It’s been a year since I’ve posted to this blog. I’ve started and stopped writing multiple different posts, but I’ve never been fully committed to any of the topics, and to be honest, I didn’t have the energy for it. To start, I want to apologize to anyone who has contacted me in the past year and hasn’t yet received a response. I promise, it’s not personal, and I greatly appreciate the time and effort you took to both read my writing and to contact me. I will be going back through all my emails and notifications to make sure I respond to each and every one of you. I’ve also changed my current email contact address to one dedicated to this website, so the emails don’t get lost in the constant influx of other notifications in my inbox. My health has gone increasingly down hill since 2015, and as I’ve mentioned previously, severe fatigue has always been my worst symptom. For anyone with unrelenting fatigue, you know it’s more than just being tired, as there is no relief, it demands attention, and cannot be ignored. In the past year, I've traveled to Texas and Minnesota (not Mayo) for medical appointments, and in July 2017, I additionally had a polysomnography (sleep study) that included a Multiple Sleep Latency Test (MSLT), which should have been done back in 2011 with my first sleep study (if not long before), and I was diagnosed with Idiopathic Hypersomnia (IH), which is similar to Narcolepsy Type 2 (Narcolepsy without Cataplexy). IH, though, is poorly understood, has been neglected by researchers, and has no FDA approved treatment. Sounds strangely similar to so many of my other diagnoses, doesn't it? This IH diagnosis, too, wasn’t new to me and was the result I expected (and had suspected since I found it myself back in 2011).
However, what I did not expect was that around this same time, my new PCP had an idea as to the missing link regarding my fatigue and numerous still unexplained neurological symptoms that were rapidly progressing. She suspected I had Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), which is a neuromuscular autoimmune disease and is the chronic form of the acute Guillain-Barré (GBS); she sent me to my fourth neurologist (in two years), who confirmed CIDP.
If you Google CIDP, it will tell you that this disease only attacks the Peripheral Nervous System (PNS) and does not involve the Central Nervous System (CNS), as is seen in Multiple Sclerosis (MS). To that information, I say ha, that’s what you think. Way to cater to the average patient, while leaving out the rest of us. CIDP can affect the CNS, as well as the Autonomic Nervous System (ANS), resulting in Dysautonomia, and can impact the cranial nerves, leading to symptoms similar to Bell’s Palsy, and have bulbar involvement as well, which for me included pseudobulbar affect (likely my third most hated symptom, with fatigue and hyperhidrosis coming in first and second); it’s also the symptom my own university tried to use against me (a horrible and despicable act of discrimination and unacceptable intolerance, but a topic for a later date) after I had the audacity to question "authority" – I'm sure everyone that knows me is completely shocked that I would dare to stand up for myself (note the sarcasm). To return to the current topic at hand though, in some cases of CIDP, usually in long-standing untreated disease (another check for me), symptoms can also occur mimicking Cauda Equina, which results from nerve roots at the end of the spinal cord being affected. Symptoms can include numbness, tingling, and/or altered sensation in the “saddle region” (the nicer term for groin), low back pain, and bladder and/or bowel dysfunction (such as urinary retention, fun times; this symptom started after I’d just finished two years of pelvic floor physical therapy for hypertonic/nonrelaxing pelvic floor dysfunction – I really can’t win). I’m (un)lucky enough to have all of these systems affected, along with both sensory and motor involvement. Finally, I had an explanation that encompassed all of my disturbing neurological symptoms, which was a gigantic relief. Given the diagnosis, I started intravenous immunoglobulin (IVIg) treatments in October 2017. IVIg is used as a treatment for a variety of disorders, including immunodeficiency, autoimmune disease, and neuromuscular disorders. It's even starting to be used as a treatment for gastroparesis, autoimmune dysautonomia, and MCAS.
[Note: My CIDP diagnosis only took the short amount of time of nearly twelve years. Let’s give a round of applause to the American healthcare system for the expedient identification of the problem. A recent CME-certified study of US-based neurologists revealed that over 50% were incompetent in both diagnosing and selecting the appropriate treatment for CIDP. Comforting knowledge, isn't it? And, people seriously wonder why I so readily question "authority."
I'd also like to pause for a moment to give a shout-out to the Wardenburg Health Services nurse practitioner at CU Boulder who, when I requested a referral to a neurologist, wrote in my medical records that I thought I had a neurological disorder (funny how accurate I was about that diagnosis – POTS...), but she really thought it was "psychosomatic." Thanks for that permanent, libelous, and inaccurate non-assessment, since there was no actual assessment, in my records. I recommend she consider reviewing the concept of do no harm, as once a medical provider suggests a patient's symptoms are all in their head, it's very difficult for the patient to ever have their symptoms taken seriously. And, hey, in my situation, I was right all along! Imagine that! A patient knowing their own body. Must be a rare find, since in medical definitions, rare = non-existent. Seriously, it really does. I've heard it a lot: "You don't have that – that's rare." Fun fact: the nursing equivalent of the Hippocratic Oath is called the Nightingale Pledge, though it has fallen into disuse – perhaps that's part of the problem?]
