Hashimoto’s Autoimmune Thyroiditis

Hashimoto’s disease is an autoimmune disorder in which your immune system inappropriately attacks your thyroid gland, causing damage to your thyroid cells and upsetting the balance of chemical reactions in your body. The inflammation caused by Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, often leads to an underactive thyroid gland (hypothyroidism). Hashimoto’s disease is the most common cause of hypothyroidism in the United States.

When You Are Diagnosed With Hashimoto’s

By the time you are diagnosed with Hashimoto’s, Hypothyroidism involving just the thyroid is no longer the primary factor. Any support you give for just the thyroid will provoke further attacks. So stop it!!! Look for the other non-thyroid factors and which of the other five patterns of low thyroid  are involved. You will respond much quicker in doing this.

Along the way, however, there can be periods where the thyroid sputters back to life, even causing temporary hyperthyroidism, then a return to hypothyroidism. This cycling back and forth between hypothyroidism symptoms and hyperthyroidism is characteristic of Hashimoto’s disease as the other Non-Thyroid Factors and/or conditions that cause the five patterns of hypothyroidism and/or 22 factors of low thyroid function caused by the neuroendocrine transmitters of the NEI Supersystem  flare up and/or calm down. Again, the thyroid is NOT directly involved.

So, for example, periods of anxiety/insomnia/diarrhea/weight loss may be followed by periods of depression/fatigue/constipation/weight gain. Did I mention the 22 different factors that can cause low thyroid function that are due to neuroendocrine transmitters of the NEI Supersystem? Again, the thyroid is NOT directly involved.

Hashimoto’s Thyroiditis Treatment Priorities

  1. Calm and Quite the immune system
  2. Quench inflammation in the body
  3. Reset the immune system
  4. Support the elimination of the other NON-Thyroid factors that provoke immune responses towards the thyroid. (Not mentioned by Kharrazian or Wentz)
  5. Address the Neuroendocrine transmitters imbalance that can cause 22 patterns of low thyroid function. (Kharrazian D. Why Do I Still Have Thyroid Symptoms. Chapter Ten, page 179; Not mention by Izabella Wentz)
  6. Support the underlying cause of whichever of the six patterns of low thyroid is present in the  body.  (Kharrazian D. Why Do I Still Have Thyroid Symptoms. Chapter Four, page 67; Not mention by Izabella Wentz)

The treatment of Hashimoto’s should not focus on the thyroid until the underlying factors provoking the immune attack are resolved. Any support that enhances the thyroid function will provoke aggressive attacks on the thyroid gland itself. Most of the factors involved in low thyroid function do not involve the thyroid gland.

It is like having a coworker that prevents you from doing your job and you have the job that gets all the attention and blame.

Hashimoto’s typically involves a slow but steady destruction of the gland  by the immune system and other NON-THYROID Factors that eventually results in the thyroid’s inability to produce sufficient thyroid hormone — the condition known as hypothyroidism. There are other NON-Thyroid factors that provoke immune responses towards the thyroid that take priority over supporting normal thyroid function.  There are six patterns of hypothyroidism (Low Thyroid) – five of which do not involve the thyroid that should be addressed.

Forbidden Cytokines Make Antibody Tests Confusing

Cytokine secretion by helper T cells is particularly important in autoimmunity because chronic autoimmune diseases, such as Hashimoto’s Thyroiditis, multiple sclerosis, diabetes, and rheumatoid arthritis are predominantly caused by Th1 cells. Th2 cells can antagonize Th1 functions and in numerous autoimmune conditions prevent autoimmune diseases from getting established.

After autoimmune conditions, such as those mentioned above, become established. Th2 is not only an inefficient suppressors of Th1, but can provoke and promote the onset of autoimmune conditions. Furthermore, neuropeptides (NPs): (somatostatin, calcitonin gene-related peptide, neuropeptide Y, and substance P), drive distinct Th1 and Th2 populations to a “forbidden” cytokine secretion: secretion of Th2 cytokines from a Th1 T cell line and vice versa. Such a phenomenon cannot be induced by classical antigenic/antibody stimulation.

Some of the NPs are produced by microbes as part of their defense strategy. Thus, focusing on restoring normal thyroid function to an autoimmune thyroid is futile.

Hypothalamic Sampling Hormones Requires Blood Flow

Sampling of hormones (including the sex hormones) by the hypothalamus requires consistent blood flow. In the body, blood carries hormones released by endocrine glands and carries them to body parts that need them.

In parasympathetic withdrawal, diagnosis is usually considered adrenal fatigue. The volume of blood shifts from the muscles and brain to the central abdominal compartment. The blood flow to the brain is not stopped when this occurs. The flow is reduced and Poiseuille’s Laws come into play.

The circulatory system provides many examples of Poiseuille’s law in action—with blood flow regulated by changes in vessel size and blood pressure. Blood vessels are not rigid but elastic. Adjustments to blood flow are primarily made by varying the size of the vessels, since the resistance is so sensitive to the radius. This is done by the Abdominal Brain through the release of NeuroEndocrine transmitters, i.e. Serotonin – sero = “blood”, tonin = “pertaining to”.

A 19% decrease in flow is caused by a 5% decrease in radius of the blood vessels. The body may compensate by increasing blood pressure by 19%, but this presents hazards to the heart and any vessel that has weakened walls.

This decrease in radius is surprisingly small for this situation. To restore the blood flow in spite of this buildup would require an increase in the pressure difference of a factor of two, with subsequent strain on the heart.

ISCHEMIC PENUMBRA OF PARASYMPATHETIC DOMINANCE

In severe and/or chronic illness, profound changes occur in the hypothalamic-pituitary-thyroid axis. Ischemia and inflammation disrupt the porous Blood-Brain-Barrier surrounding the hypothalamus. The observed decrease in serum concentration of both hormones and neuroendocrine transmitter (neurotransmitters in the blood) are not compatible with a negative feedback loop.

Ischemia is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive, healthy and functioning properly). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue or organs. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, red blood cell aggregation due to insulin resistance/diabetes). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes.

Hepatic Portal Hypertension

Parasympathetic Withdrawal (vasodilation) with blood pooling in the Abdominal Compartment makes the Movement Compartment and Brain/Spinal Cord Ischemic. At the periphery of the ischemic region, the so-called ischemic penumbra, neuronal damage throughout the body develops more slowly because blood flow arising from adjacent vascular territories (collateral flow) keeps blood perfusion above the threshold for immediate cell death. In the ischemic core, the major mechanism of cell death is energy failure caused by Oxygen/Glucose Deprivation (O2/GD). The hypothalamus and midbrain are most vulnerable to ischemia.

Neuron Vulnerability

Neurons in the most vulnerable areas cease to respond or show only faint responses and develop irreversible ischemic or post-ischemic damage. The hypothalamus responds to ischemic insults rigorously without having irreversible ischemic or post-ischemic damage.

The thalamus-hypothalamus interface represents a discrete boundary where neuronal vulnerability to ischemia is high in thalamus (like more rostral neocortex, striatum, hippocampus). In contrast hypothalamic neurons are comparatively resistant, generating weaker and recoverable anoxic depolarization similar to brainstem neurons, possibly the result of a Na/K pump that better functions during ischemia.

There is a well recognized but poorly understood caudal-to rostral increase in the brain`s vulnerability to neuronal injury caused by metabolic stress (insulin resistance).

Several brain regions, including the caudate, hippocampus, and hypothalamus, are vulnerable to hypoxic–ischemic brain injury. During O2/GD, hypothalamic neurons gradually depolarized during ischemic exposure. The O2/glucose deprivation (O2/GD) response induces failure of the Na+/K+ pump. The recovery is slow with chronic ischemic penumbrance

Without oxygen and glucose, neurons cannot generate the ATP needed to fuel the ionic pumps that maintain the ionic gradient across the neuronal membrane, mainly the Na+−K+ ATPase.

In the ischemic penumbra, the flow reduction is not sufficient to cause energy failure, and neurons remain viable for a prolonged period of time after the insult, but the neurons are stressed and critically vulnerable to pathogenic events that may tip their fragile metabolic balance. Excessive extracellular accumulation of glutamate is a major factor contributing to production of cytotoxic nitric oxide, free radicals and arachidonic acid metabolites. These events lead to necrosis or programmed cell death depending on the intensity of the insult and the metabolic state of the neurons. Injured and dying cells have a key role in post-ischemic inflammation because they release danger signals that activate the immune system.

Neurons that demonstrate particular vulnerability to ischemic challenges have been termed “selectively vulnerable neurons”. Of the entire forebrain, the neurons of the hippocampus are the most vulnerable.

