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.
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This post was published originally on Hormones Matter on July 22, 2015.
I found this article super interesting and helpful. Thank you.
Here are just a couple of things, though: LCHAD is a deficiency of the riboflavin-dependent enzyme long-chain 3-hydroxyacyl-CoA rather than of CPT. CPT is a transporter rather than an enzyme.
I didn’t understand what you meant when you talked about the synthesis of methionine. Methionine is an essential amino acid, so we don’t synthesise it. We can recycle it from homocysteine, but that doesn’t require vitamin B12. The part where vitamin B12 is involved is in converting methionine to SAMe, our methyl donor. Did you mean we need vitamin B12 to synthesise methyl groups rather than methionine?
Riboflavin deficiency also results in carnitine deficiency and liver damage. I’m not sure what the precise mechanism is. However, riboflavin is a cofactor for two methylation enzymes (MTHFR and MTRR) and for the kinase enzymes that activate vitamin B6 inside cells. So, it may be because riboflavin deficiency reduces the methyl pools and P5P necessary to make carnitine.
Salicylates deplete carnitine in addition to coenzyme A and block niacin transporters. Thus, they completely destroy mitochondrial function and fat metabolism in susceptible people, particularly those with MCADD, LCHAD, and probably VLCAD. I suspect riboflavin deficiency is also a major risk factor.
And I have my suspicions about flavonoids, fluoroquinolones, psychotropic medications, statins, and other toxicants depleting riboflavin, too.
I developed adult-onset cyclical vomiting, and it took me several months to work out that carnitine deficiency was causing it. Then, it took me a couple more years to discover that riboflavin deficiency drives carnitine deficiency. It’s fascinating stuff.
Thank you for this article, it was very useful to me as a naturopathic practitioner.
I have personally known only a handful women who experienced HG, and my observation is that all three were seriously underweight. Two I know to have had eating disorders. Could this be a factor, or would you simply consider it the reason for a severe nutritional deficiency situation?
It could be both cause and consequence. Anorexia is common with poorly functioning mitochondria, particularly thiamine deficiency. There is just not enough energy to eat, which then begins the cycle of poor nutrition. Of course, deficiencies in things like l-carnitine also play a role in the onset and persistence of HG because l-carnitine is needed for fatty acid metabolism. So, thiamine and l-carnitine are key to reducing HG and improving outcomes.
Something that has always been a “head scratcher” to me is whether parental genetics plays strongly into it somehow. I have 6 children. My first was a “normal” pregnancy with some regular first trimester NVP for a few weeks as expected. No further complications. My subsequent children all have a different father than my first, as I had him from a previous relationship before I was married. I have had moderate (to severe during first/second trimester for some) HG with all 5 of these pregnancies with my husband. Why would that be?? I have done a lot of research on different sites, but I haven’t run into any specific indications that parental genetic combinations make a difference, or perhaps they haven’t been studied enough as it is an in common occurrence? This could be anecdotal, but it seems very strange to me and a bit more than coincidental.
It is entirely possible that there is a genetic component to it as well, passed down from the father affecting the way the fetus manages/or doesn’t manage certain nutrients or waste products. There is a similar pattern with women who get pre-eclampsia, though nothing has been proven. It is also possible that with each subsequent pregnancy you become further depleted in critical nutrients.
There are a couple potential mechanisms to induce HG. One is thiamine, https://www.hormonesmatter.com/quick-thoughts-hyperemesis-early-thiamine-deficiency/ . The other is carnitine: https://www.hormonesmatter.com/hyperemesis-gravidarum-severe-morning-sickness-are-mitochondria-involved/
Thank you! I’m in my 6th pregnancy (5th HG) 3rd trimester and I believe my more severe symptoms this time are pointing to long term thiamine deficiency from my first HG in 2016 that were never replenished. I just started Allithiamine but I may be having a paradoxical reaction so I will have to titrate up to tolerate and wait it out.
This info combined with other possible connections help me to understand what is going on with my body. Thanks so much.
Thank you so much Chandler! i’m suffering from HG and I want to ask you if there is any info about administration routes different than oral or iv (topical, sublingual?). I can not tolerate almost any drug or supplement taken orally. Thanks in advance, Milena
I am not aware of any sublingual or topic formulations of l-carnitine. Look on amazon, you never know there might be something out there.