In September 2017, my EMG showed I had no reflexes in my legs or arms, and I also had no F-waves, a measure of nerve conduction velocity to and from the spinal cord, which “occurs at the interface between the peripheral and central nervous system.” After 3.5 months of IVIg treatment, my repeat EMG at the end of January 2018 showed I had very tiny reflexes and F-waves, meaning the IVIg is working, which was of no surprise to me whatsoever. I could immediately tell a massive difference, even after the first treatment. I’ll write more about this experience later, but I wanted to provide background as to why I’ve been so absentee over the past year and as to the reason I haven’t been able to respond to everyone, though trust me, I’ve been thinking about all of you. The good news is that these treatments have helped my fatigue, which is all I’ve ever wanted since 2006. The fatigue is the reason I set about researching my symptoms to begin with, and it’s rather ironic to think that if it wasn’t for the CIDP, I very well might have spent my entire life never knowing I had Hypermobile Ehlers-Danlos Syndrome (hEDS). While I still have a very long way to go recovery-wise, and I’m having to receive treatments weekly, or else I rapidly decline all over again, I’m hopeful that the fatigue will continue to improve.
In the meantime, I have a long list of topics to discuss that I hope people will find helpful. As always, I’ll add the reminder that I am not a doctor and cannot provide medical advice, but I’m aiming to post far more regularly, and hopefully, symptom-wise, this year will be full of improvement, for once, rather than decline. I’m currently taking a human nutrition course, so this post will relate to nutrition and diet and will provide an overview of some gastrointestinal and gluten-related disorders, as well as reference things I’ve found personally helpful. If you have any suggestions regarding topics you’d like me to research, feel free to let me know in the comments.
Thanks for reading.
IBS, SIBO, & Diet
Irritable Bowel Syndrome (IBS) is a complex, chronic, functional GI disorder, influenced by a variety of factors including chronic low-grade inflammation, visceral hypersensitivity, and genetic and immunological factors. Degranulation of mast cells in the intestine are also thought to play a role [see also Mast Cell Activation Syndrome (MCAS)]. IBS is an intriguing disorder to research, as approximately 37% of patients with an IBS diagnosis meet the diagnostic criteria for hEDS, which is a surprisingly high percentage.
Typically, IBS patients are advised to eat a high-fiber, low-fat diet. However, this approach is problematic, as IBS patients often may have other GI disorders, which may or may not have already been diagnosed. For example, for IBS patients who also have Gastroparesis (which is common among diabetics and in people with autonomic disorders), eating a high-fiber diet can worsen symptoms, as the additional fiber further slows digestion, resulting in increased abdominal pain. Excess fiber can also lead to bezoar formation and may result in gas, increasing IBS symptoms.
Diagnostically, IBS patients are usually further characterized into subgroups, including diarrhea-predominant, constipation-predominant, or mixed-type. Most patients report worsening of symptoms with certain foods, such as those containing lactose (e.g. milk), fructose (e.g. pears, cherries), gas-producing foods (e.g. beans, cabbage), wheat, and sweeteners (e.g. xylitol, sorbitol – meaning individuals should avoid most sugar-free chewing gum). For people with diarrhea-predominant symptoms, it’s often best to also avoid high sources of caffeine, which may include coffee, coke (fizzy drinks can exacerbate symptoms, too), and chocolate. For those with constipation-predominant IBS, a higher fiber diet may be helpful, as additional fiber softens stool. A low-FODMAP (Fructose, Oligosaccharides, Disaccharides, Monoamines, and Polyols) diet has more recently been used, frequently with good results, especially for symptoms such as abdominal bloating, pain, and diarrhea. Several clinical trials studying low-FODMAP diets in IBS have found that approximately 70% of IBS patients find relief from symptoms utilizing this diet.
