vaccines-life-expectancy-rates

Number of vaccines and infant mortality rates among wealthier nations.

Comments by Brian Shilhavy
Editor, Health Impact News

As we have previously reported at Health Impact News, in spite of the fact that the U.S. spends more on “healthcare” than any other nation in the world, our infant mortality rates are among the highest, especially when compared to developed, wealthier nations. The most recent study was published in January of 2018 in the journal Health Affairs and compared the mortality rate of children in 19 wealthy, Western countries, where the U.S. came in last. (Source.)

It is also well-known that American babies receive more doses of vaccines than any other nation.

And yet, government health agencies refuse to even consider if vaccines are part of the problem.

Within the U.S., the state with the highest infant mortality rate, Mississippi, also (coincidentally??) has the highest vaccination rates in the U.S. (Source.)

Neil Miller, a medical research journalist and the Director of the Thinktwice Global Vaccine Institute, wrote in 2014 that while there are 130 official ways for an infant to die according to official categories of death, sanctioned by the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) as published in the International Classification of Diseases (ICD), vaccines are not one of them:

There are 130 official ways for an infant to die. These official categories of death, sanctioned by the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO), are published in the International Classification of Diseases (ICD). When a baby dies, coroners must choose from among these 130 categories.

The official causes of death listed in the ICD include nearly every imaginable — and tragic — possibility.

However, there is NO category for infant deaths caused by vaccines.

This is odd because the federal government is aware that vaccines permanently disable and kill some babies — the very reason Congress established a “death and disability” tax on childhood vaccines more than 25 years ago when the National Childhood Vaccine Injury Act of 1986 (Public Law 99-660) created the National Vaccine Injury Compensation Program (VICP). (Full article.)

According to the CDC, Sudden Infant Death Syndrome (SIDS) remains one of the leading causes of death among infants in the U.S., claiming 3,700 deaths in 2015.

Dr. Viera Scheibner is one of the few scientists and researchers who has investigated SIDS and a possible link to vaccines, and she presents her research here on Health Impact News.

The real cause of cot death (SIDS)

by Dr. Viera Scheibner (PhD)
Health Impact News

Abstract

From time to time there is a flare-up of a discussion about sudden infant deaths (SIDS) or cot death.

Between 1986-1993 I was involved in recording of babies’ breathing with the standard and microprocessor-based breathing monitor (developed by my late husband Leif Karlsson) and I published the results in Journal of Australasian College of Nutritional and Environmental Medicine (Scheibner 2004).

I have also studied as much as possible of other authors’ published cot death related research from English speaking countries since the 1960s, and I feel that I can meaningfully contribute to the most recent discussion.

Cot death (SIDS) has always been presented as a diagnosis of exclusion, with minimal pathology insufficient to cause death, characterised by petechial haemorraging into lungs, pericardium, thymus and other organs.

Prone position as a position of risk for a while enjoyed popularity, with some important research conducted in the UK most of which demonstrated that the prone position was actually a position of advantage and then summarily reversed, and, more recently, bed-sharing (co-sleeping) became designated as a major risk. Smoking parents also enjoyed popularity for a while.

Vaccination was usually ignored or rejected as the cause of cot death (SIDS). Only a few authors ventured into this tabu area.

The overview of published research into cot death (SIDS)

I almost agree with professor Mitchell et al. (2009) who believe that “we already know enough” but not that “there is overwhelming evidence showing that bed sharing is a major risk for Sudden Infant Death in infants of mothers who smoke.”

Cot deaths researchers mostly published lots of articles on innumerable events in babies lives, with the exception of the paucity of one: vaccination. And even when they did, they usually, in unison, rejected it as the cause of [cot death, SIDS, infant deaths].

The exception is Torch (1982, 1986a,b), a retired pediatric neurologist from Reno Nevada, who delivered three lectures to two Conferences on Pediatric Neurology and stated clearly and without mincing words that DPT vaccination may be an unrecognized cause of sudden infant death, described the symptomatology and pathology very clearly and exhaustively and concluded that these events are causally related.

