Free Radicals Generation | Body Oxygen Is Prime Antioxidant
When thinking about good health and prevention of damage due to free radical production, many modern people are obsessed with foods and diets. Meanwhile, virtually all sick people would still have poor health and abnormally high concentrations of free radicals species (or reactive oxygen species) even if they boost their intake of herbs, supplements and super foods extra rich in antioxidants. Why? This is because they generate free radicals 24/7 and especially during early morning hours due to tissue hypoxia.
You cannot have cancer, or heart disease, or diabetes and normal oxygen levels at the same time. Cell hypoxia is the main cause of free radical generation and oxidative stress. Humans need oxygen in cells, not free unbounded oxygen that can pumped in the blood using hyperbaric oxygen therapies. (Right oxygen is delivered due to normal oxygen transport.)
Severely and moderately sick people, and most modern people, can consume pounds of antioxidants, drink canisters of super juices and eat tons of best foods, but if their automatic breathing pattern is unchanged, they will suffer from the same symptoms, pains and aches. What is wrong with their breathing?
Minute ventilation rates (chronic diseases)
click below for abstracts
|Normal breathing||6 L/min||-||Medical textbooks|
|Healthy Subjects||6-7 L/min||>400||Results of 14 studies|
|Heart disease||15 (±4) L/min||22||Dimopoulou et al, 2001|
|Heart disease||16 (±2) L/min||11||Johnson et al, 2000|
|Heart disease||12 (±3) L/min||132||Fanfulla et al, 1998|
|Heart disease||15 (±4) L/min||55||Clark et al, 1997|
|Heart disease||13 (±4) L/min||15||Banning et al, 1995|
|Heart disease||15 (±4) L/min||88||Clark et al, 1995|
|Heart disease||14 (±2) L/min||30||Buller et al, 1990|
|Heart disease||16 (±6) L/min||20||Elborn et al, 1990|
|Pulm hypertension||12 (±2) L/min||11||D'Alonzo et al, 1987|
|Cancer||12 (±2) L/min||40||Travers et al, 2008|
|Diabetes||12-17 L/min||26||Bottini et al, 2003|
|Diabetes||15 (±2) L/min||45||Tantucci et al, 2001|
|Diabetes||12 (±2) L/min||8||Mancini et al, 1999|
|Diabetes||10-20 L/min||28||Tantucci et al, 1997|
|Diabetes||13 (±2) L/min||20||Tantucci et al, 1996|
|Asthma||13 (±2) L/min||16||Chalupa et al, 2004|
|Asthma||15 L/min||8||Johnson et al, 1995|
|Asthma||14 (±6) L/min||39||Bowler et al, 1998|
|Asthma||13 (±4) L/min||17||Kassabian et al, 1982|
|Asthma||12 L/min||101||McFadden & Lyons, 1968|
|COPD||14 (±2) L/min||12||Palange et al, 2001|
|COPD||12 (±2) L/min||10||Sinderby et al, 2001|
|COPD||14 L/min||3||Stulbarg et al, 2001|
|Sleep apnea||15 (±3) L/min||20||Radwan et al, 2001|
|Liver cirrhosis||11-18 L/min||24||Epstein et al, 1998|
|Hyperthyroidism||15 (±1) L/min||42||Kahaly, 1998|
|Cystic fibrosis||15 L/min||15||Fauroux et al, 2006|
|Cystic fibrosis||10 L/min||11||Browning et al, 1990|
|Cystic fibrosis*||10 L/min||10||Ward et al, 1999|
|CF and diabetes*||10 L/min||7||Ward et al, 1999|
|Cystic fibrosis||16 L/min||7||Dodd et al, 2006|
|Cystic fibrosis||18 L/min||9||McKone et al, 2005|
|Cystic fibrosis*||13 (±2) L/min||10||Bell et al, 1996|
|Cystic fibrosis||11-14 L/min||6||Tepper et al, 1983|
|Epilepsy||13 L/min||12||Esquivel et al, 1991|
|CHV||13 (±2) L/min||134||Han et al, 1997|
|Panic disorder||12 (±5) L/min||12||Pain et al, 1991|
|Bipolar disorder||11 (±2) L/min||16||MacKinnon et al, 2007|
|Dystrophia myotonica||16 (±4) L/min||12||Clague et al, 1994|
Average minute ventilation in modern "normal subjects" is about 12 L/min and they have only about 20-25 for the body-oxygen test (see links below). Therefore, people generate free radicals "naturally". Let us now prove that abnormal breathing is the most powerful source of free radicals and oxidative stress in modern, especially sick, people.