Summary: Parasympathetic Dominance causes Ischemia to the Hippocampus, Hypothalamus, and Pituitary producing alterations in the HPA, HPT, HPD and HPG axis.

Is Your Diagnosis Being Driven By Internet Algorithms?

Is your diagnosis being driven by an Internet Algorithm bought and paid for by a Professional or Social Media Influencer? Is this Internet Algorithm catching your inescapably into a Click Funnel, conveniently linked to a sale page for a “Good-For-You” supplement. I have one question. Do you feel like you are swimming in a riptide when it come to your health?

There is a tendency at this time for Doctors and Patients alike, to jump to worst case scenarios. Especially, when the underlying factors are overlooked and ignored to create a self-fulfilling prophecy, which maintains supplement sales.

Too many believe in their diagnosis. Too many believe in their support group. There is safety in numbers. How can this many in the Support Group possibly be wrong? They are unknowingly being swept into Ad Funnels bought and paid for by Professional and Social Media Influencers.

Have you ever written something in an email or text or maybe searched for something online? Only to see your web browser inundated with advertisements for that product. Do you think that is only happening for consumer products? Professional and Social Media Influencers are paying to put their ads and websites on your electronic devices screens. The same is happening for health related topics. After they link your searches together with your friends on Social Media, they have you locked in to their funnel.

Google and Facebook algorithms are funneling Doctors and people alike into diagnosis du jours and links for purchasing supplements. Professional and Social Media Influencers are buying ad-words on Google and Facebook to sweep people into their funnels. More like whirlpools or riptides that people can’t escape from. Leaving them drowning in erroneous treatment protocols.

Google and Social Media Ad Funnels make it darn near impossible to find any information to the contrary. You will have to consciously “Red Team” (on the contrary, the opposite is true) the information you are finding. You may have to go click through ten to twelve search engine pages before finding and information that has not been “copy and pasted” from some influencers website.

Most Doctors Follow the Personality. Not the Information.

There are howles and gnashing of teeth with that quote. They follow the information published by the Profesional Influencer Personalities. They never actually checkout the information. Since the 1990s, critical thinking has not been taught. Instead, Doctors are taught the answers to their National Board tests. Essentially, puking up an answer based on what they have been told to answer. They don’t feel qualified to question the Professional Influencer. Much less tell the Empereur, they have no clothes.

Google / Social Media Algorithm Trap Snares Doctors As Well

When Doctors fall into the Google / Social Media Algorithm trap, they will go from being advocates for a supplement, recommending the supplement for all their patients; to asking their Social Media Group, what brand of supplement others use, when they are not seeing the results claimed by the Supplement Companies or Professional and Social Media Influencers. Because, obviously it isjust the brand they are using that is the problem. Never recognising that the Professional or Social Media Influencer recommending the supplement has a financial interest in the recommendation.

The Doctors never take a step back and look at the information supporting the product. I take a different attitude towards supplements. If there are consistently poor or nonexistent beneficial results. I stop recommending it. I stop wasting the patient’s resources. Even with all the pressure patients put on me. Too many patients assume I am not aware of a particular wonder supplement. When in actuality, I wonder why anyone would recommend it.

Fives Stages of Hashimoto’s Thyroiditis

Hashimoto’s is a progressive autoimmune condition and the Five stage of Hashimoto’s have been identified.

Stage 1

A person has the immune system imbalance that predisposes them to development of Autoimmune conditions, one of which is Hashimoto’s. For all intents and purposes they do not have thyroid disease or an autoimmune disease. Their thyroid function is normal and there is no attack on the thyroid.

  • Women are more at risk for autoimmune conditions due the monthly fluctuations of their hormones.
  • Women with severe morning sickness have an over active Th17 immune response.

    READ MORE... Th17

  • Women with “hip pain”, “sciatica” or “loose ligaments” during the last trimester have an overactive Th17 immune response causing bone marrow edema in the hip bones causing the aforementioned painful conditions.
  • Women put on bed rest during the last trimester have an overactive Th17 immune response.
  • Women that feel better during pregnancy are using their baby’s endocrine glands to support their NEI Supersystem deficiencies. The baby is born with over-worked, underdeveloped endocrine glands that will not be able to support them during adult life.
  • Immune / inflammatory and hormone messengers cross the placenta, which the baby’s immune and endocrine system responds to. The baby is born with an overactive immune system and possible “forbidden” Cytokines are actively disrupting the child’s immune responses. These are the children born with allergic responses or incessant crying.

Stage 2

Other Non-thyroid Factors begin provoking immune responses towards the thyroid gland. Bacteria can translocate from the mouth to the thyroid. Lectin can damage TSH receptors. Damage occurs to the thyroid gland. The immune system moves into to clear the damaged tissue. Because the oral infection is never addressed and eating a diet of non-seasonal fresh fruit and vegetables is considered healthy. The Non-thyroid factors continue to damage the thyroid with the help of the immune cells. A person will have symptoms, but their TSH, T3 and T4 may be normal. But thyroid medication will be demanded and prescribed anyway. At this point the thyroid antibody test may reveal thyroid antibodies are now being produced.

Stage 3

The neuroendocrine transmitters may lose the ability to control the blood supply. The blood may be predominantly in the abdomen with very little hormone messengers making their way to the head for sampling by the Hypothalamus. This will cause altered feedback signals to the thyroid gland.

The thyroid gland loses its ability to compensate and thyroid hormone production starts to become affected. The lack of T3 and T4 making in the blood stream to the Hypothalamus for sampling will cause a mildly elevated TSH (between 2 – 10). The T3 and T4 will be normal as they are used up by the body, decreasing their available supply. This is often described as subclinical hypothyroidism. The five Non-Thyroid patterns (underconversion, overconversion, resistance, hormone binding elevation or HPT axis), 22 patterns of Neuroendocrine transmitters imbalance and the Non-Thyroid factors will never be considered or addressed. Thyroid hormones will be prescribed leading to further inability of the thyroid gland’s need to produce thyroid hormones.

Stage 4

Ignoring the Non-Thyroid Patterns while taking Thyroid Drugs

Thyroid gland failure occurs when the thyroid gland loses its ability to make thyroid hormones. The thyroid hormone drugs are recognized during hypothalamus sampling. As far as the hypothalamus which controls the Hypothalamic-Pituitary-Thyroid Axis is concerned, you have all the thyroid hormones you need and there is no need to signal the thyroid gland by producing Thyroid Stimulating Hormone (TSH). Thus, it is expected that TSH is low while taking thyroid medications. This makes it a failure to stimulate the production of thyroid hormone problem. If you do not use it, you lose it. Your body sees no need to support unused thyroid tissue.

Too much of the thyroid gland is not maintained when the Non-Thyroid Patterns causing hypothyroidism symptoms are not addressed.

Ignoring the Non-Thyroid Factors while taking Thyroid Drugs

Thyroid gland failure occurs when too much of the thyroid gland is damaged or destroyed by the Non-Thyroid Factors and the subsequent Immune response. Too much of it has been damaged or destroyed. Supporting the “normal” function of the thyroid gland will enhance the immune response towards the thyroid gland. It is futile to cause more damage while expecting thyroid gland improvement.

Thyroid Drugs and Supplements

TSH will be low as there is no signals from the Hypothalamus for its production. T3 and T4 numbers will be ambiguous and confusing. Support will continue for the restoration of thyroid gland with confusing results.

Stage 5

You are allowed to have multiple autoimmune conditions simultaneously. It is not a matter of which came first. Most Doctors will only offer to test for autoimmune conditions based on their specialty. This leads to multiple Doctor visits, multiple diagnoses, and multiple treatment plans putting you on a slippery slope with a downward spiral.

Until the immune system is brought under control, thyroid supplements and drugs are futile. You do not worry about what color you are painting the kitchen when the house is on fire.

What is Th17?

The purpose of Th17 cells is to clear pathogens, which are not efficiently handled by TH1 and TH2 type of immunity. The induction of Th17 responses must go through three distinct steps: Induction, amplification and stabilization. The stability of Th17 population is only relevant if it is protective against a given pathogen-invader or other kind of insult. If Th17 cells loose their stability they become highly proinflammatory and promote the destruction of your body’s tissues as occurs in autoimmune conditions. In essence, your immune system chooses to sacrifice body tissues by destroying in order to preserve the rest of your body.

By promoting inflammation and attracting neutrophils, TH17-cells may help to remove microbes from the body. However, by triggering an excessive inflammatory response, TH17-cells can contribute to such inflammatory diseases as Hashimoto’s Thyroiditis, Crohn’s disease, Ulcerative Colitis, Psoriasis and many other Autoimmune conditions.

