Disclaimer: This blog is written by a patient, for patients. Any medical advice offered must be regarded as one patient trying to help other patients suffering from metronidazole toxicity. You will have to decide what to take from this information.
Update! My research has been published by Hormones Matter, an online medical magazine led by Dr. Lonsdale and Dr. Marrs! Click here to read–it’s an abbreviated version of this “Treatment” page. Dr. Lonsdale even wrote a response article in regards to metronidazole toxicity; you can read it here.
On June 13th, 2015, I lost the ability to walk and speak while taking metronidazole. This was accompanied by a mountain of other symptoms (see my homepage for more details). Despite being debilitated for several months, I was lucky to have slowly improved from my initial reaction. Nonetheless, I’ve never been back to 100% since that day in June, with lingering symptoms affecting me and also flare up’s that could put me down from time-to-time.
Then in November of 2017, I suffered one of the worst metronidazole toxicity flare up’s in almost 2 years. While I’ve said on my homepage that most people do typically recover from this toxicity, it seems that for people who do not, flare up’s are commonplace. And there are a few unfortunate people who simply never improve from metronidazole toxicity at all.
But the question as…why?
Why is this happening to us? What is the mechanism behind this toxicity? Metronidazole causes lesions to form on the back of the brain—specifically the cerebellum, brainstem and sometimes the basal ganglia—and these lesions can lead to psychiatric issues, motor control issues, nerve damage, and finally (something that is not in medical literature but everyone in our support group on Facebook has reported in some way) dysautonomia. Dysautonomia is dysfunction of the autonomic nerve system, which controls anything that’s involuntary in the body: heart rate, blood pressure, respiration, salivation, swallowing, sweating, sleep regulation, and also the body’s fight/flight response.
But what causes the lesions? What’s causing the symptoms? This question has been theorized in case studies and systematic reviews about metronidazole toxicity, and in almost every case, there is one phrase that is consistently brought up: thiamine deficiency.
So what is thiamine?
Thiamine is a fancy word for vitamin B1. It is a nutrient that the human body cannot create itself, and a deficiency in this one nutrient can cause an avalanche of—what appears to be—complex and diverse symptoms.
Thiamine is used within the “machinery of oxidative metabolism,” along with at least 17 other nutrients, and is especially important for our mitochondria (aka, the energy source of our cells). Mitochondria are found all over the body, but are in higher concentrations in certain regions, including the heart, the muscles, the gastrointestinal system and the brain—specifically high in the cerebellum and brainstem.
All 17 nutrients are essential for oxidative metabolism (aka, the process of turning food and oxygen into fuel), but thiamine—together with magnesium—”sits atop this process as a critical cofactor in the metabolism of carbohydrates, fatty acids, in the hexose monophosphate shunt pathway and the decarboxylating component of alpha-ketoglutarate dehydrogenase, and the branched chain of amino acid dehyrogenase,” explained Dr. Derrick Lonsdale and Dr. Chandler Marrs, authors of the medical textbook, Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.
In other words, thiamine plays a pivotal role in allowing other nutrients and oxygen into our cells, especially our mitochondria. It is the bouncer that opens the door and permits other nutrients to enter, essentially aiding in the first big step in the oxidative metabolism process.
“Among the nutrients involved in oxidative metabolism, evidence shows that thiamine and magnesium are the most critical” explained Marrs and Lonsdale, and then further added, “Even mild deficiency would impact downstream mitochondrial energetics and functional dynamics.”
So what does a deficiency in thiamine do to the body?
We don’t have to look far to know just how crucial vitamins are to our bodily functions. Just like vitamin C, if the body suffers a deficiency, then the consequences can lead to serious damage. When it comes to vitamin C, the condition is called “scurvy” and, if left untreated, it can be potentially fatal. For thiamine (aka, vitamin B1), the old-school name is “beriberi” and also, in severe cases, can also be fatal.
Unfortunately, in today’s society, we believe that a severe nutritional deficiency can’t happen. And—also unfortunately—conventional doctors believe the same. Other than in the case of “Wernicke’s encephalopathy,” which is a form of thiamine deficiency caused by severe alcoholism, it seems that medical professionals consider thiamine deficiency as a relic of the past.
On top of this, thiamine deficiency can manifest what, appears to be, very diverse symptoms that do not seem related until all the underlying mechanisms are fully understood. As Marrs and Lonsdale explained, “In practice, thiamine deficiency is so far afield from clinical suspicions that, even in its most severe forms, clinical diagnosis is missed in 80% of adult cases.”
