Archive for the 'Lawrence Broxmeyer MD' Category

Cancer and the Science of Denial -with Breast Cancer/Long Island Breast Cancer

August 11, 2017

By Dr. Lawrence Broxmeyer MD

Broxmeyer L. Cancer and the Science of Denial. J Tumor Med Prev 2017;1(3):1-26


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Lawrence  Broxmeyer, MD

Submitted: May 24, 2017  Published: July 14, 2017

The word ‘cancer’ is of Latin derivation and means crab. By the turn of the 20th Century organized medicine had come to the conclusion that it was not a matter of whether infectious disease caused cancer, but which one. Then, in 1910, certain American medical powers did a 180-degree rotation –abruptly deciding that cancer was not caused by a microbe. This flew in the face of over two hundred years of research in which a cancer germ had been discovered and rediscovered. Of all the infectious possibilities for cancer, unquestionably the one class of microbes that has been long recognized to most consistently mimic and imitate ‘cancer’ at both clinical and tissue levels were the mycobacteria of the family Actinomycetales of which tuberculosis and leprosy are premier examples. The association of TB with carcinoma was initially described about 200 years ago by Bayle who considered the lung malignancy ‘cavitation cancereuse’ to merely be one of the various types of tuberculosis. Ever since, almost as if in reflex to the obvious –the potential association between TB and subsequent development of cancer has drawn active investigation.

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CWD Tuberculosis Found in Spongiform Disease Formerly Attributed to Prions: Its Implication towards Mad Cow Disease, Scrapie and Alzheimer’s

May 9, 2017


Journal of MPE Molecular Pathological Epidemiology 2017 Vol. 3 No. 3: 3

Lysenko AP PhD,
Broxmeyer L MD,
Vlasenko VV PhD,
Krasochko PA PhD,
Lemish AP and
Krasnikova EL


The TSE’S or transmissible spongiform encephalopathies, include bovine spongiform encephalopathy (also called BSE or “mad cow disease”), Creutzfeldt– Jakob disease (CJD) in humans, and “scrapie” in sheep or goats (caprine spongiform encephalopathy).  They remain a mystery, their cause still hotly debated. Current mad cow diagnosis lies solely in the detection of late appearing “prions”, an acronym for hypothesized, geneless, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. And the only real evidence that prion originator Stanley Prusiner had in his original paper that the disease agent behind “Scrapie” in sheep and goats was devoid of DNA or RNA– was based upon the fact that he couldn’t find any. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed any causative microorganism and Heino Dringer, who did pioneer work on their nature, candidly predicts “it will turn out that the prion concept is wrong.” Roels and Walravens as well as Hartly traced Mad Cow to Mycobacterium bovis. Moreover, epidemiologic maps of the origins and peak incidence of Mad Cow in the UK, suggestively match those of England’s areas of highest bovine tuberculosis, the Southwest. The neurotaxic potential of bovine tuberculosis has for some time been well known. By 1911 Alois Alzheimer called attention to “a characteristic condition of the cortical tissue which Fischer referred to as ‘spongy cortical wasting” in Alzheimer’s disease (AD). But behind AD, Fischer suspected a microbe called Streptothrix which was constantly being mistaken and confused for tuberculosis. Our present investigation of the TSEs clearly shows cell-wall-deficient (CWD) tubercular mycobacteria present, verified by molecular analysis, ELISA, PCR and microscopy to cause spongiform encephalopathy.

Keywords: Prions; Scrapie; The Spongiform Encephalopathies; Alzheimer’s disease; The etiology of Alzheimer’s Disease; Mycobacterium tuberculosis Complex

Received: April 05, 2017; Accepted: April 27, 2017; Published: April 29, 2017



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Killing of Mycobacterium avium and Mycobacterium tuberculosis by a Mycobacteriophage Delivered by a Nonvirulent Mycobacterium: A Model for Phage Therapy of Intracellular Bacterial Pathogens

January 12, 2017
Lawrence Broxmeyer, Danuta Sosnowska, Elizabeth Miltner, Ofelia Chacon, Dirk Wagner, Jeffery McGarvey, Raul G. Barletta, and Luiz E. Bermudez

Killing of Mycobacterium avium and Mycobacterium tuberculosis by a Mycobacteriophage

The Journal of Infectious Diseases


Mycobacterium avium causes disseminated infection in patients with acquired immune deficieny syndrome. Mycobacterium tuberculosis is a pathogen associated with the deaths of millions of people worldwide annually. Effective therapeutic regimens exist that are limited by the emergence of drug resistance and the inability of antibiotics to kill dormant organisms. The present study describes a system using Mycobacterium smegmatis, an avirulent mycobacterium, to deliver the lytic phage TM4 where both M. avium and M. tuberculosis reside within macrophages. These results showed that treatment of M. avium–infected, as well as M. tuberculosis –infected, RAW 264.7 macrophages, with M. smegmatis transiently infected with TM4, resulted in a significant time and titer  dependent reduction in the number of viable intracellular bacilli. In addition, the M. smegmatis vacuole harboring TM4 fuses with the M. avium vacuole in macrophages. These results suggest a potentially novel concept to kill intracellular pathogenic bacteria and warrant future development.

