Things that can go wrong in the gut and how you may be able to correct them.

This is not medical advice I am posting this for educational and informational purposes.


Always remember homeostasis is the goal.

This is not finished but I need to work on other things and I figure this will give people a good foundation to research and build on.

Lipopolysaccharide (LPS) is usually used when referring to pathogens. Our commensal microbes produce LPS which our body uses to identify them. Normally they are not harmful to the body and some of the other commensal consume LPS keeping levels down. But a loss of those commensal or leaky gut can cause LPS to enter our blood streams which can lead to sepsis so it is very important to protect and maintain the health of our guts.

If we develop leaky gut and do not correct it toxins like mercury that can be in our food and usually will get excreted can now easily enter the blood stream and a person may develop high levels of mercury, cadmium or other toxins in the body.

If you have leaky gut oxalates that usually get excreted can enter the body. It is very important to heal the gut because oxalates are very damaging to the body. Calcium will bond with oxalates preventing them from being absorb and is why if a person is lactose intolerant they need to work on correcting it because milk with meals would help prevent that. Some calcium supplements are not good for you so if you decide to take that route make sure you do your research. Once oxalates build up in your body it prevents the gut from healing so it is very important to reduce oxalate levels. I have posted on reducing oxalates.

There are 2 components to the intestinal barrier. Intrinsic barrier and extrinsic barrier.

Intrinsic barrier is composed of the epithelial cells lining the digestive tube and tight junctions that tie them together.

Our gut bacteria maintain the health of our gut but damage to our gut can inhibit FUT2 production. Our gut microbiome cannot get established if we are deficient in FUT2. Lactobacillus Casei increases FUT2 production by inducing ERK/JNK. Inducing ERK/JNK stimulates FUT2. Nitric Oxide induces ERK/JNK, arginine rasises NO levels. Hypoxia induces ERK/JNK. Interleukin 10 inhibits FUT2 so a person may want to be cautious when taking probiotics that stimulate IL-10. Lactobacillus species of microbiotia stimulate IL-22 especially L Johnsii. IL-22 stimulates FUT2 secretion.

Extrinsic barrier consist of secretions and other other influences like microbes that influences the epithelial layer but are not physically part of the epithelium cells and maintain their barrier function.

Intrinsic Intestinal Barrier.

The gut is lined by sheets of epithelial cells that define the structure of the mucosa they are tied together by tight junctions, which paracellular spaces and thereby establishing the basic gastrointestinal barrier. Paracellular spaces are were nutrients are transported into the blood stream and toxins can be transported to the intestines for removal. Toxins and microbes that are able to breach this barrier have unimpeded access to the circulatory system. The tight junction layer and the mucus membrane for the most part prevents this from happening when healthy. Some cells in the epithelial are not effected by acid but others do not have the protection so count on the mucus membrane to protect them.

Extrinsic Barrier

Mucus that coats the entire epithelium. Hormones and cytokines that regulate the function of our digestive system and maintain digestive health. Our gut microbiome are a part of the extrinsic barrier. They reside in the mucus membrane.

Tight junctions encircle the epithelial cells and are an important part of the intrinsic layer. Their permeability is regulated by zonulin.

Tight junction controls the equilibrium between tolerance and immunity to non-self antigens. It is involved in macromolecular transport and tolerance and immune balance. If the tight junction layer becomes too porous a person may develop autoimmunity and their bodies immune system will turn on the body and start causing autoimmune disorders. A person will develop food allergies and food intolerances. The longer this goes without being addressed the more a persons health will decline. They will develop many metabolic, genetic and immune dysfunctions. Many things can damage this vaccines have been shown to raise B cell levels which causes the tight junction layer to become more porous. BT Toxins in GMOs have been shown to cause the body to react in a way that the tight junction layer becomes more porous. Many farm chemical cause it to become more porous especially glyphosate and glufonisate cause it to become more porous. Stress and trauma can also cause the tight junction layer to become more porous.

Zonulin is the only intercellular modulator of the tight junctions. If zonulin becomes over expressed the gut becomes more porous leading to leaky gut. It is involved in the transport of macromolecules and in balance between tolerance and immune response balance. If zonulin becomes deregulated it can cause inflammatory bowel, anemia, systematic inflammation, red sore areas on the skin known as Sweet’s syndrome that can eventually develop into blisters that eventually turn ulcerative which is known as Pyoderma Gangrenosum. They can develop swelling and sores in the mouth. The eyes can become red sore and inflamed. This condition is called sceritis it can lead to uveitis which effects the iris and can lead to blindness. Bones may thin and become brittle. Oxalates will develop causing stone formation this can also effect the liver. Not only can it cause endogenous oxalates to be produced but now oxalates consumed in our foods that are normally excreted can readily enter the body. Gall stones may form because bile production and pancreatic enzymes become inhibited and a person can develop chronic diarrhea, constipation or alternate between the two.

When the bile is inhibited it is called Primary Schlerosing Cholangitis. From food particles and toxins entering the blood stream a person could start having excessive blood clotting. A person will start developing nutrient deficiencies from being unable to absorb and break down nutrients properly. A person will eventually develop high histamines if this continues they may develop asthma, they can start developing sarcoidosis throughout the body. Mast Cells can start to degranulate leading to mastocytosis or mast cell activation syndrome. This effects our immune system as you will see below. It can lead to diabetes, heart disease and many other chronic illnesses. It can also lead to obesity or anorexia depending on how the person has been effected.

In order to restore zonulin levels to normal the genetic, metabolic, oxidative stress, changes in ph for example if you have developed acidosis or alkalosis it will have to be addressed along with infections that come along with our immune system being disabled. I have posted on most of those issues and correcting them. There are three isoforms of zonulin. ZO- 1 , ZO-2 and ZO-3.

When we get an infection it is a sign we are lacking a nutrient or gut microbe that protects us. The infection produces lipopolysaccharide (LPS) which stimulates zonulin making our guts more porous. Also antibiotics can kill the butyrate producing gut bacteria which makes our gut more porous. Butyrate keeps many things at homeostasis. We cannot restore normal zonulin levels if we do not replace the butyrate producing bacteria and feed them with fiber, oligosaccharides, galactosaccharides, and fructooligosaccharides. The lower the diversity of our gut microbes the higher our zonulin levels will be showing that our digestive system needs feedback from a variety of microbes to function properly.

The fun part of all of this is they will tell you all this in in your head until you are so ill it will take months or years to heal. In the mean time they will still continue to treat the symptoms instead of the cause. It is a common theme with allopathic medicine. I have seen this with naturopathic also but for the most part naturopaths treat the cause and not the symptoms.

Things that can reduce zonulin is meditating, if you have experienced trauma work very heard to move forward. It is difficult not to look back but constantly looking back causes stress and can increase zonulin. Anger increases zonulin so try to learn to deal with frustration and bad situations in a calm way , the calmer we are the lower our zonulin levels will be.

Replace the butyric acid producing bacteria I listed many microbes that produce it if you search my blog.

Inflammation and immune dis-regulation and can increase zonulin so the microbes that increase T regulatory cells and inflammation will reduce zonulin. If your immune system has been disabled then microbiome that stimulates IL-10 will help restore immune function.

High LPS levels will increase zonulin so we need the gut microbes that reduce LPS. Studies have shown the higher our guts diversity the less ZO-1 is express which prevents leaky gut and inflammation.

Under normal conditions things with gliadin , glutin and lactose will not effect a healthy gut but increase zonulin when the mucus membrane is damaged.

There are many molecules that interact with each other to maintain the Zonulin layer and the tight junction layer.

Occludin plays a role in tight junction maintainence and assembly which is regulated by phosporylation of serine, threonine, and tyrosine risidues. It is important for maintaining TJ stability and function. Loss of occludin can lead to leaky gut, inflammatory bowel, and hyperplasia most likely from the inflammation. Occludin also regulates cell survival or death through the intrinsic system. It is important in receiving and transmitting cell survival signals. Occludin has a strong inhibitory effect on cancer. Loss of Occludin leads to cell death.

If Phosphorylation of tyrosine, threonine and serine residues is inhibited it reduces occludins interaction with zonulin. Dephosphorylation of ser/thr residues and poor phosphorylation of tyr residues causes a reduction in occludins interaction with ZO-1 leading to it’s seperation from the junctional complex and TJ disruption. It also leads to excess ROS production which increases gut permeability. Inflammation reduces occludin levels. Endotoxins also reduce occludin. Another function of occludin is in modulating the TJ response to cytokines to protect and heal the tight junction. Occludin plays an active role in cellular location of caveolin-1. Caveolin-1 is required for cytokine induced TJ barrier changes, where it is required for TJ remodeling. So addressing endotoxins, high B cell or T cell levels and reducing inflammation is very important for preserving occludin. Many of our commensals that increase T regulatory cells balance our immune system which would restore proper T and B cell levels. Many of our commensal microbes reduce inflammation and reduce LPS (endotoxins). I have posted on my blog which of those accomplish these things. TNF-a is involved in caveiolinn-1 mediated internalization of occludin which increases occludin, alleviating cytokine induced gut permeability. This can be induced by TNF-a which is an inflammatory cytokine.

Mucous Membrane

The mucus membrane is thin in most inflammatory bowel diseases but is thick in Chron’s disease which I have not researched much on. Inflammtion usually causes the globin which are the mucin secreting cells to become depleted but for some reason this does not happen in Chron’s disease.

