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The Lyme Spiral

Published on November 15, 2023

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Two of the most commonly asked questions I face as someone with Lyme disease is “when were you bitten by a tick?” and “when did you get Lyme?” To be honest, while I have my suspicions, I really have no idea. Many people are surprised to hear that the majority of people with Lyme disease never recall being bitten by a tick. The bullseye type rash that people assume is the hallmark of Lyme symptoms also doesn’t occur in many of us with Lyme, hence why we have no idea when we first contracted the disease.

Early History

I was an active child and a competitive swimmer. By high school, I was swimming at the state and national level. I was in great shape with great health, or so I thought, and had no obvious reason to be experiencing any medical abnormalities. However, over my freshman year in high school, I started experiencing widespread joint pain. Because I was in such good health and swimming and training up to four hours per day, it came as a surprise to my parents, coaches, and doctors when I was experiencing such pain. During this time, I did get tested for Lyme by my pediatrician. While he was fine testing for rheumatoid arthritis and lupus, we had to beg him to test for a Lyme test, even though it was common in our area. It was years later when we learned that traditional doctors typically do not test for or treat Lyme disease.

My test showed that I had one positive band of Lyme. He said that this was not enough for a diagnosis, and I was sent home without any answers. My sophomore year of high school, the joint pain continued and even began to get a bit worse. I went to a rheumatologist at the Children’s Hospital of Philadelphia and was diagnosed with Amplified Musculoskeletal Pain Syndrome, also known as AMPS. Their main treatment plan was exercise, which, with swimming, I was already doing. There wasn’t much else that could be done, but by junior year it seemed like I had grown out of AMPS. Whether it was really AMPS or had it been Lyme disease all along, I have no idea.

College Dorm Flu Masked My Infections – Until My Vocal Cords Went Haywire

My freshman year of college living in a dorm I was sick constantly. I missed several of my college swim meets from contracting the adenovirus, developing severe swimmer’s ear, and coming down with strep throat and bronchitis. Another strange thing I began to notice was that I was having low grade fevers nearly every day. I got tested for the mono virus, as many college students are, at one point or another, but the test came back negative. With the constant infections, along with many headaches and slight fatigue, a blood test showed that I had an underlying Epstein Barr virus from prior contraction. I do think they missed mono, and I can’t help but wonder if Lyme played a role.

During my sophomore year of college, I began the swimming season feeling strong until I developed a nasty virus along with a bad cough within the first few weeks of the semester. Luckily, the virus died down, however the cough never went away. The cough became worse as I swam and I was led to assume I had developed sports-induced asthma. I just couldn’t get in a good full breath. During fall break, I went to an allergy and asthma specialist. When I told her I couldn’t fully breathe in, she pointed out that with asthma, you typically have trouble breathing out. She performed a rhinoscopy, where they stick a camera in your nose down into your throat, and examined my vocal cords on a very fuzzy screen before diagnosing me with vocal cord dysfunction. This was a difficult diagnosis because it was hard to explain to friends and family. It is not commonly known, and somewhat misunderstood. People genuinely had no idea that when I was breathing in, my vocal cords were spasming closed. The only thing I could link this to was the virus I had a month prior.

It took months of my vocal cord dysfunction being taken lightly or just blatantly disbelieved until I went to an otolaryngology specialist in New York City. The specialist performed a rhinoscopy as well, but recorded everything on a crystal clear screen. He was able to visibly show my parents that my vocal cords were, in fact, spasming closed when I breathed in. My parents have since admitted they didn’t fully believe me until that appointment. The recommended treatment was Botox. This meant that I had to go into the city every few months to get Botox injected into my vocal cords. Eventually, the doctor recommended surgery because folds of tissue were leaning into my airway over my vocal cords, a condition known as laryngomalacia, making my vocal cord dysfunction worse. I got surgery and continued with my Botox appointments and my vocal cord dysfunction finally calmed down a bit. Again, here I had suspicions that this was related to Lyme disease as well. My first Lyme specialist commented that vocal cord dysfunction could have been a result of the disease. After hearing Shania Twain’s story about how Lyme disease affected her vocal cords, my suspicions were stronger, but, again, I will never know for sure.

Looking For a Zebra: Fatigue, Tachycardia, and Hypertension

I took a year off of school for a few different reasons, some of them being medical. I was still experiencing low grade fevers constantly, fatigue, tachycardia, and hypertension. I was still very active, going to OrangeTheory Fitness classes a few times a week, along with lifting weights and swimming. Currently, I can barely walk my dog and my exercise consists of physical therapy. A few times, I went to OrangeTheory Fitness with my mom, and when I looked up at my name on the screen, I saw the number 212, which I thought was my score (I thought I was winning), but my mom realized it was actually my heart rate. At another point during this year, my blood pressure was in the 200s over the 200s. I went to an endocrinologist for my fevers, fatigue, and the general feeling that something was very off. She told me I was on so many psychiatric medications that they were making me “sound slow,” and that I just had fever of unknown origin. She also said that she was going to visit her family in India and could bring me back herbal supplements for the fever of unknown origin.

