Re: tumor promotion with sodium bicarbonate

March 30, 2008

,

NaHCO3 in cancers in effective when the malignant tissue is in DIRECT contact

with 5% NaHCO3. There is sea of difference between direct contact and oral

administration of NaHCO3. The studies you sent have no relevence here which were

based on systemic alkaline infusions. If you see the video of Dr.Tullio on a

lung cancer adenoCA, you could see improvement in the tumour size and the

appearance in 24 hours. So the study you sent has no relevance to the protocol

of Dr.Tullio. It makes a hell of difference local and systemic administration.

Your post is confusing and misdirecting. Go through Dr. Tullio's study protocol

to get a clear idea about how NaHCO3 is active against cancers(DIRECT CONTACT).

His results speak for themselves. My own doctor did administer NaHCO3 to a lung

cancer pt(adenocaricinoma)which you should know is rare and non responding to

conventional; it did nothing to him with chemo, mono clonal but responded

beautifully with NaHCO3 in short time. What

more evidence you need? It is DIRECT CONTACT with NaHCO3 that tumours respond

to and not oral(so forget about soda bicarb degraded in stomach with HCl). Hope

this is clear to you now i.e.DIRECT CONTACT OF MALIGNANT TISSUE WITH 5% NaHCO3.

Dr.Tullio discovery is a boon to mankind.

Rahul

List, The following abstracts speak to the probable inadvisability

of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

animal models as a tumor promoter. Table salt (NaCl) can be equally troubling.

------------ --------- --------- --------- -------

Food Chem Toxicol. 1999 Dec;37(12):1159- 66.

Effect of urinary pH on the progression of urinary bladder tumours.

<http://www.ncbi. nlm.nih.gov/ sites/entrez? Db=pubmed & Cmd=Search &

Term=%22Lina% 20BA%22%5BAuthor %5D & itool= EntrezSystem2. PEntrez.Pubmed.

Pubmed_ResultsPa nel.Pubmed_ DiscoveryPanel. Pubmed_RVAbstrac tPlus>Lina

BA,

<http://www.ncbi. nlm.nih.gov/ sites/entrez? Db=pubmed & Cmd=Search & Term=%22van%

20Garderen- Hoetmer%20A% 22%5BAuthor% 5D & itool= EntrezSystem2.. PEntrez.Pubmed.

Pubmed_ResultsPa nel.Pubmed_ DiscoveryPanel. Pubmed_RVAbstrac tPlus>van

Garderen-Hoetmer A.

TNO Nutrition and Food Research Institute, AJ, Zeist, The Netherlands.

Systemic alkalosis has been postulated to enhance tumorigenesis,

whereas systemic acidosis has been implicated to exert a favourable

influence on tumour control and regression. In the present study the

urinary pH was influenced by feeding acid-forming or base-forming

diets, and the effect of alkaline or acid urine on the early and late

progression phase of urinary bladder carcinogenicity was investigated

in male Wistar rats. Bladder lesions were initiated by

N-butyl-N-(4- hydroxybutyl) nitrosamine (0.05% BBN in the drinking

water during 4 weeks) and promoted by sodium bicarbonate (3.4% NaHCO3

in the diet during 15 or 25 weeks). After short- (15 week) and more

long-term (25 week) promotion with NaHCO3, groups of 20 rats were fed

a diet containing the acidifying salt ammonium chloride (2.1% NH4Cl)

or the control diet. All surviving rats were killed after a total

study duration of 52 weeks. Additional control groups were, after

initiation, fed diets containing NaHCO3 and killed after 15 wk or 25

wk of promotion, or at the end of the study. In rats fed diets with

added salts, water intake and the amount of urine produced were

increased and the urinary density was decreased compared to rats fed

control diet. During NaHCO3 feeding, urinary pH and sodium

concentration were increased. During NH4Cl feeding, urinary pH was

decreased and urinary chloride and calcium concentrations were

increased. Initiation by BBN followed by treatment with NaHCO3 caused

a high incidence of papillary/nodular hyperplasia, papillomas and

carcinomas of the bladder epithelium. These lesions progressed with

time or longer duration of NaHCO3 promotion. A tumour protective

effect of urinary acidification by NH4Cl was not found. In fact, both

acidification and prolonged alkalinization tended to aggravate the

malignancy of bladder carcinomas.

PMID: 10654592 [PubMed - indexed for MEDLINE]

------------ --------- --------- -------

March 30, 2008

Rahul,

For credentialed professionals the usual and

credible way to release bona fide information is

through peer-reviewed articles. There is no

conspiracy to suppress such information. An example is:

------

<http://www.sciencedirect.com/science/journal/0304419X>Biochimica

et Biophysica Acta (BBA) - Reviews on Cancer

<http://www.sciencedirect.com/science?_ob=PublicationURL & _tockey=%23TOC%234907%2\

32005%23982439998%23606512%23FLA%23 & _cdi=4907 & _pubType=J & _auth=y & _acct=C00005022\

1 & _version=1 & _urlVersion=0 & _userid=10 & md5=c2acdb1d4fb23546dd0c18621beed73e>Volum\

e

1756, Issue 1, 25 September 2005, Pages 1-24

The role of pH dynamics and the Na+/H+ antiporter

in the etiopathogenesis and treatment of cancer.

Two faces of the same coinone single nature

Salvador

Harguindey<http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6T23-4GNKKG\

M-1 & _user=10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 & _version\

=1 & _urlVersion=0 & _userid=10 & md5=91a9c33807b437898c1272b8b153701b#aff1>a,

<http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6T23-4GNKKGM-1 & _user=\

10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 & _version=1 & _urlVer\

sion=0 & _userid=10 & md5=91a9c33807b437898c1272b8b153701b#cor1>

Corresponding Author Contact Information

, <mailto:salvaszh@...>

E-mail The Corresponding Author

, Gorka

Orive<http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6T23-4GNKKGM-1 & _\

user=10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 & _version=1 & _u\

rlVersion=0 & _userid=10 & md5=91a9c33807b437898c1272b8b153701b#aff2>b,

José

Pedraz<http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6T23-4GNKKGM-1 & \

_user=10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 & _version=1 & _\

urlVersion=0 & _userid=10 & md5=91a9c33807b437898c1272b8b153701b#aff2>b,

Angelo

Paradiso<http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6T23-4GNKKGM-\

1 & _user=10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 & _version=1\

& _urlVersion=0 & _userid=10 & md5=91a9c33807b437898c1272b8b153701b#aff3>c

and Stephan J.

