For the first day of the new year, we dive into what is considered the first proposed vitamin, vitamin B1 also called thiamine.
This episode goes in-depth on the critical role thiamine plays in our bodies, and its necessary presence in adequate amounts for producing ATP, our cellular energy currency. In this episode, I go over the often-overlooked connection between carbohydrate intake and thiamine needs, and the consequences that can follow when this vitamin is in short supply.
When thiamine levels drop, it's not just our energy that's at risk – our brain health also might hang in the balance. I dive into the neurological consequences of thiamine deficiency (and even a sustained state of inadequacy...) like the development of Wernicke-Korsakoff syndrome, a two-part disorder that is usually, although not exclusively associated with chronic alcohol dependency. I will also consider thiamine's [or lack thereof] potential links to Alzheimer's and Parkinson's diseases. Other brain responses to a marginal thiamine shortage, include adaptations that could lead to reduced appetite and anorexic behavior. The theoretical rationale will be provided in this episode.
As I round out the episode, I go over the groups most vulnerable to this nutrient shortfall. Lastly, and perhaps most importantly, I will confront the silent epidemic of thiamine deficiency that has been suggested by many to be hiding behind very common symptoms or metabolic disorders. I will tackle what has been suggested now by several researchers, that less thiamine availability and bodily activity may not be because we aren’t taking in enough thiamine, but because we might be overexposing ourselves to anti-thiamine factors present all around us (dietary choices, lifestyle choices, medication use, etc.).
Join me in for this episode where I do my best to achieve adequate thiamine status and arm you with actionable insights and preventative strategies to safeguard your nutrient status.
Be sure to subscribe for future episodes covering specific nutrients and strategies for achieving optimal nutrient adequacy.
For the first day of the new year, we dive into what is considered the first proposed vitamin, vitamin B1 also called thiamine.
This episode goes in-depth on the critical role thiamine plays in our bodies, and its necessary presence in adequate amounts for producing ATP, our cellular energy currency. In this episode, I go over the often-overlooked connection between carbohydrate intake and thiamine needs, and the consequences that can follow when this vitamin is in short supply.
When thiamine levels drop, it's not just our energy that's at risk – our brain health also might hang in the balance. I dive into the neurological consequences of thiamine deficiency (and even a sustained state of inadequacy...) like the development of Wernicke-Korsakoff syndrome, a two-part disorder that is usually, although not exclusively associated with chronic alcohol dependency. I will also consider thiamine's [or lack thereof] potential links to Alzheimer's and Parkinson's diseases. Other brain responses to a marginal thiamine shortage, include adaptations that could lead to reduced appetite and anorexic behavior. The theoretical rationale will be provided in this episode.
As I round out the episode, I go over the groups most vulnerable to this nutrient shortfall. Lastly, and perhaps most importantly, I will confront the silent epidemic of thiamine deficiency that has been suggested by many to be hiding behind very common symptoms or metabolic disorders. I will tackle what has been suggested now by several researchers, that less thiamine availability and bodily activity may not be because we aren’t taking in enough thiamine, but because we might be overexposing ourselves to anti-thiamine factors present all around us (dietary choices, lifestyle choices, medication use, etc.).
Join me in for this episode where I do my best to achieve adequate thiamine status and arm you with actionable insights and preventative strategies to safeguard your nutrient status.
Be sure to subscribe for future episodes covering specific nutrients and strategies for achieving optimal nutrient adequacy.
Hello everyone, my name is William Wallace and I will be your host today as we take an overview. Look at another single nutrient compound. In fact, this was the first vitamin to ever be identified, which is a bit poetic when you consider the crucial role this vitamin plays in the production of energy in the form of ATP, which is necessary to sustain life. Although many vitamins and minerals play important roles in energy production, this vitamin is so important to those processes that it is informally known as the energy vitamin. Of course, the vitamin I am referring to is vitamin B1, also known as thiamine. In this episode, we will discuss the different functions of thiamine, notably the critical role it plays in energy production through carbohydrate metabolism and how carbohydrate intake affects one's thiamine needs. We're going to talk about what happens when we don't get enough thiamine and some of the surprisingly widespread consequences of insufficient thiamine intake. We're also going to take a look at true thiamine deficiency and how that's identified and how it's treated at this point in time. Of course, we're going to go over thiamine requirements, sources of thiamine and how different types of food might be helping us or even working against us when trying to get enough thiamine from our diets. Before I go any further. I must preface with the disclaimer that this podcast is being generated purely for educational purposes. The contents of this broadcast do not constitute medical advice and are not meant to substitute for standard medical practice. Please consult with your primary healthcare practitioner before beginning any nutrition and or supplement based protocols that may be mentioned in this episode.
Speaker 1:Thiamine is one of the water soluble B vitamins, also known as vitamin B1, but has also been called anurin in the past. This name was given to it before its chemical structure was ever determined, and once its structure was determined to consist of what's known as a theazol ring and in a mean group, it was then called thiamine. Moving forward, thiamine is found in various forms in food as well as the body. For instance, there is free thiamine. Thiamine also is found in several phosphorylated forms that include thiamine monophosphate, thiamine diphosphate and thiamine triphosphate. Phosphorylation in this case means that one or more phosphate groups get added to the thiamine, which changes the molecule structure and the way it functions in the body. Collectively, these thiamine based compounds are called thiamine vitaminers. If you listened to either of the first two episodes of this podcast, you would know the term vitaminer by now, but in case you did not. A family of vitaminers is what we call a group of compounds that are chemically related to one another. Of these thiamine vitaminers, thiamine diphosphate is the most physiologically relevant compound.
Speaker 1:This is what is known as the active form of thiamine and the primary coenzyme form of the vitamin. When I say coenzyme, I mean the form of a vitamin that is used by different enzymes to perform their functions. You can essentially think of an enzyme in the body as a tool, like a drill, for instance. To work effectively, the drill needs a bit. In this case, the bit for the enzyme is what we call a coenzyme. Thiamine diphosphate is the form of thiamine that acts as that bit for different enzymes in the body so that those enzymes can actually function properly. Thiamine diphosphate is also formerly known as thiamine pyrophosphate. So thiamine diphosphate and thiamine pyrophosphate are the same thing and those two terms can be used interchangeably. I'm going to use the term thiamine pyrophosphate, moving forward, when referencing this active form of thiamine. Thiamine pyrophosphate serves as a coenzyme for five very important enzyme complexes that most notably play a role in the metabolism of carbohydrates, as well as branched chain amino acids. You've heard of BCAAs before. Those are leucine, valine and isoleucine.
Speaker 1:All the products produced by these enzymes play critical roles in the production of energy from food through their direct or indirect connection to the Krebs cycle, which is also known as the citric acid cycle. I believe that most of you will have heard of the Krebs cycle at some point, whether that was from your time in high school or education beyond high school, but not everyone actually really understands what that is, and that's quite alright, so I'm going to do my best to explain it here. Simply, the Krebs cycle begins with a molecule called acetyl-CoA. This comes from the breakdown of sugars, fats and proteins in our food. As this molecule moves through the Krebs cycle, it gets transformed through a series of steps all involving different enzymes. You can think of this as a production line in a factory where each step is going to change the product a little bit more. At one particular step in the cycle, atp is produced. Atp is literally energy. This is what human cells directly use as and for energy. It's the energy currency of the body.
