Sulphur-reducing Bacteria

[chrismturner89]

I have a problem with this and sulphur in general. I often get hot nasty smelling flatulence and I believe that this is one of the causes of my thyroid problems and ongoing low selenium and copper.

Does anyone know any strategies to reduce these nasty bacteria and balance them out? There is so much mainstream info on probiotics etc but I'm not sure i trust it.

High iron foods seem to make it worse. Most of my fat is saturated. I eat high carb.

 

[Amazoniac]

I remember reading something about it on Kellogg's work: gut bacteria that have specialized on protein is flexible and seem to generate more heat during fermentation, so the gas isn't cool (?), it's warm and foul. You have people with lactose problems that have one type of flatulence or the other, it appears to me that the warm and foul ones suffer more because bacteria are attacking the carbs and the protein at the same time.

You must have problems with leafy greens, but I suspect it's the amino acids, not the carbs. The only difference between methionine and selenomethionine is the sulfur being replaced with selenium (Trawizard, 2017), and this can be a good diagnostic tool: if you have flatulence from selenomethionine, it means that the issue is not sulfur, but amino acids and putrefactive bactaeria.

Probably vit K1 and saturating yourself with vit C might help. Adequate B-vitamins, perhaps with thiamine and biotin topically, maybe even pyridoxine (according to Koch). Magnesium in lower doses and if you need more, topical as well; the excess can worsen infections, including fungal. His pineapple might help, and adding some molybdenum to it not only will protect it from fermentation but will join with manganese and this is the mineral combination that tyw believed was needed to correct some methylation issues [citation not need, it's tyw].

 

[Peat Tong]

sulfur-reducing bacteria Bilophila wadsworthia:
Taurine-conjugated bile used to digest the saturated fat feeds the bacteria.

 

[chrismturner89]

Thanks guys. Really helpful posts. I will definitely reevaulate my saturated fat intake.

I feel slightly frustrated because all animal protein seems to affect me negatively and I'm unsure what to do about it because I know I need to eat enough protein. I never feel great after eating a high animal protein meal.

 

[Amazoniac]

Thanks guys. Really helpful posts. I will definitely reevaulate my saturated fat intake.

I feel slightly frustrated because all animal protein seems to affect me negatively and I'm unsure what to do about it because I know I need to eat enough protein. I never feel great after eating a high animal protein meal.

I might be wrong on this, but it seems that Tong is actually getting paid to say that. Crisco.

It's true that lab animals that are fed high amounts of long-chain saturated fats experience weird changes. Yeet! This should only occur if you're eating copious amounts of it; without enough minerals in the meal, having enough calcium for example makes it possible to form the detergent soaps (Franklin, 2012); most meals without some indigestible carbs; and all that especially in the presence of constipation.

The only useful thing to get from it is that you might be deficient in taurine because it's being degraded. I don't know if it's possible to supplement it topically and how effective it is in nourishing the liver. But it's a probable deficiency.

Vitamins A and D, magnesium and zinc are important for intestinal integrity. Finding your right balance of those vitamins can be a fix.

If none of these interventions work, there must be more options available, but sometimes you just need a boost to be able to correct the problem (Tenacity, 2018) and your diet might be even nutritious with not much having to be addressed, it's just being wasted by the constant assaults and depleting you over time.

 

[Peat Tong]

hmm, I just realized you said you eat high carb. so not a lot of whole milk? undercooked eggs?

in the meantime, taking pepto-bismol occasionally will mop up sulfur.

 

[chrismturner89]

I have done the whole milk thing but it seems to make me feel bad after a while. And no I stay away from eggs. They drop my selenium and copper too much and make my thyroid swell. Selenium brings my thyroid swelling right down.

 

[chrismturner89]

I remember reading something about it on Kellogg's work: gut bacteria that have specialized on protein is flexible and seem to generate more heat during fermentation, so the gas isn't cool (?), it's warm and foul. You have people with lactose problems that have one type of flatulence or the other, it appears to me that the warm and foul ones suffer more because bacteria are attacking the carbs and the protein at the same time.

You must have problems with leafy greens, but I suspect it's the amino acids, not the carbs. The only difference between methionine and selenomethionine is the sulfur being replaced with selenium (Trawizard, 2017), and this can be a good diagnostic tool: if you have flatulence from selenomethionine, it means that the issue is not sulfur, but amino acids and putrefactive bactaeria.

