OCTN2 is upregulated by intermittent fasting, exercise, PPARalpha agonists and, I think, testosterone. It's vital for carnitine uptake (which is antiinflammatory in the gut) and butyrate metabolism (crucial for HDAC inhibition).
Drug Metab Dispos. 2009 Jun 1;
Changes in mRNA expression levels of solute carrier transporters in inflammatory bowel disease patients. Wojtal KA, Eloranta JJ, Hruz P, Gutmann H, Drewe J, Beglinger C, Fried M, Kullak-Ublick GA, Vavricka SR. University Hospital Zurich.
Inflammatory bowel disease (IBD) is an inflammatory condition that affects gastrointestinal tract. Solute carrier superfamilly of transporters (SLC) comprise proteins involved in the uptake of drugs, hormones, and other biologically active compounds. The purpose of this study was to determine the mRNA expression levels of 15 solute carrier transporters in two regions of the intestine in IBD patients. Endoscopic biopsies were taken from two locations (terminal ileum and colon) for histological examination and RNA extraction. We quantitatively measured the mRNA expression of 15 SLC transporters in 107 IBD patients (53 Crohn's disease and 54 ulcerative colitis) and 23 control subjects. Messenger RNA expression was evaluated using the quantitative reverse transciption-PCR technique. We observed that in ileum of IBD patients, mRNA levels for SERT, ENT1, ENT2, and OATP2B1 were significantly elevated while for ASBT and OCTN2 they were significantly lower. In colon, mRNA levels for ENT1, ENT2, CNT2, OATP2B1, and OATP4A1 were significantly higher, while mRNA levels for OCTN2 were significantly decreased. In inflamed colon of IBD patients the mRNA expression levels of ENT1, ENT2, CNT2, OATP2B1, OATP4A1, and PEPT1 were significantly higher. We conclude that intestinal SLC mRNA levels are dysregulated in IBD patients, which may be linked to the inflammation of the tissue and provides an indication about the role of inflammatory signalling in regulation of SLC expression.
> OCTN2 is upregulated by intermittent fasting, exercise, PPARalpha > agonists and, I think, testosterone. It's vital for carnitine uptake > (which is antiinflammatory in the gut) and butyrate metabolism (crucial > for HDAC inhibition). > > Changes in mRNA expression levels of solute carrier transporters in > inflammatory bowel disease patients...
Does the study distinguish if OCTN2 (carnitine transporter) reduction causes IBD or that OCTN2 is simply reduced during inflammation? Since carnitine is an antioxidant and is essential for metabolism of long chain fatty acids (LCFAs), lack of it could cause inflammation. On the other hand, during inflammation, cell many not want to metabolize LCFAs since they are prone to peroxidation.
In article <edd2ecbf-aa30-45c8-84fe-d0af18522...@p20g2000vbl.googlegroups.com>,
jay <jaym1...@hotmail.com> wrote: > > OCTN2 is upregulated by intermittent fasting, exercise, PPARalpha > > agonists and, I think, testosterone. It's vital for carnitine uptake > > (which is antiinflammatory in the gut) and butyrate metabolism (crucial > > for HDAC inhibition). > > > > Changes in mRNA expression levels of solute carrier transporters in > > inflammatory bowel disease patients...
> Does the study distinguish if OCTN2 (carnitine transporter) reduction > causes IBD or that OCTN2 is simply reduced during inflammation?
Given that supplemental carnitine in liposomes has alleviated TNBS colitis in mice when TNBS downregulates OCTN2, I'd say it's causative [PMID 17065219]. The other limiting factor might be glutamine (via the Atb0+ transporter).
> Since > carnitine is an antioxidant and is essential for metabolism of long > chain fatty acids (LCFAs), lack of it could cause inflammation. On the > other hand, during inflammation, cell many not want to metabolize > LCFAs since they are prone to peroxidation
> Given that supplemental carnitine in liposomes has alleviated TNBS
colitis in mice when TNBS downregulates OCTN2, I'd say it's causative [PMID 17065219]. The other limiting factor might be glutamine (via the Atb0+ transporter).
Thanks, I'll try glutamine next for the burning tongue syndrome that I have been experiencing for the last 8 years. In the last two years it has reduced mostly by avoiding trigger foods of which there are many including organic fruits and veggies.
