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Sikter András

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I am a practitioner internist/cardiologist doctor. I deal with the effects of carbon dioxide on cell physiology and pathophysiology. I have created a metabolic model on the cellular level. I also deal with stress theories. I created a brand new hypothesis. I reviewed "A 21st-century update of Claude Bernard's Theory about the Constancy of the Internal Environment." It is a brand-new hypothesis about the cellular signalling.

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Ammar Ahmed Abduh

Sana'a University

Semmelweis University

Margery Barrand

Ege University

Case Western Reserve University

Markéta Vaňková

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Papers by Sikter András

LÉLEGZÉS = LÉLEKZÉS ?�A széndioxid hiány és/vagy túlsúly szerepe egyes pszichiátriai betegségek patomechanizmusában. Sikter András belgyógyász – kardiológus – szabadon gondolkozó 2009 május 27 SE Kútvölgyi Pszichiátriai Klinikai Csoport

A citoplazmatikus ionok (K+, Mg++, Zn++, anorganikus foszfátok) hiányának aritmogén hatása

The role of carbon dioxide (and intracellular pH) in the pathomechanism of several mental disorders: Are the diseases of civilization caused by learnt behaviour, not the stress itself? [A széndioxid (és az intracelluláris pH) szerepe néhány mentális betegség patomechanizmusában: Nem maga a stress...

Chronic psychic stress can cause metabolic syndrome through mild hypercapnia

Theory, 2022

The author presents a new psychosomatic stress model. All the elements of the hypothesis are well... more The author presents a new psychosomatic stress model. All the elements of the hypothesis are well known but, in this context, are published fi rst. The following are the most critical aspects of the recommended chronic stress model. 1/ Stress contains both sympathetic and parasympathetic elements, but the latter predominate. 2/ The mediator of stress is carbon dioxide, the substance that can turn the psyche into soma. 3/ In humans, chronic stress is mainly social; people cause it to each other. Chronic social stress is created frequently due to deviations in civilisation, education and tolerance. 4/ The freeze response (or freezing behaviour) plays a subordinate role in the animal world; it lasts mainly for a maximum of minutes, while in humans, it dominates and can continue for decades. 5/ The decisive step of freeze is apnea, hypopnea, which occurs due to aversive psychological eff ects. After a more extended existence, mild chronic respiratory acidosis develops and most often appears in the clinical form of obstructive sleep apnea. 6/ Chronic hypercapnia can shape the metabolism into metabolic syndrome. 7/ After that, various cardiovascular and metabolic complications (hypertension, atherosclerosis, type 2 diabetes, depression) may develop partly due to genetic and lifestyle reasons.

Hypertension and the Interior Ion-milieu. Can we Overcome Hypertension with Regulated Breathing?

Acta Scientific Medical Sciences, May 1, 2022

The author presents a new model for age-associated diseases through a hypothesized pathogenesis o... more The author presents a new model for age-associated diseases through a hypothesized pathogenesis of hypertension. Preservation or restoration of the constancy of each original cell-specific intracellular ion-pattern is essential for upholding cellular identity and integrity. The ageing background is intracellular acidosis: low-grade respiratory acidosis elevates the intracellular HCO 3-/Clgradient and induces metabolic syndrome, while low-grade metabolic acidosis causes exhausting buffer syndrome (EBS) with a decreased intracellular HCO 3-/Clrate. The former elicits higher aldosterone levels to restore the original ion-pattern by NHE-1 (natrium-hydrogen exchange) mechanism located in the membrane of vascular smooth muscle cells (VSMCs) and by retaining NaCl. The fault of ion-status restoration leads to Salt-sensitive hypertension through cascades of events. The ion-pattern changes in EBS elicit angiotensin II levels elevation through the renin-angiotensin system, which tries to eliminate intracellular changes via NBCn1 (natrium-bicarbonate cotransporter). However, it leads to a dead-end, and Salt-resistant hypertension develops. Hypertension occurs because restoring the original intracellular ion-pattern in VSMCs by aldosterone and angiotensin II fails. These hormonal counterregulations lead to Na + retention and alkaline overcompensation in the VSMCs. There may be several explanations for the failure, but hypertension would not develop if the intracellular ion-milieu were initially neutral or slightly alkaline. Regulated breathing could overcome hypertension.

