best cancer clinical trial: medical triumph pdf short

8/20/2019 Best Cancer Clinical Trial: Medical Triumph PDF Short

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Cancer: Medical Triumph

with Self-Oxygenation Therapies Artour Rakhimov (PhD)

Copyright

Content copyright © Dr. Artour Rakhimov. All rights reserved.

This book is copyrighted. It is prohibited to copy, lend, adapt, electronically transmit, ortransmit by any other means or methods without prior written approval rom the author.

!owever, the book may be borrowed by amily members.

Disclaimer

The content provided herein is or inormation purposes only and not intended todiagnose, treat, cure or prevent cystic ibrosis or any other chronic disease. Always

consult your doctor or health care provider beore making any medical decisions. The

inormation herein is the sole opinion o Dr. Artour Rakhimov and does not constitutemedical advice. These statements have not been evaluated by "ntario #inistry o !ealth

nor by the $orld !ealth "rgani%ation. Although every eort has been made to ensure the

accuracy o the inormation herein, Dr. Artour Rakhimov accepts no responsibility or

liability and makes no claims, promises, or guarantees about the accuracy, completeness,or ade&uacy o the inormation provided herein and e'pressly disclaims any liability or

errors and omissions herein.


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ContentCancer( #edical Triumph ...................................................................................................)with *el+"'ygenation Therapies........................................................................................)

Copyright.........................................................................................................................)

Disclaimer........................................................................................................................)Content.................................................................................................................................

Introduction......................................................................................................................-

. /ody o'ygen( the key health actor.............................................................................0. 1ow body ")( the crucial actor in development o cancer...................................0

.) Acidic cellular p! or low body ")( what causes what2........................................3

. Chronic inlammation and cancer........................................................................

.- Inlammatory disorders are also based on low ")...............................................-.0 Cell hypo'ia causes o'idative stress and generation o ree radicals..................4

). /reathing norms vs. breathing in people with cancer................................................3

). 5hysiological norms or breathing at rest............................................................3

).) "ther parameters o normal breathing.................................................................)6). Dr. /uteyko norms or breathing.........................................................................)

).- /reathing parameters in people with cancer........................................................)). 7ects o overbreathing 8hyperventilation9...............................................................)0

. :asoconstriction and reduced blood low are caused by low C") in the arterial

blood..........................................................................................................................)0.) 1ow C") results in the suppressed /ohr eect...................................................6

. 1ess o'ygen or cells...........................................................................................

About the author Dr. Artour Rakhimov.........................................................................4


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Introduction

This book does not claim that all metastatic cancers can be reversed. !owever, the initial

stages o metastasis or spread o malignant cells to neighboring lymph nodes can be

successully addressed with therapies that increase body o'ygenation naturally )- hours aday, everyday. Russian and ;krainian medical doctors applied their methods on hundreds

o people with cancer and even had a published clinical trial on women with metastatic

breast cancer. This trial was not an application o totally new techni&ues and methods or people with metastasis. Their protocol involved the application o additional therapies

together with standard medical treatments such as surgery and radiation or chemotherapy.

This trial clearly demonstrated the power o natural sel+o'ygenation methods, as well asthe presence o dangerously low o'ygen content in the participants o this trial beore

they applied those powerul sel+o'ygenation techni&ues. Cancer cannot e'ist in people

with normal body ") 8o'ygen9 content.

The average o'ygen concentration in cells o the body and within tumors is a known keyactor that predicts appearance and aggressiveness o tumors. It is also a actor that in the

survival o patients who are in the last stages o cancer. There are hundreds o recent

medical studies that repeatedly claim that tissue hypo'ia or low o'ygenation o bodycells plays the leading role in the development o cancer. These researchers and doctors

do their research on a cellular level using very sophisticated techni&ues and methods to

measure the eects o o'ygen deprivation on malignant cells. They openly claim that

they are clueless about the causes o tissue hypo'ia which is ound in each and each person with cancer.

!owever, the cause o the tissue hypo'ia in people with cancer is their abnormal

breathing. This has been discovered so ar in each tested individual. $hat should happen

i some physiological parameter is about ) or more times away rom the physiologicalstandard2 Imagine i one


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1 !ody oxygen: the "ey health factor

"All chronic pain, suffering and diseases are caused from a lack of oxygen at the cell

level"

#uyton $C% The Text&oo" of Medical 'hysiology(% )ifth *dition* World’s most widely used medical textbook of any kind * World’s best-selling physiology book

5roessor ?uyton was the Dean o the ;niversity o #ississippi #edical *chool. This

?uyton


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in 5hysiology and #edicine or his discovery o the nature and mode of action of the

respiratory en#yme.

$hile Dr. $arburg only started the new era in molecular eects or micro causes ocancer 8what is going on a cell level9, there are numerous modern studies related to

cellular causes o cancer. #any practitioners o alternative therapies suggest that cancer

tumors appear and grow due to a p! which is too acidic within the cells o the human body. This acidic environment, as they assert, is created due to environmental inluenceswhere an abnormal diet with too much animal proteins and too little vegetables and

grains plays the crucial role. $hile this idea o acidic dietary inluences has some rational

oundation, the real negative eects o e'cessive protein consumption are very dierent.$e are going to e'plore this acidic p! idea and eects o diets in more detail later in this

book. At the moment, let us ocus on recent studies that e'plain the origins and cause o

cancer.

)irst groups of cancer cells can appear only at low &ody O,

$hy do irst cancer cells appear2 A group o microbiologists rom the ;niversity o

Caliornia in *an Diego had the ollowing title or their article( The hypoxia inducible factor-$ gene is re%uired for embryogenesis and solid tumor formation 8Ryan et al,

339. As we can see rom this title, tumors do not appear out o nowhere. They re&uirelow body o'ygenation that is e'pressed in the hypo'ia+inducible actor+ that is the

marker o low body o'ygenation and a necessary actor or any irst cancer cells to

multiply and orm a malignant tumor.

Cancer cells en.oy tissue hypoxia

;nder normal conditions, even a group o hypo'ic cells will die or will be easilydestroyed by the immune system. $hat about cells in malignant tumors2 Researchers

rom the ?ray 1aboratory Cancer Research Trust located in #ount :ernon !ospital,

@orthwood, #iddlese', the ;E concluded, &ells undergo a !ariety of biologicalresponses when placed in hypoxic conditions" including acti!ation of signaling pathways

that regulate proliferation" angiogenesis and death' &ancer cells ha!e adapted these

pathways" allowing tumors to sur!i!e and e!en grow under hypoxic conditions'''B8Chaplin et al, 349. These scientists say that cancer tumors like tissue hypo'ia.

!ere is another &uote rom a study done in the Fale ;niversity *chool o #edicine

8;*A9. Dr Rockwell studied malignant changes on the cellular level and wrote, The

physiological effects of hypoxia and the associated micro en!ironmental inade%uaciesincrease mutation rates" select for cells deficient in normal pathways of programmed cell

death" and contribute to the de!elopment of an increasingly in!asi!e" metastatic

phenotypeB 8Rockwell, 33G9. The title o his publication is xygen deli!ery

implications for the biology and therapy of solid tumors.

+ow O, is the crucial factor in cancer metastasis

$hen the solid tumor is large enough, and while body o'ygenation becomes critically

low, malignant cells start to invade neighboring lymph nodes and later other organs and

tissues. This process is called metastasis.

Do%ens o medical and physiological studies conirmed that low ") concentrations intumors and body cells control spread o malignant cells to other organs and tissues. !ere


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is the title o one study that claims, Tumor oxygenation predicts for the likelihood of

distant metastases in human soft tissue sarcoma 8/ri%el et al, 3349.

?erman researchers rom the the ;niversity o 1eip%ig and ;niversity o Rostockconcluded, '''Therefore" tissue hypoxia has been regarded as a central factor for tumoraggressi!eness and metastasisB 8Eun% H Ibrahim, )669.

Canadian doctors rom the "ntario Cancer Institute at the 5rincess #argaret !ospital

8;niversity o Toronto9 even measured the eects o low body ") values in chances otumors to metastasi%e. These doctors ound, n our studies of carcinoma of the cer!ix"nodal metastases were $' times more likely at diagnosis in patients with more hypoxic

tumours relati!e to those with less hypoxic tumours''' 8!ill et al, )669

/ypoxia and chances of surial

&linical e!idence shows that tumor hypoxia is an independent prognostic indicator of poor patient outcome' +ypoxic tumors ha!e altered physiologic processes" including

increased regions of angiogenesis" increased local in!asion" increased distant metastasis

and altered apoptotic programsB 8Denko et al, )669.

+ow O, is a "ey parameter in treatment resistance

There are many therapies used by modern oncologists to treat cancers. Apart rom radicaltreatment methods 8or dierent orms o surgeries9, there are other methods that include

common conservative methods that include radiation therapy and chemotherapy.