Additionally, look up thiamine/thiamine deficiency which can be consequence of HG and a fairly dangerous one at that. There are sublingual and topical versions of thiamine (vitamin B1). There is also IV or IM, which if you have been vomiting regularly, you should argue with your doctor to prescribe. Look up HG induced Wernicke’s Encephalopathy.
Thanks for your reply! I will search for all what you mention (i’m aware of b1 deficiency but didn’t know the existence of sublingual formulation). Thanks again!
Thank you for this excellent article. My daughter has a friend with severe hyperemesis, and I am printing this information for her–and have ordered up a bottle of allithiamine as well. I will post an update if she is interested in trying thiamine.
I am going to encourage her to try 100 mg daily of benfotiamine this week, and then to transition over to 100 mg allithiamine when it arrives. I am also buying l-carnitine today, and will encourage her to take whatever the suggested dose is on the bottle.
I wanted to add also that I have spent several hours searching for the book mentioned by Dr. Lonsdale in his comments– “The Natural Way to a Trouble Free Pregnancy: the Toxemia/Thiamine Connection” by Dr. John Irwin. It is not easily available; there are a couple of copies used on Amazon for just under $1,000 each. (!!!) I am copying and printing the comments on the Amazon site about the book; hopefully that will give her the confidence to try. I will keep looking for the book, but wanted to encourage you to share any pertinent information from that book here, as it is really no longer available.
Thank you again for this article–wish me luck!
Oh my goodness, the cost of the book is ridiculous. A few months back, someone said it was $400 and I thought that was bad. Now, it’s $1000? I don’t know who they think would pay that much. I understand that it is out of print, but still, it seem silly to attempt to charge that much. Having said all of that, whatever you do begin slowly. It would be best if you did this under a physician’s supervision. I am not a physician and this is just research, based upon some of the chemistry and hypothesis on my part. The carnitine connection in particular, is not well known. It does work wonders with cyclic vomiting and there is anecdotal evidence that it works for HG as well, but nothing has been tested. As far as thiamine deficiency, the earliest symptoms are vomiting and food intolerance, which, as you know, are components of HG. Given the hypermetabolism of pregnancy in general and the reduced intake/expedited excretion with HG, it makes sense that if not a causative variable, thiamine deficiency would definitely be a consequence. Indeed, the case literature is rife with reports of women, who, with severe HG go on to develop something called Wernicke’s encephalopathy – a thiamine deficiency disease. All of this is preventable, if the thiamine is addressed earlier.
AN UPDATE. The last comment is dated June 2018 and I wish to add information from recent research. We have known for a long time that thiamine presides over carbohydrate metabolism and has an important part to play in protein metabolism. It has recently been discovered that it also has importance in fat metabolism. It therefore has a choke on all forms of diet including even milk. Dr. Marrs discusses the role of mitochondria, but there is another organelle in cells that deals with the preparation of fatty acids for use as cellular fuel. Thiamine has been found to be a necessity for this. If it is deficient, there is also a substance in milk that is derived from chlorophyll (we get small amounts of this by eating meat from grass fed animals). If this is not processed (oxidized) it results in an accumulation of a substance called phytanic acid which is toxic. Interestingly, giving milk to a person suspected of being thiamine deficient and then finding phytanic acid in blood or urine would be a way of proving thiamine deficiency. Lastly, I recommend a book by John Irwin entitled “How to have a trouble free pregnancy: the thiamine connection”, published by Aslan Publications, Fairfield,CT. He had spent his career as an Ob/Gyn specialist and he had found that giving a routine dose of 100 mg of thiamine a day throughout pregnancy completely abolished ALL the complications of pregnancy, including hyperemesis. He had tried to get academic obstetricians interested but was ignored. Alas, this support of his work might also be ignored.
So many of us still, many years later trying to understand. We look for dosages and hope because our medical community gave us none. Is your work on helpher.org? That was the one place I turned to to try to treat myself when no one else would. I had 2 hg pregnancies, preterm labor with first (plus I wanted to die) and 8 weeks of prodromal labor as well with the second. My kids seem healthy as a horse but I get sick at every turn, muscle cramping and muscle strains, spontaneous sprains when no injury event occured. I have yet to find a medical professional willing to dig to help find answers. Very interesting thoughts here.