Probably vit K1 and saturating yourself with vit C might help. Adequate B-vitamins, perhaps with thiamine and biotin topically, maybe even pyridoxine (according to Koch). Magnesium in lower doses and if you need more, topical as well; the excess can worsen infections, including fungal. His pineapple might help, and adding some molybdenum to it not only will protect it from fermentation but will join with manganese and this is the mineral combination that tyw believed was needed to correct some methylation issues [citation not need, it's tyw].

So I have tested this--paying attention to when I eat animal protein and I tried the selenomethionine and, yup you're right, it is causing the hot foul gas. Regular selenium doesnt cause it. I feel like I need to change the ratio of my gut bacteria to reduce some of the putrefactive bacteria. Do you have any experience with kefir or other "good" bacteria sources?

 

[Amazoniac]

So I have tested this--paying attention to when I eat animal protein and I tried the selenomethionine and, yup you're right, it is causing the hot foul gas. Regular selenium doesnt cause it. I feel like I need to change the ratio of my gut bacteria to reduce some of the putrefactive bacteria. Do you have any experience with kefir or other "good" bacteria sources?

I doubt that probiotic foods can correct it.
Have you checked to your vitamin D status recently? Do you get enough vitamin A its cofactors?

Competition for hydrogen between sulphate-reducing bacteria and methanogenic bacteria from the human large intestine

"[..]significant populations of SRB were found only in faeces from persons who did not produce methane, suggesting that dissimilatory sulphate reduction and methanogenesis were mutually exclusive in the large gut."

"The amount of sulphate that is available in the human large intestine is unknown; it is important to identify sources of this metabolite, however. since its availability may play a key role in determining whether sulphate reduction or methanogenesis predominates in the gut. It is unclear whether any dietary sulphate reaches the colon but potential endogenous sources include the sulphated mucopolysaccharides chondroitin sulphate and mucin. Chondroitin sulphate is an acidic mucopolysaccharide that is widespread in animal tissues and is thought to be an important source of carbohydrate in the colon, due to sloughing of the epithelial cells fining the gut (Salyers & OBrien 1980). Chondroitin sulphate may also provide a source of sulphate for SRB since by weight, sulphate constitutes up to 7% of the polysaccharide (Ishioka et al. 1987). Mucins may function similarly. They are secreted into the gastrointestinal tract throughout its length and are extensively degraded by the gut microflora (Vercellotti et a/. 1977)."

"Molybdate is a specific and potent inhibitor of sulphate reduction by SRB. The addition of 20 mmol/l sodium molybdate to methanogenic faecal slurries had little effect on methane production (Fig. 2a); in the non-methanogenic slurries however, sulphide production was strongly inhibited (Fig. 2b). The inhibition of SRB resulted in the accumulation of hydrogen in large quantities in the head space gas. In the mixed slurries, inhibition of sulphate reduction enabled the methanogens to compete for hydrogen and methanogenesis predominated (Fig. 2c)."

"Competition studies with mixed faecal slurries established that SRB outcompeted MB for hydrogen. This was particularly evident when sulphate reduction was inhibited by molybdate."

"The addition of molybdate to nonmethanogenic slurries completely inhibited sulphate reduction, with the result that considerable quantities of hydrogen accumulated in the incubation bottles. These results clearly show that SRB play a major role in the colonic metabolism of hydrogen, in nonmethanogenic individuals. The inhibition of sulphate reduction in mixed faecal slurries facilitated methanogenesis and demonstrated that substances inhibitory to methanogens were not present in non-methanogenic faeces. Similarly, the activity of SRB in mixed slurries showed that methanogenic faeces did not contain inhibitors of these bacteria."

