Nutritional Interventions in Autoimmune Diseases

I was looking forward to this talk for quite a while now. It has been postponed twice during the last year until it was finally been set to happen today. Funnily it fell onto the same day that I embarked on a whole new journey, becoming a student of Integrative Medicine and meeting my tutors and fellow students this morning… quite an awkward feeling – sitting in a classroom again, I can tell you, and a day full of humble flash-backs, insightful visions and profound encounters with like minded people, promising to share eclectic knowledge with one another. Surely this blog will see more content sparked by the idea of a greater picture of health and healing.

Today I will stick to loading up the slides from the talk about Nutritional Interventions in Autoimmune Diseases this morning. I was invited by Dr Otto Thaning on behalf of the Organizing Committee of the Christiaan Barnard Memorial Hospital Academic Programme. Every Thursday morning healthcare professionals attend CME talks in the hospitals staff canteen with an amazing variety of quality speakers of all specialties. Please contact Otto Thaning directly to receive more information or to be put on the mailing list.

The talk focused on “Nutritional Interventions in Autoimmune Diseases (AD)”, the subject being hotly debated and fast progressions taking place. Established guidelines incorporate these findings increasingly as the topic gains prominence in disease prevention/ modification and are of interest to any healthcare professional.

The presentation includes:
– A brief overview of the prevalence and cost of AD,
– Problems with current treatment approaches,
– A short overview of the genesis of AD
– The role our environment (incl. our food) plays
– Finally a solution suggesting an oligoantigenic elimination diet
– A “Paleo Autoimmune Protocol” is proposed and some clinical practice insights are given.

Thanks very much to everybody who attended the talk. I am looking forward to receive your questions, concerns and feedback!

Please let me know should you be interested in any of the topics mentioned in this presentation or anywhere else on this blog. I am happy to speak and engage with any group and regularly speak to healthcare professionals, corporates, special interest groups and the lay public.

Leaking Brain or Leaky Gut? Part 2 – Communication Failure

Considering the evolution of memory in the most basic terms would look something like this: 
Stimuli (internal or external) –> attention/ focus –> info relay and selective processing (electro-chemical fluctuations, structural cell/ membrane, nucleus changes) –> cortex storage and/ or consolidation –> response and execution/ action. 

A system of overlap, integration and symbiosis, signal transduction being its most functional element. 

The groundwork: A failure to communicate 

To put it simply, a behaviour or cognitive process is based on a conscious or subconscious experience. The experience is encoded via learning, turning into memory. Memory enables optimal attentional focus as well as selective attention, which in turn relies heavily on reward-behaviour or expectancy/ fulfillment aptitude. Stimuli as well as attentional function (critical for memory and in turn reliant upon it) depend on physical capability, e.g. whether adequate energy requirements are met (for cell function and execution), inferring the optimal functioning of neurotransmitters and their environment or signal pathways (proteins, amino acids, hormones). 

If neither requirements are met or functional outcomes are mislead, our signaling pathways malfunction or stop and the system communication breaks down, much the same as a car without petrol. 

At the heart of signal transduction are the cellular receptors that respond to changes in the environment. Change implies stimulation: which could infer ‘over’, ‘under’, ‘nonexistent’ or adequate stimulation to achieving or obstructing optimal results for the functioning of the organism. In the case of memory formation, the Glutamate/ NMDA Receptor pathway has been implicated in many neurological (memory/ amnesia) disorders, such as stroke, dementia, epilepsy, Huntington’s, Alzheimer’s and Parkinson’s disease. 

While the etiology of various memory related diseases appears to be different in causality and outcome or regions affected, the pathophysiology is surprisingly similar. 