Reshkin<http://www.sciencedirect.com/science?_ob=ArticleURL & _udi=B6T23-4GNKKGM-1\

& _user=10 & _rdoc=1 & _fmt= & _orig=search & _sort=d & view=c & _acct=C000050221 & _version=1 & \

_urlVersion=0 & _userid=10 & md5=91a9c33807b437898c1272b8b153701b#aff4>d

aCentro Médico “La Salud”- c) Independencia,

13-01004 Vitoria, Spain, and Biotechnology

Institute (BTI), c) San 15-5°, 01005 Vitoria, Spain

bDepartment of Pharmacy and Pharmaceutical

Technology, Faculty of Pharmacy, University of

the Basque Country, c) Paseo de las Universidades, 7-01006 Vitoria, Spain

cLaboratory of Clinical Experimental Oncology,

Oncology Institute of Bari, 70126 Bari, Italy

dDepartment of General and Environmental

Physiology, University of Bari, 70126 Bari, Italy

Received 3 March 2004; accepted 30 June 2005. Available online 19 July 2005.

Abstract

Looked at from the genetic point-of-view cancer

represents a daunting and, frankly, confusing

multiplicity of diseases (at least 100) that

require an equally large variety of therapeutic

strategies and substances designed to treat the

particular tumor. However, when analyzed

phenotypically cancer is a relatively uniform

disease of very conserved ‘hallmark’ behaviors

across the entire spectrum of tissue and genetic

differences [D. Hanahan, R.A. Weinberg, Hallmarks

of cancer, Cell 100 (2000) 57–70]. This suggests

that cancers do, indeed, share common biochemical

and physiological characteristics that are

independent of the varied genetic backgrounds,

and that there may be a common mechanism

underlying both the neoplastic

transformation/progression side and the

antineoplastic/therapy side of oncology. The

challenge of modern oncology is to integrate all

the diverse experimental data to create a

physiological/metabolic/energetic paradigm that

can unite our thinking in order to understand how

both neoplastic progression and therapies

function. This reductionist view gives the hope

that, as in chemistry and physics, it will

possible to identify common underlying driving

forces that define a tumor and will permit, for

the first time, the actual calculated

manipulation of their state. That is, a rational

therapeutic design. In the present review, we

present evidence, obtained from a great number of

studies, for a fundamental, underlying mechanism

involved in the initiation and evolution of the

neoplastic process. There is an ever growing body

of evidence that all the important neoplastic

phenotypes are driven by an alkalization of the

transformed cell, a process which seems specific

for transformed cells since the same

alkalinization has no effect in cells that have

not been transformed. Seen in that light,

different fields of cancer research, from

etiopathogenesis, cancer cell metabolism and

neovascularization, to multiple drug resistance

(MDR), selective apoptosis, modern cancer

chemotherapy and the spontaneous regression of

cancer (SRC) all appear to have in common a

pivotal characteristic, the aberrant regulation

of hydrogen ion dynamics [s. Harguindey, J.L.

Pedraz, R. García Cañero, J. Pérez de Diego, E.J.

Cragoe Jr., Hydrogen ion-dependent oncogenesis

and parallel new avenues to cancer prevention and

treatment using a H+-mediated unifying approach:

pH-related and pH-unrelated mechanisms, Crit.

Rev. Oncog. 6 (1) (1995) 1–33]. Cancer cells have

an acid–base disturbance that is completely

different than observed in normal tissues and

that increases in correspondence with increasing

neoplastic state: an interstitial acid

microenvironment linked to an intracellular alkalosis.

------

Dr. Simoncini chose not to go the route that

would win the respect of colleagues. When there

are problems getting important clinical research

published, the researcher can put all the raw

data on his/her website or in any number of web

publications. Any clinician knows how to display

a matrix of all patients, diagnoses, stage of

disease, past and current therapies, and

assessment of results -- complete remissions,

partial remissions, stabilization of disease, and

progression of disease. From this we can draw our own conclusions.

Dr. Simoncini's claims seem to go hand in hand

with his unconventional candida theory of cancer,

but he provides very little scientific support

for either. His reporting of wonderful cures

might be one hundred percent accurate, but why

did he choose to present his information in the

same wearying way that is usually selected by scientistic hucksters.

The history of sodium bicarbonate is almost

identical to the history of hydrogen peroxide and

other oxygen therapies for cancer. It goes back

many decades and has many true

believers. Certainly some people have

benefited. In any responsible reporting we would

be told when the treatment can be expected to

fall on its face. How well does it work on the

many difficult sarcomas? on low grade

carcinomas? on the various leukemias and

lymphomas? on patients with drug resistance? in

the face of co-morbid conditions? what about

bone mets? are there ANY cases where the sodium

bicarbonate promoted cancer growth or cancer metastasis?

The way this therapy is now being presented, all

cancer patients can now say, " Whoopee! I'm as

good as cured. I just have to make a pilgrimage

to Dr. Simoncini -- or at least see a physician

who has paid for Dr. Simoncini's seminar. "

At 12:16 AM 3/30/2008, you wrote:

>,

>

>NaHCO3 in cancers in effective when the

>malignant tissue is in DIRECT contact with 5%

>NaHCO3. There is sea of difference between

>direct contact and oral administration of

>NaHCO3. The studies you sent have no relevence

>here which were based on systemic alkaline

>infusions. If you see the video of Dr.Tullio on

>a lung cancer adenoCA, you could see improvement

>in the tumour size and the appearance in 24

>hours. So the study you sent has no relevance to

>the protocol of Dr.Tullio. It makes a hell of

>difference local and systemic administration.

