vaccine adverse reactions

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.

Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors

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One of the things I most love about social media and health research is the opportunity to identify patterns of illness across different patient groups. Here is an example of finding research from one patient group, ThyroidChange, that likely spans many others (Gardasil injured, post Lupron Hashimoto’s, and Fluoroquinolone reactions – to name but a few) and offers clues to a perplexing array of symptoms. The research, is about a little known association between movement and balance disorders and Hashimoto’s thyroiditis: Ataxia associated with Hashimoto’s disease: progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis.  Some background.

Hashimoto’s Disease

Hashimoto’s is the most common causes of hypothyroidism afflicting women at a rate of 10 to 1 compared to men. It is an autoimmune disorder in which antibodies attack the thyroid gland and destroy its ability to maintain normal thyroid hormone concentrations. The most common symptoms include: fatigue, muscle pain, weight gain, depression, cognitive difficulties, cold intolerance, leg swelling, constipation, dry skin. If left untreated, goiter – a swollen thyroid gland, appears. If left untreated for an extended period, cardiomyopathy (swelling of the heart muscle), pleural (lung) and pericardial (heart) effusion (fluid), coma and other dangerous conditions develop.

Hashimoto’s and Cerebellar Degeneration

A little known risk in Hashimoto’s is cerebellar degeneration. The cerebellum is the cauliflower looking section at the base of the brain that controls motor coordination – the ability to perform coordinated tasks such as walking, focusing on a visual stimuli and reaching for objects in space. The walking and balance disturbances associated with cerebellar damage or degeneration have a very distinct look, a wide gait, with an inability to walk heel to toe. Cerebellar ataxia looks like this:

In recent years, cerebellar involvement in attention and mood regulation have also been noted. The physicians reporting the Hashimoto’s – ataxia connection present case studies of six patients with Hashimoto’s disease, presumably controlled with medication and a progressive and striking shrinkage of the cerebellum (see report for MRI images) along with progressively debilitating ataxia (walking and balance difficulties) and tremors. Here’s where it becomes interesting.

Hashimoto’s: Medication Adverse Reaction and Misdiagnosis

Hashimoto’s disease is prevalent in our research into medication adverse reactions for Gardasil and Cervarix and Lupron, with some indications it may develop post Fluoroquinolone injury as well. The symptoms are difficult to distinguish from other neurological and neuromuscular diseases such as chronic fatigue syndrome, fibromyalgia, multiple sclerosis and an array of psychiatric conditions, and so Hashimoto’s often goes undiagnosed or is misdiagnosed and mistreated for some time.

Hashimoto’s, Demyelination and Cerebellar Damage

In some of the more severe adverse reactions to medications and vaccines that would lead to Hashimoto’s, the tell tale cerebellar gait disturbances have been noted and documented, along with a specific type of tremor (discussed below).

Research from other groups shows a strong relationship between thyroid function and myelin/demylenation patterns in nerve fibers in animals. Specifically, insufficient T3 concentrations demyelinates nerve axons, while T3 supplementation elicits myelin regrowth. Myelin is the white sheathing, the insulation that protects nerves and improves the electrical conduction of messages in sensory, motor and other neurons. Like co-axial cable in electrical wiring, when the protective sheathing is lost, electrical conductance is disrupted. The early symptoms of a demyelinating disease neuromuscular pain, weakness, sometimes tremors. These can be misdiagnosed as multiple sclerosis, fibromyalgia, chronic pain, when in reality, the culprit is a diseased thyroid gland.

Back to the Cerebellum

The cerebellum is a focal point of white matter axons – myelinated sensory and motor nerves. The cerebellum is where input becomes coordinated into motor movements or movement patterns. White matter damage in the cerebellum causes cerebellar ataxia, the movement and balance disorders displayed above. Hashimoto’s elicits white matter disintegration. Adverse reactions to medications and vaccines can elicit autoimmune Hashimoto’s disease. See the connection?

The Thiamine – Gut Connection

It gets even more interesting when we add another component of systemic medication adverse reactions – nutritional malabsorption, specifically thiamine deficiency. Almost across the board, patients with medication or vaccine adverse reactions report gut disturbances, from leaky gut, to gastroparesis, constipation, pain and a myriad of other GI issues that make eating and then absorbing nutrients difficult. Gut issues are common in thyroid disease too.