Speaker 1:Now, while the Krebs cycle itself does not produce high amounts of ATP, it produces other metabolic byproducts, like the reduced form of nicotinamide adenine dinucleotide we call this NADH for short. Another important byproduct is flavin adenine dinucleotide, also called FADH2. Both of these are also coenzymes, just like thiamine. Pyrophosphate is a coenzyme. Nadh is a coenzyme derived from NAD. Nad is a coenzyme form of vitamin B3, also called niacin, and FADH2 is a coenzyme form of vitamin B2, which is riboflavin. These two molecules play a crucial role in the production of ATP in a later process called oxidative phosphorylation, where larger amounts of ATP are produced. But it really all begins with vitamin B1, thiamine, to kick the process off.
Speaker 1:One of the very first steps in the Krebs cycle is when pyruvate is transformed into acetyl coate to enter the cycle. Like I just mentioned a moment ago, this conversion is made possible by an enzyme called pyruvate dehydrogenase. This step is highly dependent on the availability of thiamine. Thiamine is so important for this step to take place that it is the rate limiting variable for the metabolism of carbohydrates. When thiamine is present, pyruvate is converted to acetyl coate and then enters the Krebs cycle, where it's converted into other molecules that are needed for the body to make key fatty acids as well as cholesterol. While thiamine, pyruvate dehydrogenase activity will go down, decreasing our ability to make energy as ATP through the Krebs cycle and oxidative phosphorylation. This would also reduce our ability to make very important lipids needed by the body for numerous different functions.
Speaker 1:There are also other dehydrogenase enzymes that need thiamine to function, for instance, branched chain alpha-keto acid dehydrogenase that's a lengthy word. Well, it's actually several words, but it's a lengthy enzyme name. It metabolizes the branched chain amino acids leucine, valine and isoleucine into acetyl-CoA, among other things. Genetic defects to this enzyme result in the condition known as maple syrup urine disease, signs manifest in the form of lethargy seizures and, like the name would suggest, maple syrup odor of the urine. One type of genetic mutation results in a loss of this enzyme's ability to use thiamine, and this type of maple syrup urine disease actually responds to high doses of thiamine as a treatment, anywhere from 10 to 200 milligrams, depending on the genetic defect and the severity of reduced enzyme activity. The other dehydrogenase enzyme that needs thiamine is alpha-ketoglutarate dehydrogenase I know these are really long words which converts alpha-ketoglutarate into susanol-CoA, both of which are really important substrates in the Krebs cycle. All three dehydrogenase enzymes need the niacin-derived and riboflavin-CoA enzymes I had mentioned a while ago, but also lipoic acid and magnesium, with thiamine being the chief companion to all of these enzymes. When there is not enough thiamine present, these enzymes' activity levels go down, and this results in a buildup of fatty acids, which can result in dyslipidemia and the formation of different pro-inflammatory molecules, both of which are common findings in people with what is generally described as metabolic inflexibility, and this is also observed in people with type 2 diabetes.
Speaker 1:Because we're on this topic, I must mention another enzyme that thiamine serves a rate-limiting role for, and that is the enzyme transketolase. Transketolase enzyme is very important to remember because its activity levels decrease very early in thiamine deficiency, and measuring its activity is one way in which thiamine status is measured today. But we're going to get into that in just a little bit. In brief, the transketolase enzyme is needed to support antioxidant capacity in the body, but also to manufacture a compound called ribose. Ribose is really important for what are called nucleotides. Atp, for instance, is one kind of nucleotide. Nucleotides are the building blocks for nucleic acids. Nucleic acids are DNA and RNA. So, just like amino acids are the building blocks of protein, nucleotides are the building blocks of nucleic acids. It's the same concept. Now take all that, take all of what I just mentioned on these thiamine-dependent enzymes, and we can sum it up into this these thiamine availability will effectively down-regulate mitochondrial energy production while up-regulating more toxic byproducts of metabolism. This happens when proteins, carbohydrates and fats are diverted away from metabolic pathways that rely on thiamine towards alternative pathways that become more active when thiamine is not available.
Speaker 1:The adult human has a somewhat limited ability to store thiamine. We hold anywhere from 25 to 30 milligrams of thiamine, depending on the nutritional and physiological state of the individual. Some estimates do go as high as 50 milligrams of thiamine stored in the body, but 30 milligrams that's the most common estimate. It's stored primarily in tissues with high metabolic needs, like skeletal muscle, the heart, brain, the liver and the kidneys. What is not stored or being used in different cells within organs would be found circulating in the blood, where 90% of thiamine can be found in red blood cells, and that will be important to remember when we get to testing thiamine status. Approximately 80% of thiamine in the body is found in the form of the active thiamine pyrophosphate.
Speaker 1:The half-life of thiamine is very short. It's approximately 12 hours. Absent regular consumption of thiamine, your storage would be depleted within two to three weeks. With an acute illness, thiamine depletion and deficiency can actually present itself in as little as 72 hours because of the body's increased need for thiamine. I should note that particular finding did come from a 2010 study looking at thiamine status in sepsis patients. Nevertheless, any illness is going to increase the body's demand for thiamine. This data supports the notion that we do require a continuous supply of thiamine from our diets.
Speaker 1:Because of how essential thiamine is to macronutrient metabolism, especially glucose metabolism, and when considering how the brain depends on glucose as its primary energy source, it comes as absolutely no surprise that thiamine plays a major role in neurological function. In fact, signs of thiamine deficiency are mainly neurological in nature. This is because thiamine plays a role in neurofunction and the electrical activity of many tissues. Actually, thiamine fryphosphate, a form that's not commonly used, active. It can donate one of its three phosphate groups to activate a protein called rapsin. Rapsin plays a very important role in what is called the neuromuscular junction. This is where neuro fibers coming from motor neurons in the brain stem and spinal cord connect with skeletal muscle to initiate muscle contractions using the neurotransmitter acetylcholine. Neurotransmitters, for those who don't know, are specialized molecules that neurons in different parts of the body use to communicate with one another or target tissues. The rapsin protein essentially helps to anchor acetylcholine receptors at the neuromuscular junction, specifically on the muscles. These receptors are needed so that, when acetylcholine is released by neuro fibers, it can bind to these receptors on muscle and enable muscle contraction. Thiamine donates phosphate groups for other synaptic proteins directly in the brain as well.
