alcohol and gluten

beer_champagneBeer (or wine) and Pizza make a classic combination – talk about umami! However that feel good effect may have more to it than the taste and the buzz of alcohol. It may in fact be a sign that opiates are being released into the brain. But how does this occur? And how can a gluten allergy be involved in this?

In my reboot! post mentioned how I was diagnosed with a Gluten allergy. At the time, I was shocked! After all, I did the test to rule out the possibility of a gluten allergy as a cause for my health problems! As such I faced having to give up my hobbies of beer brewing and bread making with gluten grains, so I looked into what could have triggered the allergy. My answer came when I looked at alcohol and below I delve into what I found out.

Allergies and Barrier Integrity

Allergies start when an unusual particle (such as a food molecule) crosses a barrier within the body. These barriers serve to keep out those particles and exist in the Gastro Intestinal (GI) Tract as well as the Brain, and they are formed by molecules that are tightly woven together and allow only particles of a certain size to cross them. Whether the barrier itself has integrity or is in a weakened state making it “leak” is a major health concern. In my studies on Allergies and Autoimmune and Digestive Health I have posted the factors that lead to leaky barriers. Of these factors, stress and alcohol are quite possibly the most important.

Stress in itself draws blood away from the digestive tract, slowing down the breaking down of food and the motility of it through the body. Just think of when someone said something that made you anxious or distressed whilst you ate – what happened inside your gut? Did you feel a tightening, a constriction in the gut and a loss of appetite? This leads to larger than normal food particles that linger in the GI tract. Having partially digested food remain in the GI tract is damaging to it, as we shall see below. And a family of food particles that we do not wanting to have lingering around are lectins, in particular wheat lectin.


Dietary lectins are present both in wheat and in beans and legumes. Like phytates, they serve as protection for plant seeds, such as grains and legumes. Lectins cause damage as they are sticky proteins that bind to other molecules in the body and in the process stimulate an immune response. And this immune response damages barrier lining and widening the junctions in it. Put another way, lectins cause holes in barriers such as the GI tract and allow unusual particles to cross it. [1]

Lectins are broken down and destroyed through sprouting or fermenting, which makes soaking and sprouting your legumes all important! However all too often these grains and legumes are not sprouted, and the lectins are still present in them. Even heating foods containing lectins, such as in making bread does not destroy the lectins in them. Thus even gluten free bread made with bean flour such as Garbanzo or Chickpea Flour contains lectins that can damage the GI lining. [2] And even fermenting (in the case of sourdough bread) almost always only ferments a small portion of the overall grain flour used in the bread. So be aware that eating any food that contains lectins (such as foods made with wheat or beans), damage may be caused to the GI lining making it more permeable.

Leaky barriers and Opiate Highs

A damaged GI wall and intestinal permeability also results from an overgrowth of pathogenic bacteria in gut caused by stress, poor gut motility or diets low in probiotic foods.With a more permeable intestinal barrier, more molecules normally prevented from crossing this barrier are allowed to cross, such as partially digested protein molecules (or peptides). These molecules can then prompt an immune reaction to their appearance leading to an inflammatory response. This inflammatory response can then lead to increased intestinal permeability in turn causing an inflammatory spiral (ie increased inflammation). This sets the stage for the immune system to form antibodies so that it can react more effectively in the future. And in the case of foods with gluten, an allergy or sensitivity to gluten is the result.

Gluten proteins may also be digested improperly and metabolized by pepsin and hydrochloric acid in the stomach into gluteomorphin peptides.  This is the case when people have low stomach acidity which leads to low production of pancreatic enzymes (which itself may be caused by stress). In turn this leads to impaired intestinal wall enterocyte and enzyme function causing problems with digesting protein in food. Most importantly Gluteomorphin peptide breakdown is inhibited[3]

When intestinal enzymes do not break down these peptides, they cross the GI barrier intact. Gluteomorphins can also cross Blood Brain Barrier (BBB) where they bind to opiate receptors in the brain. And opiate receptor binding lead to euphoria, addiction and cravings for more (and appetite stimulation)[3].  This may explain the craving for and happy buzz you get from pizza – an opiate high from Gluteomorphins! However that high and craving could be a sign of both intestinal permeability and a gluten allergy.

Leaky Barriers and Brain Health

Opiate receptor binding of gluteomorphin in the brain also has direct links to schizophrenia, autism and ADHD. In addition, partially digested  peptides crossing the GI barrier inhibit enzymes which break down used protein metabolites in body, such as hormones and neurotransmitters. This is turn leads to increased circulation of them leading to damage to tissues, organs and the brain. Gluten meanwhile is associated with several specific brain health issues[4][13]

  • Encephalopathy (brain disease) and brain destruction that leads to migraines and stroke like symptoms such as loss of use of arm, legs or speech and vision difficulties as well as dementia and peripheral neuropathy
  • Immune related damage to memory and mind, such as temporal lobes, resulting in seizures and epilepsy
  • Cerebellar ataxia caused by the binding of gluten anti-bodies in the brain to Purkinje receptors and brain cell destruction

This ataxia (impaired muscular co-ordination) you may be familiar with – it happens on those occasions when we drink too much alcohol! However alcohol also poses even more dangers. Drinking alcohol even in moderate amounts has been shown in a study to disrupt the GI lining making it leaky[5]. In addition, alcohol has been shown to disrupt and weaken the Blood Brain Barrier (BBB)[6].

Other factors, including immune mediators and inflammatory compounds can weaken the BBB leading to neural degeneration and diseases such as Alzheimer’s, Parkinson’s and epilepsy[7]. And these inflammatory compounds can stem from a leaky gut, which in itself has been shown to contribute to a leaky BBB[8]. In fact, any factor which weakens the GI barrier including stress, the use of pharmaceuticals and exposure to allergy foods and toxins can also weaken the BBB and lead to neurodegeration[9].

A key point involved in this is the additional load of toxins and peptides that are allowed into the body through a leaky gut. These then create metabolic waste as the immune system tries to tackle them. All of this waste then needs to be cleared out by the liver, and the liver shares nutrient resources for its function with the immune and adrenal systems. Thus under increased work load to process this metabolic waste, or if the nutrients it needs are being used due to stress or an immune response, the liver will take longer time to break down this waste leading to damage caused to the body as they keep circulating in it. Thus drinking alcohol will enhance the potential for this damage to the body, for it is also a toxin that the liver deals with.

Alcohol consumption in itself has been shown to have links with the development of Celiac disease[10]. However, whilst it is not clear that alcohol consumption actually causes Celiac disease, what can be assumed is that it plays a mediatory role. This same role has been shown to occur between alcohol consumption and the development of Cerebellar degeneration related to gluten (Gluten ataxia)[11]. The issue here is what triggers the development of antibodies that react both to gluten and to brain tissue. As such alcohol can prime a person for the formation of these antibodies through weakening the GI and BBB as well as through weakening the liver’s ability to process metabolic waste.

A key point to note is that brain degeneration related to Gluten is not always associated with GI related symptoms or discomfort, as studies have shown[12] [13] [14]. These studies postulate that the immune system response to gluten is different between people. Thus an allergic response to gluten could manifest in GI problems with some people and neurological (Brain) related problems with other people. Meanwhile these studies show that avoidance of gluten lowered the onset of GI and neurological problems. A gluten free diet moreover may also prevent these problems occurring at all.


Personally I never had GI problems from eating wheat or gluten grains. However my tests showed I had gluten antibodies in my brain, antibodies linked directly to Gluten Ataxia and Cerebellar degeneration. From looking into this, I see that alcohol and stress played a key role in weakening my BBB and triggering the formation of those antibodies. And I certainly don’t want to lose my muscular co-ordination and ability to exercise due to Gluten Ataxia. Nor do I want the same to happen to you!

So I offer you the following advice:

  • Ensure you are able to relax and be absorbed in good vibrational feelings whilst you eat and that you are not stressed (or distressed / made anxious) by anything. A simple habit or ritual to help with this is to say a prayer of gratitude or grace before eating and to eat mindfully and gratefully (and encourage others who eat with you to join you in this ritual!)
  • Chew thoroughly as this also both stimulates and is a key part of the whole digestion process
  • Be aware that all foods that contain grain and legumes run the risk of causing a leaky gut. This includes all breads, pastas as well as gluten free products made with bean flour. In other words, unless the grains and legumes used in the food are thoroughly soaked, sprouted or fermented to break down the lectins in them, those lectins could be causing a leaky gut
  • A glass of alcohol with food makes the barriers of the brain and gut leaky and a leaky barrier is what triggers an allergic reaction as well as both Gastro Intestinal and Brain damage
  • Love your liver! and start you day with a green smoothie



An excellent article about Lectins, GI health and the benefits of sprouting from the Precision Nutrition

An indepth study on Dietary Lectins and immune response from Laura Power, pH D

A great article about the link between Wheat and brain health from Dr Mercola

An study article about the health problems caused by wheat from GreenMedInfo

Adapted from:


Pierini , C. (no date). Lectins: Their Damaging Role in Intestinal Health, Rheumatoid Arthritis and Weight Loss.

Kharrazian, D. (2013). Why Isn’t My Brain Working? Carlsbad, C.A.: Elephant Press

Perlmutter, D. (2013). Grain Brain. New York, N.Y.: Little, Brown and Company


Campbell-McBride, N. (2004). Gut and Psychology Syndrome.  Cambridge, U.K., Medinform Publishing

Davis, William (2011). Wheat Belly: Lose the Wheat, Lose the Weight, and Find Your Path Back To Health. New York, NY: Rodale

Alcohol and Weakening of the Blood Brain Barrier


Elamin E, Jonkers D, Juuti-Uusitalo K, van IJzendoorn S, Troost F, et al. (2012) Effects of Ethanol and Acetaldehyde on Tight Junction Integrity: In Vitro Study in a Three Dimensional Intestinal Epithelial Cell Culture Model. PLoS ONE 7(4): e35008. doi: 10.1371/journal.pone.0035008

Haorah, J., Heilman, D., Knipe, B., Chrastil, J., Leibhart, J., Ghorpade, A., Miller, D. W. and Persidsky, Y. (2005), Ethanol-Induced Activation of Myosin Light Chain Kinase Leads to Dysfunction of Tight Junctions and Blood-Brain Barrier Compromise. Alcoholism: Clinical and Experimental Research, 29: 999–1009. doi: 10.1097/01.ALC.0000166944.79914.0A

Blood Brain Barrier

Stamatovic, S. M., Keep, R. F., & Andjelkovic, A. V. (2008). Brain Endothelial Cell-Cell Junctions: How to “Open” the Blood Brain Barrier. Current Neuropharmacology6(3), 179–192. doi:10.2174/157015908785777210

Aristo Vojdani and Jama Lambert, “The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II,” Evidence-Based Complementary and Alternative Medicine, vol. 2011, Article ID 984965, 7 pages, 2011. doi:10.1093/ecam/nep063

Forsgren, S. (2008). NeuroImmunology: From Leaky Gut to Leaky Brain. Public Health Alert: 3(12).

Alcohol and Gluten sensitivity

Koivisto, H., Hietala, J., Anttila, P., & Niemelä, O. (2008). Co-occurrence of IgA antibodies against ethanol metabolites and tissue transglutaminase in alcohol consumers: correlation with proinflammatory cytokines and markers of fibrogenesis. Digestive diseases and sciences53(2), 500-505.

Currie, S., Hoggard, N., Clark, M. J. R., Sanders, D. S., Wilkinson, I. D., Griffiths, P. D., & Hadjivassiliou, M. (2013). Alcohol Induces Sensitization to Gluten in Genetically Susceptible Individuals: A Case Control Study. PLoS ONE8(10), e77638. doi:10.1371/journal.pone.0077638

Gluten Ataxia

Hadjivassiliou, M., Mäki, M., Sanders, D. S., Williamson, C. A., Grünewald, R. A., Woodroofe, N. M., & Korponay-Szabó, I. R. (2006). Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia. Neurology66(3), 373-377. This study may be found by copying and pasting the following link into your browser:

Hadjivassiliou, M., Aeschlimann, P., Strigun, A., Sanders, D. S., Woodroofe, N., & Aeschlimann, D. (2008). Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Annals of neurology64(3), 332-343.


Hadjivassiliou, M., Sanders, D. S., Grünewald, R. A., Woodroofe, N., Boscolo, S., & Aeschlimann, D. (2010). Gluten sensitivity: from gut to brain. The Lancet Neurology9(3), 318-330. This study may be found by copying and pasting the following link into your browser:

Hadjivassiliou, M., Aeschlimann, P., Sanders, D. S., Mäki, M., Kaukinen, K., Grünewald, R. A., … & Aeschlimann, D. P. (2013). Transglutaminase 6 antibodies in the diagnosis of gluten ataxia. Neurology80(19), 1740-1745

auto-immune and stress study

Rheumatoid Arthritis

 by Hugo Allen-Stevens


Rheumatoid Arthritis (RA) is an auto-immune condition characterised by a cascade. Triggers in the cascade include DNA and genetic expression, Gastrointestinal Integrity and Immune homeostatis. Mediatory factors include stress response, liver detoxification and the inflammatory pathways. Intervention and treatment at any point in the cascade (including prevention) may successfully reduce symptoms and inhibit or resolve expression at any point along the RA cascade. This paper will focus on the use of Dietary and Lifestyle factors as key tools in that intervention.

This paper will also bear reference to the case of a 73 year old female with RA who has in the last year undergone operations to replace her knees which were crippled by RA. This lady has in the last 10 years undergone increased physiological stress whilst acting as carer for her husband. This paper will address how long term stress impacted this lady’s RA cascade. It will also address how the death of this lady’s husband this year and the resultant reduction in stress may be factors that can be combined with nutritional and lifestyle support to address her RA cascade and ease her symptoms. This lady is the mother of the author of this paper.