Overstimulation of the NMDA receptor (STRESSOR) can lead to increased nitric oxide and concomitant high levels of oxidative stress, making the overstimulation of the NMDA receptor at least partially responsible (Liska, 2006). Cell stressors (signals/ stimulants/ messengers) like that cause energy and mitochondrial dysfunction, oxidative stress and inflammation manifested by glial activation resulting in neurodegenerative diseases (Lamb, 2010). These carriers/ signals/ stimulants/ messengers are commonly understood to be amino acids, proteins, enzymes and hormones, which become potential system stressors when a failure in communication sets in. To cut a long story short, lost and overtly strong or weak signals are potentially dangerous, turning into organism stressors rather than facilitators such as an overexcited NMDA receptor. The excitotoxic NMDA pathway leading to oxidative damage is a direct stressor/ pathway dysfunction in relation to memory. 

Systemically seen however, the most directly observable stressor is often not the causative factor of disease but the final malfunction of the last working instance within a system. While the psychosomatic angle is well taken care of in conventional medicine, the somato-psychiatric side lacks attention. 

What is being treated, cause or symptomatic outcome? 

In the case of Multiple Sclerosis (MS), the axonal demyelinisation explains sclerosis and the scarring explains interrupted brain function. The immune system has started attacking parts of its own nerve cells, interrupting communication. Because the immune system being identified as the ‘terminator’, immunosuppressant drugs have been administered as controlling measures, initiating numerous side effects without proven efficacy (Embry, 2010), (Colman&Perlmutter, 2005). 
Parkinson’s Disease is characterised by a decrease in dopamine production as a result of neuronal degeneration in the dopamine-captiol, the substantia nigra. 
This ‘terminator’ has already dealt out its cards and disabled the production of dopamine. It would seem logical then to supplement dopamine, which the standard drug treatment of levodopa (L-dopa) attempts to do. L-dopa evokes a tolerance in the patient over time, so that the dosage has to increase rather rapidly, and with it do its side effects: rising homocysteine levels levels (causing oxidative stress) which in turn increase the risk for dementia, stroke and heart disease (Colman&Perlmutter, 2005). 
Alzheimer’s disease is characterised by the accumulation of a protein called beta amyloid in the brain, which, over time, increases free radical production and inflammation, killing neurons, resulting in a loss of memory, belatedly in a loss of body function control  and ultimately death. Low acetylcholine (AC) has been implicated as the Alzheimer ‘terminator’. Paradoxically, drugs administered to boost the AC levels seemingly lead to a ‘sudden worsening’ (Colman&Perlmutter, 2005). The cause-effect pathway considered does not answer the problems at hand satisfactorily. 

Since all diseases (MS, Parkinson’s, Alzheimer’s) have similar originating ‘groundwork’, contrary to the identified and ‘treatable’ ‘terminators’ mentioned above, the baseline should be re-assessed before treatment or preventative methods are attempted. 

In the case of Alzheimers, a relatively recent ‘rediscovery’ to treatment is a drug called memantine, blocking the action of the amino acid glutamate, which has been linked to free radical production in the brain (Colman&Perlmutter, 2005). The good thing is, that attention is being redirected to the critical role free radicals play in brain degeneration diseases. ‘Bad News’ is, a couple of more steps back are needed to be able to consider the broader picture of systemic inflammation and communication failure leading to cell death. 

Now for the food part. 

Looking at memory loss related diseases, one will find numerous commonalities, all of which involve a change in neurotransmitter release, glucose metabolism, blood flow, oxygenation and alterations in axonal structure and function. While all this might be attributed to a closed head-injury (neuronal damage, compromising of the cholinergic, dopaminergic, noradrenergic system, oxygen deficiency, etc) humans are quite capable of recreating similar impairments on their own, spanning over several decades if necessary.  Human life is dependent upon an intricate balance of minerals, water, organic molecules, and high energy bonds (Lamb, 2010). Being characterised by cellular organization, growth and metabolism, reproduction and heredity, it will not seem surprising that any stressors compromising the homeostasis of this dynamic balance would upset the system as a whole. The body’s response to acute or chronic stress, positive or negative, involves both the peripheral and the nervous system, extending far beyond memory implicated systems and structures, the ‘fight-flight’ response being exemplary. 

