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Thoughts on Inflammation, Vaccines and Modern Medicine

Published on September 28, 2017

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One of the core components of an HPV vaccine adverse reaction inevitably includes some degree of seemingly unexplainable but observable brain inflammation and white matter disintegration. The brain inflammation falls under a number of different names and diagnoses, some are regionally specific, cerebellar anomalies for example, while others demarcate a more diffuse injury including, acute disseminated encephalomyelitis (ADEM), myalgic encephalomyelitis (ME), sometimes known as chronic fatigue, multiple sclerotic (MS) type lesions and, the newest and perhaps more prescient among them, a set of conditions designated as Autoimmune/Inflammatory Syndrome Induced by Adjuvants or ASIA that denote chronic inflammation both centrally and peripherally relative to vaccine adjuvant exposure.

Is the Brain Immune Privileged?

Despite the observance of brain inflammation in many post HPV vaccine victims, many practitioners, and indeed, the FDA and CDC, seem loathe to recognize that an aluminum lipopolysaccharide adjuvanted virus vector might induce a neuro-inflammatory response, leaving patients with little recourse post injury. The difficulties attributing brain inflammation to a vaccine reaction stem from a long held belief that the blood brain barrier is stalwart in its protection against peripheral trespassers. The brain has long been considered, ‘immune privileged’ having little to no communication with peripheral immune function. Indeed, the perceived impenetrableness of the blood brain barrier is so extensive that brain-body separation might as well be complete, with a brain in bottle and a decapitated body.

Logically, we know this cannot be true. There must be crosstalk between the immune systems of brain/central nervous system and that of the body. How else could we survive if the two modalities were segregated so completely? It turns out, that logic may be prevailing. A decade of research suggests that the long held notion brain immune – privilege is completely and utterly incorrect. Indeed, the immune system not only guides early neurodevelopment (and so mom’s immune function matters) but communicates and affects brain morphological changes chronically. Likewise, signals from the brain continuously influence peripheral immune function.

The immune system appears to influence the nervous system during typical functioning and in disease. Chronic infection or severe illness may disrupt the balance of normal neural–immune cross-talk resulting in permanent structural changes in the brain during development, and/or contributing to pathology later in life. The diversity, promiscuity, and redundancy of “immune” signaling molecules allow for a complex coordination of activities and precise signaling pathways, fundamental to both the immune and nervous systems.

It should not be surprising then, that nutrient status and toxicant exposures in the periphery, in the body, affect central nervous system function and are capable of inducing brain inflammation and vice versa. And yet, it is; perhaps even more so than any of us realize.

Re -Thinking Brain Inflammation

When one reads through the definitions, research and case reports of ADEM, ME, MS or other instances of brain inflammation, the notion that biochemical lesions in the periphery are linked to observed neuro-inflammatory reactions is far from center stage. Nevertheless, if we can accept the premise what happens in and to the body does not stay in the body, then we can begin to re-frame our approach to brain inflammation. Specifically, we can look at inflammation more globally and ask not only what triggers inflammation, but allows inflammation to persist chronically, regardless of its location. If there is an on-going peripheral inflammatory response, is it not prudent to suspect that a similar response might be occurring within the central nervous system, even if our imaging tools are not yet capable of visualizing the inflammation; even if it is too premature to observe demyelination, neuronal, axonal swelling or other telltale signs of chronic brain inflammation? I think it is.

Vaccine Adjuvants: A Pathway to Brain Inflammation

With the HPV vaccine, and indeed, any vaccine, the deactivated viral vectors come with a cocktail of additional chemical toxicants and a metal adjuvant to boost the recipient’s immune response, as measured by the increase in post vaccine inflammatory markers. It is believed that without these adjuvants (and data back this up), the recipient’s immune response is insufficiently activated to merit ‘protection’ against the virus. The strength or size of the immune response is then equated with success and protection.

By this equation, an excessive immune response that continues chronically and is eventually labeled ‘autoimmune’ as innate systems begin to fail, is in some way not a failure or side effect, but an example of extreme success; the larger the immune response, the stronger the vaccine. And so, skewed as this observation may seem, within the current vaccine-paradigm there can be no ‘side-effects’, not really. By design, there should be inflammation, even brain inflammation; the more the better. Also by design, metal, lipid soluble, adjuvants cross the blood brain barrier and directly induce brain inflammation. To say vaccines don’t or somehow couldn’t induce brain inflammation is ignorant, if not, utterly negligent, and quite simply, defies logic. Again, for prudence and safety, shouldn’t we assume that an inflammatory reaction in the body might also ignite some concordant reaction in the central nervous system?

Why Aren’t We All Vaccine Injured?