Description of condition

The RA cascade involves anti-bodies that attack the synovial membrane between bones resulting in damage and degeneration of surrounding cartilage and bone tissue. Marieb notes that RA “begins with inflammation of the synovial membranes […] Inflammatory cells […] enter the joint […] and release a deluge of inflammatory chemicals that destroy body tissue […] In time […] cartilage is destroyed, scar tissue forms and connects bone ends” (2009, p. 173). Marieb further notes that “the course of RA varies as is marked by remissions and flare-ups (rheumat = susceptible to change or flux)” (2009, p. 173). Holford notes that during a remission, joints become “inflamed and enlarged, causing pain, swelling, stiffness and loss of function in the joints and possibly other parts of the body” (2009, p. 4). Holford adds that “sufferers may have a slight fever, they are likely to feel tired and generally run down” (2009, p. 5).

During RA remissions, “involved joints are characteristically quite warm, tender and swollen. The skin over the joint takes on a ruddy purplish hue. X-ay findings usually show soft-tissue swelling, erosion of cartilage, and joint space narrowing. As the disease progresses, deformities develop in the joints of the hands and feet, although deformities can [also] occur in the neck and shoulders” (Murray, 2005, p. 761). Most intriguing, however, is Holford’s assertion that RA “affects the whole body, and usually on both sides of the body (for example, both wrists, rather than simply a weight bearing joint). It often affects fingers, wrists, knees and ankles but can also affect other parts of the body such as heart tissue and muscle” (2009, p. 4). Holford provides a possible explanation for this stating that “some viruses and bacteria particularly affect joints by lodging in them and recurring when […] immune defences are low” (2009, p.13).

As such, a weakened immune system can place any part of the body at risk of RA symptoms. However the cascade that leads to that begins with antigen presentation, identification and immune response.

Cell related immune function

Choy and Panayi (2001) note that RA begins with the presentation of an antigenic protein that could be viral or endogenous. The end result of this presentation is the production of key cytokines that the authors note as being instrumental to the inflammatory process in RA. Those cytokines are: Interleukin-1 (IL-1), interleukin-6 (IL-6), and TNF-alpha (TNFa). IL-1 and TNFa are noted for stimulating neutrophil activity, and neutrophils are noted by the author for releasing enzymes that damage and degrade the proteoglycans in cartilage tissue. Furthermore, CD4 and T-Cell intermediaries, upon being stimulated by the antigen presentation, release chemical compounds that further degrade joint tissue (osteoclastogenesis). This results in the key characteristics of RA – the swelling and degradation of joints and cartilage due to the inflammatory immune response.

RA itself is characterised by periods of remission and “flare-ups” where the swelling of joints (and pain) returns. If this remission becomes prolonged, leading to chronic localised inflammation, degradation of both joint tissue and cartilage may be irreversible. Thus there is a key need to intervene before inflammation becomes chronic.

Simopoulos (2002) notes that 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. Also noted is the down-regulation in the production of Leukotriene B4 (LTB4). LTB4 is closely associated with neutrophil activity and down-regulation of LTB4 was shown to lead to down-regulation of neutrophils (neutrophils, as noted above, can damage cartilage tissue). Furthermore, down-regulation of LTB4 was prolonged after supplementation with DHA and EPA was stopped, again illustrating the possible immune regulatory effects of fish oil supplementation. Fish oil, as such, could have a function in reprogramming the immune system.

Simopoulos points out that 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 RA suffers. So could fish oil function in reprogramming the immune system? Evidence presented by Simopoulos suggests it can. He points out that both fish oil and other Omega 3 sources (such as flax seed) are shown to be rapidly incorporated into cell membranes, particularly the membranes of monocytes. Furthermore, these oils competing 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.

Simopoulous adds that 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 (needed, for example, for possible up-regulation of immune and inflammatory responses.) Over all, there is a clear function for Omega 3 in regulating inflammatory conditions where they are chronic.

Meanwhile other factors triggering a chronic inflammatory state will need to be monitored – especially in RA. These factors include the influence of stress and the adrenal hormones.

Adrenal Hormones

Kiecolt-Glaser (2003) points out over-production of pro-inflammatory cytokine IL-6 is associated with arthritis (as well as osteoporosis, type 2 diabetes, cancer and heart disease). In her study of long term caregivers looking after their spouses, she concluded that IL-6 levels rose in response to stress and remained high in many cases for years after the death of the spouse. She also notes how psychological and emotional factors can trigger the release of IL-6 leading to increased inflammatory damage from this cytokine when release is sustained over long periods of time – such as with caregivers. What is interesting to note is how psychological and emotional behavioural patterns 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 behaviour can break the same inflammatory cycle.

Straub and Cutolo (2001) note that 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. Straub and Cutolo note that 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) involved in RA. However they note that sustained cytokine release inhibits sex hormone production. Furthermore, IL-6 converts Estrogen to proinflammatory estradiol. In effect, a chronic inflammatory condition such as RA can be self-sustaining and lack regulatory control, especially when stress is chronic. This lack of regulatory control can lead to RA (or stress) spinning out of control affecting other organ systems, such as the endocrine system.

Straub and Cutolo (2001) also note that inflammatory cytokines not only down-regulate sex hormone production (via the Hypothalmic-Pituitary-Gonadal Axis) but also up-regulate ACTH release via CNS activation. This is echoed by Kharrazian (2009), who points out how Cortisol release is stimulated by inflammatory conditions. As mentioned above, 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 presumably be ignored – and stress response  stimulus of Cortisol could be chronic in itself. The danger here is not just increased risk of inflammation (pointed out by Kiecolt-Glaser) but also thyroid hormone problems and adrenal, as well as sexual hormone disruption. Kharrazian (2009) notes that either prolonged stress or chronic inflammation can lead not only to disrupted T4 function and T3 synthesis, it also leads to neurotransmitter problems. And in a sustained spiral of increasing organ system disruption, Straub and Cutolo point out how inflammatory cytokines stimulate the aromatase enzymes and disrupt steroid hormone production – in this case producing estrogen which can then be converted into the pro-inflammatory estradiol. There thus is a clear need for intervention at any point in this cascade, and especially before stress or inflammation in the RA cascade becomes self-sustaining and lacking regulation.

In the case of the mother of the author of this paper, the net effect of this stress response can be seen in the worsening of this lady’s RA condition in the last ten years whilst acting as caregiver – whereby inflammation became chronic as a result, and degradation of synovial membranes in both knees became irreversible. This resulted in the necessitation of surgery to replace those knees. Whilst the stress of acting as caregiver no doubt increased her RA inflammation and led to that joint degradation, this could continue even when that stress apparently disappears. And Kiecolt-Glaser (2003) point out the possibility of stress response being prolonged even after the death of a husband when the wife is the caregiver. They furthermore point out a worsening of the symptoms of RA and also the increased risk of diabetes and heart problems.

If sum, prolonged stress can bring the body to a 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. As pointed out above, intervention in the psychological and emotional programming that occurs during chronic stress can disrupt stress response and its influence in inflammatory conditions such as RA. And this could be effected using mind body techniques and lifestyle adjustments (which are detailed later in this paper).

Intimately related to an unregulated adrenal or inflammatory process is the risk of intestinal inflammation being triggered. In fact, intestinal health and inflammation in the Gastro Intestinal (GI) tract can itself be a trigger for the RA cascade.

GI Integrity

Nuclear Factor-κB (NF-κB) is another key cytokine and intermediary in the inflammation pathway. Vojdani and Lambert (2011) point out how factors such as stress and the use of pharmaceuticals can cause bacterial imbalance as well as bacterial crossing of the mucosal lining. They also point out how antigens (such as food allergens) can increase intestinal Tight Junction (TJ) permeability. These factors, amongst many others, trigger immune responses.

Vojdani and Lambert (2011) also point out the key roles of IL-1, IL-6, and TNF in the consequential inflammatory process. They implicate IL-1 as playing a key role in increasing TJ permeability and NFkB as playing a key pivotal role in the resultant enhancement of the inflammatory process. And this process they point out 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 either RA 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 either inflammatory pathway (RA or GI permeation). 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. This in itself is a key factor in the RA cascade – whereby bacteria enters joint synovial fluid activating the inflammatory process.

Another key potential cause of auto-immune disorders such as RA and 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 (Marieb, 2009, p. 429). In a weakened, nutrient deprived state caused by a chronic inflammatory condition, the potential for release of these “self reactive” immune cells could be enhanced and in itself become a trigger for either disorder through immune memory cell programming.

Unwinding these inflammatory processes could be effected using dietary measures. Ichikawa et al. (2006) report that Withanolides in Aswagandha root inhibit NFkB. They also identify suppression by these Withanolides of osteoglastogenesis by NFkB – thus a lowering of the joint damage in the RA cascade. Mulabagal et al. (2009) built on the work of Ichikawa et al. in proving the effective use of Aswagandha Withanolides in suppressing COX-2 enzymes in the Arachidonic Acid inflammatorial cascade. In addition, Chattopadhyay et al. (2004) point out that COX-2 enzymes may be down-regulated due to the broad anti-inflammatorial profile of Curcumin in Turmeric root: they point out that Curcumin has been proved to reduce both TNF and NFkB genetic expression, reduce COX-2 activation, and also have powerful anti-oxidant effects. In addition, Altman et al. (2001) report that Ginger root down-regulates inflammatory compounds such as TNF through inhibition of COX and LipoOxygenase enzymes in the Arachdionic Acid pathway. Meanwhile, Linos et al. (1999) point out the inhibitorial effect of Oleic Acid in Olive Oil on key inflammatorial compounds such as LTB4; their work further illustrates the beneficial effects of dietary fatty acids in flax seed and fish oil and thus adds to the beneficial effects of Omega 3 oils reported by Simopoulos (2002). Garlic, meanwhile, has well noted anti-biotic effects that may be of use in regulating or assisting the immune system involved in inflammatory responses.

Pharmacological intervention

The beneficial use of natural nutrients in treating both GI and RA cascades is well noted in the above studies – especially with regard to their avoidance of problems caused by pharmacological drug treatments of such conditions. Rakel (2007) details these treatments as including Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), Corticosteroids, DMARDs (Disease Modifying Anti-Rheumatic Drugs), as well as other immune-suppressive drugs (such as anti-TNF agents) and also Anti-biotics.

Both Rakel (2007) and Holford (2009) point out the increased risk resultant from the use of these drugs in terms of heart disease, osteoporosis and diabetes, as well as intestinal problems. Holford (2009) notes that NSAIDs decrease immune prostacyclins that act in the GI tract to both protect and repair gut mucosal lining. It should be noted that damage to this lining will increase GI permeability and the cascade that could contribute to the RA cascade. Also, Vojdani and Lambert (2011) point out that medical drugs can upset the balance of gut intestinal bacteria that leads to GI permeability. Additionally, upset caused to this bacteria will lead to and contribute to the formation of food intolerances and allergies, as well as dysbiosis of the colon. And it is these GI problems that should be avoided in treatment of RA and intervention in the RA cascade.

Dietary intervention

“Virtually any food can aggravate RA, but most common offenders are wheat, corn, milk, dairy products, beef, nightshade-family foods (tomatoes, potatoes, eggplants, peppers)”

(Murray, 2005, p. 762)

Due to the inter-relationship between auto-immune conditions like RA and food intolerance and allergenic response factors, Murray (2001, 2005), Rakel (2007) and Holford (2009) advocate identifying and removing possible food allergens. This principle cannot be emphasised enough, for health in the GI tract is needed to supply the body with the nutrients it needs to achieve homeostasis. Rakel and Murray both advocate fasting as a first step in mediating RA symptoms and possible dietary triggers of its onset. And both emphasise fasting followed by the reintroduction of foods avoiding common allergenic aggravators (such as those listed by Murray above). Murray further emphasises a vegetarian diet both as a method to avoid availability of saturated fats for use in the Arachidonic Acid pathway and to provide anti-oxidant support for immune function. It could also be noted that plant based foods down-regulate blood acidity: high blood acidity is associated both with a meat based diet and is further implicated in increasing pain and inflammation.

Kjeldsen-Kragh (1999) further notes the beneficial effects of dietary intervention. He studied the use of dietary fasting as well as the use of vegan and vegetarian diets in controlling pain and swelling in RA patients. He attributed improvements in patients’ conditions from these dietary approaches as stemming largely from beneficial effects of fiber:

“The diet changes the fecal flora and thereby alters the amount and type of bacterial substances absorbed by the intestinal mucosa. The absorbed bacterial substances in turn influence the inflammatory process in the joints.

“The cause-effect relation may be the opposite. Rheumatoid arthritis is a systemic disease that can affect almost all tissues, and a reduction in disease activity may also involve the intestine. Changed conditions in the bowel can in this way influence the growth conditions of the intestinal bacteria and thereby alter the balance between the different species of the microflora.”

(Kjeldsen-Kragh, 1999)

Kjeldsen-Kragh’s study could also have highlighted the possible beneficial effects of nutrient deprivation in a vegan or vegetarian diet, namely reduced protein intake for forming immune compounds. Kjeldsen-Kragh did not specify this, but nutrient deprivation through fasting or a restrictive diet (such as a vegan or vegetarian diet) could be used as a method for immune-suppression and down-regulating excessive immune and inflammatory activity. However it is in the opinion of the author of this paper that ensuring full support for immune function using key nutrients along with lifestyle modifications would provide better tools for addressing the RA cascade. Furthermore, fasting and nutrient deprivation should only be used under expert supervision to interrupt and reset an unregulated (ie chronic) inflammatory condition such as RA.