Available Publications Allow Us to Better Explore the Causes of Essential Hypertension

Poster, 2022

+ only follows the changes of the Clion concentrations. The goal of the regulation could be to re... more + only follows the changes of the Clion concentrations. The goal of the regulation could be to restore physiological ion conditions. One of the known causes of (mostly low-grade) chronic respiratory acidosis is persistent hypopnea induced by chronic psychic stress (e.g., during social defeat), which often appears in the clinical picture of obstructive sleep apnea syndrome. (Salt-sensitive hypertension could therefore also be called respiratory or psychosomatic hypertension.) Chronic kidney failure or age-associated kidney function deterioration causes intracellular metabolic acidosis. A regular acidogenic diet and other mechanisms (perhaps free radical activation) can also play a role. These lead to an increase in intracellular Clconcentration at the expense of HCO 3-. The decreased HCO 3-/Clratio with intracellular acidosis primarily increases the ANG II level. ANG II activates the Na +-HCO 3cotransporter in the membranes of vascular smooth muscle cells (VSMCs) via NBCn1. As a result, it also reduces the intracellular H + and Clconcentration trying to restore the physiological ion conditions. Salt-resistant hypertension is, therefore, primarily of renal origin. Subclinical kidney function damage could cause essential salt-resistant hypertension linked to the body's extreme acid sensitivity. ALD counteracts respiratory acidosis, while ANG II affects metabolic acidosis; they have opposite action in HCO 3vs Clregulation. The present hypothesis is based partly on the fact that humoral regulation also seems to restore intra-and extracellular ionic conditions. At the same time, either ALD or ANG II restoration actions fail on the ion milieu of VSMCs; ion transports continue even after pH normalising and the pH becomes overcompensated. This results in intracellular alkalosis (H + deficiency) and Na + excess, which increases the Na + /Ca 2+ exchange mechanism. These result in hypertrophy and increased tone in the arterioles (VSMCs) and the left ventricular myocardium. We can assume that if initially there is no intracellular acidosis or if the RAAS feedback mechanisms work well, then hypertension will not develop.

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes. Part 1. A Theory for Modelizing the Cytoplasm and Diseases

Acta Scientific Medical Sciences, 2019

Sodium bicarbonate as (also) medicine for COVID-19 infection

Sodium bicarbonate as (also) medicine for COVID-19 infection

Sodium bicarbonate as (also) medicine for COVID-19 infection

A new hypothesis on vascular calcifi cation: the exhausting buff er syndrome (EBS)

Neuropsychopharmacologia Hungarica, 2021

Here we propose that the Western world lifestyle disrupts phosphate metabolism and homeostasis du... more Here we propose that the Western world lifestyle disrupts phosphate metabolism and homeostasis due to caloric or acidic hyperphagia. Psychic factors such as social defeat due to stressed social coexistence characterized by reduced activity and chronic hypoventilation (hypercapnia) also play a role. At least two mechanisms mediate the harmful vascular eff ects of phosphates with intracellular acidosis being a feature in both of them. First, insufficient lifestyle and adjacent diet together with the psychosomatic mechanism of social defeat (mainly through chronic hypercapnic acidosis) lead to insulin resistance characterized by the classical Cardiometabolic Syndrome. Secondly, overload with fi xed acids caused by renal insuffi ciency or acidic diet (due to intracellular metabolic acidosis) leads to our here proposed Exhausting Buff er Syndrome (EBS) which tends to elevate serum inorganic phosphate levels. These two mechanisms overlap and are regulated through genetically determined pr...

VITIONnal stimulált feltáplálás hatása alkoholos polyneuropathiában és vascularisan decompensalt alkoholos májcirrhosisban RÓKUS KH. tudományos köri előadás

The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação: a hipocapnia no patomecanismo do distúrbio de pânico

Revista Brasileira de Psiquiatria, 2007

OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effe... more OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. METHOD: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. DISCUSSION: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2) when the late...

Can hypocapnia trigger ARDS and kill coronavirus diseased patients?