Per your advice, I recently added carnitine and alpha lipoic acid (ALA) and they both reduce the tongue burn. And of the two, ALA seems to be more effective. It also seems my "food allergies" which manifest itself as itching, sharp intermittent shooting pains and hand numbness have been reduced, at least for black pepper and raw hazelnuts. And I can ingest more beans before incurring a heartburn.
But I am wondering if I have the OCTN1 vs OCTN2 defect which would prevent the plant derived antioxidant, ergothioniene, from being accumulated in related tissues (ie skin, gut, endothelial lining, eyes, joints, immune cells, nervous system). OCTN1 variants are also linked to CD, RA, lupus, psoriasis and leukemia.
Recent I experimented with cooked vs raw bananas and strawberries. For some reason cooked cause less tongue burn than raw ones. Anyone else experience this? What might be the reason?
Have you noticed that an apple or potato turns brown when cut or bruised. Supposedly, the enzyme tyrosinase converts some polyphenols into quinones. Quinones are quite reactive and apparently have anti- viral, bacterial, insect and worm properties.
In humans, a similar process is used to produce melanin. Here tyrosine is oxidized by tyrosinase into quinones and then further into melanin. Supposedly ingested dietary polyphenols are also oxidized into quinones. And neurotransmitters (ie adrenaline) are also oxidized into quinones. Coincedentally, I get bloating and nerve pain from elevated stress. And according to some abstracts, vitiligo (white skin) may be related to quinones also.
Does anyone have links that describe the metabolism of dietary polyphenols and if it involves carnitine or ergothioniene? Also can anyone suggest some low molecular weight, non-phenolic based, antioxidants effective against quinones and hydrogen peroxide (H2O2)? Thx
Background Info: Various members in my family have suffered Crohn's Disease, Psoriasis, Dermatitis, Breast Cancer, Leukemia, Cataracts, etc. Starting 2001, I also experienced gut inflammation, rhoids/ fissures, pain near terminal ileum, IBS, CFS, neuropathy, CTS, RLS, sciatica, heartburns, sore joints and food allergies that peaked in late 2007. About half a year ago I starting developing vitiligo on my hands.
--------- Catechin metabolism: glutathione conjugate formation catalyzed by tyrosinase, peroxidase, and cytochrome p450. The metabolic pathways of dietary flavonoids are still largely unknown. In the present work, mass spectrometry and UV-vis spectroscopy studies were used to show that the naturally occurring flavonoid catechin underwent enzymatic oxidation by tyrosinase in the presence of glutathione (GSH) to form mono-, bi-, and tri-glutathione conjugates of catechin and mono- and bi-glutathione conjugates of a catechin dimer. A hydroxylated catechin adduct was also detected. Using UV spectroscopy, it was shown that the catechol B-ring of catechin was oxidized by tyrosinase to form an o-quinone which could be reduced back to catechin with potassium borohydride or reacted with GSH to form glutathione conjugates. The catechin-glutathione conjugates formed had much lower distribution coefficient values than catechin itself. When peroxidase and hydrogen peroxide were used instead of tyrosinase, only mono-glutathione conjugates were formed but not bi-glutathione conjugates or hydroxylated adducts. (1)H NMR evidence showed that three different mono-glutathione conjugates on ring B of catechin were formed by peroxidase and hydrogen peroxide. Rat liver microsomes and NADPH or cumene hydroperoxide also catalyzed catechin-glutathione conjugate formation which was prevented by benzylimidazole, a P450 2E1 inhibitor. Catechin cytotoxicity toward isolated hepatocytes was also markedly enhanced by hydrogen peroxide or cumene hydroperoxide and was prevented by benzylimidazole, suggesting that catechin could be metabolically activated by P450 peroxidase activity to form cytotoxic quinoid species. PMID: 11453730
In article <5160df3e-a793-440f-b8b6-7c780a27d...@v38g2000vbb.googlegroups.com>,
jay <jaym1...@hotmail.com> wrote: > > Given that supplemental carnitine in liposomes has alleviated TNBS > colitis in mice when TNBS downregulates OCTN2, I'd say it's causative > [PMID 17065219]. The other limiting factor might be glutamine (via > the > Atb0+ transporter). ... > Per your advice, I recently added carnitine and alpha lipoic acid > (ALA) and they both reduce the tongue burn.