In our case, we were expatriates in Argentina. My husband and I had so carefully planned to get pregnant; we really wanted to have a child. I very quickly became ill, and lost 22% of my body weight. I was already very thin. The obgyn there treated it as a psychological issue, and when I was finally hospitalized, I couldn’t lift my head without passing out. I was put on IV fluids, but that was all. They wheeled me to the newborn unit every day and enquired, “Why don’t you want to feed your baby?” as they rolled me in. I cried and sometimes when I cried but strangely there weren’t any tears. I wonder now if I wasn’t so incredibly dehydrated that I couldn’t produce tears. I longed to eat, somehow dreamt of eating spaghetti and watermelon, but nothing would stay. Water wouldn’t stay. They kept me in a dark room to think about the fetus, they said. I started to wonder about myself. I worried that my husband must have thought I’d gone crazy. Finally, a family member Stateside managed to contact a high-risk obgyn, who conveyed to my husband and then to the doctor the severity of the situation. I was dying. At this point, I didn’t even know what was happening, but the details have been told to me. I was transferred to another hospital, where I got slightly better, but still continued the hyperemesis. By then, I had choked on my vomit a number of times, tore my esophagus, had had hallucinations (movements on the ceilings and walls, apparently) and had a couple of what they thought were seizures. Of course, my bowels had long since ceased, and my muscles had wasted, my eyelids couldn’t open easily. With the little energy I had, I remember trying to sing to my unborn child. I couldn’t believe it was my fault. We had both wanted this child. With time, and PTN, I was able to sit up, but would often pass out. I finally graduated to eating slight bits, then one day I was able to return home, albeit with a nurse, and my mother flew from the States to help out. So many years later, I have an 18 year old daughter who was either impacted from it (I’m so very sorry, my sweet love, I NEVER EVER meant to hurt anyone), or who was sick to begin with. We were told initially when she was born that she had pyruvate dehydrogenase deficiency further to lactic acid/pyruvate ratios as well as many other metabolic markers and clinical features. She was very ill. While we never got a complete answer, we both tested for the mitofusin mutation MFN2, making things even more complex. She also has Ehlers-Danlos, Carnitine Deficiency and dysautonomia. The question is, which came first, the chicken or the egg? Is it my fault? She is now looking at colleges, and is somewhat disabled, but wants to kick ***. I fear for her if ever she wants children some day. Please know that we chose to have a child many years later, but were followed by a metabolic – geneticist. Through him, I used a pic line for Levo-Carnitine and general hydration. The pregnancy was still difficult, but not the lethal, life-changing type I had with my first daughter. We know now that Levo-Carnitine can have some cardiac implications, so care must be given. As for me, I never fully recovered. I try to stay active, but I think metabolically something altered in my body. I apologize for the novel. I wish I could reach out and hug some of you, and cry, because I know the lives lost and damaged. I seem to not be able to forgive myself for the damage that may have been caused by genetic predispositions.
What a horrific experience. I am so sorry that you had to go through this, but am glad someone finally recognized the severity of your illness. Please forgive yourself, this wasn’t your fault. If anything it was the result of bad medical care. Your doctors should have realized the severity the hyperemessis and given you intravenous nutrients, including thiamine. The carnitine issue is not well known, but hyperemessis induced thiamine deficiency is. Women who develop severe hyperemesis become extremely thiamine deficient and the lives of both the baby and the mother are at risk. You are lucky you survived. As far as your daughter is concerned, she will need thiamine and l-carnitine and likely other nutrients to carry a pregnancy to term. If she does this, she should be find. She likely needs thiamine now. Please read the thiamine deficiency book: http://amzn.to/2EuShXL. This will explain everything.
My heart breaks to hear of your story. Follow the research on HG on the HER Foundation site and email us if you want to share your story.
This article is amazing stuff! Thank you so much for the work you are doing here! I can’t wait to read more articles from this site as well.
I am 10 months postpartum with our latest baby, and am working to prepare for our next. I would like to try the method you list here, namely the CoQ10 and L-carnitine. Is there anything that you can tell me regarding (1) dosage, (2) preferred forms, and (3) any recommended brands? Any info would be appreciated. I am going to be taking a B-complex by Pure Encapsulations, so hopefully that should cover the B vitamins that you mention.
Have you tried posting this in the Preventing Hyperemesis Facebook group? Or, on second thought, this may be where I found this article!! If not, it would be a great place to post it. There are lots of women in there who are seriously looking for answers.
I will be posting about this article on my blog, and also adding the link to my HG informational sidebars. Thank you again for all of this information.