TH17 cells have recently emerged as a third independent type T cells which may play an essential role in protection against certain disease causing microbes.  IL-17 plays an important and unique role protection against specific pathogens. The production of IL-17 and the recruitment of neutrophils is important in protection against gram-negative bacteria and fungal infections.Th17 are highly pro-inflammatory and that Th17 cells with specificity for self-antigens lead to severe autoimmunity.

Forbidden Cytokines and Autoimmunity

T-cells secrete various cytokines through which they affect a broad spectrum of normal and pathological immune processes. Cytokine secretion by helper T cells is particularly important in autoimmunity[i] because chronic autoimmune diseases, such as Hashimoto’s Thyroiditis, Multiple Sclerosis, Type 1 Diabetes, and Rheumatoid Arthritis are predominantly caused by Th1 cells. Th2 cells can antagonize Th1 functions[ii] and in numerous autoimmune conditions prevent and/or cure autoimmune diseases.

However, recent studies found exceptions to this rule, suggesting that the behavior of a given T cell population may be unpredictable in its cytokine secretion profile. For example, (i) Th2-type T cells can be not only inefficient suppressors of autoimmune conditions induced by Th1 cells,[iii] but can cause Autoimmune conditions;[iv] thus Th1 and Th2 cells can both promote autoimmune conditions; (ii) Th0-type T cells (producing both Th1 and Th2 cytokines) can stimulate autoimmune conditions and are able to instigate Autoimmune conditions;[v] and (iii) Th2-type T cells can induce pancreatitis and diabetes in immune-compromised nonobese individuals with blood sugar problems.[vi]

The cytokine secretion of the same T cell population is different in the lymph nodes (producing both Th1 and Th2 cytokines) than in the central nervous system (CNS) environment (producing only Th1 cytokines). This observation suggests that within the CNS, specific factors (mainly IL-12 producing microglia acting as APCs, not neurons) can modulate the cytokine secretion of Tcells, can select Th1/Th2 pathway, and can control effector CD4+ T cell cytokine profile in Autoimmune conditions.[vii]

Four neuropeptides (NPs): somatostatin, calcitonin gene-related peptide, neuropeptide Y, and substance P, in the absence of any additional factors, directly induce a increased secretion of cytokines [interleukin 2 (IL-2), interferon-g, IL-4, and IL-10) from T cells. Furthermore, these NPs drive distinct Th1 and Th2 populations to a ‘‘FORBIDDEN’’ cytokine secretion[viii]: secretion of Th2 cytokines from a Th1 T cell line and vice versa. Such a phenomenon cannot be induced by classical antigenic stimulation.

The nervous system, through these NPs interacting with their specific T cell-expressed receptors, can lead to the secretion of both typical and atypical cytokines, leading to the breakdown of the commitment to a distinct Th phenotype, and a potentially altered function and destiny of T cells in vivo.

Nerve fibers that release NPs are widespread in the mammalian central and peripheral nervous systems, in certain endocrine tissues, and in all the primary and secondary lymphoid organs.[ix]

[i] Merrill, J. E. & Benveniste, E. N. (1996) Trends Neurosci. 19, 331–338.

[ii] Benveniste, E. N. (1995) in Human Cytokines: Their Role in Research and Therapy (Blackwell Scientific, Oxford), pp. 195–216.

[iii] Khoruts, A., Miller, S. D. & Jenkins, M. K. (1995) J. Immunol. 155, 5011–5017.

[iv] Lafaille, J. J., Keere, F. V., Hsu, A. L., Baron, J. L., Haas, W., Raine, C. S. & Tonegawa, S. (1997) J. Exp. Med. 186, 307–312.

[v] Krakowski, M. L. & Owens, T. (1997) Eur. J. Immunol. 27, 2840–2847.

[vi] Pakala, S. V., Kurrer, M. O. & Katz, J. D. (1997) J. Exp. Med. 186, 299–306.

[vii] Krakowski, M. L. & Owens, T. (1997) Eur. J. Immunol. 27, 2840–2847.

[viii] Mia Levite. Neuropeptides, by direct interaction with T cells, induce cytokine secretion and break the commitment to a distinct T helper phenotype (T helper cells 1 and 2). Proc. Natl. Acad. Sci. USA Vol. 95, pp. 12544–12549, October 1998 Immunology

[ix] Weihe, E., Nohr, D., Michel, S., Muller, S., Zentel, H. J., Fink, T. & Krekel, J. (1991) Int. J. Neurosci. 59, 1–23.

Somatostatin

Yeast/Fungi (ingested mold in this case) synthesize somatostatin using it as a defense mechanism to create their ideal environment. Normally, somatostatin is produce by the body in the gastrointestinal tract, pancreas and regions of the CNS. Classified as an inhibitory hormone, it has been shown to impede proinflammatory responses. Somatostatin secreted from non-neuronal cells along the digestive tract plays an important role as a mediator during mucosal inflammatory responses after physiological (induced by TNF-α) and pathophysiological (up-regulation of bacteria) stimulations. TH1, which predominates gastritis (gut inflammation), may be quelled through the increased levels of somatostatin. Through reduced inflammation, the yeast and other microbes are able to avoid attack by the TH1 immune system.

Yeast (Saccharomyces cerevisiae) used in probiotics, synthesizes an analogous peptide hormone precursor, pro a-factor, which is proteolytically processed by at least two separate proteases, the products of the KEXZ and STE13 genes, to generate the mature bioactive peptide somatostatin (SMS).[i],[ii],[iii],[iv],[v]

Expression in yeast of recombinant DNAs encoding hybrids between the proregion of a-factor and somatostatin results in proteolytic processing of the chimeric precursors and secretion of mature somatostatin.[vi]

[i] Green R, Schabern M, Shields D, Kramer R. Secretion of Somatostatin by Saccharomyces cereuisiae CORRECT PROCESSING OF AN a-FACTOR-SOMATOSTATIN HYBRID June 5, 1986 The Journal of Biological Chemistry, 261, 7558-7565.

[ii] Bourbonnais Y, Bolinn D, Shields D. Secretion of Somatostatin by Saccharomyces cerevisiae CORRECT PROTEOLYTIC PROCESSING OF PRO-a-FACTOR-SOMATOSTATIN HYBRIDS REQUIRES THE PRODUCTS OF THE KEX2 AND STE13 GENES’ Vol. 263, No. 30,Issue of October 25, pp. 15342-15347,1988

[iii] PRICE L, KAJKOWSKI E, HADCOCK J, OZENBERGER B, PAUSCH M. Functional Coupling of a Mammalian Somatostatin Receptor to the Yeast Pheromone Response Pathway MOLECULAR AND CELLULAR BIOLOGY, Nov. 1995, p. 6188–6195 Vol. 15, No. 11

[iv] Keisuke Hara, Tomohiro Shigemori, Kouichi Kuroda and Mitsuyoshi Ueda. Membrane-displayed somatostatin activates somatostatin receptor subtype-2 heterologously produced in Saccharomyces cerevisiae. Hara et al. AMB Express 2012, 2:63

[v] Hara, Shigemori, Kuroda, Ueda (2012) Membrane-displayed somatostatin activates somatostatin receptor subtype-2 heterologously produced in Saccharomyces cerevisiae AMB Express 2(1) 63

[vi]Bourbonnais Y, Bolin D, Shields D. Secrestion of Somatostating by saccharomyces cerevisiae, The Journal of Biological Chemistry, 263, October 25, 1988: 15342 – 15347

Chronic Inflammation Uncouples the Adrenals

Chronic inflammation causes the Adrenals (HPA axis) to be uncoupled from the Vasomotor Autonomic System (VAS). That’s correct. Despite the fact that the adrenals are disconnected from autonomic control; many Doctors suspect and treat adrenal fatigue in any patient who has low grade or a chronic inflammation. Why? They didn’t look any deeper, questioning why are the adrenals always showing up in their analysis.

They will tell you with inflammation, it is in your best interest to improve your adrenal function to reduce inflammation. They will say the same  with about any other condition. They always recommend doing adrenal support. The Hypothalamic-Pituitary-Adrenal (HPA) axis is a prominent focus of treatment in patients with chronic health conditions. Adrenal Fatigue Syndrome (AFS) is considered the root cause of the problem.

Adrenal / HPA axis Endocrine Pathway: Note the complete absence of any references to Cortisol as an Endocrine Hormone traveling through the blood after release by the adrenals.

This Endocrine hormone dilemma is caused by  the overactive immune response causing chronic inflammatory conditions and low cortisol levels  occurring relative to the level of inflammation the individual is experiencing.

