The horrors of polio vaccines

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The horrors of polio vaccines

Postby Firestarter » Tue Sep 12, 2017 4:41 pm

Some of the worst health malpractice stories I’ve read are about polio vaccines.

Member of Bilderberg Melinda Gates, wife of the so-called “richest man in the world”, is a real philanthropist and founded the “Bill and Melinda Gates Foundation”, that is trying to get “wild polio” out of this world.
Apparently it is really bad when (only) several hundreds of children die of “wild polio”, so ten thousands of children in India get paralysed by Non-Polio Acute Flaccid Paralysis (NPAFP), caused by the vaccine: ... aused.html
(archived here:

It isn’t fair to accuse the Gates Foundation alone (and Gates’ PATH and GAVI), because it is a joint effort with the World Health Organization (WHO).
India was declared free of the wild polio virus by the WHO in January 2011 however there has been a huge increase in cases of NPAFP.
In 2004, 12,000 cases of NPAFP were reported which increased to 25,000 in 2005, 40,000 in 2007, 61,000 in 2011, and 53,563 cases by 2012.
Government surveillance data show that India has become the nation with the world’s highest rate of NPAFP incidence. In the 13 months before December 2015, India has reported 53,563 cases of NPAFP at a national rate of 12 per 100,000 children: ... matically/
(archived here:

The best source I’ve found on this black page in history are Neetu Vashisht and Jacob Puliyel of the Department of Pediatrics at St. Stephens Hospital in Delhi.

Neetu Vashisht et al – ”Polio programme: let us declare victory and move on” (2012):
(archived here:
Furthermore, while India has been polio-free for a year, there has been a huge increase in non-polio acute flaccid paralysis (NPAFP). In 2011, there were an extra 47,500 new cases of NPAFP. Clinically indistinguishable from polio paralysis but twice as deadly, the incidence of NPAFP was directly proportional to doses of oral polio received. Though this data was collected within the polio surveillance system, it was not investigated. The principle of primum-non-nocere [First, do no harm] was violated.
The first step in understanding the issue is to clarify what the term eradication implies as distinct from elimination and control of disease.
However in 2005, a fifth of the cases of non-polio AFP in the Indian state of Uttar Pradesh (UP) were followed up after 60 days. 35.2% were found to have residual paralysis and 8.5% had died (making the total of residual paralysis or death - 43.7%) (28). Sathyamala examined data from the following year and showed that children who were identified with non-polio AFP were at more than twice the risk of dying than those with wild polio infection (27).
In 2011, an additional 47,500 children were newly paralysed in the year, over and above the standard 2/100,000 non-polio AFP that is generally accepted as the norm. (32-33).

Neetu Vashisht et al – “Trends in Nonpolio Acute Flaccid Paralysis Incidence in India 2000 to 2013” (2015): ... te-flaccid
(archived here:
Although the incidence of polio acute flaccid paralysis (AFP) has decreased in India, the nonpolio AFP (NPAFP) rate has increased. Nationwide, the NPAFP rate is 11.82 per 100,000 population, whereas the expected rate is 1 to 2 per 100,000 population. We examined the correlates of NPAFP to discern explanations for the increase. The incidence of polio AFP in India has decreased. However, the nonpolio AFP rate has increased since 2000.
Results: NPAFP increased with the number of OPV doses used. (R2=25.02%; P<0.001). When effect of cumulative doses over the previous years was examined, the non-polio AFP rate in 2013 best correlated to the cumulative doses received in the previous 7 years (R2=57.16%), excluding 2012 as data for this year was incomplete. This correlation was highly significant (P<0.001).

The following graph shows that the correlation between number of NPAFP cases and Cumulative amount of Oral Polio Vaccines

This wasn’t the first time that vaccination campaigns with polio caused controversy.
Kihura Nkuba was told by a preacher that when the WHO and UNICEF introduced the National Immunization Days in 1997, most of the children died after vaccination. After Nkuba discussed the adverse effects of Oral Polio Vaccination (OPV) on his radio shows, revolts broke out in the streets. Then the army was used to vaccinate children with polio.
In 1977, the month following polio vaccination, at the main hospital in Mbarara more than 600 children had died.

Nkuba became something of an investigative reporter after being accused of making ill-founded claims. He read that they stopped poisoning children in North America with Sabin OPV in 1996 because, it caused polio. When he was over in the USA, he called the CDC:
I said 'I am living in America and I want to go to Uganda, and my children have not received oral polio vaccination. And they said 'No, they can't receive oral polio vaccination in this country.' I said 'Why not ?' and they said 'Well, you can get polio from oral polio vaccination.' And I said 'Is this the Centers for Disease Control ?' and they said 'Yes'. 'Are you sure you are not the Centers for Disease Uncontrol ?' They said 'No, we are the Centers for Disease Control - the real McCoy.' So I said 'What if I have a history of HIV and I receive oral polio ?' They said 'That would be really pretty dangerous. It could be a death sentence.' (And I said) can I have your name ?' 'No, you can't have my name. You can have a reference number.' I said 'O.K.' but I recorded this, and when I went back I played it on radio.

