vaccine side effects

Do We Need a New Approach to Vaccine Recommendations?

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In a recent article published in the British Medical Journal, Crowcroft et al (2015) suggest we need a new approach to vaccine recommendations. Focusing mainly on the economic and ethical considerations involved in public policy surrounding vaccine programs and vaccine approval the authors write:

“We are on a steep trajectory away from an era of inexpensive vaccines for diseases that are widespread in the absence of immunisation… Technologies such as searching genetic codes for possible antigens and the development of new adjuvants to stimulate immune responses also bring considerable uncertainty about safety and effectiveness.” 

“…some sections of society are less likely to vaccinate themselves or their children. Those who hesitate to vaccinate are often highly educated, well resourced, and demand respect for their perspectives.” 

Though speaking specifically about a ‘novel vaccine’ for serogroup B meningococcal disease, Bexsero (Novartis, Basel), the issues and problems of vaccine safety and approval apply to all vaccines. Arguably, more important than the economic risk to benefit models used by healthcare policy analysts to calculate the health costs for vaccines are the very real questions associated with safety and efficacy. Those concerns neither make it to same cost/benefit calculations, inasmuch as the actual costs associated with mitigating adverse reactions are not included, nor do they appear paramount to policy makers or ethicists. The preference instead is to assume that risks of adverse reactions and ineffective vaccines are minimal compared the risks associated with the diseases vaccines purport to protect against. I would suggest that efficacy and safety are central to any risk/benefit calculation and ensuing policy decision. For without those data, neither the economic costs nor the human costs of said policy decision can be accurately assessed.

Vaccine Safety and Efficacy  

If we look at the historical data, across multiple vaccines, a pattern emerges that is quite distinct from the models proposed by many healthcare agencies and governmental institutions.

Crawcroft and Britto (2002) called whooping cough a continuing problem, which has re-merged in countries with high vaccination coverage [with inexpensive vaccines] and low mortality.  Then they contradicted themselves. “Pertussis has re-emerged…because of low coverage after a vaccine scare in the 1980s (in the United Kingdom) or the use of vaccines with poor efficacy (Canada, Sweden).”

“Germany stopped their vaccination programmes completely and only reinstated vaccination for pertussis after years of recurrent epidemics of whooping cough.” However, according to Miller and Farrington (1988), “In West Germany, unlike the UK, there are no national statistics on pertussis incidence, no national vaccination policy and no figures for vaccine uptake. Local studies have shown that vaccination rates are low and that pertussis is prevalent particularly in 2-4 year age-group, which is typical of a country with low uptake, similarly serotype 2 predominates.”

Whooping cough vaccine was introduced in the UK during the 1960s and national statistics on uptake rates are available from 1961.

“Mortality data show that death from whooping cough declined before ‘the disease was reduced by vaccination’”.

Are there any Diseases Reduced by Vaccination? 

Starting with smallpox vaccines, continuing through typhoid, diphtheria and later on DPT and other vaccines, the highest incidence of targeted diseases occurred in the vaccinated. Famously, the Leicester citizens’ boycott of smallpox vaccine stopped smallpox epidemics in their city. Outbreaks of typhoid in the army occurred right after mass vaccination (Wright 1901). A huge diphtheria outbreak in the vaccinated in the 1940s in Nazi Germany and in the Nazi occupied countries. A documented 300% increase in the incidence of whooping cough starting in the 2-months old DPT recipients in the USA in mid seventies (Hutchins et al 1988).

The US outbreaks of measles in even 100% vaccinated populations started in 1963 with the licensure and mass use (Sencer et al. 1967) of the  measles vaccines. The destruction of transplacentally-transmitted immunity (Mulholland 1995) predicted by vaccine researchers early in the piece, resulted in pertussis and measles occurring in newborn babies in all countries with high vaccination compliance. Outbreaks of provocation paralysis (infantile paralysis) provoked by all vaccinations) (McCloskey 1950) are well-documented.

Natural infectious diseases of childhood (both mortality and morbidity) were on the downward trajectory 50 years before any vaccines were administered in mass proportions. The main reasons were better nutrition (especially better vitamin C status), sanitation, clean water and uncrowded living conditions. Generational immunity acquired by repeated exposure and inherited and acquired natural immunity cannot be overlooked, either.

The largely unvaccinated Amish (claiming religious exemption) had not reported a single case of measles between 1970 and December 1987, for 18 years (Sutter et all 1991), while the well-vaccinated non-Amish communities experienced regular 2-3 year epidemics in even 100% vaccinated populations. Pro-vaccinators claimed success and set a date for measles eradication (1 October 1982). Instead, large measles outbreaks occurred in the vaccinated non-Amish, starting in 1982, and on 5 December 1987 in the Amish.  The situation simply confirmed Hedrich’s (1933) evaluation of measles epidemic cycles (2-3, 11, and even 18 years).

Pertussis followed similar dynamics motivating pro-vaccinators to claim success with early pertussis vaccination. However, it did not take long and pertussis outbreaks in fully vaccinated populations followed mass vaccination drives. Instead of abandoning the obviously ineffective vaccination, the culture of “lies, damn lies and statistics” set in.

Sweden discontinued pertussis vaccine use for 11 years in 1979; whooping cough became a mild disease and stopped occurring in babies and young children below one year of age (Isacson et al. 1993).  Very few doses of pertussis vaccine were administered, however, even those few recipients developed pertussis (one in 3).  372 (61%) of the 377 parents interviewed, reported clinical pertussis in their unvaccinated children (confirming Hedrich’s (1933) concept of herd immunity).

