The Big Zika Lies: Revisiting the Timeline, the Narratives, and the Ignored Science

We provided detailed information on Zika and microcephaly that Hotez and PLOS One thought was "not helpful". As a result, the world still believes the myths of Zika.

In 2015, global media and health authorities declared war on a new public health threat: the Zika virus. Women in Brazil, particularly in the impoverished Northeast, were warned that a bite from a mosquito could lead to devastating birth defects, especially microcephaly. The World Health Organization (WHO) declared a Public Health Emergency of International Concern. The U.S. Centers for Disease Control and Prevention (CDC) issued sweeping advisories. The panic was viral. But the so-called scientific consensus was fragile—built on rhetorical devices, not empirical rigor.

What if Zika wasn’t the cause of Brazil’s microcephaly crisis?

To understand what really happened, we must revisit the timeline, because the facts—as they played out—contradict the official story at nearly every step.

Microcephaly cases began rising in Northeast Brazil well before the first Zika infections were detected. Brazil’s live birth defect registries show microcephaly rates began to climb in 2012 and intensified in 2013–2014. Meanwhile, the Zika virus wasn’t detected in Brazil until July 2014, and even then, it was retrospective surveillance that uncovered it. The first public reports attributing microcephaly to Zika came in October 2015.

At the same time, and in the same region—Northeast Brazil—Brazil’s Ministry of Health had implemented an aggressive public health campaign targeting pregnant women in the slums. This included the deployment of a tetanus-diphtheria-pertussis vaccine. Crucially, the formulation used in these settings was the whole-cell pertussis vaccine (wP), not the acellular version (aP) used in wealthier countries. Whole-cell pertussis vaccines are known to be highly reactogenic and are no longer recommended for use in adults or pregnant women in countries like the United States due to their elevated risk profile.

This was not widely disclosed at the time. But in a personal communication to me, Dr. Wadely de Oliveira from Instituto Butantan confirmed that whole-cell pertussis vaccines were indeed administered to pregnant women in the slums of Northeast Brazil during 2014 and 2015—the very same period immediately preceding and during the microcephaly surge. This campaign was subsequently halted in 2016. Afterward, microcephaly cases plummeted. Zika virus, however, continued to circulate. No new surge in microcephaly followed.

Dr. De Oliveira Dias of Instituto Butantan also confirmed in a February 17, 2016 communication: “Whole-cell pertussis vaccine is used in Brazil in the general population to reduce cost, whereas use of the more expensive acellular pertussis is restricted to clinics.” In follow-up correspondence, she expressed concerns about the mass vaccination of pregnant women in a population with high infectious burden and nutritional deficiency, calling the campaign “unnecessary” and acknowledging that Brazil’s vaccine production infrastructure had collapsed at the height of the Zika panic. These admissions confirm not only the use of whole-cell pertussis in pregnancy but also the vulnerability of the population exposed.

Let that sink in: the birth defects stopped, but the virus remained.

To date, no international health agency has disclosed the use of whole-cell pertussis vaccines in these vulnerable populations. No public health review has reevaluated the assumption that Zika caused the microcephaly. No retraction has been issued for the sweeping claims made in 2015–2016. Instead, the narrative hardened. The myth was institutionalized.

There was no robust evidence base to begin with. In fact, Anthony Fauci himself cited the presence of Zika virus RNA in a single fetal brain as “strong evidence” of causality. That is not science. That is confirmation bias. One brain. One anecdote. That became the foundation for sweeping global vaccine development campaigns, pesticide spraying, fear-mongering, and the suspension of scientific doubt.

But there were other exposures in play. At the same time that wP vaccines were used in pregnant women, Brazil had also introduced pyriproxyfen, a larvicide, into drinking water supplies in the Northeast. This coincided with the GM mosquito release in 2011–2014 in the same region. Aluminum-containing adjuvants were ubiquitous in maternal vaccines. Malnutrition was rampant. None of these cofactors were systematically evaluated. None were studied. None were ruled out.