Growing up in Uganda, Nkuba never saw any cases of polio. Until he was 25, when he went to the cities where polio vaccination had taken place.
In Africa polio doesn’t kill anybody and is very rare to catch, and even rarer to get paralysed by polio. Every 5 seconds a child is dying of malaria in Africa. Why doesn’t Africa get life-saving anti-malaria treatment?
Nkuba reported he had a terrible car crash, when two pick-up trucks forced him off the road:
(archived here:

The horrors of polio vaccination continue. Even the WHO has admitted a recent vaccine-derived poliovirus type 2 (cVDPV2) outbreak in Syria.
Ironically there wasn’t a single Wild Polio Virus type 1 (WPV1) case reported in Syria since 21 January 2014 (according to the WHO this proves how great these vaccines are…).
A total of 58 Acute Flaccid Paralysis (AFP) cases have been reported in Syria this year until 6 June 2017. 11 of these have tested negative for polioviruses.
Syria switched from trivalent Oral Polio Vaccine (tOPV) to bipalent Oral Polio Vaccine (bOPV) for routine immunization on 1 May 2016.
Ironically, according to the WHO these polio cases show that it’s “critical to achieve the highest possible coverage during the vaccination response”: ... public/en/
(archived here:
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Re: The horrors of polio vaccines

Postby Firestarter » Wed Sep 13, 2017 4:14 pm

I’m beginning to think that the polio and AIDS “epidemics” are more similar than most people think.
From the data I’ve read it looks like either: 1) pesticides is a cause of immune deficiency which makes that people aren’t able to cope with the polio virus anymore, 2) pesticides causes polio like symptoms including paralysis.

Labelling paralysis first as “polio” and then – after introduction of the vaccine – as “Acute Flaccid Paralysis”. The following graph shows that the number of paralysis cases hasn’t only risen in India, as a result of the massive polio vaccination campaign, but also in the rest of the world, from something like 17,000 in 1996, to 100,000 in 2010. Thanks to the World Health Organisation, UNICEF and the Gates Foundation.

In 1956 the American Medical Association (AMA) instructed each licensed medical doctor that they could no longer classify polio, as vaccines had eradicated polio, or their license to practice would be terminated. Any paralysis was now to be diagnosed as AFP (acute flaccid paralysis) MS, MD, Bell's Palsy, cerebral palsy, ALS (Lou Gehrig's Disease), Guillian-Barre, etc.

In 1942, the epidemic of the first half of the century subsided, and there were fewer than 5,000 cases of polio in the United States. Around 1948, the number of polio cases began to soar. Polio reached a peak in 1949, with nearly 43,000 cases. By 1951 the number had dropped to below 28,000. Following a government-subsidised study of polio vaccine, the number soared to an all-time high of more than 55,000 cases.
Most diagnoses were based upon clinical observation, not sophisticated virological studies. After introduction of the vaccine, the number of polio cases decreased, while the number of meningitis cases increased. Most cases reported as non-paralytic poliomyelitis prior to 1 July 1958 were after that reported as viral or aseptic meningitis.
According to Jonas Salk, the live virus polio vaccine developed by Dr. Albert Sabin was:
the principal if not the sole cause of the 140 vaccine cases reported in the U.S. since 1961. At the present time the risk of acquiring polio from the live virus vaccine is greater than from naturally occurring viruses. ... doubt.html
(archived here:

Since 1940, pesticides were introduced in Europe and North America.
See what looks like correlation between the amount of insecticides and polio cases from 1912 to 1963 in England and Wales.

Mortin S. Biskind was one of the first to see the pesticides as the cause of the polio “epidemic”:
Central nervous system diseases such as polio are actually the physiological and symptomatic manifestations of the ongoing government and industry sponsored inundation of the world's populace with central nervous system poisons.
When the population is exposed to a chemical agent known to produce in animals lesions in the spinal cord resembling those in human polio, and thereafter the latter disease increases sharply in incidence and maintains its epidemic character year after year, is it unreasonable to suspect an etiologic relationship?

Biskind’s views fell into disfavour with the establishment, who favoured that polio was caused by a virus. By October 1955, Biskind’s career was destroyed.
See the correlation between the most used chemicals, DDT, BHC, Arsenic and Lead, and the number of “polio” cases from 1940 to 1970 in the USA.
Image ... olio-wrong
(archived here:
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Re: The horrors of polio vaccines

Postby Firestarter » Fri Sep 15, 2017 4:14 pm

I’ve read some general information on polio; the official story appears to contradict itself.

When most people think about the horrors of polio, they think that it’s some horrible infectious disease that causes paralysis. In reality, according to the official numbers only 0.5% of the infected suffer from paralysis. Polio can be classed in 4 severities:
1 – In more than 90% of the cases, the polio infection causes antibodies to develop, without symptoms, and the person doesn't even know that infection occurred.
2 - The majority of the remaining less than 10%, suffer some flu-like symptoms: fever, digestive upset and possibly a cough. This infection has no lasting effects, except immunity.
3 – For a small percentage, polio reaches its “second stage, and reaches the Central Nervous System (CNS), these patients get seriously ill, but don’t suffer any permanent damage.
4 - For about 1 in 200 who are exposed, that polio reaches the CNS and paralyses enough motor neurons that control anywhere from one limb to the whole spinal cord. If the infection reaches motor neurons that are high in the spinal cord or in the brain, death is the likely result.