"bviously, medical proessionals are trying to improve eiciency o these methods andind out causes o their low success rates. 1ow cell ") is one o the main actors that

reduce success rates or chemotherapy and radiation therapy.

American scientists rom !arvard #edical *chool noted ''' +ypoxia may thus produce

both treatment resistance and a growth ad!antageB 8*chmalt% et al, 339.

In their article published in Cancer 1etters, Dr. 7vans and Dr. Eoch observed, ,owtissue oxygen concentration has been shown to be important in the response of human

tumors to radiation therapy" chemotherapy and other treatment modalities' +ypoxia is

also known to be a prognostic indicator" as hypoxic human tumors are more biologicallyaggressi!e and are more likely to recur locally and metastasi#eB 87vans H Eoch, )669.

+ow O, is the central factor in cancer dynamics

?rowth o tumors and progression o any cancer is a dynamic process with changes that

can take place within 0+6 minutes in both directions. $e are going to provide practical

e'amples related to this dynamic nature o cancer later. At the present moment, let usreview relevant conclusions rom recent medical and oncological research.

?erman biologists rom the 7dinger Institute at the ohann $olgang ?oethe ;niversityin Jrankurt directly claim, Thus mounting e!idence suggests that the +. /hypoxia-

inducible factor0 system plays a decisi!e role in tumor physiology and progression intheir study 1 role for hypoxia and hypoxia-inducible transcription factors in tumor

physiology 8Acker H 5late, )66)9.

Jrench oncologists rom the Institute o *ignaling, Developmental /iology and Cancer

Research at the ;niversity o @ice also reviewed the role o cell hypo'ia in cancer


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dynamics. They wrote, +ypoxia is a common characteristic of the microen!ironment of

solid tumors and" through acti!ation of the hypoxia-inducible factor" is at the center of

the growth dynamics of tumor cells 8Dayan et al, )669.

There is so much proessional evidence about the ast growth o tumors when the

condition o hypo'ia is present that a large group o Caliornian researchers recently

wrote a paper +ypoxia - inducible factor-$ is a positi!e factor in solid tumor growth8Ryan et al, )6669.

7choing their paper, a /ritish oncologist Dr. !arris rom the $eatherhill Institute o

#olecular #edicine 8"'ord9 went urther with the manuscript +ypoxia - a key

regulatory factor in tumor growth 8!arris, )66)9.

Conclusions

As we see rom all these &uoted studies, all stages o cancer rom its birth and up to itsdeath 8andKor death o the owner9 are tightly linked to ") content in tumors and body

cells. @ote that I put these phrases together since body o'ygenation and tumor

o'ygenation correlate with each other. $hen tumors grow, its low o'ygenation e'ist onthe background o whole body hypo'ia that is an e&ual driving orce or cancer

development. I body o'ygenation improves, due to some smart things that we can do,

the tumor ") content may not remain unaected. Indeed, as we reviewed above,

appearance o very irst groups o cancer cells re&uires hypo'ia that e'ist in normal 8notmalignant yet9 cells.

0eferences

Acker T, 5late E! 1 role for hypoxia and hypoxia-inducible transcription factors in

tumor physiology" #ol #ed 8/erlin9. )66) *epL6839(04)+G0.

/ri%el D#, *cully *5, !arrelson #, 1ayield 1, /ean #, 5rosnit% 1R, Dewhirst #$,

Tumor oxygenation predicts for the likelihood of distant metastases in human soft tissue sarcoma, Cancer Research 334, 04( p. 3-+3-.

Dayan J, #a%ure @#, /rahimi+!orn #C, 5ouyssMgur , 1 dialogue between the

hypoxia-inducible factor and the tumor microen!ironment" Cancer #icroenviron. )66DecL89(0+4.

Denko @C, Jontana 1A, !udson E#, *utphin 5D, Raychaudhuri *, Altman R, ?iaccia

A, n!estigating hypoxic tumor physiology through gene expression patterns, "ncogene

)66 *eptember L ))8G9( p. 036G+03-.

7vans *# H Eoch C, 2rognostic significance of tumor oxygenation in humans, Cancer1etters )66 #ay 6L 3089( p. +4.

!arris A1, +ypoxia a key regulatory factor in tumor growth, @ational Review in Cancer)66) anuaryL )89( p. +-G.

!ill R5, De aeger E, ang A, Cairns R, p+" hypoxia and metastasis" @ovartis Jound

*ymp. )66L)-6(0-+40L discussion 40+.

Eun% # H Ibrahim *#, 3olecular responses to hypoxia in tumor cells, #olecular

Cancer )66L )( p. )+.


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Rockwell *, xygen deli!ery implications for the biology and therapy of solid tumors,

"ncology Research 33GL 384+G9( p. +36.

Ryan !, 1o , ohnson R*, The hypoxia inducible factor-$ gene is re%uired for

embryogenesis and solid tumor formation, 7#/" ournal 33, G( p. 660+60.

Ryan !7, 5oloni #, #c@ulty $, 7lson D, ?assmann #, Arbeit #, ohnson R*, +ypoxia-inducible factor-$ is a positi!e factor in solid tumor growth, Cancer Res, August

, )666L 46809( p. -66 + -60. +ypoxia-inducible factor-$ is a positi!e factor in solid

tumor growth

*chmalt% C, !ardenbergh 5!, $ells A, Jisher D7, 4egulation of proliferation-sur!i!al

decisions during tumor cell hypoxia, #olecular and Cellular /iology 33 #ay, 809( p.

)-0+)0-.

$arburg ", The 2rime &ause and 2re!ention of &ancer , Revised lecture at the meetingo the @obel+1aureates on une 6, 344.

1, $cidic cellular p/ or low &ody O,: what causes what

As it was mentioned above, many proponents o alternative therapies believe that cellular

p! is the main actor that causes cancer tumors. Indeed, there are numerous studies that

support the concept that tumor acidity is a signiicant actor that can prevent the successo conservative cancer treatment methods such as chemotherapy and radiation. Thereore,

there are numerous websites and books which promote this idea and even oer treatment

protocols to ight cancers. In this section o the book, we are going to review scientiic

evidence related to this topic( $hat is the primary actor in cancer growth( is it tissuehypo'ia or acidic cellular p!2

This &uestion o cancer origins was analy%ed in numerous published studies on cancer. A

group o American doctors rom the Department o #edicine and the Cancer Center atthe ;niversity o Caliornia in 1a olla in their conclusions wrote, These results indicatethat hypoxia and its accompanying low p+ enrich for 334-deficient cells and that loss

of 334 renders human colon carcinoma cells hypersensiti!e to the ability of hypoxia to

induce microsatellite instability and generate highly drug-resistant clones in the sur!i!ing population 8Eondo et al, )669.

A team o scientists rom the Cancer Research Institute at the ;niversity o @ice in

Jrance devoted their publication to the ollowing topic, 1 dialogue between the hypoxia-

inducible factor and the tumor microen!ironment 8Dayan et al, )669. In their abstract,they wrote, +ypoxia is a common characteristic of the microen!ironment of solid

tumors and" through acti!ation of the hypoxia-inducible factor" is at the center of the

growth dynamics of tumor cells' 5ot only does the microen!ironment impact on thehypoxia-inducible factor but this factor impacts on microen!ironmental features" such as

p+" nutrient a!ailability" metabolism and the extracellular matrix' $e can see here that

the answer is simple. +ow cellular O, causes a&normal p/ changes

Caliornian researcher Dr. 5ayne rom the *teenblock Research Institute suggested thee'act mechanism how tissue hypo'ia causes low intracellular p!. &hemo- and radio-

resistant cancer cells within solid tumors undermine the effecti!eness of these


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approaches to achie!ing oncolysis' These resistant cells and clusters of cells typically

thri!e at low oxygen tensions and are reliant on anaerobic metabolic pathways that

churn out lactate' This hypoxic state is one that can be exploited and in this paper ano!el method is ad!anced in!ol!ing tumor cell infiltration by bifidobacterium species

which should bring about prodigious lactate synthesis6 concomitant blocking of its

en#ymatic degradation by urea as well as export (from the cell) by use of %uercetin6depletion of 1T2 using exogenous thyroid6 and compromised oxidati!e catabolism of

free fatty acids and amino acids !ia oral intake of l-hydroxycitrate" melatonin and

nontoxic 5781' This anaerobic pathway cocktail" it is hypothesi#ed" will bring abouta profound reduction in intracellular p+ and a compromised state of cellular energetics

sufficient to effect oncolysis 85ayne, )66G9.

