Category Archives: Intracranial Hypertension

Nutritional Management of Biochemical Abnormalities in Idiopathic Intracranial Hypertension

Note: This is the research paper I wrote earlier this year for my Biochemistry of Nutrition graduate school class. I haven’t looked at it since I turned it in. I originally wanted to add more to it on specific IH research topics (coagulation factors, thyroiditis) that I didn’t have the time or space to write about originally, but my health took a turn this spring and I’m just now recovering from it.

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Nutritional Management of Biochemical Abnormalities
in Idiopathic Intracranial Hypertension


Idiopathic Intracranial Hypertension [IIH], historically known as Pseudotumor Cerebri and Benign Intracranial Hypertension, is a rare disorder where there is greatly increased cerebrospinal fluid pressure in the skull without an obvious cause like a head injury or chiari malformation. It can occur in any age group and any sex, but the largest population is obese women of child bearing age. IIH mimics the symptoms of a brain tumor and common symptoms include: chronic headaches, visual disturbances or vision loss from papilledema, tinnitus or pulsating heartbeat in head, nerve pain and paresthesia, dizziness and lightheadedness, nausea and vomiting, fatigue, memory and cognitive difficulties, and exercise intolerance. There are a number of hypotheses about the biochemical mechanisms involved with IIH but recent research implicates increased levels of pro-inflammatory cytokines associated with the reduction in cerebrospinal fluid drainage. High levels of cortisol and several other pro-inflammatory cytokines are also associated with impaired secretion and absorption of cerebrospinal fluid. Nutrient deficiencies and genetic polymorphisms that affect absorption of one or more of the vitamins required for one carbon metabolism are not uncommon with IIH; those vitamins include riboflavin, folic acid, vitamin B12, and vitamin B6. Typical medical treatments for IIH include: lifestyle changes like weight loss and reductions in salt and caffeine in the diet; medications like acetazolamide or loop diuretics to help reduce the build-up of fluids in the skull; and medical procedures or surgeries such as multiple lumbar punctures to remove cerebrospinal fluid, optic nerve sheath fenestration to improve visual field, and shunt or stent implantation to control cerebrospinal fluid drainage. Nutritional management of IIH includes normalizing homocysteine levels with the appropriate bioavailable forms of B vitamins and healthful, low calorie or low carbohydrate diets to promote weight loss, reduce cortisol levels, and control inflammation.

Signs, Symptoms, and Diagnosis

Idiopathic Intracranial Hypertension [IIH] involves a dysfunction in the mechanisms that secrete or absorb cerebrospinal fluid in the brain. It is a rare disease that is becoming increasingly more common. There’s some debate whether this increase is due to rising obesity rates or improved diagnostics; it is likely a combination of both. 92% of those diagnosed with IIH are obese women between the ages of 22-44, but it can be found in any population. Occurrence rates in the general population are approximately 1/100,000; however, in obese women of childbearing age the rate is 20/100,000. A small but significant population of those prone to IIH are astronauts. 29% of astronauts experience either intracranial hypertension or other visual changes related to changes in cerebrospinal fluid dynamics. NASA has partnered with The Intracranial Hypertension Research Foundation to study causes and improve diagnostics and treatment of Intracranial Hypertension.

Associated risk factors for the development of IIH include disorders like hypothyroidism, hyperthyroidism, Cushing’s disease, Lyme’s disease, and aldosteronism. Secondary intracranial hypertension has been associated with sleep apnea, pregnancy, anemia, meningitis, medications or drugs (antibiotics, lithium, vitamin A, steroids, hormone birth control), chiari malformation, and living in a microgravity environment.

Severity of symptoms vary but disabling chronic headaches is the most common symptom and permanent vision loss is experienced by nearly a quarter of IIH patients. Due to the diverse and often nonspecific nature of the symptoms, it takes an average of 5 years before the diagnosis of IIH is made. IIH is commonly misdiagnosed as chronic migraines or dismissed as symptoms of other health problems. The previous name of IIH, Psuedotumor Cerebri (meaning: false brain tumor), clearly shows the symptoms apply to other diseases. Because symptoms and treatments can be disabling, the medical profession has moved away from the name Benign Intracranial Hypertension because it undermines the seriousness of the condition.

