carnitine Archives - Hormones Matter

Lessons Learned About Recovering From Thiamine Deficiency

Published on February 1, 2023

28309 views

lessons learned with thiamine deficiency

It has been a year since I started taking high dose vitamin B1 (thiamine) for a variety of chronic symptoms including: Lyme disease, CFS/ME, endometriosis, histamine intolerance and other food intolerances, SIBO, chronic complicated migraine with aura, chronic insomnia, chronic severe light and exercise intolerance, to name a few. By traditional medicine, each of these conditions was considered unique and thus treated individually. I have learned that they are not separate conditions, but simply different manifestations of disturbed mitochondrial metabolism. In my case, all of this was related to deficiencies in thiamine and other vitamins and minerals. My recovery has been difficult and I have made many mistakes along the way, but hopefully, I learned from them. I am publishing my story here so that you may also learn from my experience. You can read my original story here.

Lesson 1: Magnesium Formulation Is Important

Magnesium is required to change thiamine from its free form to the active form called thiamine pyrophosphate (TPP). Without sufficient magnesium, supplemental or consumed thiamine remains inactive and basically useless. This means that magnesium deficiency can cause a functional thiamine deficiency. I understood this, but what I did not understand, was that there are many different formulations of magnesium supplement, each with pros and cons relative to the individual’s specific needs. I thought they were all interchangeable.

For me, and for individuals with heart related symptoms, magnesium taurate is preferred. One of my first mistakes I made was to ignore Dr. Lonsdale’s comments in which he talked about the importance of taking magnesium taurate. I understood it as meaning that magnesium was important and did not understand that it was a special form of magnesium with cardio protective effects due to the taurine content.

When I initially took magnesium taurate, I noticed an increase in my wellbeing, especially in the fatigue and headache that I would develop after walking around the house or being intellectually active, but I didn’t know that it was the taurine component that was responsible for that change. For a while, I stopped taking magnesium taurate and returned to using other forms of magnesium (magnesium citrate or malate). They did not help as much as the taurate. During this time, I also realized that I do not tolerate magnesium glycinate or bisglycinate. If I take that form, I have a terrible headache on the right side of my head. The glycine activates glutamate via NMDA receptors in the brain causing some excitatory activity. This may be why I could not tolerate it. Others do not have a problem with magnesium glycinate.

Over the last two weeks, I was that taking magnesium malate and taurine separately. I wanted to avoid spending a lot of money on magnesium taurate, so I tried to buy a cheap form of magnesium – magnesium malate – and combine it with taurine which is inexpensive when purchased in bulk. This did not provide the same benefits as magnesium taurate. I experienced chest pressure and pain and my resting pulse went back to being higher than 65-70 BPM. Once I began taking magnesium taurate again, my heart rate and chest pain/pressure disappeared.

So the lesson here, is that different formulations of magnesium work for different people. It is important to research which form may work better for you and your set of symptoms and not to assume they are interchangeable.

Lessons 2-3: TTFD Degrades with Heat and Light and Interruptions to Thiamine Repletion Cause Setbacks

One other important thing I realized was that thiamine is destroyed by UV light. This meant that in August, when I put my TTFD powder (a form of synthetic thiamine that crosses cell barriers more easily) in a transparent container on the kitchen table, and left it there all day long while sunlight shone directly on it through the big windows in my kitchen, it was being destroyed every day. I experienced a big crash during that month, especially since I was taking all the other vitamins and minerals that were serving as co-factors. I could not explain it and was thinking that even this therapy was losing its effect, that my recovery was over, and that I could no longer hope for a better quality of life.

However, in September, I received my new order of TTFD powder. The very day I received it, I took my regular dosage from this new batch. The difference was incredible in terms of my symptoms. It was night and day. The effects were truly remarkable and unmistakable. I’m very careful now with my TTFD powder and make sure it stays in an opaque container.

Lesson 4: Treating My Carnitine Deficiency. Once Again Formulation Matters.