As we learn more, and as individuals are tested, severe nutrient deficiencies are noted, in vitamin D, Vitamin B1, B12, Vitamin A, sometimes magnesium, copper and zine. We’ve recently learned of the connections between Vitamin B1 or thiamine deficiency and a set of conditions affecting the autonomic nervous system called dsyautonomia or Postural Orthostatic Tachycardia Syndrome (POTS) linked to thiamine deficiency in the post Gardasil and Cervarix injury group. It may be linked to other injured groups as well, but we do not know yet.

Thiamine and Cell Survival

Thiamine or vitamin B1, is necessary for cellular energy. It is a required co-factor in several enzymatic processes, including glucose metabolism and interestingly enough, myelin production (the Hashimoto’s – cerebellar connection). We can get thiamine only from diet. When diet suffers as in the case of chronic alcoholism, where most of the research on this topic is focused, or when nutritional uptake is impaired, thiamine deficiency ensues. Thiamine deficiency can elicit cell death by three mechanisms:

  1. Mitochondrial dysfunction (reduced energy access) and cell death by necrosis
  2. Programmed cell death – apoptosis
  3. Oxidative stress – the increase in free radicals or decrease in ability to clear them

Thiamine deficiency in and of itself can elicit a host of serious health symptoms. The cell death and disruption of cellular energy balance can be significant and lead to a totally disrupted autonomic system.

Thiamine and Myelin Growth

Add to those symptoms, the fact that thiamine is involved in the growth myelin sheathing around nerves, and we have a whole host of additional neuromuscular symptoms masking as fibromyalgia, multiple sclerosis, chronic fatigue. Like with MS, limb and body tremors are noted in dysautonomic syndromes such as POTS. (Video of POTS tremors, note the uniqueness of the POTS tremor and the similarity between it and the foot tremor shown above along with cerebellar ataxia).

Let thiamine deficiency continue unchecked for period and we get brain damage, as white matter – the myelin disintegrates in the brainstem, the cerebellum and likely continues elsewhere. One of the most prominent areas of damage in thiamine deficiency, is the cerebellum, and hence, the cerebellar ataxia (movement disorders) noted in chronic alcoholics who are thiamine deficient, but also observed post medication or vaccine adverse reaction.

The Double Whammy on Myelin and Cerebellar Function

In the case medication or vaccine adverse reactions, particularly those that reach the systemic level, we have a double whammy on myelin disintegration: from a diseased thyroid gland and a diseased gut. Hashimoto’s and the reduction of thyroid hormones, particularly T3, impairs nerve conduction by shifting from a constant and healthy remyelinating pattern to one of demyelination, while the lack of thiamine further impairs myelin regrowth, because it is a needed co-factor. Both deficiencies affect peripheral nerves, but both also hit the brainstem, the cerebellum and likely other areas within the brain.

Take Home Points

The science of adverse reactions is new and evolving and much of what I am reporting here remains speculative. However, it has become abundantly clear through our research that to address medication adverse reactions or vaccine adverse reactions in a simplistic fashion, by region, or in an organ specific manner, is to miss the broader implications of the compensatory disease processes that ensue. Moreover, to look for symptoms of adverse reactions simply by the drug’s mechanism of action and/or by the standard outcome variables listed in adverse event reporting systems, again misses the complexity of the human physiological response to what the body is perceiving as a toxin. I believe that the entire framework for understanding the body’s negative response to a medication must be shifted to a much broader, multi-system, and indeed, multidisciplinary approach. In the mean time, we will continue to collect data on adverse reactions and offer our readers points of consideration in their quests for healing. I should note, that finding these connections is entirely contingent on the input our community of patients and health activists, both via the personal health stories that so many of you have been willing to share and the data we collect through our research. You know more about your health and illness than we do.

What we Know So Far – Tests to Consider

If you have had an adverse reaction to a medication or vaccine and neuromuscular difficulties, like pain, numbness, motor coordination problems, tremors etc., consider testing for Hashimoto’s thyroiditis. Also, consider thyroid testing when fatigue, depression, mood lability (switching moods), constipation, attentional and focus difficulties are present. In fact, I would consider thyroid testing, specifically for autoimmune thyroid disease like Hashimoto’s, as one of the first disease processes to rule out.