When you read this, you must conclude that:
1) It’s impossible to know (or even estimate) how many people are infected by polio, as more than 95% doesn’t suffer from a major illness and don’t go to the doctor.
2) Because only a small percentage of the polio patients get paralysed (or even die), it’s almost impossible to know for sure that this was the result of the polio, as it’s impossible to rule out other causes. I can only imagine some horrible experiments, in which this could be determined. Determining that this percentage is 1 in 200 is completely impossible...

Because there’s no way to determine how many people are infected with polio, the number of polio cases is founded on fantasy. Furthermore the number of polio cases doesn’t even matter, as most people that are infected by it, don’t suffer anything grave.
This means that the only reasonable way to estimate how bad the polio “epidemic” is, is by the number of Acute Flaccid Paralysis (AFP) cases. By general consensus the amount of AFP cases has increased enormously.

By general consensus the polio virus had been active for hundreds of years. And until the beginning of the twentieth century never caused any “epidemics” or great calamities.
The first serious polio outbreak happened in 1916, “coincidentally” in New York, with over 27,000 known cases and over 6,000 deaths. By multiplying 6,000 by 200 (in reality according to the official statistrics, I should multiply this by even more...) this means that at least 1,200,000 people were infected with polio. This is completely ridiculous, and in a complete disregard with the “official” statistics, a maximum of 120,000 infected is named.

By general consensus, polio is easier transmitted with poor hygiene, and it is claimed that sanitation level improved in the 20th century (at least in the developed world).
This raises the contradiction that in the hundreds of years before 1916, polio would have been worse...
This means that polio's doesn’t comply with Farr's Law; big pharma invented a unique argument (which almost per definition means it’s bad science). I’ll try to explain this bizarre hypothesis as well as I can.
Supposedly when a baby is born in a “dirty” environment, it gets polio antibodies from its mother (who must have been exposed to polio). Then the baby gets infected within a couple of months after birth, and is still “protected”, and then becomes immune for polio, without anyone noticing that the baby was infected...
With better hygiene, either the mother was never infected (so cannot pass the antibodies to the baby) or the baby doesn’t get infected in the first months (when it still has the antibodies of the mother).

According to this bizarre hypothesis (which is the official explanation), with better hygiene (in particular) the number people infected with polio comes down, which means that this would be the only way to eradicate polio (never mind nutrition, which isn’t part of the agenda of our health care officials). But then because relatively more people get infected, when they don’t have the inherited protection from the mother, the consequences of polio or more grave (including more AFP cases that are caused by polio).
Just by looking at the rising number of paralysis cases, we can see that something is wrong in the state propaganda they want us to believe. It’s more probable of course that paralysis isn’t caused by polio, but by something else (like for example pesticides)...

After Mortind Biskind, in April 1949, published his study on neuropsychiatric manifestations of DDT, he was attacked with blatantly false data.

On 25 April 1955, the polio vaccination program encountered disaster when “faulty” vaccines manufactured by the Cutter Laboratory in California were discovered. The incidence rate was 17 per 100,000 for one month.
In 1958, incidence rates of over 400 per 100,000 per month were found in Detroit with the polio vaccines, which was swept under the carpet.

Alexander Langmuir lobbied Congress, to give the CDC contingent powers to deal with potential emergencies. In July 1951, he assembled the first class of the Epidemic Intelligence Service (EIS). New EIS officers were first assigned for 2 years to hospitals or state and local health departments in the US. Upon completing their field experience, EIS alumni – as agents for the CDC – infiltrated the medical community.
According to British epidemiologist Gordon Stewart, a former CDC consultant, the EIS was nicknamed the "medical CIA”:
(archived here:

In 1928, the German born Henry Kumm joined the Rockefeller Foundation for Medical Research.
In 1951, Kumm resigned from the Rockefeller Foundation to a position as assistant director of research at the National Foundation for Infantile Paralysis. He conducted field trials in the study of gamma globulin and the Salk vaccine and became the Director Of Polio Research at NFIP in 1954.
After his wonderful work on polio, Kumm rejoined the Rockefeller Foundation in 1959:
(archived here:

During 1933-1937, there were a total of 37,463 poliomyelitis cases in total (4,930 deaths).
From 1938-1942 31,993 cases in total (4,165 deaths).
In 1943 12,449 cases (1,115 deaths).
In 1944, 19,029 cases (1,433 deaths).
In 1945, 13,619 cases (1,189 deaths).

