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Healing Our Daughter, Healing Ourselves

Published on May 27, 2025

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Healing our daughter with thiamine and vitamin K2

Our Little Tadpole

Abby is our little tadpole. Sensitive to seemingly everything, she morphed into something she should never have been. Many people openly stare quietly, thankful their kids aren’t like her and go about their business without much thought. Or worse were those who only stood by saying “God, somebody DO something!” when our daughter was screaming in pain in public as if WE weren’t there. There is much to be learned from them, if we only had eyes to see. We’ve made mistakes in our journey with our daughter, but the 10 specialists we’ve taken her to in the last nine years have provided numerous test results with little to no answers. The last allergist I took her and told me to “stay off the internet” as he was handing me free pharmaceutical samples as I was walking out the door. They made it as far as the trash can in the restroom. And so began our journey of doing something different, looking for answers outside of what we’ve been told. In our journey to heal our youngest daughter, we are healing ourselves too as we all seem to be dealing with very similar issues of low stomach acid, connective tissue dysfunction, and nutritional deficiencies/dependencies. I will start with her story first, since it is because of her that we’re figuring ourselves out.

The Early Red Flags: Hypermobility, Digestive Issues, Speech Problems and Intense Reactivity

Abby was adopted from China in September 2010 at the age of 10 months. Her birth and family history is unknown. She was found in a very poor district at three weeks old, underweight and jaundiced. She also had a congenital heart defect called atrial septal defect, which later closed up on its own. She was kept in ICU for a period of time. She was bottle fed until 10 months, then introduced to gluten and dairy. Orphanage caregivers reported she had a much heartier appetite than other babies (an early red flag that we all missed).

When we adopted her, we found her to be a very happy and social baby, who transitioned well. Her eye contact was always good. We did notice, however, her hips, elbows, knees, and fingers were hypermobile. In hindsight, we recognized that she played differently with infant toys. More red flags.

In October of 2010, she had her first post-adoption doctor’s appointment.
In December 2010, she was walking on her own. She tested positive for TB exposure and put on Isonaizid. She tested negative for lead. She became ill and was in pain for 10 days with diarrhea 3x day. We switched to Rifampin for the next 6 months. She was on Isonaizid and/or Rifampin from December 2010 through July 2011. Anti-tuberculosis antibiotics required monthly liver checks. She was vaccinated during this time as well, a mistake we came to regret. Our once happy child now became stoic and would remain so for nearly a year, but things had changed.
In spring of 2011, she experienced continuous and severe congestion along with loose stools.
In July we stopped Rifampin. She was a good eater, often ravenous.
In spring of 2012 we began speech therapy, 3x per week, but progress was slow. After removing gluten she spoke her first three word sentence.
July 2012 her hearing was checked. “Possibly mild frequency decrements. Minor issues”.
July 2013, probiotics stopped her diarrhea, unless she was exposed to a problematic food.
In 2014, we found she was a MTHFR 677ct double mutation. We strongly suspect she has a CBS mutation due to very strong reactions to various things: ALA, NAC, Epsom salts, CLO, methylated B12/Folate. Though over time, some of these we have been able to get in her in small amounts.
Over the next few years, and a multitude of negative tests, all we were able to determine was that her B12 levels were consistently high, even when not supplementing much, as were her B6 levels (though iodine brought her B6 levels down into the normal range). Creatinine was low, and a few amino acids were only slightly elevated. Prostaglandin F2 were extremely high and liver enzymes were elevated.

Despite all of this, Abby is a very happy, socially engaged and intelligent girl. Her speech has always been intermittent, ranging from very slurred to full complete clear “normal” sentences. It switches at random. Her former teacher of 5 years doesn’t think it is ASD, but in truth, it doesn’t really matter. Our kids are often labeled for the convenience of others.

Altered Pain Sensitivity

Abby appears to have a high pain threshold, except stomach pain. Since she was young, she has preferred to be barefoot and wore few clothes, even in winter. Over time this has changed and she has grown more “normal” in her body’s adjustment to temperatures.

The only observable nervous system affect was that she tightens/clenches her fingers when very excited. Excitement seems to trigger degranulation in her unstable mast cells. She had been extremely reluctant to draw, write, or color when young. She’s doing all this now, not as age-appropriate, but gaining.

She has had many problems with probiotics in the past; often creating an immediate OCD/stuffing whatever she could get her hands on behavior, under furniture, peeling birch tree bark for hours, etc. Her brain was almost immediately affected.

Severe Reactions to Triggering Substances

Trying to solve her medical problems has been difficult. She has had so many reactions in the past when trying various vitamins/minerals and supplements recommended by her physicians. The results were always mixed and reactions could be extreme. We often, and still do, dose her vitamins and minerals separately, mixed together. Many reactions were not to the main ingredient, but to the binders or fillers added to the supplement. Some treatments would spur a short snippet of normal speech but only 1-2x then nothing more.

Below are the symptoms that we have been navigating.

Dry, itchy skin. Rashes, hives, angioedema, large welts from some foods/chemicals and insect bites. Her skin feels like it’s on fire and she tore at her clothing after a small amount of Pure Vegetable Glycerin (99.9% pure) was applied. In 2015, her skin peeled off her arm, wrist to shoulder in a 3” wide band of deeply reddened dry/cracked skin, after eating non-organic strawberries. It looked like a third-degree burn, minus the blisters. Epsom salts, baking soda, Vick’s Vapor Rub, various other skin oils like jojoba, or almond oil, all caused painful reactions.
Severe abdominal pain. She experiences severe abdominal distress and pain after ingestion of various foods or charcoal-grilled food. She may also develop constipation/diarrhea, headaches/migraines. Probiotics often dramatically changed her behavior within an hour to severe OCD. Fruit-based digestive enzymes would cause facial rashes and behavior changes. Pancreatic enzymes caused much less speech, very quiet per her teachers.
Urinary. She was unable to urinate 9+ hours after ingesting cough syrup on two occasions. She was not dehydrated either time. She formerly had urinary incontinence on occasions and enuresis. The enuresis resolved with the addition of vitamin K2 MK7.
Insomnia. Occasionally she would develop insomnia, often after ingesting or exposure to an offending food or chemical. Tap water seems to be particularly problematic.
Behavioral. She has experienced severe OCD, irritability, extreme aggression/anger, hyperactivity.
Heart and Lungs. She develops a rapid heartbeat at rest and persistent coughing for 6+ hours following ingestion of a trigger.
Head and nose. Congestion, puffiness/eyes, headaches/migraines (based on focused tearing behavior).
Speech Problems. Her ability to speak various greatly relative to exposures. It goes from single words to full clear “normal” sentences. With gummy vitamins, recommended by her doctor, she developed a very notable and immediate regression in speech when she was four years old. The day before she took the vitamins, she had clearly-spoken emerging speech, i.e., “I eat” “I do” “I wash”. Immediately after giving her the vitamins, she walked about the entire day just saying “mmmmmm” over and over. Unsure of the cause, I was thinking dyes, rancid hydrogenated oil, or some such. I would not make the sugar connection for a few more years.
Severe pain after exposures. She had a strong reaction to Cassia cinnamon. In class, she and other children were making Christmas ornaments with lots of Cassia cinnamon. Although none was ingested, her teacher said she was inhaling it and handling it for hours. Near pickup time, the teacher said she was not feeling well, began to be irritable, like her head hurt. As we were walking out of the building, she went down fast onto the ground and began writhing in pain (not sure if head or gut related). Teacher held her head to keep her from hitting it on the pavement, while I ran to get my Lavender essential oil rollerball. Applied it, and within a few minutes she was fine and got into the car. No further incident. Ceylon cinnamon causes no problems. Cassia can affect B1 levels, or so I read.

Our Journey to Healing Began With Vitamin K and Thiamine

In October 2018, we learned about thiamine and suspected that many of her problems may have been the results of a longstanding thiamine deficiency. We began in August slowly increasing Thiamine HCL. She began to improve at school, but results were inconsistent. We then moved to Benfotiamine for a while and results seemed better, but still inconsistent. By October, she was taking Sulbutiamine and we worked our way up slowly to 200 mg. Organic Acid Test (Great Plains) showed her lactic acid levels came down with the addition of the high dose of thiamine.

Nighttime enuresis persisted several years beyond toilet training. In 2016, we added approximately 700 mcg of vitamin K (MK7) working up slowly to this dose and her nighttime accidents completely stopped. The addition of vitamin K (MK4), reduced her food intolerances and allowed her to eat a broader diet, but that form of the vitamin did not stop the enuresis, the MK7 form did. We have since lowered her doses and now she just takes a D3/K2 liquid form with no return of the enuresis and food tolerances seem good, though we monitor her diet closely.

We use a variety of homeopathic remedies to treat reactions, illnesses, and injuries and reduce chemical exposures at home. Once her lactic acid levels came down into the normal range with the thiamine, we were able to add probiotics without negative reactions.

Her diet is mostly organic, grass-fed beef, organic chicken, wild-caught fish, cage-free eggs, local raw honey, coconut and olive oil, ghee, no GMOs. MTHFR mutations seems to be sensitive to gluten and dairy, but I wonder if that’s because of our need for the TTFD form of thiamine. She has been sugar free since July 2018.

My Big Takeaway: Healing Requires Resolving Nutrient Deficiencies Dependencies

EDS and ASD both share very similar nutritional deficiencies and/or dependencies. I wonder how much of autism isn’t simply the undiagnosed trio of EDS/MCAD/POTS. As most genetic testing is beyond the reach of most family budgets, it is difficult to know. It seems like it would be worth looking into one’s broad family history. A friend once told me that the foods we crave the most can be our biggest problems.