Adrenal Hormones Pass Through Blood – Brain -Barrier

Adrenal hormones and neuroendocrine transmitters have important influences upon the hypothalamus, and to do so they must pass through the blood–brain barrier. The hypothalamus is bounded in part by specialized brain regions that lack an effective blood–brain barrier; the capillaries at these sites has perforations to allow free passage of hormones and even large proteins and other molecules. At these sites, the hypothalamus samples the hormone composition of the blood. Some of these sites are the sites of neurosecretion, where signals are sent from the nerve cells of the hypothalamus to the posterior pituitary. The hypothalamus secretes substances known as neurohormones that start and stop the secretion of anterior pituitary hormones.

The neurons are in intimate contact with both blood and Cerebrospinal Fluid (CSF). These structures are densely vascularized, and contain receptive neurons that control hormones, regulation of fluid and electrolyte balance.

Read More - Hypothalamic Sampling Hormones Requires Blood Flow

 

Cortisol

Cortisol is a steroid hormone released into the blood stream by the adrenal glands. The adrenal glands sit on top of your kidneys. Cortisol does not get released into nerves or travel through the nerves. Inflammation damages and disturbs blood flow through out the body and the delivery of Endocrine hormones.

The  HPA axis is an adaptive response for “short-lived” inflammatory responses leading to breakdown of energy stores and energy utilization by activated immune and other cells. This becomes a disease causing factor, if it continues too long, that can drive systemic chronic inflammatory diseases such as the hypothyroid or chronic fatigue syndrome symptoms.

Which Hormone Chart is Accurate?
Technically, Both are correct. The lower is more complete. The upper chart is missing most of the hormones. Are those missing hormones important for your health? Are the missing hormones, contributing to your health condition. You may never know, unless you find a Doctor like Dr. Peterson that uses complete hormone tests.

Low DHEA

The response of the hypothalamic-pituitary-adrenal (HPA) axis to chronic inflammation is: 1) low serum levels of cortisol; 2) ambiguous lab results with respect to levels of adrenocorticotropic hormone (ACTH) and cortisol; 3) Uncoupling of HPA axis and Vasomotor Autonomic System (VAS); 4) Symptoms ranging from no symptoms to severe cases of hypoandrogenism (low DHEA which is converting into pro-inflammatory Etiocholanolone), fatigue, and/or mineralocorticoid excess; 5) altered circadian rhythm causing morning symptoms. Low cortisol is associated with problems going to sleep and waking up. Low levels of cortisol in relation to Vasomotor neurotransmitters may be proinflammatory because cooperative anti-inflammatory coupling of the two endogenous response axes is missing.

Chronic inflammation and Adrenal Fatigue are quite closely associated: inflammation contributes to and triggers common, but very subtle, symptoms of Adrenal Fatigue such as brain fog, gastric bloating, pain of unknown origin, depression, anxiety, and reactive hypoglycemia. The real truth is that stress and Adrenal Fatigue is not a mysterious entity at all that always seems to be present.

Adrenal Fatigue consists of many nonspecific but debilitating symptoms. The onset of this condition is often slow and insidious. Sufferers are told that they are stressed and need to learn to relax more. Yes, we all know that “stress kills” to a large extent. But, the question is how?

Inflammation Uncouples the HPA axis

These difficulties in understanding “Adrenal Fatigue” and the HPA axis is caused by the fact that the Vasomotor Autonomic System (VAS) axis and the Hypothalamic-Pituitary-Adrenal (HPA) axis are “UNCOUPLED”  in patients with inflammatory conditions or Hepatic Portal Hypertension (another overlooked condition) .

Cooperation between the Vasomotor Autonomic System (VAS) and the Adrenals (HPA axis) is important in chronic inflammatory diseases to efficiently down regulate inflammation in the body. Research of classical stress systems, such as the hypothalamus–pituitary–adrenal (HPA) axis and the sympathetic and parasympathetic nervous systems (SNS and PNS), is disappointing as findings are often contradicting each other, and counterintuitive, as for example, the finding of low HPA axis activity in chronically stressed and traumatized individuals. This is the basis for the meme of “Adrenal Fatigue”.

If you have chronic inflammation; the chances of Adrenal Supplements working is not good.

DHEA is converting into pro-inflammatory Etiocholanolone

Adrenal testing is popular with many Doctors. Low DHEA is often reported in the results. Complete hormone testing is rarely if ever done. When Complete Hormone testing are used. It become apparent that the low DHEA is due to its conversion into the inflammatory hormone Etiocholanolone. The hot flashes women experience may be due to Etiocholanolone surges. It is NOT a DHEA deficiency.

The reason your DHEA is low is because DHEA is converting into Pro-Inflammatory Etiocholanolone

Etiocholanolone is produced from androstenedione. It causes fever, short term hot flashes, immune stimulation and increased white blood cells. Excessive DHEA supplementation may be the cause of high etiocholanolone levels.

The Vasomotor Autonomic System (VAS) axis and the hypothalamic-pituitary-adrenal (HPA) axis are stimulated in parallel in response to stress factors under healthy conditions. This physiological synergism of the axes stimulated by the hormone Etiocholanolone aims at optimizing immune responses. With inflammatory diseases, one would expect that TNF or IL-6 (TH17) stimulates the hypothalamus, which activates the Vasomotor Autonomic System (VAS) axis and the hypothalamic-pituitary-adrenal (HPA) axis in a parallel fashion.

If lab test report shows DHEA, androstenedione and testosterone levels are low with signs and symptoms of bacterial overgrowth, high pro-inflammatory cytokines IL-1, IL-6 levels, etiocholanolone may be causing symptoms of inflammation, fever, leukocytosis, increased serum C-reactive protein, low iron (hypoferremia), increased IL-1 lymphocyte activation and increased white blood cell activity.

In some cases Etiocholanolone has been known to decrease cortisol in short bursts because it has a higher affinity for the parts of the adrenals (Zona Glomerulosa & Zona Reticularis) which effect mineralocorticoids, salt and water content of your blood, and Androgens (testosterone).

Increased etiocholanolone causes a rapid fall in serum iron and a rise in serum ferritin. This would be diagnosed as an iron deficiency. Read More… Anemia of Chronic Inflammation

Hydrocortisone Treatment

A critical confounder of “Adrenal Fatigue” and the HPA axis is the influence of previous glucocorticoid therapy (Hydrocortisone), which has long-lasting, but often ignored, depressive effects on the HPA axis. Hydrocortisone drugs decrease adrenal function, increase kidneys excretion of androgens (testosterone, DHEA) and increased binding of androgens to globulin making them inactive.

If you have previously used Hydrocortisone creams or Cortisone injections; the chances of Adrenal Supplements working is not good.

Uncoupling May Persist Even After Improvement

An uncoupling of the Vasomotor Autonomic System (VAS) and the HPA axis may persist even following clinically significant improvement. Suboptimal HAVS regulation of the HPA axis in patients, with chronic health conditions remains particularly prominent during periods of stress-induced activation of the two systems.

Uncoupling of these two axes is linked to prior corticosteroid therapy. Uncoupling is enhanced in prednisolone treated patients because prednisolone stimulates the SNS and inhibits the HPA axis even in healthy subjects.

How Should Doctors Treat Adrenal Fatigue?

Hypothalamic Pituitary Thyroid (HPT) Axis

Hypothalamic – Pituitary – Thyroid Axis (HPT) AKA: Hypothyroidism Secondary to Pituitary Hypofunction

Another more appropriate name for the Hypothalamic – Pituitiary – Thyroid (HPT) Axis is Hypothyroidism Secondary to Decreased Pituitary Output. This is the label used in Dr. Kharrazian’s book Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal.

The pituitary gland is often portrayed as the “Master Gland” of the body. Such praise is justified in the sense that the anterior and posterior pituitary secrete a battery of hormones that collectively influence all cells and affect virtually all physiologic processes.

The pituitary gland may be king, but the power behind the throne is clearly the hypothalamus. Some of the neurons within the hypothalamus – neurosecretory neurons – secrete hormones that strictly control secretion of hormones from the anterior pituitary. The hypothalamic hormones are referred to as releasing hormones and inhibiting hormones, reflecting their influence on anterior pituitary hormones.

T3 and T4 regulation

The production of thyroxine (T4) and triiodothyronine (T3) is regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary. The thyroid and thyrotropes (cells in the anterior pituitary) form a negative feedback loop: TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and secreted at an increased rate in situations such as cold (in which an accelerated metabolism would generate more heat).