Interactive Risk: Whole-Cell Pertussis as a Co-Factor in a Toxic Web

Brazil’s mass vaccination programs didn’t occur in sterile clinical settings. They were deployed in the favelas of the Northeast, regions suffering from chronic malnutrition, infectious disease burden, and environmental contamination. These areas were also subject to emergency countermeasures like pyriproxyfen treatment of drinking water and multiple concurrent vaccinations. Yet, no official risk models ever evaluated the combinatorial effects of these exposures.

wP + Aluminum + Malnutrition: Whole-cell pertussis vaccines in Brazil contained 1.25 mg of aluminum hydroxide. Malnourished mothers—common in slums—have impaired detoxification pathways. Combined, this creates a sustained neuroinflammatory state in the fetus, particularly dangerous during early brain development.

wP + Mercury (Thimerosal): Each dose included 0.2 mg of thimerosal. Ethylmercury is a mitochondrial toxin. Coupled with the cytokine storm induced by wP, fetal mitochondrial injury and apoptosis become likely. This combination was never evaluated in gestational safety studies.

wP + Pyriproxyfen: The larvicide was added to drinking water. Vaccine-induced inflammation may compromise placental integrity, increasing fetal exposure to small molecules like pyriproxyfen and amplifying any teratogenic effects.

wP + Zika Virus: Even if Zika has limited standalone teratogenic potential, it may act as a co-factor. Immune activation from wP may heighten Zika’s neuroinflammatory impact on the fetal brain.

wP + Concurrent Vaccines: Brazil’s maternal immunization schedule often included multiple simultaneous vaccines. This immune burden could exceed tolerable limits during critical gestational windows.

wP + Background Infection Burden: Superimposing vaccine-induced inflammation on a high-infection background may tip immune balance into crisis, with devastating fetal outcomes.

Not one of these interaction pathways was modeled, measured, or ruled out by the WHO or CDC. Their approach was linear, binary, and dangerously simplistic. The phrase “no evidence” was weaponized against every potential co-factor, even when the interacting variables were known teratogens, inflammagens, or immune disruptors.

In February 2016, I submitted a manuscript to PLOS ONE documenting the timeline: the rising microcephaly cases predating Zika, the introduction of wP vaccine campaigns, the environmental co-exposures, and the suspiciously timed collapse in microcephaly cases following the cessation of those campaigns. The manuscript was rejected without scientific rebuttal. The editorial team provided vague procedural objections. Around the same time, Dr. Peter Hotez remarked via peer review of our article, submitted to PLOS One article that such a paper would “not be helpful.” Helpful to whom? The women who lost their babies? The families who were told a virus did it, when no such evidence held up under scrutiny? To science?

Zika virus has existed for decades without ever causing birth defects. In Colombia, Zika spread widely in 2016. Microcephaly did not. One of my colleagues who was instrumental in keeping people reasonable about Ebola - Dr. Gavin MacGregor-Skinner- traveled to Colombia during the height of the microcephaly crisis and confirmed - Zika, no microcephaly. I called a doctor in Suriname - Zika, no microcephaly. Decades prior - Nigeria, Java, French Polynesia, similar story: many infections, no microcephaly. Only in Brazil—only in the slums, only in the years wP was administered—did this cluster of tragic birth outcomes occur.

This is not coincidence. It is a signal. And IPAK was on it in real time. Peter Hotez and PLOS One want to sanitize any potential link to vaccination; my manuscript is still unpublished, a testimonial to their destructive effect on science.

Here is our best three-factor causal hypothesis that could explain MC in Brazil from 2012-2015.

Science, if it is to mean anything, must be honest. And honesty requires that we acknowledge uncertainty, revisit our assumptions, and follow the data wherever it leads—even when the destination is uncomfortable. To this day, no major health authority has investigated whether the use of whole-cell pertussis vaccine in pregnant women caused Brazil’s microcephaly crisis. But the burden of proof does not lie on the victims. It lies on the institutions that unleashed untested interventions on vulnerable populations and then buried the consequences beneath a viral scapegoat.

Zika virus may have been present, but it was never proven to be the cause of microcephaly. Whole-cell pertussis vaccine, in contrast, was confirmed in use during pregnancy, was known to be inflammatory, was halted just before the crisis resolved, and yet has never been studied in this context. That is not “no evidence.” That is willful ignorance.