Torch (1982, 1986a,b), clearly, and others (Griffin et al. 1988) unwittingly, made the same observation: increasing numbers of deaths with the increasing interval from the vaccine injections, increasing numbers of injections and increasing age.

Munoz et al. (1981) reported on deaths in mice caused by pertussigen injected in minutest of doses (in ng) by measuring their weight gain (or otherwise); not only the studied mice stopped putting on weight, but within 8 days four of the studied five mice died. Even the one that survived, experienced leveling of the weight gain along the same (critical) days along which the other four were dying.

Needless to say, these were the same critical days that I discovered and documented during monitoring of babies’ breathing with Cotwatch.

Sadly, but not surprisingly, Munoz et al. (1981) failed to understand the meaning of their own research, by thinking that just because no mice died along certain days and not others, it represented the protective effect of pertussigen on those others days.

Indeed, a similar thing occurred in Professor Mitchell and his collaborators’ research (Mitchell et al. 1995); while their own research, properly tabulated by myself, clearly demonstrated clustering of deaths along the same critical days as I discovered and documented (Scheibner 2004): 10-14), Mitchell et al. (1995) concluded that “there was a reduced chance of SIDS in the four day period after immunisation” and hence that immunization “may even lower the risk of SIDS” (though also saying that they cannot confidentially state it as certainty).

Far from showing protection against cot death by vaccination, their data show that all those babies studied died as a direct consequence of their DPT and OPV vaccination, showing perfect clustering along the critical days, clearly showing increased numbers of deaths on the critical days 2, 7 and 10, with lower numbers of deaths in between. Fairly high numbers of deaths on day 1 reflects over-representation of such deaths due to a reluctance of reporting delayed death after vaccination.

Griffin et al. (1988) data on deaths after vaccination are of equal interest. They studied the so-called Tennessee deaths: hundreds of babies died after their vaccinations straight after DPT and OPV became mandated by individual U.S. states, in mid seventies, as a condition for enrollment.

Just as Mitchell et al. (1995), Griffin et al. (1988) failed to tabulate their data appropriately, but when appropriately tabulated, four age groups immediately emerged: Group 1 included babies aged 1.5-2.5 months (at that time, in the USA the first dose of DPT and OPV was administered at 6-8 weeks); group 2 included babies aged 2.5-4 months, who died after their second dose of DPT and OPV; group 3 included babies aged 4-8 months who died after their third dose; and group 4 included babies aged 8-12 months forming the residue of deaths after the third dose. Most babies died after the first and second vaccine doses. Most were delayed deaths (more than 31 days after vaccination).

Far from showing no evidence of the causal link between the administration of DPT and OPV vaccines, as claimed by the authors, their properly tabulated data shows three important phenomena: 1. Younger babies die earlier, the bigger babies take longer to die; 2. Sensitization (harmful, exaggerated immunological reaction – anaphylaxis) after subsequent doses of vaccines; 3. Increased number of deaths with the increasing interval from the vaccine injections – delayed reactions (deaths), which are a rule rather than an exception.

Fundamental Error of Judgment in SIDS Research

Generally, speaking, the most fundamental error of judgment displayed by cot death researchers is that they do not look at what happened to the babies who succumbed to SIDS days before they died, and instead they are trying to identify the elusive entity of “at risk” babies. The reality is that any baby may become at high risk of dying when it is exposed to stressors (toxins) which overwhelm its system.

The pneumographic studies are done without much regard to the timing of apnoeas and hypopnoeas described as the apparently life threatening episode (ALTE). In my experience, the timing of the pneumographic studies is determined by the availability of a bed in the overnight study units; this may take weeks, and by the time the baby is admitted for the study, the crisis is usually over and the results are irrelevant.

Even if the babies were admitted immediately, due to the existence of the critical days the 6-8 hour O/N study may not pick the critical day. The late Leif Karlsson and myself recorded non-stop longitudinally for weeks or months, the cot researchers monitor for 6-8 hours (overnight).

This enabled us to observe and record the effect of stressful events (vaccination) on babies’ breathing hour by hour and hence we discovered and demonstrated the existence of the critical days on which there are flare-ups of stressed breathing caused by the documented events. In the case on hand, the administered vaccinations.