However, when thiamine deficiency is put on the figurative table of consideration, the symptoms start to form a solid picture. Because this deficiency can disrupt multiple organs where mitochondria are most prevalent, the list of symptoms is vast, but the majority of them affect significant regions, especially the cerebellum and brainstem.
Let’s break it down:
Cerebellar Dysfunction Symptoms of Thiamine Deficiency
- Ataxia (loss of motor control function). With thiamine deficiency, this is almost always in the legs.
- Dysarthria (aka, difficulty speaking), particularly “overly enunciated word patterns”
- Nystagmus (rapid eye movement)
- Decreased visual acuity
- Changes in body perception
- Changes in cognitive function and attention
- Altered Mental Status
As Marrs and Lonsdale elaborated, “The cerebellum consumes enormous amounts of ATP [see below for definition of ATP]. The energy consumed by the Purkinje cells alone, the sole output neurons of the cerebellum is estimated at ~10 ATP molecules per second for each Purkinje cell. With an estimated 15 million Purkinje cells in the cerebellum, the sheer volume of energy consumption is staggering, particularly if one considers that Purkinje cells consume only 15% of the total ATP of the cerebellum. In light of these energy requirements, it is not difficult to imagine how decrements in mitochondrial oxidative metabolism might disturb cerebellar signaling and yield the telltale motor and cognitive changes.”
*ATP, short for “adenosine triphosphate,” is an organic chemical that is essentially “the molecular unit of currency” when it comes to energy transfer in the body. Thiamine and magnesium are particularly essential for ATP.
Dysautonomia (Dysfunction of the Autonomic Nervous System) – Overview
- Sympathetic/Parasympathetic Imbalance. The autonomic nervous system (ANS) is responsible for keeping your body balanced. This balance is between the sympathetic nervous system (aka, your fight-or-flight response) or your parasympathetic (your “rest” state). Thiamine deficiency—depending on the stage—will cause the patient to either shift to the sympathetic or parasympathetic, where one system unnaturally dominants over the other.
- Postural Orthostatic Tachycardia Syndrome (POTS). This is an extreme increase in heart rate when standing that can lead to lightheadedness, fainting, trouble thinking, weakness and blurry vision. This is due to the ANS’s inability to properly regulate the heart. Also, patients with POTS sometimes have “blood pooling” where the blood pools to their lower extremities when they stand.
- Vasomotor Dysfunction. This is the dilation or contraction of blood vessels regulated by the ANS. With thiamine deficiency, this could be shown with increased sensitivity to stimuli, with increased blood pressure, heart palpitations, nausea, vomiting, and “substernal oppression” (aka, pressure, tightness or pain in the chest). This can also cause “flushing” similar to traditional hot flashes.
- Cerebral Salt Wasting Syndrome. This syndrome is caused by inadequate sodium retention. This will cause frequent urination, low blood sodium concentration, excessive thirst, extreme salt cravings and dehydration.
Dysautonomia (Dysfunction of the Autonomic Nervous System) – Gastrointestinal
- A “full” sensation in the epigastrium (the part of the upper abdomen directly over the stomach)
- Hypoacidity in early stages, followed by hyperacidity during recovery before returning to normal
- Constipation (although diarrhea is possible depending on ANS imbalance)
- Anorexia. Anorexia is a telltale sign of thiamine deficiency.
Dysautonomia (Dysfunction of the Autonomic Nervous System) – Cardiac/Respiratory
- Rapid pulse. Or slow pulse, but it rapidly increases with slight exertion.
- Irregular electrocardiogram (usually in later stages)
- Blood pressure irregularities, including the left arm’s pressure being different than the right arm’s.
- Audible arterial tone (loud, hard heartbeats). Can sometimes be heard by others.
- Low oxygen concentration in arterial blood and high oxygen concentration in venous blood (this indicates a “defective transfer of oxygen from hemoglobin to the cell”).
- Vasomotor dysfunction (explained above under “ANS Overview”)
- Altered respiratory function. “Vital capacity was reduced,” explained Marrs and Lonsdale. “Oxygen and carbon dioxide measurements in the alveolar air and the arterial and venous blood showed decreases of carbon dioxide and oxygen in the alveolar air as well as in the blood, indicating that there was extensive change in the gas exchange rate in the alveoli [aka, in the lungs].”
