thiamine deficiency symptoms

Thiamine Insufficiency Relative to Carbohydrate Consumption

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high carbohydrate diets and thiamine

Thiamine (vitamin B1) is an essential micronutrient responsible for key reactions involved in the conversion of the foods we consume into the chemical energy substrate requisite for cellular function, adenosine triphosphate (ATP). Absent sufficient ATP, all sorts of metabolic functions become disordered leading to the disease processes that dominate western medicine. Chronic inflammation, altered immune function, hormone dysregulation, cognitive and mood disorders, and dysautonomias, all can be traced back to insufficient thiamine > inefficient mitochondrial function, reduced ATP, and the compensatory reactions that ensue.

Among the most common but least well-recognized contributors to thiamine deficiency is the regular consumption of a high carbohydrate/highly processed food diet. Although most of these foods are enriched or fortified with thiamine, perhaps staving off more severe deficiencies, the density of sugars overwhelms mitochondrial capacity to process these foods, both the thiamine and any other potential nutrients are excreted, while the carbohydrates themselves are stored as fat for future use. High-calorie malnutrition is a common contributor to thiamine deficiency in obesity but also may develop in presumed healthy athletes whose diets focus heavily on high carbohydrate intake.

Thiamine, along with other B vitamins is often deficient in vegetarian and vegan diets as well. Not only do fruits, vegetables, and carbohydrates contain minimal, if any, thiamine, but some have anti-thiamine factors and are high in what are called oxalates. Anti-thiamine factors found in some fruits and vegetables interfere with the absorption or digestion of thiamine. Oxalates are mineralized crystals of sorts that tend to build up and store in places like the kidneys (kidney stones), but also may store and cause problems anywhere in the body like bones, arteries, eyes, heart, and nerves. Effective oxalate metabolism and clearance requires thiamine. Since vegetarian and vegan diets are also carbohydrate intensive, thiamine deficiency and oxalate issues may be compounded. Thus, a number of common diets not only contain reduced thiamine content but cause an increased need for thiamine by at least three mechanisms; higher carbohydrate consumption overwhelming capacity, which is then magnified by poor carbohydrate and oxalate processing.

Add daily coffee, tea, and/or alcohol consumption to any diet, and whatever thiamine that is consumed is either inactivated by enzymes before being used or is unabsorbable. Add a medication or four and thiamine availability will tank simultaneously with an increased need. Medications both block nutrient uptake and/or increase the need for nutrients by inducing mitochondrial damage. Given that 70% percent of the US population takes at least one medication regularly, while 20% take four or more, it is safe to say, that a good percentage of the population is consuming insufficient thiamine to maintain mitochondrial function and health.

Are We Really Thiamine Deficient?

As an essential nutrient, thiamine must be consumed regularly to maintain sufficient concentrations. The question is how much thiamine is sufficient to maintain health? Current RDA values for daily thiamine intake suggest a little over a milligram per day is adequate for most adults. If this is true, then the minimum value can be attained through just about any diet including those dominant in highly processed, carbohydrate-dense foods, which are commonly either enriched or fortified with thiamine. Everything from bread to cereals and even junk food like Oreos have thiamine. Per the RDA values, none of us ought to be thiamine deficient and none of us ought to require thiamine supplementation, and yet, many of us are and do. Indeed, several studies, across disparate populations show that even by this minimum standard, deficiency is a serious health problem. From our book:

  • 76% of diabetics (type 1 and type 2)
  • 29% of obese patients, 49% of post-bariatric surgery
  • 40% of community-dwelling elderly, 48% of elderly patients in acute care
  • 55% of cancer patients
  • 20% ER patients (random sample, UK)
  • 33% of congestive heart failure patients
  • 38% of pregnant women, more with hyperemesis
  • 30% of psychiatric patients

It takes approximately 18 days to completely abolish endogenous thiamine stores in a diet that is completely devoid of thiamine. Except under total starvation, medical or industrial food production mishaps, and experimentally contrived situations, thiamine consumption is never completely abolished. It waxes and wanes by dietary choices and life stressors. According to rodent studies, it takes a reduction of greater than 80% of thiamine stores before the more severe neurological symptoms are recognizable. In humans, these symptoms include those associated with Wernicke’s encephalopathy, the various forms of beriberi, and dysautonomic function. These include but are not limited to: ataxia, changes in mental status, optic neuritis, ocular nerve abnormalities, diminished visual acuity, high-output cardiac failure with or without edema, high pulse pressure, polyneuropathy (sensorimotor), enteritis, esophagitis, gastroparesis, nausea and vomiting, constipation, hyper- or hypo-stomach acidity, sympathetic/parasympathetic imbalance, postural orthostatic tachycardia syndrome (POTS), cerebral salt wasting syndrome, vasomotor dysfunction, respiratory distress, reduced vital capacity, and/or low arterial O2, high venous O2.