Other uses of fasting are to provide the GI tract a chance to heal. This is especially necessary when dietary inflammatory aggravators are being ingested. Vojdani (2011) notes the effect of dietary antigens in increasing TJ permeability. Cordain et al. (2000) further expands upon this noting the effects of dietary lectins in both increasing TJ permeability as well as aggravating enterocyte function in the intestinal tract, leading to dysbiosis as well as degradation of the intestinal villi. Furthermore, with the ability to cross the intestinal tract, Cordain et al. then showed that lectins altered lymphocyte function prompting auto-immune triggering of both the RA cascade and other auto-immune disorders. Furthermore they pointed out that lectins could trans-locate after entering to the synovial membranes (of joints), again triggering the RA cascade. Cordain et al. do point out however that lectin activation of both RA and GI disease pathways is possible is some but not all cases of these disorders.

Cordain et el. (2000) back-up Murray (2005) in asserting that wheat is an aggravator of RA (albeit in some but not all cases). Cordain also point out that other lectins, such as those from red beans and other pulses such as lentils, are again aggravators of RA. And nightshade family vegetables, such as potatoes and tomatoes, are again high in lectins and thus potential aggravators as well as initiators of the RA cascade (as well as potentiating GI inflammation and permeability). Cordain et al.’s study thus shows the intricate relationship between GI health and the RA cascade. They also point to the benefits of fasting in lowering both RA and GI inflammatory processes. This combined with Kjeldsen-Kragh’s study of fasting as well as the numerous studies of fasting cited by Murray (2001, 2005), Rakel (2007) and Holford (2009) point to a possible benefit of fasting in treating RA. These studies, however, are not conclusive in their evidence for the benefits of fasting – and many patients under study achieved no benefit.

The author of this paper thus once again concludes that fasting has a potential use in treating RA patients, but under expert supervision. With that supervision, and the re-introduction of foods under supervision and testing, food allergens and aggravators may be identified and eliminated. What may be concluded with that supervision is that food poses no role in aggravating or initiating the RA cascade. However the potential for lectins as well as other potential dietary allergens such as gluten and lactose to be aggravators must be tested – under expert supervision.

Immune support and a 7 or 14 day nutritional program

The role of food nutrients in supporting immune health is the reason the author advises fasting only under supervision. Following that fast, identification and elimination of food allergens is best done with an expert – which potentially could be a 7 or 14 day dietary treatment. Another form of treatment during a 7 to 14 day treatment period could be to providing nutritional immune support. Again, the author advises this be done under expert supervision with immune marker testing. This is due to the potential to use nutrition for down-regulation as well as up-regulation of immune or inflammatory systems. For example Murray (2001) illustrates the potential use of food in up-regulating T-suppressor to T-helper ratios in auto-immune conditions such as RA, as does Haas (2006). This again points to a role of reducing nutrient intake of key foods (such as protein) in order to suppress the immune system. Again however, the author stresses that expert supervision is needed. Otherwise, and assuming GI health is intact, the author advocates immune support through adequate nutrient support.

The possible nutrients that will support immune function are outlined by both Murray (2001) and Haas (2006). Haas advises sufficient protein intake, as well as sufficient intake of Vitamins A, C, E, B1, B2, B3, B5, B6, B12 and Folic acid, the minerals Selenium, Magnesium, Zinc. Haas also advocates intake of Bioflavonoids, Carotenes, Essential Fatty Acids and judicious intake of Iodene, Copper, Iron and Zinc (considering the possibilities of them off-setting each other in absorption or having detrimental effects if taken in excess). Haas also advises intake of Garlic and the use of Goldenseal and Licorice Root as immune supporting herbs. Murray (2001) adds to this list of medicinal herbs stating Echinacea and Astralagus may be taken for short periods with beneficial effects. Meanwhile he advocates a whole food diet with reduced sugar and decrease saturated fat, all to support immune function. As noted above, in Murray (2005) he advocates reduction of meats with saturated fats in order to suppress the Arachdionic Acid pathway. In the same book, Murray advocates the use of dietary enzymes such as Papain and Bromelain in helping with the RA cascade. Holford (2009) advocates the use of Bromelain for its anti-inflammatory effects. Other anti-inflammatory foods Holford recommends are Bioflavonoids (such as Quercetin), Ginger, and the herb Boswellia, as well as Hops extract and Olive extract.

The potential therefore is for a 7 or 14 day dietary program to include a fast, followed by a food elimination program. In doing so, it could follow the “4 R” principal advocated by Bland et al. (2004). In doing so it would include a GI healing program (to “replace” dietary enzymes and stomach acid, as well as “reinoculate” the GI tract with healthy bacteria using probiotics and prebiotics). Finally it would include a “repair” process, involving the introduction of a low irritant diet and GI dietary support that includes anti-oxidants and L-glutamine.

Bland et al. (2004) also point out the use of Omega 3 oils in the Arachidonic (AA) cascade, pointing out how they may be used to attract desaturase enzyme activity  away from desaturating Omega 6 fatty acids into AA cascade. Bland et al. also point out how fish oil, flaxseed oil and primrose oil may all provide fatty acids that may be used for production of anti-inflammatory prostaglandins. Holford (2009) notes that the enzymes needed to desaturate these oils for prostaglandin production need support from Vitamins C, B3 (Niacin) and B6, as well as Biotin and the minerals Zinc and Magnesium.

The above advice echoes and adds to the findings of Simopolous (2002) regarding the use of Omega 3 in re-regulating the immune system, namely Omega 4 oils being incorporated into cell membranes. Bland et al. (2004) illustrate that the beneficial effects of Omega 3 oils being taken into cell membranes (and altering their function) depends on thyroid hormone homeostasis. However Kharrazian (2009) points outs out that thyroid hormone homeostasis may become unstable as a result of both chronic stress and chronic inflammation. In effect, the need to modulate stress once again should be a central feature of any dietary treatment.

Bland et al. (2004) also point out the use of nutritional inhibitors of enzymes in the AA cascade, namely Quercetin, Vitamin E, Turmeric, Ginger, Garlic and Onion, as well as herbal inhibitors such as Licorice, Turmeric, Boswellia, Black willow and Wintergreen. This echoes key findings from studies cited above and underscores the use of nutritional aids as substitutes for pharmacological medicines in treating patients with RA. However, full function of these nutrients requires not only additional nutritional support (to aid the desaturase enzymes for example), they also require support from hormone glands (such as the thyroid) as well as GI integrity. This should be taken into account when selecting a 7 to 14 day program for a patient with RA.

Holford (2009) points out that RA sufferers may need nutritional support for their joints, and to provide the body with the materials to form and prevent the breakdown of proteoglycans, the structural components of joints, synovial fluid and cartilage that are all damaged in the RA inflammatory cascade. In particular he points out the use of Glucosamine, pointing out how it is not only an essential component in making cartilage and produced in body, but that a Chinese study shows it has similar anti-inflammatory and pain reduction properties to ibuprofen [1] (Holford, 2009, p. 184). He also advises adequate intake of Vitamin C, D, the minerals Calcium, Magnesium, and Sulpur containing foods (such as eggs, onion and garlic) as well as supplementation with Chondriotin, all for joint health, as well as bone health. Bone health should be addressed in a dietary program as Holford notes the probability of bone damage both from RA induced inflammation and also hormone disruption (namely progesterone and estrogen).

Under supervision of a dietary expert, the correct 7 to 14 day treatment plan may be carefully chosen from any of the above ideas. Care should be taken with the allergenic foods and RA aggravators at all times. Meanwhile, care should be taken with aggressive treatment plans involving fasting, nutrient deprivation or supplementation. For example, altering the T helper to T regulatory ratio with the use Vitamin D, Fatty acids EPA and DHA, Glutathione, and SuperOxideDismutase may be useful in treating auto-immune cases, it may not be useful for all cases. For this, as with any other specific dietary advice for a 7 to 14 day period, the specifics of the diet relate to the specific situation of the patient (such as age, lifestage, stage in the RA cascade, amongst other considerations). The author of this paper cannot stress enough the need to tailor any 7 to 14 day dietary program to the specific needs of the patient.

Additional nutritional support for key body functions include liver support, anti-oxidant support and blood sugar management. All these could be built into a 7 to 14 day nutritional program – though the author emphasizes that they should be used as part of a longer term lifestyle change for RA patients that also includes stress management.

Liver support

Whilst the health of the GI tract and that of the immune system are closely inter-related (especially with relation to the RA cascade), the RA cascade, as noted above is closely related to the endocrine glands and stress response. Stress, it itself, is closely related to liver function due to the liver’s role in breaking down and eliminating stress hormones. Added, the liver plays a key role in eliminating environmental toxins such as chemical pollutants and medications, toxins that can lead to and trigger the GI permeability cascade.

What is important to note is that many of the key nutrients required for successful liver function and detoxification are exactly the same as those required by the immune system – thus enhanced immune activity, such as in the potentially chronic inflammation in the RA cascade, could lead to nutrients being deprived for use in liver detoxification and function. Conversely (and more likely given the liver’s receipt of blood and nutrients prior to the immune system) extra nutrient use in liver function in breaking down stress hormones or environmental toxins could lead to key nutrients being deprived for use in the immune system. Meanwhile, GI health again is paramount in determining the supply of the key nutrients needed by both the liver and the immune system.

Dietary fiber, as noted above, is needed for GI bacterial balance. It is also needed for assisting in bile secretions from the liver – bile being one of the most important mechanisms by which detoxification end products of the liver are taken from the liver. And fiber has a key role in assisting in preventing the reuptake of these end products in the GI tract (such as hormones that have been broken down) and ensuring their successful elimination from the body. Fiber also plays a key role in blood glucose management which plays a key role in adrenal hormone function and stress response.

Anti-oxidants, such as bioflavonoids, are required by both the liver and the immune system, and their use (and subsequent need for replacement) will be greater in the case of either liver or immune system activity. Bioflavonoids, meanwhile, are needed for collagen health which will be of paramount concern in the RA cascade. Another key nutrient used in both the immune and liver systems is Glutathione. Equally, nutrients required for methylation pathways are required for both liver detoxification and to ensuring homocysteine levels do not in themselves become inflammatory and a burden on immune system resources.

The key nutrients needed for optimal liver function include Betaine (from Beets and fish) used by the liver to process fat, prevent chemical damage ad assist in the metabolism of homocysteine. Choline from egg yolks, organ meats, orange and cauliflower) is another nutrient needed by the liver for exporting fat from the liver and preventing its build up there, as well as being used methylation reactions. Meanwhile, key liver detoxification pathways are

  • Glucuronidation (for breaking down many medical drugs, estrogen and other hormones) which requires nutritional support from sulphur containing foods (such as garlic) and limonene rich foods (such as citrus fruits, dill and caraway)
  • Glutathione conjugation and anti-oxidant activity: Glutathione is made from amino acids methionine and cysteine as well as other source nutrients (such as Selenium) that can be sourced from asparagus, avocados, walnuts, Brassica family plants, and fresh fruits, fish and meat
  • Methylation (for breaking down estrogen and other steroid hormones) which needs nutritional support from Choline, Vitamin B12, Folic acid (from green leafy vegetables); vitamin B6 (from whole grains and legumes); Vitamin B12 (from animal products and supplements)
  • Sulfation (is the main pathway for breaking down environmental toxins, microbial products, drugs and stress hormones) and which needs nutrient support from sulphur containing foods such as egg yolks, red peppers, garlic, onions, broccoli, brussel sprouts as well as amino acids methionine and cysteine

Anti-oxidant support

Both the liver and the immune system, especially during enhanced activity such as increased steroid hormone detoxification or inflammatory response, produce free-radicals. RA itself produces free radicals at sites of inflammation, free-radicals that can build up and cause collateral damage if they are not neutralised by anti-oxidants. Part of the damage done by free-radicals (or Reactive Oxygen Species: ROS) is damage to cell structure and function. ROS also damage DNA, cause the triggering of RNA, and lead to the expression of genetic predisposing factors to diseases such as RA. ROS damage thus may play a causal role in triggering the initial phase of the RA cascade.

However at any part in the RA cascade, Anti-oxidants will be needed to prevent ROS damage and build up during inflammatory immune response. They will all be needed to assist liver detoxification pathways and to support immune health. It is important to note that anti-oxidants have a synergistic effect – enhancing effects when working in combination with each other (eg Vitamin C being boosted by Carotenes). Key anti-oxidants are:

  • Carotenes found in fruits, especially darker fruits such as berries, cherries; and in vegetables: including broccoli, onions, greens, parsley; legumes; green tea and red wine; ginkgo bilboa. Carotenes also enhance immune functions, are anti-tumor, and work primarily to stimulate anti-oxidant mechanisms
  • Flavonoids found in dark-coloured vegtables such as: carrots, squash, spinach, kale, sweet potatoes; fruits such as cantaloupe, apricots. Flavonoids are also anti-inflammatory, anti-allergenic, anti-viral and anti-cancer properties, working primarily to protect cell integrity, function and response
  • Vitamins C and E, Zinc, Copper, Manganese: reduce superoxides through superoxide dismutase enzymes
  • Vitamin C – needed to enhance oxidative capacity and prevent ROS damage and acts as ROS scavenger
  • Vitamin E – very good for reducing exercise induced ROS; protects phospholipid bilayers of all cells; ROS scavenger and important for oxidative stress conditions
  • Coenzyme Q10 (CoQ10): has central role in aerobic metabolism and avoidance of ROS production through enhanced electron transfer capabilities in ATP reactions
  • Selenium: supports production glutathione peroxidase enzyme, which counteracts peroxides, stimulates immune response, and protects against toxins
  • Vitamin B2: assists in maintaining electron balance (and avoiding ROS formation)
  • Sulfur containing L-cysteine and methionine: ROS trappers
  • L-Carnithine: synthesized from lysine (needs Vitamin C) increases utilization of fats in ATP energy production, prevents oxidation and ROS formation

Stress, Pain and Blood Sugar Management:

As mentioned above, Cortisol, Adrenaline and Noradrenaline all have an immune-regulatory and anti-inflammatory effect which can be beneficial in the RA cascade. However, chronic stress leads to imbalances in other endocrine hormones (such as the thyroid and sex hormones). Long term stress  can also raise IL-6 levels that can itself trigger the RA cascade. Meanwhile triggering of the RA cascade can lead to raised levels of IL-6, THF and IL-6 that can disrupt DHEA and sex hormone production. Progesterone, needed to build bone tissue, may thus be down-regulated, with osteoporosis as well as other arthritic conditions being worsened. There is thus a clear need to manage stress during periods where the RA cascade is triggered. Key to this is ensuring liver breakdown of stress hormones through liver support. Added, stimulants such as nicoteen and caffeine not only increase the stress response, they also place an extra burden of toxic substances needed to be broken down by the liver. These stimulants also inhibit stress hormone breakdown (in the case of caffeine and its effect on adrenalin breakdown). And Heliovaara et al. (2000) further demonstrated a causal link between coffee consumption and the risk, and incidence, of RA. In effect, coffee, caffeine and smoking should be avoided and stress should be managed at any stage in the RA cascade.