Thyroid Hormones Pass Through Blood – Brain -Barrier

Thyroid hormones and neuroendocrine transmitters have important influences upon the hypothalamus, and to do so they must pass through the blood–brain barrier. The hypothalamus is bounded in part by specialized brain regions that lack an effective blood–brain barrier; the capillaries at these sites has perforations to allow free passage of hormones and even large proteins and other molecules. At these sites, the hypothalamus samples the hormone composition of the blood. Some of these sites are the sites of neurosecretion, where signals are sent from the nerve cells of the hypothalamus to the posterior pituitary. The hypothalamus secretes substances known as neurohormones that start and stop the secretion of anterior pituitary hormones. 

The neurons are in intimate contact with both blood and Cerebrospinal Fluid (CSF). These structures are densely vascularized, and contain receptive neurons that control hormones, regulation of fluid and electrolyte balance.

The hypothalamic-pituitary-thyroid axis (HPT axis) is a neuroendocrine system that regulates metabolism.  When the hypothalamus senses low circulating levels of the hormones T3 and T4 in the blood, it signals to the pituitary by releasing Thyroid Releasing Hormone (TRH) into the capillaries traveling to the anterior pituitary, which secretes Thyroid Stimulating Hormone (TSH) into the veins. The veins carry the TSH to the thyroid signaling the thyroid gland to release T3 and T4.  T4 normally is converted to the more active T3, but T4 can also be converted to reverse T3 (rT3).  Reverse T3 antagonizes the T3 receptor, so high levels can be detrimental.

 

Hypothalamic Sampling Requires Blood Flow

Sampling of hormones (including the sex hormones) by the hypothalamus requires consistent blood flow. In the body, blood carries hormones released by endocrine glands and carries them to body parts that need them. 

In parasympathetic withdrawal, diagnosis is usually considered adrenal fatigue. The volume of blood shifts from the muscles and brain to the central abdominal compartment. The blood flow to the brain is not stopped when this occurs. The flow is reduced and Poiseuille’s Laws come into play. 

The circulatory system provides many examples of Poiseuille’s law in action—with blood flow regulated by changes in vessel size and blood pressure. Blood vessels are not rigid but elastic. Adjustments to blood flow are primarily made by varying the size of the vessels, since the resistance is so sensitive to the radius. This is done by the Abdominal Brain through the release of NeuroEndocrine transmitters.

A 19% decrease in flow is caused by a 5% decrease in radius of the blood vessels. The body may compensate by increasing blood pressure by 19%, but this presents hazards to the heart and any vessel that has weakened walls.

This decrease in radius is surprisingly small for this situation. To restore the blood flow in spite of this buildup would require an increase in the pressure difference of a factor of two, with subsequent strain on the heart.

ISCHEMIC PENUMBRA OF PARASYMPATHETIC DOMINANCE

In severe and/or chronic illness, profound changes occur in the hypothalamic-pituitary-thyroid axis. Ischemia and inflammation disrupt the porous Blood-Brain-Barrier surrounding the hypothalamus. The observed decrease in serum concentration of both thyroid hormones and thyrotropin (TSH) are not compatible with a negative feedback loop.

Ischemia is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive, healthy and functioning properly). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue or organs. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, red blood cell aggregation due to insulin resistance/diabetes). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. 

Parasympathetic Withdrawal (vasodilation) with blood pooling in the Abdominal Compartment makes the Movement Compartment and Brain/Spinal Cord Ischemic. At the periphery of the ischemic region, the so-called ischemic penumbra, neuronal damage throughout the body develops more slowly because blood flow arising from adjacent vascular territories (collateral flow) keeps blood perfusion above the threshold for immediate cell death. In the ischemic core, the major mechanism of cell death is energy failure caused by Oxygen/Glucose Deprivation (O2/GD). The hypothalamus and midbrain are most vulnerable to ischemia.

Neurons in the most vulnerable areas cease to respond or show only faint responses and develop irreversible ischemic or post-ischemic damage. The hypothalamus responds to ischemic insults rigorously without having irreversible ischemic or post-ischemic damage.

The thalamus-hypothalamus interface represents a discrete boundary where neuronal vulnerability to ischemia is high in thalamus (like more rostral neocortex, striatum, hippocampus). In contrast hypothalamic neurons are comparatively resistant, generating weaker and recoverable anoxic depolarization similar to brainstem neurons, possibly the result of a Na/K pump that better functions during ischemia.

There is a well recognized but poorly understood caudal-to rostral increase in the brain`s vulnerability to neuronal injury caused by metabolic stress (insulin resistance).

Several brain regions, including the caudate, hippocampus, and hypothalamus, are vulnerable to hypoxic–ischemic brain injury. During O2/GD, hypothalamic neurons gradually depolarized during ischemic exposure. The O2/glucose deprivation (O2/GD) response induces failure of the Na+/K+ pump. The recovery is slow with chronic ischemic penumbrance

Without oxygen and glucose, neurons cannot generate the ATP needed to fuel the ionic pumps that maintain the ionic gradient across the neuronal membrane, mainly the Na+−K+ ATPase. 

In the ischemic penumbra, the flow reduction is not sufficient to cause energy failure, and neurons remain viable for a prolonged period of time after the insult, but the neurons are stressed and critically vulnerable to pathogenic events that may tip their fragile metabolic balance. Excessive extracellular accumulation of glutamate is a major factor contributing to production of cytotoxic nitric oxide, free radicals and arachidonic acid metabolites. These events lead to necrosis or programmed cell death depending on the intensity of the insult and the metabolic state of the neurons. Injured and dying cells have a key role in post-ischemic inflammation because they release danger signals that activate the immune system. 

Neurons that demonstrate particular vulnerability to ischemic challenges have been termed “selectively vulnerable neurons”. Of the entire forebrain, the neurons of the hippocampus are the most vulnerable.  

Summary: Parasympathetic Dominance causes Ischemia to the Hippocampus, Hypothalamus, and Pituitary producing alterations in the HPA, HPT, HPD and HPG axis.

HPT AXIS 

During illness, profound changes may occur in the hypothalamic-pituitary-thyroid (HPT) axis. The most consistent change is a decrease in serum tri-iodothyronine (T3) level, but in severe illness, serum thyroxine (T4) may also decrease. The persistence of a normal or even decreased serum level of thyrotropin (TSH) in the face of decreased serum thyroid hormone concentrations implies there is not an adequate concentration of T3 or T4 reaching the hypothalamus for sampling. 

Since these abnormalities of thyroid hormone concentration usually occur without any evidence of thyroid disease and disappear with recovery, they have been referred to as the `sick euthyroid syndrome’ or the `euthyroid sick syndrome’.

The downregulation at all levels of the HPT axis (decreased thyrotropin-releasing hormone (TRH) and TSH at the hypothalamic-pituitary level, and a decreased production of T3 at the peripheral extra-thyroidal level) in Non-Thyroid Illness is part of the neuroendocrine adaptation to Parasympathetic Withdrawal. In this view, attempts to restore thyroid hormone levels are detrimental and should not be undertaken. 

Immune Stimulation

There is a neuroendocrine component in the pathogenesis of the decreased activity of the HPT and somatotropic axes in prolonged critical illness. T3 can stimulate dendritic cell (DC) maturation, leading to DC-induced T cell proliferation and IFN-γ release. The cytokines IL-1β, TNF-α, IFN-γ, and IL-6 can inhibit the conversion of T4 to T3, thereby shunting T4 towards the production of the potentially detrimental rT3.

Melatonin Stimulates Parasites to Reproduce

Melatonin supports the synchronized reproduction of parasites. Parasites are attracted towards melatonin producing areas of the body during their reproductive cycles. Secretion of melatonin synchronizes the nocturnal release of microflilaria – the early larval stage of a parasitic nematode worm filarial. It follows that exogenous melatonin administration or the use of Blue Blocker Glasses during the day would also trigger release of microfilaria.

The nightly release of microfilaria into the circulation coincides with the feeding activity of parasites, a synchronization that is presumably an evolutionary adaptation favoring survival and transmission of the parasite.

88% of the cercariae (worm larvae) were shed between 11 a.m. and 3 p.m. and the average pattern is of circadian type, with the average peak at 1 p.m., and representing 27% of the total number of cercariae of the day. The rhythms of emergence are associated with nocturnal production of melatonin.

All worms were found in the distal 55% of the small intestine (ileum). During the night and morning, parasite was heavily concentrated in the jejunum and, during the day, worms are located more distally, with a heavy concentration in the ilium. Parasites have a migratory pattern that occurs with the initiation of gastric activity of the host. Worms move away from the areas producing digestive chemistry when production is initiated after eating. Two hours after feeding worms move towards the food. High fat diets result in a significant decline in worm dry weight, body area and uterine egg counts in worms. Low fat diets are conducive to increased parasite infestation.