CO2 and Cellular O2 are Best Natural Antioxidants
Normal arterial levels of CO2 have antioxidant properties. Indeed, a group of Russian microbiologists discovered 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 (free radicals) by the cells and mitochondria of the human and tissues" (Kogan et al, 1997). They suggested several independent mechanisms involving inhibition of the NADPH-oxidase activity (Kogan et al, 1997; Kogan et al, 1996), better coordination of oxidation and phosphorylation and increased the phosphorylation velocity in liver mitochondria (Boljevic et al, 1996).
Czech scientists from the Department of Medical Chemistry and Biochemistry of the Faculty of Medicine (Charles University, Center for Experimental Cardiovascular Research, Prague) published an article in the Physiological Research Journal with the title "The role of carbon dioxide in free radical reactions of the organism" (Veselá & Wilhelm, 2002). They discovered several mechanisms to explain explain the protective antioxidant role of CO2 against free radical damage (see the abstract and the link to the study below).
This is sensible since hypocapnia or over breathing reduces oxygen levels in body cells (see image of the brain).
Ineffective breathing: the key cause of free radical damage
Dozens of studies have shown that modern "normal subjects" breathe about 12 L/min at rest, while the medical norm is only 6 L/min. As result, blood CO2 levels is less than normal. Arterial hypocapnia (CO2 deficiency) causes tissue hypoxia that trigger numerous pathological effects (see links with medical studies below).
There are additional adverse biochemical effects related to mouth breathing and chest breathing that also promote free radical damage and oxidative stress.
For most modern people, there is a certain time of the day when they have lowest levels of oxygen in the brain and body cells. This is also the time when people generate most free radicals.
Sleep and free radical generation
Most people feel worst or most miserable in the morning. Furthermore, as mentioned above, severely sick, critically ill (due to heart attacks, seizures, acute asthma, strokes, etc.) and hospitalized patients are most likely to have acute episodes or even die during early morning hours (see medical research on Web page Sleep Heavy Breathing Effect). The key reason for all these abnormalities is a low body oxygen level due to overbreathing with contributions of chest/mouth breathing. What are the effects? Hypoxic cells switch to anaerobic respiration and start producing lactic acid and other incompletely oxidized chemicals or free radicals causing cellular stress and intensifying respiration.
While many people are concerned with free radicals in foods, water and air, generally sick and severely people do not eat or drink anything during or just before night sleep. How do they cause oxidative stress then? They get free radicals and free radical damage due to their low oxygen levels in the body caused by heavy breathing and low levels of CO2 in the lungs.
175 medical doctors practicing the Buteyko breathing technique suggested that
there are 2 thresholds for the body-oxygen test in relation to free radical generation:
- less than 20 s for the body-oxygen test (moderate degrees of chronic diseases)
- less than 10 s (severe forms of chronic diseases).
Therefore, taking care about light and easy breathing 24/7 (and high body oxygen levels), especially during early morning hours, is a much smarter step to prevent free radical damage and increase body antioxidant defenses than to worry about diets, "natural" supplements and pills.
Related web pages:
- CO2: Cell Oxygen Levels are controlled by alveolar CO2 and breathing. Hyperventilation, regardless of the arterial CO2 changes, causes alveolar hypocapnia, which leads to cell hypoxia (low cell oxygen concentrations).
- CO2 and Chronic Inflammation - Hypocapnia caused by hyperventilation leads to hypoxia that promotes chronic inflammation.
