Tag: autoimmune encephalitis

Dealing with depression after encephalitis. After many years of trials, this is my current depression regimen, just wanted to share.

Hello everyone, I just wanted to share my current depression regimen and some situation info, in case anyone has similar health issues. I have experienced many hospitalizations since 2015, including involuntary psychiatric hospitalizations. Finally in 2017 I was diagnosed with autoimmune encephalitis (brain inflammation), as well as autoimmune thyroiditis. I was treated with intravenous corticosteroids and that led to some improvement. I continue to experience health issues, but I have made several life style changes that have helped me and that I wanted to share. Again, I was diagnosed with autoimmune disease, and my neuropsychiatrist believes that the encephalitis greatly contributed to my depression. Clearly it’s not the case for everyone, so I am not stating that this should work for all. I have been doing better since these changes, I was able to complete a graduate degree, get back to painting, and started writing and playing guitar again. These were huge improvements for me as I was not able to enjoy any hobbies when I had severe depression and was not able to pursue graduate courses.

  1. I cut out all refined carbs and processed foods. There is sufficient evidence indicating that these foods contribute to inflammation. I am not doing keto or low carb, I am not trying to be very strict with myself, I enjoy all sorts of complex carbs such as baked plantains, potatoes, oatmeal, fruits, berries, etc.
  2. Switched to low glycemic foods – this related to #1, as cutting out refined simple carbs in general does leave one with complex carbs that have lower glycemic index.
  3. Foods that cause an immune reaction – this clearly does not occur for most people, but some do react to certain foods. I noticed that I feel physically and emotionally worse after eating gluten, dairy, or soy, so I had to drop these from my diet.
  4. I go to sleep earlier and stay away from my laptop/phone screen after 9pm. I used to stay up late, but now I go to bed around 11pm. After 9pm I usually dim the lights in the room a bit and I read on my Kindle. Kindle Paperwhite does not emit a high amount of blue light. I also installed blackout curtains so that I spend the night sleeping in the dark.
  5. Sleep is very important – so when I really can’t fall asleep, I do use a cannabis oil (NightNight CBN + CBD oil). But changing my diet, losing weight, and going to bed earlier, did reduce my insomnia, so I don’t need the oil every day.
  6. Significantly decreasing my caffeine intake – personally for me it did lower my anxiety and the occurrence of panic attacks, I now only have green tea in the afternoon, otherwise I drink rooibos tea, water, kefir, decaf tea.
  7. Intermittent fasting – I do fell less brain fog and more clear headed when I am not eating the whole day. I used to surf the internet at 1am eating Sweet & Salty bars. Then my mind would go into dark places and I would start reading about serial killers. Now I eat two to three meals a day between 9am and 5pm, I fast for 16-18 hours a day.
  8. Seeing a psychologist – going through CBT and DBT did help, and this related to #5. I still experience racing thoughts, anxiety, and other issues, but I can now more easily choose to not follow my thoughts. For example – I did used to read a lot about US serial killers and then I would freak myself out and I would start to think that someone could climb through the window. Now I choose more what I read – should I keep reading about mass murders? What is the point of that for me? Will that change anything for the better?
  9. Sunlight – I try to get some sunlight each morning, if I have no energy to come out, I still stick out of the window and get some sunlight on my face.
  10. Exercise – I experience certain pains due to autoimmune disease, and fatigue, so I don’t do extensive exercise, but I do yoga at home. And by exercise I don’t mean that I do a whole hour after work, I do certain yoga poses occasionally throughout the day. I think that’s still better than no exercise.
  11. Shrooms – I did several shroom trips, at home alone, after I was treated for encephalitis. I haven’t done shrooms for a while due to pregnancy and breastfeeding, but the positive antidepressant effects of the trips still remain for me.
  12. CBT, again – accepting that some days are better than others, some are worse, but also seeing the positive – in general I am doing much much better now than in 2016. I am female, hormones fluctuate, I do feel worse during the luteal phase, but I experience a lot more enjoyable moments than before my steroids treatment and this lifestyle change.

My previous mistake when going on a dairy-free diet: too many food restrictions and not enough calcium

I want to describe my mistakes with my previous attempt at going dairy-free. A bit of background – I started experiencing severe abdominal cramps in my 20s, then also I started to have panic attacks, fatigue, and swollen eyelids. I had problems waking up in the morning. I ended up being referred to a psychiatrist, but the medications did not help. Finally an endocrinologist checked my antibodies and found that I had very high levels of thyroid antibodies, so my immune system was attacking and damaging my thyroid. I was put on thyroid medication. I also was referred to a neurologist who then diagnosed me with autoimmune encephalitis (brain inflammation), and I was treated with intravenous steroids (for immunosuppression). At the same time I started reading online a lot about autoimmune diseases and I came across articles about the AIP diet. I was feeling to unwell, so I decided that I had to change my lifestyle, and I started following the AIP diet strictly – no dairy, no gluten, no soy, no grains, no legumes, no nuts, no chocolate, no alcohol. There were a lot of restrictions! You can google this diet, if you are curious.