For foods included in the low-FODMAP diet, I’m partial to the Gastroenterological Society of Australia’s document on the subject. I appreciate their explanations of foods, while also breaking down each category that should be avoided. The negative to this diet, however, is that it can be restrictive and planning must be meticulously done to ensure foods are either replaced with alternatives or appropriate supplements are added. For anyone avoiding milk products, calcium and vitamin D supplements may be needed. Good vegetables within this diet include spinach, carrots, eggplant, zucchini, tomatoes, and potatoes. However, as previously mentioned, if someone has additional GI disorders, diet planning can quickly become complicated, as if a low histamine diet is also required, tomatoes, for example, may be off the table. Nightshades, too, can be problematic for some people, especially for those with IBS, food sensitivities, allergies, and/or autoimmune disease, and both eggplant and potatoes (but not sweet potatoes) are nightshades. Fruit within this diet can include strawberries, bananas, blueberries, grapes, pineapple, and oranges for example, but again, the same problem exists, as bananas are high in histamine, and personally I have trouble with citrus fruits, including pineapple and oranges. Individuals on certain medications may also need to avoid foods that interact with their medications, such as citrus foods for patients on stimulants such as Adderall. Strawberries, too, for me are sometimes problematic, though I tend to tolerate them better blended in a smoothie, rather than eating them whole. When avoiding lactose products, good alternatives can be soy milk, rice milk, and almond milk. Both soy milk and rice milk are problematic for me, so I typically stick with almond milk and occasionally coconut and cashew milk. Oatmeal and bran can be good sources of fiber for anyone that can handle the fiber, and good protein sources can be tuna, salmon, eggs, and chicken, but you can get your protein entirely from plants if you choose. Meat-intake has been found to have a potentially detrimental role in inflammatory bowel disease, so it may be worth omitting. Avoiding gluten may also be helpful for some individuals, as IBS can overlap with Non-Celiac Gluten Sensitivity (NCGS). Gluten is a major symptom inducer for me, and it also triggers neuropathy in my feet.
I have found a low histamine diet, as well as a diet tailored for Gastroparesis, to be helpful. UVA Nutrition Services has a document available on dietary intervention for Gastroparesis that I found useful. I ate two meals a day for several months as smoothies, and the suggestions they offered were vital in my food decision-making process. As for the low histamine component, I utilize Whole 30’s low histamine shopping list.
Medication-wise, some people find mast cell stabilizing medications, such as Sodium Cromolyn and Omalizumab, helpful in treating IBS, because, as previously mentioned above, degranulation of intestinal mast cells are thought to contribute to gut hypersensitivity. For individuals who may have a mast cell disease (which is thought to be highly prevalent, though massively underdiagnosed), a full histamine blockade may be useful, such as an H1 (e.g. Cetirizine) and H2 blocker (e.g. Famotidine), both of which can be obtained over-the-counter without a prescription. If histamine blockers are helpful in reducing symptoms, you may wish to consider pursuing a formal mast cell disease diagnosis, though specialists are few and far between. Dr. Lawrence Afrin, a US-based Mast Cell Disease specialist, also has a book that may be a useful resource. For anyone with Gastroparesis, Erythromycin or Metoclopramide can further be helpful.
I’ve also found Quercetin to be a positive addition, especially when taken with Bromelain, which is a protein digesting enzyme obtained from pineapple that exhibits "fibrinolytic, antiedematous, antithrombotic, and anti-inflammatory” properties. Quercetin is a flavonoid, found in fruits and vegetables, that exhibits antioxidant activities, inhibits histamine release, and decreases pro-inflammatory cytokines, among other properties, and is mast cell stabilizing and helpful for people with allergies. My personal choice in brand for these supplements is BulkSupplements for Quercetin and Superior Labs for Bromelain.
Another comorbidity worth mentioning is Small Intestinal Bacterial Overgrowth (SIBO), which can go hand-in-hand with IBS, especially for diarrhea-predominant IBS, therefore treatments for SIBO may also help IBS symptoms. Studies into the relationship between SIBO and IBS are ongoing, but are thus far suggesting “there is significant association” between the two disorders. Two drugs commonly used in treatment are Rifaximin (Xifaxan) and Neomycin. The potential side effects of Neomycin scared me, so I opted for Xifaxan alone, which did help me significantly.
As far as lifestyle choices, I encountered a clinical trial reporting on yoga being helpful in reducing IBS symptoms. I find this suggestion annoying, as people love to tell you to do yoga as a solution for everything, but to each their own, if it helps someone, good for them, I’m glad they found something that works.
Gluten are the proteins found in wheat. Related proteins have also been identified in rye and barley. Gluten-related disorders are a group of diagnoses including Wheat Allergy (WA), which is induced only by wheat proteins, Celiac Disease (CD), and Non-Celiac Gluten Sensitivity (NCGS), which is equivalent to Gluten Sensitivity (GS) or gluten intolerance. Globally, 5% of the population is estimated to be affected by these conditions. Wheat is one of the five most common allergens in children, which about 65% of children outgrow by age 12, and prevalence in both children and adults is approximately 1%. Worldwide, CD is estimated to impact approximately 1:100, with 1% of the US affected. Currently, NCGS has an estimated incidence anywhere from 0.6% to 6% of the US population; a study at the Center for Celiac Research at the University of Maryland, from 2004 to 2010, found 6% of their 5,896 patients had NCGS. For both WA and CD, the diagnosis is based on a combination of the patient’s clinical history and specific tests, including blood tests, and for WA may include assays, whereas CD involves duodenal biopsies. NCGS, however, is currently still primarily a diagnosis of exclusion.