Italian scientists rom Rome were also interested, according to the title o their article in

Tumor acidity" chemoresistance and proton pump inhibitors. They wrote, 1nimportant determinant of tumor acidity is the anaerobic metabolism that allows selection

of cells able to sur!i!e in an hypoxic-anoxic en!ironment with the generation of lactate

8De #ilito H Jais, )6609. As we see, they also suggest that anaerobic respiration o cells

causes acidity in tumors.

/ritish "'ord researchers rom the Imperial Cancer Research Jund at the ;niversity o

"'ord 8Institute o #olecular #edicine9 pinpointed the key trigger o pathological

events leading to advance o cancers. +ypoxia" a common conse%uence of solid tumor

growth in breast cancer and other cancers" ser!es to propagate a cascade of molecular pathways which include angiogenesis" glycolysis" and alterations in microen!ironmental

p+''' 8?oonewardene et al, )66)9.

A study by ?erman oncologists published in the ournal o #olecular #edicine

conirmed the same conclusion about the primary driving orce o cancers. Theresearchers wrote, The +. system induces adapti!e responses including angiogenesis"

glycolysis" and p+ regulation which confer increased resistance towards the hostiletumor microen!ironment 8Acker H 5late, )66)9.

To my knowledge, there are no studies that suggest or conirm the leading role o cellular p! in creation o cell hypo'ia or in cancer dynamics. There are indeed numerous studies

claiming that low p! or acidic environment o tumors is a very potent negative actor that

makes acidic tumors very resistant to all types o conservative treatments.

#any proponents o alternative therapies promote an idea that cancer is caused by a poordiet with too many acidic oods that makes cells acidic and leads to growth o tumors.

This is the inluence o acidic diets which are usually based on animal proteins and Nunk

oods. !owever, these eects are not due to this nearly mechanical hypothetical

relationship( you eat more amino acids and less oods with minerals, thereore you getacidic body cells. The negative mechanism due to e'cessive dietary proteins, especially

animal proteins in comparison with vegetables, ruits and other oods that have lessamino acids but more minerals and other nutrients, is very dierent. There is some

rationality in having vegetarian diets provided that all re&uired nutrients are provided.

#edical research showed that diets based on animal proteins make breathing heavier incomparison with vegetarian diets. !eavy breathing, as we are going to learn later, reduces

body and tumor o'ygenation.


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0eferences

Acker T, 5late E! 1 role for hypoxia and hypoxia-inducible transcription factors in

tumor physiology" #ol #ed 8/erlin9. )66) *epL6839(04)+G0.

Dayan J, #a%ure @#, /rahimi+!orn #C, 5ouyssMgur , 1 dialogue between the

hypoxia-inducible factor and the tumor microen!ironment" Cancer #icroenviron. )66DecL89(0+4.

De #ilito A, Jais *, Tumor acidity" chemoresistance and proton pump inhibitors" Juture

"ncol. )660 DecL849(GG3+4.

?oonewardene TI, *owter !#, !arris A1, +ypoxia-induced pathways in breast cancer"#icrosc Res Tech. )66) "ct L0389(-+.

5ayne A?, 9xploiting hypoxia in solid tumors to achie!e oncolysis" #ed !ypotheses.

)66GL48-9()+.

12 Chronic inflammation and cancer

$hen we consider only appearance o inlamed tissues, we can immediately suspect that

these swollen inlamed cells have some eatures that make them similar to malignantcells. Rudolph Carl :irchow 8) O 36)9 was a amous ?erman doctor, anthropologist,

pathologist, and biologist was probably the irst doctor who in 4 suggested the link

between chronic inlammation and cancer. !e demonstrated leucocytes in neoplastictissue. Dr. :irchow is oten reerred to as the ather o modern pathology and

considered one o the ounders o social medicine.

Recent modern oncological studies have also conirmed the link using a more detailed

description o events leading to chronic inlammation and appearance o malignanttumors. There are several common key chemicals that are parts o chronic inlammatory

and developing malignant processes. Jurthermore, many researchers ound that havinginlammatory health problems increase chances o cancer. #any oncologists suggestedthat chronic inlammation is even one the key actors causing cancer.

Jor e'ample, doctors rom the The *idney Eimmel Comprehensive Cancer Center in

/altimore, #D wrote, &hronic inflammation is now known to contribute to se!eral

forms of human cancer" with an estimated :;< of adult cancers attributable to chronic

inflammatory conditions caused by infectious agents" chronic non-infectiousinflammatory diseases and=or other en!ironmental factors' ndeed" chronic inflammation

is now regarded as an >enabling characteristic> of human cancer 8*anos H De #ar%o,

)6)9.

Australian scientists rom #elbourne 85eter #acCallum Cancer Centre and Departmento "ncology at the ;niversity o #elbourne9 also observed, &hronic inflammation is a

risk factor for tumor de!elopment 8Chow et al, )6)9.

Dr. #orrison provided several common chemicals that e'plain why chronic inlammation promotes growth o cancers, ''' chronic inflammation and associated reacti!e freeradical o!erload and some types of bacterial" !iral" and parasite infections that cause

inflammation were recogni#ed as important risk factors for cancer de!elopment and


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account for one in four of all human cancers worldwide' 9!en !iruses that do not directly

cause inflammation can cause cancer when they act in con?unction with proinflammatory

cofactors or when they initiate or promote cancer !ia the same signaling pathwaysutili#ed in inflammation' Whate!er its origin" inflammation in the tumor

microen!ironment has many cancer-promoting effects and aids in the proliferation and

sur!i!al of malignant cells and promotes angiogenesis and metastasis' 3ediators ofinflammation such as cytokines" free radicals" prostaglandins" and growth factors can

induce 751 damage in tumor suppressor genes and post-translational modifications of

proteins in!ol!ed in essential cellular processes including apoptosis" 751 repair" andcell cycle checkpoints that can lead to initiation and progression of cancer 8#orrison,

)6)9.

Eorean oncologists rom the Cancer Research Institute at the *eoul @ational ;niversity

devoted their review, according to the title o their recent article to nflammation gearing the ?ourney to cancer 8Eundu H *urh, )669. In their summary, they wrote,

3any of proinflammatory mediators" especially cytokines" chemokines and

prostaglandins" turn on the angiogenic switches mainly controlled by !ascular

endothelial growth factor" thereby inducing inflammatory angiogenesis and tumor cell- stroma communication' This will end up with tumor angiogenesis" metastasis and

in!asion' 3oreo!er" cellular micro451s are emerging as a potential link between

inflammation and cancer .

Another title o the research paper written by researchers rom the Department o#olecular and /iomedical 5harmacology at ;niversity o Eentucky *chool o #edicine

in 1e'ington also suggests the same story nflammation a dri!ing force speeds cancer

metastasis 8$u H Phou, )6639.

Drs. !oseth and $argovich rom the Department o /asic 5harmaceutical *ciences atthe *outh Carolina College o 5harmacy also speciied key chemicals that participate in

promotion o chronic inlammation and development o cancer. 1t the molecular le!el" free radicals and aldehydes" produced during chronic inflammation" can inducedeleterious gene mutation and posttranslational modifications of key cancer-related

proteins' ther products of inflammation" including cytokines" growth factors" and

transcription factors such as nuclear factor kappa@" control the expression of cancer genes (e'g'" suppressor genes and oncogenes) and key inflammatory en#ymes such as

inducible nitric oxide synthase and cyclooxygenase-:' These en#ymes in turn directly

influence reacti!e oxygen species and eicosanoid le!els' The procancerous outcome of

chronic inflammation is increased 751 damage" increased 751 synthesis" cellular proliferation" disruption of 751 repair pathways and cellular milieu" inhibition of

apoptosis" and promotion of angiogenesis and in!asion' &hronic inflammation is also

associated with immunosuppression" which is a risk factor for cancer 8!oseth H$argovich, )66G9

There are so many similarities between chronic inlammation and cancer, that many

teams o scientists are even trying the same medical drugs and natural e'tracts or

substances to combat both these conditions. This relates to application o(+ andrographolide and its analogues 81im et al, )6)9

+ curcumin 8*chaer et al, )69

+ olic acid that is also known as vitamin /3 8Fang et al, )6)9,


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+ tocotrienols, the potent isoorms o vitamin 7 8@esaretnam H #eganathan, )69

+ thymo&uinone, an active ingredient isolated rom @igella sativa 8$oo et al, )6)9

+ unstable naturally derived hepo'ilins, metabolites o arachidonic acid 85ace+Asciak,)69

+ group o autacoid mediators that are the products o arachidonic acid metabolism

include( the prostaglandins, leukotrienes, lipo'ins and cytochrome 5-06 8CF59 derived bioactive products, which are all collectively reerred to as eicosanoids 8?reene et al,

)69

+ resveratrol 8trans+,-=,0+trihydro'ystilbene9, a natural polyphenol with antio'idant, anti+inlammatory, and anticancer properties 8Tili H #ichaille, )69

and some other substances.