After the corticosteroid treatment and the diet change, I did start feeling better, I l also lost 20kg, but I still experienced a lot of symptoms such as irritability, leg spasms, feeling of numbness in my fingers, and insomnia. I ended up deciding that there was no scientific evidence for my dietary restrictions, and at some point I went back to eating dairy and gluten, as well as the rest of the foods. I ended up gaining 30kg, and starting to again experiencing paranoia, panic attacks, nightmares, and fatigue.

I recently decided to look into my diet again and instead of going into the extremes – such as the very strict AIP diet, I started with excluding dairy. I also realized that when I was dairy-free the first time, I did not consume any foods with calcium, and that could have been the cause of my muscle cramps and numbness in my hands. This time I looked into non-dairy sources of calcium and calculated how much of those foods I would need to be eating. I have now been dairy free since February, I also went gluten-free and soy-free, as I noticed through multiple observations, that those foods were also causing symptoms for me. I now no longer have any pains in the lower abdomen, I have more energy and was able to attend yoga classes. I have no symptoms of low calcium this time, as I eat canned sardines, canned salmon with bones, and powdered egg shells. I am feeling much better, and I have lost around 22 pounds since February.

A great story of recovery from Anti NMDA Receptor Encephalitis

I recently had someone contact me in regards to their relative who was in a hospital, diagnosed recently with autoimmune encephalitis. It was an ongoing situation, and therefore extremely painful for them. Probably unless you are in the neurology field, or immunology, you have never heard of autoimmune encephalitis, unless it happens to you or someone you know. Most people think of brain injury being caused by a physical accident, such as a sports injury, by stroke, or by dementia. Very few people could imagine that a young person, twenty or thirty years old, could also receive a brain injury, from the immune attack of their own body.

The person who contacted me described their relative as being young, and previously completely healthy. Going from that state, to being in a hospital, held down due to severe aggression and violence, is of course shocking. I was asked whether myself I ever recovered, whether I was able to work. The person was concerned that their relative does not love them anymore. They did say after our conversation that talking to me gave them some hope, given that I also had similar symptoms of aggression and violence, swearing, believing that my close people were making plans on how to get rid of me. Not being sure if they were actually real, whether they existed, or only in my thoughts. It’s hard to describe that experience. And then going back to a much more normal state – being able to spend time with people as usual, not constantly finding secret meanings in their words, not seeing predictive signs everywhere. I also sent that person a story of recovery that I found on YouTube, and I hope it will add more hope for them as well. The young woman in the story clearly had a very severe case of encephalitis, as she was not able to recognize her parents and some point, she ended up in a coma, and currently does not remember those several months of illness. Also she provides important information on treatment in the video – for her it was specifically a combination of two chemotherapy drugs, Cytoxan and Rituximab. I think it’s important to know, as IV steroids or IVIG may not work for all cases of encephalitis. It’s good to know about other available treatment options, which as you can see, in some cases lead to great recovery.

Anti NMDA Receptor Encephalitis – Amanda’s Rare Autoimmune Disease Story

 

Beautiful schizophrenia treatment success story

I found Quentin’s successful outcome in this story very hopeful. I don’t have schizophrenia, antipsychotics did not turn out to be useful for me, but it’s great to hear how they do work for many people with schizophrenia and how the outcomes can now be so different in comparison to the times before invention of antipsychotics. My psychosis has also mostly subsided since the treatment of encephalitis with intravenous steroids, prednisone, and intravenous immunoglobulin. I do have issues remaining with depression, but definitely the psychosis is maybe at the 5% level of what is used to be, and many times of the day no psychosis is currently present at all for me. Sometimes I even have thoughts – hey, maybe it wasn’t that bad, was I really that psychotic? Maybe I am exaggerating my story? But then I look back and yes, it was terrible, it was hell.

If you listen to Quentin’s story, I had actually very similar symptoms as he describes – I had persistent thoughts that my boyfriend and my parents were in danger and that only I had to protect them with my thoughts. Then also came the idea that me being anxious about their safety is increasing the danger, so they would be safer if I didn’t exist, because it was my thoughts that were putting them in danger. And these ideas were not occasional, they were persisting every second of the day. It’s easy to realize that it’s not possible to function or have any desire to live that way, especially if you are convinced that by being alive you are putting very close people to you in danger. I don’t really want to imagine what would happen to me if I didn’t figure out that I had encephalitis and wouldn’t get the immunosuppressant treatment, or what would happen to young people like Quentin before the invention of antipsychotics. I’m glad that his treatment story is a very positive one and that currently he is doing really well, studying for his engineering degree, doing an internship at a lab, and finding interest in life.

