This is not medical advice I am posting this for educational and informational reason.
I am summarizing my notes. I will update them as I go and make spelling corrections late. Just posting them now to give people an idea what to research.
For inflammatory bowel issues and malabsorption issues.
Many with inflammatory bowel have low Catechol-O-Methyltranserase activity. (COMT). Increasing COMT activity must be done with caution if you increase it too much you can swing things too far the other way. Decreased COMPT activity can cause high estrogen levels which effects cholesterol synthesis and can inhibit bile production. If COMT activity is low adrenal hormones will become high and so will more nuero transmitting hormones. Low COMT activity can lead to inflammatory bowel.
SAMe increases COMT activity along with 5-MTHF and folinic acid. Do not take folic acid it will make it worse. Magnesium , lithium and niacin are also needed . Methyl donors are needed for COMT but if a person has sulfation issues they should address it before taking methyl donors.
Those with low COMT need to avoid Quercetin, Rutin, Luteolin, Green Tea, Catechins, Epicatechins, Fisetin, Ferrulic Acid and hydroxytyrosol until they have address the dirty COMT gene. Also L-Dopa compete for COMT so should be avoided.
For a temporary fix reducing tryptophan, phenylalanine, and serotonin reduces high catecholamine levels from low COMT.
These flavonoids can be used by those with COMT down regulation apigenin, genistein, chrysin, myricetin, tangeretin, biacelin, scutellarein and wogonin.
MAO increasing MAO can increase COMT activity. Sirt 1 can activate MAO but is usually high in inflammatory bowel. MAO is not a good route to go because it can cause many other issues.
To address the high adrenal and neurotransmitter levels adaptogenic herbs like eleuthero, ashwanga, passion flower, Lemon balm and valerian will help normalize them.
Increasing progesterone and taking magnesium malate should help also.It will also decrease estrogen levels. Low progesterone can cause problems with sleep causing insomnia or disrupted sleep cycles. It can cause fluid retention and brain fog. It causes estrogen dominance which inhibits T4 from being converted to T3 resulting in low T3 and high T4 levels. Low progesterone can cause night sweats and hot flashes. High adrenaline levels from low COMT activity can cause low progesterone levels.
Cholesterol is needed to produce Progesterone. Stress decreases progesterone. Vitamin C, Magnesium, Zinc, B6, are needed for progesterone. Fiber helps increase it by decreasing bad hormone levels. L-arganine can help increase progesterone.
MTHFR enzyme regulates the methyl cycle issues with it can impair the bodies ability to process folate. It metabolizes folate to 5-methyltetrahydrofolate (5-MTHF). 5-MTHF coverts the ammino acid homocysteine down into methionine and glutathione. Methionine is used to make proteins utilize antioxidants, and assist the liver in processing fats. It also prevents depression and inflammation. Methionine helps convert estradiol into estriol which has weaker estrogen effects. Methionine is farther converted to SAMe which is a methyl donor and reduces inflammation. SAMe supports immune function. SAMe also helps produce certain neurotransmitters such as serotonin, dopamine, and melatonin. SAMe is involved in growth, repair and maintenance of cells.
Methylation has been found to be inhibited in those with inflammatory bowel. Methylation is sometimes referred to as transmethylation. Methylation is when a methyl group is transferred from one compound to another. One example is the recovery of methionine from homocysteine. In order to sustain sufficient reaction rates during metabolic stress this reaction requires B vitamins, B12 and foliate . Mehtyltetrahydrofolate delivers the methyl groups to form the active methyl form of B12. Methycolobalamin is required for themylation of homocysteine.
B12 or folate deficiency causes increased levels of circulating homocysteine. Elevated homocysteine is a risk factor for cardiovascular disease, metabolic syndrome and autism.
Major players in methylation are S-adenosylmethionine (SAMe), and methyltransferase (MT) which include DNA methyltransferase (DNMT), and Protein arginine methyltransferase (PRMT).
Methyltransferases remove methyl group from SAM, thereby converting it to S-adenosyl-L-homocysteine (SAH). This acts as a potent feedback inhibitor of upstream methylation reactions by blocking MT activity. The reactions are reversible.
The ratio of SAM to SAH influences whether SAH is coverted back to SAM or more likely hydrolyzed by S-adenosyl-L-homocysteine hydrolase (SAHase) into andenosine and homocysteine. Blackade of SAHase activity raises intracellular SAH levels and reduces MT activity and indirectly inhibits methylation reactions. Decreased SAHase activity causes raised creatine kinase, SAH, and raised SAM levels. Symptoms are reduced by dietary calorie restriction of methionine and supplementation of creatine and phosphatidylcholine.
Arginine methylation can increase steric hindrance and hydrophobicity but in contrast to phophorylation it does not affect protein charge.
Arginine methylation occurs in histones, trascription factors, cytoskeletal proteins, cytoplasmic signaling proteins and apoptosis proteins.
PRMT substrates are ERA receptor, others are splicing and elongating factors SAP49, UIC, CA150 and FGF-2 and Ewing Sarcoma Oncoprotein.
Problems with the vitamin D receptor can reduce tolerance to methyl donors. Impaired VDR can cause a person to be senstive to methyl donors. SAMe rescues it.
Things that can hinder or block methylation are low electrolytes, and low glutathione. High sulfite levels can cause methyl donor sensitivity. High sulfites can be cause by CBS issues, BH4 causing CBS upregulation or gut dysbiosis. Low superoxide dismutase can also cause methyl donor intolerance or sensitivity. Low methionine can cause methyl donor intolerance. If B12 is not being converted to methylcolobamin it can cause a methyl trap and methyl groups will build up making a person ill.
Homocystein in methylation. In the homocysteine cycle , homocysteine needs to be converted to SAMe and glutathione. SAMe becomes a methyl donor to support healthy methylation and glutathione goes on to act as a powerful antioxidant that slows aging.
Causes of under methylation are leaky gut, nutrient deficiencies especially B12 , low methionine, betaine, choline, and homocysteine levels. The co-factors needed are B12, folate, zinc, B2, B3 and B6.
Mast cell activation syndrome can cause high histamines. Histamines can deplete methyl groups. High basophil levels can cause under methylation. High folate levels can mask B12 deficiency.
Pathways that can lead to undermethylation are CBS, COMT, VDR, MTR, MTRR.
Supporting under methylation SAMe, 5HTP, Evening primrose oil, P5P, inositol, Vitamin A, Vitamin C, Zinc, magnesium, Trymethylglycine (TMG) also known as betaine or DMG. Also using methyl forms of vitamins may help. Folate, methionine, glutathione, natural sources of calcium like stinging nettles. Do not take copper, DMAE or choline. Some say not to take manganese but many are deficient now days and I have not seen reliable sources to show it would be bad to take when an under methylator.
