Archive for the 'Ebola or African Strains of TB' Category

QUESTIONING THE ZIKA VIRUS

January 8, 2017

DR. LAWRENCE BROXMEYER, MD

QUESTIONING THE ZIKA.pdf

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

© Under License of Creative Commons Attribution 3.0 License

ABSTRACT

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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  132. The Pan American Health Organization/World Health Organization (PAHO/WHO). Epidemiological Update. Zika virus infection. 16 October 2015. http://www.paho.org/hq/index.php?option=com_docman&task=doc_view&Itemid=&gid=32021&lang=en

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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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

 

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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.

 

REFERENCES

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
8. Livingston-Wheeler V, Addeo EG. The conquest of cancer. CreateSpace Independent Publishing Platform. January 30, 2013. Pp. 288.
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.
10. De Savitsch, et al. The Influence of Orange Juice on Experimental Tuberculosis in Guinea Pigs. National Tuberculosis Association Transactions. Vol. 30 pp. 130-135. 1934.
11. Birkhaug, K.E.. The Role of Vitamin C in the Pathogenesis of Tuberculosis in the Guinea Pig. I to V. Acta Tubeculosis Scandinavica, Vol 12: pp. 89-98, 98-104, 359-372. 1938.
12. Morton, R. Phthisiologia, seu, Exercitationes de phthisi tribus libris comprehensae totumque opus variis historiis illustratum . Latin Edition. EEBO Editions, ProQuest Publishers. (Latin) Paperback – January 3, 2011. 444pp 1689.
13. Andosca JB, Foley JA. Calcium Ribonate and Vitamin C (Nu 240-10) in the Treatment of Tuberculosis Chest.1948;14(1):107-114. p.109.
14. Faulkner J, Taylor F. Vitamin C and Infection: Ann. Int. Med.. 10:1867. 1931.
15. (Baur and Vorwerk. “Beitrag sum Vitamin C Deficit bei Lungentuberculosen.” Beitr. S. Tuberk., 91: 262, 1938)
16. Borsalino, G. “Fragilite Capillare nella Tuberculose Polmonare e le sue Modificazione par azione della vitamin C.” Gior. de clin. Med., 18: 273, 1931.
17. Moore, et al. “Nutrition among Northern Manitoba Indians.” Can. Med. Assoc. J., 54: 223, 1946.
18. Kleimenhagen, P.. Effect of Ascorbic Acid on Experimental Tuberculosis in Guinea Pigs. Zeitschrift fur Vitaminforschung. Vol 11: 209-227. 1941.
19. Steinbach, M. M. and Klein, S.J. Vitamin C in Experimental Tuberculosis in Guinea Pigs. American Review of Tuberculosis. Vol 43: 403-13. 1941.
20. (Boyden, SV, Anderson, ME. Diet and Experimental Tuberculosis in the Guinea Pig. Acta Pathologica et Microbiologica Scandinavia (Kobenhavn). Vol. 39: 107-16. 1956.
21. Getz, 1951). (Getz, HA, Henderson HJ. A Study of the Relation of Nutrition to the Development of Tuberculosis; influence of ascorbic acid and vitamin A. Am Rev Tuberc. 1951 Oct; 64(4):381–393.
22. Charpy, J., and Ascorbic Acid in Very Large Doses Alone or with Vitamin D in Tuberculosis. Bulletin de I’Academie Nationale de Medicine (Paris). Vol. 83:421-3. 1948.
23. Vitorero, JRB, Doyle, J. Treatment of intestinal tuberculosis with vitamin C, Med. Wkly., 2, 636, 1938
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

SEE also: http://preview.tinyurl.com/mowcz2c