You should try reading the references and the earlier posts I've made on the subject. Carnitine might only be effective 1) if you can get it across the cell membrane (like in liposomes or by boosting OCTN2 expression via intermittent fasting, exercise, PPARalpha agonists or other means I've discussed) and 2) if you consume carnitine in conjunction with butyrate - *however* if your colitis is due to a virus then butyrate may only aggravate its replication (especially in conjunction with a vitamin D3 deficiency).
And of the two, ALA seems
> to be more effective. It also seems my "food allergies" which manifest > itself as itching, sharp intermittent shooting pains and hand > numbness have been reduced, at least for black pepper and raw > hazelnuts. And I can ingest more beans before incurring a heartburn.
Pepper is going to activate TRPV's which isn't exactly antiinflammatory for some people.
> But I am wondering if I have the OCTN1 vs OCTN2 defect which would > prevent the plant derived antioxidant, ergothioniene, from being > accumulated in related tissues (ie skin, gut, endothelial lining, > eyes, joints, immune cells, nervous system). OCTN1 variants are also > linked to CD, RA, lupus, psoriasis and leukemia.
In digestive disorders I think it might be a *gain* of function and it might be a problem due to antibodies against bacteria cross-reacting with the receptor. This has been discussed here before as well.
A loss of transport via OCTN1 might occur due to antibodies blocking it - and upregulating the receptor might only result in more antibody problems - but this is but one interpretation.
> Recent I experimented with cooked vs raw bananas and strawberries. For > some reason cooked cause less tongue burn than raw ones. Anyone else > experience this? What might be the reason?
These fruits are too sweet. Sugar feeds inflammation. Cooking fruit is particularly problematic as it generates all sorts of advanced glycation end products.
I don't see why you don't simply try eliminating these foods first if they're giving you trouble. None of them are essential to a balanced diet.
> Have you noticed that an apple or potato turns brown when cut or > bruised. Supposedly, the enzyme tyrosinase converts some polyphenols > into quinones. Quinones are quite reactive and apparently have anti- > viral, bacterial, insect and worm properties.
People actually take worm eggs to force Crohn's into remission. It works well for me. <www.ovamed.de>
> In humans, a similar process is used to produce melanin. Here tyrosine > is oxidized by tyrosinase into quinones and then further into melanin. > Supposedly ingested dietary polyphenols are also oxidized into > quinones. And neurotransmitters (ie adrenaline) are also oxidized into > quinones. Coincedentally, I get bloating and nerve pain from elevated > stress. And according to some abstracts, vitiligo (white skin) may be > related to quinones also.
Vitiligo is not simply "white skin." It's loss of pigmentation. It can happen due to loss of beta-endorphins, vitamin D3, catalase and - if I'm not mistaken - even cAMP can be involved. There appears to be a link to Parkinson's.
Might I suggest testing for anti-folate receptor antibodies and folate levels. A folate deficiency would inhibit your ability to make proper use of Vitamin D3. In combination with a carnitine deficiency, that could explain the neuropathy, the cancer, the autoimmunity and the cataracts. You might want to run a general metabolic panel if you haven't already, particularly looking at carnitine, vitamin D3 and B vitamins. I've discussed how to address various parts of these problems before.
>> [ALA] ... "food allergies" ... reduced, at least for black pepper ...
> Pepper is going to activate TRPV's which isn't exactly antiinflammatory for some people.
I didn't find any pubmed abstracts relating TRPV and Piper Nigrum (black pepper). Do you have a link? The only spice that I take frequently and which has never caused itching is turmeric. Currently I am trying black pepper since it and ginkgo may be helpful for vitiligo. Below are some abstracts for black pepper.