>Your post is confusing and misdirecting. Go

>through Dr. Tullio's study protocol to get a

>clear idea about how NaHCO3 is active against

>cancers(DIRECT CONTACT). His results speak for

>themselves. My own doctor did administer NaHCO3

>to a lung cancer pt(adenocaricinoma)which you

>should know is rare and non responding to

>conventional; it did nothing to him with chemo,

>mono clonal but responded beautifully with NaHCO3 in short time. What

>more evidence you need? It is DIRECT CONTACT

>with NaHCO3 that tumours respond to and not

>oral(so forget about soda bicarb degraded in

>stomach with HCl). Hope this is clear to you now

>i.e.DIRECT CONTACT OF MALIGNANT TISSUE WITH 5%

>NaHCO3. Dr.Tullio discovery is a boon to mankind.

>

>Rahul

>

>List, The following abstracts speak to the probable inadvisability

>of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

>animal models as a tumor promoter. Table salt (NaCl) can be equally troubling.

>

>------------ --------- --------- --------- -------

>Food Chem Toxicol. 1999 Dec;37(12):1159- 66.

>

>Effect of urinary pH on the progression of urinary bladder tumours.

>

><<http://www.ncbi.>http://www.ncbi. nlm.nih.gov/

>sites/entrez? Db=pubmed & Cmd=Search &

>Term=%22Lina% 20BA%22%5BAuthor %5D & itool=

>EntrezSystem2. PEntrez.Pubmed. Pubmed_ResultsPa

>nel.Pubmed_ DiscoveryPanel. Pubmed_RVAbstrac tPlus>Lina

>BA,

><<http://www.ncbi.>http://www.ncbi. nlm.nih.gov/

>sites/entrez? Db=pubmed & Cmd=Search &

>Term=%22van% 20Garderen- Hoetmer%20A%

>22%5BAuthor% 5D & itool= EntrezSystem2..

>PEntrez.Pubmed. Pubmed_ResultsPa nel.Pubmed_

>DiscoveryPanel. Pubmed_RVAbstrac tPlus>van

>Garderen-Hoetmer A.

>

>TNO Nutrition and Food Research Institute, AJ, Zeist, The Netherlands.

>

>Systemic alkalosis has been postulated to enhance tumorigenesis,

>whereas systemic acidosis has been implicated to exert a favourable

>influence on tumour control and regression. In the present study the

>urinary pH was influenced by feeding acid-forming or base-forming

>diets, and the effect of alkaline or acid urine on the early and late

>progression phase of urinary bladder carcinogenicity was investigated

>in male Wistar rats. Bladder lesions were initiated by

>N-butyl-N-(4- hydroxybutyl) nitrosamine (0.05% BBN in the drinking

>water during 4 weeks) and promoted by sodium bicarbonate (3.4% NaHCO3

>in the diet during 15 or 25 weeks). After short- (15 week) and more

>long-term (25 week) promotion with NaHCO3, groups of 20 rats were fed

>a diet containing the acidifying salt ammonium chloride (2.1% NH4Cl)

>or the control diet. All surviving rats were killed after a total

>study duration of 52 weeks. Additional control groups were, after

>initiation, fed diets containing NaHCO3 and killed after 15 wk or 25

>wk of promotion, or at the end of the study. In rats fed diets with

>added salts, water intake and the amount of urine produced were

>increased and the urinary density was decreased compared to rats fed

>control diet. During NaHCO3 feeding, urinary pH and sodium

>concentration were increased. During NH4Cl feeding, urinary pH was

>decreased and urinary chloride and calcium concentrations were

>increased. Initiation by BBN followed by treatment with NaHCO3 caused

>a high incidence of papillary/nodular hyperplasia, papillomas and

>carcinomas of the bladder epithelium. These lesions progressed with

>time or longer duration of NaHCO3 promotion. A tumour protective

>effect of urinary acidification by NH4Cl was not found. In fact, both

>acidification and prolonged alkalinization tended to aggravate the

>malignancy of bladder carcinomas.

>

>PMID: 10654592 [PubMed - indexed for MEDLINE]

>------------ --------- --------- -------

March 30, 2008

,

I think you know Dr.Simoncini himself a qualified oncologist and has 20 years

of experience with NaHCO3 on cancer patients.He is in the mainstream oncology

stream but different and open to new and out of the box approaches..If you think

all remedies in cancer should fall within 'the controlled fence'of the major

drug co.,and institutes then you are wrong.Dr.Simoncine did approach many cancer

centers and institutes to try his protocol but he was ignored.Just imagine one

Simoncini to fight and prove the worth of his therapy against billion dollor

industry.It is highly impossible unless people like you and me encourage to look

real into the matter before discarding blindly.I made you to understand how

DIRECT CONTACT with NaHCO3 is the key here.Just posting some articles to

disprove his theory doesn't hide the truth..Mind you,you need to seperate study

with his protocol to validate and not some unrelated scientific papers that has

no relevance.The study

with Dr.Simoncini would be supressed straight for there is threat to big cancer

industry.Also,Dr.Simoncini is not a out of the mainstream doctor.He is an

oncologist.Unless you do clinical trails using Dr.Simoncini protocol which is

impossible in this century atleast,all clinical research publications that has

no relevance to Dr.Simoncini protocol makes no sense.So try to get into his

basic psysiochemical reactions with reference to pathological

implications.Simply borrowing some unrelated article to disprove his theory is

not professional but otherwise.This is just begining.Statistics and other data

automatically follow.So Dr.Simoncini is a new hope for cancer patients.I hope

you got it now.

Rahul

March 30, 2008

What does this suggest about the Gerson diet,

which is profoundly alkaline?

VGammill wrote:

> List, The following abstracts speak to the probable inadvisability

> of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

> animal models as a tumor promoter. Table salt (NaCl) can be equally

> troubling.

>

----------[snip]

March 30, 2008

Indeed. That one extreme is bad doesn't mean that another extreme will be good.

>

> List, The following abstracts speak to the probable inadvisability

> of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

> animal models as a tumor promoter. Table salt (NaCl) can be equally

troubling.

>

> ----------------------------------------------

> Food Chem Toxicol. 1999 Dec;37(12):1159-66.

>

> Effect of urinary pH on the progression of urinary bladder tumours.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Lina%20BA\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Di\

scoveryPanel.Pubmed_RVAbstractPlus>Lina

> BA,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22van%20Gar\

deren-Hoetmer%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Resul\

tsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>van

> Garderen-Hoetmer A.

>

> TNO Nutrition and Food Research Institute, AJ, Zeist, The Netherlands.