Holford (2009) points out meanwhile that stress and stimulants (such as caffeine) increases blood  glucose levels that in turn increase inflammation – as such, excess blood glucose can make inflammation more chronic. Insulin, meanwhile, has an anti-inflammatory effect by reducing blood glucose. However, Holford notes that insulin has inflammatory effects in converting Gamma Linolenic Acid (GLA) for use in the Arachidonic Acid pathway. It therefore becomes key for a patient with RA to manage their blood sugar and curb excesses of either glucose or insulin in the blood. A key nutritional tool for this is fiber due its regulatory effect of glucose uptake to the blood in the GI tract. Holford meanwhile advises management of blood glucose via the Glycemic Index dietary principles. With relation to stress, particularly recovery from chronic stress, as well as replacing poor dietary habits (ie excessive sugar consumption) with healthier eating practices, the use of the Glycemic Index diet could be a nutritional aid to both lifestyle change and also stress management. The principle here would be to use a low stimulant, high fiber, managed Glycemic Index profile in order to effect a physiological change that could accompany and synergise with stress reducing techniques. And the author in this instance advocates using these dietary principles to effect lifestyle changes.

A key tool for managing stress, processing stress hormones, and benefiting the immune system is exercise. Kiecolt-Glaser et al. (2003) note how exercise down-regulates IL-6. Meanwhile, exercise can be used to strengthen joints, increase motility of lymph fluids and clearing of immune (and metabolic) wastes. Exercise also improves mood, increases metabolic rate and increases energy levels. Water exercises are most beneficial due to lack of joint stress – however weight bearing activity is needed to prevent bone damage and osteoporosis. Tai Chi and Yoga can be extremely beneficial for any stage of the RA cascade, as well as preventing it – especially with regards to calming the nervous system and down-regulating stress responses.

Rakel (2007) points out how mind body therapy can help with people is the RA cascade and in stress management. A key suggestion he makes is journal writing about stressful events in order to clear them. He also suggests journaling positive emotions (presumably to promote them and the sense of wellbeing). Holford (2009) echoes the value in this, pointing out the toxic side effects of repressing or holding in negative emotions (evidencing a study on the low incidence of RA in people who did not inhibit their impulses and ended up in prison [2]). Rakel also points out the value of meditation and mindfulness training, such as meditative walking, pointing out decreased pain and the possibility of recovery from a debilitating experience of RA inflammation. Murray (2001) expands upon this, indicating the value of meditative practices such as guided imagery, hypnosis, relaxation and positive mental attitude in promoting homeostasis. Murray and Rakel, meanwhile, both indicate the value of laughter, and Murray points out how positive emotions enhance homeostasis. Rakel also points out how being creative, finding meaning in life, trying new things, having positive relationships and the possible use of psychotherapy can all be useful in preventing and treating RA. What is important to note is that not only do all these therapies provide relief from the symptoms of RA, they also provide relief from stress. Meanwhile Rakel adds that Acupuncture and Laser Therapy both have low risks and high success rates in alleviating pain and swelling.


RA itself is a cascade and an individual may find themselves at any point in that cascade. Factors in that cascade include genetic predisposition, excess ROS damage triggering RNA expression, GI permeability leading to bacterial infection of joint tissue, and inflammation as well as stress responses becoming chronic and unregulated by the body. Added in that cascade are symptoms of pain, swelling and potential lack of joint mobility leading to the necessity for surgery. Intervention in that cascade and remedial treatment will depend on where the individual finds themselves. Broadly speaking, fasting, identifying and eliminating allergenic and RA aggravating foods, mind body therapy as well as stress management techniques all form part of an initial treatment of an RA flare up. And where stress has been chronic, mind body therapy becomes more important: in order to interrupt psychological and emotional patterns and engage individuals in more positive patterns, lifestyles and (supportive) relationships. With expert accompaniment, nutritional therapy can support this process.

Pharmacological drugs are noted for being useful in acute situations of inflammation and pain. However due to their damaging side effects, the use of Omega 3 oils, Turmeric, Ginger, Ashwagandha (as well as Olive Oil and Garlic) are noted for being more beneficial. These natural forms of medicine are also noted in studies for assisting RA patients to stop taking Pharmacological drugs as well as effectively treat less acute conditions.

Elimination and avoidance of toxins, as well as stimulants such as caffeine is recommended, as is key nutrient support of the liver. This support becomes more important during chronic inflammatory episodes due to the relationship between nutrient needs of both the liver and the immune system. And liver support is needed for recovery from an inflammatory flare up. Meanwhile, Anti-oxidants are needed – in prevention, treatment and recovery in all stages and phases of the RA cascade. Anti-oxidants are also needed for immune and liver support.

A plant based diet that avoids saturated fatty acids from animal products is recommended – not just to avoid the inflammatory effects of those fatty acids, but also to enhance intake of fiber. Plant fiber is needed for assisting liver functions as well as ensuring GI health – it also is needed to regulate blood glucose. Blood glucose will need to be monitored, especially with patients involved or recovering from chronic stress, and a low Glycemic Index Diet is recommended in such cases. It is further recommended by the author or this paper that these changes in diet become permanent in the lifestyle of people at any stage of the RA cascade – as is the increased regular intake of deep sea fish such as salmon due to their Omega 3 oils.

Exercise, meanwhile, should be a permanent feature of any person in the RA cascade, especially those involved in stressful lifestyles. Intense exercise training such as weight lifting, power yoga, aerobic exercises (such as running) as well as other sports involves a person in a lifestyle of exercise that may have positive and preventative effects of RA triggering. Regular surfing and contact with salt water can also be beneficial, especially in the leaching of inflammatory compounds (through osmosis) from sites of inflammation – this effect is noted by this paper’s author through his personal experience. Equally the author notes from personal experience that QiGong and advanced level training exercises, such as “Bone Marrow Washing”, are extremely beneficial in treating and preventing inflammatory disorders such as RA. Meanwhile, light exercises such as Tai Chi, Pilates, and light Yoga (as well as Yoga breathing exercises) are all beneficial for patients who are in an inflammatory RA episode, as is swimming. Above all, it is recommended that regular and ongoing exercise of any form, particularly lighter exercises, becomes part of the permanent lifestyle adopted by RA sufferers.

In addition to this, nutrient intake should be optimised – both by ensuring health of the GI tract (through avoiding allergenic foods for example) as well as taking key nutrients to support key body functions.


RA is a cascade triggered and mediated by a number of differing and inter-relating factors – stress and diet being key contributing factors to the onset or worsening of symptoms. Conversely, stress management and diet are the mediating factors where solutions, relief and preventive treatments may be found. Dietary and lifestyle change consisting of a permanent, sustainable set of practices to manage both RA symptoms, the RA cascade itself and stress effectively can be begun in a 7 to 14 day dietary therapy or treatment. However it is strongly recommended by the author of this paper that all people with RA consult a nutritional expert and begin dietary treatment under their supervision. This is due to the highly individual nature of both the testing and analysis that will need to be done, as well as the individually tailored course of treatment, therapy and lifestyle adjustments to each person’s individual requirements.


[1] Jang B.C. et al. (2007). Glucosamine hydrochloride specifically inhibits COX-2 by preventing COX-2 N-glycosylation and by increasing COX-2 protein turnover in a proteasome-dependent manner. Journal of Biological Chemistry, 282 (38), 27622-27632

[2] Study conducted by Dr Ronald Lamont-Havers whilst he was national medical director of the Arthritis and Rheumatism Foundation. “Crime doesn’t pay but keeps arthritis away”, Los Angeles Times, 23 January 1963

Bibliography and Citations:

Murray, M. (2001). Total body tune-up. New York, N.Y.: Bantam Press

Murray, M. (2005).Encyclopedia of Healing Food. New York, N.Y.: Atria Books

Haas, E. (2006). Staying Healthy with Nutrition. Berkeley, CA: Celestial Healing Arts.

Ernest H S Choy, & Gabriel S Panayi. (2001). Cytokine pathways and joint inflammation in rheumatoid arthritis. The New England Journal of Medicine, 344(12), 907-16. Retrieved May 18, 2012, from ProQuest Health and Medical Complete. (Document ID: 69894911).

Simopoulos, A.P. (2002). Omega-3 Fatty Acids in Inflammation and Autoimmune Disease. Journal of the American College of Nutrition, 21 (6). Retrieved from:

Kiecolt-Glaser, J.K., Preacher, K.J., MacCallum, R.C., Atkinson, C.A., Malarkey, W.B., Glaser, R. (2003). Chronic stress and age-related increases in the proinflammatory cytokine IL-6. Proceedings of the national academy of sciences, 100 (15).

Kharrazian, D. (2009). Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal: A Revolutionary Breakthrough In Understanding Hashimoto’s Disease and Hypothyroidism. New York, N.Y.: Morgan James Publishing

Straub, R. H. and Cutolo, M. (2001). Involvement of the hypothalamic–pituitary–adrenal/gonadal axis and the peripheral nervous system in rheumatoid arthritis: Viewpoint based on a systemic pathogenetic role. Arthritis & Rheumatism, 44: pp. 493–507. doi: 10.1002/1529-0131(200103)44:3<493::AID-ANR95>3.0.CO;2-U

Vojdani, A. and Lambert, J. (2011). The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy, Part II. Evidence-Based Complementary and Alternative Medicine. Article ID 984965. doi:10.1093/ecam/nep063

Ichikawa, H., Takada, Y., Shishodia, S., Jayaprakasam, B., Nair, M.G., Aggarwal, B.B. (2006). Withanolides potentiate apoptosis, inhibit invasion, and abolish osteoclastogenesis through suppression of nuclear factor-κB (NF-κB) activation and NF-κB–regulated gene expression. Molecular Cancer Therapeutics, 5 (6), pp. 1434 to 1445. doi: 10.1158/1535-7163.MCT-06-0096

Mulabagal, V., Subbaraju, G. V., Rao, C. V., Sivaramakrishna, C., DeWitt, D. L., Holmes, D., Sung, B., Aggarwal, B. B., Tsay, H.-S. and Nair, M. G. (2009), Withanolide sulfoxide from Aswagandha roots inhibits nuclear transcription factor-kappa-B, cyclooxygenase and tumor cell proliferation. Phytother. Res., 23: 987–992. doi: 10.1002/ptr.2736

Chattopadhyay, Ishita ; Biswas, Kaushik ; Bandyopadhyay, Uday ; Banerjee, Ranajit K (2004) Turmeric and curcumin: biological actions and medicinal applications Current science, 87 (1). pp. 44-53. ISSN 0011-3891

Altman, R. D. and Marcussen, K. C. (2001), Effects of a ginger extract on knee pain in patients with osteoarthritis. Arthritis & Rheumatism, 44: 2531–2538. doi: 10.1002/1529-0131(200111)44:11<2531::AID-ART433>3.0.CO;2-J

Linos, A., Kaklamani, V.G., Kaklamani, E., Koumantaki, Y., Giziaki, E., Papazoglou, S., & Mantzoros C.S. (1999). Dietary factors in relation to rheumatoid arthritis: a role for olive oil and cooked vegetables?The American Journal of Clinical Nutrition, 70 (6). Retrieved from:

Marieb, E.N. (2009). The essentials of human anatomy and physiology. San Francisco, C.A.: Pearson Education

Rakel, D. (2007). Integrative Medicine. Philadelphia, PA: Saunders

Holford, P. (2009). Say no to Arthritis. London, UK: Paitkus

Murray, M. (2001). Total body tune-up. New York, N.Y.: Bantam Press

Murray, M. (2005).Encyclopedia of Healing Food. New York, N.Y.: Atria Books

Kjeldsen-Kragh, J.. (1999). Rheumatoid arthritis treated with vegetarian diets. The American Journal of Clinical Nutrition, 70(3S), 608S-614S. Retrieved May 20, 2012, from ProQuest Health and Medical Complete. (Document ID: 44389682).

Cordain L, Toohey L, Smith MJ, Hickey MS (2000). Modulation of immune function by dietary lectins in rheumatoid arthritis. British Journal of Nutrition, 83, pp. 207-217. Retrieved from:

Haas, E. (2006). Staying Healthy with Nutrition. Chapter 16: Immune enhancement (pp. 633 to 640). Berkeley, CA: Celestial Healing Arts.

Bland, J., Costarella, L., Levin, B., Liska, D., Lukaczer, D., Schlitz, B., Schmidt, M., Lerman, R., Quinn, S., Jones, D. (2004). Clinical Nutrition: A Functional Approach, Second Edition. Chapter 4: Fats (pp. 69 to 94), Omega 3 and Arachidonic acid cascade (pp. 74 to 78), fatty acids and thyroid function (p. 87); Chapter 7: permeability and the 4R gastointestinal support program. Gig Harbor, WA: The Institute for Functional Medicine.

