of adenine nucleotides in the brain was higher as compared with the initial values, that was due to an increase in the ATP concentration; in the other tissues the contents of adenine nucleotides did not differ from that of the intact rats. The repeated action (48 hours after the first influences) caused no changes in the contents of adenine nucleotides in skeletal muscles and decreased them in the myocardium and liver. In the brain their amount and the content of creatinephosphate were increased as related to the intact rats. In the brain and myocardium the level of NADPH decreased after the first action and 48 hours after impact it restored up to the inital values. After repeated impact the level of NADPH in the brain restored up to initial values, in the myocardium it was increased.

Fiziol Zh SSSR 1978 Oct;64(10):1456-62. [Role of CO2 fixation in increasing the body’s resistance to acute hypoxia]. Baev VI, Vasil’ev VV, Nikolaeva EN

In rats, the phenomenon of considerable increase in resistance to acute hypoxia observed after 2-hour stay under conditions of gradually increasing concentration of CO2, decreasing concentration of O2, And external cooling at 2–3 degrees seems to be based mainly on changes in concentration of CO2 (ACCORDINGLY, PCO2 and other forms of CO2 in the blood). The high resistance to acute hypoxia develops as well after subcutaneous or i.v. administration of 1.0 ml of water solution (169.2 mg/200 g) NaHCO2, (NH4)2SO4, MgSO4, MnSO4, and ZnSO4 (in proportion: 35 : 5 : 2 : 0.15 : 0.15, resp.) or after 1-hour effect of increased hypercapnia and hypoxia without cooling.

Vopr Med Khim 1976 Jan-Feb;22(1):37-41 [Pyridine nucleotide content in the brain and myocardium of rats under combined effect of hypercapnia, hypoxia and cooling]. Baev VI, Drukina MA

In experiments with rats, subjected to single and repeated simultaneous effect of hypercapnia, hypoxia and cooling, contents of pyridine nucleotides (NAD, NADP, NAD-H2 and NADP-H2) and macroergic substances were studied and also the activity of dehydrogenases of the pentose pathway was determined in brain and myocardium. In brain NADP was not practically determined and in heart its content was increased after the first and the second treatments. Content of NADP-H2 was distinctly decreased in both tissues after the single treatment. NAD was not altered in the tissues in all the periods studied. The amount of NAD-H2 was decreased in brain after the single treatment and it was increased in myocardium after the repeated one. In the activity of dehydrogenases marked alterations were not observed. Total macroergic substances were not altered in brain after the single treatment and after the repeated one they were increased mainly due to the ATP increase. In myocardium total macroergic substances were decreased after the both treatments.

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By Team FPS – April 23, 2011

Mitochondria and mortality

by Ray Peat, PhD

Diet, exercise, and medicine, damaging or repairing respiratory metabolism

MAIN IDEAS AND CONTEXTS

  • Lactic acid and carbon dioxide have opposing effects. Intense exercise damages cells in ways that cumulatively impair metabolism. There is clear evidence that glycolysis, producing lactic acid from glucose, has toxic effects, suppressing respiration and killing cells. Within five minutes, exercise lowers the activity of enzymes that oxidize glucose. Diabetes, Alzheimer’s disease, and general aging involve increased lactic acid production and accumulated metabolic (mitochondrial) damage. 
  • The products of glycolysis, lactic acid and pyruvic acid, suppress oxidation of glucose. 
  • Adaptation to hypoxia or increased carbon dioxide limits the formation of lactic acid. Muscles are 50% more efficient in the adapted state; glucose, which forms more carbon dioxide than fat does when oxidized,, is metabolized more efficiently than fats, requiring less oxygen. Lactic acidosis, by suppressing oxidation of glucose, increases oxidation of fats, further suppressing glucose oxidation. 
  • Estrogen is harmful to mitochondria, progesterone is beneficial. 
  • Progesterone’s brain-protective and restorative effects involve mitochondrial actions. 
  • Thyroid hormone, palmitic acid, and light activate a crucial respiratory enzyme, suppressing the formation of lactic acid. Palmitic acid occurs in coconut oit, and is formed naturally in animal tissues. Unsaturated oils have the opposite effect. 
  • Heart failure, shock, and other problems involving excess lactic acid can be treated “successfully” by poisoning glycolysis with dichloroacetic acid, reducing the production of lactic acid, increasing the oxidation of glucose, and increasing cellular ATP concentration. Thyroid, vitamin B1, biotin, etc., do the same. 

Since reading Warburg’s publications in the late 1960s and early 70s, and doing my own research on tissue respiration, I have been convinced that Warbug was on the right track in seeing mitochondrial respiration as the controlling influence in cell differentiation, and in seeing cancer as a reversion to a primitive form of life based on a “respiratory defect.” Harry Rubin’s studies of cells in culture have expanded Warburg’s picture of the process of cancerization, showing that genetic changes occur only after the cells have been transformed into cancer.

It is now well recognized that defective mitochondrial respiration is a central factor in diseases of muscles, brain, liver, kidneys, and other organs. The common view has been that the mitochondrial defects are produced by genetic defects, that are either inherited or acquired, and are irreversible.

Mitochondria depend on some genes in the nuclear chromosomes, but they also contain some genes, and mutations in these specific mitochondrial genes have been associated with various diseases, and with aging. Although these aren’t the genes that the cancer establishment has focussed on as “the cause” of cancer, for people interested in the achievements of Warburg and Rubin, it is important to know whether mutations in these mitochondrial genes are the cause of respiratory defects, or whether a respiratory defect causes the mutations. Recent research seems to show that physiological problems precede and cause the mutations.

Warburg believed that mitochondria supported specialized cell functions by concentrating themselves in the places where energy is needed. This idea has some interesting implications. For example, when the amount of thyroid hormone is increased, or when the organism adapts to a high altitude, the number of mitochondria increases. But in energy deficient states such as diabetes, they don’t. How are these crucial organelles called into existence by the hormone that increases respiration and energy, and also by the hypoxic conditions of high altitudes? In both of these conditions, the availability of oxygen is limiting the ability to produce energy. In both conditions, carbon dioxide concentration in tissue is higher, in one case, because thyroid stimulates its production, in the other, because the Haldane effect limits its loss from the lungs.

 

SOME DEFINITIONS

Glycolysis: The conversion of glucose to lactic acid, providing some usable energy, but many times less than oxidation provides. Lactic acid, produced by splitting glucose to pyruvic acid followed by its reduction, is associated with calcium uptake and nitric oxide production, depletes energy, contributing to cell death. >P> Crabtree effect: Inhibition of cellular respiration by an excess of glucose; excess of glucose promotes calcium uptake by cells.

Pasteur effect: Inhibition of glycolysis (fermen-tation) by oxygen.

Randle effect: The inhibition of the oxidation of glucose by an excess of fatty acids. This lowers metabolic efficiency. Estrogen promotes this effect.

Lactated Ringer’s solution: A salt solution that has been used to increase blood volume in treating shock; the lactate was apparently chosen as a buffer in place of bicarbonate as a matter of convenience rather than physiology. This solution is toxic, partly because it contains the form of lactate produced by bacteria, but our own lactate, at higher concentrations, produces the same sorts of toxic effect, damaging mitochondria. Estrogenic phytotoxins damage mitochondria, kill brain cells; tofu is associated with dementia. .

 

Could carbon dioxide, a major product of mitochondria, help to call mitochondria into existence? My answer to this is “yes,” and it will help to briefly explain how I see mitochondria. Although I have no hesitancy in accepting that organelles can be exchanged between species, and that it is conceivable that mitochondria might have been derived from symbiotic bacteria, I am reluctant to believe that something happens just because it could happen. For example, Francis Crick proposed that life on earth originated when genes arrived here on space dust from some other world. That’s a theoretical possibility, but what’s the point? It just avoids explaining how the highly organized material came into existence somewhere else, and it probably seriously interfered with the consideration of the ways life could arise here. Similarly, some people like to think that mitochondria and chloroplasts were originally bacteria, that came into symbiosis with another kind of living material, consisting of nucleus and cytoplasm. Like Crick’s “space germs,” it can be argued that it’s possible, but the problem is that this explanation can stop people from thinking freshly about the nature of the various organelles, and how they came to exist. (How did cells originate? How did mitochondria originate? “Germs.”)

Since I have a view of how cells came to exist, under conditions that exist on earth, I should consider whether that view doesn’t also reasonably account for their various components. Sidney Fox’s proteinoid microspheres provide a good model for the spontaneous formation of primitive cells; variations of that idea can account for the formation of organelles (such as mitochondria and nuclei within cells, and chromosomes within nuclei). The value of this idea, of a self-stimulating process in mitochondrial generation, is that it suggests many ways to test the idea experimentally, and it suggests explanations for developmental and pathological processes that otherwise would have no coherent explanation.

Proteinoid microspheres and coacervates form by acquiring molecules from solution, condensing them into a separate phase, with its own physical properties. At every phase boundary, there are numerous physical forces, especially electronic properties, that make each kind of interface different from other kinds. Small changes of pH, temperature, of salts and other solutes can alter the interfacial forces, causing particles to dissolve, or grow, or fragment, or to move. In the way that carbon dioxide alters the shapes and electrical affinities of hemoglobin and other proteins, I propose that it increases the stability of the mitochondrial coacervate, causing it to “recruit” additional proteins from its external environment, as well as from its own synthetic machinery, to enlarge both its structure and its functions.

In the relative absence of carbon dioxide, or excess of alternative solutes and adsorbents, such as lactic acid, the stability of the mitochondrial phase would be decreased, and the mitochondria would be degraded in both structure and function. As the back side of the idea that carbon dioxide stabilizes and activates mitochondria, the idea that lactic acid is involved in the degrading of mitochondria can also be tested experimentally, and it is already supported by a considerable amount of circumstantial evidence. This combination of sensitivity to the environment, with a kind of positive feedback or inertia either upward or downward, corresponds to what we actually see in mitochondrial physiology and pathology.

The Crabtree effect, which is the suppression of respiration by glycolysis, is often described as the simple opposite of the Pasteur effect, in which respiration limits glycolysis to the rate that allows its product to be consumed oxidatively. But the Pasteur effect is a normal sort of control system; when the Pasteur effect fails, as in cancer, there is glycolysis which is relatively independent of respiration, causing sugar to be consumed inefficiently. Embryonic tissues sometimes behave in this manner, leading to the suggestion that glycolysis is closely related to growth. Unlike the logical Pasteur effect, the Crabtree effect tends to lower cellular energy and adaptability. Looking at many situations in which increasing the glucose supply increases lactic acid production and suppresses respiration, leading to maladaptive decrease in cellular energy, I have begun thinking of lactic acid as a toxin. The use of Ringer’s lactate solution in medicine has led many people to assume that lactate must be beneficial, or they wouldn’t put it in the salt solution that is often used in emergiencies; however, I think its use here, as a buffer, is simply a convenience, because of the instability of some bicarbonate solutions.

On the organismic level, it is clear that lactic acid is “the essence of hyperventilation,” and that it produces edema and malfunction on a grand scale: The panic reaction, shock lung, vascular leakiness, brain swelling, and finally multiple organ failure, all can be traced to an excess of lactic acid, and the related features of hyperventilated physiology. Otto Warburg apparently thought of lactate as simply a sign of the respiratory defect that characterizes cancer. V. S. Shapot at least hinted at its possible role in turning on the catabolic reactions leading to cancer cachexia (wasting). I think a good case can be made for lactate as the cause of the respiratory defect in cancer, just as it is usually the immediate cause of the respiratory derangement of hyperventilation on the organismic level.

The Crabtree effect is usually thought of as just something that happens in tumors, and some tissues that are very active glycolytically, and some bacteria, when they are given large amounts of glucose. But when we consider lactate, which is produced by normal tissues when they are deprived of oxygen or are disturbed by a stress reaction, the Crabtree effect becomes a very general thing. The “respiratory defect” that we can see on the organismic level during hyperventilation, is very similar to the “systemic Crabtree effect” that happens during stress, in which respiration is shut down while glycolysis is activated. Since oxidative metabolism is many times more efficient for producing energy than glycolysis is, it is maladaptive to shut it down during stress.

Since the presence of lactate is so commonly considered to be a normal and adaptive response to stress, the shut-down of respiration in the presence of lactate is generally considered to be caused by something else, with lactate being seen as an effect rather than a cause. Nitric oxide and calcium excess have been identified as the main endogenous antirespiratory factors in stress, though free unsaturated fatty acids are clearly involved, too. However, glycolysis, and the products of glycolysis, lactate and pyruvate, have been found to have a causal role in the suppression of respiration; it is both a cause and a consequence of the respiratory shutdown, though nitric oxide, calcium, and fatty acids are closely involved.

Since lactic acid is produced by the breakdown of glucose, a high level of lactate in the blood means that a large amount of sugar is being consumed; in response, the body mobilizes free fatty acids as an additional source of energy. An increase of free fatty acids suppresses the oxidation of glucose. (This is called the Randle effect, glucose-fatty acid cycle, substrate-competition cycle, etc.) Women, with higher estrogen and growth hormone, usually have more free fatty acids than men, and during exercise oxidize a higher proportion of fatty acids than men do. This fatty acid exposure “decreases glucose tolerance,” and undoubtedly explains women’s higher incidence of diabetes. While most fatty acids inhibit the oxidation of glucose without immediately inhibiting glycolysis, palmitic acid is unusual, in its inhibition of glycolysis and lactate production without inhibitng oxidation. I assume that this largely has to do with its important function in cardiolipin and cytochrome oxidase.

Exercise, like aging, obesity, and diabetes, increases the levels of circulating free fatty acids and lactate. But ordinary activity of an integral sort, activates the systems in an organized way, increasing carbon dioxide and circulation and efficiency. Different types of exercise have been identified as destructive or reparative to the mitochondria; “concentric” muscular work is said to be restorative to the mitochondria. As I understand it, this means contraction with a load, and relaxation without a load. The heart’s contraction follows this principle, and this could explain the observation that heart mitochondria don’t change in the course of ordinary aging.

When a person has an accident, or surgery, and goes into shock, the degree of lactic acidema is recognized as an indicator of the severity of the problem. Lactated Ringer’s solution has been commonly used to treat these people, to restore their blood pressure. But when prompt treatment with lactated Ringer’s solution has been compared with no early treatment at all, the patients who are not “rescuscitated” do better than those who got the early treatment. And when Ringer’s lactate has been compared with various other solutions, synthetic starch solutions, synthetic hemoglobin polymer solution, or simply a concentrated solution of sodium chloride, those who received the lactate solution did least well. For example, of 8 animals treated with another solution, 8 survived, while among 8 treated with Ringer’s lactate, 6 died.