>

> Systemic alkalosis has been postulated to enhance tumorigenesis,

> whereas systemic acidosis has been implicated to exert a favourable

> influence on tumour control and regression. In the present study the

> urinary pH was influenced by feeding acid-forming or base-forming

> diets, and the effect of alkaline or acid urine on the early and late

> progression phase of urinary bladder carcinogenicity was investigated

> in male Wistar rats. Bladder lesions were initiated by

> N-butyl-N-(4-hydroxybutyl) nitrosamine (0.05% BBN in the drinking

> water during 4 weeks) and promoted by sodium bicarbonate (3.4% NaHCO3

> in the diet during 15 or 25 weeks). After short- (15 week) and more

> long-term (25 week) promotion with NaHCO3, groups of 20 rats were fed

> a diet containing the acidifying salt ammonium chloride (2.1% NH4Cl)

> or the control diet. All surviving rats were killed after a total

> study duration of 52 weeks. Additional control groups were, after

> initiation, fed diets containing NaHCO3 and killed after 15 wk or 25

> wk of promotion, or at the end of the study. In rats fed diets with

> added salts, water intake and the amount of urine produced were

> increased and the urinary density was decreased compared to rats fed

> control diet. During NaHCO3 feeding, urinary pH and sodium

> concentration were increased. During NH4Cl feeding, urinary pH was

> decreased and urinary chloride and calcium concentrations were

> increased. Initiation by BBN followed by treatment with NaHCO3 caused

> a high incidence of papillary/nodular hyperplasia, papillomas and

> carcinomas of the bladder epithelium. These lesions progressed with

> time or longer duration of NaHCO3 promotion. A tumour protective

> effect of urinary acidification by NH4Cl was not found. In fact, both

> acidification and prolonged alkalinization tended to aggravate the

> malignancy of bladder carcinomas.

>

> PMID: 10654592 [PubMed - indexed for MEDLINE]

> -------------------------------------

>

> Food Chem Toxicol. 2004 Jan;42(1):135-53.

>

> Toxicity and carcinogenicity of acidogenic or alkalogenic diets in

> rats; effects of feeding NH(4)Cl, KHCO(3) or KCl.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Lina%20BA\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Di\

scoveryPanel.Pubmed_RVAbstractPlus>Lina

> BA,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Kuijpers%\

20MH%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Kuijpers

> MH.

>

> TNO Nutrition and Food Research, PO Box 360, 3700 AJ The, Zeist,

> Netherlands. lina@...

>

> The effects of diet-induced acid-base disturbances were examined in

> 4-week, 13-week and 18-month toxicity studies, and in a 30-month

> carcinogenicity study. Rats were fed a natural ingredient diet

> (controls), supplemented with 2% or 4% KHCO(3) (base-forming diets),

> or with 1% or 2.1% NH(4)Cl (acid-forming diets). Additional controls

> were fed 3% KCl (neutral diet providing K(+) and Cl(-) in amounts

> equimolar to those in the 4% KHCO(3) diet and the 2.1% NH(4)Cl diet,

> respectively). NH(4)Cl induced the expected metabolic acidosis, as

> shown by decreased base excess in blood, decreased urinary pH and

> increased urinary net acid excretion. KHCO(3) induced the opposite

> effects. KCl did not affect the acid-base balance. Clinical condition

> and death rate were not affected. The feeding of high levels of each

> salt resulted in growth retardation and increased water intake and

> urinary volume. Plasma potassium and urinary potassium excretion were

> increased with KHCO(3) and KCl. Plasma chloride was increased with

> NH(4)Cl, but not with KCl. Urinary calcium and phosphate excretion

> were increased with NH(4)Cl, but there were no indications that bone

> minerals were involved (weight, calcium content and fat free solid of

> the femur were not affected). Standard haematological and clinical

> chemistry parameters were not affected. Kidney weights were increased

> with 2.1% NH(4)Cl. Hypertrophy of the adrenal zona glomerulosa

> occurred with KHCO(3), KCl and NH(4)Cl, due to chronic stimulation of

> the adrenal cortex by either K(+) or by NH(4)Cl-induced acidosis. An

> early onset (from week 13) of oncocytic tubules was noted in the

> kidneys of rats fed KHCO(3) and, after 30 months, the incidence of

> this lesion was much higher than the background incidence in ageing

> controls. No progression to oncocytomas was noted. KCl showed only

> slight effects on the early onset of oncocytic tubules (from 18

> months). In contrast, the severity of nephrosis and the incidence of

> oncocytic tubules were decreased with 2.1% NH(4)Cl, suggesting a

> protective effect of acidosis. The feeding of KHCO(3) resulted in

> hyperplasia, papillomas and carcinomas of the urinary bladder. With

> KCl only a slight increase in proliferative urothelial lesions was

> noted. Apart from these (pre-)neoplastic lesions in the urinary

> bladder there were no treatment-related differences in tumour

> response among the groups. We concluded that most of the observed

> changes represent physiological adaptations to the feeding of acid-

> or base-forming salts. Remarkable effects noted with KHCO(3), and to

> a far lesser extent with KCl, consisted of renal oncocytic tubules

> and (pre-)neoplastic lesions of the urinary bladder epithelium.

> NH(4)Cl-induced chronic metabolic acidosis was not associated with

> dissolution of alkaline bone salts in rats. Finally, a protective

> effect of chronic acidosis on tumour development was not found.

>

> PMID: 14630137 [PubMed - indexed for MEDLINE]

> ----------------------------------

> Eur J Nutr. 2001 Oct;40(5):200-13.

>

> Diet, evolution and aging--the pathophysiologic effects of the

> post-agricultural inversion of the potassium-to-sodium and

> base-to-chloride ratios in the human diet.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Frassetto\

%20L%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Frassetto

> L,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20\

RC%20Jr%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu\

bmed_DiscoveryPanel.Pubmed_RVAbstractPlus>

> RC Jr,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Sellmeyer\

%20DE%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_DiscoveryPanel.Pubmed_RVAbstractPlus>Sellmeyer

> DE,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Todd%20K%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Dis\

coveryPanel.Pubmed_RVAbstractPlus>Todd

> K,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Sebastian\

%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Sebastian

> A.

>

> University of California, San Francisco 94143, USA.