M Heliovaara, K Aho, P Knekt, O Impivaara, & et al. (2000). Coffee consumption, rheumatoid factor, and the risk of rheumatoid arthritis. Annals of the Rheumatic Diseases, 59(8), 631-5. Retrieved May 18, 2012, from ProQuest Health and Medical Complete. (Document ID: 57941890).

stress and adrenal health study

Stress and Adrenal Health study

by Hugo Allen-Stevens

Metabolic aging


  • Fight or flight stress response hormone
  • Assists and allows the body to access structural, functional and energy bio-chemicals that enable thinking, movement as well as breathing, eating and other body function (eg through break down food for energy to perform body functions)
  • Signals breakdown of old cells to make new cells, a turnover that keeps cells younger and functioning better
  • Excess adrenaline causes cells to use bio-chemicals faster than it can replace them, leading to accelerated metabolic aging
  • Insufficient adrenaline causes insufficient access to bio-chemicals, leading to inefficient metabolism and accelerated metabolic aging

Poor nutrition and lifestyle causes adrenaline levels to be high to break down structural chemicals for use in body functions. This gives a sense of well-being and will cause turnover of structural bio-chemicals that will cause radiance and looking young e.g. shinier hair, softer skin, stronger nails – which can be addictive. Equally, if adrenaline levels are low, this may prompt self-medication with caffeine or sugar – both of which raise adrenaline levels. Again this is seeking a feeling of well-being that is addictive. However, without sufficient rest to rebuild structural compounds and without sufficient nutrients with which to build those compounds, these addictive patterns as well as high adrenaline levels cause the body to lack structural and functional compounds. The result is that accelerated aging as well as health problems are caused.

Adrenaline causes the breakdown to structural proteins – those found in muscle as well as bone. Thus sufficient protein is needed: to rebuild what is lost when adrenaline levels are high. However, excess protein intake triggers adrenaline secretion – which can result in insufficient rebuilding of structural proteins. One reason for this is that if protein intake is high (and carbohydrate or fat intake is low), the body will break down protein for energy use – especially in the brain. The breakdown process results in acid formation, which prompts adrenaline release to enhance the clearing of that acid from the body (and in the urine). Equally, over-exercise causes adrenaline levels to be high – which results in loss or lack of replacement of those same structural proteins. Compounding this problem is that adrenaline is a natural appetite suppressant.

Low Calorie diets and Low Blood Sugar causes the release of adrenaline to assist in the breakdown of glucose in the liver. Primarily this is to safeguard energy supply to the brain. Equally, breakdown of protein and fat will occur in order to prevent low blood sugar causing brain damage. Repeated incidences of insufficient calorie intake / low blood sugar and hypoglycaemia results in repeated adrenaline responses and spikes, as well as addictive resultant feelings of wellbeing that have potential catabolic (ie breakdown of structural proteins) effects.

Stress and stimulants also increase adrenaline – with bad stress and caffeine prolonging and enhancing the effects (bad stress leads to greater adrenalin release and caffeine prevents adrenaline breakdown)


Cortisol assists with maintaining blood sugar at levels constant enough to ensure sufficient supply to the brain. Again, like adrenaline, breakdown of structural bio-chemicals as well as protein and fat may occur to ensure this. Meanwhile, ant-inflammatory gluco-corticoids raise cortisol levels. Cortisol is also release in response to long term stress.

Stress responses are reflexes – the response is the same and automated no matter what the stimuli is. And each induces the release of Cortisol. For example, stress at work (eg tasks piling up) or personal stress causes same reflex as a life-threatening situation. The consequence is that structural bio-chemicals are used up whilst muscles are primed for sustained use (ie running or fighting). Equally, calorie controlled diets prompts the same life-threatening reflex response to famine – the shut-down of non-essential functions such as reproductive ability and the rebuilding of structural components such as hair, skin and nails. The result is that structural bio-chemicals are used up and not replaced – causing accelerated metabolic aging. Finally chemical threats from toxins prompt a stress related reflex response – to rid the body of the toxin. Alcohol likewise induces a reflex release of cortisol, and the cortisol helps to breakdown structural compounds to supply energy release inhibited by alcohol – alcohol prevents the breakdown of glycogen in the liver. The result is alcohol induced accelerated metabolic aging.

Other stress reflex responses include physiological stress, such as chronic over-exercising. Equally the loss of a hormone or its down-regulated release or function causes a stress response to compensate for that loss / release / function. The result of all these stress reflex responses is that in the short term, they are beneficial. However when they are sustained, accelerated metabolic again occurs as well as metabolic dysfunction / chronic illness.

One of the consequences of sustained high cortisol release is the breakdown of lean body tissue / muscle. Principally this occurs in the arms and legs whilst compensating adipose tissue is deposited round the waist. Equally, both cortisol and adrenalin increase the utilization of serotonin the neurotransmitter that cause feelings of calm and happiness – the result of serotonin use is that it is harder to eat well, avoid ingesting toxins, manage stress and the get the right amount of exercise. In effect, it contributes to metabolic stress.

Equally, stimulants and toxic chemicals are addictive because they cause the release of serotonin. The result is that serotonin is both used up and damage occurs to the cells that make serotonin. Furthermore, lifestyle factors such as watching television, using the internet, email, mobile phones and video games prompt the release of cortisol in order to manage and process the information and communication and effect responses to them. And demands upon us add to busy schedules, as well as the many cultural demands – such as achieving fun, pleasure, happiness and gratification. These again prompt cortisol release, as well as prompting relief through overeating carbohydrates (comfort eating), drinking alcohol (comfort drinking), excessive exercise as well as excessive use of stimulants. And the release of neurotransmitter dopamine (which result in feelings of pleasure) both rewards and reinforces behavioural patterns. The result is a feedback loop where patterns of behaviour are both hormone and neurotransmitters are released and used up. At the same time, structural and functional bio-chemicals are used up.

Physiological stress response

Nervous System Response

The hypothalamus is the centre point in the nervous system of the brain that is responsible for many drives and emotions, the limbic system of the emotional visceral brain. As such it plays a central role in many aspects of the autonomic or involuntary nervous system division of the Central Nervous system (CNS), the divisions of which are the parasympathetic (PNS) and sympathetic nervous systems (SNS).

The SNS is stimulated by being emotionally upset or physically stressed / challenged and acts on the following organs:

  • Digestive system: decreases activity and withdraws blood from the GI tract, constricts digestive system sphincters
  • Liver: releases glucose
  • Heart: increase rate and force of heartbeat
  • Lungs: dilates bronchioles
  • Urinary bladder: constricts sphincters (prevents voiding)
  • Kidneys: decreases urinary output
  • Blood vessels: constrict blood vessels in viscera and skin (dilates those in skeletal muscles and heart; increase blood pressure
  • Glands (salivary, lacrimal, gastric): inhibits; results in dry mouth and dry eyes
  • Eye (Iris): stimulates dilator muscles; dilates pupils
  • Eye (cilary muscle): inhibits; decreases bulging of lens; prepares for distant vision
  • Adrenal medulla: stimulates medulla cells to secrete epinephrine and norepinephrine
  • Sweat glands of skin: stimulates to produce perspiration
  • Hair arretor pili (erector muscles): stimulates to produce “goose bumps”
  • Penis: causes ejaculation
  • Cellular metabolism: increases metabolic rate; increases blood sugar levels; stimulates fat breakdown
  • Adipose tissue: stimulates fat breakdown

The sympathetic division generates conditions that enable the body and mind to cope rapidly and vigorously with situations that threaten homeostasis. Its function is to provide the best conditions for responding to some threat, challenge, or upset, whether the best response is to run, see better, or to think more clearly.

The effects of the SNS continue until the liver breaks down the hormones involved. Thus, although the neural effects of stress may be short lived, the hormonal effects may linger. The function of this lingering activation of the body serves to ensure the body is still best prepared should the original threat be immediately repeated.

Hormonal response

The adrenal glands stimulated by the Sympathetic Nervous System are chiefly responsible for the stress response in the body, however the hypothalamus gland also plays a role because it causes the pituitary gland to secrete hormones that travel to the adrenal glands and other glands that also play a part in the stress response within the body.

The Hypothalamus makes two hormones which it stores in the Posterior Pituitary Gland or PPG (which cannot itself produce hormones). Of these two hormones, Anti-Diuretic Hormone (ADH) plays a part in stress response

ADH’s release from the PPG causes the kidneys to absorb more water from urine, thus decreasing urine volume output and increasing blood volume. Increasing blood volume raises blood pressure, and ADH also increases blood pressure by causing vasoconstriction of the small arteries (arterioles).

In response to stress, the hypothalamus also stimulates the Anterior Pituitary Gland (APG) to release AdrenoCorticoTropic Hormone (ACTH) which stimulates release of corticosteroids Aldosterone, Cortisone and Cortisol:

Corticosteroids (more than 24) and the most important, Aldosterone, is a mineralocorticoid produced by outer layer of adrenal cortex:

  • regulates mineral content of the blood
  • regulates electrolytes (eg potassium and sodium, which regulate flow of electricity in nerves and cells)
  • release activates the kidney tubules to reabsorb sodium ions into the blood and secrete potassium ions into the urine
  • Water follows sodium and is reabsorbed into the blood, increasing blood volume and pressure and causing water retention
  • excess release and water retention / renal uptake can cause increased BV and BP, swelling, and excess potassium release
  • excess loss of potassium through urine due to aldosterone release causes problems in nerve transmission and muscle contraction
  • release is regulated by sodium potassium balance (more potassium ions in blood prompt aldosterone release
  • release also prompted by release of enzyme Renin by kidneys in response to lowering BP, converted to Angiotensin II that stimulates Aldosterone release

Glucocorticoids – produced in middle cortical layer

Cortisone and cortisol:

  • play central role in response to stress: release promotes cell metabolism and help the body resist long term stressors
  • released in response to raised levels of ACTH in blood (ACTH from pituitary gland)
  • have hyperglycaemic actions that increase blood sugar and trigger formation of glucose from fats and protein
  • increase mental cognition and alertness
  • maintains BV by regulating amount of water in cells
  • suppressive action on immune system: reduces pain and inflammation
  • blocks inflammation by decreasing edema
  • inhibit release of inflammatory prostaglandins
  • released in blood in high levels in morning (low in evening)
  • constant stress leads to constant secretion leading to depression, fatigue, insomnia, high blood sugar, loss of muscle and bone, poor wound healing, impaired immune function
  • elevated levels cortisol in blood linked to: atherosclerosis, chronic fatigue, fibromyalgia, high BP, hypoglycemia, hypothyroidism, menstrual abnormalities, obesity, osteoporosis, rapid aging, stress

The hypothalamus also has a direct neural effect on the Adrenal Medulla (AM) in response to stress and is as such an SNS stimulator of it. The AM releases catecholamine hormones Epinephrine (or adrenaline) and Norepinephrine (noradrenaline).

Catecholamines  are produced in inner / medulla layer of adrenal gland. Epinephrine (or adrenaline) and Norepinephrine (noradrenaline) deal with short-term stress responses

  • result in more oxygen and glucose in the blood and a faster circulation of blood to the body organs (most importantly the brain, muscles and heart)
  • enable the body and mind to deal with a short-term stressor though action or clear thinking.
  • Enhance and prolong the effects of neurotransmitters in response to stress
  • Increase heart rate
  • Increase blood pressure
  • Promote liver conversion of glucogen to glucose and release of glucose into the blood
  • Dilate the bronchioles
  • Change blood flow patterns, leading to increased alertness and decreased digestive and kidney activity
  • Increase metabolic rate
  • Increase mental cognition and alertness (norepinephrine)
  • provide short term alert response to danger
  • excess leads high BP, rapid heartbeat, high blood sugar levels, nervousness, insomnia, sweating
  • caffeine increases output of catecholamines and prevent their breakdown

Other major hormone secreted by the adrenal glands

Dehydroepiandrosterone (DHEA) – an androgen

  • produced by adrenals and is source molecule in conversion to sex hormones estrogen, testosterone and progesterone
  • anti-diabetogenic, anti-stress, and weight loss promoting effects
  • emotional stress increases urinary output of DHEA stress
  • Prolonged stress depresses DHEA levels and sex hormone levels (eg Pregnenolone stealing)

Physical and psychological stress impact adrenal glands

  • Prolonged stress increases output of hormones such as cortisol
  • Excess output over time can cause decrease in size and loss of function of adrenal glands, leading to total exhaustion

Adrenal stress


  • Fatigue, Depression, Sweet cravings, Low libido, Weak Immune system, Insomnia, Poor memory, Anxiety, PMS problems, Weight gain or loss, Joint and muscle pain
  • Slow to start in morning, afternoon headache, headaches with mental or physical stress, ulcers, feeling full of bloated, cravings for sweet / cigarette/ caffeine, blurred vision, unstable behaviour and emotions, irritable before meals, light headed or shaky if meals are missed or delayed, eating to relieve fatigue, cannot stay sleep or fall asleep, dizziness when moving from sitting or lying to standing, transient spells of dizziness, allergies, asthma

 Causes of stress

  • External: Toxic exposure (food, environment, air), psychological, diet, stimulants, smoking
  • Internal: gut dysbiosis, food allergies, anemia, faulty detoxification, heavy metals, blood sugar imbalances, allergies, infections; Gut infections, Food intolerances, chronic infections, autoimmune conditions

All these prompt body to release (or look for easy sources of) energy with which to deal with stress. Adrenal stimulators provide this – by increasing blood glucose