Under methylation can cause many health problems. This is a list of symptoms of under methylation. CBS issues need to be addressed before addressing methylation issues or the methyl donors will have no effect.
chronic degenerative diseases
obesity though lean people can be under methylators also.
Obsessive compulsive disorders
Phobias or fears
Low white blood cell count
Extremely large red blood cells
Symptoms of over methylation
headache or migraines
hypokalemia low plasma potassium levels.
Things that support over methylation are B12, folate, niacinamide, DMAE, choline, manganese, zinc, Omega 3s, DHA and EPA. Vitamin C and E. Avoid SAMe, inositol, TMG or DMG.
Oxidative phosphorylation needs restored in inflammatory bowel. OXPHOS is the final step in cellular respiration. Increasing OXPHOS increases glycolysis. The reduced OXPHOS is a result of inhibition of the citric acid cycle. Oxidative stress can also inhibit OXPHOS. Salicylate (aspirin) causes inhibition of OXPHOS. OXPHOS is used by some cancers for growth. Salicylate inhibits the Krebbs cycle and a-ketoglutarate dehydrogenase. This is dependent on ATP and ADP just as the Krebbs cycle is.
Piperine inhibits OXPHOS so should be avoided if you have issues with it or the Krebbs cycle.
OXPHOS provides the ATP used in the brain for most synaptic events including transmitter release.
In cancer that uses the Warburg effect inducing OXPHOS kills the cancer cell but it can feed other types of cancer. Complex 1 inhibitors induce OXPHOS. This causes a back up of ROS in the cells causing cell destruction so this also shows the importance of homeostasis of OXPHOS. So we should work towards restoring what may be inhibiting it for example low NADPH levels or inhibited function of the citric acid cycle or low ATP.
Need to increase Malic Acid, tamarand, apples, pears grapes, black haw and horsetail herb. Malic acid is needed for the Krebbs cycle, reduces pain, improves fibromyalgia, it prevents kidney stones and kidney disease. It also increase the guts production of GABA.
If they cannot tolerate cold this indicates low SIRT3 levels, this will cause problems with the break down of fats, cause low ATP levels, and low glucose levels. SIRT3 increases Acetyl-CoA which fuels the Krebbs cycle. It also stimulates the Krebbs cycle to produce energy by increasing IDH2 activity which which increases conversion of isocitrate to a-ketoglucarate. This is involved in metabolism of hydroxy proline. SIRT3 is involved in ketogenesis. Low SIRT3 will cause inhibited ketogenesis. Those with inflammatory bowel issues are usually low in SIRT3 . SIRT3 increased NADPH which is usually low in inflammatory bowel and malabsorption. Excess SIRT3 will inhibit protein synthesis in the mitochondria and inhibit oxidative phosphorylation. This is one you would have to be careful in manipulating because many with malabsorption have inhibited OXPHOS. Low SIRT3 levels can lead to NAFLD and COPD it increases fibrosis. SIRT3 increases pyruvate dehydrogenase activity which is usually low in malabsorption disorders but high in some cancers. SIRT3 function is PH dependent so if we have acidosis or alkalosis those must be addressed in order for SIRT3 to function properly. Excess SIRT3 will inhibit bone growth. As with anything homeostasis should be the goal.
Things that increase SIRT3 stimulating HSP70 cold will do that. Exercise, nicotinamide riboside, PQQ, Lipoic Acid, Resveratrol, berberine, bitter melon, green tea, chinese skullcap, Leucine, hydrogen peroxide, carnitine, Kaempferol, caffeic acid, chlorogenic acid.
Ketones and a Ketogenic diet inhibit SIRT3.
NPC1 is inhibited in inflammatory bowel. Which is the cholesterol transporter. A deficiency in NPC1 causes an accumulation of cholesterol in lysosomes. This can also cause a deficiency in enzymes needed to break down fats. This is evident by high fat content in stools. Lecithin increases NPC1 but most have issues that need addressed before they can take lecithin. NPC1 deficiency causes lysosomal acid lipase deficiency this causes a disruption in vitamin A homeostasis because the vitamin A receptor becomes inhibited. SP1 transcription factor and adipocyte protein 2 interact to regulate NPC1. A deficiency in either one will decrease NPC1 activity. AP2 is high in hyperglycemia and diabetes. It is also high in obesity. I suspect that may have to do with lectin issues that can be addressed. Also AP2 has been found to be overexpressed in fibrotic types diseases like COPD and NAFLD. AP2 is increased by cAMP protein kinase. Issues with phosphorylation and dephosphorylation effect the function of AP2. AP2 is also high in diabetes and obesity leading me to believe it is an issue involved with lectin sensitivy or insulin. Studies have shown a possible connection with it and insulin resistance. I also suspect there may be issues with the LXR receptors.
ATOX1 and KPNI issues causes high unbound copper levels. ATOX1 is found in cytoplasma. It binds free metals protecting cells from ROS. It also shuttles copper from cytosol to ATPase transporters. This is vital for the subsequent insertion of copper into ceruloplasmin. It is also involved in cell cycle. When it is inhibited lipogenesis becomes inhibited resulting in cell death from increased oxidative stress. Inhibited bile flow causes a decrease in ATOX1. High C-reactive levels which is common in many tick born illnesses and mycoplasma infections cause these enzymes to become inhibited preventing copper from entering ceruloplasma causing high plasma unbound copper levels.
Low Quinone oxidorecutase levels is very common in inflammatory bowel I suspect the opposite is also true in some people. It is also known as NADH dehydrogenase. It acts on NADH and NADPH. It is involved in the first step of the electron transport chain of OXPHOS. NADH is used to create H2 in order to make ATP. NADH is then oxidized resulting in NAD+. AMP is a quinone oxidoreductase inhibitor. Certain sulfur based herbicides also inhibit Quinone oxidoreductase. Low levels of AMP makes you more susceptible to viral infection. So inhibiting AMP is not a good idea but addressing what may be causing high levels of AMP should be the goal. High levels of adenosine induces sleep and as you sleep adenosine deanimase is produced which degrades adenosine this causes us to awaken. Infection causes raised adenosine levels and they believe the body does this so it can heal. Adenosine increases insulin sensitivity. Adenosine makes the blood brain barrier more porous. Low adenosine causes an increase in dopamine and glutamate. So you can see inhibiting AMP could cause some problems. It is best to increase adenosine deanimase. Adenosine deanimase deficiency has been linked to decreased IL-2 which modeulates the immunes system to help it recognize the difference between something foreign and self. Adenosine deanimase defficiency has also been linked to thymus cell death, lung inflammation and defective T cell receptor signaling.
