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Will a low sulfur diet reduce hydrogen sulfide production?

Hip

Senior Member
Messages
17,824
In another thread, Richvank posted:

There are two categories of bacteria that can produce hydrogen sulfide in the gut. There are the SULFATE-reducing bacteria, which convert sulfate to sulfide, and there are others that ferment sulfur-containing amino acids from the diet to form hydrogen sulfide.

I am just wondering whether these bacteria that ferment sulfur-containing amino acids are one and the same as SULFUR-reducing bacteria (bacteria that reduce elemental sulfur to hydrogen sulfide), and if they are a source of hydrogen sulfide in ME/CFS patients.

Furthermore, if SULFUR-reducing bacteria (as opposed to SULFATE-reducing bacteria) are involved in making hydrogen sulfide in some ME/CFS patients, might a low sulfur diet be the answer for these patients, as a means to limit the hydrogen sulfide production?

A low sulfur diet essentially involves avoiding cruciferous vegetables (cauliflower, cabbage, cress, broccoli and similar green leaf vegetables), all dairy, eggs, onions, peas, which are all high in sulfur (thiols), so the low sulfur diet is relatively easy to follow.

A full list of foods that are high in sulfur (thiols) is given here:

http://livingnetwork.co.za/chelationnetwork/food/high-sulfur-sulphur-food-list/

Could such a low sulfur diet help treat ME/CFS, by reducing hydrogen sulfide levels ??




I came out as a strong positive on de Meirleir's hydrogen sulfide urine test (the neurotoxic metabolite test).

Now, from my Genova Diagnostics Digestive Stool Test, I know have the bacterium Proteus mirabilis in my gut, and I believe I also have Proteus mirabilis as a chronic recurrent kidney infection that I can never get rid of. (The other bacteria in my gut are: alpha hemolytic Streptococcus, gamma hemolytic Streptococcus, Staphylococcus aureus, hemolytic Escherichia coli)

Anyway, since Proteus mirabilis is a SULFUR-reducing bacteria (along with Campylobacter, Pseudomonas and Salmonella), could Proteus mirabilis be making hydrogen sulfide from the sulfurs in my diet, either in my gut or in my kidneys, where this Proteus mirabilis resides?

Anyone familiar enough with the chemistry to answer this question?
 

Hip

Senior Member
Messages
17,824
I just found this webpage on sulfur-reducing bacteria that says:

Molybdate and selenate interfere with sulfur-reducing metabolism, and are used to inhibit the bacteria in non-medical applications. I've found these two supplements containing those compounds; I wonder if they would help....?

Life Link's Sodium Selenate 200 mcg 100Caps
Allergy Research Group Liquid Molybdenum

The author, however, may be confusing SULFUR-reducing bacteria and SULFATE-reducing bacteria.
 

Hip

Senior Member
Messages
17,824

ramakentesh

Senior Member
Messages
534
This is an interesting area, although I am not yet convinced that elevations in hydrogen sulfide are automatically derived from the gut. Being a vasodilator molecule that works in a careful balance with nitric oxide I dont think would take much for a pathological condition to arise where its endothelial or neuronal expression is moved out balance. When you consider the large evidence that changes in nitric oxide bioavailability can cause or exaccerbate many cardiovascular pathologies and that these are now accept etiological mechanisms, I cant see why genetic abnormalities or perhaps chronic inflammation could result in altered hydrogen sulfide expression specific to the vascular endothelium.

Many of the tests being used to detect hydrogen sulfide in CFS patients are speculative and have issues - particular the breath tests.

But in answer to your question it would be certainly worth trying as I would personally find it easier to believe that excess expression of this molecule could be effected by dietary bioavailability than that it can be effected by manipulating the bacteria in the stomach that are suggested as its source.
 

richvank

Senior Member
Messages
2,732
Hi, Hip.

I would be concerned that a diet low in sulfur-containing amino acids (methionine, cysteine and taurine) would make things worse for PWMEs, because their sulfur metabolisms are already depleted in many cases. Many already have low methionine. The methylation cycle is at the beginning of the sulfur metabolism, and glutathione is an important member of it. I think that it would be better to keep the sulfur amino acids coming in, but to make sure that the gut issues are dealt with so that dysbiotic bacteria in the gut do not divert the sulfur-containing species to the production of excess hydrogen sulfide.