If you have had an adverse reaction to a medication that includes gut disturbances, consider the possibility that you are deficient in key micronutrients such as Vitamin D, the B’s, Vitamin A, magnesium, copper, zinc. And given the modern diet, consider that you were probably borderline deficient even before experiencing the adverse reaction. These nutrients are critically important to health and healing (and no, I do not have an association with vitamin companies or testing companies). Some tests for these nutrients are more accurate than others, so be sure to do your homework first.

If you have symptoms associated with autonomic systems dysregulation such as those associated with POTS, dysautonomia and its various permutations, consider thiamine testing, especially, transkelotase testing.

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Postscript: This article was published originally on Hormones Matter on October 15, 2013. 

Reducing Brain Inflammation with Vitamin B6

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Among the many symptoms of vaccine adverse reactions is brain inflammation, often considered idiopathic or of unknown origins. There are a number of potential culprits underlying vaccine related brain inflammation, including the virus vectors, the neurotoxic adjuvants or the cocktail mistakenly presumed inert ingredients that accompany any vaccine. No matter the cause, however, once inflammation is unleashed within the central nervous system, the inflammatory response itself can become self-perpetuating, initiating secondary pathologies that are chronic, progressive and neurodegenerative.

Chronic brain inflammation, like inflammation in the rest of the body, is now considered one of the leading causes of disease. In the brain, chronic inflammation is believed to lead to Alzheimer’s, dementia and Parkinson’s, while chronic inflammation in the body is connected to heart disease, type 2 diabetes, depression and a myriad of autoimmune diseases. At the center of all inflammatory diseases are dysfunctional mitochondria that, as regulators of the cell survival and number of other functions, control immune reactions – inflammation. Mitochondria are highly susceptible to damage from pharmacological and environmental toxicants and inextricably dependent upon dietary nutrients for proper functioning. When toxicants attack mitochondrial pathways and/or nutrient depletion diminishes mitochondrial functioning, mitochondria activate the immune system and spur inflammatory cascades; cascades that can be stopped only if the exposures are removed and the nutrients restored.

In the brain, neural mitochondria and microglia (brain immune cells), regulate inflammation. Like the mitochondria, these microglia are highly dependent upon dietary nutrients. As we have written previously, the B vitamins are particularly important for central nervous system functioning. New research finds that vitamin B6 is a key regulator of brain inflammation.

Vitamin B6 and Brain Inflammation

Vitamin B6 (pyridoxine >peridoxal 5’ – phosphate) is a necessary co-factor in over 100 enzymes. It is critical for the catabolism (breakdown) of the essential amino acid tryptophan. Tryptophan is required for serotonin (well-being and GI motility) and melatonin (the sleep hormone) synthesis. Disturbances in tryptophan catabolism not only lead to disturbances in neurotransmitter activity, but also, can lead to cell death or apoptosis, in vital brain regions, like the hippocampus (learning and memory), basal ganglia (movement, motivation, intention) and in the cerebellum (motor control and balance).

When all is working well, tryptophan serves as a substrate for serotonin and melatonin. Excess tryptophan is degraded resulting in the by-products nictonic acid and nicotinamide adenine dinucleotide (NAD+)  – or as most of us recognize, niacin, vitamin B3. Niacin is an essential nutrient in many physiological functions. Loss of niacin metabolism from this pathway can lead to significant disease, including, Pellagra, a disease characterized by scaly skin lesions, delusions and confusion. In addition to a loss of niacin synthesis, when vitamin B6 is deficient and the tryptophan pathway is disturbed, the incomplete degradation of tryptophan produces several metabolites that are neurotoxic, including one called quinolinic acid.

Quinolinic acid is a potent and self-perpetuating neurotoxin when unopposed in the brain. It generates ROS (reactive oxygen species indicative of mitochondrial oxidative stress and damage) and over-activates NMDA glutamate receptors (the brain’s primary excitatory neurotransmitter) to the point of apoptosis (cell death), all the while inhibiting brain astrocytes’ ability to clean up the excess glutamate. Once that cycle becomes initiated, quinolinic acid potentiates its own release and that of other neurotoxins, ensuring continued brain inflammation and damage.