Speaker 1:Interestingly, though, while the brain is vulnerable to thiamine depletion and when I say vulnerable I mean that reduced thiamine in the brain would have serious consequences but the brain does not store substantial amounts of thiamine in it. However, different animal-based studies have shown that during periods of low thiamine intake, the brain is depleted of thiamine more slowly than other tissues. On the flip side, when therapeutic doses of thiamine are given, like in a repletion protocol, the brain isn't repleted as rapidly as other tissues, like the liver, for example. This suggests that the brain keeps some degree of what we call homeostatic control over its thiamine status. Remember, just a bit ago I'd mentioned that, under conditions of insufficient thiamine, different metabolic pathways might up-regulate themselves to help sustain energy production. One such pathway in the brain is known as the GABA-SHUN.
Speaker 1:Gaba is the most abundant inhibitory neurotransmitter in the central nervous system, but that pathway through which it's produced can also help to yield ATP under certain circumstances, when not enough thiamine is present to fuel alpha-ketoglutarate dehydrogenase. This enzyme is unable to convert alpha-ketoglutarate into suesinal CoA within the Krebs cycle. When alpha-ketoglutarate builds up, the GABA-SHUN pathway might increase its activity. This takes alpha-ketoglutarate and then converts it into glutamate, which is an excitatory neurotransmitter. This is further converted into GABA and then it's able to make its conversion into susanate and then re-enter the Krebs cycle. So under conditions of thiamine deprivation, the GABA-SHUN pathway may up-regulate to help yield energy.
Speaker 1:This phenomenon may actually explain why anorexic behavior is noted as a common characteristic of thiamine deficiency, more specifically, subclinical thiamine deficiency. Gaba activity increasing through this pathway in certain parts of the brain has been shown to inhibit feeding in animal models, and this has been tied to reduced appetite and eating observed in subclinical thiamine deficiency in humans. In fact, a loss of appetite is one of the earliest signs and symptoms of thiamine deficiency. Many early signs of thiamine deficiency are non-specific, common and actually frequently overlooked. Early signs of deficiency are not pronounced or distinct enough to warrant a diagnosis, because they could actually be attributed to a number of different diseases. For instance, never-ending fatigue, reduced appetite, changes in mood with a tendency towards hyperurability are those are all common early signs of thiamine deficiency. Sleep disturbances, mental fuzziness, if you will those are all common early signs as well. You can see here how it can be difficult to diagnose or determine a thiamine deficiency based on these. As such, when describing thiamine deficiency, it's usually the later stages that are focused on, as this actually points to a clearer picture where thiamine deficiency is the most likely culprit.
Speaker 1:There are three conditions that indicate key roles of thiamine in neurological function. Those are Wernic Korsakov syndrome, alzheimer's disease and Parkinson's disease. The first of those, wernic Korsakov syndrome, is considered to be the most severe consequence of alcohol abuse, and I'll elaborate a little bit how alcohol consumption that even moderate, can be a major contributing factor to thiamine deficiency. Wernic Korsakov syndrome consists of what are essentially two parts, with the first part, wernic's encephalopathy, being considered the acute or early phase of the syndrome. The diagnosis of Wernic's encephalopathy is characterized by a triad of symptoms that include abnormal eye movements, ataxia, which describes an unsteady gait or coordination impairments, and, lastly, cognitive impairment in the form of confusion or brain fog. Because these symptoms overlap with alcoholic delirium, wernic's encephalopathy is thought to be underdiagnosed and, if left untreated, it can result in permanent neurological damage and progress into the second part of this two-part syndrome, known as Korsakov's psychosis, which typically follows, but it can sometimes coexist with the first part, wernic's encephalopathy. This is referred to as the chronic part of the condition, korsakov's psychosis that is. This is characterized by confabulation, which would be someone doing something like making up stories to fill in memory gaps. Other characteristics of Korsakov's psychosis include psychosis, significant memory impairments to the point of amnesia, and also profound apathy coming from a person. When the amnesic state is not present. This condition is referred to as Wernic's disease, but referred to as Wernic's Korsakov's syndrome when the amnesic symptoms are actually present, with the other two symptoms of the triad, those being gait impairment and abnormal eye movement.
Speaker 1:Most obvious risk factors for this condition include alcoholism, severe gastrointestinal illness and malnutrition. Absent these risk factors, symptoms of Wernic Korsakov's syndrome share similarities with many other conditions. As such, clinical diagnoses can sometimes be difficult of note here. One particular study did a post-mortem so after death investigation of 131 cases of Wernic's encephalopathy and found that 80% of cases were missed while the patients were still alive, with the suggested reason being that only 16% of them presented with the classic triad of symptoms. In addition to that, 44% had one or two symptoms of the triad and 19% had no symptoms of the classic triad at all. But they did have brain lesions present in the parts of the brain you would expect in someone with Wernic Korsakov's syndrome.
Speaker 1:A 2013 Cochrane review of the usage of thymine to prevent Wernic Korsakov and people with alcohol abuse determined that there was insufficient evidence to guide the use of thymine by healthcare practitioners to treat or prevent this condition. This review only consisted of two randomized trials on the matter, hence the insufficient evidence to suggest actual healthcare protocols here. However, the European Federation of Neurological Societies does support the use of 200 milligrams of thymine three times daily administered intravenously to treat Wernic Korsakov. Likewise, the Royal College of Physicians in London supports the use of oral thymine hydrochloride that's a common supplemental form of thymine in amounts of 100 milligrams three times daily in people at risk for, but showing no signs of, wernic Korsakov syndrome. When symptoms are present, intravenous administration is recommended through a healthcare practitioner, of course. However, it is worth noting that this condition can be a consequence of gene mutation to the transketolase enzyme, not necessarily alcoholism, that results in reduced binding affinity of thymine to this enzyme. In this case, thymine administration in high doses seems to be effective approximately one quarter of time.
Speaker 1:Alzheimer's disease is another neurological disorder with ties to thymine deficiency through animal models, but also by observations that reductions in thymine dependent processes in the brain appear to be related to altered glucose metabolism that is seen in people with Alzheimer's disease. It's worth noting here that past research has demonstrated that glucose utilization in the brain, when measured, that can actually help predict the progression of someone from mild cognitive impairment to Alzheimer's disease. Now combine that with the information we covered earlier that thymine dependent enzymes are uniquely tied to and important for carbohydrate glucose metabolism in the body. Interestingly, case control studies one published in 2004 and another in 2017, showed that blood levels of thymine pyrophosphate so that's active thymine and thymine monophosphate, were lower in people with Alzheimer's associated dementia. But that in itself is not uncommon to say about many different vitamins for that condition, especially water soluble B vitamins. Now there was a study published in 1990 that showed 13% of 150 patients with cognitive impairments so that's pre Alzheimer's that they were considered to have a true thymine deficiency. Very few studies to this point in time have looked at true deficiency prevalence in people with Alzheimer's disease.