Reference pages: Breathing norms and medical facts:
- Breathing norms: Parameters, graph, and description of the normal breathing pattern
- 6 breathing myths: Myths and superstitions about breathing and body oxygenation (prevalence: over 90%)
- Hyperventilation: Definitions of hyperventilation: their advantages and weak points
- Hyperventilation syndrome: Western scientific evidence about prevalence of chronic hyperventilation in patients with chronic conditions (37 medical studies)
- Normal minute ventilation: Small and slow breathing at rest is enjoyed by healthy subjects (14 studies)
- Hyperventilation prevalence: Present in over 90% of normal people (24 medical studies)
- HV and hypoxia: How and why deep breathing reduces oxygenation of cells and tissues of all vital organs
- Body-oxygen test (CP test) : How to measure your own breathing and body oxygenation (two in one) using a simple DIY test
- Body oxygen in healthy: Results for the body-oxygen test for healthy people (27 medical studies)
- Body oxygen in sick : Results for the body-oxygen test for sick people (14 medical studies)
- Buteyko Table of Health Zones: Clinical description and ranges for breathing zones: from the critically ill (severely sick) up to super healthy people with maximum possible body oxygenation
- Morning hyperventilation: Why people feel worse and critically ill people are most likely to die during early morning hours
References: pages about CO2 effect:
- Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
- The Bohr effect: How and why oxygen is released by red blood cells in tissues
- Cell oxygen levels: How alveolar CO2 influences oxygen transport
- Oxygen transport: O2 transport is controlled by vasoconstriction-vasodilation and the Bohr effects, both of which rely on CO2
- Free radical generation: Reactive oxygen species are produced within cells due to anaerobic cell respiration caused by cell hypoxia
- Inflammatory response: Chronic inflammation in fueled by the hypoxia-inducible factor 1, while normal breathing reduces and eliminates inflammation
- Nerve stabilization: People remain calm due to calmative or sedative effects of carbon dioxide in neurons or nerve cells
- Muscle relaxation: Relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence
- Bronchodilation: Dilation of airways (bronchi and bronchioles) is caused by carbon dioxide, and their constriction by hypocapnia (low CO2)
- Blood pH: Regulation of blood pH due to breathing and regulation of other bodily fluids
- CO2: lung damage: Elevated carbon dioxide prevents lung injury and promotes healing of lung tissues
- CO2: Topical carbon dioxide can heal skin and tissues
- Synthesis of glutamine in the brain, CO2 fixation, and other chemical reactions
- Deep breathing myth: Ignorant and naive people promote the idea that deep breathing and breathing more air at rest is beneficial for health
- Breathing control: How is our breathing regulated? Why hypocapnia makes breathing uneven, irregular and erratic.
Physiol Res. 2002;51(4):335-9.
The role of carbon dioxide in free radical reactions of the organism
Veselá A, Wilhelm J.
Department of Medical Chemistry and Biochemistry, Second Faculty of Medicine, Charles University, Center for Experimental Cardiovascular Research, Prague, Czech Republic.
(Free full PDF file of this article is available: http://www.biomed.cas.cz/physiolres/pdf/51/51_335.pdf)
Carbon dioxide interacts both with reactive nitrogen species and reactive oxygen species. In the presence of superoxide, NO reacts to form peroxynitrite that reacts with CO2 to give nitrosoperoxycarbonate. This compound rearranges to nitrocarbonate which is prone to further reactions. In an aqueous environment, the most probable reaction is hydrolysis producing carbonate and nitrate. Thus the net effect of CO2 is scavenging of peroxynitrite and prevention of nitration and oxidative damage. However, in a nonpolar environment of membranes, nitrocarbonate undergoes other reactions leading to nitration of proteins and oxidative damage. When NO reacts with oxygen in the absence of superoxide, a nitrating species N2O3 is formed. CO2 interacts with N2O3 to produce a nitrosyl compound that, under physiological pH, is hydrolyzed to nitrous and carbonic acid. In this way, CO2 also prevents nitration reactions. CO2 protects superoxide dismutase against oxidative damage induced by hydrogen peroxide. However, in this reaction carbonate radicals are formed which can propagate the oxidative damage. It was found that hypercapnia in vivo protects against the damaging effects of ischemia or hypoxia. Several mechanisms have been suggested to explain the protective role of CO2 in vivo. The most significant appears to be stabilization of the iron-transferrin complex which prevents the involvement of iron ions in the initiation of free radical reactions.