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January 8, 2017



Broxmeyer L. Questioning the Zika
Virus. J Mol Path Epidemol. 2017, 1:1.

© Under License of Creative Commons Attribution 3.0 License


A growing body of health officials in Brazil are doubting that the Zika “virus” is responsible for the rise in birth defects in parts of that country. Zika, along with yellow fever, has been tossed into the family Flaviviruses; the Latin “flavus” meaning yellow. But unlike yellow fever, the vast majority of Zika’s symptoms for the last 70 years have been mild to non-existent. Despite disseminations by the lay and scientific press, there are serious questions whether Zika causes microcephaly at all. If by March, 2016 the Brazilian Ministry of Health reported 2,197 suspected cases of microcephaly, only 11.48% of these were Zika-positive. Zika is widespread throughout Brazil and South and Central America, yet the bulk of microcephaly cases are confined to the costal tip of Northeastern Brazil. Furthermore, despite extensive testing, no known mosquito-borne arbovirus or any other virus has to this point been proven to cause Brazilian microcephaly.

While Zika was being portrayed as “the most alarming health crisis to hit Brazil in decades”, tuberculosis and its related mycobacteria were quietly gaining a stranglehold and building an ecologic niche in the very Northeastern region being hit by epidemic microcephaly. Why was this important? With NE Brazilian microcephaly/Zika we are probably dealing with a mosquito-fueled environmental zoonosis – a disease that can be transmitted from animals to humans – such as primates, and to a lesser extent birds (Mycobacterium avium), and rodents (Mycobacterium microti), all mentioned in the Zika literature. Add to this the penchant of Brazilians to illegally capture and keep mycobacterial-laden wild monkies and exotic birds as pets or for revenue,and  you have a potential zoonotic time-bomb ready to explode once the proper vectors presents themselves. Three mosquito vectors have been steadily populating Northeastern Brazil: namely Culex quinquefasciatus, the Aedes aegypti and the Aedes albopictus – all of which have the capacity to transmit viral-like forms of the mycobacteria associated with HIV and through direct laboratory investigation with microcephaly. Perhaps it is time to rethink what’s really behind Brazilian Microcephaly and other symptomatology from the “Zika” agent.

KEYWORDS: The Zika virus; microcephaly; Aedes aegypti; Flaws in Zika diagnostics; Mycobacterium tuberculosis; Rhesus monkey; Brazil; CWD mycobacteria; Yellow fever; Flaviviruses; Systemic lupus erythmatosus; SLE; Neurtralization tests.

Received: October 07, 2016; Accepted: November 16, 2016; Published January 02, 2017


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Further Evidence for Cancer as a Cell-Wall-Deficient Mycobacterial Disease

December 5, 2016

A.P. Lysenko PhD, L. Broxmeyer MD, V.V. Vlasenko PhD, P.A. Krasochko PhD, A.P.Lemish PhD, and E.A. Krasnikova

Further Evidence for Cancer as a Cell-Wall-Deficient Mycobacterial Disease.pdf

Corresponding author:
Lawrence Broxmeyer, M.D

© Under License of Creative Commons Attribution 3.0 License


Received: October 07, 2016; Accepted: November 03, 2016; Published: November
14, 2016



In 2014, Buehring reported that Bovine Leukemic Virus (BLV), a common oncogenic retrovirus of cattle, was present in some humans, primarily localized to the breast epithelium  ―  the  very  cell  type  from  which  most  breast  malignancies  arise.  By 2015, there appeared data (Buehring, 2015) supporting that as many as 37% of human breast cancer cases could be attributable to BLV exposure. But if recent estimates suggest over 83% of U.S. dairy operations are currently positive for BLV, they also show that approximately 68% are positive for cell-wall-deficient Mycobacterium avium subspecies paratuberculosis (MAP). Although tubercular lung infection has been said to cause 11 times the incidence of lung cancer as normal control subjects, it is its cell-wall-deficient (CWD) forms (also called L-forms) that have recently repeatedly been found through genetic analysis and appropriate stains in such cancer tissue ― suggesting that CWD tuberculosis or atypical tuberculosis “is likely to be involved in the occurrence or development of lung carcinoma”. A similar relationship between tubercular L-forms and the genesis of the very breast cancer addressed in the aforementioned BLV viral trials. This is not a coincidence. L-forms (CWD forms) predominate and are crucial to the survival of mycobacteria in vivo and they have been documented by fluorescence microscopy in all intracellular macrophage-grown M. tuberculosis observed. From its origin, the very concept of the “BLV leukemic virus” has been on shaky, unstable ground. In 1969, veterinarians Janice and Lyle Miller from the University of Wisconsin-Madison spotted C-shaped “virus-like” particles in cattle lymphosarcoma insisting that these were similar to other C-type viruses “regarded as the cause of leukemia in other species.” But by 1978, scientists at Downstate reported atypical mycobacterial forms, including its preferred filterable virus-sized “L” or cell-wall-deficient (CWD) forms in not only leukemia but all other malignancies ― all having, as their common denominator the continuous presence of mycobacterial C-shaped forms.