When Sweden resumed pertussis vaccination (with acellular vaccine) in mid 1990s, not only the incidence went up, but the babies under the age of one contracted the disease already during the trials of acellular vaccine straight after the first dose of the vaccine (Olin 1995). The trial was discontinued before the expected termination date. Epidemics in the vaccinated have continued.

Japan moved the DPT & P vaccination age to two years in mid seventies with similar effect as observed in Sweden, including a substantial fall in the overall infant mortality (from 17th to the first, lowest infant mortality rate in the world (Jenny Scott 1990).

The UK experienced similar dynamics, also in mid seventies. After the first media report of brain damage linked to DPT vaccine the UK parent’s compliance fell down to 30% or even 10%), but according to Fine and Clarkson (1982), paradoxically, the inter-epidemic period did not decrease after the 1974 fall in vaccine uptake.

Pertussis incidence and hospital admissions fell markedly and so did the overall infant mortality. Macfarlane (1982) wrote, ”The postneonatal mortality fell markedly in 1976, a year on which a sharp decline in neonatal mortality rate began. Between 1976 and 1979, however, neither the late neonatal nor the post-neonatal mortality rates fell any further.  Indeed, the post-neonatal mortality rate increased slightly among babies born in 1977.  Obviously, when the compliance started climbing, so did the infant mortality rates in England and Wales and Glasgow. Epidemics in the vaccinated followed.

Preston (1994) analyzed the pertussis situation and wrote, ”In the mid-1970s, the general public and many health care professionals in Britain lost faith in the safety of whole-cell pertussis vaccine. This reaction (largely in response to fears about vaccine-induced brain damage) was unjustified, and caused vaccine uptake in infants to plunge from 80% to 30%.” Preston compared this with the situation in Massachusetts and wrote, “An apparent increase in incidence in 1989-91 was largely due to wider surveillance and the introduction of serologic diagnosis for adolescents with not less than 1 week of paroxysmal coughing…” “Stott and Davis suggested that, in the absence of a positive culture, the term “pseudo-whooping cough” is appropriate for paroxysmal cough of less than 3 weeks duration. Although the authors of the Massachusetts report express concern about the diagnosis of pertussis in fully vaccinated children, they do not tell us how many of these children had positive cultures, culture positivity being the only reliable laboratory test.

Cincinnati likewise experienced a resurgence of pertussis in 1993, with 223 culture-positive cases.  Although 82% of diagnosed “cases” between 6 months and 6 years of age had received at least three doses of (Connaught and Lederle) vaccine, the criteria for clinical diagnosis are not stated, nor are we told the number of culture-positive cases in this age group…Both consider panic measures, such as neonatal vaccination, immunisation of pregnant women and boosting with acellular vaccine.” And, we are told “The vaccine cannot be expected to protect against pseudo whooping cough.  Nevertheless, there are several good reasons for genuine failure of pertussis vaccination.”

Early Vaccination and Later Disease

In all countries with national vaccination programs, the distribution of all vaccine-preventable disease experienced deranged age distribution. The present situation is that in all developed countries with high vaccination compliance epidemics of pertussis, measles, mumps, etc. occur with increased frequency and magnitude, and, in the vaccinated.

Medical researchers documented waning vaccine ‘immunity’, changes in the serogroup, polymorphism and mutations of the causative organisms (directly linked to vaccines in a similar fashion as experienced with antibiotics and other antibacterials and antivirals) (Cassiday et al. 2000; Octavia et al. 2011; Mooi et al. 2014).

Medical research provides important scientific evidence against continued use of vaccines, which is an outdated, ineffective and unsafe technology. Moreover, the evidence of the benefits of natural infectious diseases in providing a life-long specific and non-specific immunity has also been mounting.

References

  1. Crawcroft et al. 2015. Do we need a new approach to making vaccine recommendations? BMJ; 30 January: 350; h308:1-6 (Analysis).
  2. Crawcroft and Britto. 2002. Whooping cough – a continuing problem.  BMJ; 325. 29 June : 1537-1538 (editorial).
  3. Miller and Farrington. 1988.  The current epidemiology of pertussis in the developed world: UK and West Germany. Tokai J Exp Clin Med; 13 Suppl): 97-101.
  4. Wright 1901.  On the changes affected by anti-typhoid inoculation in the bactericidal power of the blood; with remarks on the probable significance of these changes.  Lancet; Sep 14: 715-723.
  5. Hutchins et al. 1988. Current epidemiology of pertussis in the United States.  Tokai j Clin Med; 13(Suppl): 103-109.
  6. Sencer et al. 1967.  Epidemiologic basis for eradication of measles in 1967.  Pub Health Reports; 82(3): 253-256.
  7. Mulholland 1995.  Measles and pertussis in developing countries with good vaccine coverage.  Lancet; 345. Febr 4: 305-307.
  8. McCloskey,  1950,  The relation of prophylactic inoculations to the inset of poliomyelitis. Lancer. April 18: 659-663.
  9. Sutter et al. 1991.  Measles among the Amish: a comparative study of measles severity in primary and secondary cases in households.  J Infect Dis; 163: 12-16.
  10. Hedrich 1933.  Monthly estimates of the child population “susceptible” to measles, 1900-1930, Baltimore, MD.  Am J Hygiene: 613-635.
  11. Isacson et al.  1993.  How common is whooping cough in a non vaccinating country?  Ped infec Dis J; 12(4): 284-288.
  12. Olin 1995.  Acellular pertussis vaccines – a question of efficacy. J of Hospital Infections; 30 (Suppl): 503-507.
  13. Jenny Scott  1990.  US slips in infant mortality.  National Commission to prevent infant mortality.
  14. Fine and Clarkson 1982.  The recurrence of whooping cough: possible implications for assessment of vaccine efficacy.  Lancet; March 20: 666-668.
  15. Macfarlane 1982.  Infant deaths after four weeks.  Lancet; October 23: 9290939.
  16. Preston 1994.  Pertussis vaccination: neither panic nor complacency.  Lancet; 344, August 20: 491-492.
  17. Stott and Davis.  1981.  Pertussis vaccination and pseudo-whooping cough.  BMJ; 282,June 6: 1871.
  18. Cassiday et al. 2000.  Polymorphism in Bordetella pertussis pertactin and pertussus toxin virulence factors in the United States, 1935-1999).  J Infect Dis; 182: 1402-1408.
  19. Octavia et al. 2011.  Insight into evolution of Bordetella pertussis from comparative genomic analyses: evidence of vaccine-driven selection.  Mol Biol Evol; Jan 10; 28(1): 707-715.
  20. Mooi et al. 2014.  Pertussis resurgence: waning immunity and pathogen adaptation – two side of the same coin.  Epidemiol Infect. Feb 13; 142(4): 685-694.