$hile application o these products may have certain beneicial chemical reactions,

without removal o the key cause o low body ") levels, their overall eiciency will bevery low. @ote that there are oten true stories o people testiying about their magic

recovery ollowing use o some special protocols. !owever, when other people with

cancer apply to the same substances using the same dosages, very ew o them are able to

achieve the same results. The eects o various positive substances and unctional oodsdepends on body o'ygen levels that can be easily measured using the body o'ygen test

described below.

0eferences

Chow #T, #Qller A, *myth #, nflammation and immune sur!eillance in cancer"*emin Cancer /iol. )6) JebL))89()+).

?reene 7R, !uang *, *erhan C@, 5anigrahy D, 4egulation of inflammation in cancer by

eicosanoids" 5rostaglandins "ther 1ipid #ediat. )6 @ovL348+-9()G+4.

!oseth 1, $argovich #, nflammation" cancer" and targets of ginseng" @utr. )66G

anLG8 *uppl9(*+0*.Eundu E, *urh F, nflammation gearing the ?ourney to cancer" #utat Res. )66 ul+AugL4038+)9(0+6.

1im C, Chan TE, @g D*, *agineedu *R, *tanslas , $ong $J, 1ndrographolide and

its analogues !ersatile bioacti!e molecules for combating inflammation and cancer" Clin

7'p 5harmacol 5hysiol. )6) #arL389(66+6.

#orrison $/, nflammation and cancer a comparati!e !iew" :et Intern #ed. )6)

an+JebL)489(+.

@esaretnam E, #eganathan 5, Tocotrienols inflammation and cancer" Ann @ F Acad

*ci. )6 ulL))3(+)).

5ace+Asciak CR, +epoxilins in cancer and inflammation--use of hepoxilin antagonists"Cancer #etastasis Rev. )6 DecL68+-9(-3+064.

*chaer #, *chaer 5#, Pidan , /ar *ela ?, &urcuma as a functional food in the

control of cancer and inflammation" Curr "pin Clin @utr #etab Care. )6

@ovL-849(0+3G.


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*anos E*, De #ar%o A#, 2rostate cancer and inflammation the e!idence'

!istopathology. )6) anL4689(33+)0.

Tili 7, #ichaille , 4es!eratrol" 3icro451s" nflammation" and &ancer" @ucleicAcids. )6L)6(6)-.

$oo CC, Eumar A5, *ethi ?, Tan E!, Thymo%uinone potential cure for inflammatorydisorders and cancer" /iochem 5harmacol. )6) Jeb 0L8-9(--+0.

$u F, Phou /5, nflammation a dri!ing force speeds cancer metastasis" Cell Cycle.

)663 "ct 0L8)69()4G+G.

Fang , :lashi 7, 1ow 5, .olate-linked drugs for the treatment of cancer andinflammatory diseases" *ubcell /iochem. )6)L04(4+G3.

13 Inflammatory disorders are also &ased on low O,

As numerous very recent studies claim, chronic inlammatory conditions, on a cell level,

are also controlled by tissue hypo'ia or low o'ygen content in cells. Among the key

driving orces o chronic inlammation are pro+inlammatory transcription actors, suchas nuclear actor kappa / 8@J+kappa/9, activator protein 8A59+ 8*aronova H #orita,

)66L Ryan et al, )6639, and hypoxia-inducible factor 8Imtiya% H *imon, )66L

*umbayev H @icholas, )669, the same substance that is the key actor in cancer 8see5art .9.

/oth eects, chronic inlammation and low o'ygen levels in cells, are common in peoplewith many chronic diseases, such as(

+ arthritic conditions

+ Al%heimer=s disease+ asthma

+ autoimmune diseases

+ acne+ allergic reactions


15/37

+ atherosclerosis

+ chronic prostatitis

+ Crohn=s disease+ C"5D

+ dermatitis

+ hepatitis+ hypersensitivities and allergic reactions

+ insulin resistance 8diabetes9

+ irritable bowel syndrome 8I/*9 o the intestinal tract+ inlammatory bowel diseases 8I/D9

+ lupus

+ nephritis

+ obesity+ cache'ia

+ gastrointestinal ischemia

+ osteoarthritis

+ pelvic inlammatory disease+ 5arkinson=s disease

+ sarcoidosis+ sleep apnea

+ transplant reNection

+ and ulcerative colitis.

*ymptoms o these chronic diseases include inlammation, possible atigue due toe'hausted cortisol reserves, likely pain, and other symptoms. *everal other chronic

diseases 8including atherosclerosis, and ischemic heart disease9 also have their origins in

chronic inlammatory processes. The same is true or cancer as we discussed above.There are hundreds o research studies that either mentioned or proved the acts provided

above. *ome o these studies are listed below.

0eferences

Arnaud C, Dematteis #, 5epin 1, /aguet 5, 1Mvy 5, bstructi!e sleep apnea" immuno-

inflammation" and atherosclerosis" *emin Immunopathol. )663 unL89(+)0.

7lt%schig !E, Rivera+@ieves , Colgan *5, Targeting the 1:@ adenosine receptor during gastrointestinal ischemia and inflammation" 7'pert "pin Ther Targets. )663

@ovL89()4G+GG.

Jrede *, /erchner+5annschmidt ;, Jandrey , 4egulation of hypoxia-inducible factors

during inflammation" #ethods 7n%ymol. )66GL-0(-60+3.

Imtiya% !P, *imon #C, +ypoxia-inducible factors as essential regulators ofinflammation, Curr Top #icrobiol Immunol. )66L-0(60+)6.

oussen A#, Jauser *, Erohne T;, 1emmen ED, 1ang ?7, Eirchho /, 7iabetic

retinopathy' 2athophysiology and therapy of hypoxia-induced inflammation Article in

?ermanS, "phthalmologe. )66 #ayL66809(4+G6.

"liver E#, Taylor CT, Cummins 75, +ypoxia' 4egulation of 5.kappa@ signalling

during inflammation the role of hydroxylases" Arthritis Res Ther. )663L89()0.


16/37

Ramalho R, ?uimares C, The role of adipose tissue and macrophages in chronic

inflammation associated with obesity clinical implications Article in 5ortugueseS, Acta

#ed 5ort. )66 *ep+"ctL)809(-3+34. 7pub )663 an 4.

Ryan *, Taylor CT, #c@icholas $T, Aystemic inflammation a key factor in the pathogenesis of cardio!ascular complications in obstructi!e sleep apnoea syndromeB

Thora'. )663 ulL4-8G9(4+4.

*aronova ", #orita I, Transcriptome remodeling in hypoxic inflammation" Dent Res.)66 #ayL3809(-6+--. 7pub )66 #ar )4.

*umbayev ::, @icholas *A, +ypoxia-inducible factor $ as one of the signaling

dri!ers of Toll-like receptor-dependent and allergic inflammation" Arch Immunol Ther

7'p 8$ars%9. )66 AugL08-9()G+3-. 7pub )66 #ay )4.

Taylor CT, nterdependent roles for hypoxia inducible factor and nuclear factor-kappa@in hypoxic inflammation" 5hysiol. )66 *ep L0485t G9(-600+3.

$outers 7J, ,ocal and systemic inflammation in chronic obstructi!e pulmonary disease"

5roc Am Thorac *oc. )660L)89()4+.

14 Cell hypoxia causes oxidatie stress and generation of free radicals

$hen o'ygen supply is restricted, it is necessary or various bodily processes andreactions to take place in cells and organs, there are various protective but damaging

mechanisms and solutions that maintain vital unctions in various parts o the human

body. These adaptations to cell hypo'ia are dierent in various organs o the human bodyand, in addition, are speciic in duration. These are the conclusions o the study titled

ntermittent hypoxia has organ-specific effects on oxidati!e stress 8un , *avransky et

al, )669 conducted at the ohn !opkins Asthma and Allergy Center, Division o5ulmonology and Critical Care #edicine in /altimore, #D, ;*A. Jurthermore, hypo'ia+


17/37

induced chemicals can be generated in some areas and parts o the human body but cause

problems or other organs, or e'ample, the brain and heart.

!owever, there are common mechanisms related to eects o tissue hypo'ia. Fou have probably heard about antio'idants and ree radicals. Jree radicals are also called reactive

o'ygen species 8those powerul chemicals that can cause damage to hundreds or

thousands o other cells due to their inherent destructive power9. They create so calledo'ygen stress. #aybe you even take supplements that contain such known and popularantio'idants as vitamin C, %inc, vitamin A, selenium and some others. !owever, it is very

likely that you generate ree radicals in your body cells due to your ineective or

abnormal breathing.