"It has been reported that nitrate represses hydrogen and methane production by human colonic bacteria (Allison & Macfarlane 1988), and this was confirmed in the present study. However, the effect of nitrate on the activities of faecal SRB has not been previously documented. Results obtained here (Fig. 5) showed that sulphate reduction was only slightly reduced in the presence of nitrate. Supression of H, production by nitrate would not significantly inhibit the activity of SRB as a range of nutritionally distinct genera are found in the colon (Gibson et al. 1988). Furthermore, some SRB can utilize nitrate as a terminal electron acceptor in lieu of sulphate (Keith & Herbert 1983). The ability to reduce nitrate is not widespread amongst SRB but species belonging to the genera Desulfobulbus (Widdel & Pfennig 1982) and Desulfooibrio (Keith & Herbert 1983) are known to carry out the process. There is growing evidence to suggest that substantial amounts of nitrate may enter the large gut from both dietary (Walker 1975; Bartholomew & Hill 1984) and endogenous sources (Archer et al. 1981). The relative insensitivity of SRB to the toxic effects of nitrate or its reduction product, nitrite, compared with MB, suggest that nitrate could potentially play a role in selecting for SRB in the large gut."

"Some species of Desulfovibrio can grow fermentatively in the absence of sulphate (Postgate 1984) and so these bacteria might be expected to be present under sulphate-limited conditions in methanogenic individuals. In this circumstance however, the Desulfovibrio spp. would not be able to compete effectively with the MB for hydrogen (Kristjansson et al. 1982). Desulfovibrio spp. are not found in methanogenic faeces, thereby indicating that in the absence of sulphate they are unable to compete with other components of the microflora for electron donors such as lactate, pyruvate, ethanol and succinate. Competition for these fermentation intermediates must be intense in the large gut because they are found only in very low concentrations (c. 1-5 mmol/l) in colonic contents (Cummings et al. 1987). These results suggest that sulphate availability is the major factor limiting the growth of SRB in the methanogenic colon."

"Fermentation of chondroitin sulphate and mucin stimulated methane formation in methanogenic faecal slurries and sulphate reduction in the non-methanogenic slurries (Table 1). Sulphide production remained low in the methanogenic slurries, however, showing that the high levels of sulphide formed in the nonmethanogenic slurries were not produced by the breakdown of sulphur-containing amino acids, but rather, resulted from the activities of SRB."​

Perhaps molybdenum-, nitrate- and sulfate-rich meals can be combined in a way that doesn't favor the growth of one or the other, while you try to address the actual cause.

 

[somuch4food]

This weekend I had horrible gas. It seemed to be better when I had more carbs with proteins.

Going low protein, low sulfur generating food and then gradually reintroduce to the amount you were eating might work.

Also, consider upping your fiber intake it would feed other types of bacteria that might be able to dominate those nasty smelly gas producing bacteria. I ate celery when I had gas this weekend and it seemed to quiet things down a bit.

 

[Amazoniac]

I ate celery when I had gas this weekend and it seemed to quiet things down a bit.

Ahaa! It should contain those nitrates (Wagner, 2018). Celery powder is even used to preserve meats, which shows how helpful it can be in combating putrefactive germs.

Heat lamps on abdomen can also be used dissociate an eventual build-up of nitric oxide (Jaminet, 2015).

 

[Nighteyes]

Ahaa! It should contain those nitrates (Wagner, 2018). Celery powder is even used to preserve meats, which shows how helpful it can be in combating putrefactive germs.

Heat lamps on abdomen can also be used dissociate an eventual build-up of nitric oxide (Jaminet, 2015).

You are definitely onto something there amazoniac. I have noticed much less smelly gas when eating lots of rucula, beets and other greens. But dysbiosis remains. No amount of probiotics has been able to anything about it. I am starting to think fecal transplant is the way to go for lasting changes in gut flora.

 

[Amazoniac]

You are definitely onto something there amazoniac. I have noticed much less smelly gas when eating lots of rucula, beets and other greens. But dysbiosis remains. No amount of probiotics has been able to anything about it. I am starting to think fecal transplant is the way to go for lasting changes in gut flora.

How far from Netherlands in Europe? This can be it. As you get closer, not only health improves, but also your bank account, house, spouse, and even the mouse on the street that happens to be cleaner and not a vector for disease.

Vitamins A and D are very effective in normalizing the intestines, the tricky part is providing the conditions needed for them to work.

I have some doubts if the topical use of fat-soluble vitamins is a route that delivers them in adequate proportions to the body: some tissues might get a lot of one, others a lot of other, so you end up with an odd ratio in tissues in spite of applying them in reasonable balance.