With the appropriate vitamin B6, quinolinic acid is not the final product of tryptophan catabolism, NAD+ or niacin is, and any damage initiated by quinolinic acid as a natural by-product within this pathway is offset by two neuroprotective factors, kynurenine and picolinic acid. Vitamin B6 is critical for the kynurenine aminotransferase and kynurinase enzymes; enzymes that lead to neuroprotective compounds, kynurenine or picolinic acid. Kynurenine blocks the cytotoxic effects of quinolinic acid by blocking the NMDA receptor, making it unavailable to quinolinic acid, while picolinic acid is the primary metal chelator (remover) in the brain (likely critically important in post vaccine reactions). In other words, vitamin B6 controls the balance between inflammation and anti-inflammation within the brain and the body.

How do We Know Vitamin B6 is a Neuroprotectant?

Well, we’ve actually known this since the 1970s (perhaps earlier) when work on the kynurenine pathway began. Somehow though, it wasn’t recognized again until the 1990’s and has only recently become prominent over the last decade as connections between environmental and pharmaceutical toxicants and gut microbiota and mitochondrial damage are revealed.

Several studies have emerged over the last decade showing the importance of vitamin B6 (and other B vitamins) in systemic and brain inflammation. Defects in vitamin B6 metabolism are linked to seizure disorders resistant to traditional anticonvulsants but remediable with Vitamin B6.  Vitamin B6 reduces brain atrophy in Alzheimer’s patients. Low vitamin B6 is believed to play a key role in the oxidative stress associated with Huntington’s disease. One of the more interesting studies involves preventing the hippocampal apoptosis associated with bacterial meningitis using vitamin B6.

Bacterial meningitis is a life threatening disease associated with high mortality and morbidity. Of those patients who survive, up to 50% suffer serious neurological impairment including: hearing loss, seizures, cognitive decrements and sensory-motor deficits. The bacteria attack cortical and hippocampal regions of the brain. Hippocampal cell death is associated with learning and memory deficits. In an experimental version of bacterial meningitis with rodents, researchers tested whether vitamin B6 supplementation could prevent the hippocampal apoptosis by moderating the tryptophan pathway towards the B6-dependent kynurenine and picolinic metabolites versus the neurotoxic quinolinic acid. They were successful. Vitamin B6 supplementation reduced brain inflammation and hippocampal apoptosis by up-regulating the neuroprotective factors controlled by the tryptophan – kynurenine pathway. An impressive result reached simply via vitamin supplementation.

Final Thoughts

Tryptophan metabolism and the kynurenine pathway are implicated in disease processes where inflammation is prominent. Vitamin B6 may be critical to maintaining the appropriate balance between inflammatory and anti-inflammatory immune reactions. With modern nutritional deficits (high calorie, low nutrient foods), commercial agricultural practices (glyphosate doused crops are nutrient poor), estrogenic medications and environmental exposures (estrogens inhibit vitamin B6), it entirely conceivable that many of us are vitamin B6 deficient and, as a result, functioning with a constant level of inflammation. Vitamin B6 supplementation, along with the other B vitamins might be warranted.

For those individuals suffering from brain inflammation mediated by disease, medication or vaccine adverse reactions, vitamin B6 might just reduce the inflammation cascades and improve quality of life. Given its direct impact on tryptophan metabolism, vitamin B6 ought to be considered critical for brain health.

 

Poor Nutrition Stress: The Enemy of Health

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In previous posts, I have indicated that stress can initiate or exacerbate disease and medication or vaccine adverse reactions. Read that statement, you might think I am attributing the onset of serious disease and adverse reactions to a psychosocial cause. That is not the case. Stress comes in a myriad of forms, some external, some internal, and although much of what we call stress relates to psychosocial responses to perceived threats, I think stress encapsulates so much more. At its most fundamental level, stress represents a physical state where the body is performing less than optimally. Let me explain.

What is Stress?

I define the word “stress” as a physical or mental force that is acting upon you. An example of mental or psychosocial stress might be an insult from a person, meaning that the stress comes from a source outside the body. On the other hand, it might be the realization that a deadline has to be met, a mental source from within. Any form of injury is an obvious source of physical stress. Physical action such as shoveling snow is another form of stress, demanding energy consumption imposed by the individual who wishes to get rid of the snow. Being infected with a virus or by bacteria is a form of stress that demands a defensive reaction. In each of these instances, the body reacts to the inflicting stressor. Sometimes, when the resources are available, it reacts efficiently. Other times, when the resources are not available or when additional factors intercede, the body’s response to the stress is ill-adapted.