Despite the declining cases of polio in the US, in 1946, President Harry S. Truman declared the “War on polio” (where have I heard the “War on ...” before?).
In some sick experiments DDT was sprayed on cities to fight polio. For example on 27 August 1945, a bomber spayed Rockford, IL with DDT and in 1946, a massive amount of DDT was sprayed in San Antonio, TX. The results of these “experiments” were never released.
In a great effort to replicate these wonderful experiments. This month, the area of Houston has been sprayed with pesticides under the guise of fighting an outbreak of the magical Zika virus that was discovered in 1947 and then in 2015 suddenly started causing microcephaly: ... icals.html

In 1946, the number of reported polio cases hit 25,191 — nearly twice the number of 1945.
In 1947, the cases dropped to 10,737 (580 deaths).
In 1948, a huge increase to 27,680 (2,140 deaths).
During 1949-1951, the number of polio cases remained high with a total of 103,719 (an annual average of 34,573).
In 1951, DDT fumigation in the US was at a peak.
In 1952, the number of polio cases peaked at 52,879.
And then began to decline (before polio vaccination was introduced) to 35,592 in 1953, 38,476 in 1954 and 28,985 in 1955: ... -of-polio/
(archived here:

After introduction of the polio vaccine in the USA, the number of polio cases actually increased. Obviously some doctors didn’t understand that they had to report these cases differently after the vaccine had been introduced...
Vermont reported 15 cases of polio during the one-year report before 30 August 1954 (before mass vaccination), compared to 55 cases of polio in the following year (a 266% increase).
Rhode Island reported 22 cases before as compared to 122 cases after vaccination (a 454% increase).
Massachusetts went from 273 to 2027 polio cases (a 642% increase).
In New Hampshire the figures increased from 38 to 129; in Connecticut from 144 to 276;

During the 1950s, doctors and scientists on the staff of the NIH knew that the Salk vaccine caused polio and refused to vaccinate their own children. Some health departments banned the vaccination.
The Idaho State Health Director declared: “I hold the Salk vaccine and its manufacturers responsible” for the polio outbreak that killed several and hospitalized dozens more.
In the mid-1990s, during a period of less than 5 year, 13,641 adverse reactions to the oral polio vaccine were reported:
(archived here:

See the following correspondence “Non-Polio AFP Rate and Polio Eradication” (2008):
(archived here:
India has made great progress towards eradicating polio and has had excellent AFP surveillance. Since 2004 there was rapid increase in the non-polio AFP rate, which reached 8 in 2007 (Table I). The increase in non-polio AFP rate is mainly limited to the two polio hyperendemic states of Uttar Pradesh and Bihar(3).

The “Non-Polio” AFP rate in India went from 1.45 in 1998 to 8.45 in 2007 (an increase of 483% in 10 years).

On the following site the official numbers of AFP cases can be seen from 2000 to 2016, globally the numbers went from: 30,625 in 2000 to 109,807 in 2016 (an increase of 259% in 16 years).
Africa from 5,936 to 31,922 in 2016 (an increase of 438% in 16 years).
East Mediterranean from 3,253 to 11,357 in 2016 (an increase of 249% in 16 years).
South East Asia from 10,758 to 25,790 (an increase of 140% in 16 years).
India from 8,103 in 2000 to 46,579 in 2016 (an increase of 475% in 16 years):

Also see the number of polio cases in the Dominican Republic from 1978 to 1987. When the OPV vaccine was introduced in 1983, there were hardly any cases of polio. Also see the sharp low in number of cases in 1979...
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Re: The horrors of polio vaccines

Postby Firestarter » Sat Sep 16, 2017 4:28 pm

I thought that a limited topic like polio vaccines wasn’t too much information, but it looks like there’s a sheer limitless amount of dirt...

In 1972, in the US DDT was prohibited, but instead they continued to produce “dicofol” (a.k.a. Kelthane), which is really DDT in disguise.
K. Paul Stoller – AD, AFP, ALS, and DDT (2015): ... s/0151.pdf
(archived here:
DDT was/is used in the United States to control insects in crops and livestock and to combat insect-borne diseases. It was introduced as a pesticide during WWII. In the United States, the general use moratorium took place in 1972, but there is another pesticide dicofol, which is made and sold by Dow AgroSciences and carries the trademark KELTHANE® , is in fact DDT. In China dicofol is produced by the Yangzhou Pesticide Factory, which reports production quantities of 4 million pounds of dicofol per year.
This class of insecticide (organochlorine) impacts the electrical activity in the body, so it affects brain and heart, but also there are other organs that use electrical current, including the lungs. It clearly affects the immune system and causes cancer, and the best part is that it doesn’t break down in the environment other than to become DDE (and DDD).
India, which manufactures and uses the most DDT, was declared free of polio in 2011, but cases of AFP have skyrocketed.

Stoller refers to a nice paper describing research by the US Army Medical Research and Development Command (with MIT) that shows that at the 20 and 40 μg levels of DDT, the yield of polio virus per cell was increased 37 and 90%, respectively. It is reasonable to postulate that it could also increase the replication of other viruses.
Also look for Kelthane (that replaced DDT) which increases the yield of the polio virus with a whopping 430%...