The best bet is to supply plenty of B-vitamins (all of them) along with fat-solubles orally. Magnesium, vit C, taurine, bicarbonate intake and attention on calcium will be needed with supplemental vit D. Its excess tends to be put to storage, but when it's used with a rice meal for example, it might be possible to antecipate the effect; hopefully the presence of niacin also reinforces this. It can be desirable to allow vit D to be released slowly, just like it happens when it's synthesized with sun exposure.

I would also focus on what warms you up (Stone, 2013) and what gives you vigorous excrementation (fast and furious).

 

[Nighteyes]

How far from Netherlands in Europe? This can be it. As you get closer, not only health improves, but also your bank account, house, spouse, and even the mouse on the street that happens to be cleaner and not a vector for disease.

Vitamins A and D are very effective in normalizing the intestines, the tricky part is providing the conditions needed for them to work.

I have some doubts if the topical use of fat-soluble vitamins is a route that delivers them in adequate proportions to the body: some tissues might get a lot of one, others a lot of other, so you end up with an odd ratio in tissues in spite of applying them in reasonable balance.

The best bet is to supply plenty of B-vitamins (all of them) along with fat-solubles orally. Magnesium, vit C, taurine, bicarbonate intake and attention on calcium will be needed with supplemental vit D. Its excess tends to be put to storage, but when it's used with a rice meal for example, it might be possible to antecipate the effect; hopefully the presence of niacin also reinforces this. It can be desirable to allow vit D to be released slowly, just like it happens when it's synthesized with sun exposure.

I would also focus on what warms you up (Stone, 2013) and what gives you vigorous excrementation (fast and furious).

Around 500 km further north yeah vit D is important no doubt. I use sardines and flounder to cover this. Feel best when I dont supplement. But gut dysbiosis is a tricky thing I Think. You have get exactly the right critters in exactly the right place and feed Them just the right stuff, oh and then make sure there isnt a hoarde of bad guys fighting to wipe them out at the same time

B vits are more tricky for me without supps. They so easily get depleted when one seeks a wee bit of stimulation

 

[Nighteyes]

Wow, triple post... well done

 

[Nighteyes]

...

 

[Amazoniac]

Around 500 km further north yeah vit D is important no doubt. I use sardines and flounder to cover this. Feel best when I dont supplement. But gut dysbiosis is a tricky thing I Think. You have get exactly the right critters in exactly the right place and feed Them just the right stuff, oh and then make sure there isnt a hoarde of bad guys fighting to wipe them out at the same time

B vits are more tricky for me without supps. They so easily get depleted when one seeks a wee bit of stimulation

How much vit D are sardines providing you (at most)? 300 IU? If so, this is too little for an effect.
I guess few people succeed in manipulating them directly.
How do you use B-vitamins?

 

[Nighteyes]

How much vit D are sardines providing you (at most)? 300 IU? If so, this is too little for an effect.
I guess few people succeed in manipulating them directly.
How do you use B-vitamins?

Yes, I suspect it is too little. However I keep trying to convinve myself it must be possible to live without supplements. Which is probably just one big lie when living this far north.. I am seriously comtemplating salmon again but hate that being a big fish they accumulate mercury.
For the B's I use the occational water extract of brewer's yeast which feels the most natural to me. Never seriously tried topical B's besides when I used energin some years ago. was too messy/impractical. Anywho, probably derailed this thread pretty thoroughly by now.

Slightly on topic: Maybe rather than focusing too much on shoving the suposedly good guys into your system one should make sure the grounds are layed for their settlement. So not too much protein, ample amounts of beneficial fiber and carbs. Then we pray they show up once they like what they see. Too hopeful (read: naive) ? I think so...

 

[somuch4food]

Slightly on topic: Maybe rather than focusing too much on shoving the suposedly good guys into your system one should make sure the grounds are layed for their settlement. So not too much protein, ample amounts of beneficial fiber and carbs. Then we pray they show up once they like what they see. Too hopeful (read: naive) ? I think so...

That's my current approach. I might be too hopeful as you said. I have found that reducing the meal frequency can help stabilize digestion. I have less bloating, still some gas from time to time. I have stopped focusing on vitamins and food as a whole. I eat a varied diet 3-4 times a day that includes meat, milk, butter, grains, tubers, fruits and some vegetables.