Another thing that I had not been able to fix was my carnitine deficiency. This was discovered by the neurologist who suspected that I was dealing with a FAOD (fatty acid oxidation disorder) or a mitochondrial disease back in February. Free carnitine levels in blood are supposed to be between 17 and 49, while mine was 6. I tried taking various forms of carnitine (L-carnitine, acetyl-L-carnitine, l-carnitine tartrate, Optimized Carnitine, propionyl-L-carnitine) but they all had a laxative effect which was aggravating my symptoms. I asked my neurologist if there were injections with carnitine that could replace the pills, but was left to figure it out for myself. And I did.

Through much research, I found a form that worked for me. It is called Propionyl-L-Carnitine. This form of carnitine is a known agent that protects against ischemia – quote from the linked study:

Free CoA and propionyl-CoA cannot enter or leave mitochondria, but propionyl groups are transferred between separate CoA pools by prior conversion to propionyl-L-carnitine. This reaction requires carnitine and carnitine acetyl transferase, an enzyme abundant in heart tissue. Propionyl-L-carnitine traverses both mitochondrial and cell membranes. Within the cell, this mobility helps to maintain the mitochondrial acyl-CoA/CoA ratio. When this ratio is increased, as in carnitine deficiency states, deleterious consequences ensue, which include deficient metabolism of fatty acids and urea synthesis.

This form of carnitine has made a huge difference in my health, especially with one particular symptom – the wet cough that had accompanied my walking around the house since April 2021.

More Energy and Exercise Tolerance with the Correct Supplements

In October, I began taking magnesium taurate and I also added higher doses of potassium to my regimen, just to see if I tolerated them. I had taken rather lower doses of potassium on and off since starting high dose TTFD. One of the things higher potassium solved, was the aftertaste (or after smell) that I used to get with 300 mg TTFD. I know most people dislike it, since it’s a sulphur smell, although I never disliked it.

After about two weeks on magnesium taurate and higher potassium intake with every dose of TTFD, I began propionyl-L-Carnitine HCL and Optimized Carnitine again. I noticed that they no longer had a laxative effect and I doubled my dose of propionyl-L-carnitine HCL so that I was taking about 600 mg three times a day, combined with one capsule of Optimized Carnitine.

After about a week, I noticed that I had more energy. I no longer needed to eat every three or four hours, I no longer had dyspnea or wet cough during the day when I was walking around the house. All those symptoms speak of cardiomyopathy and were resolving with the supplements. I still need to avoid sleeping on my left side and instead sleep on an incline on my back to be able to sleep through the night, but it my sleep is so much better now. My headache, something that has tortured me since I attempted intermittent fasting in 2018, is now gone. This makes me think that the right-sided headache is one of the symptoms of my heart not being able to do its job properly.

One of the things that helps the most with mitochondrial biogenesis is exercise and it is highly recommended for people with mitochondrial disease. However, in many studies it is noted that if cardiomyopathy is present, then this therapeutic cannot really be used. This is important because many people recovered and improved their exercise intolerance, but still develop symptoms after too much physical effort and wonder what they could further do to improve their symptoms.

After finding the right supplements to correct my deficiencies, I’m able to walk around the house without it aggravating or triggering my symptoms. Prior to this, I was largely bedridden and would have flares every time I attempted to do anything. I have a device that measures how many steps I take and it shows that I walk at least 1000 steps per day when I do nothing and spend 95% of the day in bed.
Now I’m able to go out and walk around my apartment building, which is about 150 meters and do not suffer any consequence. I tried walking more than that and if I do, my main symptoms come back (insomnia, heart symptoms and headache). It is progress, but I still have a long way to go.

I am also capable of learning a little bit of German every day. While my memory is still very poor, at least what I learn “stays” in my brain and the knowledge/understanding of the language accumulates slowly day by day. Intellectual activity no longer triggers the terrible, hours-long headache it once did.

Improved Sleep: Correcting the “Histamine Bucket”, Insomnia, and Heart Symptoms

Since becoming ill, I have had insomnia, likely due to my heart struggling to maintain a constant rate and rhythm. One of the very first things I heard that could explain my constant awakenings especially around 2-3am in the morning is the theory of the “histamine bucket”. This theory argues that around 2-3 am, there is some shift in our body’s physiology and histamine is released. Thus, if you already have a lot of histamines in your body, due to mast cell activation or low DAO, your histamine bucket is full and it will make you wake up. While this is plausible, I do not believe it is sufficient to cause these early morning awakenings. It is not a cause in and of itself, but one of the many things that get dysregulated downstream after nutritional deficiencies are ignored for a period of time.