Civilized Behavior Leads to Chronic Stress and Alterations of Carbon Dioxide Level in the Organism which Turn Generate Diseases

A civilizációs betegségek eredete és patomechanizmusa (hipotézis)�

VITION kapszula, az "intracelluláris ionok" --együtt Balatonöszöd, 2006 Nov. 10-12

Kombinált terápia hatása az alkoholevonási szindrómára II. Addiktológiai Kongresszuson, Balatonfüred 1997. okt 16-18

Origin and Pathomechanism of Diseases of Civilization (Hypothesis) 11th IN VIVO PHYSICIAN-CONFERENCE Szent Rokus Hospital, Budapest 17th August 2016 By András Sikter Municipal Clinic of Szentendre

Modeling of the Cytoplasm (The original Hungarian version)

LÉLEGZÉS = LÉLEKZÉS ?�A széndioxid hiány és/vagy túlsúly szerepe egyes pszichiátriai betegségek patomechanizmusában. Sikter András belgyógyász – kardiológus – szabadon gondolkozó 2009 május 27 SE Kútvölgyi Pszichiátriai Klinikai Csoport

A citoplazmatikus ionok (K+, Mg++, Zn++, anorganikus foszfátok) hiányának aritmogén hatása

The role of carbon dioxide (and intracellular pH) in the pathomechanism of several mental disorders: Are the diseases of civilization caused by learnt behaviour, not the stress itself? [A széndioxid (és az intracelluláris pH) szerepe néhány mentális betegség patomechanizmusában: Nem maga a stress...

Chronic psychic stress can cause metabolic syndrome through mild hypercapnia

Theory, 2022

The author presents a new psychosomatic stress model. All the elements of the hypothesis are well... more The author presents a new psychosomatic stress model. All the elements of the hypothesis are well known but, in this context, are published fi rst. The following are the most critical aspects of the recommended chronic stress model. 1/ Stress contains both sympathetic and parasympathetic elements, but the latter predominate. 2/ The mediator of stress is carbon dioxide, the substance that can turn the psyche into soma. 3/ In humans, chronic stress is mainly social; people cause it to each other. Chronic social stress is created frequently due to deviations in civilisation, education and tolerance. 4/ The freeze response (or freezing behaviour) plays a subordinate role in the animal world; it lasts mainly for a maximum of minutes, while in humans, it dominates and can continue for decades. 5/ The decisive step of freeze is apnea, hypopnea, which occurs due to aversive psychological eff ects. After a more extended existence, mild chronic respiratory acidosis develops and most often appears in the clinical form of obstructive sleep apnea. 6/ Chronic hypercapnia can shape the metabolism into metabolic syndrome. 7/ After that, various cardiovascular and metabolic complications (hypertension, atherosclerosis, type 2 diabetes, depression) may develop partly due to genetic and lifestyle reasons.

Hypertension and the Interior Ion-milieu. Can we Overcome Hypertension with Regulated Breathing?

Acta Scientific Medical Sciences, May 1, 2022

The author presents a new model for age-associated diseases through a hypothesized pathogenesis o... more The author presents a new model for age-associated diseases through a hypothesized pathogenesis of hypertension. Preservation or restoration of the constancy of each original cell-specific intracellular ion-pattern is essential for upholding cellular identity and integrity. The ageing background is intracellular acidosis: low-grade respiratory acidosis elevates the intracellular HCO 3-/Clgradient and induces metabolic syndrome, while low-grade metabolic acidosis causes exhausting buffer syndrome (EBS) with a decreased intracellular HCO 3-/Clrate. The former elicits higher aldosterone levels to restore the original ion-pattern by NHE-1 (natrium-hydrogen exchange) mechanism located in the membrane of vascular smooth muscle cells (VSMCs) and by retaining NaCl. The fault of ion-status restoration leads to Salt-sensitive hypertension through cascades of events. The ion-pattern changes in EBS elicit angiotensin II levels elevation through the renin-angiotensin system, which tries to eliminate intracellular changes via NBCn1 (natrium-bicarbonate cotransporter). However, it leads to a dead-end, and Salt-resistant hypertension develops. Hypertension occurs because restoring the original intracellular ion-pattern in VSMCs by aldosterone and angiotensin II fails. These hormonal counterregulations lead to Na + retention and alkaline overcompensation in the VSMCs. There may be several explanations for the failure, but hypertension would not develop if the intracellular ion-milieu were initially neutral or slightly alkaline. Regulated breathing could overcome hypertension.