With a less severe thiamine deficiency, symptoms are rarely recognized as such and often attributed to psychological manifestations. A not entirely ethical study done in 1942 involving 11 women on a low thiamine diet over a period of ~3-6.5 months found striking symptoms.

  • During this time all subjects showed definite changes in personality.
  • They became irritable, depressed, quarrelsome, and uncooperative.
  • Two threatened suicide. All became inefficient in their work, forgetful, and lost manual dexterity.
  • Their hands and feet frequently felt numb.
  • Headaches, backaches, sleeplessness, and sensitivity to noises were noted.
  • The subjects fatigued easily and were not able to vigorous exertion.
  • Constipation was the rule, but no impairment, of gastrointestinal motility, could be demonstrated fluoroscopically.
  • Anorexia, nausea, vomiting, and epigastric distress were frequently observed.
  • Low blood pressure and vasomotor instability were present in all patients.
  • At rest, pulse rates were low (55 to 60 per minute) but tachycardia followed moderate exertion. Sinus arrhythmia was marked.
  • Macrocytic, hypochromic anemia of moderate severity (3.0 to 3.5 million red cells) developed in 5 cases.
  • A decrease in serum protein concentration occurred in 8 subjects.
  • Basal metabolic rates were lowered by 10 to 33 points.
  • Fasting blood sugar was often abnormally high.

The study above demonstrated a rapid and dramatic onset of symptoms relative to a diet with limited thiamine. Depending upon caloric intake, the amount of thiamine allowed was approximately 1/3 to 1/5 of the amount recommended by the RDA. Admittedly, the RDA for thiamine is low, to begin with, but even so, this was not a complete absence of thiamine. Since the study took place in the early 1940s, it is difficult to ascertain the specifics of the diet. Nevertheless, it demonstrates a clear association between general health and one’s ability to function, and thiamine insufficiency.

High Carbohydrate Diets Equal Lower Thiamine

More recently, a short and very small study (12 days and 12 participants) of active young men and women (ages 25-30) investigated the relationship between carbohydrate intake and thiamine status. Thiamine was measured in blood, plasma, urine (creatinine), and feces at four time points: at baseline, before the study began, during an adaptation phase where carbohydrate intake represented 55% of the total caloric intake, and during the two subsequent intervention phases, where carbohydrate intake was increased to 65% and 75% of the total caloric intake, respectively. Both caloric and thiamine intake was held constant throughout the study despite the increased intake of carbohydrates. Activity levels were also held constant. Across this short-term study, as carbohydrate intake increased, plasma, and urinary thiamine decreased. Excretion through feces remained unchanged. Transketolase enzyme activity was also measured but remained unchanged. Given the short-term nature of this study, the fact that transketolase remained unchanged is unexpected. In addition to the decreasing thiamine values, there were several changes in lipid profile as well. Despite the short duration of this study, however, the results show a clear relationship between carbohydrate intake and thiamine status; one that would likely be magnified over time and certainly if other life stressors and medical and environmental toxicants were added to the mix.

It is important to note current dietary guidelines suggest carbohydrate consumption should fall between 45-65% of total calories, percentages which, per this study would decrease thiamine availability significantly. From the baseline diet to the 55% adaptation phase, thiamine dropped precipitously, only to drop even further at the 65% phase. A recent study surveying macronutrient consumption showed that average carbohydrate consumption across the US population represented approximately 50% of total caloric intake. Importantly though, the study found that 42% of the carbohydrate consumption came in the form of what researchers termed ‘low-quality carbs’ e.g. sugary processed foods with no nutritional value. Thiamine is only found in pork, beef, wheat germ and whole grains, organ meats, eggs, fish, legumes, and nuts. It is not present in fats/oils, polished rice, or simple sugars, nor are dairy products or many fruits and vegetables a good source. Indeed as mentioned previously, some fruits and vegetables may contain anti-thiamine factors. A diet that is 42% empty calories, that contains limited to no nutritive value, save except what has been added post hoc via enrichment, begs for mitochondrial damage and the illnesses that ensue. And yet, that is precisely the nutritional landscape in which most of us exist.