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This article was published originally on Hormones Matter on March 19, 2015.

The Vaccine Debate: Where is the Empathy?

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Of Peanut Allergies and Petulance

A few weeks ago, a fellow social media acquaintance posted an article about peanut allergies in children. The article argued that no peanut butter sandwich is as important as a child’s life, so she urged her fellow moms not to bring peanut items to school if a classmate had a known peanut allergy. I read it: it was heartfelt and very sensible. I am of the opinion that my daughter can certainly live without peanut butter sandwiches at school. Her school is nut free, and never once has it inconvenienced me in the slightest. When I found out about the nut-free rule, my first thought was “Wow. I’m so glad that I do not have to worry about my daughter encountering such a dangerous allergy situation all the time–that must be really hard for those parents.” Apparently, that’s not such a common response. Read any of these articles on moms talking about peanut allergies and you will find comments from parents reacting in ways that range from annoyed to down-right cruel. Parents protesting that “Kids should learn to navigate their allergies in the real world” and “My child won’t eat anything else!” This poor mother is sitting there having to worry about one sticky peanut butter finger touching a door knob and her small child dying in a matter of minutes from anaphylaxis after touching that door knob. Think about that for a second: HAVING TO WORRY THAT YOUR CHILD WILL DIE EVERY SINGLE DAY AT SCHOOL FROM PEANUT BUTTER.  Thinking about that is enough to make my heart bust open with torturous sadness for that parent. The lack of empathy in those responses was astounding. In some cases, down right sociopathic.

You may be on board with the peanut butter argument, agreeing that we should have empathy for children with peanut allergies. Those kids didn’t choose their allergies, and their parents have to worry that their children will die from a product that is nearly ubiquitous in our existence. You may be one of the parents that gets that, and that’s great. But the conversation took an even darker turn, and that is what I want to really talk about in this article. One respondent wrote something to the effect of, “Why do we just have to worry about peanut butter sandwiches when there are stupid, irresponsible parents who let their child come to school unvaccinated and put our children at risk of death every day.” If you’ve read this article, you can imagine that struck a nerve with me. Although I feel like my response to that comment was both warranted and respectful, it never does any good but open Pandora’s Box, leaving me tired, discouraged, helpless and hopeless. WHY? Lack of empathy.

Vaccine Vitriol: A Pattern of Predictable Disdain

There’s a group of people in our society that is marginalized beyond belief in the most cruel and unusual ways: vaccine injured children and their families. Now before you stop reading, thinking I am some crazy “anti-vaxxer” about to do some “pro-vaxxer” bashing, please know that is not going to happen here. In fact, I am attempting to do exactly the opposite. The vaccine argument is one of the most contentious and heated debates I’ve ever seen. I’d be willing to go out on a limb and say it is worse than probably any other political issue to date: even more so than gun control or immigration.

In any vaccine discussion, it is common for phrases like “you should have your kids taken away and go to jail” and “you’re an idiot who believes in pseudoscience” to fly around the conversation. To be honest, there’s a lot of self-righteousness and indignation sometimes on both sides of the issue. So what is going on here? Why can’t we have a civil conversation about vaccines, like, EVER?

Well, I’m a psychologist, so all the obvious answers (to me) ran through my head: cognitive dissonance, belief perseverance, etc. Yes, it’s well documented in psychological science that people cling tight to their beliefs even in the face of overwhelming contradictory evidence, but these things don’t really account for why people can be so darn MEAN to each other in the process. Then (as I usually do), I started ruminating on how, at some level, every single thing that human beings do is explained by consciousness. Human beings are a product of their minds, and our minds are set up to run in very predictable ways. Human brains are pattern seekers; they constantly put things into groups or categories. Every piece of stimulus information we encounter (what we see, hear, touch, feel, taste), is organized in the brain in a way that helps us put things into logical order.

Information is stored in our long term memory in something called a semantic network, where similar pieces of information remain connected together in our brains. We create schemas, which are “templates” for objects and situations that become stored in our memory. These things help us predict and anticipate things we will encounter in the future. In other words, these processes help us navigate a world filled with overwhelming amounts of stimulus information. Usually, this works pretty well for getting around this complex world, except that life is not black and white, and dealing with the gray areas require much more effortful processing.