Mitochondrial metabolism is now being seen as the basic problem in aging and several degenerative diseases. The tendency has been to see random genetic deterioration as the driving force behind mitochondrial aging. Genetic repair in mitochondria was assumed not to occur. However, recently two kinds of genetic repair have been demonstrated. One in which the DNA strand is repaired, and another, in which sound mitochondria are “recruited” to replace the defective, mutated, “old” mitochondria. In ordinary nuclear chromosomal genes, DNA repair is well known. The other kind of repair, in which unmutated cells replace the genetically damaged cells, has been commonly observed in the skin of the face: During intense sun exposure, mutant cells accumulate; but after a period in which the skin hasn’t been exposed to the damaging radiation, the skin is made up of healthy “young” cells. In the way that the skin can be seen to recover from genetic damage, that had been considered to be permanent and cumulative, simply by avoiding the damaging factor, mitochondrial aging is coming to be seen as both avoidable and repairable.

The stressful conditions that physiologically harm mitochondria are now being seen as the probable cause for the mitochondrial genetic defects that accumulate with aging. Stressful exercise, which has been known to cause breakage of the nuclear chromosomes, is now seen to damage mitochondrial genes, too. Providing energy, while reducing stress, seems to be all it takes to reverse the accumulated mitochondrial genetic damage. Fewer mitochondrial problems will be considered to be inherited, as we develop an integral view of the ways in which mitochondrial physiology is disrupted. Palmitic acid, which is a major component of the cardiolipin which regulates the main respiratory enzyme, becomes displaced by polyunsaturated fats as aging progresses. Copper tends to be lost from this same enzyme system, and the state of the water is altered as the energetic processes change.

While the flow of carbon dioxide moves from the mitochondrion to the cytoplasm and beyond, tending to remove calcium from the mitochondrion and cell, the flow of lactate and other organic ions into the mitochondrion can produce calcium accumulation in the mitochondrion, during conditions in which carbon dioxide synthesis, and consequently urea synthesis, are depressed, and other synthetic processes are changed.

Glycolysis produces both pyruvate and lactate, and excessive pyruvate produces almost the same inhibitory effect as lactate; since the Crabtree effect involves nitric oxide and fatty acids as well as calcium, I think it is reasonable to look for the simplest sort of explanation, instead of trying to experimentally trace all the possible interactions of these substances; a simple physical competition between the products of glycolysis and carbon dioxide, for the binding sites, such as lysine, that would amount to a phase change in the mitochondrion. Glucose, and apparently glycolysis, are required for the production of nitric oxide, as for the accumulation of calcium, at least in some types of cell, and these coordinated changes, which lower energy production. could be produced by a reduction in carbon dioxide, in a physical change even more basic than the energy level represented by ATP. The use of Krebs cycle substances in the synthesis of amino acids, and other products, would decrease the formation of CO2, creating a situation in which the system would have two possible states, one, the glycolytic stress state, and the other, the carbon dioxide producing energy-efficient state.

Besides the frequently discussed interactions of excessively accumulated iron with the unsaturated fatty acids, producing lipid peroxides and other toxins, the accumulated calcium very probably forms some insoluble soaps with the free fatty acids which are released even from intracellular fats during stress. The growth of new mitochondria probably occasionally leaves behind such useless materials, combining soaps, iron, and porphyrins remaining from damaged respiratory enzymes.

When the background of carbon dioxide is high, circulation and oxygenation tend to prevent the anaerobic glycolysis that produces toxic lactic acid, so that a given level of activity will be harmful or helpful, depending on the level of carbon dioxide being produced at rest. Preventively, avoiding foods containing lactic acid, such as yogurt and sauerkraut, would be helpful, since bacterial lactic acid is much more toxic than the type that we form under stress. Avoiding the stress-promoting antithyroid unsaturated oils is extremely important. Their role in diabetes, cancer, and other age-related and degenerative diseases (and I think this includes the estrogen-promoted autoimmune diseases) is well established. Avoiding phytoestrogens and other things that increase estrogen exposure, such as protein deficiency, is important, because estrogen causes increased levels of free fatty acids, increases the tendency to metabolize them at the expense of glucose metabolism, increases the tissue content of unsaturated fatty acids, and inhibits thyroid functions. Light promotes glucose oxidation, and is known to activate the key respiratory enzyme. Winter sickness (including lethargy and weight gain), and night stress, have to be included within the idea of the “respiratory defect,” shifting to the antirespiratory production of lactic acid, and damaging the mitochondria.

Therapeutically, even powerful toxins that block the glycolytic enzymes can improve functions in a variety of organic disturbances “associated with” (caused by) excessive production of lactic acid. Unfortunately, the toxin that has become standard treatment for lactic acidosis–dichloroacetic acid–is a carcinogen, and eventually produces liver damage and acidosis. But several nontoxic therapies can do the same things: Palmitate (formed from sugar under the influence of thyroid hormone, and found in coconut oil), vitamin B1, biotin, lipoic acid, carbon dioxide, thyroid, naloxone, acetazolamide, for example. Progesterone, by blocking estrogen’s disruptive effects on the mitochondria, ranks along with thyroid and a diet free of polyunsaturate fats, for importance in mitochondrial maintenance.

 

REFERENCES

Biochim Biophys Acta 1999 Feb 9;1410(2):171-82 Mitochondrial involvement in Alzheimer’s disease.Bonilla E, Tanji K, Hirano M, Vu TH, DiMauro S, Schon EA. Rev Pneumol Clin 1986;42(5):238-41. Acid-base balance and blood lactate and pyruvate levels in albino rats bred under normobaric hypoxia or normoxia, after muscular work in a hypoxic or hypoxic-hypercapnic environment. Quatrini U, Licciardi A.

Muscle Nerve 1999 Feb;22(2):258-61. Acute exercise causes mitochondrial DNA deletion in rat skeletal muscle. Sakai Y, Iwamura Y, Hayashi J, Yamamoto N, Ohkoshi N, Nagata H.

Hum Mol Genet 1999 Jun;8(6):1047-52. Gene shifting: a novel therapy for mitochondrial myopathy. Taivassalo T, Fu K, Johns T, Arnold D, Karpati G, Shoubridge EA.

Brain Dev 1989;11(3):195-7. Effect of sodium dichloroacetate on human pyruvate metabolism. Naito E, Kuroda Y, Toshima K, Takeda E, Saijo T, Kobashi H, Yokota I, Ito M.

Mech Ageing Dev 1987 Aug;39(3):281-8. Lack of age-dependent changes in rat heart mitochondria. Manzelmann MS, Harmon HJ.

Adv Shock Res 1978;1:105-16. The effect of mitochondrial dysfunction on glucose metabolism during shock. Rhodes RS.

Biochem J 1982 Dec 15;208(3):695-701 Exercise-induced alterations of hepatic mitochondrial function. Tate CA, Wolkowicz PE, McMillin-Wood, J.

Am J Physiol 1997 Dec;273(6 Pt 2):F869-76. Neurosteroid inhibition of cell death. Waters SL, Miller GW, Aleo MD, Schnellmann RG.

J Pharmacol Exp Ther 1990. May;253(2):628-35. Protection against hypoxic injury in isolated-perfused rat heart by ruthenium red. Park Y, Bowles DK, Kehrer JP.

Environ Health Perspect 1984, Aug;57:281-7. Cell calcium, cell injury and cell death. Trump BF, Berezesky IK, Sato T, Laiho KU, Phelps PC, DeClaris N.

Anesth Analg 1996 Oct;83(4):782-8. Small-volume resuscitation using hypertonic saline improves organ perfusion in burned rats. Kien ND, Antognini JF, Reilly DA, Moore PG.

Respir Physiol 1977 Dec;31(3):387-95. Post-hypercapnia recovery in the dog: arterial blood acid-base equilibrium and glycolysis. Saunier C, Horsky P, Hannhart B, Garcia-Carmona T, Hartemann D.

Am J Physiol 1997 Nov;273(5 Pt 1):C1732-8 Glycolysis inhibition by palmitate in renal cells cultured in a two-chamber system. Bolon C; Gauthier C; Simonnet H.

Can J Appl Physiol 1998 Dec;23(6):558-69. The role of glucose in the regulation of substrate interaction during exercise. Sidossis LS.

Am J Clin Nutr 1998 Mar;67(3 Suppl):527S-530S. Effect of lipid oxidation on glucose utilization in humans. Jequier E.

Ann N Y Acad Sci 1998 Nov 20;854:224-38. Mitochondrial free radical production and aging in mammals and birds. Barja G.

Science 1999 Aug 27;285(5432):1390-3. Gene expression profile of aging and its retardation by caloric restriction. Lee CK, Klopp RG, Weindruch R, Prolla TA.

Nucleic Acids Res 1999 Nov 15;27(22):4510-6. Nitric oxide-induced damage to mtDNA and its subsequent repair. Grishko VI, Druzhyna N, LeDoux SP, Wilson GL.

Am J Physiol 1998 Jun;274(6 Pt 1):G978-83. Neural injury, repair and adaptation in the GI tract. I. New insights into neuronal injury: a cautionary tale. Hall KE, Wiley JW.

Proc Natl Acad Sci U S A 1999 Dec 21;96(26):14706-14711. Structural details of an interaction between cardiolipin and an integral membrane protein. McAuley KE, Fyfe PK, Ridge JP, Isaacs NW, Cogdell RJ, Jones MR.

J. Appl Physiol 1991 Apr;70(4):1720-30.. .Metabolic and work efficiencies during exercise in Andean natives. Hochachka PW, Stanley C, Matheson GO, McKenzie DC, Allen PS, Parkhouse WS.

J Dev Physiol 1990 Sep;14(3):139-46. Effect of lactate and beta-hydroxybutyrate infusions on brain metabolism in the fetal sheep. Harding JE, Charlton VE.

J Trauma 1999 Feb;46(2):286-91, The effects of diaspirin cross-linked hemoglobin on hemodynamics, metabolic acidosis, and survival in burned rats.: Soltero RG; Hansbrough JF.

J Trauma 1999 Apr;46(4):582-8; discussion 588-9, Resuscitation with lactated Ringer’s solution in rats with hemorrhagic shock induces immediate apoptosis. Deb S; Martin B; Sun L; Ruff P; Burris D; Rich N; DeBreux S; Austin B; Rhee P.

Am J Physiol 1996 Oct;271(4 Pt 1):C1244-9, Glucose and pyruvate regulate cytokine-induced nitric oxide production by cardiac myocytes. Oddis CV; Finkel MS.

Biochim Biophys Acta 1999 Feb 9;1410(2):171-82. Mitochondrial involvement in Alzheimer’s disease. Bonilla E, Tanji K, Hirano M, Vu TH, DiMauro S, Schon EA.

Adv Exp Med Biol 1995;384:185-94. Metabolic correlates of fatigue from different types of exercise in man. Vollestad NK.

J Biol Chem 1995 Jun 23;270(25):14855-8. Nitric oxide activates the glucose-dependent mobilization of arachidonic acid in a macrophage-like cell line (RAW 264.7) that is largely mediated by calcium-independent phospholipase A2. Gross RW; Rudolph AE; Wang J; Sommers CD; Wolf MJ.

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By Team FPS – April 23, 2011

Stress and Water

by Ray Peat, PhD

The biological idea of stress refers to the difficulty of adapting, and this involves energy, structure, and insight/orientation. Given enough energy, we can often adjust our structure to achieve full adaptation, and with insight, we can minimize the amount of energy and structural change needed, for example just by a change of pace or rhythm.

Change of structure can involve the growth of new cells, or the enlargement or modification of existing cells, and the shrinking or dissolution (apoptosis) of existing cells, allowing their substance to be used elsewhere. F. Z. Meerson’s work gave a clear framework for understanding this, especially in relation to the adapting heart, and Eli Mechnikov’s picture of the creative role of the phagocyte in growth can be seen as one of the most basic insights into biology.

A given structure makes possible a certain level of useful energy, and adequate energy makes possible the maintenance of structure, and the advance to a higher and more efficient structural level.

I have been using aging (menopause and the ovaries) and cancer (carbon monoxide as a hormone of “cellular immortality”) to explore the issue of cell renewal and tissue regeneration. Yesterday, Lita Lee sent me an article about K. P. Buteyko, describing his approach to the role of carbon dioxide in physiology and medicine. Buteyko devoted his career to showing that sufficient carbon dioxide is important in preventing an exaggerated and maladaptive stress response. He advocated training in “intentional regulation of respiration” (avoiding habitual hyperventilation) to improve oxygenation of the tissues by retaining carbon dioxide. He showed that a deficiency of carbon dioxide (such as can be produced by hyperventilation, or by the presence of lactic acid in the blood) decreases cellular energy (as ATP and creatine phosphate) and interferes with the synthesis of proteins (including antibodies) and other cellular materials.

When I first heard of Buteyko’s ideas, I saw the systemic importance of carbon dioxide, but I wasn’t much impressed by his idea of intentionally breathing less. If the hyperventilation is produced by anxiety, then a deliberate focussing on respiration can help to quiet the nerves. Knowing that hyperventilation can make a person faint, because loss of carbon dioxide causes blood vessels in the brain to constrict, I saw that additional carbon dioxide would increase circulation to the brain. This seemed like a neat system for directing the blood supply to the part of the brain that was more active, since that would be the part producing the most carbon dioxide.

In a nutrition class, in the late 70s, I described the way metabolically produced carbon dioxide opens blood vessels in the brain, and mentioned that carbonated water, or “soda water,” should improve circulation to the brain when the brain’s production of carbon dioxide wasn’t adequate. A week later, a student said she had gone home that night and (interpreting soda water as bicarbonate of soda in water) given her stroke-paralyzed mother a glass of water with a spoonful of baking soda in it. Her mother had been hemiplegic for 6 months following a stroke, but 15 minutes after drinking the bicarbonate, the paralysis lifted, and she remained normal. Later, a man who had stroke-like symptoms when he drank alcohol late at night, found that drinking a glass of carbonated water caused the symptoms to stop within a few minutes.

Realizing that low thyroid people produce little carbon dioxide, it seemed to me that there might be a point at which the circulatory shut-down of unstimulated parts of the brain would become self-sustaining, with less circulation to an area decreasing the CO2 produced in that area, which would cause further vasoconstriction. Carbon dioxide (breathing in a bag, or drinking carbonated water, or bathing in water with baking soda) followed by thyroid supplementation, would be the appropriate therapy for this type of functional ischemia of the brain.

When there is circulatory stasis, the tendency of the blood to clot is increased. Normally, the legs are where small clots form most often, but the same thing is likely to happen in the brain when circulation is too slow. Carbon monoxide poisoning mimics multiple sclerosis by causing clots to form in the brain, in association with areas of demyelination.