Admittedly, both studies were very small, but the research connecting thiamine deficiency to ill-health and carbohydrate consumption to thiamine loss is clear. Given the dominance of ultra-processed carbohydrate-dense foods in the modern diet, is likely that high-calorie malnutrition underlies much of the chronic illness that plagues western medicine. To learn more about thiamine deficiency and the havoc it wreaks on health: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

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What is Thiamine to Energy Metabolism?

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What is Energy?

Energy is an invisible force. The aggregate of energy in any physical system is a constant quantity, transformable in countless ways but never increased or diminished. In the human body, chemical energy is produced by the combination of oxygen with glucose. This reaction is known as oxidation. The chemical energy is transduced to electrical energy in the process of energy conservation. This might be thought of as the “engine” of the brain/body cells. We have to start thinking that it is electrical energy that drives the human body. The production of chemical energy is exactly the same in principle as the burning of any fuel but the details are quite different. The energy is captured and stored in an electronic form as a substance known as adenosine triphosphate (ATP) that acts as an energy currency. The chemical changes in food substances are induced by a series of enzymes, each of which combine together to form a chain of chemical reactions that might be thought of as preparing food for its ultimate breakdown and oxidation. Each of these enzymes requires a chemical “friend”, known as a cofactor. One of the most important enzymes, the one that actually enables the oxidation of glucose, requires thiamine and magnesium as its cofactors. Chemical energy cannot be produced without thiamine and magnesium, although it also requires other “colleagues”, since all vitamins are essential. A whole series of essential minerals are also necessary, so it is not too difficult to understand that all these ingredients must be obtained by nutrition. The body cannot make vitamins or essential minerals. There is also some evidence that thiamine may have a part to play in converting chemical energy to electrical energy. Thus, it may be the ultimate defining factor in the energy that drives function. If that is true, its deficiency would play a vital role in every disease.

Energy Consumption

Few people are aware that our lives depend on energy production and its efficient consumption. A car has to have an engine that produces the energy. This is passed through a transmission that enables the car to function. In a similar manner, we have discussed how energy is produced. It is consumed in a series of energy requiring chemical reactions, each of which requires an enzyme with its appropriate cofactor[s]. This series of reactions can be likened to a transmission, enabling the human body to function. If energy is consumed faster than it can be synthesized, or energy cannot be produced fast enough to meet demand, it is not too difficult to see that it would produce a fundamental change in function. Lack of function in body organs affects our health. The symptoms are merely warning the affected individual that something is wrong. The underlying cause has to be ascertained in order to interpret how the symptoms are generated.

Why Focus on Thiamine?

We have already pointed out that thiamine does not work on its own. It operates in what might be regarded as a ”team relationship”. But it has also been determined as the defining cause of beriberi, a disease that has affected millions for thousands of years. Any team made up of humans requires a captain and although this is not a perfect analogy, we can regard thiamine as “captain” of an energy producing team. This is mainly due to its necessity for oxidation of glucose, by far and away the most important fuel for the brain, nervous system and heart. Thus, although beriberi is regarded as a disease of those organs, it can affect every cell in the body and the distribution of deficiency within that body can affect the presentation of the symptoms.

Thiamine exists only in naturally occurring foods and it is now easy to see that its deficiency, arising from an inadequate ingestion of those foods, results in slowing of energy production. Because the brain, nervous system and heart are the most energy requiring tissues in the body, beriberi produces a huge number of problems primarily affecting those organs. These changes in function generate what we call symptoms. Lack of energy affects the “transmission”, giving rise to symptoms arising from functional changes in the organs thus subserved. However, it must be pointed out that an enzyme/cofactor abnormality in the “transmission” can also interrupt normal function.