Izv Akad Nauk Ser Biol. 1997 Mar-Apr;(2):204-17.
[Carbon dioxide--a universal inhibitor of the generation of active oxygen forms [free radicals] by cells (deciphering one enigma of evolution)]
[Article in Russian]
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 (free radicals) 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.
Vopr Med Khim. 1996 Jul-Sep;42(3):193-202.
[Ability of carbon dioxide to inhibit generation of superoxide anion radical in cells and its biomedical role]
[Article in Russian]
Kogan AKh, Grachev SV, Eliseeva SV, Bolevich S.
The study was carried out on blood phagocytes and alveolar macrophages of 96 persons, cells of inner organs and tissue phagocytes (liver, brain, myocardium, lungs, kidneys, stomach, skeletal muscles), as well as on mitochondria of the liver of 186 non-linear white mice. Generation of active oxygen forms (AOF) was evaluated by various methods with CO2 directly affecting the cells and bioptates and indirectly the whole organism. The results show that CO2 with tension close to that of the blood (37.0 mm Hg) and at higher tensions (60 and 146 mm Hg) is a powerful inhibitor of AOF generation by human and animal cells, as well as by liver mitochondria of mice. The data obtained allow to explain, in terms of AOF role, a number of physiological and pathophysiological (medical) CO2 effects.
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]
[Article in Serbian]
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.
Ter Arkh. 1995;67(3):23-6.
[Changes in the sensitivity of leukocytes to the inhibiting effect of CO2 on their generation of active forms of oxygen in bronchial asthma patients]
[Article in Russian]
Daniliak IG, Kogan AKh, Sumarokov AV, Bolevich S.
30 bronchial asthma (BA) patients and 15 donors were exposed to 8.3% and 20.8% CO2 to bring out leukocytes sensitivity to CO2 by generation of active oxygen (AO) in bronchial asthma. CO2 effects on leukocyte AO generation were defined by luminol-dependent chemiluminescence (CL) before and after the exposure to CO2. It was found that in healthy subjects 8.3% and 20.8% CO2 noticeably inhibits leukocyte CL. However, in 70% of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished. This was normal in 30% of BA patients. With BA aggravation, leukocyte sensitivity to CO2 tended to a decrease. Remission brought a complete or partial recovery of the above sensitivity. Thus, on the one hand, CO2 is involved in BA pathogenesis in terms of its inhibitory effect on AO generation by leukocytes; on the other hand, only in 30% of BA patients high CO2 concentrations as a treatment may be justified.
Patol Fiziol Eksp Ter. 1995 Jul-Sep;(3):34-40.
[Comparative study of the effect of carbon dioxide on the generation of active forms of oxygen by leukocytes in health and in bronchial asthma]
[Article in Russian]
Kogan AKh, Bolevich S, Daniliak IG.
The study was conducted by using leukocytes isolated from 74 apparently healthy donors and 60 patients with bronchial asthma. The generation of active oxygen forms was determined by luminolo- and lucigenin-dependent chemiluminescence techniques and NTC-reaction. The findings suggest that at the tension close to the blood tension of 37.5 mm Hg and the high tension of 146 mm Hg is a powerful natural inhibitor of leukocytic generation of active oxygen forms. At an exacerbation, the inhibitory effect of carbon dioxide on the leukocytic generation of active oxygen forms decreased in most (70%) patients with bronchial asthma, which potentiates the free radical mechanism of development of bronchial asthma. It may be held that the literature-described use of carbon dioxide for the treatment of bronchial asthma is justifiable only in a lower proportion of patients who have preserved a high sensitivity to the inhibitory effect of carbon dioxide on the generation of active oxygen forms.
If you click the above Facebook like button and "like" this page, I will be nearly "forced" to asnwer your question. You can also tweet this page. Mention this in your comment, and you can ask even more. Thanks.
Back to CO2 Effects
|Disclaimer||Copyright 2013 Artour Rakhimov||Contact details||About Artour Rakhimov (Google profile)|