Speaker 1:Several different studies have found evidence of decreased activity of thymine dependent enzymes in the brains of people with Alzheimer's. For instance, there was an autopsy study conducted in 1998, that demonstrated that alpha ketoglutarate dehydrogenase. There's that enzyme again. Its activity was decreased by more than 75% and transketolase activity was reduced by more than 45% in brains and peripheral tissues of people who died with Alzheimer's disease. There are two studies published in 1996 that highlighted decreased brain levels of active thymine pyrophosphate, even though free thymine and other thymine derivatives were found to be at normal levels in people with Alzheimer's disease. Although reasons for why that's been found to happen have not entirely been sorted out, thymine deficiency in animal models has resulted in increased brain plaque formation. These plaques are pathological hallmarks of Alzheimer's disease. In these models, thymine administration using a synthetic derivative of thymine with better bioavailability than thymine, called benphodiumine, promoted the regression of these plaques. However, the use of thymine supplements in clinical models of Alzheimer's disease has yielded very inconsistent results. As of now, there is no direct evidence to suggest the use of thymine or any of its derivatives for specific treatment purposes. But the takeaway from the available body of evidence here indicates that thymine deficiency might help drive the progression of Alzheimer's disease, and so the best thing we can do in this case is to ensure adequate thymine intake for as much of our lives as possible.
Speaker 1:The third condition that indicates an important role for thymine in neurological function is Parkinson's disease. Like I had mentioned, this idea comes from findings that patients with Parkinson's disease have reduced activity of thymine-dependent enzymes like alpha ketoglutarate dehydrogenase. Interestingly, this particular thiamine-dependent enzyme seems to be inhibited by metabolic byproducts of dopamine breakdown that are elevated in people with Parkinson's disease. So byproducts come about when dopamine is metabolized. One study published in 1999 found that Parkinson's patients given levodopa have higher levels of thiamine pyrophosphate so more active thiamine, in their cerebral spinal fluid, compared to people with Parkinson's who were not being treated with levodopa. Levodopa is the drug form of the precursor molecule to dopamine and it's part of the current standard of care for treating people with Parkinson's. For those that might not know that, the amount of thiamine in this case was not related to age at onset or duration of the disease, which was a really interesting finding. Some researchers have suggested that gene mutations to thiamine-dependent enzymes like alpha-ketoglutarate dehydrogenase may be associated with, or put one at risk for developing Parkinson's disease later in life, but research there is far sparser than research making connections to thiamine and Alzheimer's disease.
Speaker 1:Possibly the most well-known disorder to arise from thiamine deficiency is what is called baribary. Baribary is a consequence of severe thiamine deficiency. Symptoms of baribary include weakness and loss of feeling, usually in the legs. This can then progress to heart failure, breathlessness and, in some cases, edema. Because baribary comes with so many symptoms that present themselves at different time points of the disorder, it's been subdivided into several different categories. Those include cerebral, dry, wet and gastrointestinal. Cerebral baribary is considered to be more of a precursor to Warnock-Korsakov syndrome and again is especially prevalent in people who abuse alcohol. It's one of the most severe forms of baribary. Other forms, like dry and wet baribary, are thought to be rare in the United States, but, as I will explain shortly, it's probably not as rare as you would think.
Speaker 1:These forms are commonly seen in eastern countries, especially Asian countries, where diets consist of a lot of polished white rice. It's no surprise, then, that, historically, baribary became a major issue in the 19th century with the development of milling technologies that yielded polished rice. This condition has affected Asian populations at the highest rate, considering that even today, asian countries consume close to 90% of rice produced worldwide, which fulfills approximately 60% of Asia's daily energy and tick requirements. It is no surprise. Baribary was actually described in Chinese literature as early as 2600 BC, but more recent documentation of the disease leading up to the discovery of thiamine as a cure, but also thiamine as a molecule present in food would bring us back to the 1860s, where baribary was affecting 30 to 40% of the Japanese Navy.
Speaker 1:In the 1870s, a Japanese naval medical officer by the name of Dr Akane Hirotakaki I hope I'm pronouncing that right he happened to be a British trans surgeon. He had first noted an association between baribary and diet. He realized that Japanese sailors who were issued lower protein diets compared to British sailors, they were not experiencing the same disease symptoms the British sailors. So what he did was conduct an experiment at sea where he modified the sailors diets to include more meat, condensed milk, bread and vegetables at the expense of rice. This ended up cutting the severity and occurrence of baribary related symptoms dramatically, and this led to Dr Akane Hirotakaki to include that the disease must be caused by lack of protein in the diet. His recommendation was to include more protein in sailors diets and this was adopted by the Japanese Navy and baribary was nearly eliminated as a problem by 1880. This despite the fact that his initial conclusion that baribary was a consequence of insufficient protein was soon to be shown to be false.
Speaker 1:Thymeine as a molecule was not even proposed until 1906, and its structure was not determined until 1926, but the connection between thiamine and dietary protein, especially animal derived proteins, is an important one to keep in mind moving forward. The actual discovery of thiamine came about through the work of a Dutch physician who was at the time unaware of Dr Akane Hirotakaki's work. I do find the discovery history to be very interesting because it highlights how scientific discovery takes place, and it does help give us an understanding about how we came to be where we are today. But I'm not going to go more into the history of thiamine discovery here, unless that's something that you'd like me to include more of in future episodes, and please leave a comment on my YouTube page under this episode.
Speaker 1:As I had mentioned a few minutes back, baribary has several forms, one of which is dry baribary this is also called neuritic baribary which primarily occurs in adults and is characterized by peripheral neuropathy. Peripheral neuropathy is when nerves that are in other parts of the body, besides the brain and spinal cord, become damaged or do not work properly, causing symptoms that include numbness or tingling, hands and feet, pain that can be shooting or burning, muscle weakness as well as coordination problems. This form of baribary does not have a cardiac component to it wet baribary. This one is also known as cardiac baribary. With this form, in addition to neurological symptoms, there are also cardiovascular manifestations, which include a rapid heart rate, enlargement of the heart, peripheral edema, so swelling, and ultimately, congestive heart failure.
Speaker 1:Although wet baribary is not common in more industrialized countries, congestive heart failure is not uncommon, especially in the elderly. In this population, what are called loop diuretics are used for treatment. This is a medication, many of which actually increase the excretion of thiamine, potentially putting someone at risk for thiamine deficiency. There was actually one study in 2015,. It was a meta-analysis of nine different studies and it found thiamine deficiency risk was two and a half times higher in patients with heart failure compared to people without heart failure. Likewise, older people with congestive heart failure are more likely to be thiamine deficient compared to younger people with heart failure.
Speaker 1:One important measure of heart function is left ventricular ejection fraction. This measures how well the left ventricle of the heart is pumping. The left ventricle is the chamber of the heart responsible for pumping blood that is, oxygen rich to the rest of the body. The ejection fraction is how much blood gets squeezed out of the left ventricle when the heart contracts. A normal and healthy left ventricle ejection fraction, according to the American Heart Association, is between 50 and 70%. And it's worth noting here that this is relevant because improvements in left ventricular ejection fraction in heart failure patients is associated with improved survival.