As far as I know, the normal human metabolism does not utilize elemental sulfur. I would also not expect that there would be much elemental sulfur in the normal diet, though some crops, such as grapes, are dusted with elemental sulfur to keep down mildew in the vineyards, so there may be some residual elemental sulfur on table grapes.

Best regards,

Rich
 

hixxy

Senior Member
Messages
1,229
Location
Australia
What I would like to know is why these bacteria produce hydrogen in some people, but hydrogen sulfide in others. Under what conditions does this change happen?! Or am I completely missunderstanding the H2S producing bacteria issue?

hixxy
 

Dufresne

almost there...
Messages
1,039
Location
Laurentians, Quebec
I've not tried to sort out sulfate from sulfide reducing bacteria or from H2S producers. Too tedious for me, but I can offer a few observations from my experience.

When I eat carbs I end up expelling a lot of gas that has that unmistakeable H2S smell -rotten eggs. So sugar feeds H2S producers, I think that much is known.

MSM makes my ankylosing spondylitis flare up something awful. It's thought by some that A.S. is caused by a sensitization to klebsiella, which corresponds to the exacerbation with sugar intake, but the MSM flare is just as interesting. Is MSM feeding the same bacteria or is it feeding another resulting in leaking gut. Could sulfur-fed bacteria be seriously increasing intestinal permeability? If that's the case I think one would be better off going after the dysbiosis than trying to starve the bugs -I think the patient would be the one to lose. Though using bismuth with appropriate antibiotics, or directly starving bugs while using ABX might be a good short-term strategy.
 

end

Messages
263
Dufresne funny you mention that, as I have documented IP with a strongly positive H2S test. I feel from years of trial and error that dysbiosis must be corrected to lower H2S production. And more interestingly some dysbiosis can not be cultured read through Dr Usman's protocols for GI Biofilm infections/treatment. Organic Acid testing is an indicator of this type of dysbiosis.
 
Messages
3
I come from a long line of German women with gut, migraine, thyroid, and gallbladder issues. My grandma also claims to be highly sensitive to mercury. I had colic as a baby, headaches beginning in elementary school, migraines beginning at age 13, horrible sulfur-smelling gas beginning in my teens, toxic shock syndrome at 16 (despite being super responsible with tampons), diagnosed with IBS-C in college, multiple UTIs, one vaginal yeast infection, and diagnosed with SIBO (high levels of hydrogen) February of this year via a lactulose breath test. There is no breath test for determining the presence of hydrogen sulfide in the small intestine, but I really think that's what I have due to the absolutely foul smell of my gas. I also suspect that I have been suffering from CFS as of May when I had a sudden onset of brain fog/muscle weakness/fatigue that has gotten somewhat worse since then. A nutrient IV restored much of my energy initially, but subsequent IVs were not as helpful.

I have taken two rounds of Rifaxamin, Resolor prokinetic, Neem herbal antibiotic, and Allimed herbal antibiotic. Rifaxamin helped facilitate bowel movements while I was taking it, but my SIBO relapsed as soon as I stopped. Neem herbal antibiotic in high doses seems to help, but I do not know why. Natural Calm Magnesium helps me have the urge to go. Resolor prokinetic helps the stool be well-formed. My comprehensive stool test did not show any parasites or candida, but I am still suspicious due to fructose malabsorption/inability to handle any fruit. I also have leaky gut and react to nightshades, all grains, eggs, dairy, gluten, soy, legumes, and the list goes on and on.

I have been following an extremely low carb, low FODMAP Autoimmune Paleo diet for 4 months and it helped calm my digestive systems immensely. However, my T4 thyroid hormone was not converting to T3 properly and I was probably experiencing euthyroid sick syndrome. I have increased my carb intake to about 60 grams per day via coconut water, 10 raspberries, carrots, zucchini, coconut flakes, and a couple other things that don't seem to make me itch. My digestion does not like this increased carb intake, but my brain functions better and I have a little more energy.