AFTER WINTER : A Real Life Schizophrenia Treatment Story

 

SSRIs, fungi, and exotic botanicals

This post is about comparing my experiences with fluoxetine (Prozac – an SSRI), psilocybe mushrooms, lion’s mane mushroom, and yerba mate tea. Of course this is my personal experience, not a medical study. Remember that everyone is affected differently by psychoactive compounds. In fact recently my friend told me an interesting scientific theory in regards to why humans differ a lot psychologically. Have you heard of fungi that make ants climb on top of a leaf, hook themselves, and stay there without eating, basically committing ant suicide? The spores of the fungi then burst from the ant and go on to grow into new fungi. Ophiocordyceps unilateralis is called the zombie-ant fungus.

“Researchers think the fungus, found in tropical forests, infects a foraging ant through spores that attach and penetrate the exoskeleton and slowly takes over its behavior.

As the infection advances, the enthralled ant is compelled to leave its nest for a more humid microclimate that’s favorable to the fungus’s growth. The ant is compelled to descend to a vantage point about 10 inches off the ground, sink its jaws into a leaf vein on the north side of a plant, and wait for death.

Meanwhile, the fungus feeds on its victim’s innards until it’s ready for the final stage. Several days after the ant has died, the fungus sends a fruiting body out through the base of the ant’s head, turning its shriveled corpse into a launchpad from which it can jettison its spores and infect new ants.”

So what does this have to do with humans being different? The theory says that humans evolved to react differently to same psychoactive molecules in order to not become victims to simple fungi organisms. Since the infectious fungi are not very complex organisms, they can only release so many molecules. By evolving to have complex brains and having individuals react differently to the same psychoactive molecule, humans became resistant to being overtaken by simple fungi. The theory is that there is no one molecule that a fungi could produce that would make all humans act the same, stop whatever they were doing, walk to a nice moist and wooded area, lie down, and wait for fungi spores to emerge from them.

Back to fluoxetine and shrooms

Fluoxetine

Fluoxetine is a selective serotonin reuptake inhibitor. N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine.  It delays the reuptake of serotonin, resulting in serotonin persisting longer when it is released. Also dopamine and norepinephrine may contribute to the antidepressant action of fluoxetine in humans.

From wiki: Fluoxetine elicits antidepressant effect by inhibiting serotonin re-uptake in the synapse by binding to the re-uptake pump on the neuronal membrane to increase its availability and enhance neurotransmission. Norfluoxetine and desmethylfluoxetine are metabolites of fluoxetine and also act as serotonin re-uptake inhibitors, so increase the duration of action of the drug. Fluoxetine appeared on the Belgian market in 1986. In the U.S., the FDA gave its final approval in December 1987, and a month later Eli Lilly began marketing Prozac.

fluoxetine

Fluoxetine is one of medications considered to be effective for PMDD (premenstrual dysphoric disorder). Also research indicates that low doses of fluoxetine could help with PMS. PMS appears to be triggered by the fall in secretion of the ovarian sex steroid hormone progesterone that occurs towards the end of the menstrual cycle and leads to a decline in its breakdown product allopregnanolone, which acts in the brain as a potent sedative and tranquilising agent. In other words, women with PMS are undergoing a type of drug withdrawal response from an in-built, tranquilising steroid chemical in their brains. New research shows that antidepressants such as fluoxetine inhibit a specific enzyme in the brain, which deactivates allopregnanolone, therefore maintaining the chemical balance of this in-built tranquiliser in the brain. Recent findings published in the British Journal of Pharmacology, show that short-term treatment with a low dose of fluoxetine immediately prior to the rat’s premenstrual period not only raised brain allopregnanolone and prevented the development of PMS-like symptoms but also blocked the increase in excitability of brain circuits involved in mediating the stress and fear responses that normally occur during this phase of the cycle.