Stress, Immune Response and Hormonal interactions

  • Stress may be conscious or unconscious, past, present or future (eg trauma), emotional or psychological, external (involving environmental factors such as toxins) or internal (involving biological such as inflammatory immune responses to infections or allergies)
  • All will involve release of cortisol to manage larger, longer term stressors or adrenaline to deal with more immediate stressors.
  • Adrenal hormones influence the utilization of carbohydrates and fats and their conversion to energy in form of blood glucose
  • Adrenaline stimulate heart rhythm and activity, cause vasoconstriction and raise BP, as well as widening the bronchials (classic fight or flight readiness for action). Caffeine stimulates the release of adrenaline and furthermore prevents adrenaline breakdown by the liver, leading to prolonged adrenaline levels in blood and possible blood sugar issues and inflammation (caused by insulin surges)
  • Adrenal hormones regulate brain chemistry (noradrenalin causing alertness). Lack of cholesterol for the manufacture of adrenal hormones may lead both to physical and mental lethargy. This is a side effect of cholesterol lowering medication
  • Cortisol regulates blood sugar as well as inflammatory hormones and prostaglandins such as COX-1 and COX-2. COX-1 is needed for repair of mucosal lining of GI tract (that needs replacing every 5 days to maintain digestive function). Inhibition of COX-1 by Cortisol (and medications such as aspirin) stop necessary repair work in GI tract and elsewhere in body. Cortisol also involved in neurotransmitter turnover and metabolism, sex hormone production, immune function, weight gain and loss.
  • Cortisol prepares the body for action by encouraging cellular glucose uptake (energy), as well as diverting immune resources away from inflammatory compounds (that cause edema and pain) and immune activity (T helper cells).
  • Cortisol is made from Cholesterol. Involved is conversion of Cholesterol first into Pregnenolone and then into Progesterone or DHEA. Both of these later two are used in production of Testosterone. Progesterone is used to form Cortisol and Aldosterone. Under high, prolonged stress, the need for cortisol production may be greatest – leading to low DHEA, Testosterone and Progesterone – low sex hormone production. This explains how chronic stressors lead to loss of libido
  • Aromatase enzyme, that acts on Testosterone converting it to Estrogen, can become upregulated as a result of chronic stress, leading to Estrogen dominance and Aromatization of men. Aromatization involves blood sugar issues and storing of fat in belly and at extremes, breast enlargement. Also involved in Aromatization is mood imbalance, muscle loss, lowered sperm count, loss of libido
  • Aldosterone regulates sodium levels in the body and through this regulates water quantity in blood and BP. Sodium levels fall with low aldosterone output, leading to low blood pressure (and decreased potassium excretion – potassium needed for nerve function and muscle movement). High aldosterone, leads to sodium retention (by kidney cells) and likewise water retention in body, causing high blood pressure (and potassium loss from body). Whilst high blood pressure is needed for faster circulation (to oxygenate cells to encounter stress), the danger is that the loss of potassium involved (coupled with low potassium dietary intake) leads to neural and muscular lack of function
  • Key in understanding adrenal hormones is that the SNS plays a central role in (direct) influence of their release (as well as release via stimulation of the Hypothalamus on the Pituitary Gland). As such, the mind and the perceptual framing as well as understanding (as well as resolution) of stressors lies chiefly in the mind – as does the release of hormones that mental stimulus creates.
  • Key to understanding emotional influence on hormones is to understand that emotions run the body and physiology at the same time that body and physiology run the emotions. Thus emotional needs and addiction patterns will have corresponding and causitory physiological patterns – that can be remedied in the case of hormonal, and behavioral, as well as health disorder
  • Adrenals, in their role in blood sugar regulation, disregulate blood sugar balances that not only leads to insulin complications, but also depletion of serotonin and dopamine
  • Insulin, the hormone that regulates uptake and storage of glucose from the blood, is corrosive in blood vessels: it causes vascular inflammation. Receptor cells become desensitized due to overexposure to insulin, which leads to insulin resistance. Insulin also regulates uptake of glucose for storage – as body fat. Mineral cofactors for insulin recovery are vanadium, chromium, B Vitamins
  • Desire to eat all the time indicates blood sugar imbalances – due to a need to regulate blood sugar to get glucose (energy) to cells. Conversely a desire not to eat and loss of appetite indicates possible excess stress and cortisol / adrenalin dominance
  • Prolonged stress may cause high adrenal output and lead to high evening energy levels, alertness and productivity. If this pattern continues, evening levels of cortisol will be high and may disrupt sleep.
  • In the morning, adrenal output will be low (of cortisol) and lethargy or exhaustion, coupled with lack of appetite (stress causing digestion to be shut off leading to low appetite)
  • Early morning lethargy coupled with stress will cause adrenals to produce adrenalin to prepare system to encounter stress with sufficient energy / blood sugar (there may be a need or a habit to use stimulants such as coffee to achieve this)
  •  Energy levels may peak through stimulation from both adrenalin and rising cortisol: this will be more pronounced if no food is eaten in morning from which to source energy in form of blood sugar.
  • Energy peak, modulated by hormones causing release of energy from stores in the body (note, the body will become programmed to ensure it has sufficient stores leading to the need for body fat) will be modulated by insulin and could lead to blood sugar crash.
  • Blood sugar crash could be marked by nervous system problems as body may be orientated towards dealing with stress but lacking in sufficient nutrients to operate especially with no food inside from which to draw nutrients, or a GI tract that is not able to absorb nutrients due to SNS stimuli or gut inflammation (blood sugar delivering energy, minerals such as potassium and B-vitamins enabling nerve, muscle and brain as well as cellular function) – the result of the crash could be nervous problems (jitters, mental lack of clarity), emotional (irritability) and energy (parts of psychophysical being shutting down due to lack of available energy, such as the brain and concentration, or the body and feelings of vitality)
  • Blood sugar crash encourages reaching out for easy sources of energy (ie sugar and simple carbohydrates) as well as fat which can be stored to cushion body with energy reserves to deal with future energy crashes
  • Cortisol imbalance may be present due to prolonged stress and disrupted ability of adrenals to function or produce hormones: leading to more pronounced crashes in energy in early afternoon whereby energy levels do not recover as cortisol levels are low and unable to rise properly. The result is adrenal fatigue.

Stress and Immune function

  • Interleukin 6, a cytokine messenger released by T-cells and macrophages as well as adipose tissue, regulates inflammatory responses. It is increased in times of stress, leading to inflammatory conditions such as arthritis as well as diabetes. It also can pass the blood brain barrier.
  • Cortisol has both a direct and indirect effect on T helper cells TH1 (lowering it) and TH2 (enhancing it)over long periods of enhanced release (ie stress response). This, especially enhanced TH2 can lead to inflammation, allergies, chemical sensitivity and disrupted immunity (leading to cancer or prolonged illness – such as a cough that becomes bronchitis).
  • Cortisol has an effect on Secretory IgA, a protective secretion from B cells that is involved in protection and repair of the mucosal liming of the GI tract. Increased stress decreases IgA levels, leading to impaired GI mucosal function, namely Leaky Gut, Dysbiosis, and increased as well as impaired liver detoxification.
  • Impaired liver detoxification leads to impaired breakdown of hormones leading to excess hormones staying in the blood – leading to prolonged stress response and effects as well as deleterious health consequences – such as adrenal fatigue.

Adrenals and Thyroid Glands

Chronic Stress (CS)

  • Hypothalamus and pituitary over-stimulated and weakened leading to poor communication with thyroid gland, leading to decreased thyroid function
  • Causes increased binding of thyroid hormone proteins that mean thyroid hormones cannot bind to receptors / get into cells to do job
  • Causes conversion of T4 to inactive form of T3
  • Causes decreased cell sensitivity to thyroid hormones
  • Weakens barriers in GI tract, lungs and brain (and weakens muscosal lining repair) leading to increased permeability across those barriers leading to infection, inflammation, etc
  • Weakens immune system and leads to poor immune regulation, factors that can trigger genetic or acquired chronic health disorders (eg auto-immune thyroid  disorder Hashimoto’s)

Adrenals and Blood sugar

  • Blood sugar drops to low and does so repeatedly prompting need for cortisol release
  • CS leads to exhaustion of adrenal and thyroid glands, and exhaustion of brain centres (hypothalamus and pituitary) leading to functional hypothyroidism
  • CS weakens GI tract leading to dysbiosis, inflammation, infection that all leads to further thyroid weakening

Adrenals and Gut Inflammation, food intolerances and allergies

  • Infection and inflammation prompts stress response – pituitary prompts cortisol release to deal with / manage/ adapt to stress leading to inactive forms of T3 being produced (from T4) leading to hypothyroidism
  • Immune response to food prompts stress response that can lead to inactive forms of T3 that can further weaken gut lining

Adrenals and Progesterone

  • Chronic Stress will over-stimulate Pituitary leading to it becoming sluggish in releasing FSH (Follicle-stimulating hormone) and LH (Luteinising Hormone) resulting in poor reproductive hormone production by gonad glands (Progesterone, Estrogen, Androgens). Leads to poor reproductive system health
  • CS will over-stimulate production of Cortisol and less Progesterone production (in Cholesterol pathway). Leads to poor conversion progesterone to testosterone and decreased levels
  • Both lead to poor progesterone production and circulation – progesterone needed for TPO activity and thyroid hormone production

Adrenals and Estrogen

  • CS runs down ability of liver to break down estrogen for excretion, leading to increased levels estrogen in blood
  • Estrogen binds thyroid hormone proteins making hormones inactive in body (cannot bind / get into target cells)

Adrenals and Chronic illnesses

  • Viruses – immune response triggers cortisol release and chronic release and illness leads to adrenal and pituitary exhaustion which leads to poor thyroid function
  • Auto-immune – these both caused by and exacerbated by cortisol release, and lead to weakened thyroid
  • Pollutants – when act as chronic immune stimulator, also act as chronic adrenal stimulator leading to weakening of thyroid 


  • Stress response prompts adrenal hormone production, production leads to suppression of TPO, leading to decreased thyroid hormone production (Hypothyroidism)
  • Relaxation allows for progesterone production (instead of adrenal hormones), progesterone needed for TPO activity that is itself needed for thyroid hormone production 

Adrenal Fatigue

  • Stage 1 – involves release and recovery
    • If stressor is has a high and prolonged effect, cortisol levels will rise as will adrenaline to counter the stressor with sufficient energy upon demand (from stressor)
    • If mental and biophysical interpretation of the stressor is negated  / bracketed or reframed / relieved then body has a chance to recover resources and regroup hormonal, immunological, detoxification and nutritional requirements to ensure homeostasis
  • Stage 2 – involves overproduction of hormones
    • If previous step is not forthcoming or effective and stressor is prolonged (or multiplied with existing stressors) ability to produce DHEA and sex hormones declines – due to Pregnenolone “stealing”
    • The body becomes fatigued and cortisol levels come down to new potential output – whereby both cortisol and DHEA levels are low
  • Stage 3 – involves adrenal exhaustion
    • Low DHEA and Cortisol leading to sleep issues and mood imbalance and enhanced lack of recovery from stressor
    • Pituitary and Hypothalamus become dysfunctional, misregulating adrenals, enhancing the effects above, whilst also causing mental problems (memory and concentration issues) as well as Thyroid and sex hormone (reproductive) issues
    • Additional steps in the spiral down involve blood sugar issues and sweet cravings; nervousness; joint and muscle pain; needing stimulants; muscle pain in neck and back; low body temperature; overwhelm by small things all to to inability of hormones to function as well as adrenal atrophy (shrinkage) and auto-immune
    • Addison’s disease (dark skin) is a sign or this fatigue and the need for cortisol
    • A sufficient trigger (such as one traumatic event) can set off the steps to lead from stage 1 to 3 – with little in between.

Recovery and unwinding from adrenal fatigue – Anti-inflammatory diet and 4 R approach

  • 5 day lemon juice fast (with maple syrup)
  • take out all allergens: nightshades, nuts (can cause inflammation – soaking first helps digestion), eggs (due to albumin), dairy (due to casein), gluten
  • Anti-inflammatory foods
  • Blood sugar regulation: low GI
  • Fruit and sugar with care: these can feed intestinal yeasts
  • Protein (from fish and chicken), veggies, EFA’s
  • No grain, legumes – hard on digestion
  • No caffeine, no alcohol
  • Detoxification: liver support needed, as well as kidney support
  • Reintroduce legumes – fiber, and toxin clearing effects

Sleep, Circadian Rhythm and Hormones

Effect of sleep on the function of the adrenal glands and effects of the adrenal glands on sleep

Pineal gland secretes hormone melotonin which rise to highest levels at night and help regulate sleep cycle (using light as signal: sunlight in morning makes pineal gland shut off melatonin supply and darkness does opposite).

Pineal gland and melatonin regulate circadian rhythm – cycle of body temperature, sleep and appetite throughout day. Melatonin controls periods of sleepiness and wakefulness and plays a role in regulating mood.