Diana, love the title of the blog. Very apt. I am not a clinician, so I cannot give dosing information. Having said that, if you look into our articles on cyclic vomiting syndrome, either in the article itself or the comments there are suggestions regarding dosing for that condition, which is very similar. Also, additional mechanisms that might consider include thiamine deficiency, that can be a cause or consequence of the vomiting. Certainly, if the vomiting is not controlled thiamine deficiency becomes critical for both mom and baby. I encourage you to read about thiamine deficiency/mitochondria as well. We have dozens of articles on those topics too. I think I wrote one relative to pregnancy too. Regarding posting on the hyperemesis group, please share the link to this article on that group. The more women we can reach the better. Additionally, I would love to have feedback from physicians/midwives who use these nutrients to prevent/treat hyperemesis. From the comments on this post, a few have and were successful. Keep me posted.
Chandler, thank you for the reply! Love your name, by the way, as I’m currently living in Chandler, AZ! 🙂 Anyhow, I will definitely look up the articles on thiamine and also CVS, with which I am not currently familiar. Thank you so much for the information! I am so enjoying learning more about health. Every article or book adds another piece to the puzzle!
By the way, is there a way to subscribe via email to this site? I can’t find a subscribe option.
Thanks so much, and have a great weekend and Christmas!
Diana
So L-Carnitine is the correct supplement to try, rather than acetyl L-carnitine?
Yes.
So many professionals who have suffered from HG, Im just a mum of one, there was no way I could EVER go through full term again and my husband and I made the decisions to stop at one child. My mother often spoke to me of pregnancy being the most horrific experience and she only had me, I think she had HG too. I have a son and I feel so happy that he will never have to be pregnant, but I ache that he will not have a sibling to share his life story with, but thats the way it was for us and so be it. I want to thank all of you for the work you do, just to be believed by a doctor was a miracle, the pain beyond anything i can describe, I wanted to die. For me I had unbearable nausea for a while before the vomiting kicked in full force, no-one believed me apart from my husband, I lost so much weight I was skin and bone. Thank you again for your work, my boy is 8 and yet I still read about HG like it was yesterday. You can not imagine how important and valued everything you guys do is to HG mums.
I had two hyperemesis pregnancies followed cyclic vomiting with every period. Prior to my pregnancies I had no issues and thought I had a strong stomach and very rarely got sick. I started supplementing with L-cartinine just last month to increase my energy levels. I noticed a huge drop in my nausea this month and I had not linked the two until right now. Thank you so much for writing this!
As someone who has MCADD, this makes everything make sense. I have been in and out of the hospital with all 3 of my pregnancies due to sickness. It was so bad that I was unable to work. I always knew it had something to do with diease. This was on a support group of people who have a FOD and all the women say they had it during pregnancy.
I have read more and more material that claim magnesium is the main issue as it is what is needed for the uptake of these other vitamins and nutrients. I agree with Dr. John B. Irwin as mentioned in the above post by Derrick Lonsdale.
I had HG with all 5 of my pregnancies. My third baby tested positive for VLCAD which is Fatty Acid Oxidation (FOD) disorder. It is interesting to think that these two could be related. I would love to learn more about this study or how to be a part of it. Her FOD was found during her newborn screening.
I am so fascinated by this research, especially how this might relate to other deficiencies and such in both the mother and child. I had HG (as actually recognized) in my third pregnancies, and would venture to say with my first two as well, just not stated as such by my doc. Two medications and I still couldn’t function, and it got worse with each pregnancy. My two younger children as infants couldn’t keep anything down and my doctor just told me there was nothing to diagnos except “they are barfers”, not overly helpful! Perhaps there is a genetic connection and the depletion of nutrients just got worse with each subsequent pregnancy. I would love to be part of the research to help find solutions so others don’t have to suffer the way I did!