Physiologically, I think hypothyroidism, combined with high estrogen (which promotes blood clotting) is the main cause of MS, possibly overlapping with a variety of other demyelinating factors, such as tin, hexachlorophene, heme, and a deficiency of progesterone. One of estrogen’s effects is to cause edema, probably because it blocks albumin synthesis, and the loss of blood volume associated with edema increases the tendency to clot. People have examined the behavior of carbon dioxide dissolved in water when the water is in contact with the skin, as during a bath in carbonated water. Since the concentration of metabolic carbon dioxide in the living tissue was higher than the concentration in the water, it was assumed that CO2 would move from the tissue into the water, “down its gradient.” But the opposite happened, the carbon dioxide moved from the water into the tissue, against the gradient. This shows that we can draw false conclusions when we think of the body as a “watery system.” The carbon dioxide is more soluble in living tissue than in ordinary water, and solubility is what governs the situation, not a context-free concentration gradient. Many natural springs that have a reputation for healing contain carbon dioxide and carbonates, which the body absorbs when bathing in or drinking the water.

Carbon dioxide is more soluble in oil than in water. In general, gases dissolve better in cold water than in warm water, and cold water has more affinity for fats than hot water does. In many ways, the water in cells acts as though it were colder than it is, and more oil-loving. The term “structural temperature” is used to describe the behavior of cellular water which, at body temperature, behaves like ordinary water at a lower temperature–it has a “lower structural temperature.” There is a reciprocal action between the cell water and the material it dissolves, so that carbon dioxide tends to stabilize the normal high energy state of the cell. I will say more about cell water after saying a little more about Buteyko’s focus on carbon dioxide.

Although it is easy to dismiss Buteyko’s emphasis on the “Intentional Cessation of Deep Respiration” as a therapy, his work on the importance of carbon dioxide is sound. When I realized that many hypothyroid people compensate by producing huge amounts of adrenaline, which helps to sustain their blood sugar and their nervous energy, and that adrenaline tends to cause hyperventilation, I saw that “intentional regulation of respiration” might work in these people to reduce hyperventilation just as psychotherapy, reassurance, meditation, or taking a nap can help to control hyperventilation and other effects of excess adrenaline and anxiety. But using carbon dioxide, or a thyroid supplement to promote the body’s formation of carbon dioxide, seems like a more logical approach to treatment of a carbon dioxide deficiency.

I have been concerned about the probable effects on the fetus of the silly panting respiration that is being taught to so many pregnant women, to use during labor. Panting blows out so much carbon dioxide that it causes vasoconstriction. Possibly the uterus is protected against this, and possibly the fetus produces enough carbon dioxide that it is protected, but this isn’t known. Especially if the mother is hypothyroid, it seems that this could interfere with the delivery of oxygen to the fetus. Besides vasoconstriction, Buteyko points out that the Bohr effect, in which CO2 causes hemoglobin to release oxygen, means that a low level of carbon dioxide decreases the availability of oxygen. If the Bohr effect applies to fetal hemoglobin, then this suggests that the mother’s panting will deprive the fetal tissues of oxygen.

It is normal for the fetus to be exposed to a high concentration of carbon dioxide. Recent experiments with week-old rats show that carbon dioxide, at the very high concentration of 6% powerfully protects against the brain damage caused by oxygen deprivation (tying a carotid artery and administering 8% oxygen). (R. C. Vannucci, et al., 1995.)2

I have talked to several people who get mild neurological symptoms around 2 to 4 AM, and since the symptoms are like those caused by hyperventilation, I think nocturnal low blood sugar and high adrenaline might produce relative hyperventilation and poor oxygenation, possibly with lactic acidemia. A sizable part of the population responds to intravenous lactic acid with a panic attack, and I think these people are hypothyroid; if glycogen stores are low, lactic acid exacerbates the energy problem, and by displacing carbon dioxide could trigger hyperventilation. When a panic attack is induced by stress, it is probably because the stress is causing the production of lactic acid. Both sugar and carbon dioxide help to prevent panic attacks, according to some recent studies. (Dager, et al., and George, et al.)

Buteyko has made an unusual observation, which I think is important. He says that the oxygen deprivation resulting from a deficiency of carbon dioxide can cause increased arterial pressure, and also a dilation of veins, leading to varicose veins and hemorrhoids. (I discussed this behavior of the blood vessels in “A unifying principle.”) In a lecture, Buteyko argued that a deficiency of carbon dioxide causes allergies, sclerosis, psychosis, tuberculosis, precancerous conditions, and other symptoms. His list of diseases is reminiscent of Broda Barnes’ work, in which he showed that tuberculosis, cancer, and atherosclerotic heart disease are endemic in hypothyroid regions.

This is where the issue of cell water comes in. Carbon dioxide, produced by oxidative cell metabolism, is associated with the high energy state of the cell. When something interferes with oxidative metabolism, lactic acid is produced instead of carbon dioxide. If the cell stays very long in this low oxygen state, it swells, taking up water. (The fatigued muscle, for example, can take up so much water in a short time that it weighs 20% more than before it began working so intensely that its energy needs far exceeded the availability of oxygen. This swelling is what causes the soreness and tightness of intense exercise. The swelling persists long after the liver has cleared the lactic acid from the blood.) This swelling from taking up water is involved in one type of “edema,” and in inflammation, or activation of the cells by hormones, as well as by simple oxygen deprivation. When the eyes have been closed for several hours, the cornea swells, because it depends on direct contact with the air for its oxygen, and the eyelid, whose circulation provides oxygen for its own cells, doesn’t provide enough for the cornea.

Estrogen seems to work by blocking oxidative metabolism, and its first visible effect is to cause the stimulated tissue to take up water. Anything that causes cells to take up water seems to stimulate cell division. For example, just putting cells in a hypotonic medium stimulates cell division (and a hyperosmotic environment stops cell division). Years ago I noticed that various enzymes which are activated by estrogen are completely inactivated by cold, and I proposed that estrogen’s effect was to raise the “structural temperature” of cell water. If estrogen-stimulated cells have a “high structural temperature,” their ability to dissolve oxygen will be reduced. (Whatever the mechanism, estrogen does shift cells away from oxidative metabolism. I think many mechanisms are involved.)

Thyroid, which opposes estrogen’s effects on cell energy, stimulates oxidative metabolism with the production of carbon dioxide, and reduces the water content of tissues.

Buteyko suggested that carbon dioxide directly supports immunity. Increasing the availability of oxygen and the production of ATP should be good for immunity, apart from any more specific effects. If it contributes to an effect on the “structural temperature” of cell water, and helps to raise the energy charge of the cell, CO2 could be a major factor in opposing the action of estrogen. While the general effects of thyroid can be easily observed, many of its ways of achieving those effects are still not known.

Typical cancer cells are much wetter than normal cells, containing 90 or 92% water. It is possible that part of thyroid’s anti-cancer, immune promoting effect is the result of the increased carbon dioxide it produces. Since lactic acid turns out to have a variety of “signalling” functions, including effects on white blood cells, it seems possible that carbon dioxide has a different set of signalling or hormone-like functions. While I doubt that lactic acid produces intracellular acidosis (ATP hydrolysis produces acidosis; see Busa and Nuccitelli, and Sokoloff), it can produce temporary extracellular acidosis, besides any specific hormone-like action. This acidosis could be involved in autoimmune processes, since it can change cells’ immunological reactivity. (Oh, et al.)

It is very likely that cancer patients lack carbon dioxide, because tumors produce significant amounts of lactic acid, which tends to displace carbon dioxide. It would be interesting to see whether supplemented carbon dioxide would decrease the cancer’s production of lactic acid. Short-chain fats are very soluble, and are quickly metabolized, so it is likely that coconut oil, which is rich in short and medium-chain fatty acids, will tend to decrease the production of lactic acid.

High pressure tends to act as a cell excitant (e.g., it can cause a muscle to contract), and in effect is raising the “structural temperature” of cell water. This suggests that the reduced pressure of high altitude would have the beneficial (antistress) effect of decreasing the structural temperature of cell water. This means that gases would have a higher solubility in cell water at high altitudes, which would tend to slightly offset the biological effect of the relative scarcity of air at high altitude. There is some evidence (Drost-Hansen, 1972) that reduced pressure increases the solubility of oxygen in cells. The presence of carbon dioxide should increase this effect. (Drost-Hansen discusses some examples of “anomalous” concentration effects of hydrocarbon/water mixtures, p. 254, in “Anomalous temperature and pressure dependencies of gas solubilities: Laboratory and field observations,” Chemistry and Physics of Aqueous Gas Solutions, 233-256, 1975?) I think Drost-Hansen’s reasoning suggests that the short-chain fatty acids might also increase the solubility of oxygen in cell water. If this is true, it suggests that coconut oil might have a very important antistress effect, sustaining efficient respiration during demanding situations.

Some of the other implications of thinking about the special nature of cell water are discussed in the works of Cope3 and Ling.4

 

REFERENCES

1. R. C. Vannucci, et al., “Carbon dioxide protects the perimatal brain from hypoxic-ischemic damage: An experimental study in the immature rat,” Pediatrics 95(6), 868-874, 1995.

2. W. Drost-Hansen, Society Experimental Biologists Symposium Proceedings, XXVI, 61-101, 1972.

3. F. W. Cope, “A primer of water structuring and cation association in cells,” Physiol. Chem. & Physics 8, 479-483, 1976.

4. Gilbert N. Ling, A Revolution in the Physiology of the Living Cell, Krieger Publ., 1992.

5. V. V. Malyshev, et al., “Relationship between inflammation and the stress reaction,” Bull. Exp. Biol. & Med., 1194-1196, 1994.

6. U. Haussler, et al., “Role of the cytoskeleton in the regulation of Cl- channels in human embryonic skeletal muscle cells,” Pflugers Arch-Eur. J.Physiol. 428(3-4), 323-320, 1994. (The cytoskeleton filaments control the cell’s water content.)

7. D. L. Davies, et al., “Low-level hyperbaric antagonism of ethanol’s anticonvulsant property in C57BL/6J mice,” Alcohol. Clin. Exp. Res. 18(5), 1190-1195, 1994. (Increased atmospheric pressure blocks alcohol’s effects on behavior. High pressure acts as a sort of stimulant.)

8. S. R. Dager, et al., “Proton magnetic resonance spectroscopy investigation of hyperventilation in subjects with panic disorder and comparison subjects,” Am. J. Psychiatry 152(5), 666-672, 1995.

9. D. T. George, et al., “Effect of chloride or glucose on the incidence of lactate-induced panic attacks,” Am. J. Psychiatry 152(5), 692-697, 1995.

10. W. B. Busa and R. Nuccitelli, Am. J. Physiol. 246, R409-$438, 1984.

11. L. Sokoloff, Can. J. Physiol. Pharmacol. 70(Suppl.), 107-112, 1992.

12. T. H. Oh, et al., “Acidic pH rapidly increases immunoreactivity of glial fibrillary acidic protein in cultured astrocytes,” Glia 13(4), 319-322, 1995.
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By Team FPS – April 23, 2011

Part 2: Skin cancers — And Ultraviolet radiation

Part 2: Skin cancers — And Ultraviolet radiation by Barry Groves

All types of skin cancer are attributed to exposure to the ultraviolet (UV) part of the spectrum of sunlight. UV is classified as three distinct wavebands: A, B and C. They are all believed to contribute to the development of skin cancer.

  1. UVA rays constitute between 90% and 95% of the ultraviolet light that reaches the earth as it is not absorbed by the ozone layer. UVA light penetrates furthest into the skin and is involved in the initial stages of sun-tanning. UVA tends to suppress the immune function and is implicated in premature aging of the skin. [i]
  2. UVB rays are partially absorbed by the ozone layer and by the atmosphere. They do not penetrate the skin as far as the UVA rays but are the primary cause of sunburn. UVB is blamed for cataract formation. But UVB also our primary source of Vitamin D.
  3. UVC rays are the most harmful, but are almost completely absorbed by the ozone layer.

How strong is the evidence linking exposure to sunlight with melanoma?

During the 1980s and early 1990s more than a dozen studies compared histories of sunburn in patients with melanoma and people without it. The most complete data on melanoma and sunburn came in 6 studies from Australia, Europe and North America.[ii] They found the sunlight/melanoma link was unconvincing; while there was a suggestion of an association, the effect was modest; and they emphasised that brief periods of exposure seemed more risky than constant exposure.

Other clinicians agree. Pointing out that melanoma can be found on ovaries, occurs less frequently on sun-exposed areas, that there is 5 times more melanoma in Scotland on the feet than on the hands, that in Japan 40% of melanomas on the feet are on the soles of the feet, and that there is 10 times more melanoma in Orkney and Shetland than in the Mediterranean islands, Karnauchow writes: ‘The simplistic idea of a sun/melanoma relationship is based more on a belief than science. . . . As with other neoplasms [cancers], the cause of melanoma remains an enigma and most probably the sun has little, if anything, to do with it.'[iii]

Newcastle dermatology professor, Sam Shuster, isn’t convinced either. He states that the main reason for the supposed increase in melanomas was a change in diagnostic beliefs: lesions previously regarded as benign became classified first as dubious then as malignant. ‘Melanomas are being invented, not found,’ he says, ‘Exposure to screening and pigmented lesion clinics is a greater cause of melanoma than sun exposure.'[iv]

Dr Anne Kricker and colleagues, looking at studies into skin cancer other than malignant melanoma and exposure to sunlight, also say that the evidence linking skin cancers with sun exposure is weak. They note that most studies have not found statistically significant positive associations, while the few that have lacked empirical evidence that sun exposure was the cause.[v]

The sunscreen connection

But why has there been such an enormous increase in skin cancer recently? The Australian experience might provide the first clue. Queensland doctors have vigorously promoted the use of sunscreens for many years and, today, Queensland has more cases of melanoma per head of population than any other place in the world.

The numbers of cases of melanoma have risen especially steeply since the mid-1970s. The two principal strategies for reduction of risk of skin cancers during this period were sun avoidance and use of chemical sunscreens. Rising trends in the incidence of and mortality from melanoma have continued since the 1970s and 1980s, when sunscreens with high sun protection factors became widely used.

Significantly, the rises in malignant melanoma followed the rising use of sunscreens.