Another fallacy of cot researchers is the notion of false alarms. They call false alarms all alarms that occur when a baby is not dying. We called such alarms warning alarms; it takes time even for a very sick baby to deteriorate to a dying stage.

We recorded, and looked into, these “false” alarms and established that the stress-induced breathing pattern is not just just apnoeas, but it is mainly low volume, shallow, breathing. They occur in clusters and follow the pattern of critical hours and days. The recorded alarms also closely follow these critical days.

Vitamin C Deficiency: Vaccine-induced Scurvy

Dr. Innis (2009) elaborates on the scurvy (or as he calls it, hypovitaminosis C, probably to avoid using the word scurvy, a much stereotyped term) and its possible synergistic effect on smoking mothers and their babies, and hence SIDS, without elaborating what causes it beside smoking.

Pekarek and Rezabek (1959) demonstrated that the administration of DPT vaccine to rats caused them to develop immediate acute scurvy which rectified itself within 24 hours. However, human babies do not have the advantage the rats have of being able to produce their own vitamin C within their bodies: humans and other primates, fruit bats, Guinea pigs, to mention just a few important examples, do not produce their own vitamin C and depend for it on their food having adequate amount of this important essential vitamin.

When human babies are given DPT and OPV as Pekarek & Rezabek’s rats, they also develop an acute scurvy which does not rectify itself and persists unless the babies are given sufficiently large amounts of vitamin C (sodium ascorbate).

This, of course, rarely happens, because when babies with vaccine reactions are admitted in hospitals they are given hepatotoxic antibiotics and paracetamol which further aggravate their vitamin C deficiency.

As amply demonstrated by Hess (1920) in his much ahead of his time monograph, which stands up to modern scientific scrutiny, scurvy affects all systems of the body and results in depletion of collagen resulting in vascular wall fragility, blood clotting and other haematological derangements resulting in bruising, and brain, retinal and other organ haemorrhages and malfunctions, including derangement of the central control of temperature, breathing, cardiac function, blood pressure, and bizarre, but characteristic bone fractures and tissue injuries, etc.

Perhaps I mention Hess’s (1920) evaluation of bleeding into frenulum, scapula, clavicula and periosteum as one of many signs of scurvy, while such injuries are falsely evaluated as caused by inflicted trauma by “modern” researchers.

By the way, Dr. Kalokerinos, in his book “Every second child” credits Dr. Harbin of Tamworth with alerting him that the Australian Aboriginal babies were dying of scurvy which then prompted him to inject dying babies with vitamin C.

Injecting a number of toxins and foreign proteins directly into the blood stream causes immunological derangement, among others the reversal of T4 and T8 cells ration (Jefferys 2001).

Babies Need to Sleep on Their Backs – Flawed Advice

The much publicized and glorified advice to put babies to sleep on their backs is flawed: Beal (1986) mentioned without any further comment that, in Czechoslovakia, 61% of babies died of cot death while lying on their backs. I come from Czechoslovakia and confirm that we never adopted the fashion of putting babies on their tummies. We put our newborn babies to sleep in their sides or backs (yes they developed flat heads).

The meaning of this, of course, it that whatever the babies will die of will happen in whatever the preferred position is. The western world adopted the prone position for premature babies first and then applied it across the board. Indeed, important research in the UK demonstrated that the prone position is the position of benefit, because just like premature babies, normal babies breath easier and oxygenate better when sleeping prone.

Even though some authors linked cot death to the sleeping position already in the seventies (Beal and Blundell (1978), between 1989 and 1992 and in 1995 a series of important articles were published in the Archives of Disease in Childhood on the results of studies of the effects of positioning on babies breathing and temperature regulation. The idea was to explain many infant deaths in which the babies were found soaked in sweat and overheated. I refer to these articles individually.

