Research Forum

Forum Navigation
You need to log in to create posts and topics.

Vaccines + Poison/"Vitamin A" combined increasing mortality (deaths)

The main researcher connecting the increased risk of combining vaccinations and Poison/"Vitamin A" is Christine S. Benn (Benn CS on the following papers).  She's done a ton of work on this topic.  She hasn't realized that Poison/"Vitamin A" isn't a nutrient yet...but she sure is noticing the negative synergy between it and vaccines, along with the farce of serum retinol testing!

Does India Need a Universal High-Dose Vitamin A Supplementation Program?

High Dose Vitamin A (HDVA) concentrate began to be distributed in India in 1970 as a short-term, stop-gap approach to reduce clinical signs of vitamin A deficiency. As this problem declined globally, the purpose of distributing them changed to the reduction of young child mortality. However, their impact on this has also declined, if not disappeared, as suggested in India by the enormous DEVTA study. This may be because of improved protection against and treatment of the main morbidity involved, measles and diarrhea. At the same time, semi-annual provision of mega-doses of vitamin A is not without risks, in particular linked to children's vaccination status. While a single dose is inexpensive, large-scale implementation of HDVA programs is expensive, particularly the opportunity cost involved in reducing the time health workers involved have to deal with their other commitments. Balancing potential benefits, risks and costs leads us to recommend an immediate cessation of the distribution of HDVA in India.

Can HDVA Do Harm?
SR [serum retinol] is quite readily increased (for all ages) by regular vitamin A in physiological doses (the only dose considered safe for women of reproductive age) [2, 8]. But when the dose of vitamin A is as high as 200,000 IUs (over 200 times daily allowance), the liver may not be able to store it in such quantities, and the excess is broken up and excreted [32]; and vitamin A, if not stored or tightly bound (as with retinol binding protein), can be toxic to cells. A number of studies in Zambia suggest hypervitaminosis A is occurring, and Guatemala scaled back its vitamin A fortification levels due to similar concerns [33]. Kapil and Sareen [28] have summarized some of the other concerns about the possible side effects ofHDVA, including increased respiratory tract infections and harm to bone health. Lastly, as indicated above, HDVA may cause increased mortality in subgroups, e.g., in females who receive DTP vaccine. The underlying mechanisms are unknown but may be related to recent observations that vitamin A may induce epigenetic inhibitory modifications of monocytes, leading to innate tolerance [34]. It is worth noting that in India, which recommends a booster DTP vaccine at 18 mo of age, children will have DTP vaccine as their most recent vaccine in the majority of the first 5 y of life.

HDVA should be immediately discontinued in India on the basis of balancing the benefits and risks enumerated above and particularly the financial and logistic costs that could be diverted to other comprehensive and sustainable solutions. Before-after cessation studies of mortality outcomes by age and sex, if carefully planned, could provide important evidence regarding potential benefits or harms of continuing the program elsewhere in the world.

High-dose vitamin A with vaccination after 6 months of age: a randomized trial.

The mortality rate ratio (MRR) comparing VAS versus placebo recipients was 0.91 (95% confidence interval 0.59-1.41) and differed significantly between boys (MRR 1.92 [0.98-3.75]) and girls (MRR 0.45 [0.24-0.87]) (P = .003 for interaction between VAS and gender). At enrollment, 42% (3161/7587) received live measles vaccine, 29% (2154/7587) received inactivated diphtheria-tetanus-pertussis-containing vaccines, and 21% (1610/7587) received both live and inactivated vaccines. The effect of VAS did not differ by vaccine group.
This is the first randomized controlled trial to assess the effect of the policy on overall mortality. VAS had no overall effect, but the effect differed significantly by gender.

We need to cover a couple things to make sure we are on the same page for the rest of this article.

ALL the kids in the above study got vaccinated.  SOME of them got supplemental Vitamin A.

Mortality Rate Ratio - ratio between the observed number of deaths in an study population and the number of deaths that would be expected, based on the age- and sex-specific rates in a standard population.  A rate higher than 1 means more deaths (mortality) occurred than would have been expected.

The boys in the above study who got VAS *and* vaccines had nearly TWICE the risk of "non-accident death" (MRR 1.92) versus the "normal" expected rate!!!  Note that the type of vaccine didn't matter ("The effect of VAS did not differ by vaccine group.").