Drs Cedric and Frank Garland of the University of California are the foremost opponents of the use of chemical sunscreens. They point out that the greatest rises in melanoma are in countries where chemical sunscreens have been heavily promoted,[vi] and add that, while sunscreens do protect against sunburn, there is no scientific proof that they protect against melanoma or basal cell carcinoma in humans. Indeed, the Garland brothers strongly believe that the increased use of chemical sunscreens is the primary cause of the skin cancer epidemic. Recent studies by them have shown a higher rate of melanoma among men who regularly use sunscreens and a higher rate of basal cell carcinoma among women using sunscreens.[vii] This was confirmed by another study group who found that ‘always users’ of sunscreens had 3.7 times as many malignant melanomas as those ‘never using’. The reasons why chemical sunscreens may be dangerous are several:

  1. Chemical sunscreens do not stop UVA rays. UVA penetrates deeper into the skin where it is strongly absorbed by the melanocytes which are involved not only in the production of the skin-tanning pigment, melanin, but also in the formation of melanoma.20 UVA rays also have a depressing effect on the immune system.[viii]
  2. More importantly, however, may be the fact that most chemical sunscreens contain up to 5% of benzophenone or its derivatives, oxybenzone or benzophenone-3, as their active ingredient. Benzophenone, used in industrial processes to initiate chemical reactions and promote cross-linking,[ix] is one of the most powerful free radical generators known to man. Moreover, benzophenone is activated by ultraviolet light.
  3. Harvard Medical School researchers also discovered that psoralen, another UV-activated free radical generator, is an extremely efficient carcinogen. The rate of SCC among patients with psoriasis, who had been repeatedly treated with UVA light after an application of psoralen to their skin, was 83 times higher than among the general population.[x] This added weight to a study in 1991-2, in which scientists at the European Organisation for Research and Treatment of Cancer (EORTC) found that regular use of sunscreens increased cancer risk by 50% but sunscreens containing psoralen multiplied the risk by 228%. They also showed that in people with a poor ability to tan, psoralen users had almost four-and-a-half times the risk of melanoma compared to regular sunscreen users.[xi]

References

[i]. Fitzpatrick TB, Haynes HA. Photosensitivity and other reactions to light. In Harrison’s Principles of Internal Medicine. 7th ed, McGraw-Hill, 1974, 281-84.

[ii]. Marks R, Whiteman D. Sunburn and melanoma: how strong is the evidence? BMJ 1994; 308: 75-6.

[iii]. Karnauchow PN. Melanoma and sun exposure. Lancet 1995; 346: 915.

[iv]. Shuster S. Melanoma and sun exposure. Lancet 1995; 346: 1224.

[v]. Kricker A, et al. Sun exposure and non-melanocytic skin cancer. Cancer Causes and Controls 1994; 5: 367-392.

[vi]. Garland CF, et al. Could sunscreens increase melanoma risk? Am J Publ Hlth 1992; 82: 614-15.

[vii]. Garland CF, et al. Effect of sunscreens on UV radiation-induced enhancement of melanoma growth in mice. J Natl Cancer Inst 1994; 86: 798-801

[viii]. Fuller CJ, et al. Effect of beta-carotene supplementation on photosuppression of delayed-type hypersensitivity in normal young men. Am J Clin Nutr 1992; 56: 684-90.

[ix]. Kirk-Othmer. Encyclopedia of Chemical Technology. 1981; 13: 367-68.

[x]. Stern RS, Laid N. The carcinogenic risk of treatments for severe psoriasis. Cancer 1994; 73: 2759-64.

[xi]. Autier P, et al. Melanoma and use of sunscreens: an EORTC case-control study in Germany, Belgium and France. Int J Cancer 1995; 61: 749-55.

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By Team FPS – April 21, 2011

Sunlight Information: Skin Cancers and Vitamin D

Sunlight Information: Skin Cancers and Vitamin D by Barry Groves

Introduction

For the past several decades the numbers of skin cancers, and particularly the deadly one, malignant melanoma, have risen dramatically among Caucasian populations throughout the world. In the USA melanoma is the seventh most commonly diagnosed cancer with a rate of 14.2 cases per 100,000 population, (1) while in 1987 Queensland, Australia, had 55.8 cases per 100,000, the world’s highest rate. (2) The incidence of the various types of skin cancer in the general British population has been increasing at an annual rate of two to eight percent over the past 2 decades. (3) The contributory factors seem to be a light-skinned, northern European population living in areas of high ambient sunlight, and the incidence of the disease is seasonal, with more cases reported in summer than winter. Yet several clinical and epidemiological aspects of cutaneous melanoma seem anomalous because they contrast with other sunlight-associated skin cancers. For example, persons with the greatest risk of melanoma are not those with the greatest cumulative solar exposure; the anatomic areas that receive the most solar exposure are not preferentially affected; and not all light-skinned people suffer the same – albino Africans who have no pigmentation, are more likely to get sunburn and a number of other skin complaints as a result of exposure to the sun, but they don’t get melanomas. (4)

In the 1960s I lived with my family in Singapore, just 1.5 degrees from the Equator. I have blond hair, fair skin and blue eyes. It is a combination not believed to be suited to the harsh sun of the tropics. Nevertheless, I regularly went on the beach, to the swimming pool or sailing on the South China Sea with little or nothing on, in the heat of the midday sun. I don’t go brown, the best I can manage by way of a tan is a dark golden colour. I remember, in an effort to deepen my tan, I would lie out for hours with the sun to one side of me and its reflection in a mirror of cooking foil on the other to increase my exposure. Like everyone else in the ex-patriot Singapore community, I didn’t give skin cancer a thought in those days; the phrase ‘malignant melanoma’ was unheard of.

I didn’t use a sunscreen. They too were unavailable. If we used anything at all, which most of the time we did not, it was usually a well-shaken mixture of coconut oil and vinegar. This was a concoction used at the time by naturists. We smelt like a fish and chip shop, but we didn’t get burnt in the years we lived there.

Today, it seems, all that has changed. Why? What has changed in the last forty years?

Skin cancers

There are three major forms of skin cancer:

  • Basal cell carcinoma is the most common form of skin cancer. It forms small, fleshy bumps or lumps on the head, neck, and hands. Named for the lowest layer of the epidermis (top layer of skin) where the cancer originates. It occurs most frequently in men who spend a great deal of time outdoors and is usually found on the head and neck. (5) Basal cell carcinoma is not particularly dangerous as it rarely spreads throughout the body, although it can extend below the skin to the bone.
  • Squamous cell carcinoma is the second most common skin cancer. It usually affects people who sunburn easily, tan poorly, and have blue eyes and red or blond hair. Squamous cell carcinoma often develops from actinic keratoses and can metastasise (spread) if left untreated. (6)
  • Malignant melanoma is the rarest form of skin cancer but it is the most deadly. It originates in the melanocytes – the cells that produce the skin colouring or pigment known as melanin – and can be recognised by its black or grey colour. It usually grows from an existing mole, which may enlarge, become lumpy, bleed, change colour, develop a spreading black edge, turn into a scab, or begin to itch. It is more prevalent among city and office workers than among people who work out-of-doors and is thought to be linked to brief, intense periods of sun exposure such as one might get on annual holidays on sunny beaches and a history of severe sunburn in childhood or adolescence. Malignant melanoma metastasises readily and is almost always fatal if not caught in time (7) as it responds poorly to conventional therapy. (8) Malignant melanoma is growing at a rate of seven percent per year in the United States. In 1991 cancer experts estimated that there would be about 32,000 cases during the year of which 6,500 would be fatal. (9) In Canada melanoma incidence rose by six percent per year for men and by 4.6 percent per year for women during the period 1970 to 1986. (10) In Australia the rate for men doubled between 1980 and 1987 and for women it increased by more than fifty percent. (11) It is now estimated that, by the age of 75, two out of three Australians will have been treated for some form of skin cancer. (12)

Who’s at risk?

  • Whites at greater risk than other groups.
  • People who have had excessive exposure to UV radiation from the sun without protection.
  • People with fair skin are at more than twenty-times greater risk.
  • Men are two to three times more likely than women to have basal cell and squamous cell cancers.
  • People with a family history of skin cancer.
  • Workers exposed to arsenic, industrial tar, coal, paraffin, and certain types of heavy oils.

How to detect skin cancer

Consult a dermatologist immediately if you have moles or pigmented spots with these characteristics:

  • Asymmetrical (one half is not identical to the other)
  • Borders that are irregular, uneven, or ragged
  • Colour varies from one area to another
  • Diameter is larger than 6 mm

Ultraviolet radiation

All types of skin cancer are attributed to exposure to the ultraviolet (UV) part of the spectrum of sunlight. UV is classified as three distinct wavebands: A, B and C. They are all believed to contribute to the development of skin cancer. (5)

  • UVA rays constitute between ninety and ninety-five percent of the ultraviolet light that reaches the earth. It is not absorbed by the ozone layer. UVA light penetrates furthest into the skin and is involved in the initial stages of suntanning. UVA tends to suppress the immune function and is implicated in premature aging of the skin. (5) (13)
  • UVB rays are partially absorbed by the ozone layer. They do not penetrate the skin as far as the UVA rays but are the primary cause of sunburn. They are also responsible for most of the tissue damage which results in wrinkles and aging of the skin and are implicated in cataract formation (5) .
  • UVC rays are almost completely absorbed by the ozone layer. However, it is thought that as the ozone layer thins UVC rays may begin to contribute to sunburning and premature aging of the skin (5) .

How strong is the evidence linking exposure to sunlight with melanoma?

During the 1980s and early ’90s more than a dozen studies compared histories of sunburn in patients with melanoma and controls. But differences in design and definition of sunburn make it difficult to quantify a single estimate of risk.

The most complete data on melanoma and sunburn come from six studies from Australia, Europe and North America. These studies suggest an association but say that the effect is modest. They emphasise the point that episodic exposure seems to be more risky than constant exposure. (14)

British doctors R Marks and D Whiteman are unconvinced of the sunlight/melanoma link. They point out that:

  • Melanoma can be found on ovaries
  • Melanoma occurs less frequently on sun-exposed areas
  • In Japan forty percent of pedal melanomas are on the soles of the feet
  • There is 5-times more melanoma in Scotland on the feet than on the hands
  • And melanoma in Orkney and Shetland is ten times that of the Mediterranean islands.

Other clinicians agree. Karnauchow says: “The simplistic idea of a sun/melanoma relationship is based more on a belief than science.”. . . “As with other neoplasms, the cause of melanoma remains an enigma and most probably the sun has little, if anything, to do with it.” (15) And Newcastle dermatology professor, Sam Shuster states that the main reason for the supposed increase in melanomas was a change in diagnostic beliefs: lesions previously regarded as benign became classified first as dubious then as malignant. “Melanomas are being invented, not found,” he says, ” . . . exposure to screening and pigmented lesion clinics is a greater cause of melanoma than sun exposure.” (16)

Dr Anne Kricker and colleagues, looking at studies into skin cancer other than malignant melanoma and exposure to sunlight, also say that the evidence linking skin cancers with sun exposure is weak. They note that most studies have not found statistically significant positive associations, while the few that have lacked empirical evidence that sun exposure was the cause.

“Many questions remain about the relationship between sun exposure and skin cancer,” they say. (17)

The ozone hole

The stratospheric ozone layer is a delicate umbrella guarding us from the worst effects of solar radiation. One suggested cause of the recent increase in skin cancers is our use of chemicals which interact with protective layers in our atmosphere that screen us from the sun’s ultraviolet rays, of which the best example is a hole in the ozone layer which appeared over the Antarctic a few years ago.

The history of skin cancers follows the increase in the use of many chemicals now known to be harmful to the environment. Manufacturing processes which use or generate such synthetic chemicals as chlorofluorocarbons (CFCs), hydrochlorofluorocarbons (HCFCs), and other perfluorinated compounds (PFCs) all of which tend to destroy the ozone layer as well as having other deleterious effects on our atmosphere, have proliferated over the past half century.

Not only do these gases have a strong environmental effect, their chlorine and fluorine bonds make them exceptionally long-lived in the environment. For example, data show that sulphur hexafluoride may persist in the atmosphere for up to 3,200 years.

Could our increasing release of these chemicals into the atmosphere be the cause of the dramatic increase in skin cancers? Unfortunately, it seems not. In 1991 Professor Johan Moan of the Norwegian Cancer Institute made an astounding discovery: He found that between 1957 and 1984 the annual incidence of melanoma in Norway had increased by 350 percent for men and by 440 percent for women. But he also determined that there had been no change in the ozone layer over this period. His report concluded that: “Ozone depletion is not the cause of the increase in skin cancers”. (18)

But if the ozone layer has not yet changed significantly, except at the poles, then what is causing the recent, enormous increase in skin cancer?

The sunscreen connection

The Australian experience might provide the first clue. The medical establishment in Queensland has vigorously promoted the use of sunscreens for many years – and today, Queensland has more cases of melanoma per capita than any other place in the world. This is a trend seen worldwide.

Incidence rates of melanoma have risen especially steeply since the mid-1970s. The two principal strategies for reduction of risk of melanoma and other skin cancers during this period were sun avoidance and use of chemical sunscreens. Rising trends in the incidence of and mortality from melanoma have continued since the 1970s and 1980s, when sunscreens with high sun protection factors became widely used.

Sunscreens are designed to protect against sunburn which is caused by UVB; they generally provide little protection against UVA rays. There are two types of sunscreen:

  • Physical sunscreens contain inert minerals such as titanium dioxide, zinc oxide, or talc and work by reflecting the ultraviolet (UVA and UVB) rays away from the skin. This is the type seen as white or coloured bands on the lips and faces of sportsmen.
  • Chemical sunscreens contain chemicals such as benzophenone or psoralen as the active ingredient. They prevent sunburn by absorbing the (mainly UVB) ultraviolet rays. These are the sunscreens used by those on the beaches wishing to tan. A sunscreen with a sun protection factor (SPF) of 15 filters out approximately ninety-four percent of the UVB rays. Using one with a SPF of 30 does not double to protection – filtering out ninety-seven percent means that it only increases protection by about three percent. And this quoted SPF applies to UVB rays only. The protection provided against UVA rays in chemical sunscreens is much less at about ten percent of the UVB rating. (19) Drs Cedric and Frank Garland of the University of California are the foremost opponents of the use of chemical sunscreens. They point out that the greatest rises in melanoma are in countries where chemical sunscreens have been heavily promoted. (20) They say that, while sunscreens do protect against sunburn, there is no scientific proof that they protect against melanoma or basal cell carcinoma in humans.

Indeed, the Garland brothers strongly believe that the increased use of chemical sunscreens is the primary cause of the skin cancer epidemic. Recent studies by them have shown a higher rate of melanoma among men who regularly use sunscreens and a higher rate of basal cell carcinoma among women using sunscreens. (21) (22) This was confirmed by another study group who found that ‘always users’ of sunscreens had 3.7 times as many malignant melanomas as those ‘never using’.