A diagnosis of IIH is usually made after brain imaging, an ophthalmological exam, and a lumbar puncture. Brian imaging is used to rule out brain tumors, hydrocephalus, lesions, venous sinus thrombosis, or other structural problems. Signs of IIH that appear in imaging include flattening of posterior globe near the optic nerve and an empty cella. These occur 80% and 70% of the time in IIH, respectively.

An ophthalmological exam looks for papilledema, swelling of the optic disc from increased intracranial pressure. It is another common, though not universal, symptom of IIH. Permanent vision loss, either partial or full, is a serious complication of IIH. Permanent vision loss is more likely in patients who don’t receive a prompt diagnosis and appropriate treatment.

Measuring the opening pressure of cerebrospinal fluid during a lumbar puncture is the gold standard for diagnosing IIH. Opening pressure must be 250mm (25cm) or greater for a diagnosis of IIH. Occasionally a second lumbar puncture is required because the opening pressure was low on the first one and other causes for the symptoms were ruled out. A lumbar drain for 6 to 24 hours to monitor cerebrospinal fluid pressure is seldom required to make a diagnosis.

Physiological and Biochemical Mechanisms

While IIH is characterized by increased intracranial pressure, the exact physiological processes is yet unknown though four possible mechanisms of impaired cerebrospinal fluid dynamics have been suggested: increased cerebrospinal fluid secretion in the choroid plexus, increased cerebral volume, increased cerebrospinal fluid outflow resistance at the arachnoid granulations, and increased cerebrospinal venous pressure. There is no consensus though small studies show some IIH patients exhibit signs of at least one of these fluid dynamics disorders.


There are a number of hypotheses about the biochemical mechanisms involved with IIH, including endocrine dysfunction since IIH occurs most often in women. However, if hormones were the only factor involved, IIH would be more common. Another major factor in the development of IIH is obesity, with 94% of patients diagnosed with IIH falling into the clinically obese category. But again, if obesity was the only factor, there would be more cases of IIH. It is possible that both endocrine dysregulation and obesity, along with a combination of other factors, play a role in the development of IIH. Recent research implicates systemic inflammation along with glucocorticoid dysregulation, and one carbon metabolism errors due to nutrient deficiencies or genetic polymorphisms, though no group of patients exhibits abnormalities in every biomarker. However, it gives doctors and researchers alternative diagnostics using laboratory testing and can help establish new treatments.

Obesity is an established cause of low grade systemic inflammation. Numerous studies show pro-inflammatory cytokines in adipose tissue in those with obesity. Those cytokines include: CC-chemokine ligand 2 [CCL2], interleukin-1β [IL-1β], interleukin-6 [IL-6], interleukin-8 [IL-8], tumor necrosis factor-α [TNF-α], hepatocyte growth factor [HGF], nerve growth factor [NGF], and plasminogen-activtor inhibitor type 1 [PAI-1]. Resistance to the adipose hormone that controls appetite, leptin, and elevated serum leptin levels are also associated with obesity.

Pro-inflammatory cytokines associated with obesity, TNF-α, IL-1β, Il-6, and leptin also regulate the glucocorticoid enzyme 11β-hydroxysteroid dehydrogenase type 1 [11β-HSD1]. 11β-HSD1 regulates corticosteroid hormone activity by activating cortisol from cortisone. Elevated 11β-HSD1 is associated with altered lipid metabolism and insulin resistance because it controls cortisol availability which drives gluconeogenessis. Dysregulation of 11β-HSD1 can disrupt sex hormone metabolism and cortisol production. Cortisol dysregulation through altered 11β-HSD1 activity may have an effect on cerebrospinal fluid homeostasis through the regulation of the arachnoid granulation. There is also evidence of 11β-HSD1 immunoreactivity in the cerebrospinal fluid secreting cells in the choroid plexus.

Hematological and cerebrospinal fluid laboratory analysis in patients with IIH show high levels of pro-inflammatory cytokines, both ones associated with obesity and ones not associated with it. Systemic inflammation is linked to changes in cerebrospinal fluid dynamics and could be one of the underlying causes of IIH. Recent research implicated pro-inflammatory cytokines CCL2 and IL-17 in the reduction of cerebrospinal fluid outflow resistance and the association of high levels of homocysteine, cortisol, TNF-α, and IL-6 with altered compensatory mechanisms in the secretion and absorption of cerebrospinal fluid. Transforming growth factor-β [TGF- β], C reactive protein [CRP], leptin, and cortisol are also often elevated in patients with IIH. The leptin levels in patients with IIH is much greater than the levels found in obese patients without IIH.

