Perceived Sulfur Intolerance, two causes – but which one?
The issue of sulfur sensitivity has come to the fore in recent times, especially since clinicians have gained better knowledge of the methylation pathways. Even though methylation is relevant, in many cases, the more immediate issue is related to the microbiome.
If the sulfur-reducing bacteria dominate the gut, an individual may react to sulfur-containing foods or medicines. Removing sulfur-containing foods from the diet simply makes matters worse because sulfur plays many important roles in cell function and tissue repair processes. Much of what is causing confusion is the fact that there are two primary processes for addressing sulfur issues.
Sulfur is Absolutely Essential to Human Cells
Sulfur is an essential nutrient found abundantly in proteins, especially from the amino acid methionine which is also needed for synthesis of cysteine. Sulfur is found to a lesser extent in other food-derived molecules, including crucifer-derived sulforaphane (pr. Sul-4-a-FANE). Sulfur from all sources is utilised within the cells to synthesise key molecules including glutathione, taurine, homocysteine, S-adenosyl methionine, N-acetyl cysteine and glucosamine sulfate. Because these molecules are essential for normal cellular function, low sulfur status is likely to contribute to severe biochemical aberrations which readily translate to disease-causing processes. Cutting out these foods is risky!
Therefore, prolonged or medium-term avoidance of sulfur is not the way to solve problems which might appear to be caused by sulfur! Sulfur sensitivity has been traditionally associated with drugs like sulfasalazine and others – but more recently, with foods. It is not typically associated with sulforaphane. Confusing? It needn’t be – and here’s why.
Solving the Sulfur Puzzle
Even though sulfur sensitivity can be attributed to SNPs in the SUOX gene, from my experience, it is more often associated with dysbiosis and the overgrowth of H2S producers, the Sulfur-reducing Bacteria (SRB)like gram-negative Bilophila wadsworthia and Desulfovibrio spp. As with gram-negative bacteria in general, the SRB generate high levels of Endotoxin (or LPS) which promotes uncontrolled inflammation in the gut and as well as systemically. Unless dysbiosis due to these bacteria is addressed, resolution of any of the patient’s symptoms will be very difficult.
Where do I start?
The controlled introduction of sulforaphane to such dysbiotic patients almost always improves their tolerance to sulfur-containing and other foods, whether or not they carry the SUOX SNPs. Sulforaphane as a potent Nrf2 activator initially targets the gut epithelial cells where it is rapidly absorbed. By activating Nrf2, induction of several hundred cytoprotective genes occurs. Not only do these genes govern modulation of redox and inflammation processes, they also upregulate endogenous selective anti-microbial molecules of the gut.
Molecules such as the beta-defensins help to destroy ‘undesirable’ microbes without adversely affecting the commensals. Slow titration of the tolerated sulforaphane dose gradually restores gut homeostasis, correcting the dysbiosis. As homeostasis returns, the typical patient is no longer reactive to foods, including sulfur-containing foods.
What about SUOX and the Methylation Pathways?
In my opinion, too much emphasis has been placed on SUOX polymorphisms (sulfite oxidase) related to methylation without considering this in the wider context of cellular defence pathways and the microbiome.
It is easy to forget that the many variations on the popular Exclusion Diets compromise micronutrients such as molybdenum. With a diverse array of foods in the menu, molybdenum is quite easy to obtain but as soon as we exclude whole food groups like legumes and dairy (fermented), whole grains and animal meats, molybdenum deficiency can readily become an issue.
Micronutrient Inadequacies and Exclusion Diets
If dietary Molybdenum is inadequate, this can certainly compromise the SUOX enzyme, regardless of the presence of SNPs. Molybdenum is not difficult to obtain from a G.E.M.M-style whole food diet. Nevertheless, GFD which is the core prescription for G.E.M.M. patients contains 10 mcg Mo per capsule – or 40 mcg daily.
Subtle as these factors are, the patient on such a restrictive diet is already on the slippery slope to worsening health. The same principle will apply to a whole list of other micronutrients which can become readily deficient with a prolonged Exclusion Diet.
Although the recommendation to eliminate dietary sulfur may seem to be an intuitive solution for the reactive patient, a closer examination of the role of the gut microbiome reveals a more complex picture. Perhaps remarkably, sulforaphane in food-reactive patients can be used to confirm a state of dysbiosis – and then to correct it. I have seen many cases of sulfur sensitivity corrected by addressing the microbiome, regardless of whether polymorphisms exist in the various sulfur-dependent pathways.
In this way, the proportion of SRBs detected in a Gut Microbiome Analysis is typically reduced but may still be present at a lower level. The G.E.M.M. Protocol aims to achieve microbial homeostasis in accordance with the principles of Nature rather than aiming for eradication of those species which arguably play a role within the ecology of the gut.
Christine Houghton PhD.,BSc.,R.Nutr.