My chronic early morning insomnia began in 2015, when my thiamine levels dropped and the aggravated mitochondrial disease began to unfold. I remember waking up and I would feel my heart beating more strongly (though not pounding), sometimes I would hear a pulsatile “whoosh” sound in my ear. I would also feel weird sensations in my chest, though not pressure. During those months, I would experience on and off dyspnea while walking to my office. I didn’t think anything of it because I approach my health in the exact opposite manner people with real hypochondria do. I just thought it was a subjective “feeling”, thus not worthy of an inquiry into a possible objective cause for it.

The experience I had in the last few weeks with the supplements mentioned above makes me doubt that mast cell activation or histamine “bucket” overflow are the main causes of waking up constantly at 2 or 3 a.m. I believe it’s most likely connected with the impact histamines have on the heart – they are a known factor in developing heart failure and using antihistamines does help in preventing/postponing the onset of heart failure. This also explains why of all medications, antihistamines were the only ones that helped with a lot of my symptoms in 2016/2017.

When I started taking magnesium taurate, potassium in high enough doses and propionyl-L-carnitine, my heart symptoms improved and my sleep improved. Recently, I woke up at 3 a.m. and I immediately took a low dose of magnesium taurate and a little bit of potassium citrate. I fell asleep again in 15 minutes and in the morning I felt ok. In the past, when I would take something like L-theanine. It would force my body to go back to sleep immediately after 2 a.m., but I would feel much worse in the morning, more than if I just had insomnia.

Restoring Normal Heart Rate

One of the most important things has been reducing my resting pulse from 75-80 BPM to my normal, prior to 2016 resting pulse which used to be 60-65 BPM. I remember I used to complain about it and doctors or nurses just brushed me off. They would say that if it is under 90 BPM, then it is not a medical symptom of anything. I knew they were wrong, but how could I argue? Somehow these people in white coats think that heart failure or other cardiac diseases start out of the blue, when in fact these diseases represent years and years of ignored symptoms before the onset of the full-blown disease with typical manifestations is recognized.

Lessons Learned

Everything that helps my heart function better and recover faster improves all of my symptoms, no matter how much they may seem unrelated. This is what I observed about my own body and I encourage everyone to listen to their body and understand that all symptoms are related.

If one version of one supplement does not work, try another form and combine it with different forms and dosages of other supplements. By supplement, I understand all substances that are naturally found in food or produced by the body.

When I saw that simple forms of L-carnitine don’t have an observable effect, I simply started searching for better forms of carnitine and found propionyl-L-carnitine, which is the physiologically active form of carnitine. Why I looked for other forms of carnitine? Because I learned from experience that high dose vitamin B1, as thiamine HCL didn’t help, but that high dose Allithiamine (a formulation with TTFD) helped and still helps my body working again as it should.

I found taurine (again) by searching for supplements that improve heart failure symptoms. When I first heard about it while reading one of Dr. Lonsdale’s comments, I didn’t understand why it was important.

No one should ever quit trying to figure out their own matrix of symptoms. Begin with the vitamins and minerals, while at the same time addressing infections, limiting damaging diets, limiting exposure to toxic substances and so on. I firmly believe that all diseases with chronic fatigue involve some degree of mitochondrial dysfunction – inherited or acquired. The prototype documented, unquestionable illness that causes hundreds of symptoms, i.e. a multi-systemic illness, is inherited mitochondrial disease.

I know personally of two other people who were completely bedridden, suffering from constant light intolerance, having to live in my bed for two years with a sleeping mask all day and all night, unresponsive to any treatment or approach promoted by the online integrative medicine doctors and communities. I did not think I would ever be able to become house bound, not able to tolerate light, to think or cook for myself. The ability to no longer be bedridden and forced to live in total isolation in darkness and to be house bound is nothing short of a miracle. I owe that to thiamine.