$hy do researchers call it o'ygen stress2 @ormal air has only about )6> o o'ygen,while the main remaining part is neutral nitrogen that is an inert gas. 5ure o'ygen 8or

66> o'ygen9, as any respirologist can tell you, is to'ic due to its powerul abilities to

react with tissues. The damage due to breathing pure o'ygen and especially hyperbaric breathing starts in the lungs. Right o'ygen is bound with red blood cells 8or hemoglobin

cells9. It is released in tissues and saely transported to re&uired cells and parts o the cell.

"bviously, any attempts to consume o'ygenated drinks, o'ygenated bars, or even breathing hypero'ic air 8more than )6> at normal pressure9 can be lie+saving or

critically ill people, but always leads to worse health in a long run.

1et us now consider other well+proven eects o hypo'ia related to generation o ree

radicals. Abnormally low o'ygen delivery leads to anaerobic 8i.e., without participationo o'ygen9 cellular respiration, generation o lactic acid and ree radicals. There are

hundreds o research studies that claim that generation o ree radicals is a normal and

known outcome o cell hypo'ia. 8@ote that some studies simulated cell hypo'ia by

reducing o'ygen content in the inspired air, but breathing abnormalities present in most people cause e'actly the same eect( low body ") content.9 There are only some

reerences that are provided below. Their titles clearly highlight the role o hypo'ia ingeneration o ree radicals.

0eferences

Carvalho C, *antos #*, /aldeiras I, "liveira CR, *eiUa R, #oreira 5I, &hronic hypoxia

potentiates age-related oxidati!e imbalance in brain !essels and synaptosomes" Curr

@eurovasc Res. )66 @ovLG8-9()+66.

Dukhande ::, *harma ?C, 1ai C, Jarahani R, &hronic hypoxia-induced alterations ofkey en#ymes of glucose oxidati!e metabolism in de!eloping mouse li!er are mT4

dependent" #ol Cell /iochem. )6 @ovL0G8+)9(3+3G.

7steva *, 5edret R, Jort @, Torrella R, 5agVs T, :iscor ?, xidati!e stress status in rats

after intermittent exposure to hypobaric hypoxia" $ilderness 7nviron #ed. )66DecL)8-9()0+.

Javaro 7, Ramachandran A, #cCormick R, ?ee !, /lancher C, Crosby #, Devlin C,

/lick C, /ua J, 1i 1, :oNnovic /, 5ires das @eves R, ?la%er 5, Iborra J, Ivan #,

Ragoussis , !arris A1, 3icro451-:$; regulates mitochondrial free radical response tohypoxia and Crebs cycle in cancer cells by targeting iron sulfur cluster protein A&D"

51o* "ne. )66 Apr )4L08-9(e6-0.


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?iordano J, xygen" oxidati!e stress" hypoxia" and heart failure" Clin Invest. )660

#arL089(066+.

!imadri 5, Eumari **, ChitharanNan #, DhananNay *, 4ole of oxidati!e stress and

inflammation in hypoxia-induced cerebral edema a molecular approach" !igh Alt #ed

/iol. )66 JallL89()+--.

un , *avransky :, @anayakkara A, /evans *, 1i , *mith 51, 5olotsky :F,

ntermittent hypoxia has organ-specific effects on oxidati!e stress" Am 5hysiol RegulIntegr Comp 5hysiol. )66 "ctL)308-9(R)G-+.

#artin R, #o%et C, #artin !, $elt E, 7ngel C, Jit%l ?, The effect of 8inkgo biloba

extract (98b EF$) on parameters of oxidati!e stress in different regions of aging rat

brains after acute hypoxia" Aging Clin 7'p Res. )6 AugL)8-9()00+4.

#ustaa *A, Al+*ubiai *@, Davies *, ha A@, +ypoxia-induced oxidati!e 751 damagelinks with higher le!el biological effects including specific growth rate in common carp"

&yprinus carpio ," 7coto'icology. )6 AugL)6849(-00+44.

5atterson A, Wiao D, Wiong J, Di'on /, Phang 1, +ypoxia-deri!ed oxidati!e stressmediates epigenetic repression of 2C&G!arepsilonH gene in foetal rat hearts' CardiovascRes. )6) Jeb L38)9(6)+6.

5ialou' :, Joster ?7, Ahmed */, /eaudin A7, !anly 5, 5oulin #, ,osartan abolishes

oxidati!e stress induced by intermittent hypoxia in humans" 5hysiol. )6 @ov

0L0385t ))9(00)3+G.

Ramond A, ?odin+Ribuot D, Ribuot C, Totoson 5, Eoritchneva I, Cachot *, 1evy 5,oyeu'+Jaure #, xidati!e stress mediates cardiac infarction aggra!ation induced by

intermittent hypoxia" Jundam Clin 5harmacol. )6 Dec G. doi( 6.KN.-G)+)64.

*koumalovX A, !erget , $ilhelm , +ypercapnia protects erythrocytes against free

radical damage induced by hypoxia in exposed rats" Cell /iochem Junct. )66"ctL)48G9(6+G.

Wu , 1ong F*, ?o%al D, 7pstein 5@, @eta-cell death and proliferation after intermittent

hypoxia role of oxidati!e stress" Jree Radic /iol #ed. )663 #ar 0L-4849(G+36.


19/37

, !reathing norms s &reathing in people with cancer

7ach and every person with cancer has ineective or abnormal breathing pattern that

reduces their body o'ygenation. $e can make this conclusion rom all studies that

measured automatic breathing patterns in people with cancer, as well as rom clinicale'perience o medical doctors and health practitioners who measured breathing in their

patients and clients.

In order to investigate and understand what is wrong with breathing in people withcancers, let us start with an analysis o medical norms or breathing at rest, as well as

typical respiratory parameters in healthy and ordinary people. 1ater, we are going to

consider those studies that measured various breathing parameters in people with cancer.

,1 'hysiological norms for &reathing at rest

@ormal breathing is strictly nasal 8in and out9, predominantly diaphragmatic 8i.e.,abdominal9, very slow in re&uency 8see the numbers below9 and imperceptible 8no

eelings or sensation about one


20/37

I a person with normal breathing is asked about what they eel or their breathing

sensations, they will testiy that they do not eel their breathing at all 8unless their

practice yoga breathing or some other breathing e'ercises9. $hy is this so2 @ormal tidal

volume is only 066 ml or about 6.4 g o air, which is inhaled during one inspiration.

!ence, normal breathing is slow in re&uency and very small in amplitude.0eferences 5Medical and physiological text&oo"s6

?anong $J, 4e!iew of medical physiology, 0+th ed., 330, 5rentice !all Int., 1ondon.

?uyton AC, 2hysiology of the human body, 4+th ed., 3-, *uanders College 5ubl.,

5hiladelphia.

*traub @C, Aection I" The 4espiratory Aystem" in 2hysiology, eds. R# /erne H #@1evy, -+th edition, #osby, *t. 1ouis, 33.

Aummary of !alues useful in pulmonary physiology man' Aection 4espiration and

&irculation, ed. by 5.1. Altman H D.*. Dittmer, 3G, /ethesda, #aryland 8Jederation

o American *ocieties or 7'perimental /iology9.

,, Other parameters of normal &reathing

f a person breath-holds after a normal exhalation" it takes about J; seconds before

breathing commencesB 8#cArdle et al, )6669. This -6 seconds indicate normalo'ygenation o tissues. @ote that the breath holding test is done ater usual e'halation.


21/37

The current medical norm or C") content in the alveoli o the lungs and the arterial

blood is -6 mm !g C"). This number was established during the irst decade o the )6th

century by amous /ritish physiologists Charles ?. Douglas and ohn *. !aldane rom"'ord ;niversity. Their results were published in 363 article The regulation of

normal breathing by the ournal o 5hysiology 8Douglas H !aldane, 3639. This

corresponds to about 0.> 8at sea level9. Fou do not need to remember all these numbers.They are going to be used only to show that cancer patients never have these norms.

1et me note here that normal C") in the arterial blood is absolutely necessary or normal

transport o o'ygen to cells. $e are going to discuss the reasons later.

@ormal breathing is regular, invisible 8no chest or belly movements9, mainly

diaphragmatic, and inaudible 8no panting, no whee%ing, no sighing, no yawning, nosnee%ing, no coughing, no deep inhalations or e'halations9.

$ccording to numerous medical text&oo"s% this ery small and slow normal

diaphragmatic &reathing leads to nearly ideal oxygenation of the arterial &lood:

a&out 78-779 This conclusion is important or uture since many people believe in a

myth that deep breathing or breathing more air helps to increase blood o'ygenation. Inreality, one can breathe +0 times more than the morn, but blood o'ygenation will not be

improved to any essential degree. In act, since chronic automatic overbreathing leads tochest breathing, while lower parts o the lungs get about 0+4 times more blood due to

gravity, oer&reathing usually reduces &lood oxygenation.

0eferences

Douglas C?, !aldane *, The regulation of normal breathing , ournal o 5hysiology

363L ( p. -)6O--6.