Your Body is Your Fortress, Your Immune System the Soldiers

Perhaps an analogy might help to provide an explanation for the remarks that follow. I imagine the body as being like an old fashioned fortress. The people living within it go into action when the fortress is attacked by an enemy from outside. It would be of little use if the defense soldiers went to the eastern battlements if the attack came from the west and so there had to be a central figure that would coordinate the defensive reaction. The nature of the attack would be spotted by a guard on duty and the central figure informed by messenger.

The body represents the fortress and the lower part of the brain represents the central figure that coordinates the defense. The cells in the blood known as white cells can be thought of as soldiers, armed with the necessary weapons to meet the nature of the enemy. Suppose, for example, a person’s finger is stuck by a splinter carrying a disease bearing germ. The pain, felt in the brain, recognizes its source and interprets it as a signal that an attack has occurred. White cells in the area can be regarded as the “militia under local command” and a “beachhead” is formed to wall off the attack. The white cells sacrifice themselves and as they die, they form what we call pus. If the beachhead is broken and the germs manage to get into the bloodstream, it is then called septicemia and the brain/body goes into a full defensive reaction where high fever is the most obvious result. Such an illness is an attack/defense battle.

The symptoms that develop from such an infection represent the evidence for this defense, feeling ill, pain and developing a fever are excellent examples. Micro-organisms are most efficient at 37° C, the normal body temperature. The rise in body temperature, initiated by the brain, makes the microorganisms less efficient and may kill some of them. One therefore has to question the time honored method of reducing the fever, during illness, as being an example of good treatment. While reducing fever improves the symptoms caused by the infection, it also reduces the efficiency of the immune battle raging within.

The outcome against the stressor is death or recovery; although it is possible sometimes to end up in a kind of stalemate, represented by prolonged symptoms of ill health. Chronic illness may be viewed as the immune system’s inability to eradicate fully the stressor.

Poor Nutrition and Stress

As I have emphasized in previous posts, the autonomic (automatic) nervous and endocrine systems are used to carry the messages between the body and the brain that enable the defense to be coordinated. This demands a colossal amount of cellular energy, no matter the nature of the stress. That energy to fight stress comes from oxidation of the fuel that is provided from nutrition. Of course, the greater the stress the greater the energy demand, but in the end the equation is quite simple. If the energy required to meet the stress is greater than the energy that is supplied, there must be a variable degree of collapse within the defensive system. That collapse presents as intractable symptoms, where the body is unable provide the energy needed to sustain health. This is the secret of the autonomic dysfunction in the vitamin B1 deficiency disease, beriberi. It is also the secret behind the initiation of POTS because both conditions are examples of defective oxidation. You can read more details regarding thiamine deficiency, beriberi, POTS and other health issues from previous posts on this website

High Energy Demands Equal High Nutritional Demands

Nutrient density of diet might appear to be perfectly adequate for a given individual, but inadequate to meet the self-initiated energy demands of a superior brain/body combination in a highly active individual such as an actively engaged student or athlete. Our genetic characteristics, the quality of nutrition and the nature of life stresses each represent a factor that all combine together to give us a profile for understanding health and its potential breakdown.

Epigenetics and Mitochondria: The Stress of Our Parents

Epigenetics, the science of how our genes are influenced by diet and lifestyle, is relatively new. Epigenetics considers the possibility that genes can be activated and deactivated by nutrition and lifestyle. Stress can come in many forms, from psychosocial trauma, poor nutrition, environmental and medical toxin exposures, to infections. Stress impacts how our genes behave. Even though one may inherit a hard-coded genetic mutation from a parent, that mutation may not be activated unless exposed to a particular type of stress. Similarly, an individual who may have no obvious illness-causing genetic abnormalities but stress, in the form of nutritional depletion, exposures or trauma, can turn on or turn off a set of genes that induce illness. What is remarkable about epigenetics is the transgenerational nature of the stressors. The memories of stressors affecting our parents and even our grandparents can affect our health by activating or deactivating gene programs.

