It’s the body’s fundamental mass detoxifier that chronically ill patients need to stay healthy and prevent disease – yet so few people with diabetes have heard of it.

Often called the master of antioxidants, glutathione (an intracellular antioxidant) is a combination of three simple building blocks of amino acids: cysteine, glycine and glutamine. All three are produced naturally in the body, and this can affect diabetes in many ways.

Increasing evidence from research on insulin resistance shows that the pathogenesis of diabetes, among other metabolic diseases, is associated with oxidative stress. And the determination of low levels of GSH, the precursor of Glutathione, is a useful tool in studying oxidative stress.

How common is glutathione deficiency?

Glutathione deficiency is found in nearly all patients who are very ill. These include people with chronic fatigue syndromeheart diseasecancerautismneurodegenerative disorders, arthritisasthmaliver disease, and more.

People with uncontrolled type 2 diabetes have particularly low levels of glutathione, which prevents the neutralisation of free radicals created as a consequence of oxidative stress.

How important is glutathione?

Glutathione’s role is to recycle antioxidants though the sulfur chemical groups it contains. Mark Hyman, the Huffington Post’s medical editor, compares sulfur to fly paper. All the bad things in the body stick onto it, including free radicals, toxins, mercury and heavy metals so that they’re escorted into the bile and out of the system efficiently.

An elevated metabolism evidenced by abnormally high levels of Reactive Oxygen Species (ROS), or free radicals, and the simultaneous decline of GSH has been shown to trigger inflammation and contribute to insulin resistance. If left unchecked, free radicals can cause DNA and tissue damage in people with type 2 diabetes.

What depletes the body of glutathione?

Deficient synthesis of GSH is often attributed to limited precursor availability. Although the body produces and regenerate its own glutathione, problems occur when we are overwhelmed with too much oxidative stress or too many toxins.

There are a variety of things that can place demands on glutathione, such as a poor diet, pollution, medications, stress, trauma, aging, infections and radiation.

Illness can also result from a combination of factors present in our immediate environment, like the exposure to different kind of toxins. Toxicology research has showed that toxins – such as Aflatoxins B1 and Ochratoxins A – associated with gram-negative bacteria called endotoxins may act synergistically with certain types of pathogenic food microfungin, known as mycotoxins and found in refined grains, to directly destroy tissues or indirectly trigger an inflammatory response.

What are the consequences for people with diabetes?

Persistent chronic low-grade inflammation is an important factor in the pathogenesis of diabetes and metabolic disorders. A common marker of inflammation in people with type 2 diabetes, according to a 2015 research article, is changes in cell count of the signalling molecules cytokines.

They are classified as Th1, Th2 and other subsets. The exact cytokine profile in metabolic disorders such as obesity and type 2 diabetes is not clear, but we know that Th1/Th2 cytokine imbalance has been reported in metabolic syndrome. Both Th1 and Th2 cells, as well as their respective mediators can induce and sustain pancreatic islet beta-cell destruction in insulin-dependent diabetes.

People with uncontrolled type 2 diabetes have particularly low levels of glutathione, which prevents the neutralisation of free radicals created as a consequence of oxidative stress.

The association of Th1 cytokines with metabolic disease via a mediator called Interferon-gamma, has been evidenced by a 2008 study on adaptive immunity in obesity. Moreover, the overexpression of a key mediator in the development of Th2 cytokines cell response, in human muscle tissue, called TNF-alpha, has been found to contribute to insulin resistance.

There are many other hormonal changes that come about when cytokines are released. Cortisol levels may rise, for example, while recent endocrine studies suggest that elevated plasma cortisol is associated with complications and metabolic control of type 2 diabetes, particularly ischemic heart disease and raised fasting glucose risk factors.

The action pathways on how mycotoxins amplify the inflammatory response and affect parameters influencing diabetes on its own remain unclear, however, and many dismiss the mycoalkonics approach as pseudoscience.

Is the toxicity of mycotoxins being overlooked?

A 1999 WHO bulletin about mycotoxins said “Involvement of mycotoxins in disease causation should be considered in instances when a disease appears in several persons, with no obvious connection to a known etiological agent, such as microorganisms. Strict control of food and feed and appropriate public health measures are of considerable importance in reducing risks to human and animal health.”

Regulations specifying the maximum allowed concentration of mycotoxins exist, but none require measures to reduce contamination. In 2013 though, the Journal of Chemical Research in Toxicology indicated that government limits on mold toxins that present naturally in grain crops should be expanded to include so-called “masked mycotoxins” that change from harmless to potentially harmful forms in the body.

If mycotoxins really play a role in the diabetes epidemic, avoiding them might be a good idea. But in reality, it is a near-impossible mission to escape contact with mycotoxins. These are toxic chemicals produced by fungi that colonise crops. When grains are stored in today’s farming environment in large silos and kept for a long time before being processed, it creates mold growth and these chemical back mycotoxins.

A more comprehensive analysis of data dealing with epidemiological and toxicity effects in humans, looking specifically at actionable dietary habits for mycotoxin reduction and the maintenance of normal levels of glutathione, ought to be initiated.

But are public policy and preventative campaigns against these mycotoxins epidemics doing enough to inform the public about these substances, described in numbers of epidemiological studies as extremely potent hepatotoxic agents?

The short answer is not really, but in their defence, there’s still scientific ambiguity that needs to be resolved before we put public policy at the forefront. There is a huge tendency to want policy solutions before the science is clear, and that is a mistake.

General Food and Drug Administration (FDA) requirements regarding adulteration (e.g. 21 U.S.C. Sec 402(a)) stipulate that “A food shall be deemed to be adulterated if it bears or contains any poisonous or deleterious substance which may render it injurious to health”.

Under existing law, the agency is charged with the responsibility of ensuring that said food products do not result in acute injuries, but not with the prevention of chronic diseases.

In other words, the agency will only regulate an acute toxi, not a chronic toxin. Aflatoxins, for example, are chronic toxins. The liver metabolise them and doesn’t get sick after one contaminated meal. It gets sick after a thousand contaminated meals, and that is how many we eat, based on our addiction to cereal grains that have a longer shelf life and are susceptible to mycotoxin exposure.

How can glutathione levels be optimised and mycotoxins exposure reduced?

Animal studies suggest that in the context of a diet reducing or eliminating refined sugars and high glycemic foods – which also cause fungus to persist – the addition of antioxidants to the diet may assist in dealing with the toxic effects of mycotoxins. Among other antioxidants reviewed, the journal Cancer Letters recommends turmeric and curcumin for their ability to inhibit the aflatoxin production considerably (more than 90%) at concentrations of 5-10 mg/ml.

We should, however, put a pause on public policy. Instead of the government telling people to eat this versus that, rigorous research ought to be initiated in the field of nutritional science as well as a more comprehensive analysis of data dealing with epidemiological and toxicity effects in humans, looking specifically at actionable dietary habits for mycotoxin reduction and the maintenance of normal levels of glutathione.

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