That being said, I did have severe anxiety at the time and was dealing with post-traumatic stress disorder. I had no idea what this meant at the time, but my psychiatrist told me to go to my primary care doctor and tell him “we’re looking for a zebra,” and even a pheochromocytoma. I saw several doctors that year, each who ordered different types of blood work. One doctor was so unsure what was happening that she ordered twenty two vials of blood. Yet, I was still left without any answers.

And Then Came Covid

After my mental health and anxiety had not improved with medication and therapy, my mom felt there still had to be an underlying issue. This is when she found and took me to a Lyme specialist in the fall of 2019, who immediately diagnosed me with Lyme disease and bartonella, and later, mast cell activation syndrome (MCAS). Physically, my symptoms were manageable. However, I contracted the first strain of COVID-19 in May of 2020, and my life has never been the same. Within the next few months, I started experiencing joint pain, severe migraines, vertigo, severe fatigue, and continued mental health issues. I even had to drop all of my classes in the fall semester of 2020 because I missed nearly two weeks of school from having a fourteen day long migraine. I began developing neurological and cognitive issues, such as trouble focusing and thinking and I had with memory. I switched to a different Lyme specialist, and this time I even tested CDC positive, which is more uncommon than not in those with Lyme. I started yet again another regimen of antibiotics and herbs. I spent most of that year couch ridden, sleeping much of the day, and constantly in hot Epsom salt baths to ease the joint and muscle pain. It felt like my mind and body were completely outside of my control, almost like my autonomy was taken from me. I was on several combinations of antibiotics until I eventually switched doctors again. This new physician was recommended by my Lyme literate dietitian, and was extremely knowledgeable of complex cases. I still see her to this day.

The next year I went back to school part time, only taking two classes each semester. Before the fall semester, I was diagnosed with babesia, and a few months into the semester I was diagnosed with hypothyroidism. These diagnoses often come together in the case of Lyme disease, but a new diagnosis is always a lot to take in. In class, I would forget what I was saying mid-sentence, which made me self-conscious and hesitant to participate. I struggled to balance the fatigue, physical pain, and brain fog with school. Yet, I successfully completed those two semesters.

Medication-Induced Pancreatitis

Finally, my senior year began: Fall of 2022. I was still attending part-time, but was now taking three classes as well as a lab each semester. In late September, early October I started having these acute episodes of severe pain in my upper abdomen that spread to my back. Because I have been medically gaslit so many times and I also have a high pain tolerance, I was nervous to go to the doctor. These episodes felt like I should have been in the emergency room, but because they only lasted an hour I was afraid to go to the hospital in fear that they would brush me off as a young female having stomach aches. I dealt with the pain for almost four weeks before I finally went to a doctor.

As it turns out, I had pancreatitis. I had to go on a mostly liquid diet for two weeks, stop taking my antibiotics and other supplements for Lyme, as doctors believed it was drug induced, with the culprit suspected to be rifampin, or the combination of too many other medications and supplements. I had been on various psych meds for years. Initially they were prescribed for severe anxiety and panic attacks and when I began to get sick, it only worsened. Among the medications I have been prescribed and used are several SSRIs/SNRIs (Prozac, Zoloft, Lexapro, Luvox, and Effexor). I have used sleeping medications such as Prazosin, Seroquel, and trazodone, as well as a tricyclic antidepressant, some benzodiazepines, Wellbutrin, Buspar, hydroxyzine, and different ADHD medications (Concerta, Ritalin, Vyvanse, Adderall, Straterra).

While pancreatitis mostly resolved, my Lyme started to continue to progress. I was having many more neurological and cognitive symptoms, my whole body was tremoring nearly every day, and I knew that we had to take action before the Lyme and coinfections progressed any further. I went back on antibiotics at the beginning of the spring semester, but had many Herxheimer reactions. I was out of it and sweating with fevers in class, all while also managing an internship. Within a few months my tremors became much better, indicating that the antibiotics were working. It was a long and stressful year, but I graduated Magna Cum Laude after having periods of extreme sickness where I questioned whether I would ever graduate.