J. Gabliks – Studies of Biologically Active Agents in Cells and Tissue Cultures (1967):
(archived here:
insecticidal compounds DDT, chlordane, Kelthane , Dipterex malathion, and Karathane at subtoxic concentrations inhibited vaccinia virus replication in human Chang liver cellq. Under the same experimental conditions, the replication of poliovirus was inhibited only by chlordane and malthion, whereas Kelthane increased the virus yields 4 and 18 times, respectivaly, and DDT exhibited a slight stimulatory effect.
The studies described in the Annual Progress Report of 1965 indicated that human HeLa cells exposed to subtoxic concentrations of the insecticidal compounds, CygonR, DipterexR, DI-SystonR, chlordane and Karathane for 84 days were more susceptible to poliovirus infection than the corresponding control cells (1,2).
As it is recognized that residues of some agricultural insecticides persist in the body and that cells are continuously exposed to their metabolites, we investigated the possibility that these chemicals may alter certain physiological activities of cells and subsequently influence the susceptibility of hosts to virus infections.
The effects of organophosphorus, organochlorine and dinitrophenol insecticidal compounds on the replication of polio and of vaccinia viruses were studied in human Chang liver cells, using purified or analytical grade comnounds obtained from their manufacturers.
In the poliovirus test the cell response was not uniform. In comparison to the controls, the virus yield in the DDT-treated cultures was slightly increased; the yield in the chlordane and malathion cultures was reduced (32 and 18% of the controls); and the yield in the Kelthane and Karathane cultures was greatly increased (430 and 1800% respectively).
The stimulatorv effect by DDT, Kelthane, and Karathane on poliovirus replication suggests a possibility that these compounds may have some specific effects on the mechanisms of viral biosynthesis. This possibility is supported by the results of our previous report which indicated an increased yield of poliovirus in HeLa cells exposed to Karathane for 77 days(2).
Appendix Number 1
Janis Gabliks
To investiqate the effects of insecticidal comuounds on viral virus replication, we tested six insecticidal compounds in human liver cells infected with vaccinia and poliovirus.
In the presence of 20 and 40 μg levels of DDT, poliovirus yield per culture was comparable to that of the control. However, when the yield of infectious virus released is expressed per individual cell or per ig of cell protein, as shown in Figure 3, it is evident that at the 20 and 40 μg levels of DDT, the yield of virus per cell was increased 37 and 90%, respectively. Similarly, the yield per μg of protein was also increased 15 and 47%, respectively
In contrast to the inhibitory action of these two insecticides, the Kelthane-treated cultures produced about four times more virus, and the Karathane-treated cells 18 times more virus than the corresponding controls.
The stimulatory effect by DDT, Kelthane, and Karathane on poliovirus replication suggests a possibility that these compounds may have some specific effects on the mechanisms of viral biosynthesis, and the state of some latent viruses may also be altered. This possibility is supported by the results of our previous report which indicated an increased yield of poliovirus in HeLa cells, chronically exposed to Karathane for 77 days (7,8).

The following study writes about a previous study, where the Oral Polio Vaccine (OPV) raised the death rate in children (only significant for boys). But this couldn’t be repeated in this study.
This study in Guinea-Bissau is the only in its kind. Can anybody think of any reason for why big pharma wouldn’t research that the polio vaccines causes death…
This study could be completely worthless, as it wasn’t single blind (let alone double blind) and there are also admitted effects that there were other ongoing polio vaccination campaigns, for which the data was manipulated (censored); the study doesn’t describe how it was “censored” (I can’t remember that in the course statistics that I followed at university “censoring” was mentioned...).

Najaaraq Lund et al – The Effect of Oral Polio Vaccine at Birth on Infant Mortality: A Randomized Trial (2015): ... t-Birth-on
(archived here: )
Background. Routine vaccines may have nonspecific effects on mortality. An observational study found that OPV given at birth (OPV0) was associated with increased male infant mortality.
A supplementation conducted from 2002 to 2004 in Guinea-Bissau, the country experienced a period with a shortage of OPV; a total of 962 trial participants did not receive the recommended OPV0. Surprisingly, boys who missed OPV0 had significantly lower infant mortality compared with boys who received OPV0 (adjusted mortality rate ratio [MRR], 0.35 [95% confidence interval {CI}, .18–.71]) [24]. The tendency was opposite for girls (adjusted MRR, 1.14 [95% CI, .70–1.89]); thus, the effect of OPV0 differed significantly between boys and girls (P = .006). Receiving OPV0 was also associated with reduced immune responses to BCG in both sexes [25].
Children randomized to OPV received 2 drops of the vaccine orally immediately after randomization. There was no placebo or blinding. Guinea-Bissau does not have a central vaccination registry, so it was important that the vaccination card contained the correct information if a child moved from the HDSS area.
The main outcome was overall mortality (excluding accidents) within the first 12 months of life. In addition, we analyzed the “pure” effect of OPV0 on survival from enrollment to age 6 weeks, before controls were likely to receive the first routine OPV.
Furthermore, the protocol specified that if large campaigns were conducted during follow-up, analyses would also be conducted with censoring for such campaigns. Thus, we analyzed the impact on infant mortality with censoring for subsequent national OPV campaign, as OPV campaigns could potentially neutralize any differential effect of OPV0. During the conduct of the trial, there was also a national MV campaign (December 2009) and an H1N1 vaccine campaign (October 2010), both targeting children aged 6 months to 5 years. In additional analyses, we censored for these campaigns.
Based on previous observations [31], we anticipated an infant mortality rate of 50 per 1000 participants. However, during the study period, infant mortality declined to 26 per 1000 person-years. This reduced the power to detect a difference between groups. An interim report for the DSMB showed significantly higher mortality among children randomized to BCG only. As this was in favor of current policy, the DSMB recommended that the number of participants not be increased to compensate for the lower mortality.
Table 2.
Infant Mortality Rates and Hazard Ratios for Children Randomized to BCG Plus Oral Polio Vaccine at Birth or BCG Only, Guinea-Bissau, 2008–2011
Within censoring for OPV campaigns (mean duration of follow-up = 163 days), 41 died in the BCG + OPV0 group and 60 died in the BCG-only group.
Contrary to our initial hypothesis, both male and female children who received OPV0 with BCG tended to have better survival than those who received BCG only. As in a previous study, receiving OPV0 within the first days of life appeared to be associated with the strongest benefits. Many OPV campaigns occurred during the trial; when censoring for these campaigns, the beneficial effect of receiving OPV0 was borderline significant overall and significant separately in males.
A weakness of our study is that it was not blinded. However, health workers in the area were unaware of the study hypothesis and were unlikely to be influenced when treating the children. The outcome assessment was carried out by assistants unaware of the vaccination allocation. Hence, we do not believe that the lack of blinding affected the results.
In addition, national OPV campaigns could have led to environmental acquisition in children born in the period after a campaign. It is likely that, in a population-dense urban setting, indirect vaccination also occurs in the absence of OPV campaigns, through close contact with newly vaccinated children. This exposure, if anything, would be expected to dilute any differences between children who received OPV0 or no OPV0.
All background factors were evenly distributed between the 2 randomization groups and did not confound the results. OPV0 had the best effect among children enrolled early. Early enrollment could be a proxy for better socioeconomic status, as it is typically the more wealthy mothers who delivered at the maternity ward and were enrolled early.
In 2004 there were several campaigns, and none in 2007, but many during the present trial. Censoring for these campaigns made the results more comparable, as OPV0 tended to be most beneficial before additional OPV was given in campaigns.