Helminthic therapy, an experimental type of immunotherapy, is the treatment of autoimmune diseases and immune disorders by means of deliberate infestation with a helminth or with the ova of a helminth. Helminth therapy is being used as a treatment method for autoimmune and other inflammatory disorders.

There are a few studies highlighting the potential dangers of helminthic therapy. These are rare because as with Blue Blocker Glasses; no one wants to look at the dark side of Helminth therapy, hence few case studies.

Would you like to be advised of the negative potential of any therapy to consider before trying it.

Worms do not honor intestinal boundaries. They are capable of penetrating the intestinal lining. Especially, when overcrowding occurs from excess reproduction, e.g. melatonin stimulates parasite reproduction. This can also cause an obstruction by a large tangled mass of whipworms. Perforation of the ascending colon occurs as the worms expand their territory. How many people do you know that will go back to their social media friends to post something like this?

The good news is that the production and release of reactive oxygen species(ROS) stimulated by melatonin probably prevents most of the damage that normally occurs in parasitic infestation, e.g., eosinophil infiltration. This will also make the person with the parasitic overgrowth to be unable to feel any discomfort from the parasites.

Vaginal Yeast Infection

Vaginal Yeast infection symptoms can mimicked by Bacterial Vaginitis (BV). Periodontal bacterial vaginosis can cause vaginal symptoms similar to those of a Yeast Infection. Bacterial Vaginitis can be caused by various conditions, such as bleeding gums and gingivitis. Recurrent Pregnancy Loss (RPL), miscarriage, preterm birth and low birth weight are associated with oral bacterial infections.

 

Cross colonization of the openings of the human body have received little study in contemporary medicine. Because of this, there is limited practical recommendations for management of patients with both dental and urogenital tract microflora disorders. Not because nothing can be done. It is due to the compartmentalization of health care. The mouth and vagina are at opposite ends of the body. Dentist go to Dental conventions. Gynecologists go to Gynecological conventions. They never become aware of the problem at the other end of the body. Dental patients tell Dentists about their mouth. Gynecology patients – Well you get the point.

As a Functional Doctor, patients report all of their problems in the assessment forms allowing the connection between their reoccurring “Yeast” infection and bleeding, receding gums. From there, the patient can be directed to the proper treatment and support to eliminate the problems.

The current paradigm focuses on vaginal/uterine infections predominantly originating from the vaginal tract, with the microbes ascending into the uterus. An increasing number of bacterial species have been identified in vaginal/uterine infections that do not belong to the vaginal microflora. Infections in the uterus can originate from the mouth as bacteria entering to bleeding gums move throughout the body looking for a place to call their new home. There is a small association between periodontal disease and bacterial vaginosis with oral sex with a partner that has periodontal disease. Bacteria enter the blood vessels in the mouth is the primary route of infection.

Is Your Yeast Infection Really A Bacterial Infection?

Culture Lab Testing is still readily available and reasonably accurate for finding air breathing microbes, so clinicians continue to use it even though there are significant known limitations. 99% of microbes in your body are stressed out when exposed to air, going dormant or dying making them unculturable.

The same statistics apply with Vaginal Cultures. This is why Candida seems so prevalent. They are using antiquated lab tests.

This lack of growth by anaerobic microbes results in a significant change in the balance of microbes in lab test results; since those species capable of surviving exposure to air will more actively grow when there is no competition. It becomes readily apparent that Culture and the culture dependent MALDI-TOF methodology are severely limited to identifying only culturable microbes (less than 1% in the human body).

If your Doctor is using antiquated Culture tests or swabs. They are missing 99% of the microbes that could possibly be causing your “Yeast” infection. If you are experiencing reoccurring “Yeast” infections, the use of cultures and swab tests are likely wrong and leads to inappropriate treatment.

Vaginal and Uterine Infections

Oral bacteria enter into oral capillaries, especially if you have bleeding when flossing or brushing your teeth. Receding gums is another sign of oral bacteria causing problems. These conditions lead to increased bacteria in the blood, thus enhancing the opportunities for bacteria to travel to distant organs and joints in your body. The symptoms of oral bacteria infection mimic those experiences in ascending infections, i.e., with the bacteria colonizing the lining of the uterus.

Graphic of tooth with different points of entry for bacteria into the blood stream

Dental procedures such as extractions, root canals, implants, deep scaling and crowns that cause bleeding provides an entry point for bacteria to move into the blood. Unfortunately, the focus is on mercury fillings and not on the bacteria that take advantage of the new places to take up residence. Read more on Root Canals…

Bacteria being carried through the blood allows the spread of opportunistic bacteria from one location to another, i.e. uterus, joints, thyroid.  It is then plausible that opportunistic bacteria take advantage of your body’s specific chemistry and colonize wherever growth conditions are suitable. The oral and vaginal environments provide similar colonization and growth conditions in a your body for bacteria to grow. Because faulty, antiquated Culture Lab Tests continue to be used, anaerobic bacterial infections are seldom found.

These opportunistic oral bacteria setting up a new residence in the uterus become Invasive Species and Keystone Pathogens. An Invasive Species is a species that spreads to a new location they are not normally found in, becoming Keystone Pathogens and causing damage to the tissue, organs and health of the human body.

Invasive Species are able to out compete normal inhabitants due to lack of natural defenses that keep their population in check. Invasive Species become bullies in their new location, changing the environment to favor their growth and survival, i.e. a crack house moving into your neighborhood.

A “Keystone Pathogen” is a low-abundance microbe that can orchestrate inflammatory disease by remodeling a normally beneficial microbiota into a dysbiotic one, i.e. residents of the neighborhood change their behavior to avoid confrontation with the crack dealers. Once the Keystone Pathogens get a foothold, they hack into the immune system by producing chemicals that make them invisible to the immune system, i.e. crack dealers paying off the cops.

Oral bacteria invading the uterus and vagina change the environment so much so that the normal vaginal bacteria are weakened to the point where they are no longer able to out-compete the Candida/Yeast. You have invaders in the vagina and uterus arriving internally from the blood and externally from the vagina. The Candida/Yeast are opportunistic; taking advantage of the weakened normal vaginal bacteria being unable to prevent the overgrowth of Candida/Yeast. You experience temporary relief from Yeast infection products or prescriptions, but it always comes back. This is because the oral infection replenishes the bacteria to the vagina and uterus repeating the process over and over.

An increasing number of studies report intrauterine infections caused by bacterial species not found in the urogenital tract, such as F. nucleatum and Bergeyella, Eikenella, and Capnocytophaga spp., all of which are common species in the mouth.

Female Reproductive Disease and Periodontal Infection

Periodontitis is a condition in which dental bacterial plaque cause an inflammatory response that leads to loss of connective-tissue attachment, ultimately resulting in loss of affected teeth. Symptoms include bleeding when brushing or flossing, inflammation at the site, and tooth loosening and ultimately tooth loss.

Chronic generalized inflammatory and inflammatory-degenerative periodontal diseases of different severity have been detected in all female patients with gynecological diagnosis of bacterial vaginosis. The major markers of bacterial vaginosis have been also detected in oral cavity in women with periodontal conditions, i.e. receding gums, bleeding gums, canker sores, etc. Root canals, crowns and implants should also be considered if you are having reoccurring vaginal infections.

Bacterial vaginosis is a frequently occurring condition with the focus being primarily on bacteria ascending from the vagina into the uterus. Bacterial vaginosis affects nearly 30% of women between the ages of 14 and 49. Bacterial vaginosis is characterized by a decrease in the normally predominant (air-tolerant) Lactobacillus bacterial species, and a corresponding increase in a diversity of anaerobic microbes (air-hating) AKA Competitive Exclusion. Bacterial vaginosis is typically asymptomatic, but if symptoms are present, the most common complaints are discharge and odor.

Both periodontal disease and bacterial vaginosis have been linked to adverse pregnancy outcomes such as miscarriage, preterm birth and low birthweight. The process through which oral bacteria stimulate an immune response resulting in preterm birth remains overlooked.

Bacterial Vaginosis

Bacterial vaginosis (BV), a condition characterized by decreased vaginal lactobacilli and increased anaerobic bacteria, has been associated with an increased risk of miscarriage and preterm birth. The abnormal microflora typical of Bacterial Vaginosis overlaps considerably with bacterial species known to be associated with periodontal disease. For example, Prevotella and Porphyromonas species have been associated with Bacterial Vaginosis and Periodontal Disease.,

What are signs and symptoms of bacterial vaginosis?

The most common symptom is a smelly vaginal discharge. It may look grayish white or yellow. A sign of bacterial vaginosis can be a “fishy” smell, which may be worse after sex. About half of women who have bacterial vaginosis do not notice any symptoms.