Years ago when Abby was in preschool, her teacher had me in for a conference. She showed me her notebook, which sadly only had a few scribbly lines in it. She slowly closed the book and moved it to one side. She looked me straight in the eyes and said “this isn’t autism”. Her son was on the spectrum. She said “Abby is smart, very, very smart. I think she’s gifted”. I looked at her dumbfounded, asking “then why?”. She said, “I don’t know what’s going on, but she knows… she knows!” She proceeded to tell me something Abby did that proved to her unquestioningly her assessment. Giftedness and learning disabilities seem to share many commonalities.

We sort of figured some things out in reverse. For example, the MK4 form of vitamin K2 allowed for more food tolerances, and the MK7 stopped her enuresis. Bacteria in the gut (bacillus subtilus) produces K2, but then too much lactic acid was a problem because her thiamine was low and the CBS mutation seeming caused trouble as well. K2 seems to be very important in the distribution of calcium in the body.

We often see admonitions to heal the gut on the internet; so many opinions and recommendations. As Abby’s case suggests, it is far more complicated than simply taking a probiotic. It is also highly individual. Our daughter’s journey may not be applicable to someone else, but perhaps something can be gleaned.

We continue to avoid triggers, eat and live clean, heal the gut, use holistic remedies, play and laugh a lot. Thankfully, her reactions are now infrequent and fairly mild, but it was long road to get to this point. Her appetite is now normal with no real cravings or hunger extremes. We use vitamins/minerals, fish oil, and probiotics less cautiously now. She is gaining speech rapidly. She may still not be typical, but she is a far cry from what she had morphed into and much more normal than even a year ago.

We’ve been fortunate to avoid prescription drugs overall and use natural remedies, diet, and vitamins and minerals to affect change. We are avoiding further vaccinations, as our belief is her body has had enough and can’t deal with the stress at this time. Overall many people’s demeanor changes rapidly when mentioning alternative approaches to western medicine. If outside the norm, we may even be deemed a quack, but since we’ve been able to heal various family members of numerous ailments, if we’re seen as strange, so be it. We can heal our bodies, probably not 100%, but often without prescription drugs.

Perhaps even the most complicated puzzles among us are not as hard to put together after all. We are still healing and our journey is not over. We tell ourselves and our kids to eat less junk because a nutrient-dense diet is helpful to everyone, but it seems that it is even more vital to those who suffer both the blessings and curses of a good brain.

Our brightest lights are ever so vulnerable.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This story was published originally on August 19, 2020.

Health Shattered By Poor Diet and Conventional Medicine

by Tawnya Bareis

Published on May 22, 2025

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My health has declined over the last few decades, to the point that I am totally disabled and haven’t driven in 10 years. I have severe POTS with high blood pressure while sitting and laying down. Previously, it was low. I am not able to stand up as my heart rate goes too high and I feel as though I’ll pass out. I have coat hanger pain, jaw tension, and headaches daily. I am very irritable and impatient. Emotional outbursts crying spells, depression. I feel like I am a completely different person. I am in survival mode. My body cannot shift out of sympathetic dominance. All of this has developed over the last 20 years; a progressive decline until everything hit the fan.

I thought I had a relatively healthy childhood and into my early 20s. I did have mono in 7th grade. Looking back though, I ate poorly growing up and did a lot of crazy starvation diets. I also consumed a lot of alcohol in my later teens through my early 20s. I stopped drinking in 1994. However in 2006, I started drinking on and off again and the night I had the severe vertigo attack, I had been drinking. Since then I haven’t touched alcohol.

My mom passed away when I was 22 and I had my first child at 23, which was a C-section. At 26, I developed rosacea. This was really my first health problem. At 27, I was divorced (1993). I remarried a year later and had another child at 30 years old. Three months later, I had my gallbladder removed. With all of this, I was still active and healthy with only rosacea that would come and go, but it would get really bad on occasions and was very distressing. This was until 2007, when life stressors, poor diet and illness caught up with me.

Unending Vertigo and the Protracted Decline of Health

I started working again in 2000 after we relocated to Arizona. I was a preschool teacher, a wife, and was raising my two sons. I had a very full schedule. I was always a high achiever. In 2004, I opened my own school with another teacher. Things got even more stressful. In January 2007, I had a very emotional falling out with my father and a couple weeks after that I was diagnosed with viral pharyngitis. Within a couple weeks of this diagnosis, I was thrown out of bed with the worst vertigo you can ever imagine. This went on for three days and I was unable to walk for over two weeks. As things were improving, the dizziness never did go away. I sought out multiple practitioners, including neurologists and audiologists, but none were able to help.

I went back to work but I was never the same, having to deal with constant dizziness and feeling of being off-balance. In October of 2007, I wound up in the ER with a resting heart rate of 160. This had come on out of nowhere over the day and by the evening I was very frightened. They gave me lorazepam and sent me on my way. I continued with the constant dizziness and then the anxiety and panic attacks started. My GP gave me a script for benzodiazepine and offered an anti-depressant. I tried the antidepressant and I had a bad reaction. I felt completely numb. I couldn’t laugh smile or have any sort of reaction. That was after just try half a tablet. I never tried that again.

In 2009, I had an ankle injury and was wearing a boot for most of that year. In October, of that year I ended up having a surgery on it. What was interesting is that I was not experiencing much of the dizziness for most of that year. It wasn’t until a couple months later when I had a sudden onset of the dizziness during my physical therapy session. So the dizziness had come back and the anxiety and panic attacks were getting worse. In September 2010, I basically collapsed at work. It was about four or five days later at home, I experienced a severe shift of my energy. I was severely fatigued and now was experiencing POTS.

Is it Lyme? Maybe. Maybe Not.

November 2010, I was diagnosed with Lyme, however, my test was not conclusive. The Lyme literate doctor said my immune system was so weak that it was hard to get a positive result. He diagnosed me clinically. This set me off on a seven year journey of protocols that included benzodiazepines, two IV chest ports, supplements, herbs, homeopathics, bio-hormones, coffee enemas, detoxification therapies, chelation, IV and oral antibiotics, Flagyl, anti-fungal drugs, and every diet imaginable. You name it I did it. We had spent our life savings and I was still disabled and incredibly ill.

I became addicted to the benzodiazepines that he prescribed. He never told me about how addictive they were. I was on them for three years and they made me so much worse! I tried to come off of them several times. They turned me into a 3 year old. I was so fearful I couldn’t leave my bedroom even to cross the hall into bathroom. Finally, in 2014 I was able to kick the addiction. It took me six months of liquid titration.

As If Things Weren’t Bad Enough: Cancer Too.

Also in 2014, I had a huge fibroid and had a procedure called UFE ( uterine fibroid embolization ) to cut off blood supply so it would shrink. I know now I had severe estrogen dominance.

In 2017, I hit menopause and stopped menstruating. I was using sublingual progesterone at the time. The doctor also had me on hydrocortisone for adrenals and a time-release thyroid supplement. These supplements never helped and only made me worse. I was in such bad shape. I wasn’t sleeping for 3 to 4 days at a time and then when I would sleep it was only couple hours. This sleep regime went on all year.

In May of that year, I woke up one morning and left breast had shrunk significantly overnight!! The doctor I was seeing, had me come in. He physically examined me and felt that it was not anything to worry about. He said that I needed to detoxify my breast because it was probably blocked lymph. He told me to do skin brushing on it. I was in such bad shape that I wanted to believe him but I was so frightened. In October, I saw a different doctor and she said I had to get a biopsy. It was cancer. I did not see an oncologist. I did not have any lymph nodes removed or chemo radiation. I just had a surgeon remove it. I left the rest up to God. At this point, I could not endure anything else mentally or physically. The pathology report indicated the cancer was 98% estrogen driven.

A Dysautonomia Specialist Prescribed More Antibiotics

In 2018, I tried one more doctor. He was an autonomic dysfunction doctor and his protocol was quite simple. It was focused on lowering inflammation in the brain and body and balancing gut bacteria. At this point, I had suffered from chronic constipation for at least 10 years, on top of POTS and all of the other health issues. I was put on fish oil, olive oil, Rifaxamin and Flagyl for the possible SIBO and a vagus nerve stimulator. He told me not to use any other supplements of any kind. He claimed that most all supplements were fraudulent and using them would interfere with progress. I could not finish the Flagyl. I was feeling severely agitated and I thought it was due to the drug. I took most of it though. He assured me that the Rifaxamin was very safe and that they actually have renamed this antibiotic as a eubiotic. I did see my rosacea clear up. I had read some research and trials were they used Rifaxamin for rosacea and had a very positive outcome. So over the last 2 1/2 years I’ve been faithful on this protocol. It seemed like I had periods of time where I was able to stand up longer and do more around my house but I always relapsed. I was using the Rifaxamin on and off as per his direction for 10 days at a time. This year he put me on it indefinitely to use daily. I’ve been on it now for 8 months straight, but in July I started to go downhill very fast. I was having a decent spell able and had been able walk around for a a bit, do some limited chores and even able to be out in the pool, but one night my heart just went crazy and began to race. The vertigo came back too. I have been bedridden again since.

Discovering Thiamine Deficiency

After going back to doing some research, I came upon Dr. Lonsdale and Dr. Marrs’ book Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. I am thinking thiamine deficiency could be a piece of my puzzle. After reading one of Dr. Lonsdale’s articles on high B12 correlating with thiamine deficiency, I remembered two of my B12 tests. One in 2014, where it was 2000 and one in 2017 was 1600. The max upper range is 946.