Tracing back to techniques similar to Miller and Millers original BLV study we found in the very lyophilized antigens present in commercial kits for the diagnosis of BLV (AgBLV), these very same CWD (cell-wall-deficient) mycobacteria and mycobacterial DNA in all BLV samples ― which when introduced into guinea pigs stimulated the same antibody as occurred when mycobacteria-infected internal organ homogenates themselves were injected into other guinea pigs. It is therefore assumed that the Bovine Leukemic Virus (BLV) is being mistaken for viral-like forms of cell-wall-deficient (CWD) atypical tubercular mycobacteria. Since latent tubercular infection, as well as the administration of BCG and tuberculin also results in persistent CWD forms, their possible role in carcinogenesis is also considered.

KEYWORDS: Cancer; Mycobacterium tuberculosis; Bovine Leukemic Virus; BLV; Mycobacteriophages



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9    Miller JM, Miller LD, Olson C, Gillette KG (1969) Virus-like particles in phytohemagglutinin-stimulated lymphocyte cultures with reference to bovine lymphosarcoma. J Natl Cancer Inst 43: 1297-1305

10 Miller JM (1974) Animal model of human disease. Malignant lymphoma. Am J Pathol 75: 417-420.

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12  Alexander-Jackson EA (1954) specific type of microorganism isolated from animal and human cancer: bacteriology of the organism. Growth 18: 37-51.

13  Klieneberger-Nobel E (1949) Origin, development and significance of L-forms in bacterial cultures. J Gen Microbiol 3: 434-442.

14  Mattman LH (2000) Cell wall deficient forms: stealth pathogens. CRC Press.

15  Kashala O, Marlink R, Ilunga M, Diese M, Gormus B, et al. ( 1994) Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. J Infect Dis 169: 296-304.

16  Glover T (1930) The bacteriology of cancer. Canada Lancet Pract 75: 92-111.

17  Mazet G (1941) Etude Bacteriologique sur la Maladie d’ Hodgkin. Montpellier Med pp: 1-6.

18  Livingston V, Allen R (1948) Presence of consistently recurring invasive myco- bacterial forms in tumor cells. Microscop Soc Bull 2: 5-18.

19  Wuerthele-Caspe V (1949) Mycobacterial forms observed in tumors. J Am Med. Womens Assoc 4: 135-141.

20  Alexander-Jackson  E  (1976)  Progenitor  Cryptocides,  The  Specific Pleomorphic Microorganism Isolated From Cancer. J Int Acad Metab 5: 31-39.

21  Alexander-Jackson E (1978) Microscopic and Submicroscopic Phases of P. Cryptocides from Fresh Lymphocytic leukemia. J Int Acad Metab 1: 9-18.

22  Diller I, Diller W (1965) Intracellular acid-fast organisms isolated from malignant tissues. Trans Am Micr Soc 84: 138-148.

23  Diller I, Donnelly A, Fisher M (1967) Isolation of pleomorphic, acid- fast organisms from several strains of mice. Cancer Res 27: 1402-1408.

24 Seibert F, Feldmann F, Davis R, Richmond I (1970) Morphological, biological, and immunological studies on isolates from tumors and leukemic bloods. Ann N Y Acad Sci 174: 690-728.

25  Wang A, Xie J (1998) Infection of mycobacterium tuberculosis in lung cancer. Zhongguo Fei Ai Za Zhi 1: 92-94.

26  Guliang  H,  Tefu  L  (1999)  Mycobacterium  tuberculosis  L-forms. Microb Ecol Health Dis 10: 129-133.

27  Xie J, Anchao W, Xiazhi Z (1999) Isolation of acid fast bacillus L- forms from carcinoma of Lung. Acta Academiae Medicinae Bengbu 24: 145-146.

28 Song LY, Yan WS, Zhao T (2002) Detection of Mycobacterium tuberculosis in lung cancer tissue by indirect in situ nested PCR. Di Yi Jun Yi Da Xue Xue Bao 22: 992-993.

29 Yesong WXQ , Lifa X (2004)   A case report on pneumoconiotu- berculosis complicated with lung cancer and   Mycobacterium tuberculosis- L form infection. Chin J Industrial Med.