What does this have to do with meanness and lack of empathy? If our minds are naturally inclined to place things into groups, then that’s part of the reason that it’s so easy to cling to dualistic thought: right vs. wrong, bad vs. good, in-group vs. out-group, winner vs. loser. Not only are our brains pattern seekers, but we’re also social animals that seek out similar others. Both of these things help create a large “us” vs. “them” dynamic. Psychological science has also shown that we tend to have more empathy for those who are similar to us than dissimilar. In other words, when “us” encounters “them”, our brains are more inhibited from producing empathetic responses. Moreover, the anger that arises from our values being challenged activates our amygdala (our brain’s alarm system) which competes against our pre-frontal cortex (involved in self-control and rational thought). Combine all of that with the deindividuation (loss of self-awareness in a group) of the social media environment, and you’ve got a recipe for cruelty and indignation.

Beyond Us Versus Them in the Vaccine Debate: Empathy First

How can we unravel these barriers when it comes to the vaccine argument? One word (here it is again): Empathy. No, it’s not the dominant response in this situation, but research has also shown that we can call upon our executive functions like self-control and exert them upon will. It’s tough, and it depletes us when we do it, but it can be done. We need to approach these conversations by first trying to willfully control our immediate anger that results from confronting information that challenges our beliefs. Yes, that challenge is uncomfortable, but by taking a few minutes to let your mid-brain calm down and execute willful self-control, you’ll be better prepared to try to understand the other side of the argument.

One very smart commenter in that social media conversation, who was actually the first person to acknowledge that maybe I wasn’t crazy after all for speaking out against vaccinations, suggested that instead of eliciting anger and defensiveness, attempting to induce empathy with rational thought might be a better strategy. She suggested asking yourself, “Why would someone choose not to vaccinate their child?” or “Why would someone want to force everyone to vaccinate when they know some children have been injured by vaccines?” If you’ve really been able to put your anger aside (at least temporarily) then you’ll realize the answer to both questions is exactly the same: They want healthy children. Suddenly, it’s not “us” versus “them” anymore, it’s just “us”. We all want the same thing, we just have vastly different feelings about how to accomplish it.

This person also made a point that was the driving reason behind writing this article. She said something about how being “right” isn’t a strategy if you want to change the hearts of people that disagree with you.  I’ll admit, that’s all I have ever been trying to do: be right. The need to be right comes from a real and raw place deep down in my heart. I watched my daughter fight a chronic auto-inflammatory disease that was triggered by vaccinations. I held her while she suffered. I fought for her when doctors couldn’t figure it out. I’m the one who read hundreds of scientific articles, pored over her lab results, tracked every symptom, found the patterns, and put the puzzle pieces together. I demanded the referrals, I found her cure, and she’s currently in remission–not because of what her doctors knew but because of what I KNEW.  When you experience something like that, it’s really hard to hold on to the age-old notion that “doctors know best.”

When the vaccine debate emerges and I tell people our story, at best I will get “I’m sorry for what happened to your daughter, but that is rare” and at worst, “I highly doubt your daughter’s condition was triggered by vaccines, vaccines are a scapegoat for the onset of many genetic conditions”.  Neither of those responses is empathetic. I consider myself lucky that my daughter is in remission, but my heart breaks knowing that there are parents out there whose children are severely disabled or have died as a result of vaccines, and those are the responses they get from others.

On the other hand, I need to take a moment and practice what I’m preaching here. I need to show some empathy those folks who so valiantly defend vaccines, and I’m going to ask my vaccine-questioning friends to try and do the same. I understand why people defend vaccines. I really do. I understand the fear of a tiny little baby contracting a horrible disease that could end in their death and being angry thinking that some kid who could have been protected from that disease could be the culprit that led to your child’s death. That is absolutely terrifying and a real phenomenon that has happened in this world. I mean, all you have to do is go to the mall and see that people are coughing and sneezing, EVERYWHERE. The risk is real. I understand because I, too, share that fear. I have been exposed to information that has lessened that fear to some degree, but I still have it.  I understand that the rational and logical thing to do is adopt the mainstream position of highly respected doctors, scientists and health organizations who have had intense training in science and medicine. I can understand how ridiculous it sounds to think that all of these experts are somehow wrong or involved in some kind of grand conspiracy to cover up the idea that vaccines are highly dangerous or ineffective. In fact, I’m willing to say that this position is the logical position. I’m not going to tell anyone that believes this that they are wrong. I’m going to tell them that I understand. I not only understand, but I want to have faith in doctors and research and the CDC, too.

Some Things You Cannot Un-Know: The Corruption Runs High, But Not Necessarily Deep

Now, my vaccine defenders, it’s your turn. There is only one thing that has separated your position from my own: life experience. I cannot have faith in these doctors and organizations because they have failed me and they failed my daughter in very real, life-changing ways. When you or your child has been injured by something that you were told was safe, you can’t just shrug your shoulders and say, “Well I guess everything has risks and my child was one of the rare ones.” Nope. You say “How could this have possibly happened?” You start digging. You quickly find out there are thousands of research articles that contradict the mainstream opinion, even entire textbooks. You find out that there are thousands of doctors and scientists shouting from the rooftops about how the risk of what happened to your child is not uncommon. You find out that there has been so much corruption and cover-up in organizations like the FDA and CDC that congressmen are shouting on the congressional floor for our government to do something about it—but nothing ever gets done. You find out that pharmaceutical companies have all the money and the power and that they own the media and that’s why these dissenting scientists aren’t featured on the news. You find out the pharmaceutical companies also fund the research, pay the editors of the journals, pay doctors money to speak about their products, and even influence the head of the FDA.

Suddenly the once illogical argument that the mainstream is wrong is not so illogical after all. It’s not a grand conspiracy, it’s the influence of money and greed forcing the direction of science and medical opinion at the very top of the chain, and all those underneath that aren’t being funded simply go along with the “respected” opinion of those at the top. For those underneath who have discovered the truth, they have figured out that publicizing dissenting opinions runs the risk of destroying both their careers and reputation. The safe choice is to continue with the status quo. That’s how it happens. That’s how thousands of children and adults can be injured by pharmaceuticals, and the rest of us stand back and let it happen. Once you know this information, you can’t un-know it. It changes you.