There is an answer for this terrible condition. I too suffered extreme vomiting for all my pregnancies and in the third was hospitalised after not being able to eat for a good month and a half and water coming straight back up. After three days of being on a drip of fluids and anti nausea medication I was then put on oral medication of which all came back up. I was told I had to stay in hospital until I d done my first stool but they gave up waiting and sent me home still feeling as sick as I did before but thankfully less dehydrated. I threw up as I left the building. Managed to get home fed my pets then threw up and collapsed in bed for a further three days till one friend suggested trying vaporising marijuana. My children were being looked after by my family and although I d not smoked all pregnancy I decided to try it. The effects were AMAZING! I was instantly able to sit up on bed and felt the desire to eat for the first time in six weeks. It gave me the energy and drive to go into my garden and start cleaning my house where as previously I d been in my bed unable to do anything for soooo long. Building up my strength from eating again I was able to have my children back again and at last enjoy the last two weeks of the summer holiday with them. I would highly recommend it to anyone suffering like this as after all the medication I was given this was the only thing that helped me have the desire to eat and keep it down. I would only use a vaporiser when I felt sickness coming on and if I did a day without it I would automatically feel as sick as before. I am now in week 15 and haven’t had to use the vapouriser for a week and I ve been able to look after my children and work again since I used it. My heart really goes out to all the women who have suffered from HG. And using marijuana isn’t a new experimental drug of choice. In Jamaica it’s often been used for morning sickness and I m sure it’s not the only country that have reeled its benefits.
In U.S. you could get your children taken away from you if marijuana found in your system while pregnant!
Luckily not anymore in California and probably other states
I wanted to try this so badly when I had HG. I remember posting of FB about how there was no way is was worse than the promethazine, metacloprimide, and all sorts of other horrible things doctors kept trying. I got yelled at a lot by people who did not understand. Thanks for being awesome and trying it. I’m so glad it worked.
This was very helpful for my wife in her first pregnancy. However we’re now in our second pregnancy and once the symptoms started we tried it again, but it only seemed to make things much worse. I don’t know how the underlying physiology changes, but it no longer seems effective for her.
I had 3 times HG, B vitamine injections helped a little bit, if I found someone who was willing to help.
I ind the article very interesting. Now I wonder if I should test my children for any disorders. My daughter is 7, my son is 2. I guess the doctor will not be willing so I have to find a lab here in Germany which does such determinations and have to pay it by myself.
What do you suggest, what should be included?
I suffered from HG for 3 pregnancies (2010, 2012, 2014). Each episode of HG was resolved by about 20 weeks. I finally was diagnosed with CVS after the 3rd pregnancy (although I had it long before that but was never given a diagnosis) and started to treat it with L-Carnitine and CoQ10 which actually kept me symptom free for a year. I found out I was pregnant this year in March and my husband and I began quickly preparing for my HG downfall (he is a MD, I am a FNP). However, the downfall didn’t come as expected. I usually start getting sick by 5 weeks but was fine till about 6-7 weeks when I began to get night sickness which slowly progressed to all day sickness, but that is it, it was nothing close to what HG was. I was mildly nauseated but could eat and drink and fully function. Confused, I googled L-carnitine (since that is the only thing I had done differently from my first 3 pregnancies) and HG and found this article. My morning sickness was gone by 18 weeks and I am now 27 weeks along. There is nothing in the world more miserable than HG and I wish somehow this treatment option could be disclosed to all those with HG currently or trying to conceive. So much more research needs to be done on it. I am living proof that it works for at least some with HG and I would have given ANYTHING to have known about it for all of my pregnancies. I have gotten helpher.org to add it this article to their website and I recommend trying it on Facebook to anyone suffering, but I’m sure that is not enough. I really wish there was a way to do more research and get the word out that this is a potential option.
Shelly, that is such good news. I am so glad it worked. And thank you for sharing. I have tried to share amongst the HG groups but they don’t seem interested. Your success story will help, I am sure.
Do you take Acetyl L-Carnitine and what dose?
I was also wondering if you continued taking the same dose throughout pregnancy? Thanks!
How much did you take before and during pg?
This is fascinating. I had severe hg with two pregnancies. Ten years later, after medication, i fell ill with pots like symptoms and eventually was given the catchall diagnosis of fibro/me. My main symptoms are all related to lack of energy. I am deficient in vit c and d. I have some decreased liver function. Cortisol and estrogen levels are not normal. I tested positive for mthfr and am homozygous (among other snps). I experience xtreme nausea and vomiting mothly, related to a certain phase of my cycle. B12 did not seem to help me at all (in any form) nor did coq10 or some of the other supplements discussed. However, i have never tried l lysine or thiamine in any great amount: they may have been part of a multi vitamin i tried. Coincidentally i have a cold sore and was just told l lysine reduces the duration of them.