Imagine a drug that could cure a fatal disease within weeks or even days, using a small dose, non-toxic and 100% success rate. Regrettably, it does not exist and probably never will, but this is the power and potential of nutrients. 

‘They function within the genetic and evolutionary necessities of the cell to enhance and facilitate optimal biological functioning. They are vital to our very survival. Their effectiveness in curing deficiency diseases is dramatic, but their role in the prevention and management of long-latency chronic disease is increasingly relevant in daily clinical practice.’ (Hyman, Baker, Jones, 2010,pp. 56). 
Much alike the NMDA pathway scenario, neurodegenerative conditions alike suffer from oxidative stress. We are well aware of the final destructive causative factors of the disease, but what triggers the initial inflammation? The identification of the final communication meltdown culprit has not aided us much in treatment seemingly. So why not look at the necessities in overall system communication, moving away from a single-agent-single-outcome-paradigm? 
Since the status of the gut and liver has a profound effect on the functioning of the brain (Vasquez, 2010), affecting either would implicate the immune system, disrupt cellular signaling capacity by not delivering on necessary fuel or hormonal requirements and place constant stress upon the system as a whole. If the acute stress has turned into constant stress, several systems collapse, leading to cell degeneration/ death or mutation. 

‘Stress has been associated with many health conditions including cardiovascular disease, gastrointestinal disease and hormonal dysfunction’ (Tatum, 2010). 

Different stressors elicit different patterns of activation of the sympathetic, nervous and adrenomedulary hormonal systems. 
The gut has been termed the ‘second brain’ by many scientists. Not that surprising, when one considers that the GI system is the primary gateway by which the external environment interacts with the body and that the intestinal mucosa contains -+100 million neurons of which 90% conduct to the brain, whereas only 10% relay from the brain (Runow, 2011). ‘An undamaged esophagus is a potent barrier, but the selectively permeable membrane lining the GI tract from stomach to anus is critical to the homeodynamic function of the body. Even small aberrations in its function can have problematic results.’ (Sult, 2010) So let us consider the implications of a compromised GI lining. 

Leaking Brain or Leaky Gut? 

‘Not only is the gastrointestinal tract the recipient of massive amounts of ‘external information’ in the form of nutrients, toxicants, and allergens that weigh more than 700 kg per year, but the gastrointestinal tract is also a reservoir for the several hundred species and subspecies of yeast, bacteria and other microbes with the potential to modify hepatic function (e.g. detoxification) and overall health (e.g. immune response) by numerous mechanisms and with positive effects or negative consequences.’ (Liska&Lukascer, 2010, p.97). 
Compromise of mucosal integrity due to injury from antigens, infection, systemic inflammation, or toxicants (e.g. alcohol or anti-inflammatory drugs) increase the absorption of potentially harmful substances normally excluded when mucosal integrity has not been breached. 

In the case of Parkinson’s, impaired mucosal integrity would imply elevating the already Empire-State Building high toxic uptake level (one of the Parkinson triggers) even more, while disabling detoxification at the same time. 

In Feb. 2010 experiments by Dr Francisco Pan-Motojo et al at the University of Dresden established that toxins such as pesticides can reach the brain directly from the GI tract without entering the bloodstream. The animal model sets the stage for the Parkinsonian causal pathway (cited in Runow 2011).  
L-Dopa will merrily increase the toxic load if nothing is done about the GI sanitation. When rejected by the selectivity of the intestinal mucosa, materials that are harmless can serve as a source of inflammatory and immunogenic stimuli for the embedded macrophages in the liver and also for the systemic immune system and the brain’s embedded astrocytes and microglia on inappropriate absorption. (Liska&Lukascer, 2010). 
When dietary antigens like gluten cross a damaged mucosal lining (a leaky gut), thereby ‘escaping’ the liver-filtration, an inflammatory response is produced that can manifests itself clinically as a neurological disease: in this case complications and focal white matter lesions seen in the brains of patients sensitised to the dietary antigen gluten – very similar to the lesions seen in MS patients. The gut as the locus of immunogenic stimulation and neurogenic inflammation sets a better stage for disease onset and treatment than previously assumed (Runow, 2012). 