The Garland brothers suggest that this is because people using sunscreens develop a false sense of security; that because they do not get a sunburn they are encouraged to stay longer in the sun, but there may be other reasons why chemical sunscreens can be dangerous:

  • Chemical sunscreens do little to stop UVA rays. These rays penetrate deeper into the skin where they are strongly absorbed by the melanocytes which are involved not only in the production of the skin-tanning pigment, melanin, but also in the formation of melanoma. (20) UVA rays also have a depressing effect on the immune system. (23)
  • More importantly, however, may be the fact that most chemical sunscreens contain up to five percent of benzophenone or its derivatives oxybenzone or benzophenone-3 as their active ingredient. And benzophenone, used in industrial processes to initiate chemical reactions and promote cross-linking. (24) is one of the most powerful free radical generators known to man. Moreover, benzophenone is activated by ultraviolet light. UV breaks benzophenone’s double bond to produce two free radical sites. These free radicals desperately look for a hydrogen atom to make them “feel whole again”. While they may find this hydrogen atom, harmlessly, in the sunscreen, they could equally find it on the surface of the skin and thereby initiate a chain reaction which could ultimately lead to melanoma and other skin cancers.
  • Harvard Medical School researchers also discovered that psoralen, another ultraviolet light-activated free radical generator, is an extremely efficient carcinogen. They found that the rate of squamous cell carcinoma among patients with psoriasis, who had been repeatedly treated with UVA light after an application of psoralen to their skin, was eighty-three times higher than among the general population. (25) This added weight to a study in 1991-2, in which scientists at the European Organisation for Research and Treatment of Cancer (EORTC) found that regular use of sunscreens increased cancer risk by fifty percent but sunscreens containing psoralen multiplied the risk by 228 percent. They also showed that in people with a poor ability to tan, psoralen users had almost four-and-a-half times the risk of malignant melanoma compared to regular sunscreen users. There was no increase of risk for those using self-tanning cosmetics. They say: “Serious doubts are raised regarding the safety of sunscreens containing psoralens”. (26)

There is, however, some evidence that regular use of sunscreens helps prevent the formation of actinic keratoses, the precursors of squamous cell carcinoma. (27)

The dietary connection

In the 1970s, when kidney transplantation was pioneered, doctors first encountered the problem of tissue rejection. To combat it, they gave their transplant patients linoleic acid. This suppressed their immune systems very effectively, preventing their transplanted kidneys being rejected. But it also caused a large increase in cancers and this treatment was stopped.

Since then, linoleic acid and oils that contain it, have been shown time and again to increase the risk of several types of cancer, including skin cancers.

Linoleic acid is the major fatty acid in all polyunsaturated vegetable margarines and cooking oils:

  • Polyunsaturated margarines are around 40% linoleic acid
  • Sunflower, safflower, corn and soya oils are all more than 50% linoleic acid.

Drs B S and L E Mackie, working on Australia’s Sunshine Coast have a great deal of experience in skin cancers. They say: “In view of the work of Black and Erickson in mice and our own work in humans, we believe that human subjects who are at high risk of melanomas and other solar-induced forms of skin cancer should be advised to be moderate in their intake of dietary polyunsaturated fats.” (28)

Patricia Holborrow also points out that the increase in melanomas could be a result of dietary changes to PUFs.”Recently, I followed up four families that started in 1976 to use a diet with preferred oils as safflower and sunflower oil and low in salicylates and additives (that interfere with the metabolic pathway of these fats). There had been three cases of cancer resulting in two deaths in these families.” (29) “The issue is further complicated by dietary factors that are cofactors for the metabolic pathways for the fatty acids and which may in addition favour or have a negative effect on the anticancer or cancer enhancing properties of the various prostaglandins (eg the negative effects of vitamin E and the positive effects of vitamin C).” (30)

The Australians are as paranoid about heart disease as the Americans. I was in Australia in 1995 and noticed that it is even their custom to remove the cream from milk and replace it with polyunsaturated vegetable oil.

One of the recommendations for reducing the risk of skin and other cancers is to reduce intakes of fats and take vitamin supplements. But this approach doesn’t seem to work. The findings of a huge study by scientists at the Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston; the Division of Human Nutrition and Epidemiology, Wageningen Agricultural University, Wageningen, Netherlands; the Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York; and the Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, of 43,217 male participants of the Health Professionals Follow-up Study, did not support the hypothesis that diets low in fat or high in specific vitamins lower risk of basal cell carcinoma. (31)

It’s usually saturated animal fats that get the blame for all diseases today. They are not the culprits — ‘healthy’ vegetable oils are (see Polyunsaturated Fats in The Cholesterol Myth)

The benefits of sunlight

Although the medical establishment still strongly supports the use of sunscreens there is a growing consensus among progressive researchers that the use of sunscreens and heeding the current advice to cover up when out doors may promote not only skin cancers but other cancers as well.

There is very little vitamin D in any of the food we eat. Most of the body’s vitamin D supply is manufactured by the action of UVB rays on lipids on the skin. (32) Using a sunscreen drastically lowers this production. (33)

Researchers at the Occupational Medicine Department, School of Medicine, University of California, San Diego studied men in the US Navy during 1974-1984. They discovered that personnel working indoors had 10.6 cases of melanoma per 100,000 while those who worked in occupations that required spending time both indoors and outdoors had the lowest rate at 7.0 per 100,000. They also determined that there were more melanomas on the trunk than on the more commonly sunlight-exposed head and arms. Findings from this study suggest a protective role for brief, regular exposure to sunlight and fit with laboratory studies that showed that vitamin D suppressed the growth of malignant melanoma cells in tissue culture. (27)

The same team found that lack of exposure to ultraviolet sunlight may place some populations at higher risk of breast cancer. The association between total average annual sunlight energy striking the ground and age-adjusted breast cancer mortality rates in eighty-seven regions of the United States was evaluated. Annual age-adjusted mortality rates for breast cancer varied from 17-19 per 100,000 in the South and Southwest to 33 per 100,000 in the Northeast. Risk of fatal breast cancer in the major urban areas of the United States increased as intensity of local sunlight decreased. They conclude that “Vitamin D from sunlight exposure may be associated with low risk for fatal breast cancer, and differences in ultraviolet light reaching the United States population may account for the striking regional differences in breast cancer mortality”. (34)

They also evaluated the association between total average annual sunlight energy striking the ground and age-adjusted breast cancer incidence rates in the USSR and found that the pattern of increased breast cancer incidence in regions of low solar radiation in the USSR was consistent with the geographical pattern seen for breast cancer mortality in the USA and worldwide. (35)

A low blood level of vitamin D is known to increase the risk for the development of breast and colon cancer (36) and may also accelerate the growth of melanoma. (27) (28) (37) Because of this, Dr Gordon Ainsleigh in California believes that the use of sunscreens causes more cancer deaths than it prevents. He estimates that the 17% increase in breast cancer observed between 1991 and 1992 may be the result of the pervasive use of sunscreens over the past decade. (30) He also estimates that 30,000 cancer deaths in the United States alone could be prevented each year if people would adopt a regimen of regular, moderate sun exposure.

Prostate Cancer

That this could be so is confirmed by recent studies which have suggested that exposure to ultraviolet (UV) radiation may be protective to some internal cancers including that in the prostate. One such is by scientists working at the Department of Urology, North Staffordshire Hospital, Staffordshire, Stoke-on-Trent, UK. They studied 212 prostatic adenocarcinoma and 135 benign prostatic hypertrophy patients to determine whether previous findings showing a protective effect for UV exposure could be reproduced. Their data confirmed that higher levels of cumulative exposure, adult sunbathing, childhood sunburning and regular holidays in hot climates were each independently and significantly associated with a reduced risk of this cancer.(38)

Cancer Prevention

So what should you do to protect yourself as much as possible against these cancers? Summarizing current research the following recommendations appear reasonable:

  • Most important: the best protection is a natural suntan.
  • DO try to develop a moderate natural suntan unless you have extremely sensitive skin and burn easily.
  • DO build up a tan slowly over, say, a week. Aim for no more than a slight pinkness each day. You should never tan so much that your skin peels off.
  • DO remember that sunlight is strongly reflected from sand, snow, ice, and concrete and can increase your direct sunlight exposure by 10 to 50%.
  • DO cut down on the amount of polyunsaturated fat and oil in your diet.
  • DO see your doctor if you spot any unusual moles or growth on your skin — particularly if they are irregular in shape, bleed, itch, or appear to be changing. Most skin cancers can be cured if caught in time.
  • DO NOT sunbathe in the early morning or late afternoon sun as recommended by health authorities. If the sun is low in the sky, you will only receive UVA rays, which is counter-productive. Yes, UVA tans, but it also reduces the body’s vitamin D stores.
  • DO NOT use a sunscreen but DO use a moisturiser on your skin. Put it on at least fifteen minutes before going into the sun to allow it to penetrate the skin. It is a good idea to put this on all over your body before you dress to go out. That way you don’t miss bits such as the ‘bikini line’.
  • DO NOT shower in the morning before going out to sunbathe. The oils naturally produced by your body during the night are a good protection.
  • DO NOT shower for at least an hour after you have sunbathed. Vitamin D formed by the action of the sun on oils on the skin need time to be absorbed.
  • Forget ‘aftersun’ products. They are expensive and unnecessary if you have followed this advice and not allowed your skin to be burnt. But after you have showered, do use a moisturiser.
  • DO NOT wear sunglasses that filter out 100% of the ultraviolet light. They may protect you against the development of cataracts, but they stop UV entering the eyes – and that is much more important as UV through the eyes prevents cancer.

Dermatologists recommend that you do periodic self-examinations for any changes in the number, size, shape, and colour of pigmented areas of your skin, such as freckles and moles.

However, consulting your doctor or a dermatologist may be the surest way to detect skin cancer early. Physicians are trained to recognise skin cancers and are more likely to detect thinner melanomas, the most dangerous type of skin cancer, than patients who do self-examinations, increasing the likelihood that the skin cancer can be detected early enough to be treated effectively.

Having said that, however, Christopher Del Mar, Professor of General Practice, University of Queensland, Australia, may disagree. He notes that a worried public are the initiators of surgery. Doctors perform excisions of benign pigmented tissue because of pressure from their patients. He says: “The benefits of early detection programs are uncertain; such programs need to be evaluated to determine whether there are any benefits and, if so, whether they outweigh the costs.” (39)

Conclusion

Johnathan Rees, Professor of dermatology, University Department of Dermatology, Newcastle upon Tyne, appraises the current melanoma “epidemic”, saying: “Once you excise a pigmented lesion and know its histology you forfeit the chance of knowing what would have happened if you had left it in situ”. “Cohort analyses show, perhaps surprisingly, that mortality from melanoma rose from the 1890s to the 1950s and then started to decline. Changes in leisure activity don’t explain the 3-7% pa increase in melanoma incidence from mid-1950s to early 1980s.

“. . . individuals with higher continuous sun exposure have lower rates than those exposed intermittently.”

“There is after all no robust empirical evidence to defend most health promotion in this area. It has been suggested that the antithesis of science is not art but politics; melanoma is perhaps an example of the two having become mistakenly intertwined. An amicable separation is required. The certainties of health of the Nation and “slip-slap-slop” already look a little shaded: molecules care little for consensus.” (40)

Some years ago, the vicar of a parish in Devon, who was not in favour of a nearby nudist beach, wrote in his parish magazine: “If God had meant us to walk around without clothes, we’d have been born naked”! Well, of course, He did and we are — perhaps it was for a very good reason.

References

1. American Cancer Society. Cancer facts and figures 1998 . Atlanta, The Society, 1998.
2. MacLennan R, Green AC, McLeod GR, Martin NG. Increasing incidence of cutaneous melanoma in Queensland, Australia. J Natl Cancer Inst 1992; 84: 1427-32.
3. Potten CS, et al . DNA damage in UV-irradiated human skin in vivo: automated direct measurement by image analysis (thymine dimers) compared with indirect measurement (unscheduled DNA synthesis) and protection by 5-methoxypsoralen. Int J Radiat Biol . 1993; 63: 313-24.
4. Diffey BL, Healy E, Thody AJ, Rees JL. Melanin, melanocytes and melanoma. Lancet 1995; 346: 1713.
5. Harmful effects of ultraviolet radiation. JAMA 1989; 262: 380-84.
6. Hacker SM, Flowers FP. Squamous cell carcinoma of the skin. Postgraduate Medicine , 1993; 93: 115-26
7. Lee JAH. The relationship between malignant melanoma of skin and exposure to sunlight. Photochem Photobiol 1989; 50: 493-96
8. Malignant melanoma — Report of a meeting of physicians and scientists, University College, London Medical School. Lancet 1992; 340: 948-51.
9. Skolnick AA. Revised regulations for sunscreen labelling expected soon from FDA. JAMA 1991; 265: 3217-20.
10. Statistics Canada . Canadian Cancer Statistics, 1991.
11. Reynolds T. Sun plays havoc with light skin down under. J Natl Cancer Inst 1992; 84: 1392- 94.
12. Ozone depletion and health. Lancet 1988; ii: 1377.
13. Fitzpatrick TB, Haynes HA. Photosensitivity and other reactions to light . In Harrison’s Principles of Internal Medicine , 7th ed, McGraw-Hill, 1974, 281-84.
14. Marks R, Whiteman D. Sunburn and melanoma: how strong is the evidence? Br Med J 1994; 308: 75-6.
15. Karnauchow PN. Melanoma and sun exposure. Lancet 1995; 346: 915.
16. Shuster S. Melanoma and sun exposure. Lancet 1995; 346: 1224.
17. Kricker Anne, Armstrong B K, English D R. Sun exposure and non-melanocytic skin cancer. Cancer Causes and Controls 1994; 5: 367-392.
18. Moan J, Dahlback A. The relationship between skin cancers, solar radiation and ozone depletion. Br J Cancer 1992; 65: 916-21.
19. Kaidbey K, Gange RW. Comparison of methods of assessing photoprotection against ultraviolet A in vivo. J Am Acad Dermatol Vol. 16, No. 2, Pt. 1, February 1987, pp. 346-53
20. Garland CF, et al . Could sunscreens increase melanoma risk? Am J Publ Hlth 1992; 82: 614-15.
21. Garland CF, et al . Could sunscreens increase melanoma risk? Am J Publ Hlth 1992; 82: 614-15.
22. Garland CF, et al . Effect of sunscreens on UV radiation-induced enhancement of melanoma growth in mice. J Natl Cancer Inst 1994; 86: 798-801
23. Fuller, Cindy J., et al. Effect of beta-carotene supplementation on photosuppression of delayed-type hypersensitivity in normal young men. Am J Clin Nutr 1992; 56: 684-90.
24. Kirk-Othmer Encyclopedia of Chemical Technology. 1981; Vol 13, 3rd ed: 367-68.
25. Stern RS, Laid N. The carcinogenic risk of treatments for severe psoriasis. Cancer 1994; 73: 2759-64.
26. Autier P, et al . Melanoma and use of sunscreens: an EORTC case-control study in Germany, Belgium and France. Int J Cancer 1995; 61: 749-55.
27. Dover JS, Arndt KA. Dermatology. JAMA 1994; 271: 1662-63.
28. Mackie BS, Mackie LE. Dietary polyunsaturated fats. Med J Aust 1988; 149: 449.
29. Holborow P. Melanoma and polyunsaturated fat; cancer and diet. NZ Med J 1990; 103: 515-6.
30. Holborow P. Melanoma and fatty acids. NZ J Med 1991; 104: 19.
31. van Dam R M, et al. Diet and basal cell carcinoma of the skin in a prospective cohort of men. Am J Clin Nutr 2000; 71: 135-141
32. Garland FC, et al . Geographic variation in breast cancer mortality in the United States: a hypothesis involving exposure to solar radiation. Prev Med 1990; 19: 614-22
33. Koh HK, Lew RA. Sunscreens and melanoma: implications for prevention. J Natl Cancer Inst 1994; 86: 78-9
34. Garland FC, Garland CF, Gorham ED, Young JF. Geographic variation in breast cancer mortality in the United States: a hypothesis involving exposure to solar radiation. Prev Med 1990; 19: 614-22
35. Gorham ED, Garland FC, Garland CF. Sunlight and breast cancer incidence in the USSR . Int J Epidemiol. 1990; 19: 820-4
36. Martinez ME, Willett WC. Calcium, vitamin D, and colorectal cancer: a review of the epidemiologic evidence. Cancer Epidemiol Biomarkers Prev . 1998; 7: 163-8
37. Ainsleigh HG. Beneficial effects of sun exposure on cancer mortality. Prev Med 1993; 22: 132-40.
38. Bodiwala D, Luscombe CJ, Liu S, Saxby M, French M, Jones PW, Fryer AA, Strange RC. Prostate cancer risk and exposure to ultraviolet radiation: further support for the protective effect of sunlight. Cancer Lett 2003;192:145-9
39. Del Mar C. Slip, slop slap and wrap. Should we do more to prevent skin cancer? Med J Aust 1995; 163: 511-2.
40. Rees J L. The melanoma epidemic: reality or artefact. Br Med J 1996; 312: 137-8

http://www.second-opinions.co.uk/sunlight.html

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By Team FPS – April 21, 2011