Amides from Piper nigrum L. with dissimilar effects on melanocyte proliferation in-vitro. Melanocyte proliferation stimulants are of interest as potential treatments for the depigmentary skin disorder, vitiligo. Piper nigrum L. (Piperaceae) fruit (black pepper) water extract ... contains several amides with the ability to stimulate melanocyte proliferation. This finding supports the traditional use of P. nigrum extracts in vitiligo and provides new lead compounds for drug development for this disease. PMID: 17430636
UV irradiation affects melanocyte stimulatory activity and protein binding of piperine. Piperine, the major alkaloid of black pepper (Piper nigrum L.; Piperaceae), stimulates melanocyte proliferation and dendrite formation in vitro. This property renders it a potential treatment for the skin depigmentation disorder vitiligo... If UVA radiation is used with piperine in the treatment of vitiligo, application of the compound and irradiation should be staggered to minimize photoisomerization. This approach is shown to effectively induce pigmentation in a sparsely pigmented mouse strain. PMID: 17387768
Stimulation of mouse melanocyte proliferation by Piper nigrum fruit extract and its main alkaloid, piperine. During a herbal screening programme to find potential repigmenting agents for the treatment of vitiligo, Piper nigrum L. fruit (black pepper) extract was found to possess growth-stimulatory activity towards cultured melanocytes ...This is the first full report on such an activity of black pepper and piperine. PMID: 10575373
Antioxidant efficacy of black pepper (Piper nigrum L.) and piperine in rats with high fat diet induced oxidative stress. The present study was aimed to explore the effect of black pepper (Piper nigrum L.) on tissue lipid peroxidation, enzymic and non- enzymic antioxidants in rats fed a high-fat diet. ...The data indicate that supplementation with black pepper or the active principle of black pepper, piperine, can reduce high-fat diet induced oxidative stress to the cells. PMID: 15231065
Modulatory effect of Piperine on mitochondrial antioxidant system in Benzo(a)pyrene-induced experimental lung carcinogenesis. ... Oral supplementation of piperine (50 mg/kg body weight) effectively suppressed lung carcinogenesis in Benzo(a)pyrene (B(a)P) induced mice as revealed by the decrease in the extent of mitochondrial lipid peroxidation and concomitant increase in the activities of enzymatic antioxidants (superoxide dismutase, catalase and glutathione peroxidase) and non enzymatic antioxidant (reduced glutathione, vitamin E and vitamin C) levels when compared to lung carcinogenesis bearing animals. Our data suggests that piperine may extent its chemopreventive effect by modulating lipid peroxidation and augmenting antioxidant defense system. PMID: 14971727
Effect of piperine on the inhibition of nitric oxide (NO) and TNF- alpha production. Effect of piperine which is an alkaloid present in plants such as Piper nigrum and Piper longum on the production of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) level was analyzed using in vitro as well as in vivo systems. The level of nitrite in the LPS stimulated Balb/C mice (95.3 microM) was reduced in the piperine treated animals (25 microM) significantly. Nitrite level in the Concanavalin-A (Con-A) treated control animals (83.1 microM) was also significantly reduced to 18.5 microM in the piperine treated mice. The drastically elevated levels of TNF-alpha in the lipopolysaccharide (LPS) stimulated animals (625.8 pg/mL) was lowered in the piperine treated animals (105.8 pg/mL). Piperine also inhibited the Con-A induced TNF-alpha production. Piperine could inhibit the nitrite production by in vitro activated macrophages (116.25 microM) to the normal level (15.67 microM) at concentration of 5 microg/mL. In vitro L929 bioassay also revealed the inhibition of TNF-alpha production by the piperine treatment. PMID: 19180797
Black pepper and its pungent principle-piperine: a review of diverse physiological effects. Black pepper (Piper nigrum) is one of the most widely used among spices. It is valued for its distinct biting quality attributed to the alkaloid, piperine. Black pepper is used not only in human dietaries but also for a variety of other purposes such as medicinal, as a preservative, and in perfumery. Many physiological effects of black pepper, its extracts, or its major active principle, piperine, have been reported in recent decades. Dietary piperine, by favorably stimulating the digestive enzymes of pancreas, enhances the digestive capacity and significantly reduces the gastrointestinal food transit time. Piperine has been demonstrated in in vitro studies to protect against oxidative damage by inhibiting or quenching free radicals and reactive oxygen species. Black pepper or piperine treatment has also been evidenced to lower lipid peroxidation in vivo and beneficially influence cellular thiol status, antioxidant molecules and antioxidant enzymes in a number of experimental situations of oxidative stress. The most far-reaching attribute of piperine has been its inhibitory influence on enzymatic drug biotransforming reactions in the liver. It strongly inhibits hepatic and intestinal aryl hydrocarbon hydroxylase and UDP-glucuronyl transferase. Piperine has been documented to enhance the bioavailability of a number of therapeutic drugs as well as phytochemicals by this very property. Piperine's bioavailability enhancing property is also partly attributed to increased absorption as a result of its effect on the ultrastructure of intestinal brush border. Although initially there were a few controversial reports regarding its safety as a food additive, such evidence has been questionable, and later studies have established the safety of black pepper or its active principle, piperine, in several animal studies. Piperine, while it is non-genotoxic, has in fact been found to possess anti-mutagenic and anti-tumor influences. PMID: 17987447
> > ... cooked vs raw bananas, [pineapple] and strawberries. > > ... cooked cause less tongue burn than raw ones.