Although my ill health was progressive at first, over time, everything has just become unbearable. I have been bedridden now for 10 years. The POTS symptoms are severe and I think I have the hyperadrenergic POTS. My blood pressure is very high when both sitting and laying and when I stand up, both my blood pressure and heart rate climb. I feel as though I’ll pass out. As I mentioned previously, I also have coat hanger pain, jaw tension, and headaches daily. I am very irritable and impatient. Emotional outbursts crying spells, depression. I feel like I am a completely different person. I am in survival mode. My body cannot shift out of sympathetic dominance. I am hoping to get some direction and advice on using thiamine to possibly help my condition.

Supplements, Medications, and Diet

Upon learning about thiamine and mitochondria, I stopped taking the Rifaxamin about two weeks ago. Below is a list of supplements I currently take and some information about my diet.

Magnesium hydroxide, Magnesium glycinate, 100mg, magnesium citrate, 100mg and some magnesium oxide in an electrolyte drink, in some variation for the past 3 years
3000mg daily (6caps) DHA 500 by Now Foods for past 3 years
Liver capsules 4 daily past 3 months
Camu Camu powder, a natural Vitamin C, 100-300 mg just started about two weeks ago
Rice bran 1 tsp before bed started two weeks ago
Bee pollen 1/2 tsp daily, started 3 months ago
I follow gluten free diet. I eat beef, chicken, raw liver, raw dairy, raw kefir, cheese, bone broth, some fruit, oatmeal and some vegetables like tomatoes, green beans, onions.

Since learning about thiamine, I have begun using Thiamax but am having a rough time of it. I took my first half dose (50mg) of Thiamax on December 26, 2020 and continued that dose through December 31st. It seemed to increase my fatigue more than my normal, which is already pretty debilitating so I switched to 50mg thiamine HCL on January 1st. By January 3^rd, I had a big crash. Hoping to minimize these reactions, on January 4th I took 25 mg thiamine HCL with 12 mg Thiamax in two divided doses. The next evening, however, I rolled over at 2 AM and my heart rate went crazy. I was shaking and went into a panic attack. It took hours to settle down. I haven’t had anything like this in quite a few years and I can’t imagine this would be from the tiny doses of thiamine I’ve been taking. I also took 600mcg of biotin that night at around 6pm. This was for a longstanding fungal infection. The biotin may have contributed to my reaction, but I do not know. I skipped the thiamine and biotin the next day and was able to sleep. I have resumed the thiamine once again and so far, I am tolerating it. I understand that people with chronic health conditions have difficulty adjusting to thiamine and I am trying my best make it through to the other side, but these reactions are difficult to manage. Any input from others who have been through this would be appreciated. I desperately want to recover my health.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by (El Caminante) from Pixabay.

Rest in peace Tawnya, 2023.

This story was published originally on January 11, 2021.

Atomic Imprint: A Legacy of Chronic Illness

by Genie

Published on May 21, 2025

16420 views

In a sense, my complicated health history began a decade before I was born. In 1951, on a chilly pre-dawn morning in Nevada, my father-to-be crouched in a trench with his Army comrades and shielded his eyes with his hands. Moments later, an atomic blast was detonated with a light so brilliant that he could see the bones in his hands through his eyelids, like an x-ray. The soldiers were marched to ground zero within an hour, exposing them to massive amounts of radiation. My father suffered many physical issues and died of chronic lymphocytic leukemia at 61 – a far younger age than usual with this disease.

Many of the soldiers exposed to atomic tests and military radiation cleanup efforts paid dearly with their health, and the legacy was passed on to their offspring in the form of miscarriages, stillbirths, deformities, retardation, childhood cancers, and chronic health issues. I never wanted children, in part because I was concerned that my own genes were affected by my father’s radiation exposure.

Early Markers of Ill Health

Physically, I didn’t feel right as a child. I had mononucleosis as a baby and needed a prednisone shot to get well. I was sick often and lacked stamina. I had mono again in high school and relapsed in college.

I fared well as a young adult, but then hit a wall in my mid-30s when I suddenly became chronically ill with digestive issues, insomnia, brain fog, and fatigue. A hair test revealed off-the-charts mercury poisoning, so I had ten fillings replaced and detoxed. All my hormone levels crashed, so I went on bioidentical hormone replacement therapy for a time. I recovered quickly but adrenal and thyroid hormone support were still necessary. I even fared poorly with the ACTH cortisol stimulation test to assess for adrenal insufficiency (“adrenal disease” beyond so-called “adrenal fatigue”).

In 2001, a DEXA scan revealed I had osteopenia at just 40 years old and I tested positive for elevated gliadin antibodies, a marker for celiac disease, the likely cause of the bone thinning. I went gluten-free and began lifting weights – thankfully, my bone density resolved. I shifted away from a vegetarian diet and gained muscle mass and energy.

Over the next several years, I had bouts of “gut infections,” resolving them with herbal antimicrobials. About a decade ago, the dysbiosis flares became more frequent and difficult to resolve. I tested positive again for mercury. This time I did the Cutler frequent-dose-chelation protocol and reduced my mercury burden to within normal levels according to hair tests.

A Labyrinth of Health Issues

My health issues were becoming more numerous, complex, and difficult to manage as I grew older. Besides the persistent sleep and digestion issues, I often had fatigue, pain, bladder pain, urinary frequency, restless legs, migraines, Raynaud’s, chilblains, and more. Managing all these symptoms was a real juggling act and rare was the day that I felt right.

As I searched for answers, I turned to genetic testing, starting with Amy Yasko’s DNA Nutrigenomic panel in 2012 and then 23andMe in 2013 to learn which “SNPs” (single nucleotide polymorphisms) I have. A Yasko-oriented practitioner helped me navigate the complexities of the nutrigenomics approach – that is, using nutrition with genetic issues.

I learned that genes drive enzymes that do all the myriad tasks to run our bodies (which don’t just function automatically), and that certain vitamins and minerals are required to assist the enzymes, as specific “cofactors.” Genetic SNPs require even more nutritional support than is normal to help enzymes function better. So my focus shifted toward using basic vitamins and minerals to support my genetic impairments. I now understood that I needed extra B12, folate, glutathione, and more. I began following Ben Lynch’s work in elucidating the MTHFR genetic issue, as I had MTHFR A1298C.

Also in 2013, given my struggle with diarrhea, I was diagnosed with microscopic colitis via a biopsy with colonoscopy. In 2014, I learned about small intestinal bacterial overgrowth (SIBO), which gave me a more specific understanding of my “gut infections,” and tested positive for methane SIBO. I worked with a SIBO-oriented practitioner on specific herbal treatments with some short-lived success.

At the end of 2014, I learned that I have Ehlers Danlos Syndrome (EDS, Hypermobile Type), confirmed by a specialist. I came to understand that my “bendiness” likely had implications in terms of chronic illness, and I saw my bunion and carpal tunnel surgeries in a new context, as part of this syndrome.

Even with these breakthroughs in understanding, I still relentlessly searched deeper for root causes.

Genetic Kinetics

In 2018, Ben Lynch published Dirty Genes, focusing on a number of common yet impactful SNPs.

I learned that I had NEARLY ALL of these SNPs – NEARLY ALL as “doubles” and even a “deletion.” (Deletions are worse than doubles; doubles are worse than singles.) Researching further, I had doubles in many related genes with added interactive impacts. Typically people might have just a few of these SNPs.

Understanding my “dirty gene” SNPs revealed that I could be deficient in methylation, detoxification, choline synthesis, nitric oxide synthesis, neurotransmitter processing, and histamine processing. Each of these SNPs could potentially impact sleep, digestion, and much more in numerous ways. Now I potentially had a myriad of root causes.

Lynch warns people to clean up their health act before supplementing the cofactors, whereas I’d cleaned mine up years prior. Sadly, I found only limited improvements in adding his nutritional protocol. Suffice it to say I felt rather overwhelmed and disheartened.

But at the same time, I gained vital and necessary insights. I now understood why I had mercury poisoning twice: detox impairments. I understood why I had Raynaud’s, chilblains, and poor circulation: nitric oxide impairments. My migraines could be histamine overload. I needed high levels of choline for the PEMT gene to prevent fatty liver disease and SAMe for the COMT gene. Much was yet still unexplained. So I relentlessly soldiered on, following every lead, clue, and a new piece of information.

Later in 2018, a friend who also has EDS encouraged me to learn about Mast Cell Activation Syndrome (MCAS), as many with EDS also have this condition. A few weeks later, I had a three-day flare of many issues, which prompted me to delve into the MCAS world, which was just as complex as the genetic approach. In working with an MCAS specialist, I honed in on three supplements, quercetin, palmitoylethanolamide, and luteolin, to help stabilize mast cells, which improved my bladder pain, bone pain, migraines, fatigue, and generalized pain. This was the culmination of months of research and work. All of this points to further genetic involvement, even though I lack specifics.

Downward Spiral

Twenty-nineteen brought further insights. I integrated circadian rhythm entrainment work. I tried a low-sulfur diet, suspecting hydrogen sulfide SIBO, which made me feel worse; and I began taking dietary oxalates somewhat more seriously after testing positive on a Great Plains OAT test. I did glyphosate and toxicity testing, which provided a picture of my toxic load. Testing also indicated high oxidative stress and mitochondrial issues (very interrelated). Hair Tissue Mineral Analysis (HTMA) testing, with the assistance of a specialist, helped me understand my mineral status and to begin rebalancing and repleting.

In 2020, I took a hiatus from all this effort, during which time I turned my attention towards personal matters, but 2021 has been a doozy in redoubling my health efforts. My digestion had worsened, so I focused on this area. I learned about sucrase-isomaltase deficiency, a lack of certain enzymes to digest sucrose and starch. I hadn’t tolerated sugar and starch for years, and I found I had a SNP for this condition. In January, a zero-carb trial diet helped me feel much better, so I continued. I tested positive for hydrogen sulfide SIBO, and I wrestled with this “whole-other-SIBO-beast” – in February trying again the low-sulfur diet and again feeling worse. Combining the zero-starch and low-sulfur diets left few options. Despite all my best efforts, I experienced a downward spiral with a loss of appetite, nausea, and vomiting every few days.