Speaker 1:Now I had mentioned that diuretic use increased thiamine excretion and that diuretics are used to treat some congestive heart failure patients. Well, past research in patients given 80mg of a diuretic called churrosimide that showed that 98% of people in this case, so that was 24-25 patients given this diuretic long term were determined to have a clinical thiamine deficiency. Interestingly, there were two studies published in the 90s, one in 1991 and one in 1995 by the same research group. They gave congestive heart failure patients who were taking this diuretic three months or longer, 200mg of intravenous thiamine, that was, 100mg twice daily for seven days. In the first study, four out of the five patients improved left ventricular ejection fraction. In the second study, after the week of thiamine injections, patients were given oral thiamine at 200mg for six weeks and in the 27 patients who completed the seven total weeks of thiamine repletion, left ventricular ejection fraction went up by 22%. Now it is important to mention that other trials using high dose thiamine in heart failure patients found no improvement in left ventricular ejection fraction, and studies to this point have not singled out congestive heart failure patients, who indeed have or are at the highest risk of thiamine deficiency. The body of evidence here suggests that thiamine deficiency risk is high in heart failure patients or people who are taking loop diuretics, for instance.
Speaker 1:Thiamine deficiency is likely worsened by symptoms of heart failure. Probably is no surprise. We've seen now that thiamine deficiency not only affects the central nervous system but also negatively impacts the cardiovascular system. When thiamine's role in nutrient metabolism, especially carbohydrate metabolism, it comes as no surprise that diabetic vascular complications can also involve thiamine deficiency or altered thiamine dependent enzyme activity. Thiamine deficiency does seem to impair normal hormone function of the pancreas and make worse hyperglycemia, which in this case would contribute to sustained high blood glucose levels. Diabetic high blood glucose can cause vascular damage over time. That does affect the heart. It can also affect the kidneys this is known as nephropathy. It can affect the eyes this is called diabetic retinopathy and it can also damage nerves in the peripheral nervous system. This is called neropyphral neuropathy remember I introduced that had termed just a bit ago. This is one of the primary symptoms of berry berry, which is what happens when thiamine deficiency starts to become severe.
Speaker 1:Experts in the early 2000s showed that thiamine status was estimated to be 76% lower in type 1 and type 2 diabetics compared to non-diabetic people. A more recent study in 2015 showed that a frank deficiency was present in 98% of the participants that had type 2 diabetes, as determined by plasma and urine samples, but we're going to talk about biomarker testing soon and note some current limitations and different methods. There's not much literature available assessing thiamine status or administering thiamine diabetic patients. However, preclinical rodent models do show promise in thiamine's ability to possibly reduce diabetic complications, which we can assume would be most beneficial in people whose thiamine status is the lowest. As I noted just a minute ago, current evidence suggests a high percentage of diabetics are likely to be, at the very least, in a state of thiamine insufficiency, even if it's not in a frank deficiency. More data is really needed in this particular population when talking about disease or disorders with ties to thiamine.
Speaker 1:Cancer is worth having a discussion about. Thiamine deficiency and non-alcoholic related Wernic Korsokov syndrome have been observed in cancer patients with rapidly growing tumors. Cell culture data does suggest that rapidly dividing cells have a high requirement for thiamine. It turns out that some types of cancer cells rely on thiamine-dependent enzymes like trans-ketolase, because of their need for nucleic acids. Remember from earlier that trans-ketolase activity is necessary for the production of nucleic acids like DNA and RNA. Some chemotherapeutic drugs given to cancer patients, like one called 5-fluorosil those, actually can inhibit the enzyme that forms active thiamine pyrophosphate. This enzyme is called thiamine pyrophosphokinase.
Speaker 1:As such, thiamine supplementation is sometimes recommended to cancer patients on drugs like these to prevent deficiencies. However, some researchers and doctors do caution against the use of too much thiamine in cancer patients, as it's possible that malignant tumors could be using excess thiamine to fuel their growth. As such, thiamine supplementation in people with cancer is, to this point, usually only advised to people who are already in a state of deficiency. That being said, there's nothing wrong with making sure you're getting enough dietary thiamine through regular food to prevent an outright deficiency in first place.
Speaker 1:The presentation of thiamine deficiency is highly variable and affected by things like age, caloric intake, especially carbohydrate intake, which I'll explain shortly. It's also affected by the presence or absence of other micronutrient deficiencies. To be clinically diagnosed with a disease or condition caused by thiamine deficiency, there are one of two criteria that need to be fulfilled and, determined by a clinician One, at least three of the major signs and symptoms that I spent the last bit going over, or two at least two major and two minor symptoms, plus a positive response to thiamine treatment. Now here is one of the more interesting topics to cover regarding thiamine, and that is the actual rate of thiamine deficiency. Surely you think there must be hard numbers on how many of us need more thiamine. Well, if that was your assumption, you would be incorrect. In fact, the National Institute of Health's fact sheet on thiamine that was last updated in February of 2023 states that there is currently no data on rates of frank thiamine deficiency in US populations. Now, why is that? Well, some researchers make note that there are no firmly established standards for what constitutes lower or suboptimal thiamine concentrations, or even a consensus on what testing values constitute a frank thiamine deficiency.
Speaker 1:The Food and Nutrition Board of the National Academies of Sciences Medicine Division, which at the time was called the Institute of Medicine. It, did set an official recommended daily allowance, that's RDA, for thiamine, so standards exist for its intake. This was set at 1.2 milligrams a day for adult men and 1 milligram a day for women who are not pregnant. So just regular adult women. The problem with thiamine standards set thus far is that they have not been updated for over 80 years.
Speaker 1:Actually, in 1940, the Food and Nutrition Board of the National Academy of Medicine recommended that thiamine, along with other vitamins and minerals like niacin, riboflavin and iron, be added to flour. This is known as food fortification. With an average diet, even a poor one, but consisting of fortified foods, it's not difficult to meet the daily requirement of 1 to 1.2 milligrams per day of thiamine. Even a National Health and Nutrition Examination Survey conducted from 2003 to 2006 in the US suggested that only 6% of the population had thiamine intakes below the estimated average requirement. That's the amount needed to achieve theoretical sufficiency in 50% of the population, so that's a bit less than the RDA. If you removed thiamine from fortified food, this number would jump from 6% of people reporting not getting enough thiamine all the way up to 41% of people.
Speaker 1:If we were to take these numbers at face value, thiamine deficiency would seem like a rare and unlikely problem in industrialized countries like the United States. However, thiamine deficiency has been observed across multiple different groups of people, with deficiency incidents ranging from 20% all the way to 90%, depending on the specific group and the specific study. This in spite the fact that most people are consuming a diet rich in fortified foods containing thiamine that in some cases exceeds the RDA by a factor of 4. So that's a big deal, and it requires us to dive into who's at the highest risk of thiamine deficiency and what kinds of things can contribute thiamine deficiency, even when we're taking in supposed ample amounts through our diets. One of the most obvious groups at risk for thiamine deficiency that I've already brought up during this episode would be people with alcohol dependence.