I am now planning to try a low sulfur, low carb, low FODMAP, AIP diet for the next 10 days per my NDs recommendation. Something that is very interesting is that when I did IGG/IGA allergy testing last year, many of my allergies were high sulfur foods: sesame seeds, eggs, green beans, kidney beans, and coffee. Other allergies included blueberries and cranberries. Anyone have any insights on this?

I will report back how the low sulfur diet goes for me.
 

jepps

Senior Member
Messages
519
Location
Austria
This study says, that SRBs are involved in the development of IBS and Ulcerative Colitis:

http://pubs.sciepub.com/ajidm/2/3/5/

The increased number of sulfate-reducing bacteria and intense process of dissimilatory sulfate reduction in the gut can cause inflammatory bowel diseases of humans and animals[8,12,15,16]. These bacteria are often found in persons with rheumatic diseases, and with ankylosing spondylitis, etc.[1,18,19]. There is also an assumption that sulfate-reducing bacteria can cause some forms of cancer of the rectum through the formation of hydrogen sulfide[14,15,20], which affects the metabolism of intestinal cells and give rise to various inflammatory bowel diseases[

Microbiological analysis of the intestinal microflora of the rats during the twenty-five days was carried out. The samples were selected from each group of animals on the fifth, tenth, fifteenth, twentieth, and twenty-fifth day (Figure 1). The results of these studies showed that microflora of the first group of the animals (control) receiving the standard diet during twenty-five days was almost unchanged.
Addition a dose of the modified Kravtsov-Sorokin's liquid medium which contained sulfate ions (1 ml per each day) in the standard animal diet (second group) and the dose of a suspension withD.pigerVib-7 andDesulfomicrobiumsp. Rod-9 (at a ratio of 1 to 1) in the medium (third group), the changes in the microflora were already observed on the fifth day of the experiment. In this case, the injection of the medium to animal gastrointestinal tract caused a reduction in the number ofLactobacillus(20%),Peptococcus(14%),Candida(21%), and an increase in the number ofE. coli(lactose-negative) (70%),Proteus(13%),KlebsiellaandStaphylococcus(28%), and the sulfate-reducing bacteria (86%) in the second animal group on the fifth day. The injection of the dose of the suspension with the strains of sulfate-reducing bacteria to the tract led to the reduction in the number ofLactobacillus(30%),Peptococcus(22%),Candida(25%), and the increase in the number ofClostridium(40%),E. coli(lactose-negative) (78%),Proteus(26%),Klebsiella(36%) andStaphylococcus(30%), and the sulfate-reducing bacteria (92%) in third animal group on the fifth day of the detection compared to the control.
As this study shows, the qualitative and quantitative changes in the intestinal microflora depended on the time of the introduction of the dose of the sulfate containing medium or bacterial suspension. Each additional dose of the medium or the suspension caused significant violation of the bowel microbiocenosis in the rats on the 10th, 15th, 20th, 25thday of detection.
The greatest qualitative and quantitative changes in the microflora in the second and third animal groups were observed on the 25thday.
the injection of the sulfate containing medium or suspension with the sulfate-reducing bacteria in the gastrointestinal tract of the rats leads to a change in the qualitative and quantitative composition of the normal intestinal microflora (dysbiosis), which may be the result of the development of the inflammatory bowel disease, ulcerative colitis, and various pathological processes.
 
Messages
1
I come from a long line of German women with gut, migraine, thyroid, and gallbladder issues. My grandma also claims to be highly sensitive to mercury. I had colic as a baby, headaches beginning in elementary school, migraines beginning at age 13, horrible sulfur-smelling gas beginning in my teens, toxic shock syndrome at 16 (despite being super responsible with tampons), diagnosed with IBS-C in college, multiple UTIs, one vaginal yeast infection, and diagnosed with SIBO (high levels of hydrogen) February of this year via a lactulose breath test. There is no breath test for determining the presence of hydrogen sulfide in the small intestine, but I really think that's what I have due to the absolutely foul smell of my gas. I also suspect that I have been suffering from CFS as of May when I had a sudden onset of brain fog/muscle weakness/fatigue that has gotten somewhat worse since then. A nutrient IV restored much of my energy initially, but subsequent IVs were not as helpful.