Cortisol patterns are regulated by light (circadian rhythm) and control periods of wakefulness. Cortisol is  released in blood in high levels in morning (low in evening). Levels in blood rise during morning to peak at mid-day before lowering towards evening / night-time. This pattern can be shifted (by stress) causing poor regulation of hormones

  • Loss of sleep results in loss of cortisol regulation by body
  • Chronic sleep loss may set stage for poor stress response and symptoms of cortisol excess: depression, fatigue, loss of blood sugar control
  • Vicious cycle can ensue
  • High cortisol levels mean body converts less tryptophan into serotonin
  • Serotonin an important initiator of sleep
  • Serotonin also converted to melotonin
  • Insomnia and poor sleep quality associated with high cortisol levels
  • Low serotonin levels can lead to cravings for carbohydrates, depression, migraine headaches
  • Amino acid 5-hydroxytryptopan (5-HTP) can break cycle of high cortisol levels
  • Vitamin B12 in methylcobalamin form helps melatonin secretion: decreasing daytime levels leading to daytime alertness and concentration, and increasing nighttime levels leading to improved sleep quality

Herbs and foods that support healthy functioning of the adrenal glands

  • Vitamin A: adrenal and thyroid hormone manufacture and activity
  • Vitamin B3 – Niacin: manufacture of body compounds such as sex and adrenal hormones
  • Vitamin B5: as component of coenzyme A – utilization of fats and carbohydrates in energy production, manufacture of adrenal hormones and red blood cells; adrenal function (“anti-stress” vitamin)
  • Vitamin B6: maintaining hormonal balance 
  • Vitamin C: cofactor for hydroxylase enzymes in synthesis of norepinephrine
  • Zinc: critical for healthy male sex hormone and prostate function; hormone activity and receptor site function (adrenal, growth hormone, thymic hormones, insulin); hormone synthesis (adrenal hormones)
  • Magnesium: helps control sodium potassium pump in cells, thus preventing high blood pressure; plays role in enzyme ATPase which activates cellular energy metabolism, transport across membranes and vascular tone
  • Ginseng: tunes up adrenal gland and reestablishing proper cortisol levels leading to restored vitality, increased feelings of energy, boosted mental and physical performance, enhanced resistance to stress, reduced anxiety
  • Kava: treats anxiety and panic attacks that could result from excess hormones and neurotransmitters and agitation they promote, or lack of sleep that could result
    • Active compound are kavalactones, content of which should be sought out as content in natural plant can vary (3 to 20%)
    • Kava may increase the effect of prescription sleeping pills or worsen Parkinson’s disease
  • Adaptogenic herbs: substances with non-specific actions that act to promote homeostasis / have a normalizing effect through increasing resistance to adverse influences by a wide range of physical, chemical and biochemical factors
    • Rhodiola
    • Schizandra
    • Ashwaganda
    • Korean Ginseng
    • Licorice Root
    • Eleutheroccoccus
    • Astralagus
    • Rehmannia
    • Holy Basil

Nutritional support for Stress, Brain and Thyroid function

Serotonin support – for response, synthesis and activity

  • 5-HTP, St John’s Wort, SAMe, niacinamide, B6, methyl B12, Magnesium citrate

Dopamine support – methyl B12 and methylation cofactors

  • Choline, MSM, Beetroot, Betaine HCL

Hypoglycemia and Insulin support

  • Chromium, Choline, Carnitine, Vanadium, Alpha-lipoic acid, Tocopherols, Magnesium, Biotin, Inositol

Neurotransmitter balance from stress

  • To help body adapt to stress response: Panax Ginseng, Siberian Ginseng, Ashwagandha, Holy Basil Leaf, Pantethine
  • To support pituitary-thyroid axis: sage leaf, Arginine, Gamma oryzanal, Magnesium, Zinc, Manganese

Adapted from:

Schwarzbein, D.(2002). The Schwarzbein Principle II:The Transition. Deerfield Beach, Florida, Health Communications, Inc.

Marieb, E.N. (2009). The essentials of human anatomy and physiology. San Francisco, C.A.: Pearson Education

Murray, M. (2001). Total body tune-up. New York, N.Y.: Bantam Press

Murray, M. (2005).Encyclopedia of Healing Food. New York, N.Y.: Atria Books

Bland, J., Costarella, L., Levin, B., Liska, D., Lukaczer, D., Schlitz, B., Schmidt, M., Lerman, R., Quinn, S., Jones, D. (2004). Clinical Nutrition: A Functional Approach, Second Edition. Gig Harbor, WA: The Institute for Functional Medicine.

Kharrazian, D. (2009). Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal: A Revolutionary Breakthrough In Understanding Hashimoto’s Disease and Hypothyroidism. New York, N.Y.: Morgan James Publishing


  • Activates many enzymes
  • Muscle relaxation
  • Protein synthesis
  • Energy production reactions
    • Plays role in enzyme ATPase which activates cellular energy metabolism, transport across membranes and vascular tone
    • Metabolism (saturation) and synthesis of fat acids
  • Helps control sodium potassium pump in cells, thus preventing high blood pressure
  • Cardio-protective – blocks entry of calcium into cells of heart muscle and blood vessels, thus promoting efficient heart function, reducing vascular resistance and lowering blood pressure
Source and function notes
  • Best sources whole grains, nuts and green vegetables: magnesium is an important component of chlorophyll
  • Kidney’s regulate magnesium level (renal disease/disorder thus causing imbalance)
Vegetable sources Sea Kelp and Dulse; Beet greens; spinach; Swiss chard; collard leaves; sweet corn; parsley; dandelion greens; garlic, Potato with skin, Sweet Potato
Fruit sources Dried figs, Dried apricots, Dates, Avocado, Dried prunes, Raisins, Banana, Blackberry
Nut and seed sources Almonds, Cashews, Brazil nut, Peanuts, Pecan, Walnut, Coconut meat, Sunflower seeds
Absorption factors
  • Lactose and carbohydrate may increase absorption
  • Excess alcohol and caffeine increase urinary excretion
  • Supplementation – small amounts throughout day is best for absorption
    • Citrate and Glycinate most absorbable forms
Spice and herb sources
Deficiency factors
  • Weakness; muscle cramps or twitches; heart disturbances
  • Irritability, stress and mental confusion
  • Deficiency often secondary to factors that that reduce absorption or increase secretion e.g. high calcium intake, alcohol consumption, surgery, diuretic use, liver or kidney disease, oral contraceptive
Toxicity and dangers Excess can result in diarrhea and lethargy

Adapted from:

Murray, M. (2005). Encyclopedia of Healing Food. New York, N.Y.: Atria Books

Bland, J., Costarella, L., Levin, B., Liska, D., Lukaczer, D., Schlitz, B., Schmidt, M., Lerman, R., Quinn, S., Jones, D. (2004). Clinical Nutrition: A Functional Approach, Second Edition. Gig Harbor, WA: The Institute for Functional Medicine.

siberian ginseng – eleuthero


Part used Root and stem
Use 2 tsp dried root in 16oz water decoct 30 mins, steep 1 hour
  • Mild adaptogen – unlikely to cause overstimulation
  • Relieves angina, lowers blood lipids, relaxes arteries and treats stress induced hypertension
  • Strengthens immune system and regular use prevents colds and infections
  • Reverses bone marrow suppression and decreased white blood cell count in patients undergoing cancer therapy
  • Enhances athletic performance – increases endurance, enhances mitochondrial activity, speeds recovery and prevents immune suppression from excessive training
  • Good to combine with cordyceps, rhodiola and schisandra for improving alertness and cognitive function when under stress of working long hours (eg students, doctors, nurses and type A personalities who work long hours)
Dangers May cause overstimulation in sensitive people

Adapted from:

Winston, D. & Maimes, S. (2007). Adaptogens: Herbs for strength, stamina and stress releif. Rochester, VT: Healing Arts Press

stress study

Changing the interpretation of stress and the stress response to one that preserves health, allows for authentic personal expression and creates space for personal transformation

By Hugo Allen-Stevens


An event, whether it prompts a physiological stress response or not, is determined by the interpretation of that event. And that response can have damaging effects that include the diversion of biological resources for use in the stress response that leads to immune suppression. Mediating factors in this response include emotional behavior and personality types which trigger, enhance and prolong the stress response. In addition to this, prolonged or chronic stress is linked to many diseases. The central issue then becomes how it may be possible to intervene in the stress response to prevent the damaging health effects it can cause.

This paper will focus on conscious awareness, or mindfulness, that allows an individual to become aware and observe his or her behavior with regard to his or her authentic interests. Those interests include ensuring health is not damaged by the stress response. The key to this is ensuring the locus of control in response to a perceived stressor is held within the individual. And this will be explained by mindfulness training, so that automated physiological and psychological mechanisms that are beyond the individuals control in response to a stressor are trained to afford the best possible freedom and behavioral response.

Health problems and stress

Numerous writers have attested to the damaging behavioral responses to perceived stressors such as those involving aggression, emotional repression, self-pity, guilt and denial. These responses Siegel (1988)notes as having damaging effects on the health of cancer patients through the stimulating effects these emotional responses have on stress response. The danger here is that a stress response has biological superiority to the immune response, such that biological resources are diverted from the immune system during a stress response. And such a diversion promotes illness and prevents healing due to immune suppression.

The mediating factor in these behavioral responses are the emotions involved. Pert (. And from this, illness can result from immune suppression involved in the continued stress response.

Overall therefore, the diversion of biological resources and the individual’s intentions to behavior that does not serve an individual’s best interests promotes stress, causes immune suppression and can lead to illness. An example of this is the stress related illness fibromyalgia.

Rakel (2007) notes that patients with fibromyalgia often lack sufficient self-care and externalize this care by caring for others excessively. Rakel also notes how patients are highly sensitive to external stressors such as environmental toxins, a factor that indicates a weakened immune system. This indicates how biological resources are primarily used by these patients for dealing with stressors, or are weakened by the effects of stress hormones. However it is the lack of self-care that is of paramount importance, and the successful orientation of biological resources to serve a patient’s own best interests that would provide the means for healing. This is noted by Siegel (1988) who in treating patients observed that those patients who take a more proactive role in healing themselves had better recovery as well as abilities to deal with illness.

A key aspect to this healing is identifying, disabling and removing stressors that disable the immune system and the potential for healing. A further aspect is identifying and enabling behavior that orientates biological resources for use in the most effective fashion, such as healing. Meanwhile, whilst Siegel refers to the patient doctor relationship that is most healing, what is most important for a fibromyalgia patient in their healing is that they form a proactive healing relationship both with themselves and within themselves. And this has a bearing on their behavioral traits in relationships with others.

Rakel (2007) notes that caring or excessive attending to the needs of others is prevalent in fibromyalgia patients. The effect of this behavior is that it overwhelms the patient with responsibility, overwhelm that is symptomatic of stress. In this case, the stress and the symptoms of fibromyalgia can be seen as indicators that excess responsibility is being given to the caring role for others being played. It furthermore indicates a need for more self-care. Above all, symptoms and disease can be viewed as a need and opportunity for behavioral change.

Trivieri (2002) meanwhile notes that patients exhibit problems with the thalamus, such that sensory information from the body is misinterpreted. It could also mean that sensory information from outside the body is misinterpreted so that the hypothalamus is activated to trigger a stress response unnecessarily. Under these circumstances, transmission from the thalamus to the cerebral cortex could be strengthened so that sensory information is processed cognitively. Using these means, a relearning or new appraisal of sensory information (from both inside and outside the body) could occur with cognitive mediation. This will be described in more detail below by reference to mindfulness training. Beforehand, we will turn to address where habits and behavior in response to stress are automated and how they may be balanced in a manner that affords the best possible results.

Freedom and Meaning

Siegel observed miraculous healing that occurred with his cancer patients which leads him to advocate “finding your authentic self and following what you feel is your true course in life” (Siegel, p.5). Finding this authentic self and following what has most meaning is also key to successfully orientating the stress response. And finding this authentic self must first begin with a coming to awareness of who that self is.

However this awareness poses a threat to continued survival of the pre-existing and inauthentic self. Seaward (2008) notes that Freud had proposed the self censors itself from threat through the ego. The effect of this is that much of what an individual could be conscious of is filtered out by this ego and made unconscious. This corresponds to a fight or flight response seen in the stress response – an automated and largely unconscious response that serves to promote survival of the existing ego and self.

Sartre (1956) meanwhile disagreed with Freud, noting that for the ego to censor effectively, it must be aware of what it is censoring. Following this line of logic, there can be means for censorship and no unconsciousness. From this we can conclude that there are varying degrees of awareness within consciousness and that full awareness is within an individual’s capabilities. This would correspond to Buddhist theories concerning the pure state of conscious awareness, or enlightenment, that every living being possesses. Thus training in this awareness, or mindfulness training, is key to monitoring the ego that senses threat and triggers the stress response with automated and behaviorally scripted patterns that further enhance stress.

Sartre (1956) meanwhile, proposes that the individual always has an unlimited freedom to choose. This freedom relates to mediating the stress response in terms of the ability to choose perception and interpretation of sensory data. Chiefly this refers to reframing events and memories that are drawn upon with limiting and automating behavioral results in a stress response. It also refers to the ability to bring to conscious awareness, through personal choice, all factors relating to automated behavior in the stress response. Above all this freedom relates to the ability to orientate action and behavioral response towards those that serve the interests of the individual. And this mirrors Sartre’s model for authentic behavior whereby an individual embraces freedom and acts “for-itself”. Such an embodiment of freedom corresponds to placing the locus of control in a situation or event within an individual and furthermore is empowering.

In addition to this, Sartre proposes that the individual take responsibility for his or her perception of the world as if he or she were the creator of it. Such a responsibility could be empowering during a stressful event, for an individual could choose how to perceive the event. However, there is the risk that responsibility leads to feelings of overwhelm which could prompt a freezing and inability to choose, or a fleeing in panic. This fleeing and freezing can be seen in behavioral descriptions of the stress response. However, what is important to note is that the individual always has the power to choose what that response is, which could include a reframing of perception to reduce overwhelm and to an empowering point of view. And this freedom to choose perception could be used as a point of leverage by which an individual takes charge of and controls a situation so that it fully serves his or her own best interests.

Meanwhile, the responsibility that comes with freedom enables a freedom to choose the meaning. This meaning was observed by Frankl (2004) to be critical to the quality of life of an individual. And the ability to define meaning places the locus of control within an individual as they define the meaning of the event to themselves. Moreover they are able to reframe their perspective to choose a meaning that in a stressful situation allows for a response as opposed to a reaction. In other words, the meaning chosen serves the individuals best interests.

The freedom to choose the meaning of any event bears with it the responsibility for the resulting behaviors. And the effects of those behaviors are something for which the individual equally bears responsibility. This responsibility could be used so an individual realizes the part they played leading up to themselves being involved in a situation, as opposed to fighting or denying that responsibility and blaming others. Such a denial not only is disempowering due to placing the locus of control outside an individual, it also causes stress, conflict and the stagnation of a movement towards resolution of that situation.

In addition responsibility of effects of behaviors can be used by an individual so that the behaviors chosen in a situation suit his or her own best interests. For example, Siegel proposes an individual questions the meaning of an illness to them in order for a patient to find a challenge in it that “the patient has a basis for dealing with” (Siegel, p. 107). Again, the locus of control of a situation is once more brought back to an individual when they find a suitable challenge and a meaning that motivates them. And this can be used to unwind feelings of overwhelm or despair that may otherwise disable an individual during a stress response as well as in healing illness.