German Volume Training

A new look at an old way to get big and strong

by Charles Poliquin

Supersets and tri-sets allow you to perform a lot of work in a short period of time. The rest-pause method allows you to use heavier weights so you can recruit the higher-threshold muscle fibers, and eccentric training enables you to overcome strength plateaus. The bottom line is that almost any training method will work (provided you do it with intensity!), at least for the few weeks it takes for your body to adapt to it. There is, however, one training system that stands above all the rest. It’s brutally hard, but I’ve found it to be a very effective way to pack on muscle fast!
Canadian weightlifting coach Pierre Roy used GVT when he trained Jacques Demers, a silver medalist in the 1984 Olympic Games. Here Coach Roy is shown with his two 2010 Junior World Team members, Kristel Ngariem and Paul Dumais.

Canadian weightlifting coach Pierre Roy used GVT when he trained Jacques Demers, a silver medalist in the 1984 Olympic Games. Here Coach Roy is shown with his two 2010 Junior World Team members, Kristel Ngariem and Paul Dumais.

In strength-coaching circles, this method is often called the “10 sets method.” Because it has its roots in German-speaking countries, I like to call it German Volume Training. To the best of my knowledge, this training system originated in Germany in the mid-’70s and was popularized by Rolf Feser, who was then the National Coach of Weightlifting. A similar protocol was promoted by Vince Gironda in the US, but regardless of who actually invented it, it works.

In Germany, the 10 sets method was used in the off-season to help weightlifters gain lean body mass. It was so efficient that lifters routinely moved up a full weight class within 12 weeks. German Volume Training was the base program of Canadian weightlifter Jacques Demers, a silver medalist in the Los Angeles Olympic Games who was coached by Pierre Roy. Jacques was known in weightlifting circles for his massive thighs, and he gives credit to the German method for achieving such a spectacular level of hypertrophy. The same method was also used by Bev Francis in her early days of bodybuilding to pack on muscle.
The German Volume Training program works because it targets a group of motor units, exposing them to an extensive volume of repeated efforts, specifically 10 sets of a single exercise. The body adapts to the extraordinary stress by hypertrophying the targeted fibers. To say this program adds muscle fast is probably an understatement. Gains of 10 pounds or more in six weeks are not uncommon, even in experienced lifters!
Goals and Guidelines
The goal of the German Volume Training method is to complete 10 sets of 10 reps with the same weight for each exercise. You want to begin with a weight you could lift for 20 reps to failure if you had to. For most people, on most exercises, that would represent 60 percent of their 1RM load. Therefore, if you can bench press 300 pounds for 1 rep, you would use 180 pounds for this exercise.
For lifters new to this method, I recommend using the following bodypart splits:
Day 1
Day 2
Day 3
Day 4
Day 5
Chest & Back
Legs & Abs
Off
Arms & Shoulders
Off
When using this German Volume Training program or any other, you should keep a detailed journal of the exact sets/reps and rest intervals performed, and only count the repetitions completed in strict form. Here are a few more guidelines to ensure optimal progress:
Rest Intervals: When bodybuilders start with this method, they often question its value for the first several sets because the weight won’t feel heavy enough. However, there is minimal rest between sets (about 60 seconds when performed in sequence and 90-120 seconds when performed as a superset), which incurs cumulative fatigue. (Interestingly enough, you might find you get stronger again during the eighth and ninth sets. This is because of a short-term neural adaptation.) Because of the importance of the rest intervals, you should use a stopwatch to keep the rest intervals constant. This is very important, as it becomes tempting to lengthen the rest time as you fatigue.
Tempo: For long-range movements such as squats, dips and chins, use a 40X0 tempo; this means the eccentric portion of the exercise is 4 seconds and the concentric portion is done as rapidly as possible. For movements such as curls and triceps extensions, use a 3020 tempo.

Bodybuilding guru Vince Gironda used a type of GVT program with his numerous muscle building champions.

Bodybuilding guru Vince Gironda used a type of GVT program with his numerous muscle building champions.

Number of Exercises: Perform one, and only one, exercise per bodypart. Therefore, select exercises that recruit a lot of muscle mass. Triceps kickbacks and leg extensions are definitely out; squats and bench presses are definitely in. For supplementary work for individual bodyparts (like triceps and biceps), you can do 3 sets of 10-20 reps.

Training Frequency: Because German Volume Training is such an intense program, it’ll take you longer to recover. In fact, if you’re familiar with the writings of Peter Sisco and John Little, you’ll find that the average “Power Factor Rating” of the 10-sets method is about 8 billion. Consequently, one training session every four to five days per bodypart is plenty.
Overload Mechanism: Once you’re able to do 10 sets of 10 with constant rest intervals, increase the weight on the bar by 4 to 5 percent, and repeat the process. Refrain from using forced reps, negatives or burns. The volume of the work will take care of the hypertrophy. Expect to have some deep muscle soreness without having to resort to set-prolonging techniques. In fact, after doing a quad and hams session with this method, it takes the average bodybuilder about five days to stop limping.
Here are two examples of a German Volume Training workout, one for the beginner and one for the immediate-level trainee.
Beginner/Intermediate German Volume Training Program: Phase 1
This is a sample German Volume Training routine based on a five-day cycle. Once you’ve used this method for six workouts per bodypart, it’s time to move on to a more intensive program for a three-week period.
Day 1: Chest and Back
Exercise
Sets
Reps
Tempo
Rest Interval
A-1 Decline Dumbbell Presses, Semi-Supinated Grip (palms facing each other)
10
10
40X0
90 sec
A-2 Chin-Ups (palms facing you)
10
10
40X0
90 sec
B-1 Incline Dumbbell Flyes
3
10-12
3020
60 sec
B-2 One-Arm Dumbbell Rows
3
10-12
3020
60 sec
Notes: Rest 90 seconds between each “A” exercise and each superset; rest 60 seconds between each “B” exercise and each superset. Incidentally, I recommend only 3 sets of 10 in this program for the “B” exercises. The “B” exercises constitute supplementary work, and doing 10 sets of them would result in overtraining.
Day 2: Legs and Abs
Exercise
Sets
Reps
Tempo
Rest Interval
A-1 Back Squats
10
10
4020
90 sec
A-2 Lying Leg Curls Feet Outward
10
10
40X0
90 sec
B-1 Low-Cable Pull-Ins*
3
15-20
2020
60 sec
B-2 Seated Calf Raises
3
15-20
2020
60 sec
(*Get a weightlifting belt and buckle it. Attach it to the low pulley of a cable crossover machine. Lie down on your back in front of the machine, and hook your feet in the belt. Then pull your knees towards your chest.)
Notes: Rest 90 seconds between each “A” exercise and each superset; rest 60 seconds between each “B” exercise and each superset.
Day 3: Off

Day 4: Arms and Shoulders
Exercise
Sets
Reps
Tempo
Rest Interval
A-1 Parallel Bar Dips
10
10
40X0
90 sec
A-2 Incline Hammer Curls
10
10
40X0
90 sec
B-1 Bent-Over Dumbbell Lateral Raises*
3
10-12
20X0
60 sec
B-2 Seated Dumbbell Lateral Raises
3
10-12
20X0
60 sec
(*While seated on the edge of a bench with your torso bent over, raise the dumbbells out to the side, making sure the top two knuckles (the ones closest to your thumb) are in line with your ears at the top of the movement.)
Notes: Rest 90 seconds between each “A” exercise and each superset; rest 60 seconds between each “B” exercise and each superset. An “X” in the tempo means to move as fast as possible, keeping the weight under control.
Day 5: Off

Beginner/Intermediate German Volume Training Program: Phase 2
After six of those five-day cycles, I recommend you do a three-week phase in which the average set is 6-8 reps, and do only 4-6 sets per bodypart over a five-day cycle, or you can do any other split that suits your recovery pattern. After this three-week block, you can return to the German Volume Training method by doing the following routine of 10 sets of 6 reps. In the exercises that are prescribed for 10 sets, use a load with which you’d normally be able to do 12 repetitions. The goal in this phase is to do 10 sets of 6 with that load.
Sample 10 Sets of 6 Routine:
Day 1: Chest and Back

Exercise
Sets
Reps
Tempo
Rest Interval
A-1 Incline Dumbbell Presses
10
6
50X0
90 sec
A-2 Wide-Grip Pull-Ups (palms facing away from you)
10
6
50X0
90 sec
B-1 Flat Dumbbell Flyes
3
6
3010
60 sec
B-2 Bent-Over Rows with E-Z Bar
3
6
3010
60 sec
Notes: Rest 90 seconds between each “A” exercise and each superset; rest 60 seconds between each “B” exercise and each superset.
Day 2: Legs and Abs

Exercise
Sets
Reps
Tempo
Rest Interval
A-1 Bent-Knee Deadlifts
10
6
50X0
90 sec
A-2 Seated Leg Curls Feet Inward
10
6
50X0
90 sec
B-1 Twisting Crunches
3
12-15
3030
60 sec
B-2 Standing Calf Raises
3
12-15
3030
60 sec
Notes: Rest 90 seconds between each “A” exercise and each superset; rest 60 seconds between each “B” exercise and each superset.
Day 3: Off

Day 4: Arms and Shoulders

Exercise
Sets
Reps
Tempo
Rest Interval
A-1 Close Bench Presses with Chains
10
6
50X0
90 sec
A-2 Scott Close Grip EZ Bar Curls
10
6
50X0
90 sec
B-1 One arm seated external rotation
3
10-12
3010
60 sec
B-2 Incline Prone Lateral Raises
3
10-12
20X0
60 sec
(*While seated on the edge of a bench with your torso bent over, raise the dumbbells out to the side, making sure the top two knuckles (the ones closest to your thumb) are in line with your ears at the top of the movement.)
Notes: Rest 90 seconds between each “A” exercise and each superset; rest 60 seconds between each “B” exercise and each superset.
Day 5: Off
This German Volume Training program is elegant in its simplicity, but that’s what the Germans do best. Just ask any Porsche or BMW owner.

(Afterword: This article originally appeared in the July 1996 issue of Muscle Media 2000, which publisher Bill Phillips told me was the best issue in the history of the magazine. I should also note that an article about the GVT training program appeared in the June 2010 issue of Muscle and Fitness. It was called “Achtung, Baby!” and was plagiarized from my article with no reference to my original work. The article was written by Rob Fitzgerald, NSCA-CPT. An investigation by the NSCA Ethics Committee in May found that there is no such person certified by the NSCA by the name of Rob Fitzgerald, and as such the author is using a pen name with false credentials.)

http://www.charlespoliquin.com/ArticlesMultimedia/Articles/Article/441/German_Volume_Training.aspx/?Click=1727

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By Team FPS – April 18, 2011

Homemade Custard Easy Style

Homemade Custard Easy Style

Posted: April 17, 2011 by vvfitness

Remember back in the day schools dinners sucked! well apart from the sticky toffee puddings and custard! oh those were the days, nowadays pre-made custards are packed with additives and preservatives when really it should just contains a few nutritious and simple ingredients such as milk!

The fact is that us humans have been consuming milk for at least 50,000 years!. Our hunter gatherer ancestors would even store the milk in clay pots. This evidence was discovered in the high Andres where herds of Alpaca & Llama were milked. Western A. Price DDS visited the Swiss & African Masia population back in the 1930′s and found that their main source of protein was milk also! These cultures had no tooth decay and presented healthy & strong.

The benefits of dairy products – the prefect balance of calcium to phosphorous for our bones & teeth, a High quality protein, it contains essential vitamins and trace minerals and milk in particular contains an excellent balance of protein, carbohydrates and fat which helps heal the gut.

Since I started the Ray Peat program 5 months back I was drinking milkshakes which contained the same ingredients as custard these kept my blood sugar levels stable throughout the day, energy levels were good, kept me full and satisfied, They were also highly nutritious for my body. As well containing the right amount of protein, carbohydrates and fat in one serving. So custard is very similar alternative as it only contains milk, eggs, cream and sugar! So here how you can make this simple and easy food, desert or snack whichever rocks your boat!

Step 1. Get those ingredients together ! pasture fed organic whole or semi-skimmed milk, organic cream, organic free-range eggs also pasture raised, white cane sugar, vanilla essence and a pinch of salt. You can use raw milk but it needs to be scalded prior to making the custard. To scald put the milk in a double boiler and let it heat until you see the bubbles appear around the edges and the allow to cool and you can continue with the recipe.

step 2. Pre-heat oven to 160 degree C or for my lovely US peeps would be 325 degrees F.

Step 3. Beat the 3 eggs with a whisk! I if your lazy like me, I found a blender seems do the job just as good. So add the eggs and allow them to blend for about 2-3 minutes.

Step 4. Then add half a cup of sugar ! and pinch of salt, continue to blend for another minute.

Step 5. Measure out the milk 3 cups of milk but I add 2 and half cups of milk and a half cup of cream.