30 Zhang  S,  Guang-ling  Z,  Yan-sheng  T  (2009)  Detection  of Mycobacterium tuberculosis L forms infection in tissues of lung carcinoma. Chin J Public Health 25: 1317-1318.

31 Yang B, Tian Y, Cui X, Zhang W, Ma Y et al. Detection of Mycobacterium tuberculosis L-forms and MPB64 in breast cancer tissues The Journal of Practical Medicine. 2013; 29(15) p2552-2555.

32  Sheng TY, Kun CX, Tong H, Guang LH, Wei Z, et al. (2009) Study on the relationship between Mycobacterium tuberculosis L infection and lung cancer. Tumor 29: 1085-1089.

33  Tian Y, Hao T, Cao B, Zhang W, Ma Y, et al. (2015) Clinical End-Points Associated with Mycobacterium tuberculosis and Lung Cancer: Implications into Host- Pathogen Interaction and    Coevolution. Bio Med Research Intern p: 9.

34 Alexander-Jackson E (1970) Ultraviolet spectrogramic microscope studies of Rous sarcoma virus cultured in cell-free medium. Ann N Y Acad Sci 174: 765-781.

35  Van der Maaten M, Miller J (1976) Replication of bovine leukemia virus in monolayer cell cultures. Bibl Haemat 43: 360-362.

36  Lysenko  AP,  Drogun  AG,  Shurinova  (1998)  Studies  of  influence atypical mycobacterial  infection on AGID results with sera of cattle infected BLV (in Russian). Vet. nauka – proizvodstvu 33: 56-54.

37  ShivRaj L, Patil SA, Girdhar A, Sengupta U, Desikan KV, et al. (1988) Antibodies to HIV-1 in sera from patients with mycobacterial infections. Int J Leprosy 56: 546-551.

38 Lysenko AP, Vlasenko AP, Broxmeyer L (2014) Phenomenon of variability of mycobacteria and its use for detection of a tuberculosis infection.

39 Lysenko AP, Vlasenko VV, Broxmeyer L, Lemish AP, Novik TP, et al. (2014) The tuberculin skin test: how safe is safe?  The tuberculins contain unknown forms capable of reverting to cell-wall deficient mycobacteria. Clin Exp Med Sci 2: 55-73.

40  Lysenko AP, Vlasenko VV, Lemish AP (2014) Detection of mycobacteria in tissues by means of the differentiating immunoperoxidase staining. Tuberculos i bolezni legkhih 10: 55-58.

41  Duesberg PH (1987)  Retroviruses  as carcinogens and pathogens: expectations and reality. Cancer Res 47: 1199-220.

42  Demochowski L, Grey CE (1957) Subcellular Structures of Possible Viral Origin in Some Mammalian Tumors. Ann NY Acad Sci : pp 559-615

43 Laemmli UK (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227: 680-685.

44  Dameshek W and Gunz (1965) Leukemia. Am J Med Sci 249: 115.

45 Seibert  FB,  Feldmann  PM,  Davis  RL,  Richmond  IS  (1970) Morphological, Biological, and Immunological Studies on Isolates from Tumors and Leukemic Bloods. Ann NY Acad Sci 174: 690-728.

46 Mankiewicz E (1965) Bacteriophages that lyse mycobacteria and corynebacteria, and show cytopathogenic effect on tissue cultures of renal cells of cercopithecus aethiops: a preliminary communication. Can Med Assoc J 92: 31-33.

47  Seibert FB (1968) Pebbles on the hill of a scientist. St Petersburg Printing Company 1: 162.

48 Dobrindt U, Reidl J (2000) Pathogenicity islands and phage conversion: evolutionary aspects of bacterial pathogenesis. Int J Med Microbiol 290: 519-27.

49 Landman OE, Burchard WK, Angelety LH (1962) Lysogeny and bacteriophage adsorption in stable and reverting L-forms of Salmonella paratyphi B and Escherichia coli. Bacteriol Proc p: 53.

50  Falagas ME, Kouranos VD, Athanassa Z, Kopterides P (2010) Review ―Tuberculosis and malignancy. Q J Med 103: 461-487.

51  Nelson EL, Pickett MJ (1951) The Recovery of L Forms of Brucella and their Relation to Brucella Phage. J Infect Dis 89: 226-32.

52  Kruegar AP, Cohn T, Smith PN, McGuire CD (1948) J Gen Physiol 31: 477-488.

53 Takahashi S (1979) L phase growth of Mycobacteria. 1. Cell wall deficient form of Mycobacteria. Kekkaku 54: 63-70.

54  Broxmeyer L, Sosnowska  D,  Miltner E, Chacón O, Wagner D, et al. (2002) Killing of Mycobacterium avium and Mycobacterium tuberculosis by a mycobacteriophage delivered by a nonvirulent mycobacterium: a model for phage therapy of intracellular bacterial pathogens. J Infect Dis 186: 1155-60.