All these genes listed below are negatively effected by leaky gut. It is very important to reduce inflammation and work on getting the gut healed to restore the mucous membrane. Damage to the digestive system and mucus membrane causes many genes to become dis-regulated. MUC2 gene is the major gene responsible for the secretion of gel-forming mucin in the intestinal tract. It coats the endothelial surface protecting it from inflammation,chemicals, damage and infection. There are 20 MUC genes. There are many mucin categories that are enriched with proline, serine, and threonine. They are modified by o-glycosylation that creates oligosaccharides that confer on mucins their individual functions. Mucin is made mostly of fat. Those with inflammatory bowel and ulcerative colitis have low B-oxidation which is needed for the break down and use of fats. Since the mucous membrane is mostly fat this causes it to become dysfunctional. This makes people sensitive to fats and is why it is best if they consume medium chain fatty acids because the body can readily use them. Eggs yolks are a good source of phosphatidylcholine which is what the mucus membrane is mostly made of. Most with inflammatory bowel or colitis are sensitive to lecithin. I used sun flower seed lecithin and I did not react to it and it helped me a lot with my healing. Most other sources of lecithin I had to avoid. There are many studies showing that using sun flower seed as a source of lecithin has been shown to heal the gut. As for Chron’s disease I have a theory I have not had a chance to research but I believe they may be deficient in commensal microbes that digest sialic acid. Many of our commensals need it to thrive. Bacteroides Fragilis, Bacteroides Thetaiotaomicron, Bifidobacterium Bifido, Bifidobacterium Longhum, Bifidobacterium Infantis, Akkermansia Muciniphila all need sialic acid to thrive. Another theory I have about Chron’s that I have not gotten to research is they may have an overgrowth of those and that inflammation or LPS is stimulating the production of excessive sialic acid causing and overgrowth of those microbes.

Phospholipase A2 activity is higher in those with inflammatory bowel and colitis.

If a person is having trouble with methyl donors they will not produce enough phosphatidylcholine because methyl groups are used in the process of producing phosphatidylcholine for the mucous membrane. So combine that with the low B-oxidation and you see why it can be so difficult to heal. Disulfide bridges are also a component of phosphatidylcholine showing the importance of addressing things that can impair sulfation.

Phospholipase A2 is high in those with inflammatory bowel and colitis. Phospholipase is stimulated by inflammation. It is a mixture between inflammation and substance P and is why those with leaky gut have high substance P levels. When substance P levels get high the skin will have a burning sensation especially in the scalp and it may go down the spine. Substance P levels increase at night so the symptoms will worsen at night.

Annexin also known as lipocortin keeps PLA2 in check. Adrenal hormones increase Annexin but in many people with inflammatory bowel the adrenals become depleted from being over activated and they develop Addison’s disease which is a deficiency of adrenal hormones. Adaptogens help alleviate this which would help restore annexin levels. Annexin also helps repair our immune system. If annexin gets low the blood brain barrier becomes porous because it helps maintain the blood brain barrier. Annexin is also involved in protecting the brain from infection. It is very important to support the adrenals with the proper nutrients and to reduce inflammation so the adrenals can recover. Oddly Okadaic Acid a toxin found in shell fish increases annexin. This is something a person would definitely need an experienced medical professional to do. IL-6 increases annexin expression. To restore normal cortisol levels stress management is very important. Increased stress depletes cortisol. Getting rest is important, even if you cannot sleep just laying and resting can help increase cortisol. Avoid, caffeine, alcohol and smoking. Our mucosal layer will take up fats and integrate them to strengthen itself. Omega 3 oils, cod liver oil, nuts, and avocados help increase cortisol. Avoid processed sugar it depletes cortisol levels. Citrus fruits especially grape fruit increases cortisol but grape fruit inhibits certain cytochrome P450 enzymes so should not be eaten too often. Eat foods high in melatonin or take melatonin supplements at night which will increase cortisol. Non processed carbohydrates help increase melatonin. Magnesium is important for maintaining proper cortisol levels. Reducing inflammation can help normalize cortisol levels. Earth grounding and getting sunlight help to normalize cortisol levels. I still laugh when I mention earth grounding because I thought how could something so simple have so many health benefits. So I was determined to find research to show those earth grounders were crazy instead it was I who was crazy and the earth grounders are correct. I could find no research to prove them wrong but plenty of research showing the many health benefits of earth grounding.

We have to keep in mind goblet cells build our mucus membrane and when inhibited by inflammation, toxins or even damage to our digestive system our ability to produce mucin is reduced or inhibited. Bismuth even though it is a metal, is for the most part none toxic it takes very high doses for a very long time to reach toxic levels. It helps the gut heal. It kills many pathogens and can cause commensals that have turned pathogenic to go back to commensal. Mucilage helps protect the gut so it can heal. I have posted on reducing inflammation if you search my blog. Oatmeal is high in mucilage but you must get organic because they use glyphosate and glufonisate on grains and beans to dry them and those destroy our gut and kill our gut microbes. Three very good sources of mucilage is okra, arrow root and oatmeal. Make sure the oatmeal is organic. Most non organic oatmeal has farm chemicals that destroy the gut.

Here is an in depth article on mucus membranes.

Sialylation has been found to be increased in those with inflammatory bowel dieseases. Excessive sialylation increases inflammation. IL-10 inhibits Sialylation. Their are probiotics that increase IL-10 but IL-10 inhibits FUT2. So an oligosaccharide,galactosaccharride and fructosaccharide would probably have to be supplemented with it. I suspect the body is trying to increase the commensals that rely on the nutrients produced by sialylation and they have been depleted by antibiotics. Some commensals rely on FUT2 but others rely on sialylatin. Some do not produce the enzymes to break down sialic acid and rely on other commensals to produce it. A deficiency in either of them is probably what is causing the high sialylation. The body is trying to feed them. It is not getting the feedback from those commensals.

The bacteria this would help thrive are B Fragilis, B Theaiotaomicron, B Bifidum, B Longhum, B Infantis and A Muciniphila. I believe those with inflammatory bowel especially those with Chron’s will be deficient in those because those with Chron’s have a thicker mucous membrane.

The increased inflammation and infection caused by the above mentioned things results in an accumulation of ROS which can lead to further damage and it disturbs mitochondria function and autophagy. Once the mucus membrane has been damaged all the things mentioned below lose their protection and become dysfunctional. It may be necessary to take mucilage and bismuth to help protect them and restore their function. Once the mucus membrane breaks down it creates a cycle that has to be broken because the mucus membrane needs the things mentioned below to function properly and they need the mucus membrane to protect them and to function properly. Dysfunction in either of them from infection or toxins can start a cycle that has to be broken to heal. Our gut microbiome cannot become established without the mucus membrane because it also protects them. Our mucus membrane is a mediator between host and microbiota interactions. Decreased mucus membrane thickness causes a change in our gut microbiome and makes us more prone to infections.

This is where addressing sulfation issues, methyl group issues and issues with thiols comes in because the production of mucin requires all of those to be functioning. I have posted previously on how to deal with those issues. For the production of the oligosaccharides the endoplasmic reticulum and stem cell are required.

L-cysteine, L-arganine, L-threonine, L-serine, and L-cysteine increase mucin production in the digestive system and have been shown to promote gut microbiome homeostasis. Citrus fiber increases mucin especially the white part of the fruit. Pectin stimulates Goblet cell formation which secretes mucin. The microbiome that help restore gut health are Bifidobacterium Bifido, Bifidobacterium Breve, Bifidobacterium Lactis, Enterococcus Faecium, Lactobacillus Acidophilus, Lactococcus Lactis

For those who do not have glutamate issues bone broth heals the gut very quickly. Those who have high levels of sulfur digesting bacteria will have problems with the consumption of bone broth also.

The small intestine is the portal for the absorption of most nutrients in the body. The chyme which is the digested food that has exited the stomach enters the small intestine pancreatic enzymes and bile is secreted. This breaks the food down and if functioning properly it will be almost liquid when it enters the lower intestinal tract. Bicarbonate is also added by the body to reduce the acidity before it enters the large intestine. The enteric nervous system and gastrointestinal hormones regulate this process and the intestinal motility. Intestinal dysbiosis can cause incorrect communication or inhibited communication which leads to inflammation, intestinal damage and it could lead to a loss of the ability to produce bile and digestive enzymes. To restore proper function we must reduce the microbe causing the problem. Those who have high sulfur digesting bacteria will develop high hydrogen sulfide levels which interferes with sulfation and can interfere with the proper function of the CBS and BH4 pathways. This can lead to high sulfide levels in the body. BH4 levels will become low causing ammonia to build up when protein is consumed. The high ammonia levels will cause some commensals to go into protection mode and they will become pathogenic. Candida and H Pylori are two examples. To make matters worse they also start producing ammonia to protect themselves from the acidic environment. The digestive tract is supposed to be acidic. Ammonia alkalizes it this also makes us more prone to infections because the commensal microbes that protect us cannot survive in an alkaline environment. When we lose our commensal bacteria we lose proper immune function and our zonulin levels increase and our gut becomes more porous leaving things enter the blood stream that could not normally enter. Inflammation and oxalates can inhibit bile flow causing it to back up, when this happens the gallbladder is effected. Instead of addressing the problem modern medicine gets rid of the symptom by removing the gallbladder thus the illness continues to worsen and taking the gallbadder out can contribute to it’s progression.