>

> Theoretically, we humans should be better adapted physiologically to

> the diet our ancestors were exposed to during millions of years of

> hominid evolution than to the diet we have been eating since the

> agricultural revolution a mere 10,000 years ago, and since

> industrialization only 200 years ago. Among the many health problems

> resulting from this mismatch between our genetically determined

> nutritional requirements and our current diet, some might be a

> consequence in part of the deficiency of potassium alkali salts

> (K-base), which are amply present in the plant foods that our

> ancestors ate in abundance, and the exchange of those salts for

> sodium chloride (NaCl), which has been incorporated copiously into

> the contemporary diet, which at the same time is meager in

> K-base-rich plant foods. Deficiency of K-base in the diet increases

> the net systemic acid load imposed by the diet. We know that

> clinically-recognized chronic metabolic acidosis has deleterious

> effects on the body, including growth retardation in children,

> decreased muscle and bone mass in adults, and kidney stone formation,

> and that correction of acidosis can ameliorate those conditions. Is

> it possible that a lifetime of eating diets that deliver

> evolutionarily superphysiologic loads of acid to the body contribute

> to the decrease in bone and muscle mass, and growth hormone

> secretion, which occur normally with age? That is, are contemporary

> humans suffering from the consequences of chronic, diet-induced

> low-grade systemic metabolic acidosis? Our group has shown that

> contemporary net acid-producing diets do indeed characteristically

> produce a low-grade systemic metabolic acidosis in otherwise healthy

> adult subjects, and that the degree of acidosis increases with age,

> in relation to the normally occurring age-related decline in renal

> functional capacity. We also found that neutralization of the diet

> net acid load with dietary supplements of potassium bicarbonate

> (KHCO3) improved calcium and phosphorus balances, reduced bone

> resorption rates, improved nitrogen balance, and mitigated the

> normally occurring age-related decline in growth hormone

> secretion--all without restricting dietary NaCl. Moreover, we found

> that co-administration of an alkalinizing salt of potassium

> (potassium citrate) with NaCl prevented NaCl from increasing urinary

> calcium excretion and bone resorption, as occurred with NaCl

> administration alone. Earlier studies estimated dietary acid load

> from the amount of animal protein in the diet, inasmuch as protein

> metabolism yields sulfuric acid as an end-product. In cross-cultural

> epidemiologic studies, Abelow found that hip fracture incidence in

> older women correlated with animal protein intake, and they suggested

> a causal relation to the acid load from protein. Those studies did

> not consider the effect of potential sources of base in the diet. We

> considered that estimating the net acid load of the diet (i. e., acid

> minus base) would require considering also the intake of plant foods,

> many of which are rich sources of K-base, or more precisely base

> precursors, substances like organic anions that the body metabolizes

> to bicarbonate. In following up the findings of Abelow et al., we

> found that plant food intake tended to be protective against hip

> fracture, and that hip fracture incidence among countries correlated

> inversely with the ratio of plant-to-animal food intake. These

> findings were confirmed in a more homogeneous population of white

> elderly women residents of the U.S. These findings support

> affirmative answers to the questions we asked above. Can we provide

> dietary guidelines for controlling dietary net acid loads to minimize

> or eliminate diet-induced and age-amplified chronic low-grade

> metabolic acidosis and its pathophysiological sequelae. We discuss

> the use of algorithms to predict the diet net acid and provide

> nutritionists and clinicians with relatively simple and reliable

> methods for determining and controlling the net acid load of the

> diet. A more difficult question is what level of acidosis is

> acceptable. We argue that any level of acidosis may be unacceptable

> from an evolutionarily perspective, and indeed, that a low-grade

> metabolic alkalosis may be the optimal acid-base state for humans.

>

> PMID: 11842945 [PubMed - indexed for MEDLINE]

> ----------------------------

> Am J Physiol Renal Physiol. 2007 Aug;293(2):F521-5. Epub 2007 May 23.

>

> Dietary sodium chloride intake independently predicts the degree of

> hyperchloremic metabolic acidosis in healthy humans consuming a net

> acid-producing diet.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Frassetto\

%20LA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_DiscoveryPanel.Pubmed_RVAbstractPlus>Frassetto

> LA,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20\

RC%20Jr%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu\

bmed_DiscoveryPanel.Pubmed_RVAbstractPlus>

> RC Jr,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Sebastian\

%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Sebastian

> A.

>

> Dept. of Medicine and General Clinical Research Center, University of

> California, San Francisco, CA 94143, USA. frassett@...

>

> We previously demonstrated that typical American net acid-producing

> diets predict a low-grade metabolic acidosis of severity proportional

> to the diet net acid load as indexed by the steady-state renal net

> acid excretion rate (NAE). We now investigate whether a sodium (Na)

> chloride (Cl) containing diet likewise associates with a low-grade

> metabolic acidosis of severity proportional to the sodium chloride

> content of the diet as indexed by the steady-state Na and Cl

> excretion rates. In the steady-state preintervention periods of our

> previously reported studies comprising 77 healthy subjects, we

> averaged in each subject three to six values of blood hydrogen ion

> concentration ([H], plasma bicarbonate concentration

> ([HCO(3)(-)]p), the partial pressure of carbon dioxide (Pco(2)), the

> urinary excretion rates of Na, Cl, NAE, and renal function as

> measured by creatinine clearance (CrCl), and performed multivariate

> analyses. Dietary Cl strongly correlated positively with dietary Na

> (P < 0.001) and was an independent negative predictor of [HCO(3)(-)]p

> after adjustment for diet net acid load, Pco(2) and CrCl, and

> positive and negative predictors, respectively, of [H]b and

> [HCO(3)(-)]p after adjustment for diet acid load and Pco(2). These

> data provide the first evidence that, in healthy humans, the diet

> loads of NaCl and net acid independently predict systemic acid-base

> status, with increasing degrees of low-grade hyperchloremic metabolic

> acidosis as the loads increase. Assuming a causal relationship, over

> their respective ranges of variation, NaCl has approximately 50-100%

> of the acidosis-producing effect of the diet net acid load.

>

> PMID: 17522265 [PubMed - indexed for MEDLINE]

> -----------------------

> Kidney Int. 1987 Jun;31(6):1356-67.