Right now I’m on Anafranil, Buspar, Trazodone, Hydroxyzine, and Valium. As for Lyme and coinfections, I’m on clarithromycin, Tinidaloze, Valtrex, Mepron, methylene blue, (recently started), low dose Naltrexone, liposomal oil of cinnamon clove and oregano, cryptolepis, Researched Nutritionals MycP, phosphatidylcholine, vit D and C, omegas, ATP360 and CoQ10 for mitochondrial dysfunction (my doctor has suspected mitochondrial death/dysfunction after having COVID the first time, followed by long covid). I’m on a whole bunch of other supplements too to support my immune system, help with mast cell activation/histamines, digestion, brain function, etc. I’m taking between 50-70 pills per day with a few liquids mixed in there. I’m also on thyroid Armour for hypothyroidism as well as migraine medications and Zofran.

Chronic Illness Limbo: Neither Disabled Nor Able Bodied

Something that healthy people may not think about is having to choose your battles in terms of symptoms and treatments. For example, I started methylene blue shortly after graduation. Methylene blue, which is a medical dye, is a relatively newer, yet promising treatment for Lyme disease, but it is a monoamine oxidase inhibitor (MAOI). This means it can interact with psychiatric medications, and, therefore, I had to go off of all of my ADHD medications. The combination of an MAOI and a serotonergic ADHD medication can lead to both serotonin syndrome and a hypertensive crisis. The idea is that over time and with building up the dosage of the methylene blue it will minimize brain fog, a huge Lyme symptom, and help to treat ADHD symptoms. However, it takes quite a while to build up to an adequate dosage of methylene blue, and it also takes some time for it to actually show effects and improvements. Methylene blue treatment has been a bit brutal here and there with Herxheimer reactions.

One of the most daunting and frustrating things about Lyme disease, especially when it becomes chronic, is that there is rarely a trajectory or expected timeline to start feeling better or to reach remission. I’m currently still trying to find my way to remission, but cannot say I am close. Lyme Disease has turned my life upside down. At this point in my life, I thought I would be living up my twenties with either having already started graduate school or a big girl job. Something that people with Lyme disease, and those with other chronic illnesses as well, deal with on a regular basis is not being able to keep up with productivity culture leading to feelings of failure, laziness, or character flaws. Chronic illness is isolating, and, for many, it may feel like there is no place in society for us when we’re neither fully able bodied nor fully disabled. Instead of living up my twenties, I spend most days with my parents and my dog, I rarely drink alcohol or go out with friends, as it is difficult to maintain friendships when chronically ill. I am still trying to find a place to fit into society post bachelor’s degree, without a master’s or doctoral degree. I feel resentful of all of the doctors who misdiagnosed me or gaslit me, letting me go longer and longer undiagnosed, and therefore, untreated, allowing the Lyme to progress. However, I have found friends in the chronic illness community that, even though we have a variety of illnesses and different symptoms, understand the common struggles of chronic illness.

If you suspect you have Lyme, the best thing you can do is go to a Lyme literate doctor in your area, whose names and locations are usually spread through word of mouth due to the politicization of Lyme Disease, which can lead to possible repercussions for doctors who treat Lyme without CDC positive tests, which, like I said earlier, are inaccurate and are not often used as a basis for diagnosis.

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Why Fatigue Matters in Thyroid Disease

by Chandler Marrs, PhD

Published on August 1, 2017

6511 views

The notion that unremitting fatigue is a core clinical symptom is difficult for many physicians and patients to reconcile with its ubiquitous nature in illness. Here is yet another example of the importance of recognizing fatigue and the constellation of other clinical signs that manifest concurrently in thyroid disease. Here we see that fatigue represents a loss of mitochondrial function that, if left untreated, has some subtle and not so subtle effects on central nervous system functioning.

Some Background: Fatigue and the Mitochondrial Connection

Fatigue is one of the most common signs of mitochondrial dysfunction or deficit. Mitochondria, the energy factories within our cells, produce the ATP or cellular energy, that our bodies require to function. This process is called oxidative metabolism. As Dr. Lonsdale wrote about in How can Something as Simple as Thiamine Cause So Many Problems, consider each mitochondrion as a mini, combustion engine.

Fuel + Oxygen + Catalyst = Energy

Each of our one hundred trillion body/brain cells is kept alive and functioning because of this reaction. It all takes place in micro “fireplaces” known as mitochondria. Oxygen combines with fuel (food) to cause burning or the combustion – think fuel combustion engine. We need fuel, or gasoline, to burn and spark plugs to ignite in order for the engines to run.
In our body/brain cells it is called oxidation. The catalysts are the naturally occurring chemicals we call vitamins (vital to life). Like a spark plug, they “ignite” the food (fuel). Absence of ANY of the three components spells death.
Antioxidants like vitamin C protect us from the predictable “sparks” (as a normal effect of combustion) known as “oxidative stress”. Vitamin B1, is the spark plug, the catalyst for these reactions.