What becomes apparent though, is even with exposure to the most toxic brew of vaccines, not all who receive vaccines are injured, at least observably. (I would argue, however, even those who appear healthy post vaccine, had we the tools to observe brain inflammation more accurately, would show a central inflammatory response, at least acutely, and likely, progressively). So what distinguishes those individuals who seem fine post vaccine, particularly post HPV vaccine, from those who are injured severely and sometimes mortally?

More and more, I think that the fundamental differences between vaccine reactors and non-reactors rest in microbial and mitochondrial health. Indeed, all vaccines, medications, and environmental toxicants damage mitochondria, often via multiple mechanisms, while altering microbial balance. Whether an individual can withstand those mitochondrial insults depends largely upon a balance struck among three variables: 1) heritable mitochondrial dysfunction, genetic and epigenetic; 2) the frequency and severity of toxicant exposures across the lifetime; and 3) nutrient status. Those variables then, through the mitochondria, influence the degree and chronicity of inflammation post vaccine. With the HPV vaccine in particular, the timing of the vaccine, just as puberty approaches and hormone systems come online, may confer additional and unrecognized risks to future reproductive health.

Mitochondria and Microbiota

The mitochondria, as we’ve written about on numerous occasions, control not only cellular energy, but cell life and death. Every cell in the body, including neurons in the brain, require healthy mitochondria to function appropriately. Healthy mitochondria are inextricably tied to nutrient concentrations, which demand not only dietary considerations but balanced gut microbiota. Gut bacteria synthesize essential nutrients from scratch and absorb and metabolize dietary nutrients that feed the mitochondria. Indeed, from an evolutionary perspective, mitochondria evolved from microbiota and formed the symbiotic relationship that regulate organismal health. Disturb gut bacteria and not only do we get an increase in pathogenic infections and chronic inflammation, but also, a consequent decrease in nutrient availability. This too can, by itself, damage mitochondria.

When the mitochondria are damaged, either by lack nutrients and/or toxicant exposure, they trigger cascades of biochemical reactions aimed at conserving energy and saving the cell for as long as reasonably possible. When survival is no longer possible, mitochondrial sequestration, and eventually, death ensue, often via necrosis rather than the more tightly regulated apoptosis. Where the mitochondria die, cells die, tissue dies and organ function becomes impaired. I should note, as steroid hormone production is a key function of mitochondria, hormone dysregulation, ovarian damage and reduced reproductive capacity may be specific marker of mitochondrial damage in young women.

Mitochondria and Inflammation

Mitochondria regulate immune system activation and inflammation and so inflammation is a sign of mitochondrial damage, even brain inflammation. Per a leading researcher in mitochondrial signaling:

The cell danger response (CDR) is the evolutionarily conserved metabolic response that protects cells and hosts from harm. It is triggered by encounters with chemical, physical, or biological threats that exceed the cellular capacity for homeostasis. The resulting metabolic mismatch between available resources and functional capacity produces a cascade of changes in cellular electron flow, oxygen consumption, redox, membrane fluidity, lipid dynamics, bioenergetics, carbon and sulfur resource allocation, protein folding and aggregation, vitamin availability, metal homeostasis, indole, pterin, 1-carbon and polyamine metabolism, and polymer formation.
The first wave of danger signals consists of the release of metabolic intermediates like ATP and ADP, Krebs cycle intermediates, oxygen, and reactive oxygen species (ROS), and is sustained by purinergic signaling.
After the danger has been eliminated or neutralized, a choreographed sequence of anti-inflammatory and regenerative pathways is activated to reverse the CDR and to heal.
When the CDR persists abnormally, whole body metabolism and the gut microbiome are disturbed, the collective performance of multiple organ systems is impaired, behavior is changed, and chronic disease results.

Reducing Inflammation

Instinctively, we think reducing inflammation pharmacologically, by blocking one of the many inflammatory pathways, is the preferred route of treatment. However, this may only add to the mitochondrial damage, further alter the balance of gut microbiota and ensure increased immune activation, while doing nothing to restore mitochondrial and microbial health. In emergent and acute cases, this may be warranted, where an immediate, albeit temporary, reduction in inflammation is required. The risk, however, is that short term gains in reduced inflammation are overridden by additional mitochondrial damage and increased risk of chronic and/or progressive inflammation. The whole process risks becoming a medical game of whack-a-mole; a boon to pharmaceutical sales, but devastating to those who live with the pain of a long-standing inflammatory condition.

In light of the the fact that damaged mitochondria activate inflammatory pathways and that vaccines, medications and environmental toxicants induce mitochondrial damage, perhaps we ought to begin looking at restoring gut microbial health and overall mitochondrial functioning. And as an aside, perhaps we ought to look at persistent inflammation not as an autoinflammatory reaction, but for what is it, an indication of on-going mitochondrial dysfunction.