Usually people who end up in that state for so long never recover because all known alternative treatments are exhausted and high dose thiamine for chronic illness is virtually unheard of. I will make sure to do everything in my power to change this, no matter the costs, because there’s just too much unnecessary suffering out there.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image created using Canva AI.

This article was published originally on December 9, 2021.

Hyperemesis Gravidarum – Severe Morning Sickness: Are Mitochondria Involved?

by Chandler Marrs, PhD

Published on January 21, 2020

15019 views

Hyperemesis gravidarum, more commonly known as severe morning sickness, is the type of intractable vomiting that lasts well beyond morning and well after the first trimester. It affects up to 2% percent of all pregnant women and often leads to serious maternal and fetal health complications, including mortality. Although many theories abound, hormone changes and psychosocial stressors among them, the research is extremely limited and, more often than not, steeped in tried and not-so-true aphorisms of the blatantly obvious. Of course hormones play a role and of course stress is involved but neither are requisite to evoke the continuous vomiting experienced by some women.

As a result of our fealty to the obvious, we have no idea what causes the vomiting or how to treat it; leaving women to suffer and their physicians and midwives few tools to alleviate the vomiting. Nevertheless, there are clues from other disciplines and other diseases processes that if we piece them together correctly might point us towards a cause, and more importantly, new treatment options.

If you have followed my work here on Hormones Matter, you’ll know that I spend a lot of time understanding pharmaceutically and environmentally induced damage to the mitochondria. Over the years, I have come to realize that every illness involves the mitochondria in some manner or another. In some instances mitochondrial impairment precipitates illness. In others, it is a consequence of the illness and, in yet other cases, the disease processes involved are a gobbled mess with mitochondrial cascades initially meant to be protective promoting a sort of self-perpetuating damage that is difficult to unwind much less assign fundamental causation. No matter the origins of mitochondrial distress, however, it is my belief that if we look to the mitochondria first we can solve a great number of previously unsolvable disease processes, including hyperemesis.

Outside the Box with Hyperemesis Gravidarum

Not known for coloring within the lines, I often look for clues about disease processes outside the given discipline. So disregarding most of the hyperemesis research, I looked for other ways into this condition. Specifically, I wondered if mitochondrial disorders that cause vomiting independent of pregnancy, like Cyclic Vomiting Syndrome (covered here) or pregnancy complications that fell outside of the hyperemesis classification, but caused severe vomiting nonetheless, such as Acute Fatty Liver of Pregnancy (AFLP), would provide clues and treatment opportunities for severe morning sickness. Indeed, they did.

In both of these disease processes (and a few others), severe, ‘unexplained’ nausea and vomiting are present and, more importantly, share mitochondrial components in the form of deficient fatty acid oxidation. It appears that with Cyclic Vomiting Syndrome (CVS) and AFLP, a critical component of mitochondrial energy production is impaired within the liver (and likely elsewhere) that hinders the liver’s capacity to metabolize fatty acids and detoxify metabolic waste products effectively. When hepatic mitochondria are defunct, liver function is compromised leading to the nausea and vomiting. We get deficits in mitochondrial bioenergetics (made worse by the increased energy demands of pregnancy), but also, a buildup of toxins (energy starved mitochondria cannot clear waste products effectively), and an accumulation of unprocessed fatty acids, all leading to the body’s only mode of clearance, vomiting.

Mitochondrial Fatty Acid Metabolism

The mitochondria take nutrients from food, consume oxygen, and convert those nutrients into a fuel source (adenosine triphosphate ATP) that the cells use to function (learn more). There are three primary mitochondrial fuel pathways (and a whole bunch of secondary and tertiary pathways), one for carbohydrates, one for proteins, and the other for fats, disrupt one or more and all sorts of problems arise. Disrupt these pathways in the liver, the organ responsible not only for toxic waste removal but also for glycogen and fatty acid processing and storage, and the problems become exponentially worse. In the case of the severe morning sickness of pregnancy, I suspect that the mitochondrial beta oxidation pathway, the route for turning fatty acids into ATP, is disrupted.