>

> Dietary NaCl determines severity of potassium depletion-induced

> metabolic alkalosis.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22\

%20RE%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_DiscoveryPanel.Pubmed_RVAbstractPlus>

> RE,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Schambela\

n%20M%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_DiscoveryPanel.Pubmed_RVAbstractPlus>Schambelan

> M,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cogan%20M\

G%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_D\

iscoveryPanel.Pubmed_RVAbstractPlus>Cogan

> MG,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Colman%20\

J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_D\

iscoveryPanel.Pubmed_RVAbstractPlus>Colman

> J,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20\

RC%20Jr%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu\

bmed_DiscoveryPanel.Pubmed_RVAbstractPlus>

> RC Jr,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Sebastian\

%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Sebastian

> A.

>

> It is uncertain whether, in humans, potassium depletion can cause or

> sustain metabolic alkalosis of clinically important degree in the

> absence of coexisting known alkalosis-producing conditions.

> Previously we found, in normal humans ingesting abundant NaCl, that

> dietary K+ depletion alone can induce and sustain a small decrease in

> blood acidity and increase in plasma bicarbonate concentration; we

> hypothesized that more severe alkalosis was prevented by mitigating

> mechanisms initiated by renal retention of dietary NaCl that was

> induced by K+ depletion. To ascertain the acid-base response to

> dietary K+ depletion under conditions in which the availability of

> NaCl for retention is greatly limited, in the present study of six

> normal men we restricted dietary K+ as in the previous study except

> that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl

> Group) instead of high (126 mEq/day, High NaCl Group). Plasma

> acid-base composition and renal net-acid excretion (NAE) did not

> differ significantly between groups during the control period. In the

> steady state of K+ depletion (days 11 to 15 of K+ restriction),

> neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/-

> 0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/-

> 48 mEq) differed significantly between groups. During K+ restriction,

> persisting metabolic alkalosis developed in both groups, which was

> more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0

> mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement

> in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less

> than 0.003. A significantly more severe alkalosis in the Low NaCl

> Group was evident at all degrees of K+ deficiency achieved during the

> course of the 15 days of K+ restriction, and the severity of

> alkalosis in the Low NaCl Group correlated with the degree of K+

> deficiency. During the generation of alkalosis (days 1 to 7 of K+

> restriction), NAE increased in the Low NaCl Group whereas it

> decreased in the High NaCl Group. During the maintenance of alkalosis

> (days 11 to 15), NAE stabilized in both groups after it returned to

> values approximating the control values. In both groups, urine Cl-

> excretion decreased during K+ restriction even though Cl- intake had

> not been changed, with the result that body Cl- content increased

> negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in

> the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)

>

> PMID: 3039234 [PubMed - indexed for MEDLINE]

> -------------------------

> Toxicol Pathol. 1997 May-Jun;25(3):284-90.

>

> Dose-dependent amplification by L-ascorbic acid of NaHCO3 promotion

> of rat urinary bladder carcinogenesis.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Iwata%20H\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Di\

scoveryPanel.Pubmed_RVAbstractPlus>Iwata

> H,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Yamamoto%\

20S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_DiscoveryPanel.Pubmed_RVAbstractPlus>Yamamoto

> S,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Yano%20Y%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Dis\

coveryPanel.Pubmed_RVAbstractPlus>Yano

> Y,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Ohtani%20\

S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_D\

iscoveryPanel.Pubmed_RVAbstractPlus>Ohtani

> S,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Fukushima\

%20S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Fukushima

> S.

>

> First Department of Pathology, Osaka City University Medical School, Japan.

>

> The dose dependence of L-ascorbic acid (AsA) copromotion of urinary

> bladder carcinogenesis with continuous concomitant administration of

> NaHCO3 was investigated. In the first experiment, 83 male F344 rats

> were all given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for

> 4 wk and then divided into 5 groups, which received basal diet

> (Oriental MF) containing AsA at 0, 1, 2, 3.5, or 5% plus 1.5% NaHCO3

> for 32 wk. Relative urinary bladder weights in the 5% AsA group were

> significantly increased as compared to the 0 or 1% group values due

> to the development of tumors. Both the incidence and number of

> microscopic urinary bladder lesions (tumors and preneoplastic

> lesions) showed dose-dependent increases. Furthermore, the sizes of

> the urinary bladder tumors (carcinomas and papillomas) were

> significantly increased with the highest dose,

> 5-bromo-2'-deoxyuridine labeling indices showed slightly increased

> proliferation in preneoplastic lesions of the urinary bladder

> epithelium with 5% AsA treatment. In a separate experiment, scanning

> electron microscopic observation revealed that administration of 5%

> AsA plus 1.5% NaHCO3 for 8 wk, without BBN, altered the urinary

> bladder surface. Elevation of urinary bladder epithelium AsA content,

> as well as urinary AsA, was also noted. Ornithine decarboxylase (ODC)

> activity and ODC messenger RNA levels in urinary bladder epithelium

> of rats treated with 1.5% NaHCO3 plus 5% AsA for 8 wk showed no

> statistically significant differences as compared to the control

> group. The results indicate that AsA amplifies the rat urinary

> bladder carcinogenesis promotion activity of NaHCO3 and that its

> intensity of action depends on the dose, particularly at high dose.

>

> PMID: 9210260 [PubMed - indexed for MEDLINE]

>

> -------------------------------

> Carcinogenesis. 1988 Jul;9(7):1203-6.

>

> The role of urinary pH and sodium ion concentration in the promotion

> stage of two-stage carcinogenesis of the rat urinary bladder.

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Fukushima\

%20S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_DiscoveryPanel.Pubmed_RVAbstractPlus>Fukushima

> S,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Tamano%20\

S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_D\

iscoveryPanel.Pubmed_RVAbstractPlus>Tamano

> S,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Shibata%2\

0MA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_DiscoveryPanel.Pubmed_RVAbstractPlus>Shibata

> MA,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Kurata%20\

Y%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_D\

iscoveryPanel.Pubmed_RVAbstractPlus>Kurata

> Y,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Hirose%20\

M%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_D\

iscoveryPanel.Pubmed_RVAbstractPlus>Hirose

> M,

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Ito%20N%2\

2%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Disc\

overyPanel.Pubmed_RVAbstractPlus>Ito

> N.