If bile becomes inhibited it inhibits the vitamin D receptor further inhibiting bile production and adding to the problem because cholesterol production and conversion becomes inhibited. This will make bile become sludgy leading to low bile flow which will increase estrogen levels and cause high unbound copper levels in the blood. Bitter herbs increase bile flow but the vitamin D receptor has to be addressed along with balancing the microbiome in the gut and healing the intestinal tract.

This is why I often times recommend grape seed extract and bacopa to people. It prevents thrombosis. Inflammation because endotoxins can cause thrombosis. Grape seed extract and bacopa reduce inflammation and prevent thrombosis. If thrombosis occurs in the portal vein it will effect the liver, pancrease, and digestive system. This causes pain in the stomach, bloating, inflammation, pancreatic pain, pain in the gallbladder. This can lead to death. Bile flow will become inhibited speeding up the progression of portal vein thrombosis. Those with hepatitis need to use hawthorne or something else. Resveratrol activates hepatitis.

portal vein thrombosis

gastrointestinal symptoms (ex: abdominal pain, nausea, vomiting, and diarrhea), fever and constitutional symptoms (ex: fatigue, malaise, and anorexia/weight loss) [3]. We can also find hepatomegaly with elevated liver enzymes and jaundice [3], when associated with liver abscess or cholangitis [2]. Laboratory tests usually demonstrate elevated markers of inflammation [2]

If not addressed in time it can lead to portal hypertension. This results in brain swelling, abdominal swelling . Confusion, anemia and low white blood cell count.

Autophagy is very important in maintaining health and we need a proper balance. It can be disrupted if we have intestinal damage. If autophagy is inhibited we become prone to infection and mitochondrial dysfunction. Autophagy is the housekeeper of our cells. One common theme you will see is inflammation and shows the importance of reducing inflammation. Which could involve diet changes, addressing metabolic issues, reducing toxins and infections. Addressing detox issues and detoxing in an appropriate manor for the individual. Addressing gene issues which could be caused by any number of things including a lack of the microbe in the gut that may modulate that genes function.

The mucus membrane in our digestive system protects us from infection, physical and chemical harm. Our commensal bacteria cannot exist without it. It is very important to restore our mucus membrane when damaged in order to restore intestinal homeostasis. Many genes mentioned below are effected when it is damaged because it causes a dysfunction in them. Autophagy is very important for the maintenance or proper gene function.

Paneth cells are located within our mucus membranes and provide immunity, prevent damage to the digestive system and is involved with nutrient absorption. Loss of our mucus membrane from loss of microbiotia, drugs or farm chemicals found in our food can destroy our mucus membrane. This causes damage to the digestive system which can further inhibit the bodies ability to produce mucin. This makes us more susceptible to infection. Paneth cells stimulate the production of AMPs which fight infection and modulate commensal microbiome and innate immunity. A list of AMPs are defensin-like human lyzosome, defensin (HD)-5 and 6, lyzosome, regenerating islet derived gamma(Reg3y), and phospholipase A2 group 2A(sPLA2) as well as inflammatory cytokines such as Transforming Tumor Necrosis Factor A (TNF-a), Growth Factor B1 (TGF-B1), and Postaglandin E2. AMPs are sensitive to ER stress which I discuss below.

Autophagy protects against infection by producing Antimicrobial Peptides and degrading organelles that break down misfolded proteins and AMPs break down pathogens. This can ease the over activated inflammatory response and over active immune response. Some AMPs are defensin and cathelicidens which protect against microbes.

Intestinal Epithelial Cells. (IECs) – form a physical and chemical barrier involved in inflammatory response and immune reaction. IECs work as an interface between the quantitive microbial ecosystem in the intestinal lumen. Lumen is inside space or opening in a tubular structure.

There are 6 types of IECs

Goblet Cells which secrete mucin to build up the mucin barrier.

Enteroendocrine cells which produce gastrointestinal hormones that communicate with the nervous system, the brain and organs throughout the body. They respond to nutrients within the intestines. Helps restore intestinal tissue.

Absorptive Enterocytes – epithelial cells in small intestine. They are involved in nutrient absorption, absorption of conjugated bile acid, lipid uptake, Issues with Absorptive Enerocytes can inhibit glucose absorption and can result in lactose intolerance and many other food intolerances. It can also result in an electrolyte imbalance. Enterocytes secrete a series of chemokines and cytokines which regulate immune responses of subjugant mucosal. (Mucosal control)

Tuft Cells – brush cells which are chemosensory cells in the intestinal epithelial lining. Tuft refers to microvilli projecting from the cells. They increase during parasite infection. They are the sole source of Interleuken 25 which induces NF-kB activation which helps protect from infection. High levels of IL-25 raises eosinophils which causes inflammation and is suspected of causing inflammatory bowel diseases. Eosinophils have been shown to kill many types of cancer cells. Infection also stimulates Tuft Cell to produce IL-25. They are increased through a T cell response through a type of lymphatic tissue. Tuft cell also secret endogenous opioids. Eosinophils cause asthma, cardiovascular disease and can even cause headaches, mood swings and brain fog.

Microfold Villous Cells – are found in the Gut-associated Lymphoid Tissue (GALT) of the Peyers Patches in the small intestine and the Mucus-associated Lymphoid Tissue (MALT). M Cells initiates mucosal immunity. They allow the transport of microbes and across the epithelial cell layer. From the gut lumen to the lamina propria. M cells contain Epidermal growth factor which acts as a sensor to stimulate repair through the intestines including the mucus membrane , tight junction protein layer and it stimulates goblet cell differentiation and many other things in the colon.

Endoplasmic Reticulum are organelles within our cells and plays a major role in the production of proteins and lipids. So this is where our enzymes , hormones and even our detox enzymes are produced.

Endoplasmic Reticulum Stress Unfolded Protein Response (UPR) is activated in response to unfolded or misfolded proteins in the endoplasmic reticulum. It stops the production of unfolded or misfolded proteins it is the quality control mechanism. It will stop production and start cleaning the bad proteins out. If it continues for too long then it will induce apoptosis which is cell death. If overactivated which vaccines and many farm chemicals can cause to happen it can lead to prion disease. It plays a valuable role in intestinal endoplasmic reticulum survival and function. Dysfunction of endoplasmic reticulum can result from genes that have been effected from infection, toxins, or even stress can result in abnormal UPR function. This is referred to as Endoplasmic reticulum stress.

ER stress activates three kinds of proteins which reside in the ER membrane to detect UPR in ER Lumen and resolve them. Autophagy reduces ER stress.

inositol-rquiring membrane kinase endonuclease1 (IRE1) via a really long pathway that I am certain you do not want me to type out. Issues with the genes involved in these mediators in intestinal endothelial cells will change the histological structure of the intestinal epithelium.

XBP1- inhibition will exhibit impaired Paneth Cells, which leads to dysbiosis and spontaneous intestinal inflammation which may induce activation of NF-kB pathway which can lead to inflammation, anxiety, chronic depression, insulin and leptin resistance, it increases risk of cardiovascular disease and high TH17 levels which can lead to psoriasis or lupus, Many who have intersitial cystitis have high TH17 levels. It can cause bone lose and Alzheimers. On the other end of the scale not enough NF-kB can produce many health problems. Like lower cognitive function, inhibited ability to heal, inhibited nerve growth and brain plasticity. This is a good article covering it in more detail.

The second gene that can increase risk of inflammatory bowel disease is oromucoid-like3 (ORMDL3). Over expression can lead to immune/inflammatory diseases. It has been linked to childhood asthma. Over expression causes inhibited calcium buffering capacity of the mitochondria. This can disrupt endocytosis, enzyme control , cell growth and proliferation and cell apoptosis. ORMDL3 takes part in protein folding and in regulating UPR. It is believed ERs induced inflammation in paneth cells may disturb ORMDL3 levels leading to inflammation.

TREM1 (Triggering Receptor Expressed On Myeloid Cells-1) inhibits autophagy and increases ERs stress levels. This has been shown to increase the severity of inflammatory bowel diseases. Defective autophagy in the endoplasmic reticulum can predispose someone to inflammatory bowel diseases form a decreased clearance of IRE1 during ERs. High IRE1 levels impairs insulin signaling this can lead to many metabolic diseases. TREM1 can either increase inflammation or decrease it. During infection TREM1 increases inflammation. TREM1 also interacts with other inflammatory pathways which can also result in TREM1 increasing inflammation. TREM1 is high during septic shock. Sustained increased levels of TREM1 can lead to inflammatory bowel disease, cardiovascular disease and atherosclerosis. TREM1 is needed to help clear infection. Unfortunately when an infection that contains OspA protein that are difficult for the body to clear like HIV and Borellia (Lyme Disease) it can cause TREM1 levels to remain high. This is why it is very important to work on reducing inflammation and address infection. Most infectious diseases there are no test for and the test they do have has a high failure rate at detecting the microbe responsible for the illness. But the body and what genes are effected and cytokines present can indicate when there is an infectious agent present. The more difficult infections can be killed but it takes a multilevel approach because most that carry the OspA take multiple forms and have to be addressed differently for each form it has taken.

Inflammatory bowel disease have been shown to have a dis-regulation of T Cell which can be induced by toxins, drugs, vaccine injury, farm chemical or processed foods.