- Enlarged heart
Dysautonomia (Dysfunction of the Autonomic Nervous System) – Miscellaneous
- Impaired olfactory and/or taste sensations
- Impaired temperature sensation
- Excessive sweating / temperature dysregulation
- Lack of tears
- Abnormal cardiovascular reflexes
- Hyperphagia (opposite of anorexia, inability to stop eating)
- Muscular weakness
- Absent deep tendon reflexes
- Disturbances in salt and minerals regulations (imbalances)
- Breath holding
- Sleep/wakefulness disturbances
- Photophobia (extreme sensesitivity to light)
- Phonophobia (extreme sensesitivity to sound)
- Inappropriate emotional responsiveness and lability (rapid changes in mood)
What’s more complex is that one patient can present with “predominantly cardiac set of symptoms,” but another might have “predominantly gastrointestinal set of symptoms.” Or…a patient can present with “the full scope of symptoms listed: cardiac, neuropathic, neurological, and gastrointestinal,” said Marrs and Lonsdale.
“Autonomic control of basic survival is mediated via the brainstem,” they further explained, “which can be functionally divided into three regions: the medulla, the pons, and the midbrain. The medulla controls cardiac, vasomotor, respiratory and vomiting response while the pons, via cranial nerves V, VI, VII and VIII, influences hearing, equilibrium, facial sensation, motor movement, salivation, and tears. Finally, the midbrain structures house cranial nerves III and IV, together with nuclei that govern norepinephrine, dopamine and gamma-aminobutyric acid [aka, GABA] synthesis. The dense projections to and from the cerebrum and cerebellum and the periphery through the brainstem are central to homeostasis.”
Polyneuropathy (Burning, tingling and/or numbness throughout the body)
Normally, peripheral neuropathy does not typically appear in the early stages of thiamine deficiency, but as the disease progresses, it is common to manifest. As Marrs and Lonsdale explained, “Loss of sensation was characteristic in its locality, starting in the fingertips and lower abdomen and around the mouth in the distribution of the trigeminal nerve. In the legs, loss of sensation began in the dorsal aspect of the foot [the top of the foot]. In the arms, beginning in the fingertips, it gradually ascended on the lateral side [palm side], then on the medial side [pink/ring finger] and later on the flexor side.”
Thiamine deficiency can damage the myelin sheath; this is the fatty substance that insulates your nerves. Think of your nerve like a wire; the myelin sheath is the rubber that protects and insulates it. Without it, you have a “hot wire.” In your body, this leads to burning and/or tingling (pins and needles). The nerve itself can also be damaged, causing numbness.
- Edema (swelling). Also called “wet beriberi”
- Lesions on the back of the brain, specifically on the cerebellum and brain stem (only visible with an MRI)
Psychiatric Issues (aka Altered Mental Status) and Hypoxia
Although the above lists of symptoms does include psychiatric issues, it’s important to stress the significance of this problem when it comes to thiamine deficiency. It has long been determined (but constantly undervalued) in medical literature that psychiatric issues are common when it comes to neurological diseases. With thiamine deficiency, mental health issues are symptoms of serious neurological dysfunction.
As Marrs and Lonsdale explained:
“As difficult as it has been to recognize fully psychiatric and cognitive disturbances as signs of possible ANS dysfunction, it has been almost impossible to acknowledge that changes in biochemistry, particularly those emanating from disordered oxidative metabolism, may also provoke dysautonomic responses, of which psychiatric and cognition are key components. This makes little sense when one considers the totality of the ANS anatomy and physiology and its role in environmental adaptation. Whether the environment adaptations are precipitated internally or externally does not matter. Indeed, the reactions are reciprocal. The brain, as the largest consumer of metabolic energy per unit mass than any other organ, is acutely sensitive to permutations in oxidative metabolism—internal stressors that will ultimately necessitate autonomic adjustment. As such, one should expect a relationship between metabolic control and neuropsychiatric morbidity.”
It should be emphasized that when suffering from thiamine deficiency, one of the regions of the brain disrupted most, the brainstem, controls the body’s “fight-or-flight” response. This is handled through the ANS’s sympathetic system and if that system is over-activated due to an imbalance, not only will it cause an over-activation of the central nervous system, but also a paradoxal symptom—extreme fatigue. The body is not designed to run on its sympathetic nervous system long-term; it is a serious overuse of the body’s resources. This causes the patient to become both extremely anxious and extremely fatigued in unison.