#cArdle $.D., Eatch J.I., Eatch :.1., 9ssentials of exercise physiology 8)+nd edition9L

1ippincott, $illiams and $ilkins, 1ondon )666.

,2 Dr !utey"o norms for &reathing


22/37

During the 346=s or nearly the whole decade, *oviet Dr. Eonstantin /uteyko 8born in

;kraine9 was the manager o the respiratory laboratory in @ovosibirsk 8;**R9. /ased on

his studies o thousands o healthy and sick people in this laboratory, he suggesteddierent norms or breathing 8e.g., /uteyko, 339 that guarantee e'cellent health and

absence o nearly all chronic degenerative diseases, cancer included. $hat are his

medical norms2 Jor e'ample, his normal respiratory rate is only breathsKmin instead o). !ere are his numbers or normal breathing(

+ normal minute ventilation is - lKminL

+ normal tidal volume 8air volume breathed in during a single breath9 is 066 mlL+ normal breathing rate or respiratory re&uency is breaths per minuteL

+ inspiration is about .0 secondsL

+ e'halation is ) secondsL

+ automatic pause 8or period o no breathing ater e'halation9 is - secondsL+ breath holding time 8ater usual e'halation and without any stress at the end o the test9

is 46 secondsL

+ C") concentrations in the alveoli or arterial blood is 4.0> or about -4 mm !g 8at sea

level9.As we are going to study later, such easy and slow automatic breathing at rest delivers

more o'ygen to tissues o the human body than the current oicial medical norm

accepted all over the world.

,3 !reathing parameters in people with cancer

All available medical literature clearly demonstrates that virtually all people with cancerhave ineective or abnormal breathing. In one study conducted by the Division o

Respiratory and Critical Care #edicine at the Department o #edicine o the Yueen=s

;niversity in Eingston 8"ntario, Canada9, researchers measured minute ventilation in

people with cancer 8Travers et al, )669. The scientists were actually interested inrespiratory dierences related to presence o dyspnea that is one o the symptoms in

cancer patients. !owever, minute ventilation in participants o this study was the sameregardless the presence o dyspnea. /oth cancer groups 8-6 participants in total9 had

about )Z) liters o air per minute at rest, while the medical norm or adults is about 4

liters per minute. All these cancer patients also had elevated breathing re&uency o about

3+)6 breathsKmin instead o normal ) breathsKmin.

"bviously, when one breathes or ventilates much more than the physiological norm, it is

called hyperventilation. It would be logical to e'pect that their overbreathing caused

low C") levels in the airways and the arterial blood.

This Canadian study allows us to calculate the amount o air per one breath in peoplewith cancer. *ince the participants had about ) liters per minute with nearly )6 breaths

per minute, we can divide ) by )6 and get 6.4 liters or one breath or 466 ml o air or

their tidal volume. The normal value is 066 ml. Thereore, we see that this group o

cancer patients were breathing deeply at rest. They breathing was aster and deeper thanthe medical norms.

*everal other studies measured respiratory re&uency at rest in patients with cancer who

e'perienced dyspnea. All the results o these studies are summari%ed in this graph.


23/37

The same results or R 8respiratory re&uency9 are provided in this table.


24/37

@ote that some o these studies investigated patients with metastatic cancer and

terminally sick cancer patients who are oten given morphine during last weeks o their

lives in order to reduce pain and suering. #orphine is a powerul respiratorysuppressant and can dramatically reduce minute ventilation and R. These actors make

results or cancer patients dierent, but in each and every case we observe that they have

very ast breathing up to about )+ times aster than the oicial medical norm.;krainian medical doctor *ergey 5aschenko measured C") content in the e'pired air orso called end+tidal C") in )6 women with metastatic breast cancer 85aschenko, )669.

7nd+tidal C") concentrations are generally very close to the arterial C") concentrations.

The average value or end+tidal C") in these cancer patients was about ).3>, while theoicial medical norm is about 0.> that corresponds to -6 mm !g at sea level.

This study directly conirms the results o all previous studies( 'eople with cancer haea&normally low CO, leels in their lungs and arterial &lood due to too heay

&reathing at rest

0eferences

/uteyko E5, 3ethod of !oluntary elimination of deep breathing in RussianS, in @uteykomethod' ts application in medical practice, ed. by E.5. /uteyko, )nd ed., 33, Titul,

"dessa, p.-+40.

/ruera 7, #ac7achern T, Ripamonti C, !anson , Aubcutaneous morphine for dyspnea

in cancer patients, Ann Intern #ed. 33L 3( p. 364+36G.

Clemens E7, Elaschik 7, Aymptomatic therapy of dyspnea with strong opioids and its

effect on !entilation in palliati!e care patients, 5ain *ymptom #anagement )66G AprL

8-9( p.-G+-.

Clemens E7, Elaschik 7, 9ffect of hydromorphone on !entilation in palliati!e care

patients with dyspnea, *upport Care Cancer. )66 anL 489( p.3+33. 7pub )66G "ct .Coyne 5, :iswanathan R, *mith T, 5ebuli#ed fentanyl citrate impro!es patients’

perception of breathing" respiratory rate" and oxygen saturation in dyspnea, 5ain

*ymptom #anage )66)L )( p.0GO46.

#a%%ocato C, /uclin T, Rapin C!, The effects of morphine on dyspnea and !entilatory function in elderly patients with ad!anced cancer a randomi#ed double-blind controlled

trial , Annals o "ncology. 333 DecL 68)9( p.0+0-.

5aschenko *, Atudy of application of the reduced breathing method in a combined

treatment of breast cancer in RussianS, "ncology 8Eiev, ;kraine9 )66, v. , @o., p.GG+G.

Travers , Dudgeon D, AmNadi E, #c/ride I, Dillon E, 1avene%iana 5, "ir D, $ebbEA, "=Donnell D7, 3echanisms of exertional dyspnea in patients with cancer , Appl

5hysiol )66 anL 6-89( p.0G+44.


25/37

2 *ffects of oer&reathing 5hyperentilation6

$e ound that people with cancer breathe too much air at rest. Are there any problems

with overbreathing2 $hile most people assume that deep breathing or breathing more air

is beneicial or health and would mean more ") in body cells, hundreds o medicalresearch studies ound that hyperventilation causes many adverse reactions and no

beneits. Jirst o all, as we discussed above, breathing more air does not increase blood

o'ygenation in any signiicant degree. 1et us consider other eects o chronicoverbreathing 8or chronic hyperventilation9 on the human organism.

I a healthy person with normal breathing starts to breathe more or deeper than the norms,

what are the initial eects2 There are ollowing conse&uences(

+ #ore C") is removed rom the lungs with each breath and thereore the level o C") inthe airways and lungs immediately decreases.

+ In +) minutes, the C") level alls below the norm in the arterial blood.

+ In +0 minutes, due to C") diusion rom tissues, most cells o the body 8includingvital organs and muscles9 e'perience lowered C") concentrations.

+ In 0+)6 minutes, the C") level in the brain is below the norm due to a slower diusion

rate caused by the blood+brain barrier.

21 asoconstriction and reduced &lood flow are caused &y low CO, in the

arterial &lood

Do%ens o independent physiological studies ound that hypocapnia 8low C")

concentration in the arterial blood9 decreased the blood low or circulation or theollowing organs(

+ brain 8Jortune et al, 330L Earlsson et al, 33-L 1iem et al, 330L #acey et al, )66GL*antiago H 7delman, 34L *tarling H 7vans, 34L Tsuda et al, 3G9+ heart 8Coet%ee et al, 3-L Jo[' et al, 3G3L Earlsson et al, 33-L "ka%aki et al, 33L

"ka%aki et al, 33)L $e'els et al, 309

+ liver 8Dutton et al, 3G4L JuNita et al, 33L !ughes et al, 3G3L "ka%aki, 339

+ kidneys 8Earlsson et al, 33-L "ka%aki, 339+ spleen 8Earlsson et al, 33-9

+ colon 8?ilmour et al, 369.

$hat is the physiological mechanism o the reduced blood low to vital organs2 C") is a

dilator o blood vessels 8arteries and arterioles9. Arteries and arterioles have their owntiny smooth muscles that can constrict or dilate 8rela'9 depending on C") concentrations.

$hen we breathe more, C") level in the arterial blood decreases, blood vessels constrictand vital organs 8like the brain, heart, kidneys, liver, stomach, spleen, colon, etc.9 get less blood supply.


26/37

This eect o vasoconstriction is noticeable or detectable even or very small decrease in

arterial C"). This is because C") is a very potent vasodilator. *ome studies claim that

C") is a more powerul vasodilator than any chemical drug. Jor e'ample, medicaldoctors rom the Department o Anesthesia, Armed Jorces !ospital, in Riyadh 8*audi

Arabia9 suggested that Caron dioxide, a most potent cereral vasodilator!!! 8DNurberg

et al, 339.