Available Publications Allow Us to Better Explore the Causes of Essential Hypertension

Poster, 2022

+ only follows the changes of the Clion concentrations. The goal of the regulation could be to re... more + only follows the changes of the Clion concentrations. The goal of the regulation could be to restore physiological ion conditions. One of the known causes of (mostly low-grade) chronic respiratory acidosis is persistent hypopnea induced by chronic psychic stress (e.g., during social defeat), which often appears in the clinical picture of obstructive sleep apnea syndrome. (Salt-sensitive hypertension could therefore also be called respiratory or psychosomatic hypertension.) Chronic kidney failure or age-associated kidney function deterioration causes intracellular metabolic acidosis. A regular acidogenic diet and other mechanisms (perhaps free radical activation) can also play a role. These lead to an increase in intracellular Clconcentration at the expense of HCO 3-. The decreased HCO 3-/Clratio with intracellular acidosis primarily increases the ANG II level. ANG II activates the Na +-HCO 3cotransporter in the membranes of vascular smooth muscle cells (VSMCs) via NBCn1. As a result, it also reduces the intracellular H + and Clconcentration trying to restore the physiological ion conditions. Salt-resistant hypertension is, therefore, primarily of renal origin. Subclinical kidney function damage could cause essential salt-resistant hypertension linked to the body's extreme acid sensitivity. ALD counteracts respiratory acidosis, while ANG II affects metabolic acidosis; they have opposite action in HCO 3vs Clregulation. The present hypothesis is based partly on the fact that humoral regulation also seems to restore intra-and extracellular ionic conditions. At the same time, either ALD or ANG II restoration actions fail on the ion milieu of VSMCs; ion transports continue even after pH normalising and the pH becomes overcompensated. This results in intracellular alkalosis (H + deficiency) and Na + excess, which increases the Na + /Ca 2+ exchange mechanism. These result in hypertrophy and increased tone in the arterioles (VSMCs) and the left ventricular myocardium. We can assume that if initially there is no intracellular acidosis or if the RAAS feedback mechanisms work well, then hypertension will not develop.

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes. Part 1. A Theory for Modelizing the Cytoplasm and Diseases

Acta Scientific Medical Sciences, 2019

Sodium bicarbonate as (also) medicine for COVID-19 infection

Sodium bicarbonate as (also) medicine for COVID-19 infection

Sodium bicarbonate as (also) medicine for COVID-19 infection

A new hypothesis on vascular calcifi cation: the exhausting buff er syndrome (EBS)

Neuropsychopharmacologia Hungarica, 2021

Here we propose that the Western world lifestyle disrupts phosphate metabolism and homeostasis du... more Here we propose that the Western world lifestyle disrupts phosphate metabolism and homeostasis due to caloric or acidic hyperphagia. Psychic factors such as social defeat due to stressed social coexistence characterized by reduced activity and chronic hypoventilation (hypercapnia) also play a role. At least two mechanisms mediate the harmful vascular eff ects of phosphates with intracellular acidosis being a feature in both of them. First, insufficient lifestyle and adjacent diet together with the psychosomatic mechanism of social defeat (mainly through chronic hypercapnic acidosis) lead to insulin resistance characterized by the classical Cardiometabolic Syndrome. Secondly, overload with fi xed acids caused by renal insuffi ciency or acidic diet (due to intracellular metabolic acidosis) leads to our here proposed Exhausting Buff er Syndrome (EBS) which tends to elevate serum inorganic phosphate levels. These two mechanisms overlap and are regulated through genetically determined pr...

VITIONnal stimulált feltáplálás hatása alkoholos polyneuropathiában és vascularisan decompensalt alkoholos májcirrhosisban RÓKUS KH. tudományos köri előadás

The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação: a hipocapnia no patomecanismo do distúrbio de pânico

Revista Brasileira de Psiquiatria, 2007

OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effe... more OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. METHOD: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. DISCUSSION: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2) when the late...

Can hypocapnia trigger ARDS and kill coronavirus diseased patients?