But what, at its core, could be causing these over-activation of the sympathetic nervous system within the ANS, thus causing a “panicked” state?
In one word: hypoxia
Hypoxia is a deficiency in oxygen reaching the tissue in the body (or in the case of thiamine deficiency, pseudohypoxia):
“In contrast to the hypoxia state induced by an injury or obstruction that causes a deficiency in oxygen,” Marrs and Lonsdale explained, “the pseudohypoxia state is mediated molecularly by a lack of oxidation. Oxidation is the process by which mitochondria consumes molecular O2 to convert glucose into ATP. Thus pseudohypoxia is a functional disturbance in which thiamine is intimately involved. The early researchers of beriberi recognized the role of thiamine in oxygenation, observing that arterial oxygen concentration was often low while it was higher than normal in venous blood. However, Japanese researchers have learned that thiamine plays an important role in the ability of hemoglobin to pick up oxygen in the lung, deliver it to tissues and cause its consumption in the process of oxidation…
“A functional loss of oxidation will affect an organ or multiple organ systems simultaneously and those most demanding of ATP are compromised first…Regardless of the origins of the hypoxic state, however, hypoxia is dangerous to the organism. Survival reflexes are activated and the sympathetic branch of the ANS is called upon to fight.“
Here is a simple analogy: you’re eating dinner. You start to choke on a chicken bone. On a “psychiatric” level, what do you do? Like every person on this planet, you panic!—right? This is the same for when cells in your body are starving for oxygen. When they can’t “breathe” due to hypoxia, your brain jumps into action, just like the chicken bone blocking air to your lungs.
“When there is a mild degree of hypoxia or pseudohypoxia as in thiamine deficiency,” Marrs and Lonsdale continued, “this automatic control system [ANS] becomes chaotic. The automatic mechanisms, infinitely complex and about which we know surprisingly little, become distorted. In beriberi, the ANS is abnormally activated with either sympathetic or parasympathetic dominance at different stages of the disease as it progresses. For example, in the world of today the phenomenon that is diagnosed as a ‘panic attack’ represents a fragmented fight-or-flight reflex and it matters little whether it is called beriberi or panic attack as long as we understand the mechanism.”
Now, here comes the big question:
What does thiamine deficiency have to do with metronidazole?
The short answer is this:
Metronidazole and thiamine are “antagonists.”
Which means that metronidazole inhibits thiamine from being absorbed by the body.
Medical literature has theorized that metronidazole blocks the absorption of thiamine for decades (see: Enzymatic Conversion of the Antibioitc Metronidazole to an Analog of Thiamine) and they still speculate on this effect today (see: Thiamine Deficiency in Metronidazole-induced Encephalopathy: A Metabolic Correlation?).
The chemical structure of thiamine and the chemical structure of metronidazole are similar, as noted in “Meyler’s Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions.” This finding is also stated in The FEBS Journal (Federation of Euporean Biochemical Societies) in their article “Thiamin Diphosphate-Dependent Enzymes: From Enzymology to Metabolic Regulation, Drug Design and Disease Models” (page 6419, left column). If that’s the case, then the theory is, in the gut, the body mistakes metronidazole a part of thiamine, thus causing a neurotoxic effect. One of the chemical rings of thiamine is similar to that of metronidazole; metronidazole binds to thiamine, and this creates “thiaminase,” which is a direct inhibitor of thiamine:
Figure from Wiley Online Library
This theory could be further concluded as a possibility since, in our Facebook support group, metronidazole neurotoxicity typically manifests on day 5 of daily ingestion (sooner for some members). According to Marrs/Lonsdale, deficiency in thiamine due to simple lack of thiamine-intake in food should take 18 days to occur.
Regardless of the conclusions and contradictions, in most research about metronidazole, thiamine deficiency is considered to be either the partial or complete reason for the antiobitic’s neurotoxicity:
- Metronidazole encephalopathy: Uncommon reaction to a common drug.*
- • Metronidazole and Hydroxymetronidazole Central Nervous System Distribution: 1. Microdialysis Assessment of Brain Extracellular Fluid Concentrations in Patients with Acute Brain Injury
- Metronidazole Neurotoxicity
- Metronidazole-induced Encephalopathy in a Patient with Crohn’s Disease
*Encephalopathy is a blanket term for “brain dysfunction.”