55 Devadoss PO, Klegerman ME, Groves MJ (1993) Phagocytosis of Mycobacterium bovis BCG organisms by murine S180 sarcoma cells. Cytobios 74: 49-58.

56 Marcova N, Michailova L, Kussovsski V, Jordanova M (2008) Formation of persisting Cell Wall Deficient Forms M. bovis BCG during interaction with peritoneal macrophages in guinea pigs. Electronic J. of Biology 4: 1-10.

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November 20, 2014

 Dr. Lawrence Broxmeyer, MD


The CDC has quietly lowered its “critical temperature” protocols for detecting a fever ‘characteristic’ for Ebola after one health care worker slid by with a low-grade fever ― yet tested Ebola positive ― So……
“We changed to 100.4 after the first nurse presented to hospital with symptoms of disease and her temp was not the 101.5 that Ebola patients usually present when they are having vomiting diarrhea, etcetera,” CDC spokesman Thomas Skinner told the Daily Caller.
Etcetera. Etcetera. What Skinner meant is their Ebola temperature criteria has been changed to a temperature of 100.4ºF or above.
Anyway 100.4° (or above) sounds like a nice round number. So let’s examine it.
On the National Health Service’s website, put up by the UK government, the now magically designated temperature of100.4ºF or above also appears ― but not for Ebola. They are describing temperatures characteristic for tuberculosis. (

And, it might be added, temperatures characteristic for a dozen-and-a-half other illnesses.
So much for the use of temperature as an Ebola criteria.

Subsequently, by October the 20th ― World Health Organization (WHO) claimed Nigeria, which used to have the highest ‘Ebola’ death rate of any country in the world (See: – “Ebola-free” Great, but does that they can say the same about the Ebola-like symptoms originating from the African strains of tuberculosis ― namely Mycobacterium tuberculosis and Mycobacterium africanum ― still raging over there? Will they next proclaim West Africa “Tuberculosis-free?”

Extrapulmonary (outside of the lungs) tuberculosis is the most frequent cause of a prolonged Fever of Unknown Origin (FUO) and has been for a long, long time.1,2
And in patients returning from areas where tuberculosis and malaria are
Common ― such as Africa ― the index of suspicion for these diseases should be elevated.
The current question………………… is it?

1. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, Casademont J. Harrison’s Principles of Internal Medicine. 16th Edition. 2004. McGraw-Hill Professional Publishing. 2680 pp
2. Roth AR, Basello GM. Approach to the adult patient with fever of unknown origin.Am Fam Physician. 2003 Dec 1;68(11):2223-8.

See also:  Ebola & African TB – An Interview With Dr. Lawrence Broxmeyer, MD Part 1  Jeff Rense Dr. Lawrence Broxmeyer, MD 11-6-14
Ebola & African TB – An Interview With Dr. Lawrence Broxmeyer, MD Part 2
Is The Ebola Virus Real? From Dr. Lawrence Broxmeyer, M.D. © U.S. Library of Congress All rights reserved 11-9-14

Vitamin C and Its Unauthorized High-Dose Use for Ebola

November 4, 2014

Dr. Lawrence Broxmeyer, MD


© U.S. Library of Congress. All rights reserved. November 1, 2014



Vitamin C is at present untested and unapproved for treatment of the current Ebola virus outbreak. Yet its mention by many, as in past outbreaks and epidemics, is predictably being brought up. A bleeding tendency in both severe lack of Vitamin C and in Ebola is cited. Vitamin C, in moderation, is essential to our good health ― the key word being moderation. Curiously, in the current atmosphere, many believe that if Vitamin C is working to relieve a patient’s symptoms, then it must be a “virus” that it is working against ― despite repeated assurance in the literature that a “viral-like” illness does not mean a viral-caused illness. Perhaps some Vitamin C history is in order.

In 1976, two-time Nobel laureate Linus Pauling, tempered by his 1971 publication Vitamin C and the Common Cold1, published a similar sounding title ― Vitamin C. the Common Cold, and the Flu.2 And, at the same time, Pauling tossed his hat into the cancer arena by co-authoring a study regarding Vitamin C and cancer. Entitled Supplemental Ascorbate (Vitamin C) in the Supportive Treatment of Cancer, it was written with a medical doctor (Pauling was a PhD) from Scotland named Ewan Cameron.3 In the study 100 “terminal” cancer patients were treated with mega-dose 10-Grams-per-day quantities, divided throughout the day. Their results soon showed that Vitamin C helped with cancer, but not in convincing the medical establishment ― and a swirl of controversy like none he had experienced surrounded Linus Pauling.