In fact, because of inefficient energy production, the symptoms caused by thiamine deficiency occur in so many human diseases that it can be regarded as the great imitator of all human disease. We now know that nutritional inadequacy is not the only way to develop beriberi. Genetic changes in the ability of thiamine to combine with its enzyme, or changes in the enzyme itself, produce the same symptoms as nutritional inadequacy. It has greatly enlarged our perspective towards the causes of human disease. Thiamine has a role in the processing of protein, fat and carbohydrate, the essential ingredients of food.

Generation of Symptoms

Here is the diagnostic problem. The earliest effects of thiamine deficiency are felt in the hindbrain that controls the automatic brain/body signaling mechanism known as the autonomic nervous system (ANS). The ANS also signals the glands in the endocrine system, each of which is able to release a cellular messenger. A hormone may not be produced in the gland because of energy failure, thus breaking down the essential governance of the body by the brain. Hypoxia (lack of oxygen) or pseudo-hypoxia (thiamine deficiency produces cellular changes like those from hypoxia) is a potentially dangerous situation affecting the brain and a fight-or-flight reflex may be generated. This, as most people know, is a protective reflex that prepares us for either killing the enemy or fleeing and it can be initiated by any form of perceived danger. Thus, thiamine deficiency may initiate this reflex repeatedly in someone that seeks medical advice for it. Not recognizing its underlying cause, it is diagnosed as “panic attacks”. Panic attacks are usually treated by psychologists and psychiatrists with some form of tranquilizer because of the anxiety expressed by the patient. It is easy to understand how it is seen as psychological, although the sensation of anxiety is initiated in the brain as part of the fight-or-flight reflex and will disappear with thiamine restoration. It may be worse than that: because the heart is affected by the autonomic nervous system, there may be a complaint of heart palpitations in association with the panic attacks and the heart might be considered the seat of the disease, to be treated by a cardiologist. The defining signal from the ANS is ignored or not recognized. Because it is purely a functional change, the routine laboratory tests are normal and the symptoms are therefore considered to be psychological, or psychosomatic. The irony is that when the physician tells the patient “it is all in your head”, he is completely correct but not recognizing that it is a biochemical functional change and that it has nothing to do with Freudian psychology.

A Sense of Pleasure

A friend of mine has become well aware that alcohol, in any form, or sugar, will automatically give him a migraine headache. He still will take ice cream and suffer the consequences. I have had patients tell me that they have given up this and that “but I can’t give up sugar: it is the only pleasure that I ever get”. They still came back to me to treat the symptoms. We have come to understand that we have no self-responsibility for our own health. If we get sick, it is just bad luck and the wonders of modern medicine can achieve a cure. The trouble is that a mild degree of thiamine deficiency might produce symptoms that will make it more difficult to make the necessary decisions for our own well-being. Let me give some examples of symptoms that are typically related to this and are not being recognized.

  • Occasional headache
  • Occasional heartburn or abdominal pain
  • Occasional diarrhea or constipation
  • Allergies
  • Fatigue
  • Emotional lability
  • Insomnia
  • Nightmares
  • Pins and needles
  • Hair falling out
  • Heart palpitations
  • Persistent cough for no apparent reason
  • Voracious or loss of appetite

The point is that thiamine governs the energy synthesis that is essential to our total function and it can affect virtually any group of cells in the body. However, the brain, heart and nervous system, particularly the autonomic (automatic) nervous system (ANS) are the most energy requiring organs and are likely to be most affected. Since the brain sends signals to every organ in the body via the ANS, a distortion of the signaling mechanism can make it appear that the organ receiving the signal is at fault. For example, the heart may accelerate because of a signal from the brain, not because the heart itself is at fault. Hence, heart palpitations are often treated as heart disease when a mild degree of thiamine deficiency in the brain is responsible. We have known for many years that sugar in all its different forms can and will precipitate mild thiamine deficiency. It is probably the reason why sugar is considered to be a frequent cause of trouble. If thiamine deficiency is mild, any form of minor stress may precipitate a much more serious form of the deficiency.

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Connecting the Symptom Dots: Discovering My Thiamine Deficiency

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discovering thiamine deficiency

As a registered dietitian nutritionist (RDN), I was surprised to find out that I had a thiamine deficiency in December 2015. My diet wasn’t perfect, but it was close. I never imagined I’d spend so much time trying to treat my own deficiency, but it’s been over a year the first lab work showed the deficiency and I’m still struggling with it. I’ve been asked to share my symptoms and experiences, so I’ll start back around the initial diagnosis.