This isn’t to say that thiamine deficiency is listed as the only possible cause of metronidazole neurotoxicity (there are three, including damage to RNA); however, it appears that thiamine deficiency is the most documented theory and the best understood.
Furthermore, metronidazole toxicity is continuously compared to another type of thiamine deficiency—Wernicke’s encephalopathy.
Wernicke’s encephalopathy is thiamine deficiency due to chronic alcoholism. Alcohol is considered “empty calories,” so an alcoholic can suffer from malnutrition that induces thiamine deficiency. In medical literature, metronidazole toxicity (aka, metronidazole-induced encephalopathy) has striking similarities to Wernicke’s (see: Metronidazole-Induced and Wernicke Encephalopathy: Two Different Entities Sharing the Same Metabolic Pathway? from the American Journal of Neuroradiology as one example). In Annals of Indian Academy of Neurology, physicians noted that the disease most commonly “mimics” is Wernicke’s:
“Wernicke’s encephalopathy is the biggest mimicker of MIE, primarily because it also has high propensity for the dentate nuclei.”
Just like metronidazole toxicity, Wernicke’s encephalopathy causes lesions to form on the back of the brain, specifically the cerebellum and brainstem, where thiamine is especially required for mitochondrial oxidative metabolism. In metronidazole toxicity, the lesions are in the same place, (with the exception that metronidazole toxicity can also cause lesions on the basal ganglia, where Wernicke’s does not, showing these diseases are not 100% the same).
Here are the symptoms of metronidazole toxicity and Wernicke encephalopathy compared to one another:
|Wernicke Encephalopathy||Metronidazole Encephalopathy|
|Ataxia||Ataxia (predominantly in legs)|
|Changes in mental status||Changes in mental status|
|Optic neuritis||Dysarthria (difficulty speaking)|
|Ocular nerve abnormalities||Nystagmus (involuntary eye movement)|
|Loss of vision acuity|
In Wernicke’s, these lesions and corresponding symptoms are caused strictly by thiamine deficiency.
And while these symptoms are the telltale signs of Wernicke’s, it’s important to note that most patients do not present with all the symptoms listed here. However, while the list above has the most commonly known symptoms of Wernicke’s encephalopathy, a much more diverse list of symptoms have been reported as well. These include:
- Hearing loss
- Dysphagia (difficulty swallowing)
- Sleep apnea
- Lactic acidosis
- Memory impairment
- Excessive sweating
*One interesting note—metronidazole reacts violently with alcohol. You cannot take metronidazole and alcohol without suffering a serious reaction, especially warmth or redness under the skin, heart palpitations, tingling sensation, nausea and vomiting.
Here is a video about Wernicke’s, and you’ll see the similarities between it and metronidazole toxicity:
On the FDA label for metronidazole, there are warnings about four potentially dangerous conditions: peripheral neuropathy, optic neuropathy, seizures, and cerebellar lesions (with symptoms for the lesions being ataxia, dysarthria, and dizziness). This is a small example, as metronidazole has approximately 75 side effects listed on various websites like drugs.com and webmd.com.
Strangely, when it comes to metronidazole neurotoxicity, ataxia, dysarthria, dizziness and (in some case studies and systemic reviews) an “altered mental status” are considered the powerhouse of the condition.
After my own experience and listening for the last two years to the stories of other patients, however, it has become clear that metronidazole causes far more symptoms than what is in medical literature. This includes several debilitating psychiatric issues and dysautonomia (the drug causes lesions on all regions of the brainstem—the pons, midbrain and the medulla—as documented here):
- MR Imaging of Metronidazole-Induced Encephalopathy: Lesion Distribution and Diffusion-Weighted Imaging Findings
- Clinical and Neuroradiological Spectrum of Metronidazole Induced Encephalopathy: Our Experience and the Review of Literature
- Case report: MRI of the Brain in Metronidazole Toxicity
- Acute Cerebellar Syndrome Associated with Metronidazole
- Metronidazole Induced Encephalopathy in a Patient with Brain Abscess
To be frank, the fact that there is only one vague case study about a patient suffering from dysautonomia due to metronidazole toxicity after it’s clear the drug causes lesions to form on the brainstem just goes to show how much medical science doesn’t know.
At this point, you might ask the big question—I stopped metronidazole days, weeks, months or even years ago; how could it still be affecting my thiamine? Why am I not better? Why do I get flare up’s of symptoms?