Coincidentally, look at the autism rates between the sexes:

Sex differences in autism spectrum disorders

From the first published descriptions of autism, it has been a male-typical disorder: 8 of the 11 cases described by Kanner [5], and all 4 cases described by Asperger [6], were male. Prevalence surveys conducted since have reported a range of male biases from 1.33:1 male:female (M:F) to 15.7:1 [7], and a commonly referenced consensus ratio of ~4:1.

Interesting, right?  Is there research showing different reactions in the sexes to Vitamin A supplements and vaccines together?

Long-term sex-differential effects of neonatal vitamin A supplementation on in vitro cytokine responses.

High-dose vitamin A supplementation (VAS) may affect mortality to infectious diseases in a sex-differential manner. Here, we analysed the long-term immunological effects of neonatal vitamin A supplementation (NVAS) in 247 children, who had been randomly allocated to 50 000 or 25 000 IU vitamin A (15mg and 7·5mg retinol equivalents, respectively) or placebo at birth. At 4-6 months of age, we assessed bacille Calmette-Guérin (BCG) scarification, and we analysed in vitro responses of TNF-α, IL-5, IL-10, IL-13 and IFN-γ in whole blood stimulations to phytohaemagglutinin (PHA), purified protein derivative (PPD), tetanus toxoid and lipopolysaccharide. There were no differences between the two doses of NVAS, and thus they were analysed combined as NVAS (any dose) v. placebo. All analyses were performed unstratified and by sex. NVAS increased the chance of having a scar after BCG vaccination in females (NVAS v. placebo: 96 v. 71 %, proportion ratio: 1·24; 95 % CI 1·09, 1·42), but not in males (P for interaction=0·012). NVAS was associated with significant sex-differential effects on the pro- to anti-inflammatory cytokine ratios (TNF-α:IL-10) to PPD, tetanus toxoid and medium alone, which were increased in females but decreased in males. In addition, IL-17 responses tended to be increased in NVAS v. placebo recipients in males but not in females, significantly so for the PHA stimulation. The study corroborates sex-differential effects of VAS on the immune system, emphasising the importance of analysing VAS effects by sex.

So there are different reactions by sex to VAS and vaccines. This will be important, so remember that.

Because Poison/"Vitamin A" is passed to the fetus AND is transferred to the baby via breastmilk, is there any demonstrated increased toxic effect when a mother is given Vitamin A supplements AND the baby is given Vitamin A?  Yes.

Serious danger signals: Response to: The effect of neonatal vitamin A supplementation on morbidity and mortality at 12 months: a randomized trial

With respect to MVAS [Maternal Vitamin A Supplementation], Smith et al. observed that among mothers who received MVAS, NVAS [Neonatal Vitamin A Supplementation] was associated with a relative risk (RR) of dying of 1.12 (0.98–1.29), whereas among mothers who did not receive MVAS, NVAS was associated with an RR of 0.86 (0.70–1.06). The authors conclude that this result may help explain the heterogeneity of NVAS effect on mortality across different trials.1 However, their finding is contradicted by two previous NVAS trials, which randomized mothers to MVAS in factorial designs (Table 1).23 Additionally, in Guinea-Bissau no woman received MVAS; but there has been a consistent tendency for negative effect of NVAS.4–6
Smith et al. also propose that maternal HIV infection may partly explain why they found a trend of increased mortality after NVAS. It is noteworthy and worrying that the two trials which reported data by maternal HIV status1,3,7 both suggest a negative effect of NVAS in HIV-infected mothers [meta-analysis RR = 1.23 (1.02–1.49)].1 However like MVAS, HIV does not fulfil the criterion of explaining the heterogeneity of NVAS effects across trials. For instance, the Zimbabwe trial found tendencies for negative effects in women who were tested HIV-negative,3 and the Guinea-Bissau trials had low HIV prevalence and tendencies for negative effects.4–6