Let me preface my story by sharing some information about myself. I’m a 46 year old female and I’ve always considered myself fairly healthy. I’m active, and I complete a minimum of 12,000 steps/day and often much more. That includes some form of aerobic activity daily. I’ve dealt with some annoying health problems, but nothing I considered major. I’ve had issues with insomnia, depression, nerve problems, migraines, hypoglycemia and GI distress (mostly diarrhea) for years or decades. I’ve also had some discomfort on the left side of my chest, on and off, which goes unexplained. I’ve seen many different types of doctors, including cardiologists, neurologists, gastroenterologists, psychiatrists, sleep specialists, endocrinologists, allergists, etc. Also, I have very early visual symptoms of glaucoma, but my doctor said there aren’t any signs of disease in my eye. No familial history of glaucoma, and I’ve never been diagnosed with diabetes. Separately, all of these symptoms seemed minor. Only within the last few years or so, did I begin to wonder if there was some sort of connection.

In the fall of 2014, I started a post-bachelors program in dietetics. I had returned to school almost two decades after completing my bachelors, and the road to this program was a long one. My insomnia seemed to be severe the night before exams. Sleep eluded me, even with the prescription sleeping pills. Anxiety, right? It never occurred to me that it was something else. After all, I’ve had insomnia issues for at least a decade. Sometime during the semester, I had seen a neurologist for some nerve testing. I had numbness and tingling in my feet, hands and arms. It would wake me up at night. I began seeing a doctor of osteopathy for manipulations to help with the nerve problems, too. Also, I had noticed some garbled speech and numbness in my tongue, but thought I was imagining it.

During finals week in December, my insomnia became severe. My physician prescribed Xanax, but I hated the way it made me feel. I felt my anxiety actually increased.  Even after finals were over, sleep eluded me. I was piecing 3-5 hours of sleep together, if that. I had trouble eating a full meal and was losing weight. In addition, I was having discomfort on the left side of my chest, something that I had experienced in the past but was yet unexplained. All of this was attributed to anxiety. By the end of December, my physician prescribed a daily anti-anxiety medication. This medication made me nauseous and I had diarrhea. Of course, these symptoms didn’t help the weight loss. At no time did my physician do any lab work while this was happening. I was so miserable that I emailed my advisor to inquire about dropping out of the dietetics program. Fortunately, she wouldn’t entertain the idea and encouraged me to continue, noting that I could take an Incomplete if necessary.

By February of 2015, I was down to 103 pounds, (I’m 5’ 4” and 130 pounds currently). I was dragging myself to school. I had lost a lot of muscle mass, and couldn’t sit for long in class because of the lack of muscle. My face looked quite thin and my temples were hollowed out. In March 2015, I was weaned off the medications and began taking 7.5 mg Remeron, and Ambien as needed. The Remeron helped my appetite and I began regaining weight and strength. With the support of my professors, I was able to complete the semester, and even maintained a high grade point average!

Early in the fall semester, I listened to a lecture by an RDN who is an integrative and functional medicine certified practitioner (IFMCP). Based on her lecture, I knew my instincts about an underlying connection to all of my symptoms was correct. In November 2015, I had an appointment with that RDN. She recommended some blood work, which my primary care physician (PCP) reluctantly agreed to do. It was a lot of blood work, and fortunately my insurance covered it. There were many positive or problematic results, but among them was low thiamine (whole blood) at 29ug/L, a positive ANA test, TPO 693, as well as magnesium and ferritin were in the low normal range. After further autoimmune testing, it was determined that I have Hashimoto’s disease, too.

The low thiamine level could explain many of my symptoms, including, insomnia, nerve issues, migraines, precordial pain, weight loss and problems processing carbohydrate. The question is why was my thiamine level low? I had always thought my diet was relatively healthful. For years, I watched my added sugar intake because of trouble with hypoglycemia. My fiber, protein and water intake seemed adequate. I’m very careful with my fat intake because I had a cholecystectomy in 2009 and still have problems with lipid digestion. I rarely drank alcohol because of the hypoglycemia and insomnia. The only other beverage I consumed was tea, usually 1-3 cups per day. Furthermore, because of my hypoglycemia, I ate mostly whole grains and very little gluten, if any.