Many women with bacterial vaginosis have no signs or symptoms at all. When symptoms do occur, the most common include:

  • An abnormal amount of vaginal discharge
  • The vaginal discharge is thin and grayish white.
  • Vaginal odor (foul-smelling or unpleasant fishy odor)
  • The vaginal discharge and odor are often more noticeable after sexual intercourse.
  • Pain with sexual intercourse or urination (rare symptoms).

Symptoms of bacterial vaginosis, if present, can occur any time in the menstrual cycle, including before, during, or after the menstrual period. The amount of vaginal discharge that is considered normal varies from woman to woman. Therefore, any degree of vaginal discharge that is abnormal for a particular woman should be evaluated.

What problems can bacterial vaginosis cause?

Bacterial vaginosis usually does not cause other health problems. But in some cases it can lead to serious problems.

  • If you have it when you are pregnant, it increases the risk of miscarriage, early (preterm) delivery, and uterine infection after pregnancy.
  • If you have it when you have a pelvic procedure such as a cesarean section, an abortion, or a hysterectomy, you are more likely to get a pelvic infection.
  • If you have it and you are exposed to a sexually transmitted infection (including HIV), you are more likely to catch the infection.

If you are having frequent “Yeast” infections, you may want to consider the possibility it is not “Yeast“. It may be an overlooked oral bacteria infection. Theses same bacteria traveling through your blood are also falling into your digestive tract becoming Invasive Species acting as Keystone Pathogens causing digestive problems. Since Dentist do not treat gynecological conditions and Gynecologist do not treat dental conditions. You need help guiding you through the process.  Call today.

Am I TH1 or TH2 or TH17?

Some practitioners recommend the Th1/Th2 Challenge to determine if symptoms are immune related. Doing the Th1/Th2 Challenge is like checking for a gas leak with a burning match. It doesn’t account for Th17. Are you suffering from inflammatory fire searching the internet for answers? I often hear from women that they have to be their own advocates for their health. I agree you must be your own advocate.

Inflammation is a general term describing the effects of too many inflammatory cytokines and stimulating neurotransmitters unopposed by too few anti-inflammatory cytokines and inhibitory neurotransmitters.

Finding Your Immune Status

For more than thirty years, T-Helper (TH) cells have been divided by immunologists into two functional subsets: T-helper-1 (TH1) and T-helper-2 (TH2). Immunologists have also identified specific groups of chemical messenger molecules called “cytokines and chemokines” that are used to communicate between the cells of the immune system and stimulate eith the TH1 or TH2 system.

TH1/TH2 Challenge

When the activity of one subset goes up, it represses the activity of the other similar to a seesaw or teeter-totter. Some practitioners recommend the TH1/TH2 Challenge to determine if symptoms are immune related. In this test, one immune stimulating supplement is taken at a time and a journal is kept of the symptoms experienced. One supplement stimulates the TH1 side of the immune system, and the other supplement stimulates the TH2. The reactions to these supplements are used to determine which side of your immune system is out of balance. However, very few people are strictly TH1 or TH2.

Fig. 1: Provocation of Unregulated Immune Response

Very Few People Are Strictly TH1 or TH2.

People with similar symptoms can have remarkably different laboratory results, while people with comparable laboratory results often exhibit widely different symptoms. This leads to confusion and frustration when doing immune challenges. Results from the Neuroscience NEI Gold 5516 for women suffering from Hashimoto’s show how confusing and unpredictable it can be.

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Fig. 2: Immune Status Scale

Immune Status Scale

Many consider the immune system to be always working properly, even with autoimmune conditions. When it is actually compromised and experiencing the effects of too many inflammatory cytokines and stimulating neurotransmitters unopposed by too few anti-inflammatory cytokines and inhibitory neurotransmitters, while being hacking into and disrupted by microbes, bacteria and parasites.

Another favorite is to blame food or something from the environment. While they can and do serve as provocateurs in an Immune compromised individual. Microbes, bacteria and parasites hack into the NEI Supersystem damaging or altering the immune response for their survival resulting in false positive and false negative food antibody test results.

In the Immune Compromised individual, the immune response the response will depend on their immune system status. This can be best measured by the Neuroscience Stimulated Cytokine panel. The Immune Status Scale (Fig. 2) is not measurable but represents a means to demonstrate the compromised immune system.

  • Zero is DEATH through an acquired immune deficiency and an incompetent immune system.
  • From zero to 30 denotes an ineffectual immune system activity characterized by extreme weakness with tremendous loss of any immune response in the body.
  • The point 30 denotes approaching death unless an immune response can be stimulated which will give it a higher potential ability to protect oneself.
  • From point 30 to 60, there is immune suppression with a decreasing ability to respond to immune challenges with symptoms of cytokine-induced sickness behavior.
  • Symptoms of cytokine-induced sickness behavior begin appear as the body nears 60. A competent immune system will be able to return the body to above 60.
  • From 60 to 100, we note complete health, with 100being the maximum quality of perfect being.
  • From 100 to 150, we note immune stimulation with symptoms of cytokine-induced sickness.
  • From 100 to 130, there is immune stimulation in response to immune challenges. A competent immune system will be able to return the body to below 100.
  • At 130, we will note symptoms of complete cytokine-induce sickness.
  • At rate 150– death takes place through Septic shock, Anaphylaxis, or Toxic Shock

The immune system can jump from the immune suppressed range to the immune stimulated range during a cytokine storm or when provoked and back again. The tissue producing the immune cells may fatigue contributing to a yo-yo effect of cytokine storms followed by a collapse of the immune response as the tissue recovers.

Cyrex vs Neuroscience
Cytokines that enhance cellular immune responses, Th1 (INf-γ, TNFα, etc.), Th2 (TGF-β, IL-4, IL-10, IL-13, etc.), Th17 (IL-17, Il-21, Il-22, IL-26, G-CSF, TNFα), and Th9 (Il-9) favor antibody responses. Cytokines binding to antibodies create a stronger immune effect.

Cytokine Storms

Cytokine storms may occur in both Immune Suppressed and Immune Stimulated. Chances are you have if you are suffering from Hashimoto’s, autoimmune conditions or a confusing mess of symptoms, you may be experiencing your very own Cytokine Storm season where you will have bad days followed by calm days after the storm and again by bad days. You may have found yourself in the proverbial “up a creek without a paddle” in your autoimmune world.

Cytokine Storms occur when the immune system becomes and remains activated against the immune stimulants beyond the point of being helpful.

Lectin Toxicity Evades Antibody-Based Blood Tests

While it is clear that lectins have the potential to do harm, it must be emphasized that the type of harm they do is harder to diagnose than in classically defined food allergies or sensitivites. In other words, confirmation of intolerance will not be found in antibody, allergy or intestinal biopsy testing because the damage done is a direct cytokine driven response, and not necessarily immune-medicated or only secondarily so.

The diagnostic “invisibility” is why lectin consumption is rarely linked to the ailments that afflict those who consume them. While lectins are not the sole or primary cause of a wide range of disorders, them are a major factor in sustaining or reinforcing injuries or diseases once they are initiated and/or established in the body.

Fig. 3:Stimulated Cytokine Test Results Base: General Overall Immune Response

Blue: Zero to 60– Immune Suppressed or Immunocompromised (Fig. 2)
Red: 100 to 150– Immune Activated or Stimulation (Fig. 2)

As you can see from the Stimulated Cytokine Test results that you can be Immune-Stimulated and Immune Suppressed simultaneously. You may experience symptoms of both a suppressed and stimulated immune system (see Fig. 2).

All had bad reactions with the Th1/TH2 challenge. Why? All have an overactive Th17 immune response. Three have a suppressed TH1 response. One has a suppressed TH2 response. The upper right is immunocompromised. The lower right is immune stimulated to everything. The lower left is a raw vegan over-consuming Soft and Hard Lectins. The upper left TH1 immune system collapses when exposed to bacteria driving straight into TH17.

You also have to apply some common sense. Common sense would tell you with autoimmune conditions your immune system isn’t working properly. Are you going to trust it to be accurate during a TH1/TH2 challenge? Lab testing is the best way to determine your immune status.

The TH1/TH2 Challenge does not recognize the TH17 response, immune suppression or stimulation.

In recent years, a specific T-cell subset, termed TH17. TH17 contributes to the development of diseases such as multiple autoimmune diseases including allergic inflammation, rheumatoid arthritis, autoimmune gastritis, inflammatory bowel disease, Hashimoto’s, psoriasis, and multiple sclerosis. The TH1/TH2 Challenge does not recognize the TH17 response, immune suppression of stimulation. Confusing results occur when different immune status responses are not accounted for as seen in Fig. 1.