I had hg 17 years ago with my daughter
It was my second pregnancy I didn’t have it in my first just normal morning sickness
I had a 3rd pregnancy 3 years later which I sadly terminated as I just couldn’t cope as I was worse that time around and received no help from the medical staff and was even told that I was making it happen myself
My daughter was diagnosed with cyclic vomiting syndrome at the age of 7 after 5 years of investigations
I hope and pray that she will never experience hg but after reading this study and the links to cvs it seems likely that she will I just hope that the medical team will be more understanding and she doesn’t have to go through what I did
I’m so sorry that at the time your providers weren’t understanding of your severe condition, Lindsey. My wife too chose to terminate her second pregnancy because of lack of care. She had HG in the first one but it wasn’t as strong. We are now in the third pregnancy and she’s in the hospital the second time at only 10 weeks for dehydration etc.
I suffered HG both pregnancies back in 1995 /99. I have since found out I an homozygous for MTHFR 677 and I believe the fact that I took folic acid (as instructed) before and during both pregnancies caused / exacerbated the HG. Both children are also homozygous for MTHFR677. Thankfully avoiding folic acid (bread) etc and correct supplementation of B vitamins and we all have improved health wise.
Very interesting many mothers I come across have this MTHFR677 and advoiding folic acid helped ! I actually was taking extra doses before pregnancy to prevent birth defect ! I need to research this !
Thank you
Starr Andrews StrongHGactivist
I had CVS before Hyperemesis Gravidarum and had the most severe case of Hyperemesis Gravidarum that I have known . I vomited 100 X a day to the point my eyes would bleed . Vomiting 98-101 non stop was normal for me even on IV fluids and 16 NG IV push Zofran . I love your work . For years I have said Mito was involved in CVS and Hyperemesis Gravidarum Were connected. When I found out about the RYR2 factor I was actually thrilled . Please continue to research your theories are wonderful and right on track there’s no one like you that I met out there that thinks outside the box as I do . I’m not a medical doctor but a hardcore HG activist and advocate . I love to talk with you more !
Starr Andrews Strong HGactivist
That sounds absolutely horrible. I think CVS and HG are woefully under-recognized. I am not familiar with RYR2 factor but will look into it. As an activist, if you’d like to share your work here, we’re always looking for writers. So many topics deserve much more attention than we can give them. This is one of them.
I loved to write and help anyway I can ! Where do I send my work in ?
Thanks for your time it means a lot
Starr Andrews Strong HGactivist
An HG activist!! Wow, too cool. I suffered horrible hg six times. But not as severe as urs, ha never thot i would say THAT.
Pls give me info as to how to become involved too. This article is great, dont you think? Im too old to have babies but I fear for my 4 dds. My paternal grandma n my mother had it too.
My email is my_bba@yahoo.com
I suffered from HG in my second pregnancy. I could not get out of bed for 16 weeks. I could not care for my family. Zero energy. Today my son, after 8.5 mo “investigation” was diagnosed with carnitine uptake disorder. This is all very fascinating to me and I too am going to dig deeper into this. Today was a difficult day but I am happy to hear that this genetic condition is treatable.
Vanessa, that is very interesting that your son has the carnitine disorder. Was there any indication of this or any fatty liver disease during the pregnancy. Please dig deeper and let us know what you learn. If you’re interested in sharing your story on the blog we’d be interested in publishing it.
This article on a possible link between mitochondria and hyperemesis gravidarum is the most plausible explanation for this debilitating illness I have read. One symptom of HG, which is not often mentioned, is complete exercise intolerance. The need to preserve every ounce of energy in your body because normal everyday actions are so impossibly difficult. This symptom is not easily measured by medical professionals and HG is difficult to explain without reference to the complicated effects of pregnancy hormones on systems and metabolism.
Yes, the 12 spoon theory fits well here!
No spare energy left for like…walking lol
sigh, not funny rly
Charles Darwin suffered from an inherited pathological mtDNA mutation. His mother, among other ailments, suffered from hyperemesis of pregnancy. Her mother in turn was chronically unwell and nearly died with what was almost certainly fatty liver of pregnancy after a spontaneous abortion.
If interested Google: ‘Hayman thesis UniMelb’, which brings up an abstract, then click on ‘view/open’.
Would be interesting to survey mothers who had hyperemesis to see if their children have any disability, such as CVS, migraine or excessive motion sickness.
John, Thank you for the reference. That is fascinating. I will look it up.
John, would you be interested in writing a post about your theory of Darwin’s health issues?