Zinc deficiency can cause a deficiency in Adenosine deanimase. Estrogen also induces adenosine deanimase so high can most likely cause a depletion of adenosine causing the inability to sleep. Insulin Like Growth Factor 1 also increases Adenosine deanimase. Protein, casein in milk products , calcium, blue berries, resveratrol, vitmain C, cinnamon, prolactin, leucin, magnesium, selenium, astragulus, eleuthero, ursolic acid and carnitine increase adenosine deanimase.
Things that inhibit adenosine deanimase are IL-13 which is high in those with allergies. Berberine and curcumine also inhibit adenosine deaminase. Nitric Oxide also inhibits it. So if you have trouble sleeping using these may help.
ACMSD, SIRT1 and AMPK are high in inflammatory bowel and need decreased.
ACMSD is involved in the metabolism of tryptophan into NAD+. ACMSD is part of the Kynurenine pathway. Amino-B-Carboxymuconate-semiadehyde-decarboxylase limits quinolilinic acid formation by competitive production of picolinic acid. A deficiency in ACMSD can lead to depression and even suicidal behavior.
ACMSD is stimulated by iron (Fe2). Toxins and infections can cause oxidative stress which causes the iron in the body to be converted to Fe3 making it unavailable to the body for use. This can cause iron to build up in the body and become toxic. Lactoferrin and curcumin can restore iron homeostasis. Curcumine if taken too long can cause anemia because it chelates iron so should not be used long term. Lipocalin 2 also restores iron homeostasis. Knotgrass stimulates lipocalin 2.
ACMSD is also stimulated by carbondioxide. (CO2+). There are methods of increasing CO2 levels safely like holding ones breath or breathing into a bag. This should be done with caution because CO2 can cause the body to become more acidic.
A diet high in phytic acid can increase phytol in the body. This can activate PPARa which inhibits ACMSD which causes a rise in blood plasma levels of NAD. But it also increases quinolinic acid which can damage the NMDA receptor and other areas of the brain.
SIRT1 activates and silences many genes that promote health and longevity.
SIRT1 used to be called the anti-aging because it slows aging. In some cancers SIRT1 is elevated. If SIRT1 is activated for too long it will cause oxidative stress. So you can see the importance of SIRT1 homeostasis. Now those who have high SIRT1 levels should not worry about what increases it but should focus on decreasing it because just about everything increases SIRT1. Those with high SIRT1 levels tend to be under weight while those with low levels tend to be overweight. SIRT1 increases as NAD+ levels increase because it requires NAD+ to function. SIRT1 removes acetyl groups off proteins. SIRT1 turns inflammatory genes off. SIRT1 turns the genes off for fat storage and synthesis and the genes for managing blood sugar levels. Acetyl groups are added to groups in response to changes made by inflammation and oxidative stress. SIRT1 can reverse Leptin resistance which is common in obesity. SIRT1 can cause you to be sensitive to T3 which can cause high T4 levels and low T3 levels. This can cause a person to be sensitive to cold. SIRT1 can increase estrogen levels by increasing estrogen receptor signaling. SIRT1 and resveratrol makes you more sensitive to vitamin D. SIRT1 inhibits IGF-1 which is used to build muscle and is crucial for healing. But high levels of IGF-1 can promote cancer. SIRT1 inhibits mTOR which is involved in inflammation and aging. SIRT1 protects us from nitric oxide. Nitric oxide stimulates DNA repair via deacetylation of FOXO1. Without SIRT1 NO would cause cells to self destruct. SIRT1 increases adipopectin which stimulates TH17. High adipopectin has been linked to autoimmunity. High TH17 levels causes inflammatory skin diseases such as Lupus. High TH17 levels causes arthritis which is why high adipopectin levels have been linked to arthritis. Adipopectin stimulates weight loss. SIRT1 decreases NRF2 which is the master regulator of the antioxidant system. Acetylation allows NRF2 to bind to DNA better and as mentioned earlier SIRT1 removes acetyl groups which would inhibit NRF2 binding. SIRT1 decreases pancreatic B-Cell proliferation (growth or production) which can lead to diabetes. GLP-1 which is usually low in inflammatory bowel blocks the effects of SIRT1. Low nicotinamide inceases SIRT1 high doses inhibit it. High SIRT1 levels can impair liver repair.
As stated earlier do not worry about the things that increase SIRT1 because they are numerous but worry about the things that disrupt SIRT1 homeostasis like low GLP-1 levels. This is a list of things that increase SIRT1, NAD+, DHA, Cold, Forskolin, adrenaline by increasing cAMP which increases SIRT1, exersize increases SIRT1, Sunlight increases SIRT1, Fructose , olive oil, zinc, green tea, PQQ, curcumin, pterostilbene, cacitrol, lipoic acid, fisetin, berberine, Pau D Arco which contains Beta Lapachone, Gotu Kola, grape seed extract, Salicylic acid, kelp, quercetin, bitter melon, pyruvate, lycopene, and butein all stimualte SIRT1. Other things that increase SIRT1 are hydrogen peroxide usuall formed from toxins in the body or infections, fasting causes high ketone levels which increases SIRT1, Hydrogen sulfide increases SIRT1 which is produced in gut bacteria when we have gut dysbiosis and by the body. Saunas, malic acid, oxaloacetate, apagenin, Lithium, succinic acid, tryptophan, and aspartic acid which are fuels for NAD+. Those things are raised when we have metabolic issues that need addressed.
Things that increase NAD+ also increase SIRT1
Some things that inhibit SIRT1 are PPAR gamma, melatonin, IGF-1, genistein, and an antibiotic trichostatin. PPAR gamma regualates fatty acid metabolism and glucose homeostasis and has been found to be low in those with inflammatory bowel. Low levels of PPAR causes muscle fatigue. Stimulating the retinoic acid receptors increases PPAR, Honokiol found in magnolia stimulates PPAR gamma . High vitamin D levels prevents PPAR from binding to DNA which would inhibit it’s effects. We do not want to increase PPAR gamma to much because it can lead to acne, fluid and sodium retention. AMPK which is usually high in inflammatory bowel inhibits PPAR gamma. Low PPAR gamma levels makes it difficult to gain weight. Those with low PPAR gamma need more carbohydrates. Cold and nitric oxide can increase PPAR gamma.
Insulin-Like growth factor 1 (IGF-1) also known as Somatomedins and sulfation factor. It is involved in the incorporation of sulfur into cartilage for proper cartilage health. IGF-1 has been found to be low in inflammatory bowel and those with high TH17 levels like lupus. IGF-1 increases antioxidants and decreases inflammation. IGF-1 protects us from autoimmunity. IGF-1 improves memory, acts as an antidepressant and reduces anxiety. IFG-1 restores bone density. IGF-1 improves gut health and nutrient absorption. IGF-1 helps maintain electrolyte balance. High levels of IGF-1 causes acne. Excess IGF-1 causes enlargement of internal organs and excessive bone growth. High levels can lead to diabetes, headaches and blurred vision. It can also cause low sex drive and swelling in limbs.