However, Siegel (1988) also notes how patients may be disempowered by a lack of control and a lack of ability to see where they have a choice. He also notes where patients externalize the meaning in their life, such that they become dependent upon actions they perform for others. Seaward (2008) determines that this form of co-dependent behavior has cultural roots in the way many Americans today are brought up and accustomed to living. Mate (2010) sees a similar behavioral trait of externalization prevalent in addictive personality traits, whereby the yearning for relief from suffering is seen to be possible in something outside of the individual – such as in a drug high or work achievement. In all these examples, the common element is that the locus of control is placed outside an individual. And when that point of leverage is lost, so too is the ability to orientate behavior. And what is left is a feeling of suffering and loss, feelings that not only control behavior but also cause and prolong stress.

What really is missing in these cases is the bringing to conscious awareness and control behaviors that do not serve their interests. And an individual who embraces their freedom and responsibility has more power to mediate in behaviors that trigger, promote and enhance the stress response as well as behaviors that promote illness. Key to this is placing the locus of control inside an individual, whereby freedom is associated with something internal. Through this and the ability to find a personal meaning or see where that meaning may have been misplaced, space can be created for change to occur. And that change could embrace a responsibility to act in one’s own best possible interests.

Despite this however, there still remain theories that like Freud’s theory of the ego and unconscious, the full possibility of freedom available to the individual in relation to stress is limited. And these theories hinge on the interpretation of the stress response as an automated fight or fight response.

Physiological Survival

The stress response may occur at a level that is automated and does not lie in conscious control. These automated responses to an event, and the interpretation of it, occur with no or little conscious control and in a matter of milliseconds. According to Sapolsky (2004) such an occurrence is due to inherited biological survival mechanisms whereby the individual is physiologically programmed to respond in pre-existing patterns. Under this interpretation, the stress response is interpreted as a response to a threat which is automated and functions to promote survival. The question at this point is whether such a function serves all the individual’s interests, and not merely survival. The central issue however is whether those interests can be served using the interpretation of the stress response as a survival mechanism that is automated.

Automated survival responses may occur due to learned responses whereby the hippocampus and amygdala interpret sensory data through a lens of past occurrences to determine whether an event mirrors something from the past and thus warrants the same response. And the function of the stress response in this interpretation is to survive a perceived threat by either fighting or fleeing it. However the use of the stress response as a survival mechanism in limits the use of body resources to the defense of psychological and physiological self. The question that arises at this point is whether preserving the past and the behavior associated with this self and derived from it necessarily serves the individual’s best interests in either the present or the future.

From a biological point of view, the stress response triggers the release of key hormones to enhance energy metabolism in mental and physical function. The purpose of this enhanced energy availability in stress is that it serves to make fast decisions and actions. The fact that this is fast, beyond conscious control and automated in many circumstances allows theorists such as Sapolsky to limit the understanding of this mechanism to be a fight or flight function and based on perceived threats to survival. However the enhanced energy made available can have other functions, namely to guarantee decision and action. And whilst that action may be stalled in use by a freeze response, this stalling may be viewed as resulting from conflicting interests in the individual and the inability to decide clearly and orientate action effectively. The opposite to this meanwhile is a flow response, whereby actions and decisions flow and neither fight nor flee from using both the enhanced energy and the event as an opportunity for change.

Overall, limiting an event to necessitating survival has dysfunctional qualities, as Seaward (2002) points out, as an event may be an indicator of opportunity for change.  The key point here is that limiting the use of resources to preserve the biological self in itself promotes stress and enhances it due to the lack of change it enforces. In effect, stress occurs as a result of resistance to change. From this, Seaward proposes techniques for flowing and adapting to change whereby automatic responses, which include defenses of psychological self, are interrupted to allow for this adaption. Furthermore the stress response has an added function: to flow, as well as to fight or flee.

An explanation of this flow response is that alternatives to survival and defense mechanisms could be found through searching for a different interpretation or meaning attached to an event. Moreover, that meaning can be seen as part of a flow, with the psychological and physiological aspects of an individual functioning to enable and orientate that flow. The function of this flow response can be seen as using the event as an opportunity for transforming the self or transforming the event into an opportunity that serves the individuals best interests. In addition it could ensure biological resources are used in a manner that neither suppress the immune system with excess stress response nor inhibit expression of authenticity. In effect, the flow response is an opportunity to harmonize with events in a holistic manner and not merely serve interests based purely on survival but also serve those interests higher up the hierarchy of human needs such as self-actualization.

The key to this flow response is an expansion of interpretation of the stress response and what biological resources released can be engaged in. And the key to this expansion is mindful awareness and mindfulness training. Meanwhile a flow response uses the present circumstances as a lever to allow for change through upon opening up and orientating the individual toward the future. However, through the mediatory effects of ego, neuroplasticity, emotional state and molecular bonding, the decision making abilities of an individual primarily reinforce pre-existing patterns of psychological and physiological behavior. In effect they serve to narrow of conscious function to interpreting the present events through the prism of the past. This interpretation of sensory information is, as noted above, automated and with little to no conscious control. And given the automating effects of biological resources that primarily orientate the individual toward preserving the past, the expansion of both interpretation and orientation of biological resources for a flow response therefore occurs due to prior training before the event – namely in mindfulness.

At a psychological and physiological level, this mindfulness training can be seen to be developing patterns and traits that are embedded in the body and mind. For example, neural pathways could be strengthened through repetition as could neuropeptide bonding through stimulation of specific vibrational frequencies of emotional states. In this manner, they become unconscious and automated and balance both the triggering of the stress response as well as mediating its effects. An example of this training is meanwhile given by Benson (1996) for use in connecting the individual to healing resources during illness as well as the means to mediate the stress response. And the effect of this training is that the individual has the addition of an effective “Relaxation Response” in addition to a stress response in a situation (1996). A further example is found in mindfulness training of Japanese Samurai warriors so they maintained the locus of control within themselves during life threatening situations. The overall effect is one of balance – whereby an event does not overwhelm an individual’s capabilities by through excessive involvement in a stress response. And the result of this is the potentiation of authentic expression that neither stagnates, represses nor reacts. Instead that expression can be seen as a flowing authentic response. The question then becomes how such a response, as opposed to a biological survival reaction, becomes possible.

Physiological behavior

As mentioned above, the thalamus in the brain is the primary receptor of sensory information from both inside and outside of the body. Its role is then to transmit information to both the cerebral cortex and other areas of the brain, including the limbic system and the hypothalamus. Conscious awareness arises at this point of the sensory information, and interpretation of it is made at both an emotional level and a cognitive level, mediated by the limbic system and the cortex respectively. It is at this point that the stress responses are triggered and the hypothalamus is orientated to Central Nervous System (CNS) activation of stress related fight or flight response. Cognitive decisions, made by the cortex area, are then speeded up by the hormones and energy released, and the limbic system acts to promote emotional states that enhance the drive towards the use of energy released by stress hormones in the stress response, namely action and behavioral responses such as fighting or fleeing.

At this point it is worth noting that the hypothalamus may also be stimulated by the cortex and limbic systems to Peripheral Nervous System (PNS) activation which has a calming and steadying effect on both the body and mind. The key issue then becomes how the CNS and PNS become activated automatically and the degree of freedom and control the individual has over activation of either system. Breathing and mental techniques, such as mindfulness training, can be used to mediate the triggering of the CNS system as well as mediate the level to which it is triggered and grips the individual in a stress response. However there remains an issue of the point at which those techniques may be employed with any mediatory effect and where the stress response is automated and over-rides any freedom the individual has to mediate its effects.

Sapolsky (2004) points out the role of the amygdala in automating responses beyond conscious control. He further points out how neuroplasticity occurs in both the amygdala and hippocampus whereby an event is selectively interpreted according to its correlation to a previous event (or memory) and thus eliciting the same physiological response used in that previous event. Furthermore, with each repetition, further neuroplasticity occurs and traits become embedded. The key point here is that whilst repetition of stressful interpretation and response may result from these pathways, neuroplastification may be created by selective and repeated framing of events in a perspective chosen by the individual. In other words, an individual may choose the memories, or reframe and relearn existing memories, memories that are used in determining whether an event warrants a stress response. The reframing could be performed to specifically reduce the possibility of a stress response in future events using techniques such as visualization and Neuro Linguistic Programming. And this may be reinforced via the use of emotion and drive.

Amen (1998)meanwhile points out how the limbic system acts as a filter through which events are interpreted, interpretation that both governs and is set by the emotional states in generates. An explanation for this is that the limbic system includes the memory systems of the amygdala and hippocampus. The effect of this is that the limbic system selects from memories and interprets events in the light of those memories, and those memories determine emotion. Thus whilst memories of stressful events generate a stress response and emotions, relearning or reframing memories could disable this process.

Furthermore, Amen points out the functional role of emotions in causing drive or avoidance. Emotion thus provides a structure for repeated interpretation and behavior through selective reinforcement of similar, or desirable, emotional states. These, as pointed out above, may be generated at a cognitive level, through memory reframing. And they may be reinforced through encouraging emotional states that are then attached to those memories. Furthermore those emotions would provide motivation or drive.

Pert (1997) meanwhile established that neuropeptides mediate emotional life through a mind-body network of receptors that respond to peptide ligand bonding. Pert’s work established that this bonding, and the biochemical arousal it generates includes states of feeling and emotion in both the mind and body. This she likened to a bioelectrical vibration and frequency with arousal states of feeling and emotion being generated by bioelectrical frequency. What is important to note is that this vibrational frequency is held with an individual at a cellular level. And her work also established that the bonding was influenced and determined by previous arousal states. In other words, the reactions that cause emotional and feeling states occur due a previous arousal state. The key point is that the memory and selective inducer of that state is held in cells throughout the body and mind as bioelectrical frequency.

The central issue of importance here is that an arousal state will also determine frequency and cellular function. And this arousal state may be auto-generated or induced by an individual. It may also be monitored, at a sensory level, to determine which arousal states are present in the body. From there, a training could occur to identify arousal states that are stressful and those that mediate and modulate stressful states as they occur. Such training could take the form of rituals designed to release vibrational frequencies held in cells that are holding the individual in negative, namely stress related patterns. These rituals could then allow for full release of emotions and thoughts related to these frequencies. Other techniques to change cellular frequency could include ritual chanting, dance, movement and music. What is important to note is that with each repetition of this training and mediation, at a cellular level, a memory is created that promotes future repetition of emotional and feeling states in the individual. And this training may be used by the individual to diminish the receptivity of the body to stressful arousal states.


The function of mindfulness training and mediation is one of reframing memories and forming emotional attachments to feeling states. And this is to enable an individual a choice in how to frame perception of an event that may otherwise generate a defensive stress response. In doing so neuroplasticity, emotional states, and vibrational frequency may be formed that allow for alternatives to be found to being governed by emotion or automated behavior that arises during a stress response.

Meanwhile, what is paramount in the stress response is the degree of freedom an individual possesses when stress is perceived and then manifests on a psychological and physiological level. And this freedom is paramount in determining a successful response to stress such that it serves the individual’s best interests. The question becomes what degree of choice or conscious freedom does an individual possess when a stress response becomes manifest in the body?

The answer to this question lies in the degree of sensory and conscious awareness the individual has of that response as it becoming manifest. Meanwhile the degree of conscious and sensory awareness will determine the degree of freedom the individual has to mediate in the response. The training in this conscious and sensory awareness essentially takes on the same physiological pathways in their formation that classic stress responses do – namely through memory formation. And the point of this training is that it can be activated automatically during a stress response, thus providing an alternative to a fight or flight orientated stress response. This could be done to ensure the response to the stressor, whilst being an automated physiological reaction, retains some degree of conscious freedom and existential choice.

The sensory and conscious training outlined above meanwhile depends upon the sensitivity of the thalamus to sensory information from both inside and outside of the body. As outlined in the case of fibromyalgia, this sensitivity may be damaged or impaired such that sensory information is misinterpreted. And this could occur for many other individuals. There is thus a key need to enhance the sensitivity of the thalamus and suspend awareness of sensory information there before interpretation. And this is could be the function of mindfulness training. Above all though, this training is to allow for awareness to be enhanced and authentic flowing behavioral response to be made possible.


Sapolsky, R. (2004). Why Zebras Don’t Get Ulcers. New York: Times Books.

Seaward, B. (2008). Managing Stress: Principles and Strategies for Health and Well-Being. Sudbury, MA: Jones and Bartlett. 6th Edition. ISBN 978-0763756147.

Schlitz, M., Amorok, T., & Micozzi, M.S. (2005). Consciousness and healing: Integral approaches to mind-body medicine. St. Louis, MO: Elsevier Churchill Livingstone

Siegel, B. (1988). Love, Medicine, and Miracles. New York: Harper & Row

Sartre, J-P. (1956). Being and Nothingness. New York, NY: Philosophical Library

Frankl, V.E. (2004). Man’s Search for Meaning. London, UK: Rider

Mate, G. (2010). In the Realm of Hungry Ghosts: Close Encounters with Addiction. Berkeley, CA: North Atlantic Books

Amen, D.G. (1998). Change your brain, change your life : the breakthrough program for conquering anxiety, depression, obsessiveness, anger, and impulsiveness. New York, NY: Times Books

Pert, C. (1997). Molecules of Emotion: The Science Behind Mind-Body Medicine. New York: Scribner.

Seaward, B. (2002). Stand Like Mountain, Flow Like Water. Deerfield Beach, Florida: Health Communications Inc.

Benson, H. (1996). Timeless Healing: The Power of Biology and Belief. Accord, Mass:

Rakel, D. (2007). Integrative Medicine. Philadelphia, PA: Saunders

Trivieri, L., Anderson, J., Goldberg, B. (2002). Alternative Medicine: The Definitive Guide(2ndEd). Berkeley, Ca., Celestial Arts.