We go to Dr. Marrs and Dr. Lonsdale for this answer based on a lab study with rodents:
“Neurological symptoms appeared when cerebral thiamine concentrations reached 20% of normal. Recovery began when those concentrations climbed to 26% normal. This suggests that at least in rodents, 80% of normal brain thiamine stores must be depleted before overt neurological symptoms appear. Similarly it does not appear to take much to correct the deficit. In this study, a mere 6% increase in thiamine concentration set the course for improvement.”
People who suffered from acute metronidazole toxicity and then started to recover, only to have symptoms flare up, a full relapse or even worsening of symptoms later on, probably improved their thiamine (and magnesium) intake after stopping metronidazole, only to have something disrupt the thiamine and magnesium concentrations that were still in an extremely fragile state after taking the drug. This could be lack of dietary intake, illness, new medications, or a stressor like going back to school or work, or a combination of these factors.
“From this perspective,” explained Marrs and Lonsdale, “it is easy to see why thiamine deficiency disorders are nonlinear, at least until a particular point. Different exposures and triggers may decrease thiamine periodically, even to the point where overt neurological symptoms present. When those exposures are removed and, barring deficiencies in metabolism and diet, symptoms may abate, at least temporarily, and until the next threshold is crossed anew and thiamine deficiency becomes the medical emergency.”
I suffered my most serious flare up in almost 2 years just recently, and it was due to physically over-exerting myself. I was hired for a seasonal job on the weekends for the holidays, and just that extra running/stocking/standing sent me over an edge of deficiency that I’ve probably been skating on for the last 2 and a half years. I had to quit the seasonal job before it got worse, but if I had stayed, I might have suffered a debilitating emergence of my chronic condition, if not a full relapse.
Looking at all this data together, you will have to decide if you agree with my theory or not. But if my theory is correct (and if you agree), then the bottom line is this:
Metronidazole causes thiamine deficiency. Thiamine deficiency causes cerebellar dysfunction, polyneuropathy, and dysautonomia.
If you do agree with this statement, then here is the good news:
For most people, the effects of thiamine deficiency are treatable.
This can never be a guarantee for everyone (or that’ll be able to treat every symptom) but dysautonomia is considered an early stage of beriberi. With patients with Wernicke’s encephalopathy, most patients recover fully; it is only when they get to an extreme state called “Wernicke-Korsakoff Syndrome” that full recovery is unlikely (Korsakoff Syndrome causes full-blown psychosis, so if you’re reading this, you probably don’t have that). Even people with chronic thiamine deficiency can be treated and expect great improvement or even a full resolution of symptoms.
So what to do now? Here is my advice, from one patient to another:
- Don’t waste your money or time going to a conventional physician. Most don’t believe in adverse drug reactions and certainly don’t know how to treat a century’s old nutrient-related disease. (We have almost almost 1,000 members to our metronidazole toxicity support group on Facebook and have conducted a poll: 84% of responders reported that their doctors did not believe them when they experienced their adverse drug reaction to metronidazole, with another 11% reporting their doctor believed it was a possibility but no confirmation. Only 5% of patients reported their doctors believed them).
- Make an appointment with an integrative/functional doctor instead. They are also MDs but they focus on treating the underlying cause of disease, not just masking symptoms. They also use nutrient supplementation in their treatment plans. If an integrative doctor is unavailable or too costly, then getting advice from a nutritionist could be beneficial.
- Avoid or at least greatly reduce your sugar and coffee/tea intake. Coffee and tea (not caffeine itself) can inhibit thiamine and sugar-loaded foods can lead to further malnutrition.
- Eat thiamine-rich foods. These are not the leafy greens you would expect. Thiamine is found in lots of other types of food as well:
- Whole grains like oats
- Fish, like tuna (no raw fish–raw fish can deplete thiamine)
- Buy thiamine supplements. If you’re suffering from thiamine deficiency, eating thiamine-rich foods won’t be enough. But you don’t have to wait for your integrative doctor’s appointment; thiamine is readily available at health food stores and it’s cheap. A reputable company is Solaray, and also The Vitamin Shoppe verifies that all their vitamins are what they say they are. Remember, the FDA doesn’t regulate supplements, so it’s important to know what you’re getting. There are different types of thiamine, however, and while all are good, some are potentially better. Thiamine HCL is a good water-soluble version of thiamine, which means the body easily excretes what it doesn’t use; however, it doesn’t help the central nervous system as well as Allithiamine or Lipothiamine, both of which are are more potent for the central nervous system (both are synthetically created but are derived from garlic, so avoid if you have a garlic allergy). You can call the manufacturer (link: Ecological Formulas) and order either these supplements directly (tell them you are a Vitamin Shoppe customer and ask for 20% off). Allithiamine and Lipothiamine are not water-soluble; they are fat-soluble, which means they can enter your cell membranes without assistance from the body, making them better absorbed and more potent versions of thiamine. Start slow! 100 mg’s of thiamine HCL is a good start, but please see the chart below to see how I built up before taking 50 mg’s of Allithiamine.