Things that increase IGF-1 are high calorie intake, protein consumption, casein in milk products, vitamin C, blue berries, growth hormone, cortisol, dhea, parathyroid hormone, prolactin, cinnamon, magnesium, eleuthero, ursolic acid, carnitine, dried plums.
Things that reduce IGF-1 are fasting, protein restriction, royal jelly, glucosamine, berberine, luteolin, curcumin, resveratrol, apagenin, lycopene, green tea, boron, inflammation, and histamines.
AMPK- 5, andenosine monophosphate-activated protein kinase. It plays a role in cellular glucose homeostasis, it is the bodies energy sensor. It activates glucose and fat uptake oxidation in cells when energy is low. It is stimulates fatty acid oxidation and ketogenisis. It inhibits cholesterol synthesis and lipogenesis and trygliceride synthesis , and inhibits adipocyte lipogenesis and inhibits activation of lipolysis. This results in low cholesterol levels with HDL being lower then LDL. This inhibits the breakdown of food into energy. It also inibits protein synthesis leading to many issues especially pheylketonuria. Lypolysis is how our bodies store energy and when inhibited we will have severe weight loss. This takes place in the CBS pathway. High levels of AMPK is common in inflammatory bowel and malabsorption. AMPK is activated by AMP and inhibited by ATP. Hypoglycemia and hypoxia stimulate AMPK. So if we have low glucose levels AMPK will be high causing the CBS pathway to become upregulated which causes high sulfide levels resulting in many health problems and we will start developing a sensitivity to meat and sulfur containing drugs and foods. AMPK levels are low in those with type 2 diabetes and those who are obese. Upregulation of the CBS pathway also causes high hydrogen sulfide levels which can cause low blood pressure and the production of excess free radicals. It also increases nitrosative stress. Excessive weight gain could indicate low AMPK levels excessive weight loss could indicate high AMPK levels. High AMPK levels can result in a lower body temperature. High AMPK levels inhibit PPAR which I discussed earlier. High AMPK levels can make us more prone to viral infections.
Panex Ginseng , green tea, black tea , snow lotus , salicylate and Curcumine should be avoided by those with upregulated CBS or high AMPK levels because these increase AMPK levels. This may help those with type 2 diabetes or obesity because they would increase fat oxidation. S-adenosyl-L-methionine (SAM) inhibits AMPL decreasing the upregulation of the CBS pathway. Nitrosative stress and oxidative stress activate AMPK. Low AMPK levels can cause glycogen storage disease.
Things that increase AMPK are exercise, fasting or calorie restriction, cold exposure increases AMPK. Resverotrol, quercetin, genistein, berberine, curcumin, anthycyanines found in purple fruits, bitter melon, fish oil, carnitine, astragalus, olive oil, creatine, biacalin found in sculletaria, fleabane and plantain herb, fucoiden all stimulate AMPK.
Things that inhibit AMPK are consumption of proteins especially branch chained proteins, high glucose consumption, saturated fat and insulin. For those who have high levels of AMPK it is important to address the cause because the foods that upregulate it are numerous and we cannot avoid them, also they are needed to remain healthy so avoiding them would only add to the problem and prolong our illness. Glucose consumption and increasing ATP will reduce AMPK.
The Krebbs cycle is needed to produce ATP so issues with the Krebbs cycle need addressed. If COMT is low it will lead to issues with the Krebbs cycle and so can low glucose levels. High hydrogen sulfide levels from gut dysbiosis can cause issues with the Krebbs cycle and the CBS pathway. CoQ10 can increase ATP levels. Medium chain fatty acids can increase ATP levels. Glutathion, Vitamin C and vitamin E indirectly increase ATP levels. Cordyceps mushrooms increase ATP levels. Raising ATP levels also improves cognitive function. Pyruvate, cratine and L-carnitine also increase ATP levels. Ribose helps increase ATP production. The B vitamins are needed for ATP production. Magnesium is also needed for ATP production. Strength training improves the bodies ability to produce ATP. Adrenal fatigue can cause low ATP levels. Adaptogenic herbs help restore normal adrenal levels.
Hypoxia, chemicals especially glyphosate and heavy metals can decrease ATP. Dehydration inhibits ATP production so we must stay hydrated with fluoride free water.
Thiol persulfuration is high causing an increase in H2S which can cause inflammation and low blood pressure. This can be caused by frataxin overexpression. This can result in iron accumulation in the cells and increased oxidative stress. P5P, and ubiquinol help.
If you are deficient in flaxatin iron can build up in the cells reducing excess iron in the body and vitamin C help. Curcumine, and lactoferrin can help by reducing iron levels. Curcumin should be used with causion. Taking it for too long can cause anemia. Lipocalin 2 helps restore iron homeostais. Knotgrass stimulates lipocalin 2. It is needed to generate heme groups so we do not want to inhibit frataxin production. We need to focus on reducing oxidative stress and inflammation. HDAC inhibitors increase frataxin. Iron regulatory protein 1 and 2 regulate flaxatin levels. Increased Irp1 and Irp2 expression increases flaxatin. Hepciden regulates Irp1 and Irp2. During infection and inflammation hepcidin increases inhibiting the ability of iron to be absorbed. This causes hypoferremia a type of anemia. It does this to decrease inflammation and to inhibit the pathogens ability to use iron. A hepcidin deficiency can cause iron overload. Though there are no studies on it, it is clear that hepcidin levels can effect thiol persulfuration. So low hepcidin levels would most likely increase persulfuration and high levels would decrease persulfuration. Low levels of iron increase hepcidin and high levels increase hepcicin. High hepciden levels are linked to inflammatory bowel diseases which leads me to believe there is a link to infection that is being overlooked. High hepcidin levels can lead to atheriosclerosis. High hepcidin levels can cause sleep apnea. Hepcidin is high in psoriasis. Low hepcidin levels can increase iron absorption into the body causing iron toxicity.
Things that decrease hepcidin. Vitamin D , STAT3 inhibitors, salicytic acid, Reducing IL-6, alcohol, smoking, testosterone and estrogen.
So if we need to increase heocidin increasing STAT3, IL-6 and other things that cause inflammation should increase hepcidin.
increasing intrinsic factor to improves nutrient absorption especially B12. Gentian root increases intinsic factor. A sign if malabsorption is swelling of the tongue. It is one of the first nutrients to become deficient in malabsorption. Avoid acid blocking drugs. Stomach acid is needed to absorb B12. Increasing stomach acid helps to absorb B12. Apple cider and bitter herbs help increase intrinsic factor. Thyme increases stomach acid. Dandelion and sea salt also promote stomach acid production.