Dilation of &lood essels means more O,% glucose% and other ital nutrients and

chemicals for all organs of the human &ody !reathing more air causes constriction

of &lood essels This slows down deliery of all these "ey chemicals to organs and

tissues of the &ody

*ince all people with cancer are heavy breathers, they naturally have reduced blood lowand reduced o'ygen delivery to all vital organs and tissues.

+ow CO, increases pulse

@umerous studies have ound that when cancer advances, it is very common or suerers

to have elevated heart rates or pulse. There are even statistical data claiming that lower

heart rates and lower respiratory rates in people with advanced orms o cancer are predictors o their better survival. !owever, we can show that these two parameters relate

to each other.

In act, during the irst decades o the )6th century, the respiratory and cardiovascular

systems were not divided yet. The leading physiologists and main medical te'tbooks othe time studied the cardiorespiratory system as one mainly due to the intimate links

between the systems

!ow are they linked2 $hile the eects and interactions between them are numerous,

there is one main relationship that is based on the eects o C") to dilate blood vessels.The state o arteries and arterioles controls the total resistance to the systemic blood low

in the human body. !ence, when the arterial C") is normal or high, the arteries andarterioles are dilated, and it is easy or the heart to push blood or the total circulation.!owever, low C") or hypocapnia increases total resistance and the strain on the heart.

Thereore, breathing patterns directly participate in regulation o the heart rate.

The ather o cardiorespiratory physiology, Fale ;niversity 5roessor Fandell !enderson

8G+3--9 was the author o the irst medical te'tbooks on respiration. !e knew aboutthis C") eect on the heart rate. During one o his physiological proNects, he perormed

e'periments with anaestheti%ed dogs on mechanical ventilation. The results were


27/37

described in his article 1capnia and shock' - ' &arbon dioxide as a factor in the

regulation of the heart rate. In this 36 article, published in the 1merican Kournal of

2hysiology, he noticed, ''' we were enabled to regulate the heart to any desired rate from J; or fewer up to :;; or more beats per minute' The method was !ery simple' t

depended on the manipulation of the hand bellows with which artificial respiration was

administered''' 1s the pulmonary !entilation increased or diminished the heart rate wascorrespondingly accelerated or retarded 8p.)G, !enderson, 369.

@ote that the eects o changes in breathing on heart rate, as well as blood pressure, are

individual in a short run. !owever, when there are chronic changes in automatic

breathing patterns in the direction o hyperventilation, nearly all people develop higher pulse. Is there any signiicance in these variables or cancer patients2

?enerally, when doctors try to identiy the key actors that predict survival o cancer

patients, they choose various blood parameters that re&uire special laboratory testing,

dyspnea score, presence o edema, delirium, loss o appetite, and some other variables.!owever, in one study conducted by *panish researchers, they decided to use those

actors that can be easily measured. The title o their study was 2alliati!e performance

status" heart rate and respiratory rate as predicti!e factors of sur!i!al time in terminallyill cancer patients 8*Xnche% et al, )6649. They tested 3 patients, and in the conclusions

wrote, The median sur!i!al was L: days' n the multi!ariate analysis" three independent

!ariables were identified 2alliati!e 2erformance Acore of ; or under" heart rate of

$;;=minute or more" and respiratory rate of :J=minute or more' The !ariables that were found to be prognostic in our study are ob?ecti!e" easy" and %uick to measure" and do not

re%uire that the professional ha!e special training or experience.

Thereore, it is logical to e'pect that i people with cancer slow down their breathing

closer or back to the medical norms, they can e'pect reduced average respiratoryre&uencies 8slower breathing9 and decreased heart rates, at the same time. Jurthermore,

these numbers or the heart rate and breathing re&uency are in complete agreement with parameters or the terminally sick people that are provided by the /uteyko Table o!ealth Pones.

This is &uite consistent with what Dr. /uteyko discovered in the 346


28/37

these problems2 Fes, i we know that they breathing becomes aster and heavier. I a

healthy person starts to hyperventilate or breathe very heavy and ast at rest, what are the

eects on the brain2 As a result o voluntary hyperventilation, this person would eeldi%%y and could easily aint or pass out in about )+ minutes.

$hat are the causes o di%%iness and ainting2 #any people believe that too much

o'ygen in the brain is the cause o these eects, and we already know that very small andslow normal breathing results in having the near ideal o'ygenation o the arterial blood8about 3+33>9. $e cannot increase blood o'ygenation by taking a deep breath or many

deep breaths. The illustration below shows a brain scan undergoing two conditions(

during normal breathing and ater minute o voluntary hyperventilation. The red colorrepresents the most "), dark blue the least. This illustration shows that a person


29/37

DNurberg !?, TNan ?T, Al #outaery ER, 9nhanced catheter propagation with

hypercapnia during superselecti!e cerebral catherisation" @euroradiology. 33

ulL-68G9(-44+.

Jo[' 5, Ryder $A, 9ffect of &: on the systemic and coronary circulations and oncoronary sinus blood gas tensions, /ull 7ur 5hysiopathol Respir 3G3 ul+AugL 08-9(

p.4)0+4.

Jortune /, Jeustel 5, de1una C, ?raca 1, !asselbarth , Eupinski A#, &erebral blood

flow and blood !olume in response to : and &: changes in normal humans, Trauma.

330 *epL 389( p. -4+-G.

JuNita F, *akai T, "hsumi A, Takaori #, 9ffects of hypocapnia and hypercapnia on

splanchnic circulation and hepatic function in the beagle, Anesthesia and Analgesia 33AugL 438)9( p. 0)+0G.

!ashimoto E, "ka%aki E, "kutsu F, The effects of hypocapnia and hypercapnia on

tissue surface 2: in hemorrhaged dogs Article in apaneseS, #asui 33 "ctL 869(

p. )G+)G-.

!enderson F, 1capnia and shock' - ' &arbon dioxide as a factor in the regulation of theheart rate, American ournal o 5hysiology 36, )( p. )4+04.

!ughes R1, #athie RT, Jitch $, Campbell D, ,i!er blood flow and oxygen consumption

during hypocapnia and 22I in the greyhound , Appl 5hysiol. 3G3 AugL -G8)9( p. )36+

)30.

Earlsson T, *tNernstrQm 71, *tNernstrQm !, @orlMn E, $iklund 1, &entral and regionalblood flow during hyper!entilation' 1n experimental study in the pig , Acta Anaesthesiol

*cand. 33- JebL 8)9( p.6+4.

1iem ED, EollMe 1A, !opman C, De !aan AJ, "eseburg /, The influence of arterial

carbon dioxide on cerebral oxygenation and haemodynamics during 9&3 innormoxaemic and hypoxaemic piglets, Acta Anaesthesiol *cand *uppl. 330L 6G( p.0G+

4-.

1itchield 5#, 1 brief o!er!iew of the chemistry of respiration and the breathing heart

wa!e, Caliornia /ioeedback, )66 *pring, 389.

#acey 5#, $oo #A, !arper R#, +yperoxic brain effects are normali#ed by addition of&:, 51o* #ed. )66G #ayL -809( p. eG.

#cArdle $D, Eatch JI, Eatch :1, 9ssentials of exercise physiology 8)+nd edition9L

1ippincott, $illiams and $ilkins, 1ondon )666.

"ka%aki E, "kutsu F, Jukunaga A, 9ffect of carbon dioxide (hypocapnia andhypercapnia) on tissue blood flow and oxygenation of li!er" kidneys and skeletal muscle

in the dog , #asui 33 Apr, 8-9( p. -0G+-4-.

"ka%aki E, !ashimoto E, "kutsu F, "kumura J, 9ffect of arterial carbon dioxide

tension on regional myocardial tissue oxygen tension in the dog Article in apaneseS,#asui 33 @ovL -689( p. 4)6+4)-.


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"ka%aki E, !ashimoto E, "kutsu F, "kumura J, 9ffect of carbon dioxide (hypocapnia

and hypercapnia) on regional myocardial tissue oxygen tension in dogs with coronary

stenosis Article in apaneseS, #asui 33) JebL -8)9( p. ))+))-.

de #iguel *Xnche% C, 7lustondo *?, 7stirado A, *Xnche% J:, de la Rasilla Cooper C?,

Romero A1, "tero A, "lmos 1?, 2alliati!e performance status" heart rate and

respiratory rate as predicti!e factors of sur!i!al time in terminally ill cancer patients" 5ain *ymptom #anage. )664 unL849(-0+3).

*antiago T: H 7delman @!, @rain blood flow and control of breathing , in +andbook of 2hysiology" Aection L The respiratory system, vol. II, ed. by A5 Jishman. American

5hysiological *ociety, /etheda, #aryland, 34, p. 4+G3.