Step 6. Pour in the milk slowly while it’s still blending oh and (try not to make a mess) !

Step 7.  add the vanilla essence and blend for another minute. transfer mixture over to glass tray try not to use alumium as the chemicals when heated can leak into the food. Add a larger tray this is where you pour boiling water at about 1-2 cm deep. Cook for about 1 hour or more if needed a good test to know if its done is to run a knife and it should come out clean from the custard.

Step 7. Remove and allow to cool, you can store in the Fridge this will allow it to go more solid or reheat if you like it runny. Either way still taste good.

This custard works out to 6 servings in total if you’re not greedy and want to eat the whole thing like me! You can eat it alone or add whipped cream or some ripe fruit! nom nom… Enjoy!

http://vvfitness.wordpress.com/2011/04/17/homemade-custard-easy-style/

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By Team FPS – April 18, 2011

Three Efficient Ways to Put 5 Pounds On in Record Time.

by Charles Poliquin

Muscle growth is not a linear process. Give each one of those strategies at least a fair three weeks to show their effects.

1.    Do a calves & forearms workout only, once every 5 days.
I suggest you specialize just on calves and forearms for a single hours. Keep rest intervals short. You should knock 18 sets of calves and 18 sets of forearms during that time. Do one set of calves, one set of forearms. Crank the density up.

2.    Deadlift twice the same day.
Do long range deadlifts in the morning and short range deadlifts in the evening. For example, snatch deadlift on a podium and deadlifts from the blocks in the evening.

3.    Train legs 3 times on Saturdays.
Workout 1: 9 AM
Neural Drive
A-1 Front Squats 10 x 3 on 30X0 tempo, rest 2 minutes
A-2 Lying Leg Curls Feet Inward 10 x 3 on 40X0 tempo, rest 2 minutes

Workout 2: 1 PM
Tear some for more fibers up

A-1 Back  Squats with Chains 5 x 4-6 on 50X0 tempo, rest 2 minutes
A-2 Eccentric Lying Leg Curls Feet Neutral 5 x 4-6 on 40X0 tempo, rest 2 minutes
You will need a training partner to assist through concentric range

Workout 3: 5 PM
Bust the envelope

A-1 Leg press with feet high on plate 3 x 15-20 on 20X0 tempo, rest 30 seconds
A-2 Lying Leg Curls Feet Outward 3 x 6-8 on 40X0 tempo, rest 30 seconds
A-3 Dumbbell Walking Lunges 3 x 10-12 per leg on 20X0 tempo, rest 30 seconds
A-4 Leg press with feet externally rotated at 45 degrees, heels 4-6 inches apart 3 x 15-20 on 20X0 tempo, rest 30 seconds
A-5 Medium box step ups 3 x 10-12 per leg on 10X0 tempo, rest 30 seconds
A-6 Jump Squats with barbell 3 x 10-12  on X0X0 tempo, rest 30 seconds, use no more than 25% of bodyweight for load, go for height.
http://www.charlespoliquin.com/Blog/tabid/130/EntryId/289/Three-Efficient-Ways-to-Put-5-Pounds-On-in-Record-Time.aspx

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By Team FPS – April 18, 2011

Resistance Curves VS Force Curves

https://www.youtube.com/watch?v=Z2P0-4M9fQM

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By Team FPS – March 24, 2011

What if there was a Cure for Alzheimer’s Disease and No One Knew?

WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?

A Case Study by Dr. Mary Newport July 22, 2008
There is a growing epidemic of obesity, type II diabetes, cardiovascular disease, and predictions that 15,000,000 people in the United States alone will have Alzheimer’s Disease by the year 2050.

In 2001, Dr. Richard L. Veech of the NIH, and others, published an article entitled, “Ketone bodies, potential therapeutic uses.”1 In 2003, George F. Cahill, Jr. and Richard Veech authored, “Ketoacids? Good Medicine?”2 and in 2004, Richard Veech published a review of the therapeutic implications of ketone bodies.3 These articles are not found in journals that the average physician would read, much less the lay public. Unless you are researching the topic, it is unlikely that you would ever randomly come across this information.

My husband Steve, age 58, has had progressive dementia for at least five years. He had an MRI in May 2008 showing a diffuse involutional change of the frontal and parietal lobes and moderate left-sided and severe right-sided amygdala and hippocampal atrophy with no ischemic change, which would support a clinical diagnosis of Alzheimer’s Disease. For non-medical people, this means that he has shrunken areas of the brain. Many days, often for several days in a row, he was in a fog; couldn’t find a spoon or remember how to get water out of the refrigerator. Some days were not so bad; he almost seemed like his former self, happy, with his unique sense of humor, creative, full of ideas. One day I would ask if a certain call came that I was expecting and he would say, “No.” Two days later he would remember the message from so-and-so from a couple of days earlier and what they said. Strange to have no short-term memory and yet the information was filed somewhere in his brain. My gut feeling is that diet has something to do with the fluctuation, but what. I knew that he was locked up in there somewhere, if only there was a key to open up the areas of his brain that he didn’t have access to.

Steve has a BSBA in accounting, and did billing, bookkeeping and accounting for my neonatology practice from home, so that he could stay with our girls. He loved computers and was a fast typist. He could open computers up to repair them and fix practically anything else without ever having instruction. If he did not have a tool to do something he would “invent” it and make a usable prototype. He loved to kayak and made an attachment to keep his kayak moving in a straight line. About five years ago he began to have trouble organizing to do his accounting work. He would procrastinate as much as possible. He made mistakes with the payroll and I began to sit with him to help him get it right. I thought it was just that our practice had gotten more complicated with more employees. He knew that something was wrong and depression set in. We took him to a neurologist about 4 years ago, who did a Mini Mental Status Exam (MMSE,) and Steve scored a 23 out of 30, putting him into the mild range of dementia. On this test, the lower the score is, the worse the dementia. His MRI was reported as normal at that time.

About three years ago, Steve started taking Aricept and two years ago Namenda. We were hopeful that, if we could slow his decline enough, a treatment would come along that would turn things around for him. He was changed over from Aricept to Exelon in August 2007 after losing ten pounds over several weeks. In the past 12 months there was a noticeable change. He can no longer cook for himself, remember to eat a good meal, use a calculator or even perform the simplest addition, however he still keeps busy all day working in the yard or in his garage and he is still in good physical condition. I now do all the cooking for a man who used to cook for his family regularly. I give him the medications because he can’t remember to take them, much less take the right pills. Every night, we hold each other before we go to sleep and I wonder how many more times we will get to do this. It has been a nightmare to watch his decline and feel helpless to do anything but watch it happen. He is fully aware of his dementia, and we talk about it frequently. He is no longer depressed, probably with the help of counseling, Lexipro and Wellbutrin, or maybe worsening of his disease.

I subscribe to various alerts and check the website www.clinicaltrials.gov periodically to look for drug studies that he may qualify for. Two years ago we tried to get him into a study for a promising anti-inflammatory drug, Flurizan, but he did not qualify because he had a history of depression within the previous two years. Wouldn’t you be depressed if you knew you had Alzheimer’s? In fact, depression may be a symptom or precursor of Alzheimer’s.

Until very recently, I didn’t see anything regarding the potential use of medium chain triglycerides (MCT oil), or ketone bodies (also called ketoacids,) the end product of their metabolism, which may not only treat, but also prevent Alzheimer’s disease. Further, this is a potential treatment for Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease), drug resistant epilepsy, brittle type I diabetes, and diabetes type II, where there is insulin resistance. Ketone bodies may help the brain recover after a loss of oxygen in newborns through adults, may help the heart recover after an acute attack, and may shrink cancerous tumors. Children with drug resistant epilepsy sometimes respond to an extremely low carbohydrate ketogenic diet. MCT oil appears to be useful as an aid in weight loss and body builders use it already to improve their lean body mass (MCT oil can be easily purchased on the internet.) Athletes and soldiers could use MCT oil as a source of fuel when the body runs out of carbohydrates, which occurs rather quickly when food is not readily available.

What do these entities have in common? Our cells can use ketone bodies as an alternative fuel when glucose is not available. Brain cells, specifically neurons, are very limited, more limited than other cells, in what kinds of fuel they can use to function and to stay alive. Normally, they require glucose (sugar), but they can also use ketone bodies. Humans do not normally have ketone bodies circulating and available to the brain unless they have been starving for a couple of days or longer, or are consuming a ketogenic (very low carbohydrate) diet, such as Atkins. In Alzheimer’s disease, the neurons in certain areas of the brain are unable to take in glucose4, 5 due to insulin resistance and slowly die off, a process that appears to happen one or more decades before the symptoms become apparent. If these cells had access to ketone bodies, they could potentially stay alive and continue to function. It appears that persons with Parkinson’s disease,6 Huntington’s disease, 7 multiple
need to take 35 grams or just over two tablespoons (about 35 ml or 7 level teaspoons) of coconut oil. The following morning, around 9 A.M., I made oatmeal for breakfast and stirred two tablespoons, plus more for “good luck,” into his portion. I had some as well, since I cannot expect him to eat something that I won’t eat.

On the way to the 1:00 P.M. screening, I tried to prepare Steve by asking him the season, the month, the day of the week, reminding him that we were going to Tampa, in Hillsborough county. He couldn’t remember the word “spring,” came up with April instead of May for the month every time I asked him and he couldn’t remember it was Wednesday. During the hour-long drive, we went through these facts at least 10 times, but he still couldn’t remember. Shortly after we arrived he was whisked away for the test, about 4 ½ hours after consuming the coconut oil. When he returned, he was very unhappy about his performance. Laura, the research coordinator, returned shortly thereafter and began to take his vital signs and blood pressure, and, suspecting that we were continuing with the screening process, I asked her if she could share his score with us. She said, “Didn’t he tell you? He scored an 18!” more than he needed to qualify for the vaccine study. He remembered it was spring, it was May, it was Wednesday, that he was in Tampa, in Hillsborough county and that we were at the Byrd Institute, all points that he missed on the previous attempt at USF. As a result of the screening, we learned that he is positive for APOE4, but do not know at this time if he has one or two copies.

According to the Ketasyn studies, Steve should not have improved, but rather he should have stayed about the same. Since then he has retested for the Eli Lilly study drug, now available closer to home and scored an MMSE of 17 – he even remembered the date of July 2, 2008 this time. We have decided, after looking at the potential side effects of the vaccine for APOE4+ people, to go with the Eli Lilly drug.

At the time of this writing it has been 60 days since he started taking coconut oil (May 21, 2008.) He walks into the kitchen every morning alert and happy, talkative, making jokes. His gait is still a little weird. His tremor is no longer very noticeable. He is able to concentrate on things that he wants to do around the house and in the yard and stay on task, whereas before coconut oil he was easily distractible and rarely accomplished anything unless I supervised him directly, a source of some contention between us!

After about two weeks, and again at 37 days, after starting the coconut oil, I asked him to draw a clock (see Clocks #2 and #3.) There is an obvious marked improvement. I promise that I did not help him. He tells me that he could not even picture a clock at the St. Pete screening, but with the last two attempts, he was very concerned that the 6 was opposite the 12 and the 9 opposite the 3 on the face of the clock. He drew “spokes” to and ALS9 have a similar defect in utilizing glucose but in different areas of the brain or spinal cord.

MCT oil is digested differently by the body than other fats. Instead of storing all MCTs as fat, the liver converts them directly to ketone bodies, which are then available for use as energy. Oral and intravenous administration of MCT oil produces hyperketonemia, 10 or circulating ketone bodies, which are then available to the brain for energy, in the absence of glucose19 and even in the presence of glucose.22 In addition, hyperketonemia results in a substantial (39%) increase in cerebral blood flow, 18 and appears to reduce cognitive dysfunction associated with systemic hypoglycemia in normal humans. 19

About 2 months ago, we took Steve to the Johnny B. Byrd, Jr. Alzheimer’s Institute at University of South Florida (USF) in Tampa, Florida for an annual evaluation and screening for a vaccine study (Elan.) He was fasting for blood work and had an MMSE of 12, much too low to qualify for the vaccine study – a minimum score of 16 was required. We were very disappointed, but were advised that we could come back another time to try again, since he met all of the other criteria.

We made an appointment in mid-May 2008 in St. Petersburg, Florida to screen Steve for an Eli Lilly gamma-secretase inhibitor and made another appointment for Steve to be screened for entry into the Elan study at USF the following day. The evening before the first screening in St. Pete, I researched the two drugs to help us decide which drug to choose, should he qualify for both studies. I came across another drug, Ketasyn, or AC-1202, that was also recruiting healthy older people to test the tolerability of three different formulations. Investigating further, I learned that this treatment brought about significant improvement over a 90-day period in about half of the subjects who had a certain genetic profile (APOE2 or APOE3.) The APOE4 group remained about the same, whereas the controls (people taking the placebo) continued to show decline. The results were even more impressive for people who were already taking certain Alzheimer’s medications. In a pilot study, some people improved on memory testing with the very first dose. Upon doing an internet search for Ketasyn, I found a January 2008 patent application (see www.freepatentsonline.com ,)10 a continuation of a 2000 application, 75 pages long, with a well-written and thorough description of the science of Alzheimer’s disease and description of the “invention,” including these study results and numerous potential formulations in combination with other substances that may enhance its effect.

I learned that the promising “ingredient” in Ketasyn is simply MCT oil, and that a dose of 20 grams (about 20 ml or 4 teaspoons) was used to produce these results. The MCT oil that these researchers used was obtained from Stepan Company and consists of primarily 6 and 8 carbon chains, however they state that MCT of any combination of medium chains (6 to 12 carbon chains are medium chain) would also be effective. Just once in this application, the author mentions that MCT oil is derived from coconut or palm oil (this is incorrect, the author should have stated palm kernel oil.)
I didn’t know at that point that I could easily purchase MCT oil online, so I researched coconut oil and found out that coconut oil is about 60% medium chain fatty acids (MCFA), contains no cholesterol and also contains omega-6 fatty acids and some other short and long chain fatty acids of up to 18 carbon chains. 11 Coconut oil can be found in many health food stores and even some grocery stores. Wal-Mart sells a non-hydrogenated (no transfat) brand of coconut oil in a one-liter size (almost 32 ounce containers) for about $7 in our area of Florida. It can be purchased in quantities as small as a pint and up to five gallons online. It is important to use coconut oil that is non-hydrogenated and contains no transfat. There is a widely held misconception that coconut oil is the “artery clogging oil,” a term coined in the mid-1900’s by the president of Proctor and Gamble, the manufacturer of Crisco and other hydrogenated vegetable oils. The early studies in animals used hydrogenated coconut oil, which we now know produces the notorious trans-fats, and the essential fatty acids were excluded from the diet. 13

The largest producer of coconut oil is the Philippines, where coconut and its oil are food staples, and it is also produced in India, Thailand and other parts of Southeast Asia, the Caribbean islands and even in south Florida. The Philippines has one of the lowest incidences of cardiovascular disease in the world. Studies have shown that total cholesterol to HDL ratio improves with non-hydrogenated coconut oil.14, 15, 16, 17 The people in this part of the world also eat fish regularly, providing them with omega-3 fatty acids, which probably contributes as well to the lack of cardiovascular disease. My nurse friends from the Philippines tell me that many of their relatives back home cook everything in coconut oil and have coconut in one form or another at nearly every meal.