Go Beyond the Feedback Loops: Walk in Another’s Shoes

In many ways experiences hand us our reality, but in many ways we also create it. The things we Google appear on our Facebook feed; the things we like on Facebook are tracked and used to send us similar material. It’s easy to see how once we adopt a position it’s constantly being reinforced by more and more exposure to the same information. It’s unlikely that we ever truly expose ourselves to the other side of any argument—but that may be the key in fostering the empathy we need to drive the change we seek in the vaccine debate. Psychological science has demonstrated the social influence of reciprocity, where one concession leads to the concession of the other side. This is a powerful psychological phenomenon. So, I’m conceding. Instead of begging vaccine-defenders to listen to us and focusing on trying to be right, let’s for one second, focus on their position. Put yourself in their shoes. Show them that you understand that they have fears for their children, too. Showing empathy is the only way they will show us that in return. Being right cannot be our strategy, because it’s not their minds we need to change—it’s their hearts.

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The Flu Vaccine, Molecular Mimicry, Narcolepsy: Clues to Gardasil Injury

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What do molecular mimicry, the H1N1 Flu vaccine and the HPV vaccines Gardasil or Cervarix have to do with the brain neurons involved in narcolepsy or hypersomnia? Plenty. Researchers are learning that vaccine induced immune reactions can destroy innate cells via molecular mimicry and in the case of the flu vaccine, the hypocretin/orexin neurons responsible for maintaining wakefulness are attacked. Idiopathic hypersomnia, a derivative of narcolepsy is one of the many side effects reported by post Gardasil girls and women. Could the HPV vaccine be attacking those same neurons? Is molecular mimicry at play in the HPV vaccine too? The answers are yes and possibly, but with the HPV vaccine, the molecular mimicry is more widespread and the research only beginning to delineate its effects.

What is Molecular Mimicry?

Molecular mimicry is the notion that foreign pathogens like bacteria, viruses and vaccines can be so similar in structure or function to innate, ‘self’ peptide sequences that they evoke an autoimmune response in the exposed individual.  Molecular mimics are thought to be involved in the onset of Type 1 Diabetes, Lupus, Multiple Sclerosis and other diseases, including some neurological disease processes.

Molecular mimics are snippets of protein code embedded within the pathogen that are either functionally similar and contain sequences of identical code to those found innately in humans, or structurally similar and because of their shape can bind to and activate an immune cell receptor. The protein codes, called motifs, are instructions that govern all aspects of the cell’s activity levels, and indeed, our very health and survival. Some codes tell the cell to live and how to function, others tell the cell to die and even how to die. The thought is that when external pathogens contain protein motifs that mimic internal and innate protein motifs, our immune system recognizes the foreign invader and attacks not only the dangerous pathogen, but the innate molecules that contain those same protein motifs too, evoking all sorts of damage to potentially many different tissues and organs. When there is structural similarity between the pathogen and immune cells, the process for immune activation is quite easy. The pathogen slips in, binds to a receptor and initiates the inflammatory immune response. In either case, the immune response to the environmental pathogen results in a disease process identified as autoimmune – the immune system attacking itself. It should be noted that connection between molecular mimicry and autoimmune disease onset is hotly debated.

Narcolepsy or Hypersomnia, the Immune System and the Flu Vaccine

In 2010, amidst the fears of the H1N1 swine flu pandemic, citizens in Scandinavia and Europe were given the adjuvanted (MF-59 a squalene based adjuvant plus ASO3 – squalene-α-tocopherol mix) flu vaccine called Pandemrix. Shortly thereafter physicians began noting an increase in new onset cases of narcolepsy, especially in Scandinavian children.

Narcolepsy is the lifelong disorder characterized by excessive sleepiness with abrupt and sudden transitions to REM sleep.  It affects approximately ~ 1 in every 3000 individuals worldwide. Individuals with narcolepsy/hypersomnia have sudden and very strong urges to sleep throughout the day, though at night insomnia may develop. Patients may fall asleep as many as 20-30 times per day, for brief periods, making regular functioning difficult without wake stimulating medications.

Often co-occurring with narcolepsy is a condition called cataplexy. Cataplexy denotes the muscle tone and behavioral changes that precede the narcoleptic sleep incident. Cataplexy symptoms can range from the barely perceptible loss of facial muscle tone or twitches to full muscle paralysis and collapse. Approximately 70% of patients with narcolepsy also have cataplexy.

Hypersomnia, or more specifically, idiopathic hypersomnia, is a central nervous system disorder similar to narcolepsy. Like with narcolepsy, the brain is unable to regulate sleep-wake cycles, only here instead of bouts of uncontrollable sleepiness and periods of sudden onset sleep, with idiopathic hypersomnia, the sleepiness is severe, excessive and continuous. Both narcolepsy and idiopathic hypersomnia have long been thought to be autoimmune in nature, triggered by environmental factors. Bacterial infections such as streptococcus pyogenes, the bacteria responsible for strep throat/pharyngitis and skin infections like impetigo can elicit narcolepsy in some individuals, as well as autoimmune rheumatic fever and kidney disease in others.