It seems that a combination of dietary antigens and molecular mimicry inducts immune dysfunction, in which instance a suppressed immune system (MS immune suppressant therapy) will render the whole system more susceptible to attack and inflammation, whilst not targeting the right invaders successfully at all (Embry, 2010). 

Alzheimer’s Amyloid Plaques are triggered by free radicals, in itself enhancing radical proliferation. Similar to the Parkinson-Gut connection, it has been established, that Beta Amyloid can quite comfortably make its way from GI to the brain without needing to cross the blood brain barrier. Similar to the prions held responsible in Creutzfeld-Jakob disease (cortical dementia) being ingested, so is the responsive pattern of the beta-amyloid plaques tested in animal models. On injection with an ‘infectious’ protein intraperitoneally (in the GI tract), the plaques were found in between neurons in the brain of rodents. (Runow, 2011). 

To resist or not to resist. 

Leaky gut has not yet assumed the status of ‘low GI’ or ‘Bipolar’ in the media, but ‘Insulin Resistance’ and Metabolic Syndrome’ certainly have. Widely unknown, insulin is one of the main instigators within the inflammatory process of the gut leading to systemic complications. When hormone signaling breaks, it is the beginning of problems ranging from cancer to accelerated aging to neurological degeneration (Wolf, 2011). 
Insulin signaling, metaphorically speaking, is rendered partly ‘inaudible’ while being ‘deafeningly loud’ on impairment. When an organism is subjected to abnormally elevated (or subminimal) levels of signals, it will down-regulate its response and vice versa. Exercise increases our ability to sense it (provided the amount of exercise is within moderation) and the hormone cortisol decreases the ability to sense insulin, resulting in a loss of hormonal sensitivity, resulting in suboptimal functioning. Insulin is essential for our energy metabolism, therefore stands in direct relation to our GI system and the mitochondrial functioning of our neurons. Loss of insulin sensitivity can lead to chronically elevated insulin levels and a whole-host of health problems. 
Cortisol decreases insulin sensitivity, causes loss of collagen in the skin and other connective tissues and lowers the rate of bone formation. It increases blood pressure and acts as an anti-inflammatory by lowering the activity of the immune system. The breakdown of muscle mass by converting protein (amino acids) into glucose is triggered by cortisol (Wolf, 2011). 

Commonly referred to as the stress-hormone, it seems logical that it would influence the energy cycle, or metabolism. 

Being crucial as an anti-inflammatory, chronic systemic stress (e.g. gut inflammation, GI mucosal permeability, antigens, prions) will trigger prolonged elevated levels of cortisol and eventually insulin-resistance. It is this loss of hormonal (and a host of hormones are part of this but not possible to include within the scope of this article) communication that leads to an inability to sense our ’I‘m full’ signal and a degradation of insulin sensitivity. 
Despite the fact that the liver is ‘drowning’ in glucose (because of overeating on account of the lacking satiety signal), it perceives the ‘lack of insulin’ as low blood sugar and cortisol is brought to the rescue; more glucose is made by cannibalising body tissues (muscles and organs). Chronically high insulin levels are directly associated with diseases such as Parkinson’s and Alzheimer’s (Wolf, 2011). 

Although Glucose is critically important for brain functioning, it is also a toxic substance. 

‘Sugars have a nasty habit of reacting with proteins in our bodies. These complexes become oxidised and form ’advanced glycation end products’ – damaging proteins, enzymes, DNA and receptor sites on the surface of our cells (Wolf, 2011).  We have now encountered the cause of a massive communication system meltdown. If our diet is too heavy in carbohydrate (especially simple sugar carbohydrates), the damage accumulates faster than it can be repaired. We exist in a state of ‘über-oxidative’ stress with detrimental effects: neurodegenerative disease being ‘only’ one of them. 


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