One carbon metabolities, namely homocysteine, are also often elevated in patients with IIH, indicating B vitamin deficiencies or genetic polymorphisms that affect one carbon metabolism. Two genetic polymorphisms have been identified as increasing the risk for elevated homocystine as well as increasing the risk of developing IIH: gene MTRR with one or two G alleles and gene SHMT1 1420 with C alleles. The two identified genetic polymorphisms affect absorption of one or more of the vitamins required for one carbon metabolism; those vitamins include riboflavin, folic acid, vitamin B12, and vitamin B6. Improving the nutritional status of patients with elevated homocysteine could improve IIH symptoms and reduce the likelihood of recurrence.

Conventional Medical Treatments

Since IIH is linked to obesity, conventional treatment for IIH includes a recommendation for weight reduction. Besides extreme dieting that includes very low caloric intake, weight loss surgery is often suggested. More reasonable dietary advice for patients with IIH is to reduce sodium and caffeine intake in order to improve fluid dynamics. Excess sodium can increase intracranial pressure while caffeine increases the production of cerebrospinal fluid.

Besides lifestyle changes, medications are the first line of treatment. Carbonic anhydrase inhibitors act as a mild diuretic as well as reduce the reabsorption of bicarbonate and sodium chloride thereby slowing down fluid transport and reducing intraocular and intracranial pressure. Two popular carbonic anhydrase inhibitors used to treat IIH are acetazolamide and topiramate. Topiramate has the added benefits of reducing chronic headaches and acting as an appetite suppressant, which can aid in weight loss. If carbonic anhydrase inhibitors are not tolerated, loop diuretics that reduce the production of cerebrospinal fluid are used. Furosemide is the most popular loop diuretic prescribed for IIH. Glucocorticoids like Prednisone are sometimes used on a short term basis to reduce inflammation. They are thought to improve the outflow of cerebrospinal fluid at the arachnoid granulations in the brain. Other drugs used to treat migraines may be prescribed since chronic headaches is one of the most debilitating symptoms of IIH.

Medical procedures aren’t uncommon in severe cases of IIH that are resistant to treatment with medications. Repeated lumbar punctures to remove excess cerebrospinal fluid are often used on a temporary basis before surgical interventions are attempted or scheduled. Repeated lumbar punctures aren’t without risk. There’s always a possibility of permanent nerve damage and increased risk for serious infection.

Optic nerve sheath fenestration is used after rapid or progressive vision loss occurs due to increased pressure on the optic nerves. Incisions are made in the meninges in order to relieve the intracranial pressure on the optic nerve and improve the visual field. It’s not a cure for IIH but it can reduce further vision loss from chronic papilledema due to high intracranial pressure. Optic nerve sheath fenestration can lead to permanent blindness or other complications.

Venous sinus stents are a relatively new procedure in the treatment of IIH, but they’re gaining in popularity. A tubular support is placed in the venous sinus in order to widen an area narrowed by either intracranial pressure or blockage in order to improve cerebrospinal fluid flow. They seem to be nearly as effective as shunts but with fewer complications. The biggest complication is the risk for blot clots but that is usually controlled with medication. In IIH patients with confirmed venous sinus stenosis that impedes cerebrospinal fluid absorption, venous sinus stenting across the arachnoid granulation normalizes cerebrospinal fluid pressure and reduces IIH symptoms. Long term studies are still required but currently stenting is a surgical alternative to shunts.

Two different type of shunts are used to improve cerebrospinal fluid drainage with IIH. Shunts involve the placement of a catheter either in the brain or the spine connected to a drain tube in the peritoneal cavity in the abdomen in order to drain cerebrospinal fluid more effectively. Neuronavigation-assisted ventriculoperitoneal (VP) shunts with programmable valves are have a slightly higher risk of initial failure (14% vs 11%), but revision rates of lumboperitoneal (LP) shunts is much higher (60% vs 30%). Both often require multiple surgeries and the risk of infection is high. Shunts should be considered as a last resort.

Nutritional Management

There are three nutritional targets for the management of IIH: weight loss, reduction of inflammation, and normalization of homocysteine levels. Low sodium and limited caffeine intake may also be helpful in the management of IIH.