Discovering Thiamine

Around this time, I read an article about low thiamine (Vitamin B1) lowering intracellular potassium – I had been trying unsuccessfully to raise my potassium level in my HTMA work. I began following author Elliot Overton’s articles and videos on thiamine deficiency and oxalates. I was finally persuaded to take oxalates seriously. I then read the definitive book “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition” by Drs. Derrick Lonsdale and Chandler Marrs. I learned how B1 was key in many processes involving energy, digestion, and much more. I found that I had multiple SNPs in the B1-dependent transketolase gene, which is pivotal in several pathways. I gained some understanding of how all this related to some of my other genetic impairments, and why I might need high dose thiamine to overcome some issues.

All this was quite a revelation for me. It fit perfectly with my emphasis on vitamins and minerals to assist genes…but why hadn’t I learned of B1’s significance sooner?

In early March, I began my thiamine odyssey with 100 mg of thiamine HCL, upping the dose every couple of days. At 300mg HCL, I added 50 mg of TTFD, a more potent and bioavailable form of B1, then continued to up the TTFD dose every few days.

Similar to my experience with other vitamins, I was able to proceed rather quickly in dose increases. Many other people are not so fortunate and must go much more slowly. I already had in place most of thiamine’s cofactors (such as glutathione, other B vitamins, and methylation support) – so perhaps this helped me proceed more readily. Without these cofactors, peoples’ thiamine efforts often fail.

Magnesium is one of the most important thiamine cofactors, and for me, the most challenging. My gut cannot handle it, so I must apply it transdermally two or more times a day. At times, I had what I interpreted as low magnesium symptoms: racing and skipping heart, but these resolved as I continued.

Additionally, one must be prepared for “paradoxical reactions.” Worse-before-better symptoms hit me the day after thiamine dose increases: gut pain, sour stomach, headache, fatigue, and soreness.

My symptoms improved as I increased the dosing. When I added 180 mg of benfotiamine early on, my bit of peripheral neuropathy immediately cleared. This form of B1 helps nerve issues. As I increased my thiamine dosing, the nausea abated, my appetite came roaring back, and gastritis disappeared. Diarrhea, fatigue, and restless legs improved. I was able to jog again. My digestion improved without trying to address the SIBO and inflammation directly; the strict keto and low oxalate diets may have also helped.

In June, I attained a whopping TTFD dose of 1500 mg but did not experience further resolution beyond 1200mg, so I dropped back down. At 1200mg for a month, a Genova NutrEval test revealed that I was not keeping pace with TTFD’s needed cofactors, especially glutathione and its substrates. Not too surprising, given my malabsorption issues and my already high need for these nutrients. I dropped the TTFD to 300 mg, but quickly experienced fatigue. I’m now at 750 mg, which is still a large dose, and clearly, there is more to my situation than thiamine can address. I still have diarrhea and insomnia, and continue working to address these.

The Next Chapter

With TTFD, its cofactors, and my new gains in place, I’ve turned my attention towards a duo of genetic deletions that I have in GPX1 (glutathione peroxidase 1, one of Lynch’s dirty genes) and CAT (catalase). Both of these enzymes break down hydrogen peroxide (H2O2), a byproduct of numerous bodily processes. This unfortunate double-whammy causes me a build-up of damaging H2O2 and lipid peroxides – in other words, oxidative stress, a major factor in mitochondrial impairment, many diseases, and aging. This might be one of my biggest and yet-unaddressed issues, and I am digging deep into the published medical literature. This new chapter is currently unfolding.

I believe these two deletions are related to my father’s radiation exposure, for reasons beyond the scope of this article. But what about all the other SNPs? Many questions remain unanswered.

All my gains have been so hard-won, involving much research, effort, and supplementation. Yet what other options do I have, besides playing whack-a-mole and spiraling downward? Looking back, my improvements have been substantial, given the multitude of issues I’ve had to deal with. Perhaps now at 60, my life can start to open again to more than just self-care.

I hate to think of where I would be now, had I never come across the thiamine deficiency issue. I believe a number of factors had driven my thiamine status dangerously low earlier this year, such as malabsorption, oxidative stress, and hydrogen sulfide SIBO. I’m forever grateful to Lonsdale, Marrs, and Overton for their invaluable thiamine work that helped guide me back from the brink, and to the numerous doctors and practitioners who have helped me get this far. Perhaps my story can help others struggling with chronic health issues.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Image credit: First U.S. nuclear field exercise conducted on land; troops shown are a mere 6 miles from the blast. Nevada Test Site, 1 November 1951. This image is a work of a U.S. military or Department of Defense employee, taken or made as part of that person’s official duties.

As a work of the U.S. federal government, the image is in the public domain in the United States.

This article was published originally on September 23, 2021.

SIBO, IBS, and Constipation: Unrecognized Thiamine Deficiency?

by Elliot Overton, DipCNM CFMP

Published on May 13, 2025

160616 views

In many of my clients, chronic upper constipation and gastroesophageal reflux disease (GERD) are misdiagnosed as bacterial overgrowth. Unfortunately, they are often non-responsive to antimicrobial treatments. Yet, sometimes the issues are fixed within a few days of vitamin B1 repletion. This has shown me that often times, the small intestinal bacterial overgrowth (SIBO) is simply a symptom of an underlying vitamin B1 or thiamine deficiency.

GI Motility and Thiamine

The gastrointestinal (GI) tract is one of the main systems affected by a deficiency of thiamine. Clinically, a severe deficiency in this nutrient can produce a condition called “Gastrointestinal Beriberi”, which in my experience is massively underdiagnosed and often mistaken for SIBO or irritable bowel syndrome with constipation (IBS-C). The symptoms may include GERD, gastroparesis, slow or paralysed GI motility, inability to digest foods, extreme abdominal pain, bloating and gas. People with this condition often experience negligible benefits from gut-focused protocols, probiotics or antimicrobial treatments. They also have a reliance on betaine HCL, digestive enzymes, and prokinetics or laxatives.

To understand how thiamine impacts gut function we have to understand the GI tract. The GI tract possesses its own individual enteric nervous system (ENS), often referred to as the second brain. Although the ENS can perform its job somewhat autonomously, inputs from both the sympathetic and parasympathetic branches of the autonomic nervous system serve to modulate gastrointestinal functions. The upper digestive organs are mainly innervated by the vagus nerve, which exerts a stimulatory effect on digestive secretions, motility, and other functions. Vagal innervation is necessary for dampening inflammatory responses in the gut and maintaining gut barrier integrity.

The lower regions of the brain responsible for coordinating the autonomic nervous system are particularly vulnerable to a deficiency of thiamine. Consequently, the metabolic derangement in these brain regions caused by deficiency produces dysfunctional autonomic outputs and misfiring, which goes on to exert detrimental effects on every bodily system – including the gastrointestinal organs.

However, the severe gut dysfunction in this context is not only caused by faulty central mechanisms in the brain, but also by tissue specific changes which occur when cells lack thiamine. The primary neurotransmitter utilized by the vagus nerve is acetylcholine. Enteric neurons also use acetylcholine to initiate peristaltic contractions necessary for proper gut motility. Thiamine is necessary for the synthesis of acetylcholine and low levels produce an acetylcholine deficit, which leads to reduced vagal tone and impaired motility in the stomach and small intestine.

In the stomach, thiamine deficiency inhibits the release of hydrochloric acid from gastric cells and leads to hypochlorydria (low stomach acid). The rate of gastric motility and emptying also grinds down to a halt, producing delayed emptying, upper GI bloating, GERD/reflux and nausea. This also reduces one’s ability to digest proteins. Due to its low pH, gastric acid is also a potent antimicrobial agent against acid-sensitive microorganisms. Hypochlorydria is considered a key risk factor for the development of bacterial overgrowth.

The pancreas is one of the richest stores of thiamine in the human body, and the metabolic derangement induced by thiamine deficiency causes a major decrease in digestive enzyme secretion. This is one of the reasons why those affected often see undigested food in stools. Another reason likely due to a lack of brush border enzymes located on the intestinal wall, which are responsible for further breaking down food pre-absorption. These enzymes include sucrase, lactase, maltase, leucine aminopeptidase and alkaline phosphatase. Thiamine deficiency was shown to reduce the activity of each of these enzymes by 42-66%.

Understand that intestinal alkaline phosphatase enzymes are responsible for cleaving phosphate from the active forms of vitamins found in foods, which is a necessary step in absorption. Without these enzymes, certain forms of vitamins including B6 (PLP), B2 (R5P), and B1 (TPP) CANNOT be absorbed and will remain in the gut. Another component of the intestinal brush border are microvilli proteins, also necessary for nutrient absorption, were reduced by 20% in the same study. Gallbladder dyskinesia, a motility disorder of the gallbladder which reduces the rate of bile flow, has also been found in thiamine deficiency.

Malnutrition Induced Malnutrition

Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals. In fact, this is indeed something I see frequently. And sadly, as thiamine is notoriously difficult to identify through ordinary testing methods, it is mostly missed by doctors and nutritionists. To summarize, B1 is necessary in the gut for:

Stomach acid secretion and gastric emptying
Pancreatic digestive enzyme secretion
Intestinal brush border enzymes
Intestinal contractions and motility
Vagal nerve function

Based on the above, is it any wonder why thiamine repletion can radically transform digestion? I have seen many cases where thiamine restores gut motility. Individuals who have been diagnosed with SIBO and/or IBS and are unable to pass a bowel movement for weeks at a time, begin having regular bowel movements and no longer require digestive aids after addressing their thiamine deficiency. In fact, the ability of thiamine to address these issues has been known for a long time in Japan.