It is time to ask the questions that were never allowed. Who authorized this? Who funded it? Who ignored the outcomes? And why have the people of Brazil not been told the truth?

The public deserves answers. And science demands accountability. Even for vaccine iatrogenic disease and death.

Keep objectivity in science alive. Become and IPAK Science Hero today with your monthly donation.

Summary of Key Mechanisms Identified in Glyphosate-Induced Teratogenicity

A landmark study by Paganelli et al. (2010) offers critical mechanistic insight into how glyphosate-based herbicides (GBHs) can produce microcephaly and other neural defects—findings that mirror the patterns observed during the microcephaly surge in Northeast Brazil.

Microcephaly and Cephalic Defects from GBH Exposure

In both Xenopus laevis (frog) and chicken embryo models, sublethal exposure to GBH—at concentrations far lower than those used in agricultural settings—resulted in striking developmental abnormalities. These included microcephaly, cyclopia, and severe craniofacial malformations. Gene expression analyses revealed that key developmental markers such as slug, krox-20, N-tubulin, shh (Sonic Hedgehog), and otx2 were all significantly downregulated in exposed embryos. Additionally, the migration of neural crest cells—essential for craniofacial patterning—was visibly delayed or disrupted. These experimental outcomes directly parallel the clinical phenotypes reported in microcephalic infants born during the Zika-associated outbreak in NE Brazil.

Mechanistic Driver: Disruption of Retinoic Acid Signaling

The study identified a central mechanistic driver: disruption of the retinoic acid (RA) signaling pathway. Using a RA-responsive reporter assay (RAREZ), the researchers demonstrated that GBH exposure caused a significant increase in endogenous RA signaling. This hyperactivation of RA is known to induce developmental defects that resemble those seen in retinoic acid embryopathy. Notably, the teratogenic effects induced by GBH were rescued when embryos were co-treated with Ro 41-5253, a known RA pathway antagonist. This confirms that the observed neural and craniofacial defects are, at least in part, mediated through retinoid dysregulation. The phenotypic outcome mimicked well-documented human syndromes such as holoprosencephaly and otocephaly—both of which involve impaired midline brain development and neural crest function.

Interaction with Other Stressors

The study further raises concerns about synergistic toxicity. It demonstrated that the teratogenicity of glyphosate is potentiated by adjuvants—especially surfactants—commonly included in commercial formulations to improve absorption. Glyphosate alone was capable of impairing mitochondrial function, triggering apoptosis through the activation of caspases 3 and 7, and further suppressing Shh signaling, which is critical for neural tube and facial development. When these effects occur in tandem, they likely compound embryonic damage and increase the probability of severe birth defects. In real-world contexts—especially in vulnerable populations exposed simultaneously to vaccines, malnutrition, infections, and chemical agents—these interactions could explain the geographic and demographic clustering of microcephaly.

• Paganelli, A., Gnazzo, V., Acosta, H., López, S. L., & Carrasco, A. E. (2010). Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling. Chemical Research in Toxicology, 23(10), 1586–1595.
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• World Health Organization. (2016, February 1). WHO statement on the first meeting of the International Health Regulations (2005) Emergency Committee on Zika virus and observed increase in neurological disorders and neonatal malformations.
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• Centers for Disease Control and Prevention. (2016, January 15). Zika virus spreads to new areas — Region of the Americas, May 2015–January 2016. Morbidity and Mortality Weekly Report, 65(3), 55–58.
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• Dórea, J. G., Marques, R. C., et al. (2013). Distribution of aluminum in hair of Brazilian infants and correlation to aluminum-adjuvanted vaccine exposure. Biological Trace Element Research, 155(1), 132–140.
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• de Oliveira Dias, W. D. (2016, February 26). Personal communication to James Lyons-Weiler.

• NPR. (2016, February 18). Did a pesticide cause microcephaly in Brazil? Unlikely, say experts.
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• News-Medical.net. (2019, September 18). Concerns over GM mosquitoes released in Brazil.
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• PubMed. (2022). The tendency of stunting among children under five in the Northern Region of Brazil, 2008 to 2017.
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