Civilized Behavior Leads to Chronic Stress and Alterations of Carbon Dioxide Level in the Organism which Turn Generate Diseases

A civilizációs betegségek eredete és patomechanizmusa (hipotézis)�

VITION kapszula, az "intracelluláris ionok" --együtt Balatonöszöd, 2006 Nov. 10-12

Kombinált terápia hatása az alkoholevonási szindrómára II. Addiktológiai Kongresszuson, Balatonfüred 1997. okt 16-18

Origin and Pathomechanism of Diseases of Civilization (Hypothesis) 11th IN VIVO PHYSICIAN-CONFERENCE Szent Rokus Hospital, Budapest 17th August 2016 By András Sikter Municipal Clinic of Szentendre

Modeling of the Cytoplasm (The original Hungarian version)

Available Publications Allow Us to Better Explore the Causes of Essential Hypertension

+ only follows the changes of the Clion concentrations. The goal of the regulation could be to re... more + only follows the changes of the Clion concentrations. The goal of the regulation could be to restore physiological ion conditions. One of the known causes of (mostly low-grade) chronic respiratory acidosis is persistent hypopnea induced by chronic psychic stress (e.g., during social defeat), which often appears in the clinical picture of obstructive sleep apnea syndrome. (Salt-sensitive hypertension could therefore also be called respiratory or psychosomatic hypertension.) Chronic kidney failure or age-associated kidney function deterioration causes intracellular metabolic acidosis. A regular acidogenic diet and other mechanisms (perhaps free radical activation) can also play a role. These lead to an increase in intracellular Clconcentration at the expense of HCO 3-. The decreased HCO 3-/Clratio with intracellular acidosis primarily increases the ANG II level. ANG II activates the Na +-HCO 3cotransporter in the membranes of vascular smooth muscle cells (VSMCs) via NBCn1. As a result, it also reduces the intracellular H + and Clconcentration trying to restore the physiological ion conditions. Salt-resistant hypertension is, therefore, primarily of renal origin. Subclinical kidney function damage could cause essential salt-resistant hypertension linked to the body's extreme acid sensitivity. ALD counteracts respiratory acidosis, while ANG II affects metabolic acidosis; they have opposite action in HCO 3vs Clregulation. The present hypothesis is based partly on the fact that humoral regulation also seems to restore intra-and extracellular ionic conditions. At the same time, either ALD or ANG II restoration actions fail on the ion milieu of VSMCs; ion transports continue even after pH normalising and the pH becomes overcompensated. This results in intracellular alkalosis (H + deficiency) and Na + excess, which increases the Na + /Ca 2+ exchange mechanism. These result in hypertrophy and increased tone in the arterioles (VSMCs) and the left ventricular myocardium. We can assume that if initially there is no intracellular acidosis or if the RAAS feedback mechanisms work well, then hypertension will not develop.

Az „intracelluláris ionok” (K, Mg, Zn, P) együttes hiánya szívbetegségekben. A szupplementáció egyik lehetősége: VITION kapszula

A szerző elméletének a Magyar Gerontologiai És Geriatriai Társaágának XXIX Naggyűlésén, Zalakaros... more

Az "intracelluláris ionok" (K, Mg, Zn, foszfátok) együttes hiánya időskori manutritioban

A szerző elméletének időskori vonatkozásait tárgyalja, különös tekintettel a malnutritiora- Magya... more

LÉLEGZÉS = LÉLEKZÉS ? A széndioxid hiány és/vagy túlsúly szerepe egyes pszichiátriai betegségek patomechanizmusában . Sikter András belgyógyász – kardiológus – szabadon gondolkozó 2009 május 27 SE Kútvölgyi Pszichiátriai Klinikai Csoport DOI: 10.13140/RG.2.2.21319.29603

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes. Part 1. A Theory for Modelizing the Cytoplasm and Diseases E-Book

E-BOOK, 2019

Abbreviations In the first part, the author presents his cytoplasmic model, which was first publi... more Abbreviations In the first part, the author presents his cytoplasmic model, which was first published in Hungarian in 2007. He modelized the cy-toplasm of the animal/human cells with three constituents: 1) Cytoplasm Builder Ions (as K + , Mg 2+ , Zn 2+ , HPO 4 2-, and H2PO 4-), 2) ATP, and 3) Functioning Proteins (enzymes). The three parts of cytoplasm are equally vital-they can only increase or decrease in unison. The author presents four models that were born at different eras and based on various logics-independently of each other, but they point in the same direction. The author's model suggests well the relations of anabolism vs. catabolism as well as the occurrence of vicious and virtuous circles. It is presented how could this cytoplasm model be of some help in modelizing diseases and healing. Even a quick recovery from an illness can be dangerous, even deadly if the physician does not consider the hazards of instability. It is known the second messenger and signaling functions of almost all physiologic ions of the cell, so it is not too bold to assume that the prevailing Momentary Intracellular Ion-Pattern as a whole has an essential, perhaps the primary signaling function. It would be the so-called 'software of the cell.' It seems that H+ concentration (pHi) is the most crucial of all ions to maintain homeostasis, Therefore, regulation wants to preserve the permanence of pHi. The endeavor to keep original pHi at all costs can develop metabolic dysregulation. (See Part 2.) Practically essential issues such as Refeeding Syndrome are also analyzed. The author points out that there are so many errors about diagnosis and treatment in this issue because the pathogenesis does not refer to one but several disorders; therefore suggests a new terminology classification. The author also reinterprets Locus Minoris Resistance (the Place of Less Resistance) theory and declares that the occurrence of a vicious circle in biology is not random; it is a consequence of the Second Law of Thermodynamics, and such it is a frequent phenomenon. In all these issues, the cytoplasmic model guides us. Total Body Kalium content; TBW: Total Body Water; T2D: Type 2 Diabetes.