I have taken two rounds of Rifaxamin, Resolor prokinetic, Neem herbal antibiotic, and Allimed herbal antibiotic. Rifaxamin helped facilitate bowel movements while I was taking it, but my SIBO relapsed as soon as I stopped. Neem herbal antibiotic in high doses seems to help, but I do not know why. Natural Calm Magnesium helps me have the urge to go. Resolor prokinetic helps the stool be well-formed. My comprehensive stool test did not show any parasites or candida, but I am still suspicious due to fructose malabsorption/inability to handle any fruit. I also have leaky gut and react to nightshades, all grains, eggs, dairy, gluten, soy, legumes, and the list goes on and on.

I have been following an extremely low carb, low FODMAP Autoimmune Paleo diet for 4 months and it helped calm my digestive systems immensely. However, my T4 thyroid hormone was not converting to T3 properly and I was probably experiencing euthyroid sick syndrome. I have increased my carb intake to about 60 grams per day via coconut water, 10 raspberries, carrots, zucchini, coconut flakes, and a couple other things that don't seem to make me itch. My digestion does not like this increased carb intake, but my brain functions better and I have a little more energy.

I am now planning to try a low sulfur, low carb, low FODMAP, AIP diet for the next 10 days per my NDs recommendation. Something that is very interesting is that when I did IGG/IGA allergy testing last year, many of my allergies were high sulfur foods: sesame seeds, eggs, green beans, kidney beans, and coffee. Other allergies included blueberries and cranberries. Anyone have any insights on this?

I will report back how the low sulfur diet goes for me.

Any update on how your progress went?
 
Messages
1
I am not a microbiologist, but my limited understanding is that the sulfur reducing bacteria use the sulfur atom in place of the oxygen atom under anaerobic conditions to burn food. I had heard of this process happening in bacteria in the depths of oceanic trenches, and it was interesting to find out that it actually occurs in our guts, and that a large percentage of the healthy population harbors various strains of these sulfur reducing bacteria.

I am assuming that instead of H2O, or water, they produce H2S,the hydrogen sulfide gas, which can regulate mitochondrial function in a dualistic manner. In miniscule low concentrations, hydrogen sulfide has regulatory effects, and in high concentrations, it inhibits mitochondrial respiration. Please see below.

Higher doses are very toxic, and in the course of our planet's evolution, large amounts of hydrogen sulfide gas released from the ancient oceans have lead to mass extinctions... This is just to realize how toxic this gas can be in larger volumes. So it may be the type of the sulfur reducing bacteria, how much hydrogen sulfide is produced by each strain, individual diet (please see below), and individual genetics (i.e. mitochondrial function, and capacity to get rid of the intestinal hydrogen sulfide produced by the bacteria) that determine when the intestinal colonization by these bacteria can lead to chronic fatigue.

http://www.ncbi.nlm.nih.gov/pubmed/23991749
Regulation of mitochondrial bioenergetic function by hydrogen sulfide. Part II. Pathophysiological and therapeutic aspects

Abstract
Emerging work demonstrates the dual regulation of mitochondrial function by hydrogen sulfide (H2S), including, at lower concentrations, a stimulatory effect as an electron donor, and, at higher concentrations, an inhibitory effect on cytochrome C oxidase. In the current article, we overview the pathophysiological and therapeutic aspects of these processes. During cellular hypoxia/acidosis, the inhibitory effect of H2S on complex IV is enhanced, which may shift the balance of H2S from protective to deleterious. Several pathophysiological conditions are associated with an overproduction of H2S (e.g. sepsis), while in other disease states H2S levels and H2S bioavailability are reduced and its therapeutic replacement is warranted (e.g. diabetic vascular complications). Moreover, recent studies demonstrate that colorectal cancer cells up-regulate the H2S-producing enzyme cystathionine β-synthase (CBS), and utilize its product, H2S, as a metabolic fuel and tumour-cell survival factor; pharmacological CBS inhibition or genetic CBS silencing suppresses cancer cell bioenergetics and suppresses cell proliferation and cell chemotaxis. In the last chapter of the current article, we overview the field of H2S-induced therapeutic ‘suspended animation’, a concept in which a temporary pharmacological reduction in cell metabolism is achieved, producing a decreased oxygen demand for the experimental therapy of critical illness and/or organ transplantation.