How to Damage Mitochondria: Let Me Count the Ways

Mitochondrial function can be disturbed by a number mechanisms. Sometimes there are heritable genetic mutations, but not always. Heritable genetic mutations are called primary mitochondrial disorders and occur in up to 1 in every 200 individuals. Fortunately, not all mutations result in illness, but when they do, the results are often devastating.

More frequently, researchers are seeing what are called secondary, acquired, or functional mitochondrial damage evoked lifestyle variables. Epigenetic injuries, sometimes from generations past, have become increasingly common routes to disease. Epigenetic injuries do not induce mutations per se, but rather, aberrantly turn on or turn off gene activity that then influences mitochondrial function. Epigenetic activation or deactivation occurs relative to environmental influence, exposure to toxicants, stressors and/or other variables.

Among the least well recognized secondary mitochondrial injuries are those that are purely environmental; cumulative dietary and lifestyle exposures that damage multiple aspects of mitochondrial functioning. Many environmental and pharmaceutical chemicals evoke mitochondrial damage by leaching critical nutrients needed for mitochondrial energy production and other mitochondrial and cellular functions, but they also damage the structural or functional integrity of these organelles. The cumulative damage of everyday exposures when combined with genetic, epigenetic and/or poor dietary choices, render many individuals susceptible to mitochondrial illnesses. I suspect many of the idiopathic pregnancy complications, like hyperemesis, have their roots in mitochondrial dysfunction.

Although most of this paper, and indeed, most of the popular press focuses on mitochondrial bioenergetics, we must keep in mind that the mitochondria regulate a number of other important and endlessly reciprocal cellular functions, namely: steroidogenesis, immune signaling and cell death. Disturbances in mitochondrial bioenergetics, thus, would be expected impair hormone regulation, induce uncontrolled inflammation (chronic inflammatory and autoinflammatory diseases) and initiate tissue and organ injury. Individuals with mitochondrial issues would be expected to have a broad range of subtle and not-so-subtle health issues; many of which are endemic and epidemic in Western cultures.

Clues for Hepatic Mitochondrial Dysfunction in Hyperemesis Gravidarum

Backing up a bit, let’s connect some dots from the AFLP research. From the research on AFLP, we know that a mutation in the mitochondrial enzyme responsible for processing an important mitochondrial transporter evokes some, but not all of the cases of this disease process. Notably, in some women with hyperemesis, the fetus carries the mutation and evokes the vomiting, while mom is simply a heterozygous carrier.

The mutation (L-3-hydroxyacyl-CoA dehydrogenase deficiency – LCHAD) involves an enzyme (carnitine palmitoyltransferase I – CPT I) responsible for synthesizing the protein that acts as key transporter for fatty acids across the mitochondrial membrane. The protein involved is called carnitine.

When a fetus carries the CPT I mutation, the fetus’ inability to metabolize fatty acids and the associated bi-products are kicked back into maternal circulation effectively overriding the mom’s capacity to process these compounds. The increased load on the mom’s liver induces the vomiting, leading, in some cases, to the compensatory reaction of fat deposits within the liver cells – AFLP. Since AFLP is relatively rare, developing in only 7-10 per every 100,000 pregnancies, is not present in all hyperemesis cases (50% of women with severe vomiting show some liver damage), and the fetal mutation is even rarer, we can deduce that neither AFLP nor the mutations that impair fetal fatty acid metabolism account for the totality of hyperemesis cases or even the morning sickness of early pregnancy.

Nevertheless, this research provides several important clues about hyperemesis. First, given the right set of circumstances, e.g. pregnancy or another high intensity stressor, carriers of a particular mutation may become symptomatic. We often view heterozygous carriers as being asymptomatic or less symptomatic than their homozygous counterparts. This may not be true. We may be simply viewing the symptom status incorrectly. Secondly, mitochondrial fatty acid metabolism is likely impaired and in some manner related to carnitine. Thirdly, maternal hyperemesis may not be a primary mitochondrial disorder in the classical sense (those definitions are changing, however). Even though there are a number of possible genetic mutations involved with the carnitine pathway, most are either severe enough to be identified during infancy (save except CPT II, which may remain latent until adolescence or early adulthood) and/or present differently (with muscular weakness and cardiomyopathy), and therefore preclude them from our differential. For all intents and purposes, hyperemesis presents during pregnancy, mostly in women with no known fatty acid oxidation or carnitine-related mutations, suggesting non-genetic mechanisms at play. In other words, I think we’re looking for functional mitochondrial disturbances in fatty acid metabolism related to carnitine.