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes Part 1. A Theory for Modelizing the Cytoplasm and Diseases E-Book

ASMS, 2019

Abbreviations In the first part, the author presents his cytoplasmic model, which was first publi... more Abbreviations In the first part, the author presents his cytoplasmic model, which was first published in Hungarian in 2007. He modelized the cy-toplasm of the animal/human cells with three constituents: 1) Cytoplasm Builder Ions (as K + , Mg 2+ , Zn 2+ , HPO 4 2-, and H2PO 4-), 2) ATP, and 3) Functioning Proteins (enzymes). The three parts of cytoplasm are equally vital-they can only increase or decrease in unison. The author presents four models that were born at different eras and based on various logics-independently of each other, but they point in the same direction. The author's model suggests well the relations of anabolism vs. catabolism as well as the occurrence of vicious and virtuous circles. It is presented how could this cytoplasm model be of some help in modelizing diseases and healing. Even a quick recovery from an illness can be dangerous, even deadly, if the physician does not consider the hazards of instability. It is known the second messenger and signaling functions of almost all physiologic ions of the cell, so it is not too bold to assume that the prevailing Momentary Intracellular Ion-Pattern as a whole has an essential, perhaps the primary signaling function. It would be the so-called 'software of the cell.' It seems that H+ concentration (pHi) is the most crucial of all ions to maintain homeostasis, Therefore, regulation wants to preserve the permanence of pHi. The endeavor to keep original pHi at all costs can develop metabolic dysregulation. (See Part 2.) Practically essential issues such as Refeeding Syndrome are also analyzed. The author points out that there are so many errors about diagnosis and treatment in this issue because the pathogenesis does not refer to one but several disorders; therefore suggests a new terminology classification. The author also reinterprets Locus Minoris Resistance (the Place of Less Resistance) theory and declares that the occurrence of a vicious circle in biology is not random; it is a consequence of the Second Law of Thermodynamics, and such it is a frequent phenomenon. In all these issues, the cytoplasmic model guides us.

Psychosomatic Molecular Mechanism of Metabolic Syndrome and Type 2 Diabetes. Part 4. A Recovery Strategy from Chronic Hypercapnia and Metabolic Syndrome-Related Disorders, (a Research Proposal) E-Book

Keywords: Healing with Ion-Mixture Compositions; HPO 4 2-as the Second Messenger of Insulin; Modi... more Keywords: Healing with Ion-Mixture Compositions; HPO 4 2-as the Second Messenger of Insulin; Modified Method of Sodi-Pallarés; Momentary Intracellular Ion-Pattern Signaling Abbreviations According to the hypothesis of the author, the Metabolic Syndrome and Type 2 Diabetes are mainly consequences of chronic low-grade hypercapnia and related intracellular acidosis. The altered pCO 2 status changes the Intracellular Ion-Pattern and, consequently, the metabolism. The author has developed a recovery strategy based on his metabolic model, experiences, and data of literature. The primary goal is to increase the minute-ventilation to achieve low-grade hypocapnia (~ 35 mmHg on average) and to maintain it in the long run. As a consequence of the decreased pCO 2 level-according to the hypothesis-an intracellular alkaline pH develops and results in increased metabolism, ATP production, and consequently, phosphate, Mg 2+ , K + , and Zn 2+ influx into the cytosol. Serum Ca 2+ levels may also decrease due to increased calcium and phosphate uptake into the 'hungry bones.' It is expected that both the carbohydrates and fats will be burned more intensively in mitochondria, which would also mean a decrease in insulin resistance, serum glucose, and lipid levels. The essence of the method is that regular daily administration of monobasic phosphate (H 2 PO 4

