In search of the Primary Cause
One of the greatest challenges facing today’s clinicians lies in identifying the primary cause of the many symptoms described by the patient during the consultation. And if that is not already difficult enough, then finding the appropriate solution is equally challenging, especially when the many symptoms seem unrelated. Tempting as it is to prescribe according to the patient’s most distressing symptoms, a more comprehensive approach would aim to harness the inbuilt defences within every single cell.
Identifying the primary cause implies the need for a clinical solution that can capably target the same level of cellular dysfunction; this is where enzymes really shine. This article describes the role of key enzymes at the core of chronic disease – and then, explains how a clinician can take advantage of these inbuilt ‘powerhouses’.
How the ‘Antioxidant’ Narrative has Evolved
Human cells are enormously complex in their ability to combat the myriad stressors that confront them daily. For decades, we have considered that cells require additional antioxidants as supplements to combat such oxidative assaults; modern science shows that there are better options – options that mimic the processes of Mother Nature herself.
In a scientific breakthrough in the late 1960s, researchers discovered an enzyme present in every cell of the body and appeared to be associated with signficiant protection against free radical attack and related inflammation. Its potential was not at first appreciated but later when it was realised that Superoxide dismutase (SOD) is the ‘primary antioxidant enzyme’ of all cells, its clinical potential was embraced.
Antioxidant Enzymes as Pharmaceuticals
SOD soon became available as an injectable pharmaceutical (Orgotein®), recognised for its ability to intercept many seemingly-unrelated disease processes. Several clinical trials showed its value in inflammation-based conditions. Its application as an injectable in rheumatoid joints showed it to be superior to methylprednisolone in relieving inflammation and pain. In is oral form, it was shown to protect against radiation injury in patients irradiated for prostate and bladder cancer. Other trials demonstrated the value of SOD in chronic diseases.
But an unfortunate quirk of fate changed the course of SOD history. Because the new SOD drugs were derived from bovine serum, the arrival of so-called Mad Cow Disease in the mid-1980s called a halt to further development at that time.
The Rebirth Begins
By the late 1990s, a group of French scientists reasoned that if they could find a way to reactivate SOD activity in ageing and unhealthy cells, the damaging effects of an excessive oxidative burden could be minimised. It was already clear that an antioxidant enzyme could achieve clinical benefits not possible with a direct-acting vitamin antioxidant like ascorbate, tocopherol and others.
The advantages of an enzyme antioxidant are that one SOD enzyme can quench literally millions of superoxide species per second –
and then continue to recycle itself. Compare that with a molecule like reduced Vitamin C which can quench just a few radical species before it has been oxidised.
In healthy cells, SOD is produced continuously around the clock, increasing in response to various environmental and metabolic stresses. Age, sickness and single nucleotide polymorphisms (SNPs) can all severely reduce a cell’s ability to produce adequate SOD. For the antioxidant enzyme genes to be upregulated, the cell needs a stress signal to which it can respond by producing more antioxidant enzymes.
The goal of the French research was to produce an oral SOD supplement capable of nutrigenomically activating human cells to increase their own production of SOD – just the way Nature intended.
GliSODin® is Born
The product of their research became GliSODin®, a patented combination of a high-SOD melon extract and a biopolymer of gliadin. The gliadin serves two purposes: 1) It protects the SOD enzyme from degradation by gastric secretions and 2.) it acts as the mild stressor to activate synthesis of SOD by human cells. A series of peer-reviewed, published Proof-of-Concept studies, has confirmed that only the SOD Melon/Gliadin as the combination is capable of clinically activating synthesis of all three Antioxidant enzymes, SOD, Glutathione peroxidase (GPx) and Catalase (Cat.) In addition, GliSODin® activates synthesis of the essential anti-inflammatory cytokine, IL-10.2
The Changing Focus on Gluten
Contrary to current opinion, this unique SOD Melon/Gliadin combination does NOT impair the gut barrier; in fact, both its antioxidant and anti-inflammatory effects support the dynamic nature of the tight junctions. A growing body of research considers the tight junction as an intelligent, dynamic gateway, integral to healthy digestive function. Its dynamic nature is such that it is continuously responsive to its local environment, expanding and contracting like a spring-loaded gate as appropriate. Any factor, dietary or metabolic which creates an oxidative or inflammatory local gut environment will impair its function; gluten is just one small factor in a much more complex picture.
To put this into perspective, the 8.3 mg of gliadin per capsule of GliSODin® is roughly equivalent to the amount of gluten in a tiny breadcrumb. While even this small amount of gluten is not recommended for patients with Coeliac disease, those with gut dysbiosis or inflammation-based intestinal disorders typically improve when they take GliSODin at the recommended doses.
Important Changes in our Thinking
Only a few decades ago, we held the view that all free radicals are bad – and all antioxidants are good. It seemed logical that we should intervene with high dose antioxidant vitamins. As we have learned more about the intricate signalling chemistry of human cells, we have come to understand that the antioxidant, detoxification and other enzymes that cells make for themselves are the real drivers that maintain healthy cell function. Knowing how to activate these enzymes is the domain of the rapidly-growing science of nutrigenomics, on which GliSODin® is based.
Optimising the Effects of GliSODin®
Because GliSODin®’s nutrigenomic signalling goes well beyond the activation of SOD alone, it can influence numerous protective and anti-inflammatory pathways. Oxidative stress and uncontrolled inflammation are hallmarks of chronic disease and as such underpin a broad range of conditions for which our patients seek clinical assistance.
Such conditions extend from arthritis to asthma, autism, cardiovascular disease, type 2 diabetes, infertility, mitochondrial disorders, hormonal imbalances and psychoneurological conditions, to name just a few of the presentations that regularly present to clinicians. (Refer database www.glisodin.org)
What these conditions all have in common is cellular dysfunction at the most fundamental level, essentially a component of the primary cause of disease. The clinician’s ability to activate SOD, GPx, Catalase and IL-10 via GliSODin® provides a foundation on which to build an effective treatment plan.
 McCord JM, Fridovich I. Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein). J Biol Chem. 1969 Nov 25;244(22):6049-55.
 McIlwain H. et al. Intra-articular Orgotein in osteoarthritis of the knee: a placebo-controlled efficacy, safety, and dosage comparison. Am J Med. 1989 Sep;87(3):295-300.
 I. Vouldoukis, M. et al. “Supplementation with gliadin-combined plant superoxide dismutase extracts promotes antioxidant defenses and protects against oxidative stress,” Phytotherapy Res Mar 1;18(12) (2004) 957-962
 I. Vouldoukis. Et al. “Antioxidant and anti-inflammatory properties of a Cucumis melon extract rich in superoxide dismutase activity.” J. Ethnopharmacology. 94 (2004) 67-75 PMID: 15261965.