When there is dysfunction within this pathway, which is also called the OXPHOS or oxidative phosphorylation, when the engine doesn’t get the fuel it needs or the spark plugs don’t work, fatigue and other symptoms arise. Fatigue is an important clinical sign that something is amiss in our cellular combustion engines.

Mitochondria and Hypothyroidism – Beyond One Test One Drug

In chronic hypothyroidism, chronic mitochondrial deficits are clinical signs that can be recognized, if one is looking for them. They present as fatigue, and when chronic, as balance and gait disorders. Recall our discussion and videos on Hashimoto’s disease associated with walking and balance difficulties: Adverse Reactions, Hashimoto’s Thyroiditis, Gait Balance and Tremors – those examples pointed to mitochondrial dysfunction. Here is yet another example of the importance of recognizing subtle clinical signs of mitochondrial damage.

Watch and listen for the clinical signs. How many do you have?

Notice, he speaks of the importance of proper nutrition, of reducing inflammation, and of exercise and other modalities to correct the functional deficits of hypothyroidism and mitochondrial dysfunction. Notice also, the improvement in functioning after only eight weeks of treatment.

Datis Kharrazian: Developing the Clinical Eye to Discover the Causes of Fatigue from The Institute for Functional Med on Vimeo.

If you or a loved one suffers from chronic and unremitting fatigue rule out thyroid dysfunction and its sister condition mitochondrial damage. A simple TSH test, as is commonly considered, is not sufficient to find thyroid dysfunction. A full panel must given. Once a diagnosis is reached, remember thyroid medications, though they may be necessary, are not enough to correct mitochondrial damage. Diet and nutrients must considered. Put it all together and live healthier.

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This article was published originally on Hormones Matter on November 7, 2013.

Thresholds and Tipping Points in Thiamine Deficiency Syndromes

by Chandler Marrs, PhD

Published on May 29, 2014

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I recently stumbled upon on a research paper published in 1968. It was not that long ago in the overall course of modern medicine, perhaps even its heyday, when all things were still possible and before the complete fealty to pharmaceuticals arrived. To the youngsters and to those coming of age in the last 20 years, however, anything published pre 1990 is ancient history. What could such old paper tell me about medicine that is new and useful? It turns out an awful lot.

Back in the day, research was a little simpler and more focused, not on finding out which drug could be fit to which symptoms, but on how things worked. Good experimental design, answered mechanical questions, like if we apply X to Y or if we remove X from Y what happens?

In this paper, Encephalopathy of Thiamine Deficiency: Studies of Intracerebral Mechanisms, the researchers identified a very important component about Vitamin B1/thiamine deficiency – the time course of the disease process. That is, with a diet deficient in thiamine, how long does it take before symptoms emerge, what is the corresponding level of deficiency in the brain, and at what point, after supplementation, does recovery begin; important questions clinically.

Vitamin B1 – Thiamine Deficiency

Remember, vitamin B1 or thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Thiamine deficiency was originally observed in only chronic and severe alcoholics or with severe nutritional deficits as seen in famine. Fortification of food stuffs was thought to relieve much of the nutritional risks for deficit, especially in impoverished regions. More recent research, however, indicates that thiamine deficiency has reared its ugly head once again and this time in modern, non-impoverished, regions where the food supply is ample. How can that be?

Non-Alcoholic Wernicke’s Encephalopathies

Thiamine deficits can be mediated by a number of factors, including by less obvious nutritional deficits where food supply is abundant but nutrition is lacking (a diet of highly processed, carbohydrate and fat laden foods), with thiamine blocking factors found in medications/vaccines, environmental toxicants and some foods, after bariatric surgery and in disease processes like AIDS. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

What has always struck me about the thiamine deficits we observe is the differential expression and time course of the symptoms. In some people, the reaction leading to thiamine deficit appears linear, progressive and rapid. In others, the symptoms appear to wax and wane and to evolve more slowly. How is that possible? Certainly, individual predispositions come into play. Some individuals may be somewhat thiamine deficient prior to the trigger that initiates the full expression of symptoms, while others have higher baseline stores. Additionally, anti-thiamine environmental exposures and other medical conditions/medications may also come into play. In the literature, however, the progression of symptoms from bad to worse is almost always direct and rapid, perhaps mistakenly so. Indeed, Wernicke’s Encephalopathy is a medical emergency necessitating immediate IV thiamine. How is it then, that we see more chronic, remit and relapse patterns of thiamine deficiency, even in some cases where thiamine concentrations are being managed medically?