http://www.ncbi.nlm.nih.gov/pubmed/23898195
Metabolic niche of a prominent sulfate-reducing human gut bacterium
Abstract

Sulfate-reducing bacteria (SRB) colonize the guts of ∼50% of humans. We used genome-wide transposon mutagenesis and insertion-site sequencing, RNA-Seq, plus mass spectrometry to characterize genetic and environmental factors that impact the niche of Desulfovibrio piger, the most common SRB in a surveyed cohort of healthy US adults. Gnotobiotic mice were colonized with an assemblage of sequenced human gut bacterial species with or without D. piger and fed diets with different levels and types of carbohydrates and sulfur sources. Diet was a major determinant of functions expressed by this artificial nine-member community and of the genes that impact D. piger fitness; the latter includes high- and low-affinity systems for using ammonia, a limiting resource for D. piger in mice consuming a polysaccharide-rich diet. Although genes involved in hydrogen consumption and sulfate reduction are necessary for its colonization, varying dietary-free sulfate levels did not significantly alter levels of D. piger, which can obtain sulfate from the host in part via cross-feeding mediated by Bacteroides-encoded sulfatases. Chondroitin sulfate, a common dietary supplement, increased D. piger and H2S levels without compromising gut barrier integrity. A chondroitin sulfate-supplemented diet together with D. piger impacted the assemblage’s substrate utilization preferences, allowing consumption of more reduced carbon sources and increasing the abundance of the H2-producing Actinobacterium, Collinsella aerofaciens. Our findings provide genetic and metabolic details of how this H2-consuming SRB shapes the responses of a microbiota to diet ingredients and a framework for examining how individuals lacking D. piger differ from those who harbor it.
_______________
There is some literature indicating how a combination of cipro or flagyl along with a type of bismuth (maybe peptobismol will work?) can get rid of at least some strains of these sulfur reducing bacteria. I see some have pointed to lemon grass, but I have not had a chance to find scientific data on that.
We need studies. In the meantime, I imagine a low sulfur diet should help; and would speak with my physician to see if a trial of such a combination regimen with Bismuth and flagyl/cipro may be considered.

In another thread, Richvank posted:

I am just wondering whether these bacteria that ferment sulfur-containing amino acids are one and the same as SULFUR-reducing bacteria (bacteria that reduce elemental sulfur to hydrogen sulfide), and if they are a source of hydrogen sulfide in ME/CFS patients.

Furthermore, if SULFUR-reducing bacteria (as opposed to SULFATE-reducing bacteria) are involved in making hydrogen sulfide in some ME/CFS patients, might a low sulfur diet be the answer for these patients, as a means to limit the hydrogen sulfide production?

A low sulfur diet essentially involves avoiding cruciferous vegetables (cauliflower, cabbage, cress, broccoli and similar green leaf vegetables), all dairy, eggs, onions, peas, which are all high in sulfur (thiols), so the low sulfur diet is relatively easy to follow.

A full list of foods that are high in sulfur (thiols) is given here:

http://livingnetwork.co.za/chelationnetwork/food/high-sulfur-sulphur-food-list/

Could such a low sulfur diet help treat ME/CFS, by reducing hydrogen sulfide levels ??

I came out as a strong positive on de Meirleir's hydrogen sulfide urine test (the neurotoxic metabolite test).

Now, from my Genova Diagnostics Digestive Stool Test, I know have the bacterium Proteus mirabilis in my gut, and I believe I also have Proteus mirabilis as a chronic recurrent kidney infection that I can never get rid of. (The other bacteria in my gut are: alpha hemolytic Streptococcus, gamma hemolytic Streptococcus, Staphylococcus aureus, hemolytic Escherichia coli)

Anyway, since Proteus mirabilis is a SULFUR-reducing bacteria (along with Campylobacter, Pseudomonas and Salmonella), could Proteus mirabilis be making hydrogen sulfide from the sulfurs in my diet, either in my gut or in my kidneys, where this Proteus mirabilis resides?

Anyone familiar enough with the chemistry to answer this question?
 
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