The study, performed in Scotland, a country with an extremely high cancer rate reported that while 22% of cancer patients taking these huge doses of Vitamin C survived for more than a year after being labeled terminal ― only 0.4% of similar patients during that same time survived without the Vitamin. On average cancer patients taking the Vitamin C survived 4 times longer ― but in most cases this could be measured in days or months.

Pauling wanted the National Cancer Institute (NCI) to let him repeat the study in the US, but instead the NCI chose scientists at the Mayo Clinic. Results there under E.T. Creagan showed little going for the use of high dose Vitamin C in cancer.4 Pauling immediately objected on the grounds that most of the Mayo patients had received chemo and radiation, which weakened the very immune system needed for Vitamin C to be effective. This led to a repeat trial headed by Creagan’s second-in-command at Mayo, Charles Moertel, whose results led him again5 to denounce the use of megadose Vitamin C in advanced cancer ― even in patients with no prior chemotherapy.

This time Pauling and Cameron bounced back by saying that even this second study fell short as the vitamin was stopped prematurely if there were signs it wasn’t working. (Cameron and Pauling had continued Vitamin C indefinitely throughout their study). Also they criticized the Mayo study regarding the rebound effect that this could lead to and for not taking routine urine tests for Vitamin C prior to beginning the trial to make sure that control patients weren’t taking Vitamin C independent of the study. The controversy continued to swirl.

Actually Linus Pauling’s interest in Vitamin C grew from the research of biochemist Irwin Stone. Stone6 would eventually publish The Healing Factor: “Vitamin C” Against Disease. In the book Stone related that thru a mutation which occurred long ago man could not manufacture Vitamin C in his body.

This was a serious change, since organisms who can’t manufacture ascorbic acid (Vitamin C) were in danger of extinction. Stone placed this mutation as having occurred 55 to 65 million years ago.Ibid Scurvy, the disease resulting from too little Vitamin C could and would result.



Vitamin C

Stone’s popular book “The Healing Factor: Vitamin C Against Disease” – with a Forward from Linus Pauling, who Irwin Stone Inspired To Go On To do Vitamin C Research. Stone’s Cover Caption rightfully begins with: “Vitamin C may save your life!”



Daily Vitamin C – Necessary in Every Way


Stone captured that lack of Vitamin C could present as everything from a mild “not feeling right” to much, much more serious events called acute scurvy. The latter began with change of complexion (pale or muddy), loss of accustomed vigor, quick tiring, breathlessness and a desire for sleep, but progressed in severity to fleeting limb and joint pains, sore and bleeding gums, and small reddish spots (representing hemorrhaging), especially on leg hair follicles progressing at times to nosebleeds and blood in the urine. As the disease called scurvy advanced, teeth become loose and bones become so brittle that they could be broken by merely moving in bed. The body’s joints in the end became so damaged that the noise from the bones grinding upon on another could actually be heard as a rattling noise ― and death came by either sudden collapse on mild exertion or from secondary infection such as pneumonia.Ibid



Scurvy, a disease of significant Vitamin C deficiency becomes rapidly noticeable. Among its signs and symptoms are weakness, anemia, bruising, bleeding gums and loose teeth.

Scurvy, a disease of significant Vitamin C deficiency becomes rapidly noticeable. Among its signs and symptoms are weakness, anemia, bruising, bleeding gums and loose teeth.



For millennia, Stone said, man has suffered from lack of Vitamin C, and when the Hungarian Szent-Györgyi isolated it at Cambridge in 1928 and proved his findings in 1931, others were free to derive its chemical structure and produce it synthetically. Albert Szent-Györgyi came away with a Nobel Prize ― in research that began about as unexpectedly as Fleming’s find of penicillin.7




Chemical Formula of Vitamin C. Thanks to Szent-Gyorgyi, this Compound was Isolated and Could be Mass Produced.

Chemical Formula of Vitamin C. Thanks to Szent-Gyorgyi, this Compound was Isolated and Could be Mass Produced.



In The Healing Factor, Stone underscored that Vitamin C cannot adequately be stored. Therefore man needed to constantly replenish it through foods rich in Vitamin C. He felt the daily Vitamin C (ascorbic acid) recommended by the National Research Council of 60 mg. daily was woefully inadequate ― citing many scientists and doctors who agreed with him. Szent-Gyorgyi was among them, feeling that “the daily dosage of ascorbic acid should be much higher.”