TTFD and Gut Motility

While there are many formulations of thiamine for supplementation, the form of thiamine shown to be superior in several studies is called thiamine tetrahydrofurfuryl disulfide or TTFD for short. One study investigated the effect of TTFD on the jejunal loop of non-anesthetized and anesthetized dogs. They showed that intravenous administration induced a slight increase in tone and a “remarkable increase” in the amplitude of rhythmic contractions for twenty minutes. Furthermore, TTFD applied topically inside lumen of the intestine also elicited excitation.

Another study performed on isolated guinea pig intestines provided similar results, where the authors concluded that the action of TTFD was specifically through acting on the enteric neurons rather than smooth muscle cells. Along with TTFD, other derivatives have also been shown to influence gut motility. One study in rats showed an increase in intestinal contractions for all forms of thiamine including thiamine hydrochloride (thiamine HCL), S-Benzoyl thiamine disulphide (BTDS -a formulation that is somewhat similar to benfotiamine), TTFD, and thiamine diphosphate (TPD). A separate study in white rats also found most thiamine derivatives to be effective within minutes.

Most interestingly, in another study, this time using mice, the effects of thiamine derivatives on artificially induced constipation by atropine and papaverine was analyzed. The researchers tested whether several thiamine derivatives could counteract the constipation including thiamine pyrophosphate (TPP), in addition to the HCL, TTFD and BTDS forms. Of all the forms of thiamine tested, TTFD was the ONLY one which could increase gut motility. Furthermore, they ALSO showed that TTFD did not increase motility in the non-treatment group (non-poisoned with atropine). This indicated that TTFD did not increase motility indiscriminately, but only when motility was dysfunctional. Finally, severe constipation and gastroparesis identified in patients with post-gastrectomy thiamine deficiency, was alleviated within a few weeks after a treatment that included three days of IV TTFD at 100mg followed by a daily dose of 75mg oral TTFD. Other symptoms also improved, including lower limb polyneuropathy.

To learn more about how thiamine affects gut health:

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This article was first published on HM on June 1, 2020.

How Can Something As Simple as Thiamine Cause So Many Problems?

by Derrick Lonsdale MD, FACN, CNS

Published on April 29, 2025

164109 views

I have read a criticism that thiamine deficiency is “too simple” to explain the devastating nature of the post Gardasil illnesses or the systemic adverse reactions to some medications. Sometimes, it is the simple and overlooked elements that are the most problematic.

Understanding Thiamine’s Role in Complex Adverse Reactions – The Limbic System

The lower part of the brain, called the brainstem, is a like computer, controlling the most basic aspects of survival, from breathing and heart rate, hunger and satiety, to fight or flight and reproduction. This computer-like function within the brainstem is called the autonomic system (ANS). The ANS together with the limbic system act in concert to regulate our most basic survival functions and behaviors. Both require thiamine to function.

Postural Orthostatic Tachycardia Syndrome or POTS , a type of dysautonomia (dysregulation of the autonomic system) seems to be the among the commonest manifestations of the Gardasil effect. Many cases have been diagnosed already, while others present all of the symptoms but have yet to receive a diagnosis. Dysautonomia and POTS have also been observed with adverse reactions to other medications, as well. Dysautonomia and POTS, at the most basic level, represent a chaotic state of the limbic-autonomic system. Let me explain.

Fragmented Fight or Flight

The brainstem autonomic system together with the limbic system enable us to adapt to our environment, presiding over a number of reflexes that allow us to survive. For example, fight-or-flight is a survival reflex, triggered by perception of a dangerous incident that helps us to kill the enemy or escape. This kind of “stress event” in our ancestors was different from that we experience today. Wild animal predators have been replaced by taxes/business deadlines/rush hour traffic etc. These are the sources of modern stress. The beneficial effect is that the entire brain/body is geared to physical and mental response. However, it is designed for short term action and consumes energy rapidly. Prolonged action is literally exhausting and results in the sensation of fatigue. In the world of today where dietary mayhem is widespread, this is commonly represented as Panic Attacks, usually treated as psychological. They are really fragmented fight-or-flight reflexes that are triggered too easily because of abnormal brain chemistry.

Thiamine and Oxidative Metabolism: The Missing Spark Plug

Our brain computers rely completely on oxidative metabolism represented simply thus:

Fuel + Oxygen + Catalyst = Energy

Each of our one hundred trillion body/brain cells is kept alive and functioning because of this reaction. It all takes place in micro “fireplaces” known as mitochondria. Oxygen combines with fuel (food) to cause burning or the combustion – think fuel combustion engine. We need fuel, or gasoline, to burn and spark plugs to ignite in order for the engines to run.

In our body/brain cells it is called oxidation. The catalysts are the naturally occurring chemicals we call vitamins (vital to life). Like a spark plug, they “ignite” the food (fuel). Absence of ANY of the three components spells death.

Antioxidants like vitamin C protect us from the predictable “sparks” (as a normal effect of combustion) known as “oxidative stress”. Vitamin B1, is the spark plug, the catalyst for these reactions. As vitamin B1, thiamine, or any other vitamin deficiency continues, more and more damage occurs in the limbic system because that is where oxygen consumption has the heaviest demand in the entire body. This part of the brain is extremely sensitive to thiamine deficiency.

Why Might Gardasil Lead to Thiamine Deficiency?

We do not know for sure how Gardasil or other vaccines or medications have elicited thiamine deficiency, but they have. We have two girls and one boy, tested and confirmed so far. More testing is underway. Thiamine deficiency in these cases may not be pure dietary deficiency. It is more likely to be damage to the utilization of thiamine from as yet an unknown mechanism, affecting the balance of the autonomic (automatic) nervous system. It is certainly able to explain POTS (one of the many conditions that produce abnormal ANS function) in two Gardasil affected girls. Beriberi, the classic B1 deficiency disease, is the prototype for ANS disease. Administration of thiamine will not necessarily bring about a cure, depending on time since onset of symptoms, but it may help.

Thiamine Deficiency Appetite and Eating Disorders

Using beriberi as a model, let us take appetite as an example of one of its many symptoms. When we put food into the stomach, it automatically sends a signal to a “satiety center” in the computer. As we fill the stomach, the signals crescendo and the satiety center ultimately tells us that we have eaten enough. Thiamine deficiency affects the satiety center, wrecking its normal action. Paradoxically it can cause anorexia (loss of appetite) or the very opposite, a voracious appetite that is never satisfied and may even go on to vomiting. It can also shift from anorexia to being voracious at different times within a given patient. That is why Anorexia Nervosa and Bulimia represent one disease, not two.

Thiamine Deficiency, Heart Rate and Breathing

The autonomic nervous system, responsible for fight or flight, regulates heart activity, accelerating or decelerating according to need. So heart palpitations are common in thiamine deficiency. Its most vital action is in control of automatic breathing and thiamine deficiency has long been known to cause infancy sudden death from failure of this center in brainstem.

Thiamine Deficiency and Sympathetic – Parasympathetic Regulation

The hypothalamus is in the center of the brain computer and it presides over the ANS, as well as the endocrine (hormone) system. The ANS has two channels of communication known as sympathetic (governs action) and parasympathetic (governs the body mechanisms that can be performed when we are in a safe environment: e.g. bowel activity, sleep, etc.). When the ANS system is damaged, sometimes by genetic influence, but more commonly by poor diet (fuel), our adaptive ability is impaired. A marginal energy situation might become full blown by a stress factor. In this light, we can view vaccines and medications as stress factors. From false signal interpretation, we may feel cold in a warm environment, exhibiting “goose bumps on the skin”, or we may feel hot in a cold environment and experience profuse sweating. The overriding fatigue is an exhibition of cellular energy failure in brain perception.

Sometimes, it really is the simple, overlooked, elements that cause the most devastating consequences to human health. Thiamine deficiency is one of those elements.

To learn more about thiamine testing: Thiamine Deficiency Testing: Understanding the Labs.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Photo by Robina Weermeijer on Unsplash.

This article was published originally in October 2013.

Rest in peace Derrick Lonsdale, May 2024.

Thiamine, Epigenetics, and the Tale of the Traveling Enzymes

by Chandler Marrs, PhD

Published on April 23, 2025

10912 views

For some time now, we have been covering all the ways in which thiamine deficiency influences disease. The primary mechanisms are through the down regulation of mitochondrial enzymes critical for ATP production. The lack of thiamine impairs mitochondrial functioning significantly leading to complex, debilitating, chronic, and sometimes, deadly illnesses. With mitochondrial energy a requisite for cell functioning and survival it is easy to see how the diminishment of mitochondrial functioning would negatively impact health and how high-energy physiological systems like the nervous and cardiovascular systems might be particularly hard hit. More than just just derailing cell function, as if that wasn’t problematic enough, when mitochondrial energy production slows, the adaptive cascades that ensue include epigenetic modification, not only at the level of mitochondrial DNA (mtDNA), but also, at the level of gene expression from the cell nucleus or nDNA. This is a huge discovery with broad implications about health and disease. It means that all sorts of things considered innocuous, are directly influencing gene activation and deactivation by way of the mitochondria.

Epigenetics: How the Cells Adapt to the Environment

Epigenetic modification refers to the activation or deactivation of chromosomal gene expression absent mutation. These changes can be heritable and often are. Strictly speaking, epigenetics involves changes in methylation, histone modification and/or alterations in non-coding RNA that affect transcription. Epigenetics is the way our genome adapts to environmental circumstances and prepares our offspring to do the same. The majority of epigenetic work focuses on genomic changes. That is, those variables that affect gene expression from the cell nucleus or nDNA. There is a growing body of evidence, however, that mitochondrial DNA (mtDNA) are affected by epigenetic factors in much the same way as nDNA. In fact, given the mitochondria’s role in cell survival, one might suspect that mitochondria are more susceptible to environmental epigenetics, perhaps even the first responders and/or the initiators of chromosomal genetic changes.