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes. Part 3. Is Type 2 Diabetes a Decompensated Form of Metabolic Syndrome

Insulin is one of the most important of anabolic hormones. Type 2 Diabetes (T2D) is characterized... more Insulin is one of the most important of anabolic hormones. Type 2 Diabetes (T2D) is characterized by persistent, stealth catabol-ism, as well as impaired glucose and phosphate uptake. The phosphate transporting capability of insulin has been known for a long time, although it has been studied mainly since the 21 st century. According to the logic of the Momentary Intracellular Ion-Pattern Signaling, insulin should increase of HPO 4 2-in the cytosol-and does it, indeed. (It is not clear that this is a one-or multistep membrane transport phenomenon.) Insulin does not only stimulate the transport of phosphate (Pi) into the cytosol but alkalinizes it, as well. Cytoplasmic alkalinization is a vital process by insulin, which mechanism has not been studied in detail. Insulin is one of the most important players in the regulation of intracellular pH, which, together with phosphate transport, is crucial for maintaining its anti-catabolic effect. Acidotic cytoplasm of the pancreas beta-cells increases while alkalotic decreases insulin secretion, which may be a feedback mechanism. All insulin-mediated vital anabolic processes use energy derived from ATP. The impaired mitochondrial ATP production capability is a consequence of insulin resistance, which develops during the early stage of Metabolic Syndrome, and can persist for decades without a manifest of T2D. Decreased ATP productivity is compensated by increased lipid availability. T2D develops when high trigly-ceride availability cannot compensate for insulin resistance and reduced ATP production. The guiding principle is that mitochondria have to provide near-normal ATP content at all costs in the cytoplasm of the cells; otherwise, the cells will be severely ill or killed. Catabolism rises to increase ATP production. The liberated amino acids allow gluconeogenesis to proceed and raise serum glucose levels. Pathophysiologically, both hyperglycemia and increased food uptake have compensatory roles in ATP production, though many vicious circles are generated.

Psycosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes. Part 2. Psychosomatic Mechanism of Metabolic Syndrome (a Theory) E-Book

Part 2. Psychosomatic Mechanism of Metabolic Syndrome (a Theory) E-Book, 2020

The author had hypothesized that the prevailing Momentary Intracellular Ion-Pattern as a whole ha... more The author had hypothesized that the prevailing Momentary Intracellular Ion-Pattern as a whole has an essential, perhaps the primary signaling function. (See Part 1.) The concentration of intracellular H + (pHi) is the most critical of all ions to maintain homeostasis; that is why regulation wants to preserve the permanence of pHi. Recent researches have shown that caged rodents can be well-modelizing for human hypoarousal diseases of civilization, which may correspond to Metabolic Syndrome or Depression. Repeated Social Defeat results in such psychic mechanisms that induce persistent hypoventilation among most of the observed rodent populations. Hypoventilation continued for weeks, even after stress, and presumably associated with hypercapnia. It may correspond to a larval version of the freeze response well known in the animal world, but it becomes chronic at people. The author., et al. previously presented in their papers how social or mental stress can be converted into an increased or decreased arousal by the body's closed-loop systems. Human 'low-grade hypercapnia' usually lasts for decades-to the end of life. One of the results is the Metabolic Syndrome, which often tends to the classic Type 2 Diabetes or other Related Disorders. Persistent elevation of the pCO 2 level launches a compensational cascade through chemical and hormonal-humoral alterations that can lead to various forms of readjustment. The Metabolic Syndrome is a latent, stealth catabolic state of the body that develops due to slight but chronic hypercapnic acidosis. Although chronic hypercapnia is usually compensated, a moderate intracellular acidotic state persists in continuing. Metabolic Syndrome is often the result of a learned 'civilized behavior'; the Social Defeat can also develop in captive animals due to chronic or repeated stress. The point is that this type of load does not increase but decreases arousal through hypercapnic acidosis, which can also cause Depression. Slight cytosolic acidosis also results in reduced metabolism, which is associated with moderately reduced anabolic and increased catabolic activity in the body with insulin resistance and reduced ATP producing capacity. As a consequence, the whole metabolism has become remodeled and dysregulated because of the disturbed Intracellular Ion Pattern.