 

[Amazoniac]

Yes, I suspect it is too little. However I keep trying to convinve myself it must be possible to live without supplements. Which is probably just one big lie when living this far north.. I am seriously comtemplating salmon again but hate that being a big fish they accumulate mercury.
For the B's I use the occational water extract of brewer's yeast which feels the most natural to me. Never seriously tried topical B's besides when I used energin some years ago. was too messy/impractical. Anywho, probably derailed this thread pretty thoroughly by now.

Slightly on topic: Maybe rather than focusing too much on shoving the suposedly good guys into your system one should make sure the grounds are layed for their settlement. So not too much protein, ample amounts of beneficial fiber and carbs. Then we pray they show up once they like what they see. Too hopeful (read: naive) ? I think so...

I don't think it's off-topic because for the fat-solubles to work the needed ground is ample B-vitamins, and a temporary supernutrition might be needed. It can be quite difficult to get this from food, and it only takes one stimulation for the reserves to be drained (Nighteyes, 2018).

With too much but especially too little B-vitamins you have problems. Oftentimes all of them should be present for a coordinated action.

The work of High_Prob was available for free this entire time:
Cholesterogenesis To Steroidogenesis: Role Of B2 In The Biosynthesis Of D

"Flavins [] assist in the catalytic activation and degradation of other vitamins. For example, flavoenzymes affect de novo biosynthesis of ascorbic acid (2, 3), control the conversion of pyridoxine and vitamin K to their physiologically active forms (4–7), protect vitamins from oxidative degradation (8–10), and function conjointly with other vitamin-dependent enzymes, e.g., pyruvate dehydrogenase complex and respiratory chain complexes (11). Such interactions are the basis for the interdependency among vitamins and an underlying cause of secondary vitamin deficiencies. This interconnection ultimately results in the overlapping clinical signs and multiple sequelae that occur during vitamin deficiencies. In view of these interactions, the availability of riboflavin, its conversion to FMN and FAD, and their association with flavoenzymes can markedly affect the metabolism of folate, pyridoxine, vitamin K, niacin, and ascorbate."

"Riboflavin serves as the precursor for both FMN and FAD and is the functional moiety that accepts electrons. Both FMN and FAD coenzymes in association with their client flavoproteins participate in critical cellular processes that include energy and lipid metabolism, redox signaling, programmed cell death, growth regulation, xenobiotic defense responses, and regulation of biologic rhythms (15–19). These processes depend on the unique ability of the isoalloxazine moiety to react with NAD(P)H, molecular oxygen, electron-rich metabolites, and occasionally with UV light to catalyze 1- and 2-electron transfers. The heterocyclic nature of the isoalloxazine ring system coupled with its photodynamic properties enable flavin coenzymes to become potent oxidizing agents with a wide range of electron-donating substrates (20)."

"CPR [NAD(P)H-dependent 'cytochrome P450 reductase'] was the first member of the diflavin family to be isolated and the most extensively characterized. In mammals, a single CPR is responsible for the electron transport to a diverse array of P450s that are involved in the synthesis of biologically important endogenous compounds such as steroids, FAs, and prostaglandins. Thus, knockout mouse models are embryonically lethal (31)."

"Given the obligatory role of CPR as the primary electron donor for a variety of CYP enzymes, deficits in flavin availability other than those caused by dietary deficiency would also have far-reaching metabolic and developmental consequences. Riboflavin deficiencies can be caused by endocrine abnormalities such as adrenal or thyroid hormone insufficiencies, overexposure to certain tri- and tetracyclic drugs, or excessive ethanol consumption. These deficits in riboflavin would manifest with deformities similar to those occurring in patients with CPR missense variants, V492E and R457H. Such abnormalities would impair riboflavin status by blocking conversion of the vitamin to its physiologically active forms, by interfering with intestinal absorption and transport, and by enhancing renal excretion. Reviews of factors that adversely affect riboflavin metabolism have been published elsewhere (1, 35, 38)."