Considering that nDNA accounts for over 90% of the proteins involved in mitochondrial functioning, how could damaged mitochondria, even functionally inefficient mitochondria, not affect gene expression in the cell’s nucleus? Though we tend to think of mitochondria as self-contained and discrete entities, black boxes of sorts, where stuff goes in and ATP magically comes out, this is not only not the case, it seems biologically illogical to think that way. So much of mitochondrial functioning is related to its environmental milieu. In fact, increasingly researchers are finding that the mitochondria are the center of the organismal universe, sensing and signaling danger, and effectively, regulating all adaptive responses, including epigenetic modification of the proteins encoded by the cell nucleus.

Beyond the strict definition of epigenetics, it seems to me that any factor that altered mitochondrial function, would eventually alter gene expression by any number of mechanisms, not just the direct ones. That is, because the mitochondria produce the energy required for cell survival, anything that derails their capacity to produce ATP, pharmaceutical and environmental chemicals, for example, should be considered, ipso facto, epigenetic modulators. Energy is a fundamental requirement for life. How could energy depletion not affect gene expression? It does, and now we know how.

Starve the Mitochondria, Alter the Genome

It turns out, when the mitochondria are starving and/or damaged the key enzyme complex that sits atop the entire energy production pathway and is critical for the production of the substrates involved directly (yes, I said directly) with gene expression, migrates from the mitochondria across the cell and into the cell’s nucleus where it then sets up shop and begins its work there. Sit with that for a minute. The entire enzyme complex decides that things are not working where it is, so it hitches a ride with some transporter proteins, several of them along the way, to find a more suitable home. The enzyme complex ‘knows’ that its functions are critical for survival and so it must move or die. What an incredible bit of adaptive capacity. A symbiosis, if you will.

To make matters even more interesting, the traveling enzyme complex just so happens to be the pyruvate dehydrogenase complex (PDC) and you guessed it, the PDC is highly, and I mean highly, thiamine dependent. But wait, there’s more. Several other enzymes involved in mitochondrial bioenergetics are also thiamine dependent. These include: alpha-ketoglutarate dehydrogenase (α- KGDH) in the tricarboxylic acid (TCA) or citric acid cycle, transketolase (TKT) within the pentose phosphate pathway (PPP), the branched chain alpha-keto acid dehydrogenase complex (BCKDC) involved in amino acid catabolism and, more recently, thiamine has be identified as a co-factor in fatty acid metabolism via an enzyme called 2-hydroxyacyl-CoA lyase (HACL1) in the peroxisomes (organelles that break down fatty acids before transporting them to the mitochondria). So thiamine deficiency is problematic. It not only causes dysfunction in the mitochondria, reducing bioenergetic capacity, but if severe enough and/or chronic, it alters the genome. And those changes are likely heritable. That is, your thiamine deficiency likely will affect your children’s ability to process thiamine.

Thiamine Deficiency and Gene Expression

Without sufficient thiamine, the PDC enzyme complex does not function well and because of its geographic position at the entry point into the citric acid cycle, when it is not working at capacity, everything below it eventually grinds to a halt resulting in severe neurological and neuromuscular deficits. Absent congenital PDC disorders, however, when it simply is inefficient or starved for its cofactors, metabolic disorders ensue because we cannot convert carbohydrates into ATP and the sugars that normally would be converted into energy, remain unmetabolized, floating around outside the cells and causing the whole cascade of effects that mark type 2 diabetes. When the PDC is inefficient, ATP levels wane and fatigue ensues. Systems that are highly energy dependent are hit the hardest. Think brain, heart, muscles, GI tract. When mitochondria are inefficient or damaged, reactive oxygen species (ROS) increase. Anti-oxidant capacity decreases and further damage to the PDC ensues. Inflammation increases, immune function decreases. Cell level hypoxia grows. Alternative energy pathways are activated, those that are endemic of cancer. Yes, cancer can be considered a metabolic disorder.

When the PDC is inefficient, mtDNA heteroplasmy, the balance between mutated mtDNA and healthy mtDNA grows with each mitogenic cycle. This, of course, further derails mitochondrial capacity (and increases the need for thiamine). Absent available resources, mitochondrial death cascades are initiated. And now, we know at some point in this disease and death spiral, when ATP diminishes and the litany of adaptive measures fail to maintain sufficient energy availability, the PDC up and leaves its mitochondrion and sets up shop in the cell nucleus, in what is presumably a last ditch effort to save its cell and the organism as a whole. What a remarkable bit of adaptive capacity.

The researchers, who discovered this, ruled out the possibility that the PDC enzyme complex was already in the cell nucleus. It wasn’t. It traveled by way of several transporter proteins. They also found that once in the nucleus, it began producing acetyl-coenzyme A (CoA). Acetyl-CoA is requisite for the acetylation and deacetylation of histones, post translational changes in DNA, but also lysine acetylation, which further affects metabolism – mitochondrial energy homeostasis. With insufficient acetyl-CoA and insufficient acetylation, DNA replication is aberrant. Moreover, without sufficient acetyl-CoA, acetylcholine synthesis, an incredibly important transmitter for nervous system functioning, diminishes.

A Constitutively Active Enzyme: What Could Possibly Go Wrong?

Even more interesting, the PDC in the cell nucleus appears to be constitutively active. Unlike in healthy mitochondria where checks and balances prevail, when the PDC travels to the nucleus it has no feedback control to temper its activity. The enzymes that normally shut down PDC production (pyruvate dehyrodgenase kinase) in the mitochondria, were not present in the cell nucleus, and thus, once the PDC was turned on, it stayed on. That means when the PDC translocates to the cell nucleus it operates independently much like a Warburg effect in cancer metabolism; one that fully supplants healthier metabolic pathways. Can you say tumorogenesis?

This research has enormous implications for everything from cancer to Alzheimer’s disease and everything in between that involves metabolic disturbances like diabetes and heart disease. Metabolism begins and ends with the mitochondria, at the PDC, and the PDC is highly dependent on thiamine. Every pharmaceutical and environmental chemical damages the mitochondria in some manner or another and that damage inevitably reduces ATP capacity. Some chemicals also deplete thiamine directly, thus downregulating the activity of the PDC and the other thiamine dependent enzymes. Even when these chemicals don’t deplete thiamine directly, the western diet is more often than not thiamine deficient, sometimes only marginally, others time quite significantly so with symptoms already expressed, but very rarely recognized. We have known that thiamine was critical for health and survival for some time. Now we have one more reason to tread carefully with lifestyles and exposures that deplete thiamine.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

David Goodsell, CC BY 3.0, via Wikimedia Commons

This article was first published on April 25, 2017.

Mystery Illness: You Are Not Alone

by Derrick Lonsdale MD, FACN, CNS

Published on April 21, 2025

13367 views

Hormones Matter is a health oriented website edited by Chandler Marrs, PhD. She has long recognized the need for people to report their “mystery illnesses”, simply because they are slipping through the cracks in modern medicine. My association with Dr. Marrs is a very fruitful one because we both have the same viewpoint. This viewpoint embraces the concept that the present disease model is antiquated and badly needs to be revised. In a recent post, I have defined what we mean by a “medical model”. We both have found that a common health problem, largely unrecognized for its true cause, is a polysymptomatic illness that is almost invariably labeled psychosomatic. I will try to explain.

Food, Energy, and Illness

Much of our food is broken down to glucose, the primary fuel of the brain. This has given rise to a common concept that taking virtually any form of sugar is a way to develop “quick energy”. Before the processing of sugar in the body was understood, athletes would sometimes load up on it. We now know that this defeats the purpose. Very much like a car where an excess of gasoline “chokes” the engine, an excess of sugar has a very similar effect, particularly in the brain. An additional effect of sugar is the extremely sweet taste that sends a signal from the tongue to centers in the brain that gives the person an extreme sense of pleasure. It has been shown in animal studies that sugar is more addictive than cocaine and a book was published in 1973 entitled “Sweet and Dangerous”. The author, Dr. John Yudkin, was a professor of nutritional studies in a major London hospital. He was able to show that sugar was the cause of many modern diseases. It is indeed hard for people to understand that such an appreciated delight is dangerous to our health. If we turn to nature, you will find that sugar is never found in its free state. It is always found in fruit and vegetables where fiber is a vital component in its processing. The sweet taste from eating a banana or an orange is the way that Mother Nature designed it and it is a healthy way of experiencing a sweet taste.

Glucose is burned (oxidized) in cellular “engines” (mitochondria) and it is a very complex process. The net result is energy that is stored in a chemical substance known as adenosine triphosphate (ATP). The nearest analogy would be a battery because the energy that drives all our mental and physical functions is electrical in nature.

By far and away the commonest personal story posted on Hormones Matter is a polysymptomatic illness that is the result of inefficient energy transduction and its major effect is in the brain. To put it as simply as possible, food is not being converted into energy in sufficient amount to meet the stresses of merely being alive. The most susceptible part of the brain that is affected is the part that controls our ability to adapt to living in an environment that is essentially hostile. Using a specialized nervous system and a bunch of glands that produce hormones, this part of the brain signals every organ in the body to participate. Now obviously, if no energy were produced we would die and that is indeed a major cause of death. However this common polysymptomatic illness affecting so many people is based on an inefficient energy production, not a complete lack. It can vary in its degree of severity depending on nutritional and genetic factors. The dominant effect is “psychological”, symptoms such as undue fatigue, depression, anxiety and anger. It can run the gamut of our emotional reactions. In fact, because of its emotional implications, I have suggested that the common state of violence in America is a reflection of our uncontrolled hedonism. Can a person nursing a perceived grievance become violent if the emotional controls are too easily activated?