Wailoo et al. (1989) studied sleeping body temperatures in 3-4 months old infants. They continuously recorded rectal, skin and ambient temperatures overnight from 3-4 months old normal infants in their homes under conditions of room temperature and wrapping chosen freely by parents. It was found that rectal temperature was above 37 centigrades when infants were put down, but fell rapidly to 36.4 centigrades within one and a half hours, then stabilised for a few hours before rising steadily towards the waking time.

This pattern was tied more closely to the time of putting babies down to sleep than time of the day. The extent and rate of temperature fall did not correlate with any feature of the thermal environment. They also found that skin temperature changed much less than rectal temperature over the night, and, for the first two hours in the cot, there was no relation between skin and rectal temperature.

They concluded that there is therefore a well organised, and stabilized, endogenous rhythm of temperature in 4 months old infants.

Levene and McKenzie (1990) used pulse oximetry to measure transcutaneous arterial oxygen saturation in infants aged 2 to 11 months prone and supine in quiet sleep. Groups of healthy infants (n=34), infants with upper respiratory tract infections (n=13) and infants with generalised moderately severe lower respiratory tract infections (n=17) were studied.

No clinically important differences were demonstrated in any of these groups, although there was a small advantage in the prone position in the group with lower respiratory tract infection. The effects of posture in infants with more severe lower respiratory tract infection and during active sleep has yet to be determined.

Rawson et al. (1990) made continuous rectal temperature recordings from 32 babies the night after their first diphtheria, pertussis, and tetanus vaccination and compared it with recordings made before vaccination. Tog values of clothes and wrapping and room temperatures were also recorded. They found that vaccination the day before disturbs the normal night time rhythm of deep body temperatures. Rectal temperature of vaccinated babies was significantly higher than non-vaccinated babies from two hours into the night.

They also found that there were considerable individual variations in the extent of disturbance of temperature rhythm. They were not correlated with thermal environment. Despite these findings, the authors gave a disclaimer that there is no reason to suppose that these mild physiological responses to vaccination are in any way harmful.

Petersen et al. (1991) assessed the effect of sleeping position upon body temperature by continuous monitoring of rectal temperature in 137 babies sleeping at home under conditions chosen by their parents. They had three groups of babies: 1) normal babies aged 12-22 weeks whose temperature rhythms were developed, 2) normal babies aged 6-12 weeks who were developing their night time temperature rhythms, and 3) babies the night after diphtheria, pertussis, and tetanus vaccination, whose temperature rhythms were disturbed.

Sleeping in the prone position was not associated with higher rectal temperatures at any time of night in young babies, nor did it exaggerate the disturbance of rectal temperature rhythm after vaccination. In older normal babies the prone position did not disturb rectal temperature in the first part of the night, though the prone sleepers warmed a little faster prior to waking, especially in warm conditions. Prone sleepers were, however, born earlier in gestation and tended to be of lower birth weight.

The authors concluded that normal babies can therefore thermoregulate effectively whatever their sleeping posture, even in warm conditions, though the prone position may make it slightly more difficult to lose heat. Importantly, they also wrote that it is difficult to see how the prone position, even interacting with warm conditions, could induce lethal hyperthermia in otherwise normal babies, and, that “Perhaps the prone position is associated with other risk factors for sudden infant death syndrome.”

Heimler et al. (1992) studied the effect of positioning on the breathing pattern of preterm infants. They established that respiration, as judged by gas exchange and pulmonary function, is improved in preterm infants kept in the prone rather than the supine position. The influence of position on the breathing pattern as documented by the pneumogram was studied in 14 stable preterm infants with recent clinical apnoea.

Ten of the infants had oximetry and nasal flow studies simultaneously with the impedance pneumogram. Each infant had consecutive nocturnal pneumograms, one in the prone, one in the supine position. The infants were kept for more than six hours in the assigned position.

A significant increase in apnoea density and in periodic breathing was found in the supine versus the prone position. There was no positional difference in the incidence of bradycardia and prolonged apnoea. The examination of obstructive apnoea, mixed apnoea, and cyanotic spells did not reveal a consistent disparity between the two positions.