Autophagy is a conserved lysosome-dependent catabolic process involved in degrading and recycling aggregates as well as damaged organelles. Enhancement of autophagy promotes the survival of various cells including intestinal endothelial cells, and nuetrophils by protecting them from microbial toxins. A disturbance in autophagy could disturb the function of intestinal endothelial cells and influence inflammatory response, immune response, ROS levels and endoplasmic reticulum stress. This can lead to inflammatory bowel diseases. Autophagy plays a vital role in alleviating of intestinal inflammtion, degredation of damage associated molecular patterns (DAMPS), which can help prevent inflammatory bowel diseases. PAMPs refer to various kinds of endogenous materials produced by stress, impaired or dying cells covering DNA, RNA, ATP, histones, hyaluronan, uric acid, heparin sulfate, the S100A calgranulins, IL-1, HSP, and chromatin-associated high motility box1(HMGB1).

Basal autopaghy occurs in nearly every cell to maintain homeostasis of the ammino acid pools. There are three types of autophagy.

Macropahy – targets material such as cytoplasmic components or invasive bactria which are surrounded by a double-membrane bound autophagosome.

Autophagosome when combined with lysosomechanges into a single-layer membrane autolysome with a strong degradative and digestive ability.

Microautophagy – during the process of microautophagy lysosomal/vacuolar membranes invaginate (fold in on itself) to engulf intracellular components via a non-selective degradative mechanism.

Chaperone-mediated autophagy transports organelles and proteins into lysosomes only with the assistance of chaperones which are located in lysosomal lumen. Chaperons are proteins that assist in convalent folding or unfolding and the assembly or disassembly of other macromolecular structures. They assist in the assembly of nucleosomes which are basic units of DNA.

Two steps of Autophagy.

The first step of autophagy cup-shaped double membrane phagophores are shaped in the cytoplasma of the cell, and then misfolded proteins, damaged organelles or bacteria are engulfed to become sperical double membraned autophagosomes. Autophagosomes are usually considered to be produced from the nucleation and membrane expansion of phagophores.

During the second step autophgosomes fuse with lysosomes and endosomes to form a single-lipid layer autolysome, which is regard as basal units for degradation and digestion. Autophagy process is induced by the detection of various specific cues such as starvation or invasion by pathogens.

Two proteins are known to participate in autophagy which include Mammaian Target of Rapamycin (mTOR) as an inhibitor and adenosine monophosphate activated protein kinase as an indicator. mTOR is often activated by lower levels of Adenosine Triphosphate (ATP) caused by nutrient sufficiency or several growth factor stimulations. mTORC1 inhibits autophagy in the presence of nutrients. mTORC1 regulates glycolysis, lipid biosynthesis, and the pentose phosphate pathway has been found to be under the control of mTORC1. mTORC1 mediates upregulation of SREBP-1 activity which is necessary for lipid biogenesis. mTORC1 increases mitochondrial DNA copy number and as well as encoding many genes involved in oxidative metablolism. It has been found that mTORC1 promotes transcriptional activity of PPARy coactivator (PCG-1a) which is usually low in those who have inflammatory bowel diseases. This leads to the inability to break down fats and cholesterol causing many health problems because lipids are needed by almost all cells of the body especially the digestive system to maintain proper function and health. Ironically mTORC1 inhibition leads to longer lifespan. mTORC1 inhibits autophagy. mTORC1 increases NRF2 activity the master regulator of the antioxidant system.

Excess mTORC1 activation can cause endoplasmic reticulum stress and excess ROS production.

Low ATP levels inhibits mTORC1. Inhibiting mTORC1 increases glucose uptake. Hypoxia (oxygen deprivation) inhibit mTORC1. Amino Acid deprivation can inhibit the citric acid cycle (TCA cycle) this also inhibits mTORC1. The body inhibits mTORC1 when it senses DNA damage. Autophagy reactivates mTORC1 whose activity then promotes the replacement of lysosomes consumed during autophagy.

Symptoms of excess mTORC1 . Since there is no information on what excess mTORC1 does I will have list the symptoms of inhibited autophagy and high ROS levels since those are issues caused by high mTORC1 levels.

Symptoms of inhibited autophagy. Nuerological problem , inhibited autophagy can lead to inflammation in the brain, mental illness. Mitochondrial dysfunction, decreased antioxidant function which can lead to high levels of ROS. Pancreatic inflammation. Fat accumulation throughout the body and can lead to fatty liver disease. Issues with lysosomal storage, diabetes and sickle cell anemia. Frequent illness from infectious agents.

Symptoms of high ROS. ROS is needed for redox signaling but becomes damaging if levels get too high. High levels of ROS cause inflammation. Leaky gut and can cause a leaky blood brain barrier. This also can lead to nuerological damage and brain inflammation causing mental illness. Can cause liver damage resulting in a hepatic liver. Fatigue from reduced energy levels. Mitochondrial dysfunction which can lead to MS. Here is a link to a good article on oxidative stress.

Things that stimulate mTORC1. Resistance training, amino acid L-Luecine, Beta Hydroxy Beta-methylbutyric acid which is a precursor of butyric acid. High intake of Iron stimulates mTORC1.

Inhibitors of mTORC1 are green tea, resveratrol, curcumin, caffeine and alcohol. Iron deficiency inhibits mTORC1. Green tea can damage the liver if taken for too long and curcumin chelates iron so can make a person anemic if consumed too long.


Vitamin D receptor (VDR) mediates the activities of vitamin D3 which is the activated form of vitamin D. A deficiency can effect our digestive system in many ways. The VDR is involved in regulating 33% of the genes in the body so problems with it can effect many things. VDR and Retinoid X receptor interact to with each other and can activate each other so issues with either one can effect vitamin D homeostasis. Inhibited VDR effects calcium homeostasis, electrolyte balance, and blood pressure.

Vitamin D3 acts as a hormone a hormone and helps regulate innate and adaptive immune responses. Those with low vitamin D levels or inhibited VDR receptor are prone to infection with Mycoplasma Tuberculosis. VDR is involved in producing the antimicrobial peptide/IL-37, defensin beta B, CLDN2 encoding claudin 2 and ATG16L1 related autophagy which protects us from inefection.

The VDR receptor is involved in gut microbiome balance and autophagy. Autophagy is the house keeper of our cells it helps clean them out, protect them from infection and helps to prevent misfolded proteins. Inhibited vitamin D receptor can cause inhibited bile flow and a decrease in LDL and increase in HDL. The reduced LDL causes bile to become sludgy which leads to biliary issues and gallbladder problems and can result in gall stones and biliary blockage.

When the VDR receptor is inhibited or there is a vitamin D deficiency we can develop inflammatory bowel diseases. IKBa is an inhibitor of pro-inflammatory NF-kB.

VDR inhibition or vitamin D deficiency alters the composition of intestinal microbiome. Butyrate producing bacteria become less numerous. Butyrate increases expression of VDR so a deficiency in Butyrate would further add to the inhibition of the VDR receptor. Butyrate also suppresses intestinal inflammation and enhances AMPs. AMPs help protect us from infection.

Toxins, mold toxins, infection and a lack of nutrients can inhibit the vitamin D receptor. High levels of vitamin D3 indicates the body has recognized an infection and is trying to fight it.

Farm chemicals especially glyphosate and glufonisate inhibit the vitamin D receptor. Many toxins found in processed food can also inhibit the vitamin D receptor.

Symptoms of inhibited VDR.

If the VDR is inhibited a person may experience problems with methyl donors and low dopamine levels. They may experience frequent infections and be low in GcMAF. Inhibited VDR can cause bone loss, hair loss, brain fog, increased TH17 levels resulting in lupus, psoriasis and/or skin rashes, tooth decay and poor oral health, inflammation throughout the body, can lead to high blood pressure. Low LDL which inhibits bile production resulting in biliary and gall bladder problems and can lead to stone formation. Electrolyte imbalance and iron deficiency. Low dopamine and GABA levels is a result of VDR inhibition. Prolactin level become low when VDR is inhibited. Gut dysbiosis and inflammation in the digestive system. Increased creatine and albumin levels and decreased alkaline phosphatase are symptoms of low vitamin D or inhibited vitamin D receptor. VDR inhibition or vitamin D deficiency can result in mast sell activation syndrome. CYP3a4 an enzyme needed for detoxing xenobiotics and drugs becomes inhibited. Hormonal imbalance is also a result of VDR inhibition. Hashimoto’s syndrome can result from VDR inhibition. Heart disease can be a result of VDR receptor inhibition or vitamin D deficiency. In more severe cases VDR inhibition can lead to liver and kidney disease.

Symptoms of Vitamin D deficiency.

Joint stiffness or pain, back aches, tooth decay, bleeding gums or gum disease, muscle cramps, hair loss, bone loss, weakening of bones, increases risk for cancer, sleep apnea, brain fog, fatigue, depression, leaky gut, excess sweating especially in the head area.

Excess vitamin D can lead to many health problems and can result in loss of bone from a disruption in the mechanisms that control calcium homeostasis. Though it is needed for calcium absorption high doses can have the opposite effects. High levels of vitamin D can lead to oxalate formation. Many studies show anything over 5000 IU a day can lead to oxalate formation and many health problems.The recommended daily allowance of vitamin D is 600 IU. It is best to get vitamin D from food sources. Exposure to sunlight, far infrared, halogen lights can increase the bodies production of vitamin D. Short term raised levels have been found to be beneficial but long term raised vitamin D levels have been found to be harmful to our health. High levels of vitamin D can contribute to the inhibition of the VDR. Excess vitamin D can result in high levels of calcium in the blood resulting in calcium deposits forming in the organs including the lungs.