WA is a hypersensitivity reaction to wheat protein (including gluten) specifically, and treatment is based only on elimination of wheat grains. WA includes IgE-Dependent WA, IgE-Non-Dependent WA, and Wheat-Dependent Exercise-Induced Anaphylaxis (WDEIA), which is rare (allegedly). Wheat-related allergic disorders are further classified as food allergies, respiratory allergies, and skin allergies. The first stage of testing for WA is an oral food challenge, with the patient eating whole wheat in small doses with increasingly larger hourly doses. If symptoms occur within two hours of ingestion, the test is considered positive. Next, skin testing is done for wheat-specific IgE, usually using wheat flour. Serum concentration can also be drawn for whole wheat extract-specific IgE. Within WA, gluten-specific IgE can be assessed during testing, but the testing will only be positive in the case of a wheat allergy and will be negative for other allergies to gluten-containing grains, as the testing only contains wheat gluten proteins. This disorder is treated by a wheat-free diet. Most patients can still tolerate other gluten-containing cereals, such as rye, barley, and oats. There are also ongoing studies exploring oral immunotherapy to desensitize these patients to wheat.
While allergy classifications consider CD to be a wheat-related allergic disorder, technically speaking, CD is a T-cell mediated autoimmune disease, not an allergy, and is therefore usually treated by gastroenterologists, rather than allergists. In CD, gluten activates an inflammatory reaction within the small bowel, which causes intestinal damage and malabsorption. Currently, the only CD treatment is a gluten-free diet.
NCGS was first documented in 1980, but an international consensus was not reached until 2011. NCGS is defined as a “non-allergic and non-autoimmune condition in which the consumption of gluten can lead to symptoms similar to those seen in CD.” This gluten sensitivity is relieved by dietary exclusion of gluten, and symptoms return when gluten is reintroduced. There is thought to be a significant overlap between NCGS and IBS. WA and CD must be excluded before NCGS can be diagnosed, which is done before the removal of gluten from the diet. The patient must eat a gluten-containing diet for 6 weeks, at which point wheat-specific IgE and skin prick testing is completed, and blood tests are performed for CD. Duodenal biopsy is done if the blood testing for CD is positive and/or if the clinician is highly suspicious of CD. There are patients with false negative blood tests for CD. Once WA and CD are excluded, the patient eats a gluten-free diet for six weeks and monitors symptoms. If symptoms improve without gluten, gluten is then re-introduced to determine if symptoms return. If symptoms do return, the patient is diagnosed with NCGS. Biomarkers have been identified to aid in the diagnosis, including IgG-AGA and Zonulin, but these markers can unfortunately also be elevated in CD.
The cause of NCGS is still being researched, though it may relate to an innate, rather than adaptive, immune system response. It is also possible that eating gluten changes the gut microbiome and leads to NCGS. Further, there is evidence that genetics may play a role. Overall, research indicates NCGS involves not only gut inflammation but systemic inflammation as well. In my opinion, I would not be surprised if MCAS plays a significant role in NCGS. There are unsurprisingly still, in 2018, doctors that (wrongly) claim that NCGS does not exist, and media continually hyping that gluten-free diets are fads for everyone, except in the case of CD, do not help matters.
Massachusetts General Hospital has an informative document on a gluten-free diet, how to identify gluten-containing foods, and lists of foods to both allow and avoid. Examples of foods to avoid include wheat, flour, whole wheat flour, couscous, spelt, rye, barley, oats, pasta, noodles, spaghetti, bread, crackers, cake, pancakes, donuts, pretzels, beer, and much more. The Celiac Disease Foundation also has a helpful introduction as to what people can eat while on a gluten-free diet, including naturally gluten-free foods such as fruits, vegetables, meat and poultry, fish, seafood, dairy, beans, legumes, and nuts. Eliminating gluten seems like a daunting task when you first start, and I most definitely spent at least three times longer at the grocery store wandering around, reading labels, and Googling things on my phone. Honestly, the easiest method is likely to shop only on the outskirts of the grocery store, avoid the middle with the processed foods, and cook everything yourself. It’s exhausting, but at the very least, you know what’s in your food, and that factor alone saves you time and energy.
I hope this review was helpful, and let me know if there are other GI disorders or nutrition-related topics you’d like me to research and discuss. Feel free to comment with any tactics you’ve found helpful in treating your own GI symptoms.
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