asthma, hay fever, arthritis and the science of immunity

Asthma and Hay fever: Asthma affects bronchi of lungs causing swelling of mucous lining and excess production mucus leading to breathing difficulties; Hay fever involves allergenic reaction of nasal passages

  • Reduce exposure to airborne allergens
  • Identify and eliminate food allergies and synthetic additives – taxing immune system
  • Eliminate or reduce intake of animal products – saturated fat has suppressive effect on immune system whilst also enhancing inflammation and inflammatory responses
  • Eat more fish
  • Increase intake of B6, Selenium, Magnesium (eg in multi-vitamin and mineral supplement)
  • Increase intake of Vit C
  • Increase intake of bioflavonoids – from rich sources like grape seed, pine bark, green tea, gingko biloba due to anti-oxidant protection

Rheumatoid Arthritis (RA): Possible causes are genetic abnormalities, dietary factors, food allergies, bacterial overgrowth, leaky gut syndrome, immunization

  • Affects connective tissue (collagen structure) of bones, muscles, cartilage, tendons, internal organs
  • Treatment involves removing food allergens and lipid profile of diet (eliminating / lowering saturated fats, boosting essential fat acids)
  • Food allergies and aggressors in disease can be nightshade family foods (tomato, eggplant, pepper)
  • Omega 3 EFAs suppress production of inflammatory compounds involved in disease (and response to allergens) – Flaxseed and fish oil needed in diet; Animal foods such as wild game (venison, elk, buffalo) and fish have good lipid profile and EFA content
  • Autoimmune disease inflammation can be caused by ROS damage necessitating Vit C, E, Vit A, Selenium, Beta-carotene
  • Bromelain, Curcumin, Ginger recommended for anti-inflammatory compounds
  • Cat’s claw helps reduce swelling in joints
  • Copper and Zinc: component of anti-oxidant superoxide dismutase that help reduce inflammation
  • DHEA depletion seen to be predisposing factor to lupus and RA – supplementation needed to prevent them, counter long term corticosteroid use and prevent bone loss (osteoporosis)

Cell related immune function

  • Antigenic protein presentation (that could be viral or endogenous) results in the production of key cytokines that are instrumental to the inflammatory process. Those cytokines are: Interleukin-1 (IL-1), interleukin-6 (IL-6), and TNF-alpha (TNFa). Dietary intake of fatty acids EPA and DHA from fish oil have been shown to modulate IL-1 as well as TNF production. The studies note prolonged down-regulation of IL-1 and TNF with supplementation. They also noted prolonged down-regulation of these cytokines after supplementation was stopped – indicating how fish oil supplementation can have a regulatory effect on excessive immune activity, returning activity to homeostasis. Fish oil, as such, could have a function in reprogramming the immune system.
  • Incorporation of fish oil into the cell membrane of cells throughout the body is closely associated with the function of fish oil in regulating the immune system. Studies evidenced IL-1 and TNF numbers directly relating to the amount of EPA in cell membranes. Correspondingly, increased EPA in cell membranes necessitated less anti-inflammatory medication in patients with Rheumatoid Arthrititis
  • Fish oil and other Omega 3 sources (such as flax seed) are rapidly incorporated into cell membranes, particularly the membranes of monocytes. Furthermore, these oils compete with and displace other fatty acids, namely Arachidonic Acid (AA), for incorporation into cell membranes. When they do, they alter cell function by displacing proteins on cell membranes. This is turn results in altered expression by the cell as well as altered interaction with other cells. Furthermore, Omega 3 acids, as composites of cell membranes, suppress RNA genetic expression by monocytes and down-regulation of IL-1 and TNF production is a result of this. The net effect is that Omega 3 oils both down-regulate antigen presentation and the resulting immune cascade.
  • The incorporation of Omega 3 oils into cell membranes is, itself, down-regulated over time. This suggests that Omega 3 oils reprogram the immune system and down regulate inflammatory responses, after which the body returns to homeostasis and recovers the ability to self-regulate the incorporation of other oils into cell membranes. Over all, there is a clear function for Omega 3 in regulating inflammatory conditions where they are chronic.