Hypocretin/Orexin Neurons Damaged in Patients with Narcolepsy/Hypersomnia

From an autoimmune standpoint, key to triggering narcolepsy in some individuals, is presence of a particular gene variant in immune cells called human leukocyte antigens (HLA). The variant is labeled HLA -DQB1*0602.  Fully 98% of patients with narcolepsy exhibit the DQ0602 haplotype (DQA1*0102/DQB1*0602) versus 18-25% of the general public who have the mutation but do not experience narcolepsy. DQ0602 impairs and often destroys the brain neurons that secrete a peptide hormone that is required to maintain wakefulness. The wake-promoting hormone released from the hypothalamus, is called orexin or hypocretin.  Orexin and hypocretin are the same molecule that was discovered simultaneously by two separate research groups and then named independently.  Readers will see research articles on both orexin and hypocretin linked to narcolepsy (and the flu vaccine, migraine, glucose metabolism, feeding behavior, to name but a few other areas of research).

Molecular Mimics in the Flu Vaccine Attack Hypocretin Neurons and Induce Narcolepsy

Researchers from Stanford found molecular mimics in the adjuvanted Flu vaccine, Pandemrix, both sequence code and structural similarities that initiated immune system attacks on the hypocretin/orexin system in narcolepsy patients but not healthy controls. It should be noted in this particular study, only the adjuvanted version of the flu vaccine was studied, as that was the product distributed in Europe and Scandinavia. The non-adjuvanted version of the Flu vaccine sold in the US was not tested.

For the present study: CD4+T Cell Autoimmunity to Hypocretin/Orexin and Cross-Reactivity to a 2009 H1N1 Influenza A Epitope in Narcolepsy, the researchers used confirmed narcolepsy patients and controls who were all positive for the DQB1*0602 gene variant associated with narcolepsy. Here, despite having the variant, only the patients had a reactivation of the immune attack on the hypocretin neurons. The control group, who were also positive for the variant, but who had no active symptoms or diagnoses of narcolepsy, did not demonstrate the same immune response.  This suggests that other factors in addition to the molecular mimics and a personal predisposition must align to initiate the immune response or, in this case, what is deemed the autoimmune response. It also suggests, that in predisposed individuals, vaccine introduced molecular mimics can trigger immune system attacks and initiate disease states that may or may not have been symptomatic pre-exposure.

What this research does not explain is whether the new onset cases observed in the Scandinavian population post vaccine exposure were solely in individuals with the pre-disposing genetic variant. Was the increase in narcolepsy post flu vaccine exposure indicative of a latent disease state simply triggered by the vaccine? Or is it possible that there are other molecular mimics embedded within the flu vaccine, not yet identified, that might also trigger narcolepsy? Finally, and most importantly, could there be additional factors native to this and other vaccines, to the individual, or with the combination thereof, that evoke an attack on the neurons responsible for regulating wakefulness and inducing narcolepsy, or evoke an attack on other cells and elicit different disease processes? If the answer is yes to any of these questions, then our approach to vaccines ought to be rethought.

Molecular Mimicry and the HPV Vaccines Gardasil and Cervarix

Here is where it gets interesting for those interested in post Gardasil injury. The flu study, as limited and focused as it was, provides important clues to how and why the HPV vaccine might also induce an array of side effects, including, but not limited, to hypersomnia in some individuals but not in others.

Researchers have begun investigating molecular mimics in the HPV vaccines Gardasil and Cervarix. Thus far, they have identified 82 pentamer (5) level  mimics and 34 heptamer (7) level mimics in the HPV 16L component. The offending motifs control a variety of cell behaviors related to cardiac functioning, cell permeability and cell death. An immune system attack on any of these motifs could elicit serious illness. Indeed, the researcher postulates that the mimicked motifs controlling cardiac functioning could be culprits in the post HPV vaccine incidences of sudden death.

To my knowledge, the full HPV vaccine to human proteome has not been mapped and so how or if there are mimicked protein motifs within the HPV vaccine that are capable of attacking the hypocretin/orexin neurons is not known. Nevertheless, idiopathic hypersomnia, a derivative of narcolepsy, is one of the core symptoms of post Gardasil injury, though it is sometimes misdiagnosed and mischaracterized as excessive fatigue and sleepiness. Additionally, a number of other symptoms post Gardasil are influenced by the hypocretin/orexin system, including feeding behavior, gastroparesis (perhaps via galanin) migraine, and all over pain (via dynorphin) – more on this in subsequent posts. Since we now know that molecular mimics can evoke reactions, it is only a matter of time before researchers match the vaccine protein motifs and structural homologies to individual gene variants, environmental predispositions and the clinical symptoms/syndromes that develop.

Perhaps even more interesting, when we dig into the hypocretin/orexin system we see that the neurons are especially susceptible to changes in ATP. Intracellular ATP in hypocretin/orexin neurons must be maintained at much higher levels than in other cells. Diminished ATP stores inhibits hypocretin/orexin firing and thereby reduces sustained wakefulness. We know from other research and patient reports that severe thiamine deficiencies are present in post Gardasil injury (whether the deficiencies existed pre-Gardasil, but were asymptomatic is not clear). Thiamine is a required co-factor in the production of ATP. Reduced thiamine would impair functioning in the hypocretin/orexin neurons and induce the hypersomina and hypophagia and many of the other symptoms we see post vaccine.

In subsequent papers, I will explore the myriad functions the hypocretin/orexin neurons regulate and how damage to those neurons, either directly as indicated in the flu vaccine study, or indirectly, via targeting critical co-factors provides clues to the constellation of post Gardasil injuries. Additionally,  I will address the molecular mimicry debate and how it will reshape the framework for understanding autoimmunity.

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Obesity and Childhood Vaccines: Is there a Connection?

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The staggering increase in obesity affecting mainly people of the industrially developed world is an indisputable fact. Researchers have put forward a number of ideas of which overeating and/or eating too much sugar/carbohydrates and fats are the most popular. However, orthodox medical research points to some other factors and phenomena starting with a growing incidence of infantile and pediatric hyperinsulinemia.