>

> First Department of Pathology, Nagoya City University Medical School, Japan.

>

> The promoting activities of NaHCO3 and NaCl in two-stage urinary

> bladder carcinogenesis in rats initiated with

> N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) were investigated. Male

> F344 rats were given 0.05% BBN in their drinking water for 4 weeks

> and then treated with basal diet containing either 3% NaHCO3, 1% NaCl

> or no added chemical for 32 weeks. NaHCO3 significantly increased the

> induction of neoplastic and preneoplastic lesions of the urinary

> bladder, whereas NaCl did not. NaHCO3 produced elevation of urinary

> pH and urinary Na+ concentration. NaCl increased urinary Na+

> concentration without the elevation of urinary pH. In an additional

> experiment, DNA synthesis in the urinary bladder epithelium was

> significantly increased in the groups given 3% NaHCO3, 5% sodium

> L-ascorbate and 1% NaCl. These results confirm that urinary

> components, increase in urinary pH and Na+ concentration play an

> important role in the promotion of urinary bladder carcinogenesis in rats.

>

> PMID: 2838196 [PubMed - indexed for MEDLINE]

>

March 31, 2008

The Gerson Diet is an anti-cancer diet not necessarily because it alkalizes but

because:

1. It is a calory restrictive diet (starves the cancer).

2. It is made mainly of fruits and vegetables (particularly their juices) which:

a: Contain many cancer fighting phytonutrients (fight cancer)

b. Are not energy consuming. They are easily digested, processed and

assimilated (important in chronic diseases)

Gubi

Re: [ ] tumor promotion with sodium bicarbonate

What does this suggest about the Gerson diet,

which is profoundly alkaline?

VGammill wrote:

> List, The following abstracts speak to the probable inadvisability

> of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

> animal models as a tumor promoter. Table salt (NaCl) can be equally

> troubling.

>

----------[snip]

March 31, 2008

No one on the list has addressed the lack of

data in support of Dr. Simoncini's claims. No

one wants to address the basic science as so well

presented by Dr. Simoncini's own Italian

colleagues (below). The abstracts that I have

posted are not intended as a refutation of

Simoncini. They do show that the relationship of

pH and cancer is quite complex.

It is unnecessary for clinicians to understand

the chemistry that would buttress their

claims. It is necessary for them to show their

raw data in an intelligible form -- if they want

the respect of the professional world. This is

all the more important when one's claims run

counter to conventional science and understanding.

I get a terrible feeling of deja vu when looking

at Simoncini's website. We have been here before

with other European MDs who had the absolute best

cure for cancer. Whatever happened to Gonsalvez

and his thioproline cure? to Danopoulos and his

urea cure? Bonous and his whey cure? to DiBello

and his somatostatin cure? to Olivisatos and his

niacin cure? to Hamer and his trauma resolution cure?

What do these physicians have in common with

Simoncini? With their confidence, enthusiasm,

and testimonials they attracted many followers

and defenders, but none of these physicians saw

fit to publish supporting data. Their therapies

would slowly lose their shine and their

sycophants and proteges would drift off to find

new heros. The hangers on would talk darkly of conspiracies.

Simoncini would likely find more professional

favor were he to answer the questions in the

comments below the abstract. List members might

ask themselves why this cure hasn't been heralded

before when alkalosis is such a common

electrolyte disturbance. One would think

that subsequent " spontaneous remissions " would

be de rigeur. Why not just alkalinize by hyperventilating?

At 11:59 AM 3/30/2008, wrote:

>For credentialed professionals the usual and

>credible way to release bona fide information is

>through peer-reviewed articles. There is no

>conspiracy to suppress such information. An example is:

>------

>

><<http://www.sciencedirect.com/science/journal/0304419X>http://www.sciencedirec\

t.com/science/journal/0304419X>

>Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

>Volume 1756, Issue 1, 25 September 2005, Pages 1-24

>

>The role of pH dynamics and the Na+/H+ antiporter

>in the etiopathogenesis and treatment of cancer.

>Two faces of the same coinone single nature

>

>Salvador Harguindey, Gorka Orive, José

>Pedraz, Angelo Paradiso, and Stephan J. Reshkin

>

>aCentro Médico “La Salud”- c) Independencia,

>13-01004 Vitoria, Spain, and Biotechnology

>Institute (BTI), c) San 15-5°, 01005 Vitoria, Spain

>bDepartment of Pharmacy and Pharmaceutical

>Technology, Faculty of Pharmacy, University of

>the Basque Country, c) Paseo de las Universidades, 7-01006 Vitoria, Spain

>cLaboratory of Clinical Experimental Oncology,

>Oncology Institute of Bari, 70126 Bari, Italy

>dDepartment of General and Environmental

>Physiology, University of Bari, 70126 Bari, Italy

>Received 3 March 2004; accepted 30 June 2005. Available online 19 July 2005.

>

>Abstract

>

>Looked at from the genetic point-of-view cancer

>represents a daunting and, frankly, confusing

>multiplicity of diseases (at least 100) that

>require an equally large variety of therapeutic

>strategies and substances designed to treat the

>particular tumor. However, when analyzed

>phenotypically cancer is a relatively uniform

>disease of very conserved ‘hallmark’ behaviors

>across the entire spectrum of tissue and genetic

>differences [D. Hanahan, R.A. Weinberg, Hallmarks

>of cancer, Cell 100 (2000) 57–70]. This suggests

>that cancers do, indeed, share common biochemical

>and physiological characteristics that are

>independent of the varied genetic backgrounds,

>and that there may be a common mechanism

>underlying both the neoplastic

>transformation/progression side and the

>antineoplastic/therapy side of oncology. The

>challenge of modern oncology is to integrate all

>the diverse experimental data to create a

>physiological/metabolic/energetic paradigm that

>can unite our thinking in order to understand how

>both neoplastic progression and therapies

>function. This reductionist view gives the hope

>that, as in chemistry and physics, it will

>possible to identify common underlying driving

>forces that define a tumor and will permit, for

>the first time, the actual calculated

>manipulation of their state. That is, a rational

>therapeutic design. In the present review, we

>present evidence, obtained from a great number of

>studies, for a fundamental, underlying mechanism

>involved in the initiation and evolution of the

>neoplastic process. There is an ever growing body

>of evidence that all the important neoplastic

>phenotypes are driven by an alkalization of the

>transformed cell, a process which seems specific

>for transformed cells since the same

>alkalinization has no effect in cells that have

>not been transformed. Seen in that light,

>different fields of cancer research, from

>etiopathogenesis, cancer cell metabolism and

>neovascularization, to multiple drug resistance

>(MDR), selective apoptosis, modern cancer

>chemotherapy and the spontaneous regression of

>cancer (SRC) all appear to have in common a

>pivotal characteristic, the aberrant regulation

>of hydrogen ion dynamics [s. Harguindey, J.L.