Damage to the gut which is common now because of the BT Toxin and glyphosate in our food causes a loss in intrinci factor production because the pareital cells that generate intrisic factor becomes damaged. Once B12 levels drop it can start a cycle that is hard to break. Sublingual B12 can help , putting it under the tongue can help the body to absorb it. In some the nutrient deficiencies caused may cause issues with converting B12, P5P may be needed also to help with the conversion of B12 to a form the body can use. The B12 deficiency causes inflammation in the gut which farther inhibits nutrient absorption.
We must work on protecting and restoring the mucous membrane for parietal cells to regenerate. Bismuth can help protect the gut permitting it to repair.
Histamine, acetylcholine and gastrin regulate intrinsic factor production. Many are deficient in choline which would inhibit the production of intrinsic factor. Also H2 inhibitors will inhibit histamines which will inhibit production of intrinsic factor.
BHMT (Betaine homocysteine S-methyltransferase is usually low in those with inflammatory bowel but if they have PEMT issues it can cause problems. Betaine taken with pepsin help break down food better and increase gastric acid which should reduce GERD caused by inhibited bile. Hypothyroidism, high estrogen levels, low COMT disrupts hormone levels which can cause low stomach acid levels. Betaine is also know as trymethylglycine or TMG. Betaine increase BHMT levels. Betaine also increases methionine. Vitamin B6 , magnesium and zinc deficiencies can cause low stomach acid levels. Also if you are low in choline needed for neurotransmitters it could slow stomach acid production down. to increase BHMT lysine, choline, creatine, ursodeoxycholic acid, thiamine, mirocholic acid, methylfolate, and methionine are needed. The supplement trymethylglycine also known as TMG is betaine that was extracted from plant sources. Pineapple , beets and golden rod are high in betaine. Betaine, along with glutathione. TMG lowers the burden on the CBS pathway and also helps reduce ammonia levels. It helps the body to recycle phenylalanine preventing it from being converted to ammonia.
PCYT2 inhibition causes weight gain and overexpression can cause weight loss. Low PCYT2 Expression can cause diabetes type 2 and obesity. Phosphate Cytidylyltransferase 2 deficiency causes increased lipid absorption. PCYT2 is found to be common in polycystic fibrosis. PCYT2 deficiency causes a rise in PUFA which causes inflammation. PCYT2 is inhibited by Liver X Receptor activation, vitamin D3 activates the LXR. Oxeysterols also inhibit PCYT2. Oxysterols are cholesterol derivatives.
Leptin causes problems in inflammatory bowel and improving leptin sensitivity is important. Being sensitive to leptins can cause weight loss. Leptin resistance is different it causes obesity. It is important to decrease leptins until the issue is resolved. When you eat leptin it signals that you are full, it lets the brain know to stop eating. High leptin levels will cause the brains letpin receptor to become desensitized to leptin. Processed sugar can desensitize the leptin receptors. When that happens we will keep binge eating. High testosterone and high estrogen levels can cause leptin resistance. High insulin levels can cause leptin resistance. Leptin resistance can cause carbohydrate cravings. Leptin resistance can cause high C-reactive proteins in the body. That causes inflammation and can cause high unbound copper levels in the blood.
High leptin levels can cause osteoperosis and joint damage. Leptin increase metalloproteinase enzymes which cause cell death of the chondrocytes the cells that produce cartilage. High Leptin levels can cause autoimmunity. Leptin resistance also causes elevated free fatty acids.
When functioning properly as we eat and fat levels rise leptin goes up signaling that we have enough calories. When fat levels drop leptin levels go down signaling we need calories. When a person becomes leptin resistant they will feel sluggish because the body tells them to rest to preserve calories because the brain thinks they are starving. Losing weight causes a drop in leptin which will increase hunger. Inflammation, infection, high free fatty acid levels and high leptin levels can cause leptin resistance. This can lead to type 2 diabetes, hypertension, atherosclerosis and insulin resistance. Low melatonin levels can cause this. Studies have shown those who have leptin resistance improve when they get more sunlight. Being deficient in certain gut bacteria can also cause leptin resistance. The gut bacteria that keep us from developing leaky gut and the ones that produce short chain fatty acids prevent leptin resistance. Also health conditions like acidosis and alkalosis can cause changes in FFA levels. Acidosis can reduce FFA levels in the blood. Alkalosis can increase FFA levels. Those with acidosis should not drink alcohol because it increase acidosis. Alcohol consumption causes an increase in acetate which causes the PH of the blood to become more acidic over consumption can cause lacticacidosis.
Things that help with leptin resistance are avoiding processed foods, avoiding consumption of processed sugars including fructose and even processed honey can contribute to it. High T4 levels can cause leptin resistance which could indicate COMT deficiency and high estrogen levels. Honey that is raw does not seem to have these effects. Increasing protein consumption improves leptin sensitivity.
Leptin sensitivity is different, it is caused by leaky gut and causes fatigue, mental illness, skin rashes, allergies, nausea, muscle weakness, numbness and you become more prone to illness. You will also develop gas, bloating, headache, indigestion , diarrhea/constipation and may develop autoimmune or generative disease. Lectins should not be mistaken for Leptin which is different.
This will make you sensitive to nuts, grains, eggs, milk products, legumes, seeds, potatoes, melons, squash and other high lectin foods. Those with lectin sensitivity will usually be underweight but not always. High ketone levels can cause leptin resistance.
Herbs that reduce inflammation and also Omega 3s which help reduce inflammation increases leptin sensitivity. Correcting things that can cause disrupted sleep patterns increases leptin sensitivity. Also addressing infections will improve leptin sensitivity.
Leptin is produced in fats cells in the body. When a person loses weight the fat cells release leptin which makes the body think it is starving. High leptin levels makes us more sensitive to pain. It can also makes us more susceptible to allergies. High leptin levels can cause inflammation.
Phospholipase A needs reduced it is high in inflammatory disease especially inflammatory bowel. High Phospholipase can be caused by infection, toxins like mercury and fluorquinolone injury. Farm chemicals found in our food especially glyphosate can also cause high PLA levels. This leads to leaky gut, gut inflammation, it can eventually lead to many metabolic issues, it can cause arthritis, heart disease, it can damage the liver and pancrease. It can also damage cells and cause cell death.
Those with high PLA levels should avoid Omega 6 fatty acid. PLA increases the fatty acids in the body that causes inflammation and it also increases inflammatory cytokines. It can also increase substance P levels which increase inflammation. It also causes lipids to be oxidized which can prevent the body from being able to properly use fats which are very important for our health. Our brains need fat so it can lead to mental illness. It also causes oxLDL levels to become high.
Some things that inhibit PLA are bitter melon, Omega 3 fatty acids, butyrate found in butter, magnesium, P5P, curcumin, indole, Ginkgo Biloba, Gotu Kola, Ashwangha, Tamarind and natural COX inhibitors reduce PLA.
HSP70 Stimulation helps resolve many issues with inflammatory bowel.