Speaker 1:Alcohol use disorder appears to be the most common cause of thiamine deficiency in more industrialized countries like the United States. Past research does suggest that up to 80% of people with chronic alcoholism develop a true thiamine deficiency. What's really interesting here is the role of regular alcohol consumption as a contributor to thiamine deficiency, even under levels that would be classified as alcoholism. It's underappreciated, regardless of the amount of alcohol somebody is taking. In ethanol in alcohol inhibits the enzyme thiamine pyrophosphokinase. This again is the enzyme that converts free thiamine to the active thiamine pyrophosphate.
Speaker 1:Data in rodents suggest that even acute alcohol intake might transiently reduce thiamine availability in the body by up to 54%. There are three ways in which alcohol hurts thiamine status in the body. One, this is the most obvious one, being that alcohol generally reduces thiamine intake by displacing thiamine rich foods. Two, by impairing thiamine absorption and utilization, alcohol abuse impairs intestinal absorption of thiamine and many other nutrients. Likewise, like I just stated a few moments ago, ethanol in alcohol impairs enzyme function needed to produce active thiamine in the body. The last way in which alcohol hurts thiamine status is by increasing one's need for thiamine. When maintaining a high fluid intake, urine flow rate increases, and this would increase the loss of thiamine. In addition to that, alcohol consumption is associated with the concomitant intake of carbohydrates which, as I will discuss in just a few moments, it increases one's need for thiamine.
Speaker 1:Obese individuals also experience high rates of thiamine deficiency. It seems that here, the prevalence of official diagnoses ranges from 15 to 29% of people. Now consider that in 2018, the Centers for Disease Control and Prevention reported that over 42% of the US adult population was obese, with a clear upward trend. That's a staggering amount of people with possible thiamine deficiency. An estimation of the world's population over the age of 5, who is currently obese, by the way, is 38 to 39%. It's not surprising that thiamine deficiency rates are also high in people with diabetes, both type 1 and type 2, like we talked about just a couple of minutes ago. But to reiterate on that point, thiamine levels in plasma have been observed to be up to 76% lower in people with type 1 diabetes compared to people without, and 50 to 75% lower in people with type 2 diabetes.
Speaker 1:It's thought that hyperglycemia so high blood glucose as part of the diabetic etiology impairs thiamine uptake and increases clearance by the kidneys. Women who are pregnant are often at an increased risk for several different types of deficiencies, with thiamine being one of them. There was a very troubling finding in a 2019 review that looked at 177 pregnancy cases and concluded that thiamine depletion in pregnant women developed between 10 and 15 weeks gestation. After six or fewer weeks of vomiting, this was the case for nearly half the women. This number jumped up to almost 65% of women if they were vomiting for seven weeks. None of these women received thiamine as a treatment, but some did receive IV glucose which, as we discussed just a minute ago, can make worse thiamine deficiency if thiamine is also not given alongside glucose. I'm going to elaborate on that point in just a minute. But glucose increases one's need for thiamine. I'm going to keep hammering that point home.
Speaker 1:Older adults are one of the top groups at risk for thiamine deficiency. One study in community dwelling older adults found that 50% of the subjects in this particular study were considered thiamine deficient according to biomarker testing, even though these adults were consuming thiamine amounts greater than the current RDA, as I suggested earlier. Any illness would increase one's need for thiamine. As such, people who have been hospitalized likely have a greater need for thiamine and are also at a greater risk for thiamine deficiency. For people with heart failure, like we talked about, thiamine status is rarely tested for, but deficiencies are to be expected in a lot of people. Deficiency prevalence in this group has ranged from 30% to 90%, depending on the study, in intensive care. There is research that demonstrates that upon intensive care admission, 10% of people are more maybe thiamine deficient, although, again, thiamine deficiency is usually missed or not tested for under these circumstances, but only after a few days in intensive care, that deficiency prevalence likely doubles. The key takeaway here, considering hospitalizations, is that even though thiamine deficiency may not be present upon admission, its likelihood for developing raises dramatically in a very short period of time. We just whenever groups at risk for deficiency, but equally, if not more important is identifying potential causes of deficiency that exist independently of disease or illness that can cause or accelerate a deficiency.
Speaker 1:The most obvious cause of thiamine deficiency is inadequate thiamine intake, which is thought to be the primary cause of thiamine deficiency in most countries, especially among lower income populations. People of lower socioeconomic status tend to have diets that are very rich in carbohydrates but very low in thiamine content. Alcoholism, again, is strongly tied to lower thiamine intake. Another obvious cause is an increased requirement for thiamine. Any illness, as we already discussed, increases your need for thiamine. Pregnancy, breastfeeding and adolescent growth are all conditions under which thiamine need is increased. Strenuous physical activity, as is the case for athletes, in combination with higher carbohydrate intakes, result in a greater demand for thiamine. Actually, people with very high carbohydrate intake intakes in general need more thiamine. High carbohydrate diets diminish thiamine stores, regardless of the source or quality of the carbohydrates.
Speaker 1:Because of thiamine's critical role in carbohydrate metabolism, thiamine need rises proportionally to the amount of carbohydrates someone is consuming. There was a study published in 2021 that took men and women and held their caloric intake constant, but then increased their carbohydrate intake to account for proportionally more of their energy intake without affecting overall calories. For instance, carbohydrates initially accounted for 55% of energy intake. Patients were kept this for four days and then they increased their carbohydrate intake to account for 65% of energy intake for four days and then again another increase increased to 75% of their energy for four days. Thiamine intake, energy intake and physical activity were all held constant during this study. Over the course of the study, thiamine emplacement and urine decreased substantially. As carbohydrates increase, thiamine continued to decrease.
Speaker 1:Thiamine deficiency has been observed as a complication of what is called refeeding syndrome. In this case, the introduction of carbohydrates to severely starved individuals leaves to an increased demand for thiamine and glycolysis and the Krebs cycle, and that has made worse thiamine deficiency in past clinical observations. As a very general guideline, only 330 micrograms, that's 3300s of one milligram, are needed for every 1000 calories of energy consumed from carbohydrates. Again, that's a very general recommendation. Not getting enough magnesium in your diet can also be a cause or contributor to inadequate thiamine activity in the body. In order to synthesize active thiamine pyrophosphate using free thiamine, the enzyme thiamine pyrophosphokinase needs to use magnesium as a cofactor. This reaction also requires energy in the form of ATP. Nearly all reactions in the body that use magnesium implicate ATP in some way. As such, thiamine and magnesium are considered to be the primary energy, vitamin and mineral respectively. That is an oversimplification of their function, but the label is not entirely off base.