Energy lack is quickly recognized as dangerous by the brain. It causes a sense of panic to be felt by the affected person. That is why “panic attacks” have been recognized incorrectly as a “psychological disease that requires a medicine to tranquilize the patient” whereas they really represent a fight-or-flight reflex, naturally designed to get the affected person “out of perceived danger, i.e. energy deficiency”. The affected person seeks medical help, but this effect in the brain is seen by most physicians as “psychological”, as though the patient is inventing the symptoms. The diagnosis is, “it’s all in your head”. The irony is that although the symptoms are indeed the result of a function “in the head”, they are evidence of a sick brain lacking in adequate energy and therefore have an understandable origin and meaning. Also, the symptoms are easily erased by administration of non-caloric nutrient supplements when they are initially experienced. If allowed to continue unchecked, sometimes for years, they may lead to the irreversible damage characterized as a neurodegenerative disease.

Because the dominant effect is in the part of the brain that controls the specialized nervous system, it begins to send out exaggerated “panic” signals to the organs of the body. The result is a variable assortment of physical effects— heart palpitations, breathing problems, diarrhea, often alternating with constipation, whole body pain, migraine headaches, nasal congestion, nausea with or without vomiting, chest or abdominal pain, pins and needles etc. In other words, any organ in the body may be activated or non-activated because the pattern of our adaptive mind/body machinery is adversely affected. The very important point is this: each and every action of the brain/body union requires energy, even sleep!

Perhaps the most common symptom is severe fatigue and this has given rise to a common diagnosis of Chronic Fatigue Syndrome (CFS). It is worth noting that it is often associated with Irritable Bowel Syndrome (IBS) and it seems to be medically accepted that two diseases, both of “unknown cause” can occur in a patient at the same time. That seems to be a product of illogical thinking based on the present medical model.

Share Your Story

Anyone encountering this website is encouraged to write his or her health story and share it as a blog post. These stories help raise awareness about the scope of illnesses affecting us all and add to the knowledge base. To share your health story, send us a note here.

If you have specific questions about health and illness, we recommend that you “surf” the site because there are many posts on a variety of topics with long and detailed comment threads, one or more of which may be similar to your own story and may answer your questions.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by Leandro De Carvalho from Pixabay .

This article was published originally on December 2, 2019.

Rest in peace Derrick Lonsdale, May 2024.

Oxalate Degrading Microbes: Reconsidering Pathogenesis

by Susan Owens

Published on April 8, 2025

41823 views

oxalate degrading bacteria - lactobacillus

An exciting new paper was published recently which should turn the oxalate world upside down. The authors hunted public databases and compiled a list of microbes that possess variations of a gene called oxalyl CoA decarboxylase. That gene makes a protein that degrades oxalate.

Oxalate is an ion used by microbes for communication between fungus and bacteria, but it is found at varying levels in plant food. Our bodies also manufacture oxalate during a stress response. Everybody makes some amount of oxalate in their bodies and eats sometimes huge amounts of oxalate in foods like spinach, beets, nuts and seeds, and also (alas!) chocolate. When oxalate in our bodies gets too high, it causes dysbiosis and becomes dangerous, tangling with mineral metabolism, and delivering harsh changes to mitochondrial function, adding in distressing levels of oxidative stress.

Humans lack any oxalate-degrading gene in our own genome. That means we cannot degrade oxalate using our own talents. Instead, we are reliant upon our microbes in the gut to degrade oxalate. From studying isolated human beings who have never seen an antibiotic, scientists have realized that like them, our ancestors had plenty of oxalate degrading microbes in the gut (termed oxalotrophic microbes). The job of these microbes was to keep oxalate from food from getting into the inside of their bodies. That system worked well even when the diet was high in oxalate, but things changed when our microbiome began to be damaged by antibiotics and antifungals, and other hits.

In this discussion, I would like to examine findings from this recently published study from China: Abundance, Functional, and Evolutionary Analysis of Oxalyl-Coenzyme A Decarboxylase in Human Microbiota where they identified the microbial species that possess one of the two genes that we know are used to degrade oxalate in our intestines. We will also examine some other issues that this new knowledge unwraps.

Oxalate Degradation Is Dependent upon Thiamine and Is Impaired by Antibiotics

The protein oxalyl coenzyme A decarboxylase is dependent upon thiamine. It requires thiamine that is in other forms to be converted into thiamine diphosphate (TPP). Scientists have told us that this is the primary form of thiamine that microbes will make and use.

Some of us have inborn errors in our thiamine chemistry. Those errors might limit our delivery of thiamine to the inside of our gut so that our oxalate degrading microbes can use it. Another issue is that some antibiotics kill bacteria by attacking those microbes with a direct hit to their thiamine chemistry.

I had my own tangle with these issues very many years ago. Back in 1967, I was given two rounds of chloramphenicol, an antibiotic that attacks the thiamine chemistry in bacteria. In March of the following year, four months after I stopped taking the antibiotic, I developed bone marrow failure and almost died. The same blood disease, called aplastic anemia, has been found on occasion in primary hyperoxaluria, which is a genetic disease where the body makes fatal levels of oxalate coming mostly from producing oxalate in the liver.

Chloramphenicol was taken off the market in the US in 1968 because so many people died from blood problems that came on slowly like mine. Another antibiotic that attacks thiamine chemistry is Alinia and it is used broadly by functional medicine doctors. There may be even more antibiotics that would also cause this problem, but no one has done a systematic review of vitamin deficiencies caused by antibiotics. If someone would do this type of analysis of all licensed antibiotics, then doctors would have a list of antibiotics to avoid if their patients had a genetic weakness or a deficiency in thiamine or other vitamins. Also, some viral infections may purposefully impair thiamine chemistry to weaken the host. Polio is an example. That is why after certain infections, someone may actually develop a new oxalate problem.

Oxalate Degrading Species May Not Be Pathogenic

In the paper mentioned above, the researchers found 1739 Oxalate degrading species in humans. All of the different species they identified were equipped with oxalyl-Coenzyme A decarboxylase that allows microbes like oxalobacter formigenes to degrade oxalate. You may be surprised to learn that you have probably never heard of most of these species. Because I was curious about their identity, I looked for how many oxalate degrading bacteria show up on the GI Microbial Assay Plus (GI-MAP) test from Diagnostic Solutions Laboratory, or were found on the comprehensive-digestive-stool-analysis-(CDSA) from Genova Diagnostics. These are tests frequently ordered by functional medicine doctors or naturopaths. I have noticed how often these tests are ordered when a patient has some sort of GI distress because I routinely review that sort of lab work during consults and find out from the patient what his doctor prescribed after seeing the results of the test. Most often, the patient was given antibiotics. Of course, which antibiotic the doctor chose varied significantly.

Included in the list of bacteria that degrade oxalates, were many species that are believed to be pathogens because they were elevated on tests that were ordered at a time of increased symptoms. It is natural to assume these microbes were the primary cause of the symptoms, however, I cannot help but wonder if the relationship between these bacteria is what we thought it was. If oxalate is a communication method between microbes, how many of those symptoms could have been caused by the elevated oxalate or the effect of that oxalate on intestinal microbes? If oxalate is a favored food for these types of microbes, might they expand their population whenever oxalate is increased? This might be similar to how ants or flies may show up in numbers when you uncover food at a picnic. Flagging the increased count of these species on lab tests might have persuaded the doctors to treat with antibiotics, and there was no other game plan. Would reducing oxalate have helped solve the problem without antibiotics?

Oxalobacter Formigenes: An Oxalate Obligate

Within the oxalate field, a great deal of attention has been given to the microbe oxalobacter formigenes. The man who discovered this microbe, Dr. Milt Allison, had a lot to do with inspiring me to start looking more carefully at oxalate in autism and other conditions, and that grew to include pain conditions, autoimmunity, and gastrointestinal distress.

The uniqueness of oxalobacter formigenes, as far as we know, has been that it is the only microbe that requires oxalate to survive. Its dependency on oxalate is why scientists call it an oxalate obligate. This trait is why this microbe has received the most attention from scientists and became the launching point of this Chinese paper.

In a different study that I have reviewed before in the TLO Research Corner on the Trying Low Oxalates Facebook group, scientists looked at the differences in the diversity of microbes that survive in a very high oxalate condition (which in this case was chronic kidney stones) and compared that to normal controls. These scientists found out that oxalobacter doesn’t tolerate a high oxalate environment very well. Please note that their title implies that oxalate causes dysbiosis and not the reverse.

In the last two decades, a company called Oxthera and its predecessor have spent millions of dollars trying to develop oxalobacter as a drug for primary hyperoxaluria. Sadly, they still have no product on the market. Oxalobacter formigenes may have been the wrong microbe to pursue because the paper on dysbiosis found that this microbe really doesn’t like extremely elevated oxalate. This may be like humans having a hard time eating a hundred hamburgers in one sitting. This Chinese paper shows that scientists now have many more choices of oxalate-degrading microbes to study for research.

What Might Cystic Fibrosis Teach Us About Oxalates?

I have talked to our TLO group about this before, but cystic fibrosis is a genetic condition very important for oxalate research. This condition involves a broken intracellular regulator which governs the secretion of oxalate and sulfate among its other duties. This is why people with cystic fibrosis are elevated in oxalate. If someone has this gene defect, the mucus becomes very thick in the lungs and it is prone to infection. People with CF often live from cradle to grave with antibiotics. Pseudomonas aeruginosa often becomes their most common infection, and yes, this microbe showed up on the Chinese list of microbes that degrade oxalate. Might pseudomonas aeruginosa be growing too high levels and turning pathogenic just because it is responding to oxalate as its favorite food?