Most with imflammatory bowel need to increase CO2 levels.
Natural calcium channel blockers like hawthorn and magnesium help with inflammatory bowel.
Increasing Ghrelin and motilin improves digestion and gut motilility.
Almost all with inflammatory bowel have high benzoic acid levels and need to reduce it.
Most with inflammatory bowel have high estrogen levels. Inhibiting Sulfatse helps reduce estrogen.
SULTE1 is inhibited and needs increased.
NRF2 activation will increase estrogen sulfotransferase which will decrease estrogen. Selenium is needed.
Chaste berry reduces estrogen and increases progesterone.
Passion Flower is high in chrysin which reduces estrongen but long term use can damage the liver. It also reduces pain and anxiety.
Ellagic Acid reduces estrogen
Maca root restores hormone homeostasis and so does suma root. Kudzu does but should not be used by those with high acetaldehyde levels.
MOGAT3 is disregulated in inflammatory bowel. High levels cause weight gain and low levels cause weight loss.
Heme is usually low in inflammatory bowel but Fe3 levels are usually high. Lactoferrin and curcumin help with this. They restore iron homeostasis but if you take curcumin for to long it can chelate iron from the body causing anemia. Stimulating lipocalin 2 with knotgrass can also restore iron homeostais in the digestive system.
UDP-Glucose is usually low in inflammatory bowel and needs increased.
Many have problems with vitamin D mushrooms have a type of vitamin D the body can easily convert and use and usually will help those who have vitamin D issues.
Oxesterol is usually high in inflammatory bowel.
Cholecystokinin is usually high in inflammatory bowel. Things that reduce CCK are trypsin, capsaicin, amylase, stimulation from cold, calcium channel blockers like magnesium and hawthorn, or calcium chelators.
PKC,Pka, CamK2, cAMP and Calmodulin are low in inflammatory bowel.
T4 is high in inflammatory bowel. Reducing IL1, IL-b, IL-6, TNF-a, and interferon B will reduce T4. Increasing iodotyrosine, deiodinases help recycle thyroid hormones restoring homeostasis. Iodine, selenium and tyrosine are needed. This can cause high B-OHB levels, high ketone levels and can eventually lead to ketoacidosis. This also causes increase in glucokinase. This can cause high Glucose-6-Phosphate levels which will disrupt lipid homeostasis. N-acetylcysteine decreases G6P activity.
High Aspirin and high heperin can cause high T4 and may need reduced.
High T4 levels is usually and indication of high porphyrin levels which can be caused by metabolic issues or high acetaldehyde levels.
Reduce arginine vasopressin if plasma glucose and sodium levels are high increase it if they are low.
Quinolinic acid is high in inflammatory bowel this is caused by tryptophan issues. Tryptophan is needed so we cannot avoid it 5-htp supplement will usually prevent this.
Glycyl-Alanyl-Histidine is usually low and needs increaseased.
Many with inflammatory bowel have high oxalates. Sodium Benzoate used in pickles will increase hippuric acid which reduces oxalates. Also phenolic compound will decrease oxalates these are high in fresh fruit juices.
SLC2bA1 is low in inflammatory bowel. It needs B1, B2, B3, B6, calcium, colbalt,and alpha lipoic acid. Inhibited SLC2bA1 caused poor B6 activity. B1 needs magnesium and manganese. B2 needs ATP and magnesium. B6 needs zinc, lysine, magnesium, thiamine, and niacin.
Most with inflammatory bowel have low methionine synthase levels. This will cause D3 to not be converted and the body will change it and store it instead of using it. This can lead to parathyroid issues.
Most with inflammatory bowel are low in vitamin K2 levels.
Inflammatory bowel causes Alanine glyoxalate and glyoxalate reductase deficiency. These need increased.
P5P stabilizes AGT
Need to get your gut bacteria straightened out it is causing high H2S levels which binds to cytochrome oxidase which slows the metabolism down.
You need to avoid all oils as much as possible and only get medium chain fatty acids like coconut oil and palm oil. Cod liver oil would help also but make sure it contains lemon juice, it usually oxidizes quickly if it doesn’t.
Fulvic acid and humaric acid are the same but the body can more readily use fulvic acid. Continue to use it.
I believe if you supplemented Oxaloacetate it would help your citric acid cycle and bile flow.
Acryl-CoA:cholesterol acetyltranseferase is reduce in inflammatory bowel which effect bile production. It also inhibits function of the Krebbs cycle. Malic acid and B12 are needed to restore ACAT.
Many with inflammatory bowel have SOUX upregulation which upregulates the CBS pathway which leads to high sulfide levels which can inhibit sulfation. Reducing high sulfur goods and getting sulfate a form of sulfur the body can readily use will help. Water from volcanic sources and hot springs are high in sulfates. This can cause low NADH , low ATP levels and low vitamine E levels. It can also deplete malic acid. P5P, molybdenum, manganese, selenium, and magnesium usually help with this. Also soaking in epsom salt and getting 20 minutes of sunlight will help more if you are dark complected.
Inflammatory bowel causes Serine Dehydratase deficiency so it needs increased.
Diglycinate incereases stomach acid levels, it is a type of glycine. Those who have glyoxalate issues may not be able to take this one.
Hexokinase is low in inflammatory bowel. Increasing it helps .
MT-Kinase is low in inflammatory bowel.
GLP-1 is high and GLP-2 is low in inflammatory bowel.
Increasing GIP helps with inflammatory bowel.
DPP4 regulates dipeptidyl peptidase. Upregulating helps with inflammatory bowel. IL-1a increases DDP4 activity. It is also known as fibroblast growth factor.
Protectin 1 is low in inflammatory bowel.
Gycogen synthase is high in inflammatory bowel. Bioavailable copper is needed to reduce it, lithium, zinc, melatonin, curcumin, quercetin, cinnamon, and angelica reduce it.
Stimulating PGC1 helps restore glucose homeostasis. It also stimulates HNF4a. PQQ, curcumin, green tea, vegetables and fresh fruit juice stimulates PGC1.
HNF4 gene regulates TCF7L2. Increasing TCF7L2 improves blood glucose levels, and strengthens intestinal barriers. Most fats inhibit TCF7L2 medium chain fatty acids are required to prevent inhibiting TCF7L2.
Arginine methyltransferases (PRMT) enhances HNF4a. P38 is needed to phophorylate HNF4a.
High Tyrosine Kinase levels inhibit HNF4a.
Inceased cAMP/PKA activity inhibits HNF4a activity.
AMPK inhibits HNF4a.
PGC1a activates HNF4a.
SRC1-3 are steroid receptors. Enhance activity increase HNF4a activity.
Hes6 is a transcriptional factor in HNF4a displaces cofactors of PG1a and CBP from HNF4a. Ketones causes it to become down regulated.