I have also learned that after coconut and palm kernel oil, the food that medium chain triglycerides are most concentrated in is human breast milk. 12 It is also found in smaller concentrations in goat and cow’s milk, as well as the butters from these milks. In fact, we used to add MCT oil 20-25 years ago to premature formulas to add calories, and MCT, coconut and palm oils are currently added to premature and full term infant formulas, along with ARA and DHA to mimic breast milk.

Back to Steve, it was too late to find coconut oil before the first screening. On the way, I reminded him repeatedly that we were in St. Petersburg, in Pinellas County. On the MMSE, he remembered the city but not the county, and he couldn’t remember the season, the month or day of the week, much less the date, even though he had to initial and date numerous pages of consent forms before the MMSE. He had to be reminded on every single page where to initial and what the date was and even how to write out the date. He scored a 14, too low for entry into the study. Dr. Margarita Nunez spent considerable time with us and asked Steve to draw a clock (see clock #1), which she said was a specific test for Alzheimer’s. She took me aside and told me that his “clock” indicated he was leaning more towards severe than moderate AD, a devastating, but not surprising revelation to me, considering that I am his wife of 36 years and now his caretaker.

Thinking, what have we got to lose, we stopped at a health food store on the way home and picked up a quart of 100% “virgin” coconut oil. I calculated that in order to provide 20 gm of MCT, he would
help them line up. I did not ask him to try to put in a time, the next part of that test.
Steve has not been able to type for at least two years, but he feels that he can picture the position of the letters on the keyboard. At this point he is afraid to sit down and try to type, worried that he will be discouraged if it doesn’t come back right away. We are considering trying occupational therapy to see if he can relearn some of the skills he has lost. I cannot explain why he has improved, except that perhaps the 10 and 12 carbon chains are important, or the APOE4 people in the Ketasyn studies were not taking omega-3 fatty acids. We eat salmon at least twice a week and take fish oil supplements twice a day and have for at least the past two years.

I have been researching on the internet everything I can find about coconut oil, MCT oil, fatty acids, ketone bodies, fatty acid composition of breast milk, ketones and various disease states. When I researched ketone bodies, I came across the name of Dr. Richard Veech of the National Institutes of Health. I contacted him to ask questions about all of this and he very kindly spoke with me and emailed me articles he had written on the subject. I have had numerous questions and ideas, and he has continued to provide me with answers and more papers to read. I am thinking not only about people with neurodegenerative diseases like my husband, but also the sick and premature newborns that I take care of, and potential uses for those at both ends of the spectrum of life and everyone in between. I wonder about autism and whether something very important is missing in infant formulas and in the diets of women who are breastfeeding. 23

Beta-hydroxybutyrate is the primary ketone body that is the end product of fatty acid metabolism and appears to protect neurons when glucose is not available. 20 Dr. Veech can make an ester form of beta-hydroxybutyrate in his lab from MCT oil that can be taken orally and converted to energy by neurons and other cells. Potentially, higher levels of ketone bodies could be obtained by ingesting beta-hydroxybutyrate directly. He has done studies on animals, but needs to produce this in quantity to be able to do human studies. He could start testing this year, if only he had the funding. He needs $15 million to build a plant to produce his beta-hydroxybutyrate. That is a lot of money, but not so much if you consider that it is $1.00 for every person that is expected to have Alzheimer’s disease by the year 2050.

We visited Cincinnati at the end of June and all of my family and Steve’s family noticed a very significant difference in how he interacted with them socially compared to a year ago. Instead of looking lost, he was involved and interested in what they had to say. He recognized relatives (brothers-in-law, nieces and nephews) by name immediately that were unfamiliar to him a year ago. His facial expression was more animated. He participated actively in conversations, understood jokes immediately and even came up with his own humorous comments. He still had difficulty finding some words, but he was talking in sentences and even stringing sentences together. In the morning he would come to the kitchen and ask me to walk the “big hill” with him before breakfast to get some exercise. He is a very different person than he was a year ago and perhaps even two or three years ago. He has serious atrophy of his brain and will never be “normal,” but for now we are very pleased with where he is at and, should coconut oil stop or slow down the progress of his disease, it will be worth every drop that he takes.

My sister Lois told a lady she works with about the coconut oil and Steve’s response to it. Her father began to give this to her mother, who has Alzheimer’s and she has had a similar response, with more alertness, conversation and sense of humor.

On July 9, 2008, Steve had blood samples drawn at various times before and following breakfast and dinner. He received 35 ml of coconut oil at each of those meals. He did not receive any other coconut oil or other coconut products during the rest of that day. Normally, he receives more coconut oil than that on the average day. Steve’s ketone body levels began to increase after breakfast over 3 hours, but at relatively low levels, dropped again before dinner and were steadily rising about 3 hours after dinner. We do not know when his levels peaked because we did not draw any further levels thereafter. Dr. Veech stated that it is surprising that Steve would improve with these relatively low levels of ketones. This study reaffirms his belief that it is necessary to go forward with the production and testing of his ketone body b-hydroxy butyrate esters, since considerably higher levels of ketone bodies, timed and controlled could be achieved, and more ketones would be available for the neurons to use, and therefore greater improvement could be expected.

It is urgent that funding become available to move forward for the sake of the millions who currently suffer, and will in the future suffer, from Alzheimer’s disease, Parkinson’s disease, Huntington’s chorea, multiple sclerosis, ALS, type I and type II diabetes, as well as any number of other conditions that involve a defect in transport of glucose into neurons and other cells.

Until Dr. Veech’s beta-hydroxybutyrate is tested and available for use, a simple dietary change to coconut oil could make a difference for people who believe they are at risk and for those who already have one of these diseases.

To duplicate the dose of MCT taken in the Ketasyn study, about 7 level teaspoons should be taken at one time, once a day, which should circulate ketone bodies for about 24 hours. I do not know if it is necessary to take this much at one time or if the dosage could be spread out over the course of the day. Studies obviously need to be done to determine this. We actually give this amount to Steve at least twice a day to make sure that there are no periods without ketone bodies circulating. Many days he receives at least 50% more than this. The amounts we are taking would not be excessive in areas of the world where coconut is a staple. If a person can tolerate more, or can work up to tolerating more, it may be a good idea to do so. As an alternative, one could take 4 teaspoons of MCT oil once or twice a day, or more often as tolerated.

Some people may experience a sense of “fullness” or even have diarrhea after taking this much to start, but this problem can be reduced by starting with one or two teaspoons and increasing over a week or so to the full amount. We put it in oatmeal, combine it with salad dressings, use it to cook with, and put it on anything that one would normally put butter on, such as potatoes, sweet potatoes, rice, pasta or noodles. Coconut ice cream can be purchased at Asian stores, contains coconut oil and is the most pleasant way I can think of to make ketone bodies. Likewise, coconut milk is a combination of coconut oil and coconut water and can be found in the Asian and condensed milk sections of many grocery stores. It is a pleasant substitute for milk, and can be added instead of milk, for example, to make scrambled eggs, French toast, and mashed potatoes. You can figure out portion sizes of various combinations of foods containing coconut and coconut oil equivalent to at least 35 grams of fat from coconut oil.

If you are using any type of hydrogenated vegetable oil or any oil with transfat, do not use any more and get rid of it! Extra virgin olive oil, butter and other natural, non-hydrogenated oils are okay to use along with the coconut oil. It is possible to use coconut oil in place of all other oils, however, since it contains no omega-3 fatty acids, it is very important to eat salmon twice a week or get enough omega-3 fatty acid from other rich sources such as fish oil capsules, flax meal, flax oil (not for cooking) or walnuts.

It is inconceivable that a potential dietary prevention and cure for Alzheimer’s disease, and other neurodegenerative diseases, has been out there for so many years, and yet has gone unnoticed. It is very likely that these diseases are becoming more prevalent due our current diet. The American diet has changed drastically from what it was before the 1950’s, when our parents and grandparents used lard and coconut oil to cook. Cardiovascular disease was rare at the beginning of the 20th century, and has skyrocketed, along with other devastating diseases, such as Alzheimer’s, diabetes type II, obesity, since mass produced hydrogenated vegetable oils containing trans fats were introduced into our diets and replaced these other natural fats. Sadly, the incidences of cardiovascular and other serious diseases are becoming more and more common among people in other areas of the world who have changed over from their indigenous foods to the “western” diet.

I plan to tell everyone I can and get this information to persons in positions to investigate this with the hope that Dr. Veech and other MCT oil and ketone body researchers get the funding they need. Feel free to make copies and pass this write-up on.
If you have a loved one or a patient with

Alzheimer’s or one of these other degenerative neurologic diseases, consider trying coconut oil.
Dr. Veech suggests that, if possible, a videotape of the person before starting and at various points after starting the coconut oil would be very useful to document change. He suggests including segments of the persons face, speech and gait (walking). He also advises to have ketone bodies
measured. What have you got to lose?

Dr. Mary Newport
10030 Orchard Way
Spring hill, FL 34608
Home: (352) 666-1025
Cell: (352) 428-0251
Preemiedoctor@aol.com
Coconut oil and MCT oil websites:
www.coconutoilresearch.com
www.nutiva.com • www.amazon.com
www.tropicaltraditions.com
www.oilsbynature.com
www.cheapvitamins.com
Palm kernel oil website:
www.oilsbynature.com
Coconut oil and coconut milk are also available at most health food stores and many grocery stores.

References:
1. “Ketone bodies, potential therapeutic uses,” RL Veech, B Chance, Y Kashiwaya, HA Lardy, GC Cahill, Jr., IUBMB Life, 2001, Vol. 51 No.4, 241-247
2. “Ketoacids? Good Medicine?” George F. Cahill, Jr., Richard L. Veech, Transactions of the American Clinical and Climatological Association,
Vol. 114, 2003.
3. “The therapaeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism,” Richard L. Veech, Prostaglandins, Leukotrienes and Essential Fatty Acids, 70 (2004) 309-319.
4. “Diminished glucose transport and phosphorylation in Alzheimer’s Disease determined by dynamic FDG-PET,” M Piert, et.al., The Journal of Nuclear Medicine, Vol.37 No.2, February 1996, 201-208.
5. “Glucose metabolism in early onset versus late onset Alzheimer’s Disease: an SPM analysis of 120 patients,” EJ Kim, et. al., Brain, 2005,
Vol. 128, 1790-1801.
6. “Cerebral glucose metabolism in Parkinson’s disease with and without dementia,” RF Peppard, et.al., Archives of Neurology, Vol. 49 No.12,
December 1992.
7. “Cortical and subcortical glucose consumption measured by PET in patients with Huntington’s disease,” Brain, October 1990, Vol 113, part 5, 1405-23.
8. “Reduced glucose metabolism in the frontal cortex and basal ganglia of multiple sclerosis patients with fatigue: a 18F-fluorodeoxyglucose positron emission tomography study,” U Roelcke, et. al., Neurology, 1997, Vol. 48, Issue 6, 1566-1571.
9. “ALS-linked Cu/Zn-SOD mutation impairs cerebral synaptic glucose and glutamate transport and exacerbates ischemic brain injury,” Z Guo, et. al., Journal of Cerebral Blood Flow Metabolism, March 2000, Vol. 20 No. 3, 463-8.
10. “Combinations of medium chain triglycerides and therapeutic agents for the treatment and prevention of Alzheimer’s disease and other diseases resulting from reduced neuronal metabolism,” United States Patent 20080009467, Inventor Samuel T. Henderson, Accera, Inc., Broomfield,
Colorado (Ketasyn).
11. Nutrient analysis of coconut oil (vegetable), NDB No: 04047 – www.nal.usda.gov/fnic/foodcomp .
12. “Lipids in (human) milk and the first steps in their digestion,” M Hamosh, et. al., Pediatrics, 1985, Vol. 75, 146-150.
13. “Nutritional factors and serum lipid levels,” EH Ahrens, American Journal of Medicine, 1957, vol. 23, 928 (used hydrogenated coconut oil).
14. “Trans fatty acids and coronary artery disease,” NEJM, 1999, Vol. 340, 1994-1998.
15. “Effect of mixed fat formula feeding on serum cholesterol level in man,” SA Hashim, American Journal of Clinical Nutrition, 1959, Vol. 7, 30-34.
16. “Modified-fat dietary management of the young male with coronary disease: a five-year report,” JL Bierenbaum, JAMA, 1967, Vol. 202, 1119-1123.
17. “Cholesterol, coconuts and diet in Polynesian atolls-a natural experiment; the Pukapuka and Toklau island studies,” IA Prior, American Journal of Clinical Nutrition, 1981, Vol. 34, 1552-1561.
18. “Changes in cerebral blood flow and carbohydrate metabolism during acute hyperketonemia,” S.G. Hasselbalch, et.al, Am J Physiol, 1996,
Vol. 270, E746-51.
19. “Effect of hyperketonemia and hyperlacticacidemia on symptoms, cognitive dysfunction, and counterregulatory hormone responses during hypoglycemia in normal humans,” T. Veneman, et. al., Diabetes 43:1311-7 (1994).
20. “D-b-Hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease,” Y Kashiwaya, et. al. including RL Veech, PNAS, May 9, 2000, Vol. 97 No. 10, 5440-5444.
21. “High carbohydrate diets and Alzheimer’s disease,” Samuel T. Henderson, Medical Hypotheses, 2004, Vol 62, 689-700 (Another article of interest).
22. “Effects of b-Hydroxybutyrate on cognition in memory-impaired adults,” MA Reger, ST Henderson, et. al., Neurobiology of Aging, 2004,
Vol. 25, 311-314.
23. “Breastfeeding, infant formula supplementation, and Autistic Disorder: the results of a parent survey,” ST Schultz, et. al., International Breastfeeding Journal, 2006, Vol. 1 No. 16.
Other Important Resources
“Ketones: Metabolism’s Ugly Duckling,” TB VanItallie, TH Nufert, Nutrition Reviews, Vol 61, No 10, 327-341.
“Fuel Metabolism in Starvation,” GF Cahill, Jr., Annual Reviews in Nutrition, 2006, 26:1-22.
“Ketone Bodies as a Therapeutic for Alzheimer’s Disease,” ST Henderson, Journal of the American Society for Experimental NeuroTherapeutics,
Vol 5, 470-480, July 2008.

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By Team FPS – March 4, 2011