"With regard to cholesterol biosynthesis, flavoproteins have an obligate role within the postsqualene pathway, which is divided into the Bloch and the Kandutsch-Russell branches (44, 45). Squalene monooxygenase and DHCR24 exhibit FAD-binding domains that are the intermediate electron recipients reacting with NAD(P)H. CYP51A1, the sole P450 participant in cholesterogenesis, receives reducing equivalents directly from CPR. These reactions occur before formation of 7-dehydrocholesterol, a branch point metabolite in the cholesterol pathway which functions as the previtamin D."

"Squalene monooxygenase (EC 1.14.99.7), an FAD-dependent enzyme, is a potential regulatory site in cholesterogenesis that relies on CPR for reducing equivalents." "Squalene monooxygenase appears to play a central role in overall regulation of cholesterol biosynthesis."

"Deficits in riboflavin intake and metabolism as well as defects in flavoenzyme activity result in marked structural alterations within the skeletal and central nervous systems similar to those of disorders (inborn errors) in the biosynthetic pathways that lead to cholesterol, steroid hormone, vitamin D, and their metabolites."

"The activation of vitamin D to its major circulating form, 25(OH)D, and its hormonally active form, 1α,25(OH)2D, requires both type I and type II CYP heme proteins. The reliance on flavin-dependent heme proteins in this process supports further the association between riboflavin and vitamin D status (115)."

"As discussed previously with the cholesterogenic (type II) microsomal enzymes, vitamin D 25-hydroxylases require reducing equivalence from the FAD/FMN oxidoreductase, CPR, which is tethered to the membrane of the endoplasmic reticulum. CPR is the exclusive flavoprotein that donates electrons to all 5 of the microsomal hydroxylases, and thus mutations in CPR would be expected to present clinically with overlapping symptoms such as those observed with apparent pregnene hydroxylation deficiency, Antley-Bixler skeletal malformation syndrome, Shprintzen-Goldberg syndrome, and DHCR7 deficiency, which manifests phenotypically as Smith-Lemli-Opitz syndrome (121–126)."

"Clinical investigations that examine metabolism of micronutrients often find that deficiency symptoms of vitamins tend to be multiple. The impact of a single vitamin deficiency on the efficacy of another is best examined by using animal models where pair-feeding regiments as well as eucaloric and control diets can be maintained. Aside from rare genetic defects in riboflavin transport such as the Brown-Vialetto-Van Laere syndrome, which is characterized by progressive sensorineuropathies, paralysis, and eventual respiratory failure, isolated deficiencies of riboflavin are not widely prevalent in the general population."

"Several physical and clinical symptoms that manifest during riboflavin deficiency are not pathognomonic or exclusive to deficits in riboflavin. In this regard, only 1 study was found in the literature that addressed the impact of riboflavin deficiency directly on vitamin D metabolism (132). In this animal study, riboflavin deficiency caused a moderate decline in serum calcium as well as a decrease in the active transport of calcium through the small intestine. Measurements of 25(OH)D in the blood serum, the formation of 24,25-dihydroxyvitamin D [24,25(OH)2D] in kidney slices and the content of nuclear receptors for 1α,25(OH)2D in intestinal mucosa were significantly lower than those of control animals. Administration of vitamin D to riboflavin-deficient rats 6 d before death restored calcium homeostasis."

"The other enzymes reliant on flavoproteins and critical for vitamin D metabolism are located exclusively in mitochondria. Accordingly, CYP27A1, CYP27B1, and CYP24 thus rely on type I oxidoreductase reactions within the mitochondrial matrix."

"CYP27A1 is the only ubiquitously expressed mitochondrial enzyme that conducts a 25-hydroxylation with cholecalciferol. Thus, as a mitochondrial enzyme, its electron transfer partners are FAD-dependent adrenodoxin reductase and 2Fe-2S-adrenodoxin (133). CYP27A1 is located primarily in the liver, kidney, intestine, ovary, lung, and skin and the human CYP27A1 gene is under modest regulatory control by growth hormone, insulin-like growth factor-1, thyroid hormones, and dexamethasone (134)."