Studies show that weight loss using a short term (3 months) very low carbohydrate diet improves abnormal 11β-HSD1 activity and normalizes cortisol levels. Very low calorie diets have also shown to improve IIH symptoms, though biochemical markers weren’t checked. While doctors often recommend surgical weight loss procedures in the treatment of IIH, diet based weight loss has fewer complications as long as micronutrient needs are met.

Research into diets that mitigate pro-inflammatory cytokines and other pro-inflammatory biochemicals have identified a few factors that should be included in a diet in order to reduce systemic inflammation. Those factors include: monounsaturated and omega-3 fatty acids like those found in avocados, olive oil, nuts, flaxseed, chia seed, and oily fish; a greater quanity of fruits, vegetables, and nuts; minimally processed whole grains; and polyphenols including tea, cocoa, red wine, and berries. Studies suggest that diets with higher fruit and vegetable intake are associated with reduced levels of pro-inflammatory cytokines including IL-1, IL-6, and TNF-α and CRP.

Dietary factors that increase inflammation include: trans fats and omega-6 fatty acids like those found in vegetable oils; highly processed foods with a high glycemic index; and diets without adequate fruits, vegetables, and nuts.

New research shows that diets which contain mostly fresh foods with limited sugar and processed foods reduce inflammation. A Mediterranean style diet and a Paleolithic style diet were used in the trial and both decreased CRP. Pro-inflammatory cytokine levels weren’t tested.

Normalization of homocysteine levels can be managed through diet alone if genetic polymorphisms aren’t present. The micronutrients required for one carbon metabolism can easily be gained from food as long as genetic polymorphisms don’t hinder the conversion of them into usable forms. Bioavailable or coenzymated vitamins may be added to the patient’s treatment regime if vitamin conversion is a problem. Folate can be obtained from leafy greens, citrus, beans, nuts, and whole grains. Vitamin B12 is in mollusks, liver, red meat, fish, poultry, eggs, and dairy products. Vitamin B6 can be found in organ meats, fish, beans, potatoes, and bananas. Riboflavin (vitamin B2) is most plentiful in dairy products, nuts, red meat, fish, eggs, and pork.

Designing a diet that the patient can turn into a lifestyle change for the long term is key to any nutritional management of disease. Neither very low carbohydrate nor very low calorie diets are easy or safe for long term, though both can be used for short term weight loss in order to improve biomarkers and symptoms of IIH. For the treatment of IIH, a whole food diet rich in omega-3 fatty acids, vegetables, fruits, nuts, and nutrient rich meats and low in highly processed foods with high glycemic index and high omega-6 fatty acids seems to be the best place to start.


Idiopathic Intracranial Hypertension is a disabling disease that can cause permanent vision loss and chronic headaches that mostly affects obese women between the ages of 22-44. While the cause of the symptoms are well documented, increased cerebrospinal fluid pressure, the underlying causes of the abnormal cerebrospinal fluid dynamics are still heatedly debated and researched. Newer research implicates a number of biochemical changes including systemic inflammation, glucocorticoid dysregulation, and one carbon metabolism errors. Conventional medical treatment for IIH currently does little to identify or treat these underlying biochemical abnormality. Nutritional management of the biochemical irregularities though a carefully designed diet and supplemental vitamins, if required, is a good adjunct treatment to conventional medicine that should reduce symptoms and recurrence of IIH.


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Intracranial Hypertension and Thyroid

I started graduate school last month with the intention of earning an MS in Human Nutrition. For my Biochemistry of Nutrition class I have to do a research project on a metabolic disease. Originally I planned to do one on mitochondrial disease but from my Pathophysiology class I’ve learned that mitochondrial dysfunction underlies nearly every chronic illness from autoimmune diseases to cardiovascular disease to Parkinson’s disease to Alzheimer’s disease. Now I plan to do it on Secondary Intracranial Hypertension, if my professor agrees. The causes of Idiopathic Intracranial Hypertension are unknown but there have been multiple risk factors found for SIH, including endocrine disruption due to pituitary gland dysfunction, hormone birth control, steroids, hyperthyroidism, and hypothyroidism. Endocrine disruption makes some, not all, SIH a metabolic disease.

I believe quite strongly that facultative hyperthyroidism due to improper/negligent medical care was the cause of my SIH. This post lists all the reasons I believe this. Unfortunately there is no way to prove it since I didn’t have many labs done in the five months I was taking the wrong dosage of thyroid medication (or if I did, I don’t have copies of the results).