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This post was published originally on Hormones Matter on September 22, 2014.

The Paradox of Modern Vitamin Deficiency, Disease, and Therapy

by Derrick Lonsdale MD, FACN, CNS

Published on March 17, 2014

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In order to understand why this article is about “paradox”, the concept of vitamin therapy must be appreciated. Hence, the explanation of the title is deferred to the end. Although vitamin deficiency disease is believed by most physicians to be only of historical interest, this is simply not true. When we think of a vitamin deficiency disease, we envision an individual living in a third world country where starvation is common. Such an individual is imagined as being skeletal, whereas an obese person is considered to be well fed with vitamin enriched foods. For this reason, common diseases, some of which are associated with obesity, are rarely, if ever, seen as potentially vitamin deficient.

The Calorie Rich and Nutrient Sparse Modern Diet

Our food is made up of two different components, the caloric and the non-caloric nutrients. When we ingest high calorie foods (e.g. a doughnut) without even a vestige of non-caloric nutrients, we refer to this as “empty” or “naked” calories. For our food to be processed into energy that enables the body and brain cells to function, there must be a ratio of the calorie bearing component to that of the non-caloric nutrients. When we load the calories together with an insufficiency of non-caloric nutrients, we alter this ratio and produce a relative vitamin deficiency. The trouble with this is that it does not result in the formation of the classic vitamin deficiency diseases as recorded in the medical literature. There is a gradual impairment of function, resulting in many different symptoms. Because modern medicine seeks to make a diagnosis by the use of imaging techniques and laboratory data and because of the physician’s mindset, if the tests used are normal, the possibility of a relative vitamin deficiency is ignored.

The Brain as a Chemical Machine

We have two different nervous systems. One is called “voluntary” that enables us to do things by will-power. This is initiated and controlled by the upper brain, the part of the brain that thinks. The other system is known as the autonomic nervous system (ANS). This is initiated and controlled by the lower part of the brain, the limbic system and brainstem. This system is controlled automatically. Although it collaborates with the other system, it is not normally under voluntary control. The limbic system and brainstem are highly sensitive to oxygen deficiency, but since the oxygen is useless without the non-caloric nutrients, their absence would produce the same kind of phenomena as oxygen deficiency. Thiamine (vitamin B1) has been found to be of extreme importance as a member of the non-caloric nutrients. The brain, and particularly the limbic system and brainstem, is highly sensitive to its deficiency.

Since the ANS is automatic, we are forced to think of the limbic system and brainstem as a computer. For example, when it is hot, you start to sweat. Evaporation of the sweat from the skin produces cooling of the body, representing an adaptive response to environmental hot temperature. When it is cold, you may start to shiver. This produces heat in the muscles and represents an adaptive response to environmental low temperature. If you are confronted by danger, the computer will initiate a fight- or- flight reflex. This is a potential lifesaving reflex. It is designed for short term use, consumes a vast amount of energy and prepares you to kill the enemy or flee from the danger. Any one of these reflexes may be modified by the thinking brain. For example the lower brain, also known as the reptilian system, initiates the urge to copulate. It is modified by the upper brain to “make love”. The reptilian system, working by itself, can convert us into savages. There is an obvious problem here because our ancestors were faced with the dangers of short term physical stress associated with survival. In the modern world the kind of stress that we face is very different for the most part. We have to contend with traffic, paying bills, business deadlines and pink slips. The energy consumption, however is enormous, continues for a long time and it is hardly surprising that it is associated with fatigue, an early sign of energy depletion. It has been shown in experimental work that thiamine deficiency causes extensive damage to mitochondria, the organelles that are responsible for producing cellular energy.

Autonomic Function

The autonomic nervous system, controlled by the lower brain, uses two different channels of neurological communication with the body. One is known as the sympathetic system and the other is the parasympathetic. There are also a bunch of glands called the endocrine system that deals with the brain-controlled release of hormones.

We can think of the sympathetic branch of the ANS as the action system. It governs the fight-or-flight reflex for personal survival and the relatively primitive copulation mechanisms for the survival of the species. It accelerates the heart to pump more blood through the body. It opens the bronchial tubes so that the lungs may get more oxygen. It sends more blood to the muscles so that you can run faster and the sensation of fear is a normal part of the reflex. When the danger is over and survival has been accomplished, the sympathetic channel is withdrawn and the parasympathetic goes into action. Now in safety and under its influence, body functions such as sleep and bowel action can take place. That is why I refer to the parasympathetic as the “rest and be thankful system”.