Also see the rising numbers in reported AFP cases from 1993 to 1995 in Cambodia, China, Lao PDR, Philippines, in the 6 countries totally from 2674 to 5644 (more than double in 2 years).
Rudolf H. Tangerman et al – Poliomyelitis Eradication in the Western Pacific Region (1997): ... CSM3hhCOWA
(archived here:
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Re: The horrors of polio vaccines

Postby Firestarter » Sun Sep 17, 2017 1:57 pm

Firestarter wrote:The following study writes about a previous study, where the Oral Polio Vaccine (OPV) raised the death rate in children (only significant for boys). But this couldn’t be repeated in this study.

Benn et al – Sex-Differential Effect on Infant Mortality of Oral Polio Vaccine Administered with BCG at Birth in Guinea-Bissau... (2008): ... ne.0004056
(arvchived here:
The effect of OPV at birth on overall child mortality was never studied. During a trial of vitamin A supplementation (VAS) at birth in Guinea-Bissau, OPV was not available during several periods. We took advantage of this “natural experiment” to test the effect on mortality of receiving OPV at birth.
A total of 962 (22.1%) of the 4345 enrolled children did not receive OPV at birth; 179 children died within the first year of life. Missing OPV at birth was associated with a tendency for decreased mortality (adjusted MRR = 0.69 (95% CI = 0.46–1.03)), the effect being similar among recipients of VAS and placebo. There was a highly significant interaction between OPV at birth and sex (p = 0.006). Not receiving OPV at birth was associated with a weak tendency for increased mortality in girls (1.14 (0.70–1.89)) but significantly decreased mortality in boys (0.35 (0.18–0.71)).
Furthermore, we also conducted one study of an OPV campaign; receiving OPV in the campaign compared with not receiving OPV was associated with significantly decreased mortality among the youngest children [9].
A total of 962 children (22.1%) of the 4345 enrolled children did not receive OPV at birth (Appendix S1). There were significant differences between those who did and those who did not receive OPV at birth (Table 1). Not having received OPV at birth was associated with low age at enrolment, no maternal school education, low arm circumference, being enrolled at the Belem Health Centre, and dry season (Table 1).
The cumulative mortality curves for all children and for boys and girls separately, are illustrated in Figures 2A–C. The effect of not receiving OPV at birth on mortality up to 2 months of age (53 deaths) was 0.39 (0.12–1.29) among boys and 1.38 (0.54–3.57) among girls (p = 0.099). However, the effect of not receiving OPV at birth was not limited to the first months of life, but appeared to continue throughout the first year of life.
We studied the effect of missing OPV at birth on the major causes of death: malaria, diarrhoea, respiratory diseases and septicaemia; 58 deaths had other less common causes of death or had no verbal autopsy conducted because the family had moved. Though none of the differences reached statistical significance, the sex-differential effect of OPV at birth was seen for all four major causes of death (Table 3).
Among study children, a total of 366 hospitalisations took place from enrolment to 12 months of age. We found no effect of missing OPV at birth on the risk of hospitalisations within the first year in either sex; the adjusted IRR among boys being 0.84 (0.59–1.20) and 1.05 (0.68–1.63) among girls. The effect of missing OPV at birth on hospital case-fatality also did not differ between boys and girls, the adjusted relative risks being 1.04 (0.45–2.40) and 1.30 (0.55–3.07), respectively.
It strengthens the observation that the effect of not receiving OPV was comparable during the two major independent periods without OPV. Though no significant associations were observed between not receiving OPV at birth and major causes of death, hospitalization or hospital case-fatality, the pattern was the same. For all major causes of death there was lower mortality for boys and higher for girls if they had not received OPV; for both hospitalization and case-fatality there was a 20–25% difference between boys and girls which went in the same direction as the overall result. Hence, the results are compatible with the hypothesis that OPV at birth increases mortality of infant boys. Many factors influence a mother's choice to bring the child to the hospital, and hospitalizations may not be the best proxy for severe disease. The vast majority of children died outside the hospital.
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Re: The horrors of polio vaccines