With respect to sex, we have previously raised the hypothesis that the effect of NVAS becomes negative in females once they start receiving diphtheria-tetanus-pertussis (DTP)-containing vaccines, recommended at around 6, 10 and 14 weeks of age.8,9The hypothesis was based on populations with low HIV prevalence and no MVAS. In the Tanzania study, the authors make an analysis by sex in the total group of participants, which shows that by 12 months of age, the RR for males is 0.95 (0.82–1.11) and the RR for females is 1.16 (0.97–1.39).
A closer look at the Tanzania trial may indicate support for the hypothesis that NVAS interacts negatively with DTP-containing vaccines in females. In the first months of life, when mortality is very high, the children will have BCG and oral polio vaccine (OPV) or no vaccination as their most recent vaccine, but from around 6 weeks of age, DTP becomes the predominant vaccine. Thus, if NVAS interacts negatively with DTP in females,8,9 we should expect that a possible sex-differential effect of NVAS increases with age as DTP becomes the predominant vaccine. Smith et al. report mortality results by 6 and 12 months, and if we calculate NVAS effects by age group (Table 2, calculated based on figures from Smith et al. 20161), the sex-differential effect of NVAS becomes stronger after 6 months of age, when the most children will have received DTP.

We have previously pointed out that this seems to be a consistent feature of all the NVAS trials with follow-up to 12 months.13 Apart from our NVAS-DTP-sex-interaction hypothesis, no other explanation has been proposed for this consistent pattern of increasing female mortality with increasing length of follow-up.
As noted by the authors, MVAS is no longer World Health Organization policy.
We find it very important that the Tanzania trial not be taken as evidence for a beneficial effect of NVAS in children without MVAS, a conclusion which might pave the road for a policy of providing NVAS.15 NVAS should not be made policy—either overall or in children of mothers who do not receive MVAS. There are several important danger signals.

First, there is no overall beneficial effect of NVAS on mortality. Second, there is evidence for negative effect in HIV-positive mothers, and as long as there is no universal HIV screening, an NVAS policy would inevitably lead to supplementation of children of HIV-positive mothers. Third, more important in terms of numbers, is the danger signal of an increasingly negative effect of NVAS in females aged from 6 to 12 months. We need to exclude negative NVAS-DTP-sex interaction and find a good and avoidable explanation for this signal, before an NVAS policy anywhere would be acceptable.

So far, a negative NVAS-DTP-sex interaction is the best explanation for the heterogeneity across the existing NVAS trials. As vitamin A is an immunomodulator, there may very likely be other effect modifiers.9 In the search for these effect modifiers, consistency across trials and ability to resolve contradictions in the existing data should be the guiding light—not P-values.

That last sentence is the best one.  Let's summarize all the bad (negative) findings about Poison/"Vitamin A" supplements, shall we?

  1. Mothers who had VAS (MVAS), who then had babies that had VAS (NVAS), had an increased risk of the baby dying.
  2. Multiple studies show that giving babies VAS (NVAS) increases their risk of dying.
  3. Studies have shown that VAS increases risk of dying in both HIV positive women, yet also in HIV negative women.
  4. The DTP vaccine and VAS together shows an increased risk of dying in girls.
  5. There is actually NO reduced risk of dying from giving babies VAS.

No benefit, lots of risk.  How many holes have to be poked in this ship before it sinks?  Why does the World Health Organization keep pushing this stuff?

These findings highlight a gap between the sophisticated mechanistic understanding of vitamin A-induced tolerance and the real-world consequences of vitamin A supplementation (VAS).

It's not a gap.  It's an ocean-sized chasm.

This lack of presentation by sex is unfortunate as numerous studies have documented major differences in male and female immune systems, and the way they respond to health interventions such as vaccines and VAS early in life.4, 5 Alternatively, the different results may be due to interaction with other interventions to which the Guinean children were exposed, as only girls who concurrently received bacille Calmette-Guérin vaccination (BCG) had atopy potentiated by VAS.2 There is also evidence for interactions between VAS, vaccines and sex in relation to susceptibility to infectious diseases: VAS impairs the innate immune training enabled by BCG; and for females, it interacts with subsequent diphtheria–tetanus–pertussis vaccine in a harmful way, and with subsequent doses of VAS or measles vaccine in a beneficial way.4

An enigma: why vitamin A supplementation does not always reduce mortality even though vitamin A deficiency is associated with increased mortality

Background: Vitamin A deficiency (VAD) is associated with increased mortality. To prevent VAD, WHO recommends high-dose vitamin A supplementation (VAS) every 4–6 months for children aged between 6 months and 5 years of age in countries at risk of VAD. The policy is based on randomized clinical trials (RCTs) conducted in the late 1980s and early 1990s. Recent RCTs indicate that the policy may have ceased to be beneficial. In addition, RCTs attempting to extend the benefits to younger children have yielded conflicting results. Stratified analyses suggest that whereas some subgroups benefit more than expected from VAS, other subgroups may experience negative effects.