Adrenal Hormones

  • Over-production of pro-inflammatory cytokine IL-6 is associated with arthritis, osteoporosis, type 2 diabetes, cancer and heart disease. IL-6 levels rise in response to long term stress or trauma and remain high for long periods of time after that trauma has passed. Psychological and emotional factors can set up conditions by which pro-inflammatory cytokines such as IL-6 will be automatically released and levels sustained. This leads to the possibility that the opposite is true – that the adoption of new emotional patterns of behavior can break the same inflammatory cycle.
  • Long term release of IL-6 disrupts the function of the Hypothalamus and Pituitary glands and their release of both ACTH (AdrenoCorticotropic Hormone ) and CRH (Corticotropin-Releasing Hormone) – effectively leading to disrupted adrenal hormone response. Such a factor could lead to disrupted energy patterns leading to blood glucose imbalances. More important is the disruption to the anti-inflammatory effects of adrenal and gonadal hormones. Cortisol, DeHydroEpiAndrosterone (DHEA), Adrenaline, Testosterone (as well as CNS neurotransmitters adenosine and norepinephrine) all have a regulatory effect on key inflammatory cytokines (IL-1, IL-6 and TNF). Sustained cytokine release inhibits sex hormone production. Furthermore, IL-6 converts Estrogen to pro-inflammatory estradiol.
  • Inflammatory cytokines not only down-regulate sex hormone production (via the Hypothalmic-Pituitary-Gonadal Axis) but also up-regulate ACTH release via CNS activation. In effect, Cortisol release is stimulated by inflammatory conditions.
  • Sustained IL-6 circulation eventually leads to down-regulation of Cortisol (via disruption to the Hypothalmic Pituitary axis). However this delicate balance of regulation (presumably functioning to force the body to withdraw from stressful encounters in order to recuperate fully) could be ignored – and stress response stimulus of Cortisol could be chronic in itself. The danger here is not just increased risk of inflammation but also thyroid hormone problems and adrenal, as well as sexual hormone disruption. Prolonged stress or chronic inflammation can lead not only to disrupted thyroid hormone T4 function and T3 synthesis, it also leads to neurotransmitter problems.
  • A chronic inflammatory condition can be self-sustaining and lack regulatory control, especially when stress is chronic. This lack of regulatory control can lead to the inflammatory condition (or stress) spinning out of control affecting other organ systems, such as the endocrine system. In a sustained spiral of increasing organ system disruption, there is thus a clear need for intervention, and especially before stress or inflammation become self-sustaining and lacking regulation.
  • In sum, prolonged stress can bring the body to an unregulated pro-inflammatory state, and also disrupt and pose a danger to the endocrine system homeostasis.  There is a thus a clear need for intervention to disrupt stress, the stress response and the dangers they pose. Intervention in the psychological and emotional programming that occurs during chronic stress can disrupt stress response and its influence in inflammatory conditions. And this could be effected using mind body techniques and lifestyle adjustments
  • Intimately related to an unregulated adrenal or inflammatory process is the risk of intestinal inflammation being triggered.

GI Integrity

  • Nuclear Factor-κB (NF-κB) is another key cytokine and intermediary in the inflammation pathway. Factors such as stress and the use of pharmaceuticals can cause bacterial imbalance as well as bacterial crossing of the mucosal lining. Antigens (such as food allergens) can increase intestinal Tight Junction (TJ) permeability. These factors, amongst many others, trigger immune responses. And cytokines IL-1, IL-6, and TNF play key roles in the consequential inflammatory process.
  • IL-1 plays a key role in increasing TJ permeability and NFkB as plays a key pivotal role in the resultant enhancement of the inflammatory process. This process can lead to increasing gut permeability, up-regulated immune stimulation, and an inflammatory cascade that involves permeability of the Blood Brain Barrier and Gastrointestinal Dysfunction.
  • Due to infection, illness or the inflammatory response to GI aggravation, the resulting increased circulation of IL-1, IL-6 and TNF may lead to an enhanced sensitivity and triggering of the immune processes involved in any inflammatory pathway (GI permeation or due to infection). Effectively, one can affect the other, causing an increasing up-regulation of inflammatory processes – both working synergistically to increase each other’s inflammatory cascade. An important factor to note is that GI permeation and inflammation will cause nutritional deficiency (due to decreased absorption) which will detrimentally starve all organs and body functions of key nutrients for homeostasis. Of those functions, immune system homeostasis, if detrimentally affected, could lead to down-regulation and bacterial invasion of body tissues.
  • Another key potential cause of auto-immune disorders such as GI permeability could be immature lymphocyte T and B cells being released before they are sufficiently programmed and thus are “self reactive” to body tissues. In a weakened, nutrient deprived state caused by a chronic inflammatory condition, the potential for release of these “self reactive” immune cells would be enhanced and in itself become a trigger for auto-immune diseases due to faulty immune memory cell programming.
  • Unwinding these inflammatory processes could be effected using dietary measures. Fasting and removing allergenic foods is a first step in that process.
  • Gluten, Casein, Soy and Lactose are known allergenic foods. Added to this are dietary lectins that both increase intestinal permeability as well as aggravate enterocyte function in the intestinal tract. This aggravation leads to dysbiosis as well as degradation of the intestinal villi. Furthermore, with the ability to cross the intestinal tract, lectins alter lymphocyte function prompting triggering of auto-immune disorders. Lectins are present in wheat, red beans and other pulses such as lentils. Nightshade family vegetables, such as potatoes and tomatoes, are again high in lectins and thus potential aggravators as well as initiators of auto-immune disorders (as well as potentiating GI inflammation and permeability). However lectin aggravation is possible is some but not all people. The same is true for any allergenic food. This points to a clear need for testing and removal of any suspected foods, preferably under expert nutritional supervision.
  • Subsequent treatment can be provided with Withanolides in Aswagandha root which inhibit NFkB. Aswagandha Withanolides are also effective in suppressing COX-2 enzymes in the Arachidonic Acid inflammatorial cascade. And COX-2 enzymes may be down-regulated due to the broad anti-inflammatorial profile of Curcumin in Turmeric root which has been proved to reduce both TNF and NFkB genetic expression, reduce COX-2 activation, and also have powerful anti-oxidant effects. In addition, Ginger root down-regulates inflammatory compounds such as TNF through inhibition of COX and LipoOxygenase enzymes in the Arachdionic Acid pathway. Meanwhile, Oleic Acid in Olive Oil inhibits key inflammatorial compounds such as LTB4 which adds to the beneficial effects of dietary fatty acids in flax seed, fish oil and Omega 3 oils. Garlic, meanwhile, has well noted anti-biotic effects that may be of use in regulating or assisting the immune system involved in inflammatory responses.

Adapted from:

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