By 1969, Stone had documented laboratory tests conducted at the National Cancer Institute which showed that ascorbic acid was lethal to certain cancer cells and harmless to normal tissue. This was all being carefully monitored by Dr. Virginia Livingston’s group at Rutgers’s ― which was at the time pulling in sizable grants from major corporations in her quest to prove that cancer was from a tubercular-like cancer germ, which stained acid-fast (as opposed to other microbes) and appeared routinely as the cause of cancer in both her laboratory animals and biopsied human tissue specimens.8

But after the discovery and isolation of Vitamin C in 1928, and the establishment of its underlying relationship to scurvy, the declining incidence of this disease has led to complacency, scurvy being thought of as a well-nigh extinct disease. All of this has resulted in failure to recognize and treat subclinical forms of this disease and its complicated relationship to other disease. Scurvy and its bleeding tendencies were caused by lack of Vitamin C of course. Why go further?



A Germ With “Particular Sensitivity” to Destruction Through Vitamin C


But actually the antiseptic and bacterial qualities of ascorbic acid have long been known and mycobacteria such as TB are heavily influenced by them. Moreover there began to appear laboratory proof that TB itself depleted Vitamin C levels badly and could in itself cause subclinical scurvy. According to Stone:
“The bacteria causing tuberculosis (Mycobacteria tuberculosis) is particularly sensitive to the lethal action of ascorbic acid”.Op.cit.

Two decades before its discovery and isolation, said Stone, ascorbic acid’s effect on mycobacteria such as tuberculosis began to seep into the literature empirically. As early as 1933, McConkey and Smith9 took guinea pigs fed tuberculous sputum daily and split them into two groups. The first group was subjected to a Vitamin C deficient diet, while the second group, fed two teaspoonfuls of Vitamin C rich tomato juice, completed the study. McConkey’s idea came from his clinical observation that patients hospitalized with the intestinal form of the tubercular disease, some of which were hemorrhaging, improved when tomato juice was added to their menu. In the Vitamin C deficient cohort group 26 of the animals died from intestinal ulcerations, while only 2 succumbed while taking tomato juice ― despite the small amounts (2mg) daily. This is what Stone meant when he said that TB was “particularly sensitive” to the lethal action of ascorbic acid.

McConkey’s work was confirmed by de Savitch10 ― with orange juice as the Vitamin’s source (deSavitsch et al.1934) and Birkhaug in 193811 ― both studies using what Stone felt were woefully inadequate amounts of C. Birkhaug was on to something quite important. Not only did Vitamin C protect against “the initial invasive onslaught of”Ibid progressive tubercular disease ― but the disease itself was depleting Vitamin C levels in the body.

Actually, such linkage of TB to scurvy, historically, was nothing new. No later than in 1689 did Richard Morton, one of the earliest writers on scurvy, mention in Phthisiologia, a book which gained him almost a century of fame, say:
“Scurvy is wont [accustomed] to occasion a consumption [tuberculosis] of the lungs.”12

Birkhagh though, was essentially saying that tubercular disease caused subclinical scurvy, mentioning:
“Our study has shown that by compensating for the inevitable state of hypovitaminosis [too little] C which occurs in progressive tuberculosis, we render the animal organism more resistant against the inflammatory-necrotizing effect of tuberculosis and the initial invasive onslaught of virulent tubercle bacilli.” (Birkhaug, 1938). But what Birkhaug was not picking up, according to Erwin Stone, was that that Vitamin C was drop-dead lethal to tuberculosis.

Like Birkhaugh, Andosca and Foley13 realized that tuberculosis itself created Vitamin C deficiency. Andosca: “Most authors maintain that there is a deficiency of vitamin C in tuberculous patients.” Faulkner and Taylor14, for example, disclosed an increased demand for Vitamin C with infection. Patients with tuberculosis required more than 200 mg. of ascorbic acid a day to keep the plasma level normal.

Subclinical Scurvy from TB

Bauer and Vorwerk15 found vitamin C deficiencies of from 1 to 4 grams in the tubercular, finding a direct parallel between the activity of tuberculosis and the extent of vitamin C deficiency. Borsalino16 reported a study of 140 tuberculosis patients, in which administration of vitamin C rapidly increased capillary resistance and stopped hemoptysis ― the spitting up of blood or blood-tinged sputum. However such blood loss reappeared when treatment was discontinued. By 1946, in a survey of nutrition among the northern Manitoba Indians, Moore et al17 reported a very high mortality rate from tuberculosis and pneumonia among these Canadian Indians ― which they attributed to a diet extremely low in Vitamin C.