Methods and Results: We reviewed the potential modifiers of the effect of VAS. The variable effect of VAS was not explained by underlying differences in VAD. Rather, the effect may depend on the sex of the child, the vaccine status and previous supplementation with vitamin A. Vitamin A is known to affect the Th1/Th2 balance and, in addition, recent evidence suggests that vitamin A may also induce epigenetic changes leading to down-regulation of the innate immune response. Thus VAS protects against VAD but has also important and long-lasting immunological effects, and the effect of providing VAS may vary depending on the state of the immune system.

Conclusions: To design optimal VAS programmes which target those who benefit and avoid those harmed, more studies are needed. Work is ongoing to define whether neonatal VAS should be considered in subgroups. In the most recent RCT in older children, VAS doubled the mortality for males but halved mortality for females. Hence, we urgently need to re-assess the effect of VAS on older children in large-scale RCTs powered to study effect modification by sex and other potential effect modifiers, and with nested immunological studies.
Key Messages:

  • A number of observations contradict the interpretation that vitamin A supplementation acts merely to prevent vitamin A deficiency. The effect of vitamin A supplementation is not associated with the degree of deficiency, and the effect is modified by factors unrelated to deficiency, such as sex of the child and the vaccines he or she has received.
  • The existing evidence supports that besides preventing vitamin A deficiency, vitamin A supplementation also has long-lasting immunological effects; and, worryingly, the effect of vitamin A supplementation may be harmful in some subgroups.

The common interpretation is that VAD is associated with increased mortality—and that VAS works by preventing and treating VAD. The lack of effect in two of the original eight trials and the lack of association between the degree of VAD and the effect of VAS should perhaps have raised concern about this compelling but rather simple interpretation.

There have been numerous RCTs carried out to test whether the observed beneficial effects of VAS could be extended to younger children. Most RCTs providing VAS to children between 1 and 5 months of age found no beneficial effects of providing VAS, even when VAD was prevalent (reviewed in 9). Several RCTs of neonatal VAS (NVAS) have yielded conflicting results.10 Very recently, three WHO-commissioned RCTs of NVAS from Ghana,11 Tanzania12 and India13 were individually powered to show a 15% reduction in mortality by 6 months of age, but found no overall benefit; the random effect meta-analysis estimate of these three trials by 6 months of age and 12 months of age being 1.03 [95% confidence interval (CI) 0.88-1.19) and 1.02 (0.92-1.13), respectively. Furthermore, two new large RCTs of VAS to children above 6 months of age in Guinea-Bissau and India found no overall beneficial effect of VAS.14, 15

All RCTs except one14 hypothesized that the overall effect of VAS would be beneficial. Hence, when so many recent RCTs produce unexpected results there is reason to pause and reflect. Moreover, many of the RCTs found interactions between VAS and various background factors. Noteworthy, VAS was even more beneficial than anticipated in some subgroups, but worryingly associated with negative effects in other subgroups. The subgroup analyses have usually been dismissed as post hoc analyses. However, since VAS is being provided to millions of children with little or no assessment of the effect, it should be a concern when our expectations of universal beneficial effects are contradicted and potential explanations should be pursued.

Combining vitamin A and vaccines: convenience or conflict?