Postby Firestarter » Thu Sep 21, 2017 4:09 pm

I finally found something positive to post about polio prevention...
Generally speaking you could prevent polio paralysis, by: getting enough vitamin B1 (thiamine), vitamin C, Calcium and cut the intake of sugar.
There is only information on this in “scientific” papers going back to the 1950s or even before. Why would the pharmaceutical industry stop the research into prevention of paralysis by other methods than vaccines that cause more harm than they do good?
It’s not sure however that what worked, also has beneficial effects with all of the pesticides used today, some even worse than DDT.

McCormick’s report from 1938 shows that vitamin B deficiency possibly increases the susceptibility for polio, and that Adrenalin, Cortin and Vitamin C destroy the polio virus. It is a pretty good literature review.
Zingher, in a report on over one thousand cases of poliomyelitis under 5 years of age, found over 80 per cent to be Schick-positive. Baginsky says: "I have been struck with the very extraordinary sensitivity of children suffering with such diseases of the central nervous system as poliomyelitis, spastic cerebrospinal paralysis, hemiplegia, etc. One is scarcely able to keep these children in the hospital wards free from infection with diphtheria." The situation in this respect at the present time may be somewhat altered owing to the general adoption of toxoid immunization.
In a comparative study of poliomyelitis and diphtheria Jungeblut4 reports poliocidal substances occasionally demonstrable in the serum of monkeys actively immunized against diphtheria toxin. He and his associates also found that contact in vitro with adrenalin, cortin and vitamin C is equally destructive for both the toxin of diphtheria and the virus of poliomyelitis.
On the assumption of possible exogenous factors in susceptibility, based on nutritional imbalance, the recent work of Jungeblut and Toomey is of interest. The former, in experimental poliomyelitis in monkeys, has obtained a fair degree of protective effect from vitamin C when administered within a rather definite range of dosage. The latter has demonstrated increased susceptibility when vitamin D is withheld in conjunction with a diet otherwise rich in vitamins. But, strange to say, little or no work of a conclusive nature has been done in this respect with the anti-neuritic vitamin B. With the established anti-paralytic effect of vitamin B in beriberi it would seem that this pioneer in the vitamin field should offer the most hope of protective value in poliomyelitis.
Based on the obvious assumption of a vitamin B deficiency, a radical change in the native dietary was instituted. The sale of white flour and polished rice was forbidden in the native stores, whole-meal flour and brown rice being substituted, and the use of whole wheat bread was encouraged. Sweet potatoes were introduced, and the value of eggs and condensed milk was stressed. The sale of sugar was restricted to 1 lb. per adult per week. The use of the yeast-laden cocoanut-sap beverage was again permitted, and the sick babies were treated with an emulsion of the yeast in cod-liver oil. As a result of these measures the infant death rate rapidly fell from 50 to 7 per cent, at which level it has consistently remained.

JUNGEBLUT (1936 & 1939)
McCormick references an earlier paper by Jungeblut.
I have found 2 of his papers documenting research on the effects of vitamin C in monkeys infected with polio. The results appear to indicate that vitamin C has positive effects in fighting polio.

The limited data which formed the basis of this preliminary report naturally precluded the drawing of any definite conclusions. They seemed to suggest, however, that vitamin C when administered in the proper dose may possess distinct therapeutic properties in experimental poliomyelitis.
4. A summary of the results obtained in all three groups shows: (a) that among a total of 62 treated monkeys, 19 survived without paralysis and 43 succumbed to the disease, while of a total of 38 untreated controls, only 2 failed to develop paralysis and 36 succumbed to the disease; (b) that treatment with large doses of vitamin C was without any beneficial effect (all 10 monkeys which had received 700 to 100 rag. developing paralysis), that the administration of intermediate doses was followed by occasional survival without paralysis of the treated animal (3 monkeys surviving of a total of 19 which had received 50 to 10 rag.), and that nearly one-half of the animals which had received small doses escaped the disease (16 monkeys surviving of a total of 33 which had received 5 rag.).