I had hyperemesis during both of my pregnancies, one in 2011/12 and the other in 2015. My first son, now 4, started having vomiting issues 9 mos. ago, and the same pattern has followed every 1-2 mos for the last 9 mos. I am suspecting CVS as he meets nearly all of the signs. I just happened upon this article as I googled ‘HG and CVS’, because I couldn’t help but wonder about a connection. I wish I would have come across this discovery sooner, but better late than never. I will be digging into this deeper.
Neither hyperemesis nor CVS are as well researched as they should. Do look at our articles on CVS. The daughter of one of our writers (Philippa Bridge-Cook) had severe CVS until we stumbled upon the work a pediatric geneticist Dr. Richard Boles. His work showed that coQ10 and l-carnitine were able to treat CVS successfully. Philippa’s daughter has been using those supplements now for several years and has been largely free of the vomiting whereas before the supplements was suffering greatly. Her entire story is on the blog. Keep us posted.
I will. Thank you. I assume she supplements daily, not just during CVS episodes?
Yes. Here are the posts that I was speaking about. https://www.hormonesmatter.com//?s=cvs
I also wanted to add that while I don’t have a history of CVS or migraine as an adult or child, I have always been plagued by motion sickness. It also appears that I may have a MTHFR genetic mutation, not sure if there is a correlation.
Many mothers have CVS before pregnancy get Hyperemesis Gravidarum , or get Hyperemesis Gravidarum and get CVS after or have Hyperemesis Gravidarum and their child has CVS . More needs to be research on the RYR2 factor that the her foundation found the link of CVS and Hyperemesis Gravidarum . The connection is real but more people need to look into this !
Being a CVS sufferer since I was 15 years of age the symptoms and feeling of cvs and Hyperemesis Gravidarum are identical!
Oh my! I have 1 with car sickness! One of my worst pgs.
This post may be too technical for many people. I agree completely with the principles that are given but I may be able to simplify it to give a direction for anyone with this disease called hyperemesis gravidarum. It has always been tacitly accepted that emesis (vomiting) in pregnancy is a normal phenomenon. Hyperemesis is used to indicate that the vomiting is excessive. As readers on this post know, I have talked a great deal about thiamine and perhaps it will surprise noone that I have to indicate its use here. Recently I received an email from a specialist in ob/gyn by the name of John B.Irwin M.D. Now at the age of 92 he is long since retired but from our correspondence I became aware that he was very frustrated by his many years of attempting to describe the advantages of thiamine in pregnancy. He sent me a copy of his book which is entitled “The Natural Way to a Trouble-Free Pregnancy” published by Aslan publishing, 2490 Black Rock Turnpike, #342 Fairfield CT 06825. I will not steal his thunder because it is a book that any pregnant woman should have, but I will give you some quotes: “I will describe how large doses of thiamine (100 mg daily) have been essentially 100% effective in preventing toxemia of pregnancy in my patients”. In his book he does not mention hyperemesis but I have had personal experience with this. Some years ago I saw a patient with hyperemesis who could not even keep water down. I gave her a series of water-soluble vitamins intravenously and she went home completely free of vomiting for she was an out-of-town patient. Later on in the pregnancy the vomiting returned and she received another short course of intravenous vitamins with the same result. The last time that I saw her was only because she came to show me the baby. What we are saying here is that the present dose of obstetric vitamins is ridiculously too low. Dr. Irwin in his book, addresses the use of vitamin supplements in pregnancy. Lastly, I want to say that the lower part of the brain which contains a center called the vomiting center, is exquisitely sensitive to thiamine deficiency. A healthy dose of thiamine and magnesium with a well-rounded multivitamin seems to be a necessity in pregnancy
This is really interesting. I am a doctor but I also suffered from HG in my first pregnancy so I have done a lot of research in preparation for a 2nd pregnancy. What would be the recommended dose of magnesium?
What doses were you giving her ? How much was she vomiting ? I am very intrigued by this! I ended up with a severe thiamine deficiency while suffering from Hyperemesis Gravidarum and almost died of (WE) I would vomit 98 hours at a time without a break ! This post is not to technical for me, writing a book on Hyperemesis Gravidarum and my journey and interested in how much she was vomiting as nothing seemed to stop my vomiting even 16 mg of Zofran at one time along with other meds !
Not too technical for those motivated to understand it! 🙂
There’s a short and simple recap towards the end of the article.