> These fruits are too sweet. Sugar feeds inflammation. Cooking fruit is particularly problematic as it generates all sorts of advanced glycation end products.
No doubt sugars feed inflammation. And I too would have expected cooked fruits to be more inflammatory. But for some reason cooked fruits cause me less problems. In fact, others in the crohns-colitis group have also suggested eating cooked vs raw fruits and veggies, especially when flairing. Could this is related to the polyphenol- generated quinones? In addition, regular vitamins with citrus bioflavonoids and soy derivatives (www.iherb.com/Now-Foods-Vit-Min-75- Iron-Free-180-Tablets/829) give me heartburn, hand numbness and restless legs. But not hypoallegenic ones (www.iherb.com/Twinlab- Allergy-Multi-Caps-200-Capsules/2315).
> I don't see why you don't simply try eliminating these foods first if they're giving you trouble. None of them are essential to a balanced diet.
In my case, it seems all foods cause problems to varying degree, including hypoallegenic-, amino acid-, MCT-, glutamine-, taurine-, carnitine-based nutritional formulas (EleCare, which does have some soy oil). Milk products (inc yogurt, kefir), red meats, eggs, tropical & citrus fruits, brassica veggies, onion, chilies, some beans (soy & kidney), nuts (esp peanuts & cashews), chocolate, extra virgin olive oil, black tea, alcohol (inc red wine), MSG and processed foods are most offensive to me. I have tried a number of diets. The most inflammatory were Atkin & Paleo-type (chol = 450). Least inflammatory was the lettuce diet. Fasting to skin and bones, even less. The least inflammatory, practical diet thus far has been high in beans (lentils, pinto), salads, limited fruits and no oils/fats (chol < 170). While diet has been an important factor, it does not seem to fix some underlying problem.
> > apple or potato turn brown when cut or bruised. .. tyrosinase converts polyphenols into quinones. Quinones are quite reactive and apparently have anti- viral, bacterial, insect and worm properties.
> People actually take worm eggs to force Crohn's into remission. It works well for me. <www.ovamed.de>
I was also consindering this route at one time, but the cost is prohibitive. What are you most allergic to? What have you found most effective? Have you had any luck with antioxidants such as ALA, NAC, CoQ10, E, C, taurine, melatonin, etc?
>> ... vitiligo (white skin) may be related to quinones also.
> Vitiligo is not simply "white skin." It's loss of pigmentation. It can happen due to loss of beta-endorphins, vitamin D3, catalase and - if I'm not mistaken - even cAMP can be involved. There appears to be a link to Parkinson's.
Since I get lots of sun exposure, I don't think D3 is a factor. Thanks for other possible factors that I can follow up on. Below pubmed article are mainly tyrosinase related, however they could also indicate insufficient antioxidant capacity due to OCTN polymorphisms.
PM Abstract: Vitiligo puzzle: the pieces fall in place. Over the years, the role of biochemical, immunological, genetic, and other biological aspects in the pathogenesis of vitiligo has been studied. So far, no convincing model describing the interplay of these contributing factors has been formulated. Based on existing research, we propose that vitiligo has a multi-factorial etiology, characterized by multiple steps, but always involving an increase of external or internal phenol/catechol concentration, serving as a preferred surrogate substrate of tyrosinase, competing with its physiological substrate tyrosine. The conversion of these substrates into reactive quinones is reinforced by a disturbed redox balance (increasing hydrogen peroxide). Such reactive quinones can be covalently bound to the catalytic centre of tyrosinase (haptenation). This could give rise to a new antigen, carried by Langerhans cells to the regional lymph node, stimulating the proliferation of cytotoxic T cells. However, the activation of such cytotoxic cells is only a first step in skin melanocyte killing, which also depends on a shift in the balance between immune defence and tolerance, e.g. resulting from a decrease in properly functioning T-regulatory cells. With this new model, based on a synthesis of several of the existing theories, in mind, the external and internal factors involved in the etiopathogenesis of vitiligo are reviewed, against the background of reported clinical data, experimental studies and existing and potential new therapies. A similar complex mechanism may also lead to some other autoimmune diseases. PMID: 17850508