- Buy magnesium. Thiamine won’t work without magnesium; these nutrients go together. Natural Calm Magnesium Powder is magnesium citrate, which is considered a cheapy version and not all that great, but it you’re in a money-pinch, it’s acceptable. You can also get Magnesium Oil, which you can put into a foot soak and your skin will absorb it. But my personal favorite (recommended by people in our support group) is magnesium L-threonate, which has less chance of digestive issues and affects the central nervous system better. The Vitamin Shoppe has a good version you can buy in-store or online called Neuro-Mag.
- Do NOT rely on regular B1 blood tests offered by most health care professionals. Thiamine deficiency is incredibly hard to determine and regular B1 blood tests only test what is in the blood, not the cell itself. And whole blood cell tests, while more accurate, will not fully determine enzyme activity. The best test is the transkelatose test, which tests the enzyme activity dealing with absorption. You must refrain from supplementation before the test (I believe it’s 4 weeks, but I need to verify), and fast prior to the test itself. It’s not readily available, which is why I typically discourage people to bother with testing and instead diagnose through symptoms (after all, if you have metronidazole toxicity, aren’t all your tests coming back “normal” or are not being correlated to the toxicity? You know something is seriously wrong–the health care system says you’re fine. Testing is helpful but clearly, it can’t see everything. But if you are interested in the test, here is a link to the one in London, UK (click here).
- I would greatly suggest buying the medical textbook, “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition” by Dr. Derrick Lonsdale and Dr. Chandler Marrs. Almost all my research about thiamine came from this book. This blog merely scratches the surface of what’s in this wonderful text, and they have far more advice on what to do about thiamine deficiency, especially if you have a severe case of it and require more medical intervention, like thiamine “megadoses” with supplementation or even possibly an IV infusion of thiamine and other nutrients. They literally have a list of nutrients to follow, like a cook book, that an intergrative doctor can help you with. I should also say, I’m not getting paid a dime for promoting this book. It’s a little expensive, though (it’s a medical textbook, so that’s to be expected).
Dosing your Thiamine and Magnesium
If a person is healthy with no deficiency at all, then having 1.5 mg’s to 2 mg’ of thiamine daily is enough to support oxidative metabolism. Despite the little amount needed for most people, thiamine supplements come in 50 to 500 mg doses, over the counter at your local health food store. But if you’re deficient, especially if it’s severe and/or chronic, then you’ll probably need to “megadose” your thiamine. Megadosing, as described in Dr. Lonsdale’s book, can go pretty high, with patients taking 1200 mg’s of thiamine HCL or 250 mg’s of the most potent version, Allithiamine (again, with the guidance of an integrative physician. Get medical advice before megadosing!). However, I’ve had the privilege to speak with Dr. Lonsdale directly, and you can go much higher than this if neccessary. It’s upping the dose until your symptoms start to lessen some, and what you’re comfortable with. It is very “trial and error.”
Overdose on thiamine is rare and, according to Dr. Lonsdale, he’s never seen thiamine toxicity in his practice. Thiamine is non-toxic and most versions are water-soluble vitamin, which means your body will take what it needs and it will expel what it doesn’t. However, just like anything, people can have odd reactions when it comes to “megadosing” so it would really be in your benefit to see an integrative doctor about your case and how you should proceed with treatment. And again, I’d suggest getting the book that covers all of this.
As a patient, I can’t tell you what dose is right for you. I can only tell you what I’ve done and how I started my treatment. And remember, I supplemented magnesium along with thiamine at every level:
- Week 1 (end of November, 2017): 100 mg’s thiamine mononitrate (HCL is good, too–mononitrate was just what was readily available to me at the time). No change.