In the 1939 report, Jungeblut describes a range of experiments with vitamin C and the polio virus, again in monkeys.
Since the very beginning of this investigation it had been realized that the measure of therapeutic success attainable by vitamin C administration depended upon certain variables the operation of which was not clearly understood. Most important among these was the kind and dosage of vitamin C, optimal results being obtained only with optimal doses of natural vitamin C.
It will be seen from Table II that all of the monkeys receiving the vitamin C-virus mixtures remained free from paralytic symptoms while both control monkeys injected with the virus-distilled water mixtures developed complete paralysis on the 7th and 8th day, respectively. This experiment therefore confirms our previous observation that small amounts of vitamin C suffice to inactivate multiple paralytic doses of poliomyelitis virus in vitro.
Somewhat different results were obtained in the three series with a less drastic mode of infection. Not only was the disease produced by the droplet method of instillation much less severe than that induced by the pressure method, but the symptoms became progressively lighter from series to series in both groups of animals, treated and untreated. Undoubtedly, the droplet instillation created conditions under which only minute amounts of virus reached the olfactory area, allowing for a variable number of animals to develop typical paralysis of the extremities while the remainder showed either slight transitory involvement of the central nervous system or escaped paralysis entirely.
TABLE IV Effect of Vitamin C Treatment in Monkeys Infected Intranasally
The results recorded in this paper serve to affirm and extend our previous observations on the effect of crystalline vitamin C on poliomyelitis virus. They clearly show that small amounts of ascorbic acid, either natural or synthetic, are capable of inactivating in vivro multiple paralytic doses of two different strains of this virus. This virucidal action of vitamin C, however, is by no means limited to poliomyelitis virus.
With a less forceful method of droplet instillation, the picture of the disease in control animals becomes so variable that the results cannot be easily interpreted; but the available data suggest that vitamin C treatment may be a factor in converting abortive attacks into an altogether non-paralytic infection. 3. The administration of synthetic vitamin C to monkeys infected intracerebrally with small doses of the RMV strain gives results comparable to those previously obtained with this substance in monkeys infected intracerebrally with the Aycock strain of poliomyelitis virus.

Jungeblut found out that a therapy with vitamin C only works if it’s not too low or too high. Jungeblut also discovered that if the polio virus is given too abundantly, the vitamin C therapy doesn’t work. It’s obvious that in a “normal” situation somebody gets infected with only a limited amount of the polio virus.
Knowing this, the pharmaceutical industry can easily manipulate a “scientific” trial to “prove” that vitamin C is useless for a polio therapy…

KLENNER (1949 & 1951)
Fred R. Klenner was a doctor who experimented with vitamin C treatment for polio and other viral diseases, but unfortunately from a “scientific” point of view his work is worthless.
Here’s one of his papers from 1949, where he claims that vitamin C cured all of his polio patients in a couple of days: ... /polio.htm

Klenner’s paper from 1951 is better. The problem is that Klenner apparently developed a therapy for his patients, but without a control (placebo) group this is “scientifically” worthless: ... 4-p101.htm
It is of more than academic interest to review the findings of McCormick in 50 confirmed cases of poliomyelitis in and around Toronto, Canada, during the epidemic of 1949. This report is that children of families eating brown bread who came down with poliomyelitis did not develop paralysis; whereas in those families eating white bread many of the children having poliomyelitis did develop paralysis. The point here is that brown bread has 28 times more vitamin B1 than does white bread. Obviously, then, the paralysis which complicates acute poliomyelitis appears to be due to a B1 avitaminosis. Vitamin C by removing edema fluid relieves from pressure these vessels that supply nutriment to the horn cells, thus allowing the normal complement of vitamin B1 to reach these cells.
After 96 hours the child was moving both legs. The flexion was slow and deliberate. She was discharged from the hospital at this time, vitamin C being continued by mouth — 1000 mg. every two hours with fruit juice for seven days. On the 11th day of treatment the child was walking about the house, but her gait was slow and her posture was poor, being bent forward. Vitamin C was discontinued and vitamin B1 started — 10 mg. before meals and bed hour. Carbonated drinks were encouraged for their sugar content and mild stimulating action. Nineteen days after starting treatment there was complete return of sensory and motor function which has persisted to this date.
Calcium, in vivo, duplicates the chemical behavior of vitamin C in many respects. Calcium gluconate and calcium lexulinate were used in conjunction with vitamin C therapy in a small series of pulmonary virus infections and in mild cases of influenza.

Jonas Salk is known for creating the first polio vaccine; coincidentally it was the same Salk who was involved in the cover-up of the research of Claus Jungeblut.

On 18 September 1939, Time magazine reported that Jungeblut, showed the correlation between vitamin C deficiency and polio.
Within 2 years after the discovery of vitamin C (a.k.a. ascorbic acid), Jungeblut showed that ascorbic acid could inactivate the polio virus.
In 1936-1937, there was a rapid succession of medical scientists, who showed that vitamin C inactivated a variety of viruses: Holden et al (herpes); Kligler and Bernkopf (vaccina virus); Lagenbusch and Enderling (hoof-and-mouth disease); Amato (rabies); Lominski (bacteriophage); and Lojkin and Martin (tobacco mosaic disease).
Thus, already in the 1930s it was known that vitamin C was potentially a wide-spectrum antiviral agent.
It was none other than Dr. Albert B. Sabin, who in 1939 published a paper that demonstrated that vitamin C had no value in combating polio viruses. His 1939 paper showed that vitamin C had no effect in preventing paralysis in rhesus monkeys infected with polio.
Klenner said that there was a simple reason for Sabin's well-reported failures: the dosage was far too low:
(archived here:

Maybe I will post about the effects of sugar on polio at another time…
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