The present thesis is based on 11 papers from 1995-2010. The studies have mainly taken place at the Bandim Health Project in Guinea-Bissau, West Africa, but a reanalysis of a randomised trial from Ghana is also included. My research has explored the consequences of combining high-dose vitamin A supplementation and childhood vaccines. Vitamin A deficiency is associated with increased mortality. To protect against the consequences of vitamin A deficiency the World Health Organization recommends that high-dose vitamin A supplements be given together with routine vaccines to children between 6 months and 5 years of age in more than 100 low-income countries. The recommendation is based on logistical considerations. The consequences of combining vitamin A and vaccines were not investigated in randomised trials prior to the implementation of this policy - it was assumed that the interventions were independent. My first project aimed to study the effect on the immune response to measles of providing vitamin A together with measles vaccine. We found that the two interventions were not independent. Vitamin A enhanced the antibody response to measles vaccine given at 9 months of age significantly, especially in boys. The effects were sustained over time; the children who had received vitamin A with their measles vaccine were more protected against measles at 6-8 years of age. Though vitamin A supplementation had a beneficial effect on the immune response to measles vaccine, it intrigued me that the effect of vitamin A supplementation on overall mortality was not always beneficial. While vitamin A was beneficial when given after 6 months of age, and two studies had shown a beneficial effect when given at birth, all studies testing the effect between 1-5 months of age had found no effect. These time windows are dominated by three different childhood vaccines: BCG vaccine given at birth, diphtheria-tetanus-pertussis (DTP) vaccine given between 1-5 months of age, and measles vaccine given at 9 months of age. These vaccines have been shown to have strong effects on mortality from infectious diseases in general, so-called non-specific effects. The live BCG and measles vaccine protects against more mortality than can be ascribed to the prevention of tuberculosis and measles, respectively. The inactivated DTP vaccine worryingly has been associated with increased mortality from other infectious diseases. Both positive and negative effects are strongest for girls. I proposed the hypothesis that vitamin A amplifies not only the specific vaccine effects, as we saw for measles vaccine, but also the non-specific effects of vaccines on mortality from other infectious diseases. According to my hypothesis, vitamin A would enhance the non-specific beneficial effects on mortality of BCG and measles vaccine, but also the negative effects of DTP vaccine. Hence, the hypothesis offered an explanation for the mortality-age pattern after vitamin A supplementation. Since it was formulated, I have aimed to test this hypothesis. Since it is associated with ethical problems to randomise children above 6 months of age to vitamin A supplementation, and to randomise children in general to recommended vaccines, we have had to be pragmatic when designing the trials. Hence, our studies have taken many different forms. We conducted an observational study during a vitamin A campaign in which missing vaccines were also provided, and a randomised trial testing the effect of two different doses of vitamin A during another campaign; we tested the effect of providing vitamin A with BCG at birth in two randomised trials, and we reanalysed data from one of the original randomised trials of vitamin A supplementation from the perspective of vaccination status. In all studies the main outcome was mortality. The results document that vitamin A supplements do more than protect against vitamin A deficiency. They support the hypothesis that vitamin A supplements interact with vaccines with important consequences for mortality. First, a smaller dose of vitamin A was more beneficial than a larger dose for girls. Second, the effect of vitamin A given with DTP vaccine was significantly different from the effect of vitamin A given with measles vaccine, and children, who received vitamin A with DTP vaccine, had higher mortality than children, who had received vitamin A alone, or who did not receive anything. Third, vitamin A given with BCG at birth interacted negatively with subsequent DTP vaccines in girls. Fourth, the effect of vitamin A to older children in Ghana depended on vaccination status, being beneficial in boys, but harmful in girls who received DTP vaccine during follow-up. The results also show that boys and girls respond differently to vitamin A and vaccines. It is a common assumption within public health in low-income countries that interventions can be combined without producing unexpected consequences. The work presented in this thesis confronts this assumption; the results show that vitamin A and vaccines should be seen not only as specific interventions with specific and independent effects, but as immuno-modulators, which can interact with important consequences for overall mortality. Combining interventions can be convenient and lead to synergistic health benefits, but we documented several examples, where it also leads to unexpectedly increased mortality. Thus, to optimise the child health intervention policy in low-income countries a shift in paradigm is needed. Health interventions should no longer be seen as merely specific and independent, and the policy should probably not be the same for boys and girls. Though more complex, it is necessary to evaluate all health interventions in terms of their effect on overall mortality - and their potential interactions with other health interventions and potential sex-differential effects should always be investigated. Only in this way can we assure that the children in the poorest countries get the best possible treatment and avoid using large amounts of money and resources on interventions which may, in worst case, kill them.

To fit this into my Unified Theory of Modern Chronic Disease, the glyphosate/Roundup causes the inability to breakdown Poison/"Vitamin A", and it is this effect in causing accelerated Poison/"Vitamin A" toxicity in particular that really sets a child or adult up for the strongest type of vaccine side effect...that being death.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona, home of the Love Your Liver program
YouTube - FaceBook - Instagram - Twitter