Deficinecy in HNF4a dcreases bilea dn raises T4 levels. Stimulating PXR helps resolve this.
Increasing phosphorylatiohn of FOXO1 by insulin P13K pathway reverses repression of HNF4a via SREBP+FOXO1.
Inflammation and metabolic issues decreases HNF4a.
Increasing SHBG reduces estrogen.
Increasing prohormone convertase 2 enzyme helps restore glucose homeostasis.
Reducing glycetin helps restore gut motility and reduce excess insulin.
High AMPK levels inhibits protein producion and is high in inflammatory bowel.
Oxaloacetate is low in inflammatory bowel witch cause high B-hydroxylbutyrate, it also causes Acetyl-Coa to be shunted towards ketone body production which inhibits histone deacetylase. This also leads to inhibited gluconiogenesis, inhibited urea cycle, inhibited glyoxalate cycle, inhibited bile acid production, inhibited amino acid synthesis and inhibited citric acid cycle.
Increasing NADHP and decreasing NADH increases citrate cynthase and can help restore proper citric acid cycle function.
AGT function is usually inhibited in inflammatory bowel causing high oxalates and inhibited mitochondrial function.
Increasing P5C reductase and Proline oxidase helps with inflammatory bile. They require ornithine.
After the citric acid cycle is functioning increasing Hydroxy Proline Oxidase to help with inflammatory bowel.
KIM1 levels are high in inflammatory bowel which can damage the liver.
All these need increased to help with the many health issues caused by inflammatory bowel. L-Propyl-L-Proline, N-acetyl putrescine proline, taurine, uric acid, L-Pipecolic Acid, L-methionine, N-Acetyl-L-Methionine, 3-Methoxytyrosine, 7-methylguanine, unsaturated fatty acids like decatrienic acid and sebacic acid. Phenylacetic acid and phenylacetyl-glycine need increased.
Nicotinate and nocotinamide are low and need increased.
Need to increase B vitamins using bioavailable forms works best and should be taken with food to prevent a sugar crash and flushing.
Cindoxyl,3-hydroxyquinoline, 3-methyl oxyindole, indoleacryilic acid, indolxylsulfuric acid and xanthurenic acid need increased.
Taurocholic acid needs increased.
Kynurenine needs increased to prevent high quinolone levels.
Taurine needs increased to prevent high ammonia levels, reduce oxidative stress, increase bile flow. Glycine helps for those who do not have glycine issues.
Chondroiton sulfate helps reduce oxalates. I had sulfation issues but it did not seem to raise my sulfide levels.
Need to increase Taurocholic acid and taurodeoxycholic acid.
Need to increase carnitine to improve B-oxidation of fatty acids. This should increase Propionyl-L-carnitine which reduces NOX4 mediated oxidative stress and restore endothelial function.
Need to increase protein metabolism, betaine, bromelain, P5P, magnesium, molybdenum, manganese, cobalt , selenium usually help with that.
Vitamin C needs increased to help with metabolic processes but should be used in moderation in those with inflammatory bowel because to much vitamin C in those with inflammatory bowel can cause excess to convert to oxalates. That is the result of ascorbate 2-sulfate deficiency.
Inhibiting HAO1 prevents excess D-ammino acid activity. It prevents glycolate from being converted to glyoxylate.
Increasing Lactate dehydrogenase reduces oxalate in the renal system.
AGXT (serine-pyruvate aminotransferase) is needed to detox glyoxalate. Marshmallow root increases AGXT.
Increasing Etholamine pretects cells from ROS, restores cellular membrane function and signaling and improves bile flow.
Increasing D-bifunctional protein prevents muscle weakness, seizures, fatty acid accumulation, decreases palmitoyl CoA oxidase, peroxisome thiolase and branch chain acyl-CoA.
Increased phytanic acid oxidase prevents fatty accumulation in the liver. Excess branced chain fatty acids inhibit phytanic acid and cause it to accumulate in the liver which leads to hyperkerotosis. Increasing urea can help with this. This can also lead to adrenoleukodystrophy which causes the enzymes for fatty acid to not to function properly causing very long chain fatty acid build up. This is caused by ABCD1 issues and can result in cerotic build up.
Lorenzo’s oil can correct this conditon. It is 4 parts glyceral trioleate and 1 part glycerol. These are forms of oleic and euric acid made from olive oil and oil from olive seed. If not corrected ti can lead to the accumulation of VLCFA which causes A-Methylacyl-CoA Racemase deficiency. This can cause an accumulation of bile acids. Reducing phytanic and pristanis helps.
Dequaliniun Chloride helps resolve AGT deficiency and AGT misdirection.
By correcting issues causing excess ketone it will reduce acetoacetate, beta-hydroxybutyrate and acetone.
Increasing Pyridine nucleotides improves redox status.
Increasing NADPH oxidase increases SOD. This also blocks inflammatory causing enzymes, reduces cyclogenases and prevents thrombosis.
Increasign Lipoxin A4 decreases inflammation
Increase NADK to improve NAD binding and improve phosphorylation. Magnesium, zinc and CO2 are required.
Reduce PKC to reduce inflammation and gene overexpression.
NADPH oxidase over activation depletes NADPH. Inhibiting it can raise NADPH levels. Tripterygium wolfordii and magnolia inhibit NADPH oxidase. Nitric Oxide also inhibits NADPH oxidase. Gingko biloba inhibits NADPH oxidase but there are studies showing using it for three months or more may damage the liver.
Iron overload decreases NADPH. Lactoferrin, curcumin, and lipocalin 2 help restore iron homeostasis. Taking curcumin for to long can make you anemic because it chelates iron .
Reducing hemolysin prevents thrombosis and fibrosis and reduces H2S. When H2S levels are high it can lead to inflammation and low blood pressure.
Gut bacterias effects on inflammatory bowel.
Those who have inflammatory bowel are defecient in Short chain fatty acids. Akkerinmania municiphila, roseburia intestinalis hominis, inulinivorans faecis ceciola regulates metabolism, produce butyrate and SCFA. They also help restore our beneficial gut bacteria.
Lactobacillus Casei and L Longhum have to be taken together one cannot exist without the other. They keep the antioxidant system at homeostasis and also regulate autophagy.
Lactobacillus reuteri produces folate.
Bacillus infintas reduces inflammatory bowel
Bacillus subtilis produces antibiotics and protects the gut from infection.
Bacillus Clausii prenents diarrhea and reduces inflammatory bowel.
Most with inflammatory bowel have high copper these are some things that may help. This also improves bile flow.
4 ounces of fresh orange juice
¼ teaspoon of sea salt
8 ounces of coconut water
60 mg whole food vitamin C
3 teaspoons of cream of tartar.