Sources of vitamin D. Sunlight, halogen lights, far infrared light increases the bodies production of vitamin D. Excess sunlight has been shown to cause high levels of vitamin D and is why life guards have some of the highest rates of kidney stones. Fish oil contains vitamin D. Sardine , salmon and cod liver oil are good sources. I try to make sure the fish is not from contaminated areas. Most sea food is high in vitamin D. Mushrooms and eggs are a good source of vitamin D. Animal liver is another good source of vitamin D. Cestrum Diurnum, Waxy leaf nightshade (solanum glaucophyllum), yellow oat grass (trisetum flavescens) are plant sources of vitamin D. Those plants are so high in vitamin C that they cause calcinosis in grazing animals. Brown and read seaweed are also sources of vitamin D and cholesterol. Mercury found in fish is for the most part only a problem if we have leaky gut. When the gut is intact only about 5% of the toxins like mercury get absorbed that have been consumed and when healthy the body can easily detox that amount unless it is shot directly into the blood stream. I mention this because even though they claim vaccines do not contain mercury some still do.

Things needed for the body to be able to use vitamin D. Vitamin K2, Vitamin A, zinc, sulfur is needed to sulfate vitamin D so sulfation issues need to be addressed. Magnesium increases the bodies response to vitamin D. Boron increases vitamin D in the blood stream. Water is needed, dehydration inhibits many receptors in the body. Silica helps improve the function of many receptors in the body. Sunlight helps to sulfate nutrients. DAO and lysine are also needed to sulfate vitamin D. Boron is touchy, low levels reduce estrogen high levels increases estrogen.

Things that enhance vitamin D receptor activity. Parathyroid hormone, Sirt 1, Dopamine, Omega 3 , Omega 6, Phytoestrogens, Testosterone, Postaglandulins and bile activates VDR. Bitter herbs stimulate bile production. Even if you do not swallow bitter herbs just tasting them stimulates bile production. Resveratrol activates the vitamin D receptor. Querciten enhances vitamin D receptor activity. Curcumin stimulates the vitamin D receptor but if taken for too long it can lead to anemia because it chelates iron from the body. So one may use it at first to help stimulate the VDR receptor but probably should just take maintenance doses to make sure it continues to function. Human Growth Hormone stimulates the vitamin D receptor. Sleep, fasting, and strength training increase HGH.

Things that can inhibit VDR are cortisol/glucocorticoids, high prolactin levels, imbalance in thyroid hormones, TGF-Beta, phosphatonins which regulate phosphate homeostasis, and ubiquitin can inhibit VDR. Many of these things are inhbited by autophagy which would prevent them from inhibiting the VDR receptor. Caffeine can also inhibit the VDR. High TGF-B levels can be an indication of T cell imbalance and/or B cell imblance. Probiotics that reduce inflammatin and increase T regulatory cells should reduce TGF-B. High phosphatonins is a sign of low klotho levels. Exercise increases klotho, Most Acidophilus bacteria and Lactobacillus Lactis increases klotho. Cordyceps mushrooms increase kltoho. PPAR Gamma activators stimulate klothos, Some PPAR gamma activators are berberine, magnolia, and Omega 3s. Those who are obese should not stimulate PPAR gamma because they are usually PPAR gamma dominant. Adaptogenic herbs like suma root and maca root can help normalize adrenal levels. Ubiquitin levels are reduced by autophagy. High prolactin levels can result from toxins in plastic containers used to store food and some farm chemicals found in our food supply. There are also chemicals in processed foods that can cause high prolactin levels. Those who are taking drugs should not use berberine or things that contain it because it inhibits the cytochrome P450 enzymes needed to detox medications.

Fulvic acid and nobiline induce autophagy. We do not want to overstimulate autophagy. Fasting also stimulates autophagy but those who are Type1 diabetics have to be careful fasting can induce ketoacidosis in them. Branch Chain fatty acids can inhibit autophagy. Tumeric, ginger, berberine, gensing, mushrooms and elderberries can stimulate autophagy.

NOD2 – Nucleotidebinding Oligomerization Domaincontaining Protein 2 whew that was a lot. A member of the NLP family which is a group of immune regulating proteins. It is a sensor of muramyl dipeptide which is a constituent of both gram negative and gram positive bacteria. It is found in macropages and paneth cells. When inhibited a-defensin numbers are decreased, lower sensitivity to bacteria infection, and altered immune function from Toll Like Receptors becoming suppressed. This results in the inability to clear bacteria infections from the intestines. Inate and adaptive immunity is impaired. Nod2 induces autophagy through the NOD2 pathway. NOD2 is induced by NLP or bacteria infection, this promotes the delivery of NOD2 which enhances inflammation. Showing that if You have high NOD2 levels you would not want to induce autophagy. NOD2 prevents infection in cells which is mediated by ROS and MAPK pathways. NOD2 altered expression can lead to inflammatory bowel disease. Many cellular proteins interact with NOD2 directly and regulate it’s function positively or negatively. Among these proteins is Erbin. Erbin regulates Erbb2 if Erbin is inhibited Erbb2 levels can go up resulting in cancer growth. Centaurin B1 which I have no idea what it’s function is. Angio-associated migratory protein which is involved in endothelial tube formation and endothelial cell migration. It is involved in angiogenesis. Carbamoyl-phosphate synthase 2 is involved in the production of nucelotides in cells. Mitogen-activated protein 1 which helps down regulate NOD2. Heat shock protein 90 interacts with NOD2. HSP90 is involved in folding , intracellular transport and the degradation and maintenance of proteins. I have post on heat shock proteins like HSP90 and HSP70.

NOD deficiency. NOD2 is involved in maintaining balance between the microbiome and immune response. NOD2 deficiency results in loss of epithelium integrity, and increased susceptibility to intestinal inflammation. NOD2 deficiency can cause dysfunction in intestinal paneth and goblet cells. Deficiency increases IFN-y, and decrease ROS production which protects from infection so we need a balance because excess ROS can damage tissues in the body.

NOD2 upregulation. Vitamin D supplementation has been shown to increase NOD2 which helps to fight infection. Excess NOD2 can lead to rheumatoid arthritis, and systematic inflammation. Excess NOD2 has been linked to cardiovascular disease and pulmonary disease. NOD2 prevents inflammation in the eyes.

NOD2 deficiency causes low TH17 levels, inhibited immunity, and will be more prone to cancer. NOD2 is also involved in the detection and eradication of viruses.

Excess NOD2 causes systematic inflammation and sarcoidosis. Often times it is mistaken for cancer or copd. High NOD2 levels is a sign of infection.

Damage to the mucus membrane and intestinal tissue can cause it’s dis-regulation. This shows the importance of restoring mucus membrane and work on healing the gut.


Autophagy-Related Protein 16-like Protein 1 – Deficiency in Atg16L1 impairs recruitment of Atg12-Atg-5 complex which impairs the engulfment of pathogens and cellular organelles during the process of autophagic catabolism. Atg16L1 defeciency cause Paneth cell dysfunction and increases inflammation. Atg16L1 causes high leptin and adiponectin levels. A deficiency in Atg16L1 leads to intestinal lesions. Leptin tells the brain we do not need to eat. Leptin increases inflammation in the body. High leptin levels lead to chronic fatigue. Leptin can cause Th1 dominance. Those with high IL-10 levels would want to avoid probiotics that increase IL-10 because leptin increases IL-10. Leptin causes mast cells to become more inflammatory. Leptin causes lower T regulatory cells which keep our immune system at homeostasis. Leptin can cause excess blood clotting (throbosis). Leptin can cause high blood pressure. Leptin increases estrogen levels. Adiponectin is a protein hormone involved in glucose levels and fatty acid breakdown. High adiponectin levels causes a loss of appetite it causes weight loss and works synergistically with leptin. Adiponecton decreases gluconeogenesis. It increases B-oxidation of fats. It protects against endothelial dysfunction. It increases insulin sensitivity. So you can see the importance of Atg16L1 homeostasis.

Mir223 restores autophagy and Atg16L1 homeostasis. Mir233 downregulates inflammation. Mir233 is reduced in sepsis. Mir233 increase HDL cholesterol levels. But Mir233 is upregulated in inflammatory bowel diseases. Increasing Claudin-8 inhibits Mir233 inflammatory effects.

ROS (Reactive Oxygen Species)

ROS or Reactive Oxygen Species modulates cellular function under normal conditions. ROS is produced during the process of oxidative phosphorylation and can be handled by instracellular antioxidants. Injury, toxins , vaccine injury, infection, and stress can cause an over production of ROS which can exceed the generation of antioxidants leading to oxidative stress which can cause a lot of damage throughout the body. It causes inflammation, cell damage and even cell death. When the mitochondria become dysfunctional this can cause a rearrangement of the cytoskeleton which is framework of the plasma membrane and effects the balance between kinases, and phosphatases which promotes the ability of microorganisms to enter the cell and contributes to many inflammatory diseases. Excess ROS increases the permeability of intestinal epithelial. When levels of ROS are normal it will induce autophagy and microphagy which reduces inflammation. Reducing ROS levels too low can have the opposite effect because it would prevent it from inducing autophagy and we would lose the protection it gives us from infection.