We are used to watching with distress as flies and ants discover our food at a picnic. Does oxalate become a picnic for certain microbes?

Have we made other mistakes assuming the worst about microbes when they were actually providing a benefit to us? I recently reviewed a paper in the TLO Research Corner that showed that intestinal infections with candida protected mice from systemic infections, including systemic infections with candida. Using antifungals destroyed that protection. Have we been confused about what was going on in microbial communities, putting black hats on microbes that might be trying to protect us from something worse?

Counting Microbial Species In Cystic Fibrosis

I used PubMed to discover that many of the oxalate degrading microbes identified in the Chinese paper have been commonly reported as infections in cystic fibrosis. This is what I found:

Pseudomonas – 7838
Burkholderia – 1624
Mycobacteria – 708
Achromobacter – 206
Klebsiella – 118
Pandoraae – 59

Is there a chance that excess oxalate in cystic fibrosis patients (which is known to occur) could be attracting and feeding these microbes in the lungs? Might the antibiotics used to kill these microbes be accomplishing something equivalent to killing the policeman or fireman who is trying to get rid of the flames to save your house? Could we have been making similar kinds of mistakes by not knowing which issues (like oxalate) were encouraging particular microbes to prosper?

Because of this Chinese paper, scientists may now have a very new direction to pursue. Unfortunately, this direction may be politically risky for them because antibiotics have been the main thrust of treatment for decades and are considered to be lifesaving in cystic fibrosis.

Is it too late in this game for a shift of focus to happen?

Pathogenic Bacteria in Stool Tests: Maybe Not

I went through the list from this Chinese paper and identified microbes that showed up on the standard stool-sample-based test that a lot of doctors are now ordering rather routinely. Here is the count of bacterial species that are covered on these tests but which the Chinese paper identified as being microbes capable of degrading oxalate. The number of species is coming from the oxalate paper and not from the lab tests.

Escherichia – 252
Mycobacterium – 221
Lactobacillus – 70
Shigella – 46
Bifidobacterium – 38
Proteobacteria – 6
Salmonella – 6
Klebsiella – 4
Enterobacter – 3
Pseudomonas – 3
Yersinia – 2
Bacillus – 1
Bacteroides – 1
Citrobacter – 1
Clostridium – 1
Prevotella – 1

I discovered that this list of microbes from stool tests covered 48% of the species that the Chinese study identified. Other species they found that degrade oxalate will be less familiar to everyone.

Probiotics and Oxalate Degradation

The Chinese study found that 78 species of lactobacillus and 38 of bifidobacteria possess the oxalyl-coA carboxylase that degrades oxalate. These two types of bacteria are included in most probiotics, and now we know why this sort of probiotic has been so helpful maybe for centuries. Of course, our ancestors who began to use yogurts and kefirs certainly had no idea that a chief mode of their action was degrading oxalate. Were people with this habit the people who routinely ate potatoes or beets or Swiss chard? The following article on kefir also helped to identify the bacteria from kefir that the Chinese article found could degrade oxalate: acetobacter and pseudomonas as well as lactobacillus and bifobacteria.

Rethinking Our Relationship with Bacterial Oxalate Degraders

What do we know about other species they mentioned and when those species might show up? Did this list of species expand in the intestines in people after those people became high in oxalate? Might the bacteria also have increased when oxalate was leaving tissues where it had been stored during a phenomenon that our oxalate project calls dumping? This involves a sudden increase of blood and urine oxalate when previously stored oxalate comes out of tissues in a kind of rush. Scientists have described this happening but never named it.

Could a mobilization of stored oxalate also have happened when someone was fasting while getting ready for surgery, or maybe fasting for their health? How do these bacterial populations shift when someone goes carnivore, and do we know if and when and how such a change may induce dumping?

Many previously unnoticed populations of microbes could have expanded because someone recently took an antibiotic that either killed the competitors of these microbes, or perhaps killed other oxalate-degrading microbes. Do we have any idea how these microbes would share an oxalate burden? Do we know under which circumstances one of them, versus another, would increase their population to meet that challenge? Scientists suddenly have so many questions they need to answer.

The most glaring question is whether the symptoms that prompted a doctor to order a lab test, instead of being a response to “overgrowth”, were instead caused by the disturbances made by the way elevated oxalate affected both our microbes and our intestinal cells. Could the symptoms have arisen due to the conversations taking place between our microbes and our intestinal cells about a distressing level of raised oxalate?

Urinary Tract Infections: E. Coli

It didn’t take long for me to recognize that the genus the Chinese paper reported as the most largely represented among the oxalate degraders was E. coli, with a record number of 252 species identified. Did you know that E. coli is the most frequent microbe identified in urinary tract infections? Of course, the urinary system is where oxalate can reach a critical concentration that may provoke kidney stones. Is the E. coli showing up there in order to protect us from the oxalate in urine?

Many doctors routinely do urine tests to identify bacteria in urine during well woman visits. If they find bacteria present like E. coli, they may prescribe an antibiotic. Most frequently, this will be Cipro, a fluoroquinolone that may especially target oxalate-degraders, but it also likes to damage tendons. Previously, I have reported in the TLO Research Corner that scientists found that when doctors prescribe antibiotics for non-symptomatic urinary tract infections, it actually leads to a worsened patient outcome. That becomes glaringly obvious after a future symptomatic infection takes place after the microbes that were targeted by the antibiotic became antibiotic resistant. There is much here to think about.

Oxalate and Dysbiosis

I am listing next the species that were found to be present at higher levels in those with kidney stones versus controls in a paper I reviewed. That paper boldly stated that oxalate causes dysbiosis, rather than the reverse. Recently I looked again in their supplementary materials and found their list of species that were much more prevalent in those with kidney stones than in their control population. Those kidney stone patients had greatly elevated oxalate compared to controls. I looked for which of the microbes from that list had been identified in the Chinese paper as oxalate degraders, and these microbes made the cut:

Bacteroidales
Bacteroides
Bifidobacterium
Burkholderiales
Clostridia
Enterobacteriaceae
Gammaproteobacteria
Prevotella

Please note that many of these oxalate-degrading microbes are also on the tests for microbial overgrowth.

Are you, like me, gnawed by the question of whether these microbial populations increase merely because they found excesses of oxalate to degrade? When your doctor or practitioner orders a stool test, if these species seem to be in overgrowth compared to their reference population, will your doctor think about first suggesting that you try a low oxalate diet or identify other sources of oxalate in you BEFORE he considers the use of antibiotics? Might addressing oxalate first be safer for your long-term intestinal health? We have learned that antibiotics might make your situation worse by perpetuating your issues with a longer term dysbiosis. Unfortunately, no one knows how to restore the anaerobic bacteria you lose with antibiotics. Probiotics won’t help you there since probiotics are cultured where air is present.

Rethinking the Role of Thiamine

We have all been in the habit of thinking that vitamins were in our diet just for our own benefit. It is a bit odd to think of vitamins also being there to nourish and equip our microbes. A new paper recently made it more certain that microbes in our colon actually make vitamins that can nourish our own colon cells and I am talking about the cells called colonocytes.

Other scientists have identified yet another thiamine requiring gene in a type of bacteria that generates acetic acid, which is a substance most of us know better as vinegar. This other protein is called oxalate oxidoreductase. They explain that the protein called oxalate oxidoreductase (OOR) metabolizes oxalate using thiamine pyrophosphate (TPP). The reaction generates two molecules of CO₂ and two low-potential electrons. The gene is there to help the bacteria make acetic acid from oxalate.

This simple but elegant mechanism explains how oxalate, a molecule that humans and most animals cannot break down, can be used for growth by acetogenic bacteria.

So oxalate is good for those particular microbes, but only because they have this special gene that is only found in this type of bacteria.

A Giant Rethink Is In Order

If we have misunderstood the purpose of so many microbes, perhaps it is time that we change our thinking!

In much of the world this last year some of us learned that there were prejudices we were taught that gave us different points of view about many groups that we thought we understood. We learned that many of us needed to listen to people from other groups to find a different perspective. Groups we had belonged to had taught us to define ourselves by membership within their ranks, but those groups also perpetuated our having a narrow point of view.

Similar human influences have shaped what scientists and the public and even doctors were able to notice within scientific findings. Instead of realizing that microbes were a beneficial part of our bodies, we instead assumed they were dangerous. Why? We didn’t understand what exactly the microbes were doing with their superset of genes that outnumbered our genes by at least 140 to one. We had no tools to recognize ways that they were doing good things for us.

Now we are learning how they degrade oxalate and we are learning that their job of ridding us of oxalate is apparently a lot more important to human life than anyone ever knew before. We also learned that their task was accomplished by a much more diversified team of players than we thought. Scientists are diligently working to understand relationships that were unknown to us before. These relationships are being revealed as we rid ourselves of some major assumptions.

So much of what we learned through these scientists deserves a giant rethink…like so many things that have happened to us this past year.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Photo by CDC on Unsplash.

This article was published originally on June 7, 2021.

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Oxalate Degradation Is Dependent upon Thiamine and Is Impaired by Antibiotics

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Oxalobacter Formigenes: An Oxalate Obligate

What Might Cystic Fibrosis Teach Us About Oxalates?

Counting Microbial Species In Cystic Fibrosis

Pathogenic Bacteria in Stool Tests: Maybe Not

Probiotics and Oxalate Degradation

Rethinking Our Relationship with Bacterial Oxalate Degraders

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