"With regard to understanding the role of riboflavin and the importance of flavoenzymes in mitochondrial vitamin D metabolism, consideration must be made of the bioavailability and delivery of riboflavin into mitochondria and the activation of the nascent apoflavoenzyme within the matrix. In this regard, CYP27A1, CYP27B1, and CYP24A1 are dependent on the reducing equivalents delivered by adrenodoxin reductase and adrenodoxin to the P450 heme complex. Thus, a coordination of protein import and cofactor supply to the mitochondrial matrix is indispensable for mitochondrial function. Although more in-depth information is required, recent studies have focused attention on the subcellular distribution of riboflavin and its coenzymic forms between the cytosolic, mitochondrial, and peroxisomal compartments (157)."

"In contrast to the multiple P450 isoforms, the FAD-dependent adrenodoxin reductase and the 2Fe-2S heme-dependent adrenodoxin exist as single isoforms and are expressed in concentrations lower than those of the CYPs. Studies in adrenal cortex mitochondria have shown that the average relative molar ratio of adrenodoxin reductase, adrenodoxin, and CYP is 1:3:8 (167). In view of this molar ratio and interaction among these components, activation of vitamin D and its subsequent degradation appear to be influenced primarily by the availability of substrate within the mitochondrial matrix and the mobile independence of the CYPs. Further analyses show that the process of electron transfer in the mitochondrial metabolism of vitamin D is most dependent on the formation of transient partner protein complexes with adrenodoxin reductase, which rely critically on the proximity of the redox domains and the availability of FAD within the mitochondrial matrix (168–171)."

"It is important to note that the mitochondrial CYP system in the presence of unbound FAD or in the presence of excess riboflavin can function as a nonproductive electron transport system and react with molecular oxygen (183). As noted previously, unscheduled electron transfer via P450s and molecular oxygen can produce superoxide and other reactive oxygen species (184). Thus, a coordination among imported proteins, coenzymes, and cofactors within the mitochondrial matrix is indispensable for “correct” CYP function. Flavins unaffiliated with their client proteins or not confined within their proper domains in the electron transport chain may force unscheduled electron shunting within the chain and result in inappropriate formation of reactive oxygen species (185). Leakage of electrons within the matrix is the major source of reactive oxygen in the mitochondria. The generation of superoxide occurs at both the matrix side of the inner mitochondrial membrane as well as the cytosolic side (186). Riboflavin transported into mitochondria requires immediate transformation to FMN and FAD by the mitochondrial flavin biosynthetic enzymes."

"A compromised reduction in activities of the flavin biosynthetic enzymes (flavokinase and FAD synthetase-1), an altered FMN:FAD ratio, or a defect in an export protein could result in accumulation of free riboflavin that may contribute to formation of excessive reactive oxygen species (187). FMN and FAD serve as coenzymes and are stabilized against photoreactivity and electron transfer while buried within their protein domains. Unlike its coenzymic derivatives, FMN and FAD, the parent compound, riboflavin, does not share the same extent of privileged binding domains and thus can interfere with scheduled electron transfers. Human motor neurons are particularly susceptible to injury if marked changes occur in components involved with mitochondria electron transfers (188). Thus, unattended riboflavin present within the inner compartments of mitochondrial membranes may short circuit the tightly controlled flow of electrons through heme transport and would be expected to interfere with vitamin D metabolism."​

@tankasnowgod

 

[Nighteyes]

Thank you for that @Amazoniac ! Interesting connection between B2 and vit D. I was not aware of that. It really seems that if you look close enough everything is somehow connected to everything else. Maybe this is true for all things... Anyway, you have inspired me to retry supping some b's beyond the occational yeast (dont like the taste anyway). I just dug out the Premier Max B-ND that I had in the back of the cabinet. Will trial it for a few weeks.

That's my current approach. I might be too hopeful as you said. I have found that reducing the meal frequency can help stabilize digestion. I have less bloating, still some gas from time to time. I have stopped focusing on vitamins and food as a whole. I eat a varied diet 3-4 times a day that includes meat, milk, butter, grains, tubers, fruits and some vegetables.

Seems like a solid diet. I can add that for me I have to be careful with stuff like brocolli, raw onions and other cruceficerious vegetables. They mess with digestion. But I do think some cooked vegetables are key to providing some safe fiber to avoid protein fermentation down there. Green beans, capsicums, turnips, butternut squash... Oh and shiitake shrooms are really great for gut health too imho. Regular white button shrooms have too much iron and toxins for me. Now that I think of it, it seems mushrooms always take care of excess gas. I just instinctively use them every day.