As Irwin Stone pointed out, “There were many more reports in this sickening mass of continued repetition of ineffectual clinical tests where the investigators were correcting a nutritional deficiency instead of using ascorbic acid to actually combat the disease.”ibid In the meantime, the extent of Vitamin C deficiency or hypovitaminosis documented by Birkhaug with mycobacterial disease was soon realized to be equivalent in cancer, still another similarity in the two wasting diseases. (Carneron & Pauling, 1979)

Further positive animal studies that Vitamin C was a potent anti-tubercular were run separately by Kleimenhagen, Steinbach, and Boyden.18,19,20 culminating with Getz’s study21 of over 1000 men which intimated that were there were adequate Vitamin C blood levels ― there was no Mycobacteria tuberculosis. Still, persisted Stone: “The dogma of the vitamin theory kept these clinicians from thinking of ascorbic acid as an antibiotic and using it in the necessary antibiotic dosages.”ibid

That was until Charpy’s 1948 study22, in which a truly massive l5 Grams or 15,000 milligrams a day were given to terminal consumptive patients. These tubercular patients were so gone that one of them died before the study got underway, but the others survived and improved strikingly despite the fact that they seemed in Charpy’s words: “unaware of the enormous tuberculosis lesions they harbored”, a situation apparently again found analogous in studies of Vitamin C and cancer. Charpy does not go into possible toxicity of such high Vitamin C, nor the kidney stones that could result from it. Vitorero and Doyle23, on the other hand, found excellent results in the treatment of intestinal TB merely by injecting 500 to 600 milligrams of ascorbic acid a day initially, which was reduced to 400 milligrams as improvement was shown, and then further reduced to 200 milligrams a day. Vitorero and Doyle were quite positive about the benefits of this treatment in their few cases and recommended its use for intestinal tuberculosis.

Fast Forward to 2013

In her cancer diet, physician Virginia Livingston Op. cit used vitamins which included Vitamin C to combat her modified mycobacterial cancer germ, but not nearly to the extent of the high doses suggested by Pauling and others. But just how well Vitamin C, at the proper concentration killed even drug resistant TB had to wait until 2013.24

In an unexpected discovery, researchers at Albert Einstein College of Medicine determined that Vitamin C, all by itself, killed both TB and drug resistant TB on culture plates. The finding suggested that Vitamin C, added to existing TB drugs could enhance and possibly shorten TB therapy. The study was published in the online journal Nature Communications.

The molecular mechanism by which vitamin C exerted its lethal effect was that Vitamin C induced what is known as a Fenton reaction, causing iron to react with other molecules to create reactive oxygen species (ROS) that kill the TB (Mtb) mycobacteria.

Peculiar and Unique to TB above other microbes, Vitamin C -Through a Fenton reaction - Kills Tuberculosis (Mtb) by Causing Iron (Fe) to Create Reactive Oxygen Species (ROS) - Which Destroy Even Drug Resistant Strains of TB.

Peculiar and Unique to TB above other microbes, Vitamin C -Through a Fenton reaction – Kills Tuberculosis (Mtb) by Causing Iron (Fe) to Create Reactive Oxygen Species (ROS) – Which Destroy Even Drug Resistant Strains of TB.

What Irwin Stone had so long ago said and predicted ― that TB was “particularly sensitive” to Vitamin C ― was now recognized scientific reality.



1. Pauling, Linus. Vitamin C and the Common Cold. Bantam Books. New York. 1971.112pp.
2. Pauling, Linus. Vitamin C, the Common Cold, and the Flu. W.H. Freeman and Company. San Francisco. 1976.230pp
3. Pauling and Cameron, 1976). Pauling, Linus and Cameron, Ewan. Supplemental Ascorbate in the Supportive Treatment of Cancer. Proceedings of the National Academy of Sciences, Vol.73: pp.3685-89. 1976.
4. Creagan ET, Moertel CG et al.Failure of high-dose vitamin C (ascorbic a N Engl J Med1979 Sep 27;301(13):687-90) therapy to benefit patients with advanced cancer. A controlled trial.
5. Moertel CG, Fleming TR, Creagan ET, Rubin J, O’Connell MJ, Ames MM. High-dose vitamin C versus placebo in the treatment of patients with advanced cancer who have had no prior chemotherapy. A randomized double-blind comparison. N Engl. J Med. 1985 Jan 17; 312(3):137-41)
6. Stone, Irwin. The Healing Factor- “Vitamin C” Against Disease. Grosset & Dunlap Publishers. New York. 1972.)
7. Kyle, R. A.; Shampo, M. A. (2000). “Albert Szent-Györgyi–Nobel laureate”. Mayo Clinic proceedings. Mayo Clinic 75 (7): 722
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9. McConkey, M. and D.T. Smith. The Relation of Vitamin C Deficiency to Intestinal Tuberculosis in the Guinea Pig. Journal of Experimental Medicine. Vol.58: pp. 503-12. 1933.
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16. Borsalino, G. “Fragilite Capillare nella Tuberculose Polmonare e le sue Modificazione par azione della vitamin C.” Gior. de clin. Med., 18: 273, 1931.
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24. Vilchèze C, Hartman T, Weinrick B, Jacobs WR Jr. Mycobacterium tuberculosis is extraordinarily sensitive to killing by a vitamin C-induced Fenton reaction. Nat Commun. 2013, May;4:1881. 23 pp.

© U.S. Library of Congress
All rights reserved
November 1, 2014

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