Infantile hyperinsulinemia is sometimes considered a rare congenital disorder where excessive insulin secretion creates a state of hypoglycaemia – low blood sugar. Severe hypoglycemia in the newborn can lead to a myriad of health issues including severe neurological handicaps and seizures. The symptoms are recognized generally at around six months of age and are believed to develop in 1/50,000 births.
In regions where consanguinity are common the rate may be as high as 1-2/500. However, there are non-genetic, iatrogenic (medically induced) mechanisms of hyperinsulinemia that must be considered also.

An emerging body of evidence suggests a connection between infantile hyperinsulinemia and the administered vaccines, the use of antibiotics and other medical and environmental factors. The timing of infant vaccines, in particular, corresponds closely to the recognition of infantile hyperinsulinemia. Could there be a connection between vaccines and/or antibiotic use and insulin dysregulation in infants and children? Moreover, would this also predispose children to obesity later in life?

Vaccine Induced Hyperinsulinemia?

With the pertussis portion of the DTP vaccine (diphtheria, tetanus and pertussis; and now DTaP [aP=acellular]) pertussis vaccine, there have been longstanding questions regarding safety. In 1978 Hannik and Cohen wrote, “There is a considerable concern about the reactions that sometimes occur in children following the injection of pertussis vaccine. Reactions have been observed and reported since 1933 (1) and range from the slightest minor reactions to status convulsivus resulting in permanent cerebral damage.”

Hannik and Cohen’s review cites a number of studies identifying adverse reactions to the pertussis portion of the vaccine and a relationship to insulin homeostasis, including: Parfentjev and Schleyer (1949), Szentivanyi et al. (1963) Tabachnik and Gulbekian (1968), Tabachnik and Gulbekian (1969). Respectively, these studies dealt with the influence of histamine on the blood sugar level of normal and pertussis vaccine sensitized animals (rats and mice), adrenergic changes due to pertussis [vaccine], insulin, glucose and free fatty acids and encephalopathy following pertussis vaccine prophylaxis. The pertussis vaccine proved to be the principal precipitating pathogen in all cases.

Hannik and Cohen (1978) wrote, “Infants injected with DTP-Polio vaccine with a pertussis component of 16 International Opacity Units per dose showed slight but significant elevation in concentration of plasma insulin and temperature.” They concluded that the phenomena (i.e. the elevation in concentration of plasma insulin and increased temperature) are not interrelated. They suggested that “infants who show serious reactions following pertussis vaccination suffer from a failure to maintain glucose homeostasis.” They also noted, “low blood sugar level and extremely low CFS-glucose concentration have been reported in children who developed convulsions 3 and 36 hours after receiving pertussis vaccine.”

A few years later, Katada and Ui (1981) wrote, “Islet-activating protein is a new protein isolated from the culture of Bordetella pertussis as one of the pertussis toxins. It interacts with islet cells slowly to give rise to striking reversal of alpha-adrenergic inhibition cAMP accumulation in, a consequent insulin release from the islet cells.” In other words, a protein toxin within the pertussis portion of the DTP/DTap vaccine was found to initiate insulin release, providing additional evidence connecting the vaccine to infant hyperinsulinemia.

Deranged Glucose Metabolism in Childhood

Interestingly, Zametkin et al. (1990) demonstrated that adults with hyperactivity of childhood onset suffer derangement of cerebral glucose metabolism affecting the prefrontal cortex and superior prefrontal cortex, the parts of the brain that control attention and motor activity. Could the pertussis protein toxin that activates insulin release identified by Katada and Ui (1981) be responsible for childhood derangement in sugar metabolism and not the consumption of sugar, as such, that is implicated? Even though the authors considered the cause of the altered glucose metabolism unknown, it is clear to me that impaired glucose homeostasis may be a result of childhood vaccination. The consequences of this impairment may then be related to many of the conditions plaguing modern society, including obesity. Indeed, the product insert for Tripedia Sanofi Pasteur DTaP vaccine lists autism (SIDS and other serious reactions) detected during post-marketing surveillance.

From Vaccines to Hyperinsulinemia to Obesity

Hughes (1997) demonstrated a significant increase in both the height and weight of the 5 to 11-year old English and Scottish children and called for an urgent need to realistic intervention to reduce obesity in this population.

Freedman et al. (1997) described secular increases in relative weight and adiposity among children over two decades, from 1973 to 1994 in a biracial community of Ward of Washington Parish, Louisiana, USA.

According to Medical Observer (2005; May 12), “Alarming levels of hyperinsulinism, fatty liver, dyslipidaemia and other complications are present in Australian primary school children with high body mass index (BMI)”.

According to Dunne et al. (2004), “hyperinsulinemia promotes hepatic and skeletal muscle glucogenesis, which decreases the amount of free glucose available in the blood stream and results in suppression of the formation of free fatty acids. Fatty acids do not cross the blood brain barrier and cannot be used by the brain as an energy substrate. The combination of hypoglycaemia, reduced fatty acids availability for cardiac and skeletal muscle metabolism and reduced ketones for cerebral metabolism result in adrenergic and neuroglycopenic symptoms with severe neurological dysfunction. Seizure activity will also manifest. Repeated episodes of severe prolonged hypoglycaemia can result in permanent neurological damage, including developmental delay, mental retardation, and/or focal CNS deficits.”