We also have to consider the state of our mitochondria, the “engines” in each of our cells that produce the energy for cellular function (to learn more about mitochondria and health, see previous posts on this website). Mitochondria have their own genes that are inherited only from the mother. Damage to the DNA that makes up these genes sometimes explains the similarity of symptoms that affect a given mother and any or all of her children. For example, although this damage may be inherited, we also have scientific evidence that thiamine deficiency, known to be the result of poor diet, can damage mitochondria. A bad gene might be the solitary cause of a given disease, but even where this is known as the cause, the symptoms of the disease are sometimes delayed for many years, suggesting that other variables must play a part. A minor change in cellular genetic DNA might be alright to meet the demands of normal living, but impose a risk factor that could be impacted by prolonged stress or poor nutrition, and disease emerges.

Nutrition is the Only Factor that We can Control

The imposition of stress on any given individual is variable, most of which is accidental and out of our control. Therefore, if we represent these three factors, genetics, stress and nutrition as three interlocking circles, all of which overlap at the center of such a figure, there is actually only one circle over which we have control and that is nutrition. We now know from the science of epigenetics that nutritional inadequacy can affect our genes. By examining the mechanism by which we defend ourselves against stress, we can also see the effect of poor nutrition.

Poor Nutrition Equals a Poor Stress Response

Using these three variables, perhaps we can begin to understand several unanswered questions. Why does a vaccination negatively affect a relatively small percentage of the total population vaccinated? Or why do some medications negatively impact only some individuals? It might be because of a genetic risk factor or because of a collapse of the coordinated stress response related to quality of nutrition or a combination of both. Why does a vaccination tend to “pick off” the higher quality students and athletes? Again, the same kind of answer; high quality machinery demands high quality fuel. Since the limbic system of the brain has a high energy demand and represents the computer that coordinates a stress response we can understand the appearance of beriberi or POTS and cerebellar ataxia, all examples of a deviant response to stress. Nutrition, therefore, should not be looked at as supplement to good health, but as the foundation of health. When disease or medication and vaccine reactions emerge, efforts to identify and then restore nutritional deficiencies must be the first line of immune system health. Without critical nutrients, the body simply cannot mount a successful stress response and the battlefield will expand and eventually fall.

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Medication Safety and Efficacy Studies: Share Your Experience

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Is this Medication or Vaccine Good for Me?

That is the question on everyone’s mind; is this medication good for me? How does one decide? The mandated medication package inserts tell one story. The online drug reaction and interaction lists are long and complicated. Adverse events data are incomplete and patient stories reflect individual reactions. Where are the reports that put numbers to the side-effects and adverse reactions? Where are the real world data that show risks for patients of different age groups, men versus women, or on multiple medications? Lucine Health Sciences and Hormones Matter are collecting those data and you can help.

Understanding Side Effects

While we cannot make your medication decisions for you, we can collect more complete side-effect data from patients like you, from around the world and we can offer those data reports to patients, physicians and industry. We think everyone deserves to know the frequency, severity, and chronicity of side-effects. We think everyone deserves to know whether a the benefits of a medication or vaccine outweigh the risks. Don’t you?

How You Can Help

Take a Health Survey

Take a few minutes to complete a survey about the medications and surgical procedures you have utilized. Take as many health surveys as are applicable and share the surveys with your friends. All surveys are anonymous and completely voluntary. We’re adding more surveys every month, so check back frequently or sign up for our weekly newsletter to keep abreast of the latest research news.

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Lucine Health Sciences and Hormones Matter, are unfunded and are run by Dr. Chandler Marrs along with a cadre of dedicated volunteers. We know the work we do is important and needed and so we’re doing it anyway, despite the lack of funding. We’re bootstrapped to the nth degree*, but determined to fill the critical data void in healthcare, one study at a time.

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Hormones Matter – Legal Structure

Hormones Matter is the health media arm of Lucine Health Sciences. We leverage the broad educational and social media reach of Hormones Matter to crowdsource critical, direct-to-patient research. Lucine is a C-corporation by federal standards, a B-Corp (for benefit corporation) in the state of Nevada. What this means is that any money you contribute, either through the donate or the subscribe buttons, is not tax deductible; for that we would have to be a not-for-profit enterprise.

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Lucine neither collects nor distributes personally identifying patient information, see our Ethics and Privacy for more details. We will, however, publish trended reports for open access and custom reports for industry. For more information, see Research Services.

  • In February of 2016, Lucine received a grant to conduct a multi-phased study on the risks for blood clots with hormonal birth control. All other research remains unfunded.