Dysautonomia, Dysfunctional Oxidation and Disparate Symptoms

When there is mild to moderate loss of efficiency in oxidation in the limbic system and/or brainstem they become excitable. This is most easily accomplished by ingesting a high calorie diet that is reflected in relative vitamin deficiency. The sympathetic action system is turned on and this can be thought of as a logical reaction from a design point of view. For example, if you were sleeping in a room that was gradually filling with carbon dioxide, the gradual loss of efficiency in oxidation would be lifesaving by waking you up and enabling you to exit the room. In the waking state, this normal survival reflex would be abnormal.

High calorie malnutrition, by upsetting the calorie/vitamin ratio, causes the ANS to become dysfunctional. Its normal functions are grossly exaggerated and reflexes go into action without there being any necessity for them. Panic attacks are merely fragmented fight-or-flight reflexes. A racing heart (tachycardia) may start without obvious cause. Aches and pains may be initiated for no observable reason. Affected children often complain of aching pain in the legs at night. Unexplained chest and abdominal pain are both common. This is because the sensory system is exaggerated. One can think of it as the body trying to send messages to the brain as a warning system.

Nausea and vomiting are both extremely common and are usually considered to be a gastrointestinal problem rather than something going on in the brain. Irritable bowel syndrome (IBS) is caused by messages being conveyed through the nervous system of the bowel, increasing peristalsis (the wave-like motion of the intestine) and often leading to breakdown of the bowel itself, resulting in colitis. Of course, the trouble may be in the organ itself but when all the tests show that “nothing is wrong”, the symptoms are referred to as psychosomatic. The patient is often told that it is “all in your head”.

Emotional instability seems to be more in keeping with psychosomatic disease because emotional reactions are initiated automatically in the limbic system and thiamine deficient people are almost always emotionally unstable. A woman patient had been crying night and day for three weeks for no observable reason. A course of intravenously administered vitamins revealed a normal and highly intelligent person. Intravenously administered vitamins are often necessary for serious disease because the required concentrations cannot be reached, taking them by mouth only.

The Vitamin Therapy Paradox

The body is basically a chemical machine. But instead of cogwheels and levers, all the functions are manipulated through enzymes that, in order to function efficiently, require chemicals called “cofactors”. Vitamins are those essential cofactors to the enzymes. If a person has been mildly to moderately deficient in a given vitamin or vitamins for a long time without the deficiency being recognized, the enzyme that depends on the vitamin for its action appears to become less efficient in that action. A high concentration of the vitamin is required for a long time in order to induce its functional recovery.

Although the reason is unknown, doctors who use nutritional therapy with vitamins have observed that the symptoms become worse initially. Because patients expect to improve when a doctor does something to them and because drugs have well-known side effects, it is automatically assumed by the patient that this worsening is a side effect of the vitamins. If the therapy is continued, there is a gradual disappearance of those symptoms and overall improvement in the patient’s well being. Unless the patient is warned of this possibility he or she would be inclined to stop using the treatment, claiming that vitamins have dangerous side effects and never getting the benefit that would accrue from later treatment. This is the opposite effect that the patient expects. This is the paradox of vitamin therapy.

If we view dysautonomia as an imbalance in the functions of the ANS and the vitamin therapy as assisting the functional recovery by stimulating energy synthesis, we can view this initial paradoxical as the early return of the stronger arm of the ANS before the weaker arm catches up, thus worsening an existing imbalance. However, this is mere speculation. I did not learn of the “paradox” until I actually started using mega dose vitamins to treat patients.

The Paradox and Thiamine

In this series of posts, we are particularly concerned with energy metabolism and the place that thiamine holds in that vital mechanism. It is, of course, true that worsening of serious symptoms is a fact that has to be contended with and vitamin therapy should be under the care of a knowledgeable physician. The earlier the symptoms of thiamine deficiency are recognized, the easier it is to abolish them. The longer they are present the more serious will be the problem of paradox and a clinical response will also be much delayed and may be incomplete.

Beriberi and Thiamine Deficiency

I will illustrate from the early history of beriberi when thiamine deficiency was found to be its cause. Many of the patients had the disease for some time before thiamine was administered, so the danger of paradox was increased. It was found that if the blood sugar was initially normal, the patient recovered quickly. If the blood sugar was high, the recovery was slow. If the blood sugar was low, the patient seldom recovered. In the world of today, an abnormal concentration of glucose in the blood would make few doctors, if any, think of thiamine deficiency as a potential cause. It is no accident that diabetes and thiamine metabolism are connected. Education of the doctor and patient are both absolutely essential. I believe that the ghastly effects of Gardasil, and perhaps some other medication reactions covered on Hormones Matter, can only be understood by thinking of the body as a biochemical machine and that the only avenue of escape is through the skilled use of non caloric nutrients.

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