PM Abstact: The reaction of alpha-synuclein with tyrosinase: possible implications for Parkinson disease. Oxidative stress appears to be directly involved in the pathogenesis of Parkinson disease. Several different pathways have been identified for the production of oxidative stress conditions in nigral dopaminergic neurons, including a pathological accumulation of cytosolic dopamine with the subsequent production of toxic reactive oxygen species or the formation of highly reactive quinone species. On these premises, tyrosinase, a key copper enzyme known for its role in the synthesis of melanin in skin and hair, has been proposed to take part in the oxidative chemistry related to Parkinson disease. A study is herein presented of the in vitro reactivity of tyrosinase with alpha-synuclein, aimed at defining the molecular basis of their synergistic toxic effect. The results presented here indicate that, in conformity with the stringent specificity of tyrosinase, the exposed tyrosine side-chains are the reactive centers of alpha-synuclein. The reactivity of alpha-synuclein depends on whether it is free or membrane bound, and the chemical modifications on the tyrosinase- treated alpha-synuclein strongly influence its aggregation properties. On the basis of our results, we propose a cytotoxic model which includes a possible new toxic role for alpha-synuclein exacerbated by its direct chemical modification by tyrosinase. PMID: 18390556
Pubmed: The metabolism and toxicity of quinones, quinonimines, quinone methides, and quinone-thioethers. Quinones are ubiquitous in nature and constitute an important class of naturally occurring compounds found in plants, fungi and bacteria. Human exposure to quinones therefore occurs via the diet, but also clinically or via airborne pollutants. For example, the quinones of polycyclic aromatic hydrocarbons are prevalent as environmental contaminants and provide a major source of current human exposure to quinones. The inevitable human exposure to quinones, and the inherent reactivity of quinones, has stimulated substantial research on the chemistry and toxicology of these compounds. From a toxicological perspective, quinones possess two principal chemical properties that confer their reactivity in biological systems. Quinones are oxidants and electrophiles, and the relative contribution of these properties to quinone toxicity is influenced by chemical structure, in particular substituent effects. Modification to the quinone nucleus also influences quinone metabolism. This review will therefore focus on the differences in structure and metabolism of quinones, and how such differences influence quinone toxicology. Specific examples will be discussed to illustrate the diverse manner by which quinones interact with biological systems to initiate and propagate a toxic response. MID: 12093358
> I didn't find any pubmed abstracts relating TRPV and Piper Nigrum > (black pepper).
That's because capsaicin in pepper is the TRPV1 agonist. You'll find plenty on that.
If Parkinson's is due to an autoimmune targetting of neuromelanin then boosting your melanin production without quelling your autoimmunity will cause problems.
> No doubt sugars feed inflammation. And I too would have expected > cooked fruits to be more inflammatory. But for some reason cooked > fruits cause me less problems. In fact, others in the crohns-colitis > group have also suggested eating cooked vs raw fruits and veggies, > especially when flairing. Could this is related to the polyphenol- > generated quinones? In addition, regular vitamins with citrus
I think it's related to fiber and fermentation in the gut.
> > People actually take worm eggs to force Crohn's into remission. It > > works well for me. <www.ovamed.de>
> I was also consindering this route at one time, but the cost is > prohibitive.
Do it the natural way. It's free.
> inflammatory were Atkin & Paleo-type (chol = 450). Least inflammatory > was the lettuce diet. Fasting to skin and bones, even less. The least
Try an intermittent fast.
> prohibitive. What are you most allergic to? What have you found most > effective? Have you had any luck with antioxidants such as ALA, NAC, > CoQ10, E, C, taurine, melatonin, etc?
I react to all but about a dozen foods.
I literally take dozens of supplements.
You might try low-dose naltrexone, folinic acid shots (Tregs have folic acid receptors), carnitines, a PPARalpha agonist (which fasting will give you), testosterone, melatonin (although there's evidenc it's dangerous in Parkinson's), magnesium, butyrate. A lot of this depends on what a nutritional panel shows you.
CoQ10 can be a problem if you have a yeast issue.
> Since I get lots of sun exposure, I don't think D3 is a factor.
It is if you can't convert it. For instance, low folic acid will lead to a much faster vitamin D breakdown. You might even have adequate serum levels of folate and a problem with anti-folate receptor antibodies preventing enough folate from getting into the CNS. If that's the case, all your serum levels might be normal but you could have a considerable deficit for vitamin D and folic acid in the brain.
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