In July of 2009 I started seeing a naturopathic “doctor” because none of the multiple treatments I tried with my Internal Medicine PA, even experimental ones like Viagra, helped relieve the “Fibromyalgia” (I usually call it mold induced myalgia now) and I was getting sicker and sicker. It culminated with my PA taking me off all medications and admitting she couldn’t help me. The ND could prescribe a promising medication I had researched, Low Dose Naltrexone, that my PA was unable to prescribe since it came from a compounding pharmacy. Unfortunately I allowed the ND to talk me into trying many more things, most of which made my symptoms worse or caused new problems. Even though my hypothyroidism was very mild and I’d taken a low dose of Synthroid for years without any problems, she thought I needed to take both slow acting T4, like Synthroid, and a fast acting T3 thyroid medication because my body wasn’t converting the T4 to T3 properly. It’s possible this is true since mold illness increases systemic inflammation and interferes with the function of the pituitary gland which signals the thyroid gland to produce more T4 and T3 with Thyroid Stimulating Hormone (TSH). Inflammation can also inhibit the body’s ability to convert T4 into T3. Not everyone with hypothyroidism requires a T4/T3 medication, but there are some health issues that make it a better choice. A full thyroid serum panel that includes TSH, Free T3, Free T4, and Reverse T3 can help a doctor find the best treatments for a patient. Thyroid antibodies can also be tested if an autoimmune disease is suspected.

Instead of switching me to a natural dessicated thyroid medication that comes in standardized doses from a pharmaceutical company like Armour, Naturethroid, or Westhroid, my ND prescribed an 80/20 T4/T3 drug from a compounding pharmacy. Here’s where the negligence comes in. I was taking 37.5mcg of Synthroid and I switched to 40mcg of 80/20 T4/T3 combination in mid-September. This breaks down to 32mcg of T4 and 8mcg of T3. The problem with this dosage is that T3 medications are almost 4x as potent as T4 medications. Most thyroid medication conversion charts equates 12.5mcg of T3 to 50mcg of T4. Using that conversion, I was prescribed the equivalent of 32mcg (8×4) T3 along with another 32mcg of T4 for a total of 64mcg, almost twice the dose I was taking before. If the conversion had been done properly, I should have been prescribed 25mcg of T4 and 5mcg of T3 (5×4=20+20=40). I know math is hard, but it is a doctor’s job to know how to prescribe medications at the right doses. This is doubly so if the drug is compounded and not standardized. This dosage mistake had huge repercussions for my health.

I don’t like to play “what if” games because it would drive me insane. There are too many decisions that were made either by me or my health care providers that contributed to the worsening of my  health, from where I lived to what medications I took, but a dosage mistake is not the same thing as hidden mold or unforeseen medication side-effects. It is negligence and possibly malpractice.

At the end of December 2009, my IH headaches began and continued to worsen. Based on the location of the headaches at the top of my head, I thought they were thyroid related. My mom gets similar headaches when her thyroid meds are out of balance. I asked my ND to test my thyroid levels in early February 2010. She said everything was within normal range but I still wasn’t converting T4 to T3 properly. She convinced me to take the herb chaste tree to help regulate my period, which had been irregular and sometimes occurring twice a month since January. My health continued to decline and the headaches got worse. The problems with my period are also hallmarks of hormone/thyroid imbalance for me. Often that’s my first major sign that something is wrong since fatigue and muscle pain are normal for me.

By early March I knew the compounded thyroid meds were making me more ill, even if I couldn’t prove it; my fatigue and muscle pain were almost unbearable, I had severe sleep issues, I bled constantly, I lost weight very fast (over 10lbs in one month), and the headaches were uncontrollable. I finally saw my PA on March 12th and switched back to Synthroid at my previous dose of 37.5mcg. Of course it was too late by then; I already had IH. March 19th I tried a migraine medication in an attempt to stop the pain cycle. The next day the left side of my face and my left forearm went numb and the headache expanded to encompass my entire head. On March 23rd I started losing vision in my left eye. On March 24th I saw my PA and had an emergency MRI of my head. She talked me into trying an opiate in an attempt to stop the headache cycle. The MRI didn’t show any abnormalities so on March 26th I had an emergency appointment with an eye doctor. My eye pressure was elevated and there was bulging on my optic nerves indicating elevated cerebrospinal fluid in my skull. He diagnosed me with Pseudotumor Cerebri aka Intracranial Hypertension. Later that day it was confirmed with a lumbar puncture with an opening pressure of 35 (normal is under 25). 30cc’s of CSF was removed in an attempt to reduce the pressure in my skull and ease the four weeks of continuous headache.