- Week 2: 200 mg’s thiamine mononitrate. Small improvement. Reduced anxiety, more clear-headed, more energy.
- Week 3: 300 mg’s thiamine HCL. More improvement. Less symptoms, all anxiety resolved.
- Week 4: 450 mg’s thiamine HCL. More improvement, less symptoms.
- Week 5: 50 mg’s Allithiamine. First night, had mild paradoxical reaction (see below for details about paradoxical reaction). No improvement, no worsening of symptoms after first night. (Nowadays, I take Lipothiamine instead of Allithiamine. It’s better absorbed and doesn’t have a garlic taste. But either supplement is good!).
- Week 6: 100 mg’s Allithiamine. Improvement, able to play games with family, more energy, brain fog improved, breathing improved.
- Week 7: 150 mg’s Allithiamine. Great improvement, all symptoms relatively mild now.
- Week 8: 150 to 200 mg’s Allithiamine. Most symptoms resolved, with only “breakthrough flare up’s” that would last 20 minutes to a couple of hours.
- Summer 2018: In summer of 2018 (see more description below), I upped my Allithiamine to 250 mg’s, and continued taking magnesium L-threonate at the recommended daily dose. But I also added a B-complex (which has other B-vitamins) at the recommended daily dose. It is important to eventually add a B-complex to make sure your B-vitamins remain balanced in the long-term. You can imbalance your B-vitamins if you megadose B1 long-term; they work together.
At this level, with this vitamin-combo, my symptoms have resolved 99% with only infrequent flare up’s and very few, mild symptoms. The only symptom that seems to not have improved much is my ear ringing, which still seems to be sticking around (both my parents have ear ringing, so I might have been predisposed to this anyway).
More details: As I’ve continued my thiamine regimen, trying different doses and different types of thiamine, I still experienced flare up’s throughout the spring, almost all short-lived, but still there. I spoke directly to Dr. Lonsdale, and switched to Lipothiamine and increased my dose to 250 to 300 mg’s and could go higher if needed.
People who either have a severe case of thiamine deficiency and/or chronic deficiency (it’s been going on for months or even years), could suffer from a paradoxical reaction when they start their thiamine regimen, even at a small dose of 50 to 100 mg’s. If that happens, it’s further confirmation that you are deficient and your body has adapted to not having thiamine, so when you suddenly give it what it needs, it rejects it. Think about a starving man–you don’t give him a big meal when he hasn’t eaten for a month. It’ll make him sick! But that doesn’t mean he doesn’t need food! His body has adapted to not having what it requires and it needs to be, for lack of a better word, reprogrammed. Thiamine is not like an herb supplement that changes the way your body functions (like a drug would)–your body needs thiamine to live; it’s one of the essential nutrients. So if you feel worse on thiamine treatment, scale it back, even if it means taking as little as 25 mg’s and then move up from there. If even that small amount of thiamine feels like too much, then you can continue the magnesium and eat thiamine-rich foods for a few weeks to get your body prepared. Nutritional yeast is a great source of vitamin B1 and can be put into fruit smoothies.
Again, being monitored by a doctor or nutritionist is a good idea!
You can overdose on magnesium (it’s a mineral, not a vitamin). If you take an oral supplement—pill or powder—and you begin to have loose stools, cut back. If you’re absorbing it through your skin, be conservative because there is no warning signs like with oral supplementation.
Again, a lot of this will be trial and error. What does your body need? Can it work on peripheral neuropathy vs. dysautonomia vs. cerebellar dysfunction? Is my case considered “mild” when I feel this sick, but there are other people who are even sicker? I don’t know this; it’s new to all of us.
If you’re really sick and debilitated, you might not see significant improvement with thiamine supplementation for months. You might need an IV, megadoses and also other nutrients (points highlighted in the textbook). For some people with severe or chronic deficiency, the enzymes that absorb thiamine might require megadosing to “reactivate” them. Overtime, they can deteriorate like anything else the body isn’t using, but that doesn’t mean they can’t be strengthened or even healed.
This will take time. I’m on this journey with you, trying this out myself, putting medical theory and facts into practice. I hope and pray it helps all of us who have struggled so much with metronidazole toxicity. I can only hope and pray that this is the answer. Only time will tell if I’m right.
A special thanks to Dr. Derrick Lonsdale and Dr. Chandler Marrs for their eye-opening textbook, “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition,” for which the article was made possible.