Although the research groups noted above identified hyperinsulinemia in the studied populations, none investigated the role of the administered vaccines, in the induction of hyperinsulinemia. Given the research highlighted previously, it seems plausible that protein toxins contained in the pertussis vaccine are capable of evoking hyperinsulinemia and by way of association may be responsible for the increasing rates of childhood obesity. To that end, Smith and Furman (1988) wrote, “Pertussis vaccine, pertussis toxin, and the alpha-adrenoreceptor blocking drug phentolamine augment glucose-induced insulin secretion. The present study was carried out to determine the relationship between the action and the ability of these agents to prevent the inhibitory action of adrenaline. Pertussis vaccine augmented glucose-induced secretion in rat islets ex vivo and prevented the inhibitory actions of adrenaline and clonidine.”

Antibiotics and Obesity

Another class of medications – antibiotics – might also be linked to the increase in childhood obesity. Antibiotics are widely prescribed for a great number of conditions. Most children suffer a series of ear infections and lower respiratory and urinary infections in the first year of life after vaccination, as documented by Craighead (1975) and may, as a rule, be given several rounds of antibiotics.

Antibiotics are used prolifically in the animal food industry to enhance the protein (flesh) production and weight in animals. These have the same effect on children as they have on young food animals: antibiotics make them fat and muscular.

Garly et al. (2006) unwittingly documented the fattening effect of antibiotics in children in a developing country. They wrote, “The group that received prophylactic antibiotics had less pneumonia and conjunctivitis and has a significantly higher weight gain in the months after inclusion.”

Conclusion

Although not consistently considered a culprit in the widespread childhood obesity epidemic, iatrogenically impaired infant and childhood glucose homeostasis may be a contributing factor. Administration of DTP/DTaP and possibly other vaccines, alone or together with antibiotics could predispose children to chronic states of impaired insulin metabolism and glucose regulation irrespective of dietary considerations.

References

Kumaran et al. (2010). The clinical problem of hyperinsulinemic hypoglycemia and resultant infantile spasms. Pediatrics; 126(5): e1231-1236.

Hannik and Cohen. 1978. Changes in plasma insulin concentration and temperature of infants after pertussis vaccination. Third International Symposium on Pertussis. (Part 3): 297-299.

Parfentjev and Schleyer. 1949. Influence of histamine on the blood sugar level of normal and sensitized mice. Arch Biochem. 20: 341-346.

Szentivanyi et al. 1963. Adrenaline mediation of histamine and serotonin hyperglycemia in normal mice and the absence of adrenaline induced hyperglycemia in pertussis sensitized mice. J Infect Dis; 113: 86-98.

Tabachnik and Gulbekian. 1969. Adrenergic changes due to pertussis, insulin, glucose and free fatty acids. Eur J Pharmacol, 7(2): 186-195.

Toshiaki Katada and Michio Ui. 1981. Islet-activating protein. J Biol Chemistry; 16 (August 25): 8310-8317.

Zametkin et al. (1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. NEJM; 323 (November 15): 1361-1366.

Hughes et al.(1997). Trends in growth in England and Scotland 1972-1994. Arch Dis Child; 76:182-189.

Freedman et al. 1997. Secular increases in relative weight and adiposity mong children over two decades, from 1972 to 1994, residing in Ward 4, Washington parish, Louisiana. Pediatrics; 99(3): 420-426.

Smith and Furman. 1988. Augmentation of glucose induced insulin secretion by pertussis vaccine, phentolamine and benextramine: involvement of mechanism additional to prevention of the inhibitory actions in rats. Acta Endocrinologica; 118:89-95.

Dunaif et al. 1989. Profound peripheral insulin resistance, independent of obesity in polycystic ovary syndrome. Diabetes; 38(9): 1165-1174l

Nestler et al.1990. A direct effect of hyperinsulimemia on serum, sex hormone-biuding globulin levels in obese women with the polycystic ovary syndrome.

Gambineri et al. 2002. Obesity and polycystic ovary syndrome. Journal of International Association for the study of obesity. 26(7): 883-896.

Scott et al. 1997. Characteristics of youth-onset of non-insulin dependent diabetes mellitus and insulin-dependent diabetes mellitus at diagnosis. Pediatrics; 100: 84-91.

Dunne et al. 2004. Hyperinsulinism in infancy. From basic science to clinical diseases. Physiology Rev; 84: 239-275.

Valdyula et al. 2006. Platelet and monocyte activation by hyperglycemia and hyperinsulinemia in healthy subjects. http://informahealthcare.com/doi/abs/10.1080/09537100600760814: 17(8): 577-585.

Burghen et al. 2013. Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease. J Clin Endocrinol and metabolism; 50 (issue 1). Published online July1, 2013,

Takizawa et al. (2001) Gender differences in the relationships among hyperleptinemia, hyperinsulinemia, and hypertension. Clinical and Experimental Hypertension; 23(4): 357-368.

Hussain et al. 2004. Infantile hyperinsulinemia associated with enteropathy, deafness and renal tubulopathy: clinical manifestations of a syndrome caused by a contigous gene deletion located on chromosome 11p. J Pediatr Endocrinol Metab; 17(12): 1613-1621.

Michaud et all; 2014. Acetaminophen-induced liver injury in obesity and non-alcoholic fatty liver disease. Liver Int; 34(7): e171-179. doi.1111

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Goulding 1973. Acetaminophen poisoning. Pediatrics; 52(6):883-885.

Craighead 1975. Report of a workshop: Disease accentuation after immunisation with inactivated microbial vaccines. J Infect Dis; 1312 (6): 749-754.

Garly et al. (2006). Prophylactic antibiotics to prevent pneumonia and other complication after measles, community based randomised double blind placebo controlled trial in Guinea-Bissau. BMJ, doi:10.1136/bmj.38989.AE published 23 October 2006.