Cerebral Thiamine Deficiency: Crossing the Black Line

It turns out, there is black line with regard to thiamine deficiency, that when crossed overt symptoms emerge, and a similar black line, that demarks recovery. It is possible then that barring a continuous blockade of thiamine, one can move above and below those lines and the corresponding symptoms may wax and wane. The paper from 1968, cited above, found those black lines, in rodents, but we can extrapolate to humans.

The research. The investigators took three groups of female rodents, a paired group of thiamine deprived and thiamine supplemented, along with a group fed ad lib (as desired) and assessed the time course and concentrations of cerebral thiamine deficiency relative to the initiation and progression of the observable neurological symptoms associated with Wernicke’s encephalopathy in rodents (ataxia, loss of righting, opisthotonos –rigid body arching). The experiment lasted about 6 weeks.

Neither the control group (thiamine supplemented) nor the ad lib group demonstrated neurological deficits at any time during the study. The thiamine deprived group, on the other hand, demonstrated symptoms that began with weight loss, progressive anorexia, hair loss (recall our observations about hair loss) and drowsiness at about 2.5 weeks into the experiment. Interestingly, no neurological signs of thiamine deficiency were seen at that time.

The results. At 4.5 weeks in, the researchers noted a rapid progression of symptoms and decline of health over the course of the next 5 days (the black line). These symptoms included: incoordination with walking, impairment of the righting reflex, reluctance to walk, walking backwards in circles, imbalance, rigid posturing and eventually a total loss of righting activity and severe drowsiness.

One can imagine, if a similar deprivation of thiamine were observed in humans, the corresponding symptoms might also include the initial hair loose and weight loss, perhaps noticeable, perhaps not depending upon the time frame and severity of the thiamine deficiency. It would also include incoordination and difficulty with walking, balance and voluntary movement, perhaps tremors, excessive fatigue or sleepiness and the myriad of neuro-cognitive disturbances noted in Wernicke’s syndrome.

In the cited experiment, one injection of thiamine reversed these symptoms to a nearly normal, or apparently normal neurological state within 24 hours.

Brain Thiamine Thresholds

Animals from each of the groups were sacrificed and examined at each of the stages of the experiment. Brain thiamine and other markers of thiamine metabolism were assayed to determine the cutoff levels of thiamine that demark symptoms and recovery. This is really interesting and the beauty of this entire study. Neurological symptoms become apparent when cerebral thiamine concentrations reach 20% of normal. Recovery begins when those concentrations climb to 26% of normal. At least in rodents, one has to deplete 80% of the brain thiamine stores before overt neurological symptoms become apparent; 80% – that is a huge deficit. Similarly, it doesn’t appear to take much to right that deficit, only a 6% increase in thiamine concentration set the course for improvement.

If we extrapolate to humans, where life span, genetic and environmental factors likely moderate the degree of thiamine stores and consumption, we still contemplate a rather large thiamine deficit needed before overt symptoms of Wernicke’s emerge. Similarly though, it is also evident that a rather small change in thiamine can have enormous effects on neurological functioning. In the case of the rodents, a mere 6% point change reversed the symptoms. One might suspect equivalent deficit/recovery thiamine parameters in humans.

Waxing and Waning Symptoms: A Case for Persistent Thiamine Deficiency

If we consider the possible course of non-alcoholic thiamine deficiency, where no extraneous variables like bariatric surgery or thiamine deficient parenteral feeding are present and where dietary thiamine varies daily and is not held constant as it is during experimental conditions or during famine, we can begin to see how thiamine related neurological symptoms may wax and wane. Different exposures and triggers may decrease thiamine periodically, even to the point where overt neurological symptoms present. When those exposures are removed and barring deficiencies in metabolism and diet, symptoms may abate, at least temporarily, and until the next trigger or until the black line is crossed anew and thiamine deficiency becomes the medical emergency observed in overt Wernicke’s.

In contrast, the more persistent or chronic thiamine deficits that do not cross the 80% depletion cutoff (or the human equivalent), may also wax and wane and show all the core neurological symptoms expected in overt Wernicke’s though to a much lesser degree. Additionally, as we have speculated, persistent thiamine deficiency might disable mitochondrial functioning in such a way that the patient presents with a myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as cardiac dysregulation, gastroparesis, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. These too may be related to thiamine deficiencies. Although, we cannot and should not rule out other causes as well, sub-optimal thiamine may be involved with a host of complex disease states and medication adverse reactions where neurological symptoms are present. Thiamine deficiency should be tested for and ruled out before more invasive therapeutic options are contemplated.

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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.

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