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes Part 1. A Theory for Modelizing the Cytoplasm and Diseases E-Book

Abbreviations In the first part, the author presents his cytoplasmic model, which was first publi... more Abbreviations In the first part, the author presents his cytoplasmic model, which was first published in Hungarian in 2007. He modelized the cy-toplasm of the animal/human cells with three constituents: 1) Cytoplasm Builder Ions (as K + , Mg 2+ , Zn 2+ , HPO 4 2-, and H2PO 4-), 2) ATP, and 3) Functioning Proteins (enzymes). The three parts of cytoplasm are equally vital-they can only increase or decrease in unison. The author presents four models that were born at different eras and based on various logics-independently of each other, but they point in the same direction. The author's model suggests well the relations of anabolism vs. catabolism as well as the occurrence of vicious and virtuous circles. It is presented how could this cytoplasm model be of some help in modelizing diseases and healing. Even a quick recovery from an illness can be dangerous, even deadly, if the physician does not consider the hazards of instability. It is known the second messenger and signaling functions of almost all physiologic ions of the cell, so it is not too bold to assume that the prevailing Momentary Intracellular Ion-Pattern as a whole has an essential, perhaps the primary signaling function. It would be the so-called 'software of the cell.' It seems that H+ concentration (pHi) is the most crucial of all ions to maintain homeostasis, Therefore, regulation wants to preserve the permanence of pHi. The endeavor to keep original pHi at all costs can develop metabolic dysregulation. (See Part 2.) Practically essential issues such as Refeeding Syndrome are also analyzed. The author points out that there are so many errors about diagnosis and treatment in this issue because the pathogenesis does not refer to one but several disorders; therefore suggests a new terminology classification. The author also reinterprets Locus Minoris Resistance (the Place of Less Resistance) theory and declares that the occurrence of a vicious circle in biology is not random; it is a consequence of the Second Law of Thermodynamics, and such it is a frequent phenomenon. In all these issues, the cytoplasmic model guides us.

A 21st-century update of Claude Bernard's Theory about the Constancy of the Internal Environment

The discovery of intracellular and extracellular ion compartments and cell membrane functions ope... more The discovery of intracellular and extracellular ion compartments and cell membrane functions opened the possibility of extending Claude Bernard's theory to the intracellular ion milieu. By contrast, many misconceptions have become dominant due to underestimating the role of ions. The intracellular ion patterns characteristic of tissues were created during the species' phylogeny and are genetically determined. The concentrations of ion components are sensed by specific tissular ion sensors and maintained at a constant level by different ion exchangers and transporters, and these are often under hormonal control. So, the intracellular ion levels are also the equipment for humoral-hormonal regulation; they are second messengers. The author points out that maintaining the constancy of carbon dioxide is especially important because CO2 is one of the most decisive signalling molecules, among others, a mediator that connects bodily and soul functions. The pCO2 level also interacts with intracellular pH, Ca2+, H2PO4- and HPO4-- ions. Exactly said, the intracellular ion pattern, as a whole, has a primary signalling function. Chronic stress changes the intracellular ion patterns, increasing or decreasing the pCO2 level. According to the author, chronic parasympathetic stress results in durable slight hypercapnia and an increased HCO3-/Cl- ratio, which could lead to Metabolic Syndrome. Chronic sympathetic stress results in long-lasting or repetitive hypocapnia, decreasing the HCO3-/Cl- ratio, and could induce hyperarousal mental disorders. These functional alterations could remain reversible for decades. However, at around 50, the organism starts to get exhausted, and chronic respiratory alkalosis — induced by chronic sympathetic stress — may transform into metabolic acidosis. (Hypothesis.) This ion milieu is more stable because it requires less energy to maintain the balance. At the same time, the kidneys become reactor organs. The background of these stress-induced age-related diseases is the threatening intracellular acidosis and the organism's fighting against it. With chronic hyper- vs hypocapnia, the humoral counter-regulation cannot fulfil its function correctly and can result in (among others) salt-sensitive vs salt-resistant hypertension, respectively. Preserving the original ion pattern is essential but impossible without euventilation. We could control respiration (pCO2 level) and stress by administering H2PO4- and HPO4-- ion salts. The lifespan correlates with the Body Cell Mass (BCM), which we should maintain as long as possible.