Speaker 1:Very intake of what are considered common food compounds may actually be hindering the absorption of thiamine and contributing to insufficient thiamine status. These are called anti-thiamine factors. Different foods contain anti-thiamine factors that can react with thiamine to break it down to form an inactive product or inhibit its absorption in the gut. Some compounds found in tea or coffee may inhibit thiamine absorption. For instance, aphic acid, chlorogenic acid and tannic acid in coffee and tea can oxidize thiamine in the gut and that would render it less likely to be absorbed. Some of these compounds are included in energy drinks that have added sugars which, as we just went over, further increase somebody's thiamine need. This does not mean I'm advising you not to use things like coffee, tea or energy drinks in moderation, but consuming a lot of them and frequently may contribute to less thiamine uptake through food and less thiamine activity in the body. Nicotine in tobacco products can also reduce thiamine activity because it antagonizes thiamine transporters. There's one particular cell study that suggests nicotine inhibition of thiamine transporter activity of pancreatic cells by as much as 40%. Now consider that nicotine use through vaping or tobacco products is often co-administered with recreational alcohol use, and thiamine activity is like to be opposed even further.
Speaker 1:Another anti-thiamine factor that is not given much attention but is relevant is an enzyme present in some protein sources. In their raw state, this enzyme is called thiaminase, and this breaks down thiamine, which would make it unusable in the body. This enzyme is found in freshwater fish and shellfish, so high intakes of raw fish could limit thiamine availability. However, thiaminase is what's known as a heat libel enzyme, meaning that it is inactivated or destroyed by cooking. In this way, cooking animal-based protein sources like fish helped preserve thiamine in one sense, but in another way, high temperatures also destroy thiamine. So I think the main takeaway here is that if you consume raw fish, do so in moderation. Raw protein sources being causal to thiamine depletion is more of an issue in some countries in Africa, like places in Nigeria where African silk worms that contain thiaminase are considered a high protein food. To conclude on this point here, remember I had said that although people report adequate thiamin intakes through diet, there is research showing that at times they can still present with thiamine deficiency. It's thought that many people in developed countries are not necessarily suffering from a lack of thiamin intake. Rather, many of us may be overexposing ourselves to anti-thiamine factors Not technically considered anti-thiamine factors in food, like the ones I just went over but still antagonistic to thiamine status would be the use of specific medications.
Speaker 1:Several different pharmaceuticals can deplete thiamine, either directly or indirectly. Medications that pose a risk to thiamine status include the commercially popular pharmaceutical metformin. A 2020 study showed that metformin, along with 146 other commonly prescribed medications, inhibit what's called thiamine transporter 2, or TRTR2 is usually how it's abbreviated. This transporter is needed for thiamine to make its way into different tissues in the body, including brain tissue. Thiamine transporters are very important for thiamine status because thiamine is a water-soluble compound. This means that it cannot passively diffuse through a cell membrane that's made from different lipid or fat-based materials. It requires transporters to enter cells.
Speaker 1:Non-steroidal anti-inflammatory drugs, also called NSAIDs, tylenol, aspirin those can all contribute to thiamine depletion through reducing liver tissue retention times, reducing gut absorption or increasing the excretion of thiamine. So it's important to monitor use of compounds like these and to use them appropriately and in moderation. Of course, like I mentioned earlier, diuretics also increase the excretion of thiamine Because of the generalness or vagueness of symptoms of thiamine deficiency. Testing confirmation is needed to establish a frank deficiency. Of course, deficiency rates in different populations are based on testing assays and cutoff values. Those change from study to study. The definition of deficiency varies based on the purpose of a specific study. There's actually no consensus for exactly what testing values constitute a true thiamine deficiency, which obviously means that the same can be said of what testing values constitute a subclinical and marginal thiamine deficiency.
Speaker 1:There are two general categories of biomarker testing that exist to assess thiamine status, one of which is tissue metabolite level biomarkers. This includes looking at blood serum, plasma or urine levels of thiamine and the different metabolites that include thiamine, thiamine pyrophosphate, free thiamine, thiamine monophosphate and thiamine triphosphate. Of these, active thiamine pyrophosphate is the most informative. Thiamine in this form accounts for 90% of circulating thiamine, 80% of which is found in red blood cells. Whole blood tests of thiamine pyrophosphate are the most common tests. A healthy individual usually has whole blood thiamine pyrophosphate levels between 70 and 180 nanomoles per liter. However, reference ranges for blood levels of active thiamine they do vary a bit from lab to lab. There really is not an read upon standard for what thiamine pyrophosphate levels indicate nutritional adequacy either. Sometimes levels of other thiamine metabolites will be reported, but they aren't very useful when trying to assess actual thiamine status.
Speaker 1:Of all biomarker tests, the most accurate are the ones that measure active thiamine pyrophosphate from red blood cells, either directly or indirectly. When measuring directly, active thiamine itself is being measured. When measured indirectly, we then get into the second category of thiamine status testing, and that is functional biomarker testing. For this, the degree of thiamine pyrophosphate saturation of thiamine dependent enzymes is measured. In this case, the activity of thiamine dependent enzyme transketolase in red blood cells is what's measured.
Speaker 1:This test takes advantage of the fact that red blood cell transketolase can actually bind active thiamine in vitro, which basically means that it's happening outside of the body once being tested. This test measures the activity of the enzyme at baseline and also the activity of the enzyme when thiamine pyrophosphates added to stimulate more enzyme activity. If someone has sufficient amounts of thiamine in their body, then the addition of thiamine should not increase transketolase activity by more than 15%. If added thiamine stimulates the enzyme's activity more than 15%, this usually means that less thiamine was bound to the transketolase enzyme and thus the person's transketolase activity was operating under levels it should have been, which is indicative of some level of thiamine deficiency. If transketolase activity increases by more than 25% in the presence of added thiamine, this is thought to be reflective of a true and severe deficiency. Increases in enzyme activity over 40%, those are seen in people with Wernich's encephalopathy. So that's severe, severe deficiency. In essence, this test measures how saturated the enzyme is with active thiamine. In summation, there are two general categories of tests that assess thiamine status, and those include tissue metabolite biomarkers and functional biomarkers. The two biomarker tests that are the most useful are blood levels of thiamine pyrophosphate, which is a tissue metabolite biomarker, and red blood cell transketolase activity, which is a functional biomarker.
Speaker 1:To this point, I didn't say anything about urinary thiamine excretion testing, even though that's a commonly used measure of thiamine status. This test provides information on dietary intake of thiamine, but not necessarily thiamine stores. Urinary levels of thiamine metabolite levels increase when you're taking in sufficient amounts of thiamine through diet. For adults, excreting less than 100 micrograms a day, thiamine and urine suggest that you're not getting enough dietary thiamine, and excreting less than 40 micrograms a day and urine suggests very, very low thiamine intake through your diet. I already discussed limitations of the recommended dietary allowance established for thiamine intake, but I will list them here, as it's important still to hit these numbers at a minimum, and many organizations do agree with these numbers.
Speaker 1:For infants, the RDA of thiamine is 0.2 milligrams per day for those age zero six months and 0.3 milligrams a day for those age seven to 12 months. As children grow, their thiamine needs increase. Children aged one to three years require 0.5 milligrams per day, and those aged four to eight years need 0.6 milligrams per day. For older children, the RDA is 0.9 milligrams a day for those who are aged nine to 13 years old. In adolescents and adults, the RDA for thiamine differs by gender. Males aged 14 years and older should consume at a minimum 1.2 milligrams of thiamine per day, while females in the same age group require a minimum of one milligram per day. For women, these needs change during pregnancy and breastfeeding. Pregnant women of any age should increase their intake to at least 1.4 milligrams per day, and breastfeeding women should consume 1.4 milligrams per day.