In January 2016, I began taking a B vitamin complex, magnesium, lipothiamine and some other supplements, including Ortho-Digestzyme to aid in lipid digestion. I made changes to my diet, including dairy free and gluten free. I began seeing some health improvements. Eventually, I added yogurt and cheese back into my diet, but remained gluten free. I was having fewer migraines and began sleeping without Ambien. That spring I was taken off the lipothiamine, but continued the B vitamin complex and magnesium. I graduated from the dietetics program in May 2016, something I feared wouldn’t happen only one year earlier.

At the end of October 2016, I had an infection (perhaps, due to an insect bite) on my outer ear which wouldn’t go away. My PCP prescribed a cephalosporin antibiotic for 10 days. Towards the end of November and into December, I was having increased nerve issues, occasional insomnia, mild apathy and anxiety, which was strange given I had nothing to be anxious about. Also, I had the same chest discomfort again. My thiamine level was tested and it was low at 32 ug/L. I was taking the B vitamin complex and magnesium all along, so my PCP was unsure what to do. I’ve since learned that some antibiotics, like the one I took, can deplete thiamine.  I saw the RDN again and began taking lipothiamine again on 12/23/2016. I was taking 50 mg, twice a do with magnesium, in addition to the B vitamin complex.

My PCP planned to retest in a month to see if it was working. However, on January 20, 2017, I had an emergency appendectomy. During the surgery, I was given a cephalosporin antibiotic, but it was only during the surgery, not afterwards. It should be noted that I only missed one day of supplements because of the surgery. By the end of the first week, I strongly suspected my thiamine level had bottomed out, because my symptoms of anxiety, insomnia, nerve pain, etc., reminded me of what happened two years earlier. During that week, I was taking 50 mg lipothiamine twice a day, 200 mg magnesium and a potent multivitamin. Personally, I think the antibiotic, surgical procedure and recovery, and resulting diarrhea contributed to the low thiamine despite supplementation. I almost went to the ER in hopes that they’d give me a thiamine injection or IV, but decided to wait until Monday to see my PCP. Her suggestion was that I continue my supplements, then we’d retest in a month. One month later, my thiamine level was low still at 32 ug/L. My PCP said she isn’t comfortable giving intramuscular thiamine injections and suggested I see a gastroenterologist. I mentioned information I found on Hormones Matter, but I don’t believe my PCP was interested in reading the material.  I feel like I’m being bounced around from one doctor to another. I’m going to see the gastroenterologist, whom I’ve seen before but I’m not hopeful that she’ll be able to help. I saw a neurologist recently, who was very kind and listened intently, but could only suggest an MRI and a DO, who “might” be able to help me, but that DO’s office is 1.5 hours away. Next week, I’ll go back to the cardiologist for a check-up because of the ongoing discomfort on the left side of my chest.

For now, I’m sleeping at least 6 hours a night, which feels like a lot to someone who’s experienced severe insomnia. My hypoglycemia is under control. I’m not sure if that’s because of the thiamine supplementation, the gluten free diet or both. The last time I had gluten, I experienced both mild insomnia and hypoglycemia, but again, my thiamine was likely low too. I feel I still have occasional memory issues, but maybe that’s age related. Also, the numbness and tingling in my extremities continues. Migraines occur much less and are less severe, usually. The mild vision problems linger, as well.

The RDN I’m seeing is uncomfortable with me taking more than 100 mg lipothiamine per day. At this time, she is recommending supplements to treat continued GI inflammation too.  Here is my current regimen: 100 mg lipothiamine/day, 200 mg magnesium/day, multivitamin 1/day (RDN wants me to take 2/day), 28 mg iron w/vitamin C, sodium butyrate 600mg 4/day, NAC 600mg 2/day, Ortho-Digestzyme 2 capsules before each meal to help with lipid absorption, and about 4000 IU vit D3.

Unfortunately, I feel I’m just one missed dose of my supplements away from problems all the time now. I’m not sure how to find a physician who can help me solve this ongoing thiamine problem and don’t know where to turn next. Again, I’m going to see a gastroenterologist and cardiologist this month, but feel it may be more of the same. My father died at 45 years old of cardiovascular disease. I know thiamine deficiency can lead to cardiovascular problems too, which is why I’m going back to the cardiologist.

Any suggestions are welcomed!

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