*tarling 7 H 1ovatt 7C, 2rinciples of human physiology, -+th ed., 34, 1ea H Jebiger,5hiladelphia.

Tsuda F, Eimura E, Foneda *, !artmann A, 7tani !, !ashikawa E, Eamada T, 9ffect of

hypocapnia on cerebral oxygen metabolism and blood flow in ischemic cerebro!ascular

disorders, 7ur @eurol. 3GL )G89( p.00+4.

$e'els C, #yhre 7*, #N\s "D, 9ffects of carbon dioxide and p+ on myocardial blood- flow and metabolism in the dog , Clin 5hysiol. 30 DecL 0849( p.0G0+0.

2, +ow CO, results in the suppressed !ohr effect

There is an additional negative eect o low C") on o'ygen delivery. $e now know that

hypocapnia decreases blood supply to all vital organs. $hy do hemoglobin cells or red

blood cells release o'ygen in the tissues, but not in the arteries, or arterioles, or veins2$hy is more ") released in those tissues o the human body that use more energy2 Jor

e'ample, the heart, due to its constant work, gets more ") than those muscles that are at

rest.The answer is in the /ohr=s law 8or /ohr eect9. The /ohr eect was irst described in36- by the Danish physiologist Christian /ohr. !e was the ather o amous physicist

@iels /ohr. Christian /ohr discovered that due to higher C") content in tissues and

capillaries 8more acidic environment than in arteries and arterioles9, hemoglobin is bound

to o'ygen with less ainity. !ence, o'ygen is released in tissues due to higher C")levels in those tissues.


31/37

There are many modern proessional investigations devoted to various aspects o the/ohr eect 8e.g., /raumann et al, 3)L /Qning et al, 3G0L /ucci et al, 30L Carter et

al, 30L di/ella et al, 34L D%hagarov et al, 334L ?rant et al, 3)L ?rubb et al, 3G3L

?ersonde et al, 34L !lastala H $oodson, 3L ensen, )66-L Eister et al, 3LEobayashi et al, 33L 1apennas, 3L #atthew et al, 3G3L #eyer et al, 3GL Tyuma,

3-L $inslow et al, 309.

!yperventilation causes reduced C") tissue tension, and this leads to reduced ") release

and reduced o'ygen tension in tissues 8Aarnoudse et al, 3L #onday H TMtreault,36L ?ottstein et al, 3G49. In simple terms, low absolute C") values prevent eective

release o o'ygen by red blood cells in tissues o the human body, and the blood carries

o'ygen away rom tissues when there are no C").

In order to improve the release o o'ygen by red blood cells in tissues, cancer patients

re&uire normal 8or even slightly above the norm9 arterial C") values.

0eferences


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Aarnoudse ?, "eseburg /, Ewant ?, Pwart A, PiNlstra $?, !uisNes !, nfluence of

!ariations in p+ and 2&: on scalp tissue oxygen tension and carotid arterial oxygen

tension in the fetal lamb, /iol @eonate 3L -680+49( p. )0)+)4.

/raumann E#, /Qning D, Trost J, @ohr effect and slope of the oxygen dissociationcur!e after physical training , Appl 5hysiol. 3) unL 0)849( p. 0)-+0)3.

/Qning D, *chwiegart ;, Tibes ;, !emmer /, nfluences of exercise and endurance

training on the oxygen dissociation cur!e of blood under in !i!o and in !itro conditions,7ur Appl 5hysiol "ccup 5hysiol. 3G0L -89( p. +6.

/ucci 7, Jronticelli C, 1nion @ohr effect of human hemoglobin, /iochemistry. 30 an

0L )-8)9( p. G+G4.

Carter A#, ?r\nlund , &ontribution of the @ohr effect to the fall in fetal 2: caused by

maternal alkalosis, 5erinat #ed. 30L 8-9( p.0+3.

di/ella ?, *candariato ?, *uriano ", Ri%%o A, xygen affinity and @ohr effect responsesto :"L- diphosphoglycerate in e%uine and human blood , Res :et *ci. 334 #ayL 4689( p.

)G)+)G0.D%hagarov /#, Eruk @@, The alkaline @ohr effect regulation ofthnded hemoglobin

+b(:)L Article in RussianS /ioi%ika. 334 #ay+unL -89( p. 464+4).

?ersonde E, *ick !, "verkamp #, *mith E#, 5arish D$, @ohr effect in monomericinsect haemoglobins controlled by : off-rate and modulated by haem-rotational

disorder , 7ur /iochem. 34 un )L 0G8)9( p. 3+-6-.

?rant /, nfluence of @ohr-+aldane effect on steady-state gas exchange, Appl 5hysiol.

3) #ayL 0)809( p. 6+G.

?rubb /, ones !, *chmidt+@ielsen E, 1!ian cerebral blood flow influence of the @ohr

effect on oxygen supply, Am 5hysiol. 3G3 #ayL )4809( p. !G--+G-3.

?ottstein ;, Pahn ;, !eld E, ?abriel J!, Te'tor T, /ergho $, 9ffect of

hyper!entilation on cerebral blood flow and metabolism in man6 continuous monitoringof arterio-cerebral !enous glucose differences 8author=s transl9 Article in ?ermanS, Elin

$ochenschr. 3G4 Apr 0L 0-89( p. G+.

!lastala #5, $oodson RD, @ohr effect data for blood gas calculations, Appl 5hysiol.

3 *epL 0089( p. 66)+66G.

ensen J/, 4ed blood cell p+" the @ohr effect" and other oxygenation-linked phenomenain blood : and &: transport , Acta 5hysiol *cand. )66- @ovL )89( p. )0+))G.

Eister , #arden #C, /ohn /, 5oyart C, .unctional properties of hemoglobin in human

red cells ' 7etermination of the @ohr effect , Respir 5hysiol. 3 *epL G89( p. 4+G.

Eobayashi !, 5elster /, 5iiper , *cheid 5, Aignificance of the @ohr effect for tissueoxygenation in a model with counter-current blood flow, Respir 5hysiol. 33 unL G489(

p. )GG+).

1apennas ?@, The magnitude of the @ohr coefficient optimal for oxygen deli!ery , Respir

5hysiol. 3 @ovL 0-8)9( p.4+G).


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#atthew /, !anania ?I, ?urd JR, 9lectrostatic effects in hemoglobin @ohr effect and

ionic strength dependence of indi!idual groups, /iochemistry. 3G3 #ay 0L 869(

p.3)+34.

#eyer #, !olle 5, *cheid 5, @ohr effect induced by &: and fixed acid at !ariousle!els of : saturation in duck blood , 5lugers Arch. 3G *ep )3L G489( p. )G+)-6.

#onday 1A, TMtreault 1, +yper!entilation and !ertigo, 1aryngoscope 36 unL 3684 5t

9( p.66+66.

Tyuma I, The @ohr effect and the +aldane effect in human hemoglobin, pn 5hysiol.3-L -8)9( p.)60+)4.

$inslow R#, #onge C, $inslow @, ?ibson C?, $hittembury , 5ormal whole blood

@ohr effect in 2eru!ian nati!es of high altitude, Respir 5hysiol. 30 AugL 48)9( p. 3G+

)6.

22 +ess oxygen for cells

*ummari%ing these above+discussed physiological C") eects, we conclude(. !yperventilation cannot increase ") content in the arterial blood to any signiicant

degree 8normal hemoglobin saturation is about 3+33>9, but it instead reduces C")

concentrations in all cells and the blood.). !ypocapnia 8or C") deiciency9 leads to constriction o blood vessels, and that

reduces blood supply to vital organs o the human body.

. !ypocapnia 8or C") deiciency9 also leads to the suppressed /ohr eect that causes

urther reduction in o'ygen delivery.-. !yperventilation causes low ") levels in cells.

/ence% the more cancer patient &reathes% the less oxygen is proided for all ital

organs This generates free radicals% causes more pro&lems with chronicinflammation% and fueling adance of cancer

The discussed eects o low C") due to hyperventilation o'ygen transport are

summari%ed in these two graphs.


34/37


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$&out the author Dr $rtour 0a"himo

] !igh *chool !onor student 8?rade AB or all e'ams9

] #oscow ;niversity !onor student 8?rade AB or all e'ams9

] #oscow ;niversity 5hD 8#athK5hysics9, accepted in Canada and the ;E

] $inner o many regional competitions in mathematics, chess and sport orienteering

8during teenage and ;niversity years9

] ?ood classical piano+player( Chopin, /ach, Tchaikovsky, /eethoven, *trauss 8up to

now9

] Jormer captain o the ski+" varsity team and member o the cross+country skiing

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] Jormer individual coach o world+elite athletes rom *oviet 8Russian9 and Jinnishnational teams who took gold and silver medals during $orld Championships

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