Two Different Rheumatoid Arthritis Patients

It is much better to provoke an immune response in a laboratory setting than suffer the consequences of a failed TH1/TH2 challenge. The Neuroscience NEI Gold (5516) determines the baseline immune status and whether lectins (PHA) or bacteria (LPS) provoke a TH1, TH2 or TH17 response. As seen in Fig. 1 the immune system can fail when provoked (blue color) resulting in a suppressed immune system. Measurement of stimulated cytokines can identify the presence of an excited or suppressed immune status.

Are Edible Enemies contributing to poor health and inflammation? Lectins cause a plethora of damage to the body, promoting chronic inflammation and sensitivity. Take the Edible Enemy Quiz to test your knowledge on lectins.

Use the Lectin Control Formula to reduce the inflammatory response that occurs due to lectin consumption. Take two capsules with each meal.

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TH1

Th1-lymphocytes are primarily made in response to microbes that infect or activate macrophages and Natural Killer cells, and in response to viruses.

Th1-type cytokines tend to produce the proinflammatory responses responsible for killing intracellular parasites and for perpetuating autoimmune responses. Interferon gamma is the main Th1 cytokine. Excessive proinflammatory responses can lead to uncontrolled tissue damage, so there needs to be a mechanism to counteract this.

TH2

TH2-lymphocytes are primarily made in response to helminths (worms), allergens, and extracellular microbes and toxins. The TH2-type cytokines include interleukins 4, 5, and 13, which are associated with the promotion of IgE (severe allergies) and eosinophils response, and also interleukin-10, which has more of an anti-inflammatory response. In excess, TH2 responses will counteract the TH1 mediated microbial killing action. The optimal scenario would therefore seem to be that we should produce a well-balanced Th1 and Th2 response, suited to the immune challenge.

 

TH17

The purpose of Th17 cells is to clear pathogens, which are not efficiently handled by TH1 and TH2 type of immunity. The induction of Th17 responses must go through three distinct steps: Induction, amplification and stabilization. The stability of Th17 population is only relevant if it is protective against a given pathogen-invader or other kind of insult. If Th17 cells lose their stability they become highly proinflammatory and promote the destruction of your body’s tissues as occurs in autoimmune conditions. In essence, your immune system chooses to sacrifice body tissues by destroying in order to preserve the rest of your body.

TH17 and Vaccine-Related Injuries

Mercury or aluminum is put into vaccines to stimulate an immune response the contagious bacteria with the intention of developing immunity to the disease causing microbe. However, if a child is born with an over active TH17 response from the mother during pregnancy. A reaction, small or catastrophic may occur leaving the child impaired or worse. It is important to determine the immune status of the woman prior to or during pregnancy. Dr. Peterson can provide the answers to this.

TH17 is not included in the TH1/TH2 Challenge

The TH-1/TH-2 Challenge as noted in the book “Why Do I Still Have Thyroid Symptoms?” was printed prior to understanding of TH-17. The TH-1/TH-2 Challenge may provoke a TH-17 response. The TH-17 destroys tissue rather than allowing it to be inflamed; analogous to a suicide bomber attack that you can not defend against.

We can and do use laboratory testing to determine your autoimmune response. We recognize the impact of autoimmune conditions and the possibility of false positives and false negatives when using such labs. We start by using H.I.S.S.

  • History
  • Information
  • Signs
  • Symptoms

By utilizing a step-wise approach: Ask questions first. Lab test second. Immune challenges should be done in a laboratory – not your body. The physicians at Wellness Alternatives can determine the most likely scenario involving your immune system without provoking an uncontrolled immune response.

Very few are strictly TH-1 or TH-2.

Those with TH-1 dominance creating symptomatology usually feel better with coffee or caffeine. But feel worse with immune stimulators – Echinacea, goldenseal, immune-boosting mushrooms or probiotics. A person with TH-2 dominance creating symptomatology are the opposite. They will feel better with immune stimulators – Echinacea, goldenseal, immune-boosting mushrooms or probiotics and feel worse with coffee or caffeine.

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Very few are strictly TH-1 or TH-2. This leads to confusion and frustration when doing immune system challenges. More often than not a person will be both TH-1 and TH-2 with multiple autoimmune conditions, i.e. >80% with Hashimoto’s also have Autoimmune Gastrointestinal Disease. This happens when different autoimmune diseases are actively provoking both sides of the immune system to be overactive and the regulatory part of the immune system can’t regulate either side. When a person has both TH-1 and TH-2 creating symptomatology, they often come into the office saying: “I’m always sick” or “I’m allergic to everything.” When TH-1, they will feel worse with immune stimulators – Echinacea, goldenseal, immune boosting mushrooms or probiotics and feel better with little amounts of coffee or caffeine. Which causes a shift pushing them into an overactive TH-2 response were they will feel worse with coffee or caffeine but feels better with little amounts of immune stimulators – Echinacea, goldenseal, immune boosting mushrooms or probiotics.

This eventually drives them into a place where neither TH-1 nor TH-2 creates symptomatology but both are over reactive and under reactive at the same time. They will happily report, “I never get sick” in addition to “But I know I’m not well.” This is scary because their immune system is no longer able to protect them. They are slip sliding away down the slippery slope of autoimmune diseases because their immune system is too fatigued for any appropriate response. Those that add, “I feel good” are doing Green Allopathy often fall into this category. When we look at their labs they will have low absolute neutrophils (<1800) and lymphocytes (<1500). Some will have only one low – others both. Those with an underactive TH-2 will tell us they feel better with a little coffee, or caffeine but feel worse with moderate amounts of coffee, caffeine – as they are driven into TH-2 dominance. At the same time they also have an underactive TH-1 where they feel better with a little immune stimulators – Echinacea, goldenseal, immune boosting mushrooms or probiotics but feel worse after a time with moderate amounts of immune stimulators – being driven into TH-1 dominance.

Reregulating the immune system

Rather than supporting either the TH1 or TH2 while ignoring the TH17 dominance. Wellness Alternatives recommends Quieting the Immune system and doing everything we can to not provoke any immune response. Think of it as if you are being quiet after finally getting a cranky baby asleep. You don’t want to do anything to wake it up. In addition to this we support the T-Helper, T-regulatory cells and inhibitory neurotransmitters and cytokines to re-regulate the TH1, TH2 and TH17 immune response.

Now a quick jump back to the antibody story. It has been proposed that antibodies are normally inactive in a healthy individual. It has been said that 60% or more of the action of a healthy immune system is to deal with the leakage of larger food molecules from the gut. There is, after all, a high degree of similarity between various mammalian animal proteins in our diet and those found in our bodies. If our immune system were to attack all instances of these proteins, we would all have arthritis, lupus, and many other autoimmune diseases. Yet, in some people this type of antibody based damage does occur.

Calm & Quiet, Don’t Suppress or Stimulate Your Immune System

Taking supplements to stimulate one side because you did a TH-1/TH-2 challenge will only make both sides overactive. Yes, in theory taking supplements stimulating the TH-2 is supposed to control the TH-1 after immune regulation has been achieved. The reason you have an autoimmune disease is largely due to an inability to control your immune response. If the immune regulation was not working before the challenge, chances are very high, it will not work by provoking the other side.

It is ill-advised to provoke an immune system that cannot regulate.

Do not write checks your body cannot cash.

The physician at Wellness Alternatives utilize supplement protocols to quiet and re-regulate your immune system. This may involve supporting the regulatory or helper T Cells or the inhibitory cytokines and neurotransmitters. Care must be taken as noted previously as sometimes supporting the regulatory/helper T cells can provoke the inhibitory cytokines and neurotransmitters or vice versa into having an adverse response.

Find out WHAT is the root cause; what initial incident, infection, chronic or otherwise, is provoking and perpetuating this immunological alert status. Then deal with it!

  • DO whatever is necessary to QUIET, not suppress or stimulate, your immune system.
  • DO rotate your diet.
  • DO try to avoid many of the immune stressors in your environment.
  • KEEP a diary so you can LEARN what those stressor are! Start comparing them, you may find common ingredients, which are the provoking your immune system. This too, gives you more slack, as you can then use things without those ingredients.

For effective strategies to prevent immune-mediated disorders, including food allergy, it is essential to understand the external variables that influence immunological programming and how they interact with genetic predisposition to disease. Knowing that Autoimmune processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing intestinal barrier function. The physicians at WA use the following 4 principles to re-establish the intestinal barrier function.

  • Restore the Gastrointestinal Barrier Variables
  • Restore the Gastrointestinal Digestive Sequencing
  • Restore the Gastrointestinal Terrain
  • Re-Regulate the Immune system
  • Re-Regulate the Neurotransmitter imbalance
Concerned about your Health?
Call today! 530-615-4083