Antioxidants can reduce oxidative stress but when homeostasis is achieved a person should only take maintenance doses. Over use of antioxidants can promote cancer by protecting it from apoptosis it also increases our risk of infection by reducing ROS levels too low.


Xenophagy is the clearance of pathogens regulated by autophagy. Reduces Xenophagy leads to alterations of intestinal microbiota. This leads to a higher rate of infection. The microbiotia induce xenophagy in basal paneth cells which is induced by INF-y to maintain intestinal integrity. This impairs sensing of intracellular micro organisms in the intestinal endothelial cells and contributes to the progression of inflammatory bowel disease. Showing the importance on healing the intestinal tract so that the mucus membrane can be restored. Prebiotic fiber and the tryptophan metabolizing gut microbiota increases IFN-y. The commensal strains of E Coli increases IFN-y. Lactobacillus Gasseri increases IFN-y. Bacteroides Fragilis increases IFN-y and has been found to protect from many types of infections. Butyric Acid must be present to maintain IFN-y homeostasis. So it would also be a good idea to make sure the butyrate producing microbes are established.

IRGM (Immunity Related GTPase Family M protein) – is involved in killing of bacteria, vacuolar trafficking and acidification, it is also involved in autophagy. It is involved in fighting mycoplasmas. Damage to the digestive tract can impair it’s function which wold make you susceptible to mycoplasma infection. Inflammation inhibits IRGM. Our digestive tract needs to be acidic. If it becomes to alkaline then it creates an environment that promotes infection and dysbiosis and we lose our commensal microbiota.


My summarized notes.

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.

Addictive behavior

allergic reactions









chronic degenerative diseases


poor detoxification



muscle pain

low nuerotransmitters

obesity though lean people can be under methylators also.

Obsessive compulsive disorders

Phobias or fears


mental illness

Thyroid dysfunction

Low white blood cell count

Extremely large red blood cells

andrenal fatigue

copper overload

Symptoms of over methylation

headache or migraines



increased anxiety

joint pain

muscle pain







stomach pain



hypokalemia low plasma potassium levels.

Heart palpitations

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.

The microbes that help heal the gut.


This is not medical advice I am posting this for informational and educational purposes.

Most with inflammatory bowel disease have too many bacteriodes which is caused by excess meat consumption, antibiotics, glyphosate, glufosinate and other farm chemicals. This results in nutrient deficiencies which lead to metabolic and gene problems. Before you can get your gut bacteria reestablished you have to address those health issues because our gut microbes communicate with and modulate our genes. These are the bacteria that was found to help restore intestinal health in those with inflammatory bowel disease or leaky gut. They also help those with autoimmune issues and chronic illness.

Studies have shown that by alternating probiotics and taking lower doses of them and taking a break from them to leave them balance out is more effective at establishing a balance of our gut bacteria.

Each of our triggers are different so it is important to keep a food diary on how various food effects you.

Our gut bacteria modulate our genes. So an imbalance in them or a deficiency has effects on our genes,

We need a diversity in our gut bacteria for them to stay established.

A loss of short chain fatty acid and butyrate producing bacteria cause inflammatory bowel disease and constipation.

Our diets influence out gut bacteria for example meat alkalizes the gut producing an environment that will permit the rise of certain bacteria that can lead to health problems. If we consume too much meat it can lead to inflammatory bowel diseases because it raises bacteroides levels and kills the bacteria that produce the good fats we need and the short chain fatty acids the body needs. High bacteroides levels can also lead to heart disease, diabetes, and even autoimmunity. Also a diet high in meat can increase the bacteria in our guts that cause inflammation.

Transfats and oils like vegetable oil and canola oil were found to raise bacteroides levels and decrease our good short chain fatty acid producing bacteria. Oils like olive oil, coconut oil and fish oil have been found to promote good gut bacteria.

Whey protein and the glycoproteins found in mushrooms have been found to reduce bacteroides and increase the good gut bacteria.

Lactose has been found to increase the good bacteria that helps produce butyrate and short chain fatty acids. This is why it is important to address lactose intolerance, it can be corrected.

Sugar increases Bifidobacterium, this could be bad for those who are over weight but good for those who are under weight and need to gain weight.

Prebiotics like resistant starch, oligosaccharides, fructosaccharides increase our short chain fatty acid producing bacteria. Short chain fatty acids are very important keeping us healthy. They have also been found to increase the microbes that protect and strengthen the health of our digestive system.

Polyphenols found in fruit especially berries, promote good bacteria while reducing the bad.

Artificial sweeteners especially aspartame has been shown to increase bacteroides to the point it could lead to irritable bowel syndrome.

A list of foods that increase our good gut bacteria.

In order to establish our good bacteria we need FOMAPs I found introducing them very slowly worked best for me as my gut bacteria received the food they needed and increased I could increase my FODMAP intake. If we stay on a FODMAP diet too long it will make it difficult to reestablish our good bacteria. Adjust the diet to your body do not stick strictly to diet but base it on how your body responds. I used a paleo diet after the FODMAP but did not stick to either diet strictly but based them on how my body responded.

paleo diet.

Akkermana Muciniphila It is found in the upper part of the intestines and helps regulate bile acid production. Bile acids help regulate our pancreatic enzymes so indirectly it also regulates our digestive enzymes. It is believe to restore the mucous membrane in the digestive system. Polyphenols from berries helps to feed it and increase it’s numbers. Oligosaccharides also increase A Muciniphila. It has been found to be low in those with obesity. A deficiency in A Muciniphila will cause a deficiency in short chain fatty acids and inhibited lipogenesis. A person deficient in A Muciniphila will develop insulin resistance and low glucose levels.

Oligosaccharides and inulan have been shown to increase A. Muciniphila. This is why green algae and seaweed have so many health benefits they are high in oligosaccharides.

Roseburia species help produce butyric acid, short chain fatty acid and protects us from diabetes and obesity. They help prevent inflammatory bowel disease. Beta Glucan in mushrooms and oats , chitan and inulin help raise Roseburia levels. Butyric acid protects the gut and our brains. It also protects our nerves and is important in the absorption of nutrient. If we are deficient in butyrate we will not absorb nutrients. Butter and ghee are good sources of butyrate until the gut bacteria are restored.

Faecalibacterium Prautsnitzii increases IL-10, this is important because Lyme and other illnesses that carry the OspA protein inhibit IL-10 to stealth themselves from the bodies immune defense. There isn’t much known about it except that it is low in many types of digestive disorders. We get it from being around others who have it.

Clostridium Butyricum is a butyrate producing bacteria . Clostridum butyricum kills it’s cousin that cause negative health effects. It also increases IL-10 . It also decreases inflammatory cytokines. There are studies that have shown if the other healthy gut bacteria are not present this one like many of the bacteria species used in probiotics could start causing health problems.

It promotes better bowel movements.

E Coli Nissle 1977 doesn’t only protect us from it’s cousins that cause ill health effects it also protects against other types of infections. It has been shown to put inflammatory bowel disorders into remission. It has too many benefits to mention. The only way I know of getting this one is through a probiotic called Multaflor.

E Coli Nissle 1977’s cousin can cause many health problems if not kept in check.

Lactobacillus Casei and L. Longum have been find to be deficient in many types of digestive disorders. They do not establish well of one or the other is missing it is best if they are taken together if you use a probiotic. The improve the bodies antioxidant capacity. We need SOD to produce H2O2 which the body uses to detox cells and transport nutrients and enzyme into and out of the cells. When deficient in these cellular macrophagy is inhibited. This help protect against cancer and other illnesses.

If we are deficient in them we can develop liver disease, lysosomal storage disorders and glycogen storage issues, insulin resistance and lose the ability to absorb nutrients. Our blood sugar levels will become low because insulin levels will increase. Bifidobacterium Bifidum has many of the same benefits and probably would benefit from taking it along with these. Also we cannot absorb proteins without the Lactobacillus strains.

They also help protect us from mold toxins.!divAbstract

Lactobacillus Longum also produces folate for us.

protects our lungs.

Insulin and glycogen issues.;year=2016;volume=7;issue=1;spage=102;epage=102;aulast=Sharma;type=3

Protein absorption.

A species of bacteria called lactobacillus casei shiroto is important in regulating our tryptophan levels. A deficiency in this strain will cause reduce tryptophan levels resulting in anxiety and the inability to sleep. A deficiency in this one can result in phenylketonuria which causes high ammonia levels in the body. A person who has this issues will get ill when they eat meat , potatoes or other things high in phenylalanine. Low levels of tryptophan can cause a loss of the beneficial bacteria in the Roseburia family which can lead to leaky gut and inflammatory bowel disease and sever constipation.

Fermented milk like butter milk and kefir help them get established.

Many have been found to be deficient in Streptococcus Salivarius protects us from lung, oral and nasal infections. It also protects us from inflammation. Those who are deficient in S Salivarius will be prone to infection especially from it’s cousins in the streptococcus family that cause negative health effects. The only way I know to safely increase this is with lozenges that contain it because too much can cause health problems so you would want to avoid taking capsules of this.

Lactobacillus Rhamnosus helps prevent diarrhea , has been shown to reduce symptoms of inflammatory bowel disease. It helps protect us from infection. Helps protect us from allergies,obesity and diabetes. It also helps protect us from staph infection.