Speaker 1:Thiamine need, like I stated earlier, is directly related to one's carbohydrate intake, with approximately 1.3 of a milligram being needed for every additional 1,000 calories from carbohydrate. Food sources of thiamine include meat, fish and whole grains. Like I had mentioned earlier, whole grain fortification with thiamine and other B vitamins began in the 1940s and actually the most common sources of thiamine in the US diet are from thiamine fortified cereals and breads. It's estimated that more than one third of thiamine in the US food supply is provided by grain products, with animal meats providing around one quarter. I mentioned earlier that a 2019 study suggested that if not for thiamine fortified foods in the United States, 41% of people would not be getting enough thiamine when considering the RDA Because of fortified foods. Only approximately 5% to 6% of US adults report not taking in enough thiamine but, as we already went over, data exists suggesting that people reporting intake of four times the RDA are still considered deficient at times.
Speaker 1:Thiamine can also be naturally present in reasonable concentrations in whole grains, like brown rice, for instance. Brown rice is considered a whole grain because it includes all three parts of a grain kernel. These are the bran, the germ and the endosperm. In brown rice, these three parts are present and intact. Thus it's considered a whole grain, which naturally contains thiamine approximately 200 micrograms per 100 grams of rice. Actually, however, thiamine is unevenly distributed. In most whole grains like brown rice.
Speaker 1:Typically, thiamine and several other micronutrients are stored in what are called allurone cells. These storage cells are rich in nutrients that support early growth stages of a plant. Allurone is found in the bran layer, which is the outer layer that envelopes the germ and the endosperm. But because the germ is rich in unsaturated oils, the food product is susceptible to these oils oxidizing, which would spoil the final product. Because of this, rice grain is typically milled to remove this issue altogether and improve the shelf life of the rice and other grain products, like wheat. What you end up with is polished white rice and white flour, which is nearly devoid of thiamine and other micronutrients that were previously present. White rice contains about 1 1⁄10 of the thiamine content of brown rice, unless it's enriched with thiamine after its initial processing.
Speaker 1:In grain-based foods, the most abundant sources of thiamine are cornmeal, oats, whole grain wheat, rye flour and brown rice, ranging from 200 to 800 micrograms of thiamine per 100 grams of food. Vegetables are very low in thiamine content and most thiamine found in vegetables is in the form of free thiamine In animal tissue. So animal meats, 80% or more of thiamine is found in its active form thiamine pyrophosphate. Animal meats highest in thiamine are pork and ham, both having close to one milligram of thiamine per 100 grams of meat. Different types of fish, beef, chicken and turkey all also contain appreciable amounts of thiamine. The richest sources of dietary thiamine are yeast like dried brewers yeast and bakers yeast.
Speaker 1:Food preparation can alter thiamine content. The stability of thiamine depends on the form it's found in, as well as the pH of its environment. When food is dry and at room temperatures, thiamine is stable. Thiamine content can be lost when cooking food or when some foods are processed to remove water due to thiamine's water solubility. Thiamine is also sensitive to UV light when not bound to protein, like it is in animal-based foods. This will be relevant to dietary supplements of thiamine. As a general rule, you don't want these sitting out in sunlight for long periods of time, which, intuitively, most people don't allow to happen, but it's still worth mentioning.
Speaker 1:As for dietary supplements, there are two very common forms of thiamine that you see in supplements, and those are thiamine mononitrate and thiamine hydrochloride. Thiamine mononitrate is more stable than the hydrochloride form, but it's less soluble in water. Because of this, you will typically see the mononitrate form in multivitamins or when the thiamine is found in a pill, because the shelf life is preserved a bit more in this form. This form is also common in food and pharmaceutical preparations. Because of its better stability, the hydrochloride form is more water soluble, meaning it mixes better in water. Essentially, and because of this, it's more common to see this form in powder formats like electrolyte, workout or vitamin and mineral supplements that you would scoop and then mix in some kind of liquid. Both forms are equally suitable for supporting thiamine status.
Speaker 1:There is another form of thiamine that you may have seen or heard of, and that is benphodiuming. This is a synthetic form of thiamine. In other words, this is not a naturally occurring form of thiamine, but made to imitate the natural form while having potentially greater absorubility compared to other forms of thiamine. This form of thiamine is more fat soluble, which does allow it to pass more easily through cell membranes in the intestines. It was also made to last longer in the body compared to regular thiamine. This form of thiamine does also seem to be well tolerated. Supplementation of thiamine is really the only time you'd find yourself taking in very high concentrations of thiamine. That might lead you to wonder whether or not you're taking in too much thiamine.
Speaker 1:Thiamine, when taken orally, is generally well tolerated. Your body excretes excess amounts of thiamine very effectively through urine. The food and nutrition board of the National Academy of Medicine did not set a tolerable upper intake level, also called the UL or upper limit, for thiamine. The reason being is that there's no well-established toxic effects from long-term consumption of thiamine through food or supplementation up around 50 milligrams per day. The current leading thought on the matter suggests that absorption of thiamine declines rapidly when ingesting over 5 milligrams at a time. Now, to be clear, there don't seem to be many negative effects from taking in higher doses of thiamine orally. However, there are reported instances of potentially life-threatening allergic reactions and seizures when thiamine doses that are 100 to 200 times the RDA are given intravenously, so through an IV. There are many public organizations that support the current RDA for thiamine intake.
Speaker 1:There is also a perception that thiamine deficiency has been erased or is uncommon in more developed countries, like those in the United States and Europe. However, there is a growing body of evidence that paints a bit of a different picture, one where subclinical and even true thiamine deficiency hides behind more common symptoms of metabolic disorders, and that less thiamine availability and bodily activity may not be because we aren't taking in enough thiamine, but it might be because we're overexposing ourselves to anti-thiamine factors present in the diet but also present in other forms, like routine use of some medications, alcohol or tobacco and nicotine-based products. In sum, make sure you focus on thiamine intake through food items like animal meats and or whole grain products. Even beans and nuts and seeds can provide some thiamine. Limit alcoholic beverages, tobacco slash, nicotine use and potentially unnecessary use of certain everyday medications like NSAIDs Medications like that. They can be very helpful, but here I'm advocating for responsible use of those things. Also, remember to stay within calorie boundaries. This helps to limit excessive carbohydrate intake that may further increase thiamine need to a point where it's more difficult to meet under the suboptimal dietary conditions.
Speaker 1:That does wrap up this episode on thiamine. I hope you did learn a bit about this important and essential micronutrient. I hope that I can earn your subscription to this podcast on whatever podcasting platform you're listening on. If you've not already, please go subscribe to my YouTube channel, as that will be the best place to go and place questions about these episodes, where you'd be most likely to get a response. Thank you for taking the time to listen and I do hope to see you again here soon.