I won’t go into depth about my experience with IH in this post since I’m building a chain of evidence that the IH and my thyroid problems are linked. It took several years for the IH symptoms to ease up and mostly disappear, but my thyroid problems weren’t over. In late 2011, I once again had issues with irregular periods despite doing okay on 37.5mcg of Synthroid since switching back to it in 2010. My TSH was too high, which meant my body wasn’t getting enough thyroid hormones. My Synthroid dose was increased to 100mcg. My energy levels were greatly improved for about a month and I weighed less than I did at age 16, but then my TSH dropped too low, which meant I was taking too much medication. My dosage was adjusted downward and I gained most of that weight back in the space of two months. In late 2012, I tried Armour thyroid, a natural dessicated thyroid medication that contains both T3 and T4 hormones. I didn’t do well on it and the IH headaches, which were mild at that point, got much worse. They eased up once I was back on Synthroid.

After a year of struggling to get my thyroid levels balanced with Synthroid I asked to try a T3 medication, Cytomel, alone in late 2013. By that time my IH symptoms were basically gone. I’d get an IH headache a few days a month around my period, but that was it. I was no longer on Nortriptyline for neuropathy nor diuretics to remove extra CSF, both of which were used to treat my IH. Within a few days of slowly increasing the dosage of Cytomel, I knew it was a problem. After two weeks the IH headaches were too severe for me to continue on Cytomel. I switched back to Synthroid and soon the IH headaches were gone again. My MD still wanted me to try both T4 and T3 medications since blood tests showed I wasn’t converting T4 to T3 properly. I have copies of that lab work showing it to be true. At that point I was taking between 93.75mcg and 87.5mcg of Synthroid. We dropped Synthroid down to 50mcg and added 5mcg of Cytomel twice a day.  Even though the conversion of this dose was close to what I was taking of Synthroid (10×4=40+50=90mcg), once again the IH headaches returned. I dropped the Cytomel dose down to 5mcg in the morning and 2.5mcg in the evening and the headaches became bearable, though they were a constant presence. I’ve stayed fairly close to that dose since then though I still have to adjust the doses of Sythroid and Cytomel several times a year to find the best dose that keeps the headaches away, yet keeps my energy levels up enough I can function. If one or both of the doses gets too low or too high, not only does the IH headaches worsen, my fatigue gets worse, so do my PMS symptoms, and eventually my periods become irregular. Currently I’m taking 56.25mcg of Synthroid and 5mcg of Cytomel in the morning and 2.5mcg in the evening and I have a constant, yet mild, IH headache. I took 62.5mcg of Synthroid and 5mcg of Cytomel in the morning and 1.25mcg in the evening for several months but my fatigue worsened. Somewhere between 6.25mcg and 7.5mcg of Cytomel is my perfect dose, but I can’t cut the 5mcg tablets that small. I may ask my MD about trying a sustained release compounded form of T3 in 6.75mcg.

In the process of writing this, I realized that I’m having so much trouble adjusting my thyroid medications and keeping it balanced due to pituitary gland problems. I’ll have to ask my MD about this as well. I’m not sure there’s anything we can do to treat it directly, but it is something that mold illness affects and it’s the gland responsible for MSH production, and we know my MSH levels are much too low.

Anyway, all my experiences with Cytomel and how tiny dosage changes make my IH symptoms return made me go back and take a hard look at the compounded thyroid medication I was taking when the symptoms began. I’ve read a lot about hypothyroidism and how the body converts T4 into T3 since 2012, and I have a much better understanding of how my body reacts when my thyroid levels are out of balance. Too bad I didn’t have this knowledge before my health was ruined by IH and the treatments for it. Dealing with mold illness was bad enough without adding thyroid problems and IH on top of it. Without the lab reports or copies of the prescription, I don’t think I can prove any of my suspicions to the state naturopath licensing board, but I wonder how many other prescribing mistakes she’s made. We trust health care practitioners, especially if they call themselves doctors, to know what they’re doing. We literally put our lives in their hands. They should be at least be reasonably competent. If I can figure out dosing conversions after looking at a couple of charts online, a medical professional should have even better resources they can reference.