>Pedraz, R. García Cañero, J. Pérez de Diego, E.J.

>Cragoe Jr., Hydrogen ion-dependent oncogenesis

>and parallel new avenues to cancer prevention and

>treatment using a H+-mediated unifying approach:

>pH-related and pH-unrelated mechanisms, Crit.

>Rev. Oncog. 6 (1) (1995) 1–33]. Cancer cells have

>an acid–base disturbance that is completely

>different than observed in normal tissues and

>that increases in correspondence with increasing

>neoplastic state: an interstitial acid

>microenvironment linked to an intracellular alkalosis.

>------ Comment

>Dr. Simoncini chose not to go the route that

>would win the respect of colleagues. When there

>are problems getting important clinical research

>published, the researcher can put all the raw

>data on his/her website or in any number of web

>publications. Any clinician knows how to display

>a matrix of all patients, diagnoses, stage of

>disease, past and current therapies, and

>assessment of results -- complete remissions,

>partial remissions, stabilization of disease, and

>progression of disease. From this we can draw our own conclusions.

>

>Dr. Simoncini's claims seem to go hand in hand

>with his unconventional candida theory of cancer,

>but he provides very little scientific support

>for either. His reporting of wonderful cures

>might be one hundred percent accurate, but why

>did he choose to present his information in the

>same wearying way that is usually selected by scientistic hucksters.

>

>The history of sodium bicarbonate is almost

>identical to the history of hydrogen peroxide and

>other oxygen therapies for cancer. It goes back

>many decades and has many true

>believers. Certainly some people have

>benefited. In any responsible reporting we would

>be told when the treatment can be expected to

>fall on its face. How well does it work on the

>many difficult sarcomas? on low grade

>carcinomas? on the various leukemias and

>lymphomas? on patients with drug resistance? in

>the face of co-morbid conditions? what about

>bone mets? are there ANY cases where the sodium

>bicarbonate promoted cancer growth or cancer metastasis?

>

>The way this therapy is now being presented, all

>cancer patients can now say, " Whoopee! I'm as

>good as cured. I just have to make a pilgrimage

>to Dr. Simoncini -- or at least see a physician

>who has paid for Dr. Simoncini's seminar. "

>

March 31, 2008

Symptoms of alkalosis include irritability and muscle

spasms/weakness/twitching. Gerson therapy is not profoundly alkaline.

At 02:15 PM 3/30/2008, you wrote:

>What does this suggest about the Gerson diet,

>which is profoundly alkaline?

>

>VGammill wrote:

>

> > List, The following abstracts speak to the probable inadvisability

> > of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

> > animal models as a tumor promoter. Table salt (NaCl) can be equally

> > troubling.

> >

March 31, 2008

The human body is quite complex and the theories out there just help us in

understanding but can't answer all questions in the vivo. Experiments in mice

wouldn't justify the results in human beings. When a therapy as simple as NaHCO3

is put forward it is rejected for the simple reason that it would become a home

remedy.

I am trying to explain that the complex machanism of alkalinity and Ph with

NaHcO3 is not the issue here and there may be tons of study on that, and few

intellectuals are unable to catch simple things as cancer in direct collision

with sodium bicarbonate. I would like to know from anyone in the list if any

paper has been done on the results of DIRECT CONTACT OF NAHCO3 with the

malignant tissue. I would appreciate it and not anyone again borrowing and

blowing up with the alkalanity-ph-cancer issues, we are talking about the

fungus-cancer connection here and not ph-cancer connection.

Whether or not hyperventilating should raise alkalanity as a physiological

response makes no sense in cancer pathology. You would die if you hyperventilate

for 24 hours. Controlled alkalosis in cancer patients deaths are not known. An

open mind approach is needed and if results are there about direct contact of

cancer mass with the NaHC03, why doesn't anyone do research on this and come out

with more defined protocol. Sure, fear is the factor here that may blow up big

pharma and the cancer industry. So the solution: Snub the results before it

takes over. Simple!!! Would like to know/Figure it out- Dr.Simoncini approach to

research centers and institutes to carry out trials with his protocols were

turned down.

Simply posting lengthy unrelated confusing papaers just to prove someone is

wrong when results are always there makes no sense. Do some digging, if you find

any research paper about the study of histochemical reactions of cancer tissue

in direct contact with NaHCo3, post it and I would appreciate it rather than

some misdirecting, unrelated documents like

ph-alkalinity-hyperventilation-e.t.c, which has no relevance in Dr.Simoncini

protocol. Yes,I understand bitter truth is hard to assimilate after going

through previous posts on the subject.

Rahul

Mon, 3/31/08, VGammill wrote:

No one on the list has addressed the lack of

data in support of Dr. Simoncini's claims. No

one wants to address the basic science as so well

presented by Dr. Simoncini's own Italian

colleagues (below). The abstracts that I have

posted are not intended as a refutation of

Simoncini. They do show that the relationship of

pH and cancer is quite complex.

It is unnecessary for clinicians to understand

the chemistry that would buttress their

claims. It is necessary for them to show their

raw data in an intelligible form -- if they want

the respect of the professional world. This is

all the more important when one's claims run

counter to conventional science and understanding...........

March 31, 2008

Indeed. If one study says something is, that doesn't mean that it really is.

For the last 15 years I've been reading almost daily that cancer cell can't

survive in an alkaline environment. Has sometning changed or were all those

posts wrong?

rb2717 <robert-blau@...> wrote:

Indeed. That one extreme is bad doesn't mean that another extreme will

be good.

>

> List, The following abstracts speak to the probable inadvisability

> of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in

> animal models as a tumor promoter. Table salt (NaCl) can be equally troubling.