The authors concluded that these findings indicate an increase in central apnoea in preterm infants kept predominantly in the supine position. In other words, the prone position was a position of an advantage, while the supine position a position of disadvantage. They discussed possible relations of positional changes to lung mechanics. They advised that when evaluating pneumograms, attention must be given to the position in which they were performed.

The above research represented solid and honest observations under controlled conditions. All authors concluded that the prone position is actually a position of advantage and not of disadvantage, thus seriously challenging the unresearched speculative conclusions about the possible causal role of prone position in SIDS.

Indeed, Beal (1986) unwittingly confirmed this by writing that in Czechoslovakia 61% of SIDS babies were found on their backs. She made no comment on this important fact, probably because the Czech researchers ascertained that the numbers of cot deaths in former Czechoslovakia were very small. However, there is another important factor; I come from former Czechoslovakia and I can confirm that we never had the fashion of putting babies on their tummies; rather we put them on their backs or sides.

The whole issue of the prone position and its role in SIDS boils down to the following: when you have a fashion to put babies on their back, most of them will be found dead on their backs; when most babies are put on their tummies, most of them will be found on their tummies after suffering SIDS. The prone position as such does not cause or contribute to cot death.

Based on the above quoted research, it may actually prevent cot death. My considered personal opinion is that the fact that babies sleeping both supine and prone (which is the position of advantage) and dying means that there is a different factor causing these deaths other than the position.

Despite the above well-documented and relevant research, North et al (1995) published an article which cut across the above research and maintained that the prone position was the position of advantage. The look at their figures and graph, however, only shows what the figures of others who studied the subject show: the sudden fall in temperature as the babies fall asleep, and then a slow increases in the temperature from about 3am onwards as the babies are slowly waking up.

What then does cause SIDS?

The answer is in the name: SIDS – Sudden Immunisation Death Syndrome.

About the author

Dr Viera Scheibner is Principal Research Scientist (Retired) with a doctorate in Natural Sciences from Comenius University in Bratislava. After an eminent scientific career in micropalaeontology during which she published 3 books and some 90 scientific papers in refereed scientific journals in Australia and overseas, she studied babies’ breathing patterns with the Cotwatch breathing monitor developed by her late husband Leif Karlsson in the mid 1980s. Babies had alarms after vaccination, indicating stress. This introduced her to the subject of vaccination. She then started systematically studying orthodox medical papers dealing with vaccination issues. To this day she has collected and studied more than 100000 pages of medical papers.

References

Scheibner 2004. Dynamics of critical days as part of the dynamics of non-specific stress syndrome discovered during monitoring with Cotwatch breathing monitor. J ACNEM; 23 (3): 10-14)

Torch WC. 1982. Diphtheria-pertussis-tetanus (DPT) immunization: A potential cause of the sudden infant death syndrome (SIDS). Neurology; 32 (2): A169-170.

Torch WC. 1986a. Characteristics of diphtheria-pertussis-tetanus (DPT) postvaccinal deaths and DPT-caused sudden infant death syndrome (SIDS): a review. Neurology; 36 (Suppl 1): 148.

Torch 1986b. Diphtheria-pertussis-tetanus (DPT) immunization may be an unrecognized cause of sudden infant death (SIDS) and near-miss syndrome (NMS): 12 case reports. Neurology; 32 (2): 149.

Griffin MR, Ray WA, Livengood JR, and Schaffner W. 1988. Risk of sudden infant death syndrome after immunization with diphtheria-tetanus-pertussis vaccine. New Engl J Med; 319: 618-613.

Munoz JJ, Aral H, Bergman RK, and Sadowski PL. 1981. Biological activities of crystalline pertussigen from Bordetella pertussis. Infection and Immunity; 33. Biological activities of crystalline pertussigen from Bordetella pertussis. Infection and Immunity; 33): 820-826.

Mitchell et al. 1995. Immunisation and sudden infant death syndrome. Arch Dis Child; 73: 498-501

Innis MD. 2009. SIDS: should epidemiology be questioned? Yes! BMJ.com (18 October).

North RG, Petersen SA, and Wailoo MP. 1995. Lower body temperature in sleeping supine infants. Arch Dis Childhood; 72: 340-342.

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