H Pylori is commensal but without Lactobacillus Rhamnosus to keep it in check it can cause gastric ulcers.

We also need fungus for example Saccharomyces Cerevisiae know as brewers yeast helps prevent diabetes. They used to think S Boulardii was a separate species but it has been found to be the same. I couldn’t afford the supplement so I bout a package of brewers yeast and consumed it. Wasn’t sure it would make it through my stomach acid but I felt improvement so I believe it does. Now this is one you do not want to increase too much, also you do not want to take this if you have autoimmune issues or leaky gut. It can act as a pathogen if it gets into the blood stream, many of our microbiome can if they get too high in numbers or get into our blood stream.

S Cerevisaiae helps reduce vaginalis and candida.

Lactobacillus Rueteri produces folate those who have folate deficiency have been found to be low in folate and have high inflammation levels. L Rueteri also regulates our oxytocin which can give us a feeling of self worth and well being. A deficiency in L Rueteri can lead to extreme depression.

Our gut bacteria produce B vitamins for each other and maintain each other. If the ones who produce the B vitamins are missing then the microbiome will get them from our foods which will prevent us from receiving them. This is why it is important to eat foods high in B vitamins and to protect our gut bacteria from antibiotic, farm chemicals and toxins in our foods like artificial sweeteners.

Lactobacillus Acidophilus prevents diarrhea, helps protect against clostridium infections. Those with interstitial cystitis are usually deficient in this one. It helps reduce symptoms of inflammatory bowel disorder. Acidophilus regulates our ph of our digestive system and bladder and keeps it at the correct ph. Our bladders and digestive system need to be acidic. An akaline environment can cause a loss of our good gut bacteria and promote the growth of the bad. It can also cause candida to go from commensal to a pathogenic form. Many with interstitial cystitis have found relief using L Acidophilus suppositories. Those who are having difficulty gaining weight usually have excess L acidophilus levels because it speeds up metabolism and those who have problems with weight gain are often deficient in acidophilus. Fermented foods are high in this but those with high histamine must reduce their histamine before eating fermented food I addressed that in my autoimmune post.

Bifidobacterium increased the acid levels of our digestive tract which inhibits bad bacteria from growing and help keep our digestive tract acidic. It has been shown to reduce symptoms of irritable bowel disease.

Bifidobacterium Infantis protects us from autoimmune disorders by regulating our T cells. B infantis also helps protect our digestive tract.

This is an in depth discussion of probiotics.

more information on microbiome and folate production.

Bifidobacterium Breve reduces symptoms of celiac disease.

Frequent constipation is a sign of a deficiency in the bifidobacterium species.

If we are deficient in the lactobacillus species we are more prone to salmonella infection.

Lactobacillus Bulgaris increases T Regulatory cells which prevents on over active immune response.

Too many Lactobacillus Delbrueckii can cause urinary tract infection.

Our gut microbiome produce many of our nutrients so a deficiency in a specific strain can cause nutrient deficiencies especially in the B vitamins.

Quinones like PQQ is needed by our gut bacteria to thrive and balance out. They convert it to vitamin K2.

Phylloquinone (vitamin K) is also used by our gut bacteria and converted to vitamin K2. Animal products and leafy green vegetables are good sources of vitamin K . Many should be cooked especially spinach and kale because they are very high in oxalates.

Some food sources of quinones are. Natto, Green Tea, Parsley, Paypaya and green peppers. Some may benefit from supplementing PQQ because many of the foods that contain it are very high oxalate like kiwi.

Soil based probiotics have been shown to improve digestive health.

Bacillus Subtilis produces and antibiotic that protects us but is none toxic to the good bacteria. B Subtilis has antioxidant properties. B Subtilis has been shown to restore normal gut flora. B Subtilis has been shown to relieve constipation and diarrhea. It has reduce symptoms of inflammatory bowel disease. It boost immunity and fights H Pylori. It improves the health of the liver. It promotes the production of digestive enzymes which improves gut health.

Bacillus Coagulans improves insulan sensitivity. High insulin levels are common in inflammatory bowel disease, this would help reduce insulin levels. It helps reduce diabetes symptoms. B Coagulans improves muscle recovery and prevent arthritis. It helps increase the beneficial microbes in the gut. It relieves intestinal pain inflammation and constipation. B coagulans reduces the risk of urinary tract infections.

Bacillus Clausii protects us from respiratory infection. It fights the infections that cause diarrhea. It reduces symptoms of inflammatory bowel disease.–the-probiotic-of-choice-in-the-treatment-of-diarrhoea-2157-7595-1000211.php?aid=63792

Two soil based probiotics to watch out for because they can cause major health problems are bacillus Licheniforms and Enteroccocus Faecium.

Those with inflammatory bowel disorders have high bacteroides. They produce high levels of Beta Glucuronidase. This inhibits glucuronidation which is needed to detox mold toxins.

What is Beta-glucuronidase?

It’s not your genes it is your gut microbiome.

This is not medical advice and should not be taken as such. I am posting this for educational and informational reasons.


This is a list of gut microbiota and the conditions they help with.

Probiotic Guide.

I state this often to people. You should not take the same strains of probiotic everyday. It will lead to SIBO which causes major health problems. You have to alternate the strains you take and take a break from probiotics once in a while to let the microbiome balance out. Sibo can lead to metabolic acidosis and many other health problems.

Your gut bacteria not your genes is what makes you predisposed to illness. I am going to cover some candida myths at the end of this.

Before you read this you need to understand many scientist fabricate and falsify research. Much of what we believe is not true if you start questioning things you will start seeing through the smoke screens. Many things that have been proven wrong they teach as if they are fact. Germ theory is one of them it has been proven wrong many times.

People do not take it lightly when their perception of the reality of things has been challenged. They have killed people for exposing the truth behind fake science and for publishing true science. We also have the corruption in this political system involved.

Our gut bacteria tell us what to eat.

Ok now for the information. One mistake people make if their histamine levels go up when they take a probiotic they panic. When you first take a probiotic it sends out a molecule to tell your body to produce histamines. That makes the mucous membrane more porous. It does this so it can enter and establish itself in the mucous membrane. Once it is in and has set up camp it will continually send out a molecule telling the body not to produce too many histamines so it does not kill the good gut bacteria. So initially histamines will rise for a day or two then after they are established they will drop back down. You may bloat when you first take probiotics. It is best to alternate the types you take or you will develop gut dysbiosis. That is as bad if not worse then having Candida. Your gut bacteria keep your bladder and digestive system acidic. If it becomes alkaline which is usually caused by high ammonia levels in the body. High ammonia levels can be a result of inhibited sulfation or having too many sulfur digesting, methane producing bacteria. High ammonia levels can also be the result of high endotoxin or afloxin levels. I experienced Candida and dysbiosis . I found grapefruit seed extract helped a lot. But you can only take it for a few days and you cannot take it more then two days a week because it inhibits cytochrome P450 enzymes. Yogurt , fermented foods and aged meets should be avoided they have histamine producing bacteria in them and will raise histamine and inflammation levels. Once you get things straightened out you can eat those. I take 3 days a week where I do not take any probiotics to prevent dysbiosis. Some Probiotics that reduce histamines.

Bifidobacterium Infintus

Lactobacillus Rhamnosus

Lactobacillus Salivarius

Lactobacillus Sporogenes

Lactobacillus Saccharomyces

Lactobacillus Bouldardii

Lactobacillus Acidophilus

These bacteria are needed by the body but should be avoided if you have high histamines.

Lactobicilli Casie

Lactobicillus Reuteri

Lactobacillus Plantarum

This is a good article on probiotics and histamines.

An imbalance of gut microbiome can result in allergies.

This is another good article on lowering histamines it mentions s few strains of probiotics.

High Substance P levels can make our skin peel and cause gut issues. One of the major causes of high substance P is stress. Probiotics that reduce stress reduces substance P. High substance P causes burning skin , it will get worse at night. The worst burning will be in the scalp and down the spine. Because high substance P can make the skin itch it gets mistaken for high histamine.

This is a very informative article on probiotics.

Good information on choosing probiotics.

Antibiotics and farm chemicals kill this and it protects and heals our gut.

H Pylori prevents allergies and asthma.

You can balance your gut bacteria but it takes time and persistence.

If you bloat from taking a probiotic it could be you are taking too many or too often, or it could be die off of a pathogen.

Information on selecting probiotic strains.

This is a link to the human microbiome project. You can find many studies on the gut bacteria here.

It is very important to balance our gut bacteria they regulate gene expressions. They are involved with methylation and metabolic pathways. A disruption in them cause problems throughout our bodies. Supposed inherited imperfection are really a lack of certain commensal microbiota. Much of what they claim is genetic can be corrected by getting the correct microbiota.


Our gut bacteria is important for bone health.

Many diseases can be link to our gut bacteria.



The microbiome in our guts is what causes chronic illness.

Our emotions

Correcting autism

Our gut bacteria regulate our circadian rhythm.

The list of things modulate by our gut bacteria goes on and on.

Our gut bacteria regulate our immune system especially in our lungs. We have a gut lung axis.

Our gut bacteria train our immune system to impart immunity.

Many in science still have not come to realized this. They believe that B Cells and T cells are involved in our developing immunity even though this has been proven false many times.

Breast feeding is also important because the mother imparts immunity to the child this way.