What is Carnitine?

Carnitine is an essential micronutrient derived from the amino acid lysine with the help of methionine (an essential amino acid derived from diet). It is highly expressed in liver, testes and kidney. Dietary carnitine from meats, dairy and other sources yield carnitine. (L-carnitine is biologically active isomer. The research nomenclature varies considerably. For consistency, the word carnitine will be used throughout except when speaking of supplementation, where L-carnitine is more appropriate.) Carnitine is then shuttled off to skeletal and cardiac muscle where fatty acids are used as a primary fuel source. Although it is believed that endogenous carnitine homeostasis is maintained to some extent despite dietary contributions, there are number of conditions that override the internal synthesis of carnitine. These include genetic mutations that limit carnitine synthesis, difficulties with nutrient absorption (leaky gut or bacterial imbalances), kidney dysfunction which limits carnitine re-absorption, pharmacological inhibition of carnitine transporters, and nutrient deficiencies that disrupt any of the many enzymes involved in carnitine biosynthesis or metabolism.

In addition to its direct role in fatty acid metabolism, carnitine is also involved in glucose metabolism (the other major source of mitochondrial ATP) via its potentiating role in the pyruvate dehydrogenase complex, its modulation of acyl-coenzyme A (CoA) and the storage of acylcarnitine. So when we disrupt carnitine availability, by whatever mechanism, not only is fatty acid metabolism derailed, but the other primary pathways for mitochondrial energy production are negatively impacted, as are the storage and clearance pathways.

Carnitine, Fertility and Pregnancy

We know very little about carnitine during pregnancy except that it generally declines. Below is a review the literature.

In women undergoing in vitro fertilization, higher maternal carnitine concentrations are associated markedly improved fertilization rates and overall better outcomes. Competent fatty acid oxidation is required for oocyte and embryonic development.

During pregnancy maternal carnitine concentrations diminish significantly. Indeed, at delivery, plasma carnitine concentrations have been reported 50% lower than in non-pregnant women. Researchers don’t know why carnitine decreases so much during pregnancy. There is some indication that carnitine concentrations are inversely related to iron status. Iron is needed for carnitine biosynthesis and so the increased demands for iron during pregnancy, if not met, may negatively impact carnitine synthesis. Since carnitine crosses the placental barrier, maternal carnitine deficiency would lead to fetal carnitine deficiency. The research, however, is all but nonexistent.

From animal research, we know that supplementing with L-carnitine, maintains carnitine concentrations across the pregnancy and improves a number of variables associated with reproductie function. Supplementation with L-carnitine also appears to offset liver damage and improve liver function in a mouse model of acetaminophen induced liver toxicity. Similar to the human IVF research mentioned above, L-carnitine supplementation improves oocyte development while increasing overall fatty acid oxidation capabilities.

Carnitine Deficiency with Nutrient Depletion

Population data for carnitine deficiency are unknown but nutrient deficiencies in general are postulated to be non-existent in the developed world, except with poverty. This assumption is erroneous and dangerous in the land of nutrient stripped processed foods. What little data exist for different nutrients, show that a significant portion of the Western population is deficient in one or more nutrients. Nutrient deficiencies impact enzyme function and the mitochondria’s ability to produce ATP and perform other critical functions. Carnitine synthesis alone requires five different enzymes, each with their own nutrient demands. This is in addition carnitine’s requirement for lysine and methionine. Given such demands, it is entirely conceivable, and in fact likely, that Western women come to pregnancy deficient, either marginally or grossly, in any one of the many nutrients involved in the carnitine pathway. Here are just a few.

Possible Nutritional Culprits in Functional Carnitine Defiency

Endogenous carnitine synthesis requires methionine. Methione concentrations in foods have steadily decreased (by as much as 60%) in parallel with the increase in glysophate (Roundup) used in conventional agricultural practices. Methionine synthesis also requires vitamin B12, a nutrient deficiency common with the Western diet and exacerbated by many medications.