For the adrenal fatigue caused by high copper adaptogens like maca root and suma root help. Magnesium, boron, sodium bicarbonate and B vitamins from mushrooms or bee pollen, kelp for iodine and eggs for biotin. Taurine for the liver, molybdenum chelates excess copper. Do not take high doses of vitamin D it inhibits cerruloplasmin raising unbound copper levels. Fluoroquinolones, fluoride, glyphosate can cause high unbound copper levels and will need to be detoxed. Silica helps reduce unbound copper levels.
SULTE1 upregulation improves bile flow and reduces estrogen and reduces high levels of biounavailable copper. Increasing Adenylcyclase also helps.
Increase vitamin K2 to prevent oxalates.
BH4 is needed for proper eNOS function. BH4 inhibits excess gluconeogenisis. AMPK suppresses effects of BH4. High AMPK levels lead to high ketone levels.
GTP (quanosine trisphosphate) is the rate limiting enzyme for BH4 enzyme. Increasing GTP reduces excess succinate in the TCA cycle. Restoring NO bioavailablility and increasing DHFR with folinic acid restores BH4 levels. 5-HTP will also help restore BH4 levels.
A deficiency in BH4 can cause a B12 deficiency.
AMPK Kinase inhibits cholesterol production which negatively impacts bile production, Excess Nitric Oxide activates AMPK Kinase
Fumarate increases oxidative phosphorylation in the Krebbs cycle to reduce ketones, and lactic acid. This will increase adenosine monophosphate.
Cholestasis needs resolved . Increasing bile salts and medium chain fatty acids help and improves bile flow.
Cyclohexancaroxaloic acid, propanoic acid, buranoic acid, decanoic acid and hexanoic acid. Cicetic and Petane. Reduce inflammatory bowel.
NAC and threonine can help.
Allicin reduces acetic acid producing bacteria.
Pantothenic acid cannot function if biotin is low.
If Lipoate is deficient the antioxidant system cannot function.
Biotin requires butyrate and acetate to be absorbed. Low biotin levels causes high B12 levels because your body will be unable to convert it. Brewers yeast and eggs are high in biotin.
Hydroxylase syntase deficiency cause a loss in the ability to metabolize proteins, fats, and carbohydrates. It is dependent on biotin.
When you have inflammatory bowel you have to take nutrients in this order. First biotin, adenosylcobalamin then choline. Then sunflower seeds, mushrooms, small amounts of whole grains, bioavailable forms of B vitamins, and methyl groups.
N-methyl transferase needs increased in those with inflammatory bowel.
N-methylglycine needs increased to prevent psychosis and depression.
Increasing Alkaline Phosphatase increases the guts good bacteria. Cissus Quadrangularis increases it and so does curcumin, cod liver oil, zinc also increase ALP.
ALP stimulates bone growth.
FXR needs stimulated it is inhibited in inflammatory bowel. This corrects cholesterol production, bile production and reduces inflammation.
Motilin needs increased to improve bowel motility and prevent GERD.
Metlatonin needs increased to correct many issues.
Things that may decrease estrogen.
Inhibiting ERa receptor decreases estrogen. Genistien, diadzein, ursolic acid, green tea, kaempferol and narigenin, and phloretin found in apple leaves inhibit ERa. These also reduce Cholecystokinin.
Other things that reduce CCK are ursolic acid found in apple skins and leaves which also contain phloretin which inhibits CCK. Grapes, tomatoes, squash, thyme,rosemary , lettuce, St Johnswort, aloe vera, moringa, elderberries and endive reduce CCK.
Stimulating complement protein C2 reduces estrogen. Cod liver oil, phytoestrogens found in plants, DIM, B12, P5P, Magnesium, and increasing SAMe will increase C2 . It is found a part of the immune system so you do not want to overstimulate it.
To repair cells fructooligosaccarides and glycerophopholipids are needed. Also fructans, pectin, Beta glucans and resistant starches are needed. Many of these can be found in raw milk, clostridium, and whey protein, along with mushrooms and seaweed.
SHBG-sex hormone binding globulin is a protein when found in high levels will cause obesity , type 2 diabetes. Low levels cause hyperthyroidism and autoimmunity. To much SHBG binds up testosterone. SHBG is the master regulator of testosterone and estrogen. High SHBG levels raises estrogen. Low levels will cause hardening of the arteries and inflammation. Low LDL levels and high tryglicerides. High insulin and high prolaction levels. Can raise estrogen and thyroid hormones. High estrogen and high Thyroid hormones increase SHBG.
ABCB4 if inhibited will inhibit bile. ABC proteins transport molecules across membranes. Phosphatidylcholine is it’s substrate. T3 activates ABCB4,
Cyp7a1 inhibition will inhibit key liver bile enzmes. LXR activators increase Cyp7a1. Taurine enhances Cyp7a1 activity.
IBAT inhibition helps with inflammatory bowel. It improves cholestatic pruritus, helps with biliary cholangitis. It also increases ursodeoxycholic acid which increases bile production.
Increased FGF19 increased bile.
Most with inflammatory bowel have a pyruvate carboxylase deficiency. To increase it phosphatydil choline, biotin, chloroacetic acid which is found in asparagus, red algae and seaweed are needed. Also medium chain fatty acids are needed. Thiamine, phosphate, and magnesium are needed. Read apples and cheese also increase it. Triheptanoin also known as C7 will increase it. This helps restore the citric acid cycle function.
Most with inflammatory bowel have disregulated insulin and glucose levels. Bitter melon taken with sinocrassula indica restore insulin levels and glucose homeostasis.
To break down carbohydrates amylase, brush border enzymes, lactase, maltase, isomaltase, and sucrose activity are required.
SGLT1 deficiency with inhibit glucose absorption causing low glucose levels. This can lead to high ketone levels.
Need to correct issues causing SCFA deficiency and need to reduce branch chain amino acids in obesity but increase them in those who are under weight.
It is very important to reduce estrogen because it increases biounavailable copper. Low oxidizers also have high biounavailable copper. Low oxidizers are usually too alkaline.
Things that help with adrenal fatigue caused by high biounavailable copper is meditation, reduce stress, reduce fear, molybdenum, manganese, selenium, B Vitamins, Vitamin C and vitamin E.
Gut dysbiosis and candida can cause high acetaldehde levels. This can cause you to become intoxicated.
Nad-linked aldehyde removes excess acetaldehyde. ALDH2 gene regulates ALDH.
Other enzymes that remove excess acetaldehyde are adehyde oxidase, xanthine oxidase, glyceraldehyde-3-phosphate dehydrogenase oxidises acetaldhyde. Those who have high acetaldehyde should not use Kudzu it raises acetaldehyde levels. Vitamin B1 is also needed to reduce acetaldehyde. Xylitol inhibits bacteria production of acetaldehyde.
Things that can inhibit enzymes that break down acetaldehyde are biogenic amines, noneal, dopamine, noradrenaline, serotonin, and long chain lipid aldehydes.