If a child does not get a variety of bacteria early in life they will become prone to chronic illness.

Our gut bacteria protect us from pathogens. We have commensal bacteria related to the pathogens. The commensal protect us from their cousins. Many are lacking E Coli Nissle 1917. Also bacteria in our nasal cavities and other areas of the body.

They protect us from urinary tract infection.

Our gut bacteria protect us from inflammation

Our metabolic issues can effect our gut bacteria.

Your gut bacteria regulate your body mass.

Infants get their microbiome from their mother and environment.

The western diet has caused many species of bacteria we need to keep us healthy. With the antibiotics, and farm chemicals many species of bacteria that preserve our health is now extinct in the US.

There is even evidence that our bodies and gut bacteria are meant to eat a seasonal diet.

This is a review of the effects of synbiotics, probiotics and prebiotics.

Our gut bacteria determine if we are happy and mentally healthy.[Jour]+AND+2013[pdat]+AND+Hsiao[author]&cmd=detailssearch

Strokes have been tied to our gut bacteria.

Autism has been linked to our guts.

Mental illness has been linked to our guts.

Liver disease is from inherited gut bacteria.

When born by C section the infant does not get the beneficial bacteria.

Many toxins in our foods especially BT Toxin, glyphosate and glufonisate can inhibit FUT2. This is an enzyme that we secrete that keeps our gut bacteria healthy. Medications like fluoroquinolones can slo inhibit it along with endotoxins from pathogens and afloxin from fungus. This causes food intolerances, food allergies and chronic illness from gut dysbiosis which produces high sulfite and hydroxy radicals which raise ammonia levels in the bladder and digestive system. Ammonia alkalizes our bladder and digestive system. It should be acidic to prevent pathogens. Candida and H Pylori are normally commensal but when we become alkaline they become pathogenic. Also many pathogens prefer an alkaline enviroment. This also leads to gluten, milk and protein intolerance.

Antibiotics and farm chemicals are causing more virulant pathogens.

Not only that but there is the possibility of the transgenes of the GMOs transferring to our gut bacteria making them into a pesticide factory.

Oligosaccharides help when someone is not producing FUT2 enzymes.

If we get the correct nutrients our gut bacteria will produce non toxic antibiotics for us.

Our gut bacteria protect each other and secrete and enzyme that protects them from Reactive Oxygen Species. When the above mentioned causes a loss of those bacteria then the other gut bacteria is defenseless and also dies.

Toxins also damage our tight junction layer in our guts letting food particles enter our blood stream along with toxins that would usually be inhibited by the tight junction protein layer.

E Coli Nissle 1917 regulates our tight junction protein layer. E Coli

Our gut bacteria protect us from oxalates. If they get high we become prone to kidney stones and chronic illness.

When H Pylori is commensal it prevents allergies and inflammation.

We also have protozoa that are part of our gut microbiome and protect us.

Our gut bacteria protect us from toxins. So if we are lacking them we lose that protection.

Our gut bacteria has been linked to TMAO disorder. Fish smell disorder. Causes the urine and body odor to have a fishy smell.

Eating the right foods reduces TMAO.

High TMAO levels can cause chronic illness.

Vaccinations cause a change in our protective bacteria making us lose protection from illness.

Our gut bacteria has been linked to liver disease.

If the bacteria get out of balance bladder dysbiosis can develop resulting in interstitial cystitis.

Viruses are a part of our commensal microbiome and help protect us.

Lacking certain gut bacteria is the reason we get food poisoning.

We have commensal yeast. Taking this one helped me a lot.{bb454dd3-01bf-4720-a01e-912c62d09062}/probiotic-yeast-improves-abdominal-pain-bloating-in-ibs-c-patients

We have friendly fungus that protects us.

Our gut bacteria protect us from cancer.

Our gut bacteria regulate our T cells which would prevent autoimmunity and allergies.

Our diet effects our gut bacteria and vice versa.

This in turn effects our health.

Spore based probiotics help heal leaky gut. So does E Coli Nissle 1917.

Even our oral microbiome can effect the health of our whole body.

Our gut bacteria has been linked to MS.

Our gut bacteria has been linked to chronic fatigue syndrome.

Notice the metabolic pathways in this study are all ones that are regulated by our gut bacteria.

Gut bacteria regulate our cholesterol levels.

They use scare tactics to get us to fear viruses but they also protect us.

Now the part that kind of creeped me out. Even parasitic worms can be used to heal the gut.

Our gut bacteria will produce vitamins for us if we give them the right nutrients.

Probiotics help with aging.

Some gut bacteria feed others.

Our appendix houses backup stores of our microbiome. Antibiotics kill them making us more prone to appendicitis.

Appendectomies increase our risk of kidney disease.

Appendectomies increase our risk for infection.

Things that help with IBS.

A link to a study earlier mentioned how our microbiome regulate our zonulin levels. When things get through out of wack it can effect the whole body .

Herbal therapy has been shown to be very effective against SIBO. This would keep the good gut bacteria from being killed by antibiotics.

Gut dysbiosis can result in gall stones.

It can also result in cardiovascular disease.

If we do not get enough fiber our gut bacteria will digest our mucous membrane making us prone to infection.

Our gut bacteria is even linked to our endocanabinoid system.

Drink a little red wine and our gut bacteria will lower oxLDL.

Our gut bacteria is involved in the regualtion of bile acids. If we do not get enough bile we get constipate to much bile and we will get diarrhea.

Bile acid issues have been connected to NAFLD.

Those with sickle cell have gut dysbiosis.

Candida Myths busted.

There are many myths about candida for example you should alkalize the body to fight it. If you do that you will feed it and many other pathogens. Our bladder and digestive system is supposed to be acidic. When you alkalize them which is very hard then you would be feeding candida. When we get high ammonia levels from metabolic issues or from gut dysbiosis it alkalizes our bladder and digestive system causing candida to go from a friendly fungus we need to a pathogenic form. To get it back to the friendly form we need to fix the metabolic issues or the any other number of issues that can cause high ammonia levels. Once Candida is in the pathogenic form it will raise the PH to an alkaline one and it does it in a very short period of time.

If you are dealing with candida brewers yeast helps a lot. Candida is not in the yeast family, that is another myth that if you eat yeast you will feed candida. The opposite is true, brewers yeast gets candida back to commensal.

Burdock root also helps with candida.

I used the things in this article and they also helped.

Mushrooms help with candida.

Biotin helps with candida.

Uva Usa helps with a lot of things but I have not had a chance to research the safety of long term or high does usage.

There is a lot of confusion concerning candida and gut dysbiosis.

Nutrients needed when fighting candida.

Candida can cause sugar cravings.

Omega 3 is needed but Omega 6 must be avoided to prevent endotoxemia.

These links speak about the benefits of various probiotics.

Microbiome is transferred between sexual partners.

Our diet can change our gut microbiome and cause inflammation.


Some microbiome can cause weight gain.

There are probiotics that increase hormones such as oxytocin which helps with depression and healing.

You have to balance your gut microbiota. To much of one or another can cause problems.

if we lose some strains of bacteria it can cause TMAO disorder.

These are the probiotics that help me with my dairy issues.

For those with interstitial cystitis and urinary issues you need the right probiotics.

I had difficulty eating fruit. Probiotic yeast helped correct that.

Our gut microbiota protects us from toxins.

Peroxisomes help recycle reactive oxygen species which protects our cells from damage. Some microbiome produce peroxisomes.

Many food additives has negative effects on the gut microbiome which effects the body.

You have to balance your gut microbiota. To much of one or another can cause problems.

Because our microbiome regulates gene expression antibiotics that kill our gut microbiome causes gene damage.

Our microbione regulates inflammation in our bodies.

Some protect us from tick born illness.

Antibiotics and toxins also destroy the gut microbiome that protects us from pathogens.

Those prone to urinary tract infection have been shown to have a microbiome imbalance.

They protect us from cavities.

Some microbiome make vitamins that are needed.

They falsely claim some bacteria are pathogenic but they are needed to protect us.

Gut dysbiosis is a major cause of arthritis

Our bodies secrete an enzyme FUT2 that keeps our microbiome healthy. It also helps modulate our immune system. Many things now days can inhibit this enzyme and in some completely disable their ability to produce FUT2 Enzymes. The result can be autoimmune dysfunction and we will not be able to establish a healthy colony of gut microbiome.

There are two things that help with a FUT2 non secretor. Take a symbiotic that contains an ologosaccharide or a probiotic that produces What you need.

Here is a good article on various diseases and microbiota.

The probiotic we use has to be unique to what issues we are dealing with.


Probiotics and cancer. It is better to prevent cancer. Many who have cancer have been found to have acidosis which indicates an underlying health is. That can be from metabolic issues, leaky gut, toxins especially heavy metals and the BT Toxins found in GMOs and the herbicide used on it glyphosate. All those can cause leaky gut which can cause high histamines which also leads to acidosis. Cancer has also been found to create it’s own micro acid environment. Keeping our gut balanced protects us from cancer and many other illnesses. This can also lead to acidosis from dybiosis or akalosis (hyperammonemia)from fungal infection which also causes cancer.

Even type 1 diabetes has been linked to the gut.

Opium Lettuce helps with spastic colon.

Those who have issues with their digestion that causes the food to sit and ferment instead of digesting properly my not want to use apple cider vinegar. It delays digestion even more.