One of the only accepted treatments said to reduce the nausea in hyper-emetic women is vitamin B6 supplementation. Vitamin B6 is involved in carnitine synthesis. It is also an important anti-inflammatory, especially in the central nervous system.

The other nutrients required to maintain active enzymes for carnitine synthesis include: iron, niacin (B3) and vitamin C.

Finally, with pregnancy in general, but especially, with pregnancies involving severe nausea and vomiting, the risk of nutritional deficits is exacerbated as the intake of nutrients diminishes. Not only would we expect carnitine depletion but deficits in many of the other vitamins and minerals required by the mitochondria to produce ATP either via fatty acid metabolism or via glucose metabolism. The vomiting itself depletes nutrient stores, and thus, becomes self-propagating; fewer nutrients > more vomiting, more vomiting > fewer nutrients.

Connecting the Dots: Potential Treatment Options for Hyperemesis Gravidarum

Thus far, the clues point to some sort of functional, epigenetic, or even an unrecognized, but latent, genetic derailment of fatty acid metabolism involving carnitine. The deficit in carnitine then precipites the severe morning sickness of pregnancy known as hyperemesis gravidarum. The nausea and vomiting worsen nutrient deficiencies and continue the cascade. If this is true, and I think it is, then the question becomes, can we support the carnitine system and mitochondrial function in general, to alleviate or completely eliminate the vomiting. I think we can.

I mentioned cyclic vomiting syndrome in the early sections of this post but haven’t spent any time on the topic. It is from the cyclic vomiting research that we find our treatment options. Specifically, Dr. Richard Boles has successfully treated pediatric patients who have cyclic vomiting syndrome with L-carnitine and Co-Enzyme Q10 (CoQ10), as have others. Indeed, we have personal experience with Dr. Boles’ work, as the daughter of one our writers had treatment refractory cyclic vomiting syndrome; that is, until the L-carnitine and coQ10 eliminated the constant vomiting. Cyclic vomiting syndrome is believed to be a mitochondrial disorder falling under a category of disorders called dysautonomias. And though a specific mitochondrial genotype has not been linked to CVS, Dr. Boles’ clinical data shows a clear association with mitochondrial fatty acid oxidation (L-carnitine supplementation) and the electron transport function (coQ10 supplementation).

Other Bits and Pieces

Fatty acid and carbohydrate metabolism within the mitochondria are closely tied to each other, with multiple interleaving levels of reciprocity. Both pathways demand nutrients to power their enzymes. A nutrient that is particularly high on food chain for mitochondrial function, is vitamin B1 or thiamine. We’ve written about thiamine deficiency repeatedly, as it seems to be leached from the mitochondria by a number of medications and vaccines and is implicated in a wide variety of adverse medication reactions. As a core nutrient in the pyruvate dehydrogenase enzymes, thiamine is critical for ATP production. Thiamine is also critical for fatty acid metabolism. A borderline thiamine deficiency would impair fatty acid metabolism and is linked to hyperemesis related liver damage and Wernicke’s Encephalopathy. Thiamine deficiency also impairs brainstem control of vomiting, thereby exacerbating the already difficult-to-control pregnancy hyperemesis. Thiamine supplementation should also be considered for hyperemesis gravidarum. Our own Dr. Lonsdale tells us that he has used thiamine in clinical practice to reduce cyclic vomiting in pediatric patients. The research on hyperemesis gravidarum, however, is extremely limited, focusing solely on the use of thiamine to curb the effects of hyperemesis-induced Werknicke’s syndrome.

Final Thoughts

Although there is little direct evidence linking a functional carnitine deficiency in pregnancy to hyperemesis gravidarum, there are a enough indirect data to suggest this may be a mechanism worth investigating. If this work bears fruit, L-carnitine, CoQ10, thiamine, vitamin B6 and likely other nutrients may be all that are needed to alleviate the nausea and vomiting across pregnancy.

Please note, I am not a medical doctor and this should not be construed as medical advice. Please speak to your healthcare practitioner before beginning any treatment protocol.

If there are any physicians or midwives who have used L-carnitine in patients with hyperemesis, please comment below.