Enzyme identified that could lead to targeted treatment for PMS

A review of studies found that fluoxetine was more tolerabled by female patients than tricyclic amine antidepressants (Amitriptyline, Imipramine). ” In this study, a retrospective analysis of 11 randomized, double-blind, well-controlled trials was done to compare data from 427 female patients on fluoxetine and 423 female patients on TCAs. Both fluoxetine and TCAs significantly reduced the HAMD17 total mean score from baseline to end point, week 5 (fluoxetine, 24.35 to 14.37; TCAs, 24.57 to 14.43; p < 0.001). Both treatment groups were associated with significant reductions in the HAMD17 anxiety/somatization and insomnia subfactor scores. Abnormal vision, constipation, dizziness, dry mouth, and somnolence occurred more frequently (p < 0.05) in the TCA group. Insomnia and nausea were the only adverse events more common (p < 0.05) in the fluoxetine group. This study demonstrates that fluoxetine is an effective and tolerable agent for the treatment of major depressive disorder in women.”

Fluoxetine vs. tricyclic antidepressants in women with major depressive disorder

My experience with fluoxetine – the first time that I took 10mg of fluoxetine, I felt a difference in less than three hours. It was as if I was taken out of a dark basement and into a sunny day in July. Unfortunately I also experienced insomnia that did not go away and I had a sense of apathy, in the end I stopped taking fluoxetine, but I know many women who swear by it.

Psilocybin

Next I will mention psilocybin. Psilocybin is a psychedelic compound produced by more than 200 species of mushrooms. Psilocybin is quickly converted in human body to psilocin. Psilocin is a prtial agonist for several serotonin receptors. An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response. Recently there has been increased reseach interest in psilocybin and how it could help with depression.

“A landmark study conducted by the Beckley/Imperial Research Programme has provided the first clinical evidence for the efficacy of psilocybin-assisted psychotherapy to treat depression, even in cases where all other treatments have failed. We gave oral psilocybin to 20 patients with treatment-resistant depression, all of whom had previously tried at least two other treatment methods without success. Participants had suffered from depression for an average of 18 years, with severity ranging from moderate to severe. Each patient received two doses of psilocybin (10 and 25mg) 7 days apart, accompanied by psychological support before, during, and after each session. All participants also underwent brain scans to investigate the neural underpinnings of psilocybin mechanisms of action on depression. Follow-up examinations were carried out at 5 weeks, and three and six months. Results highlights All patients showed some reductions in their depression scores at 1-week post-treatment and maximal effects were seen at 5 weeks, with results remaining positive at 3 and 6 months. Notably, reductions in depressive symptoms at 5 weeks were predicted by the quality of the acute psychedelic experience. The drug was also well tolerated by all participants, and no patients sought conventional antidepressant treatment within 5 weeks of the psilocybin intervention. While it is important to note that this was a relatively small study with no control group, placebo, or ‘blinding’ (meaning participants were fully aware what they were getting), the results are extremely encouraging and confirm that psilocybin is safe to give to depressed patients, warranting further research into this area.”

Sceletium tortuosum (Kanna) – a plant commonly found in South Africa.  Laboratory studies have found that Sceletium alkaloids are selective serotonin reuptake inhibitors (SSRIs). Thus, they have the same action as pharmaceutical SSRIs such as Prozac. Animal studies have found that Sceletium can improve mood and reduce anxiety-related behaviours.

 

 

Restarting probiotic foods

So I am restarting probiotic foods. I suppose I had a bad start when I went all in and started consuming everything at once – yougurt, kefir, sourdough, yeast supplements, probiotic capsules. I was also fermenting apples, vegetables, plantains, trying to make my own chickpea tempeh. Home fermentation could go wrong at some point, also I think the supplements were a bad choice. Maybe taking saccharomyces boulardii for a week could improve gut microbiome, but taking the capsules everyday for several months I think for me led to SIBO (small intestinal bacterial overgrowth, in this case there was also yeast).

I think at first when I started eating goat yougurt and drinking homemade kefir, I felt better. I remember there were several days when I was helping put up posters for a missing person – the man was my close friend’s co-worker. He was last seen at a bar on a Friday night but never made it home. I didn’t personally know the guy, but since I was putting up the posters and was part of a Facebook search group, I’ve learned a lot of details about his girl friend, his parents. A week later his body was found in lake Ontario and it really got to me. I know that this tragic ending of a search for a missing person would be painful for anyone in the search group, but with depression I think such event further triggers a cascade of negative thoughts about your own life. I didn’t know the guy, I didn’t know his parents, nor his girl-friend. It was their loss, this was not about me, but anxiety and depression always find a way to relate events to your own personal issues. I remember feeling overwhelmed with anxiety and physical pain, as if it was me who let something bad happened and now I would be punished for it. I couldn’t let go of the fear of punishment for things that were happening in the world. There was a sense that I had to fix them. Maybe when I was younger I would imagine that I have these feelings because I am a morally better person, but now I know that no, feelings of guilt and fear of punishment is depression showing through.

That weekend coincidentally was also when my first batch of goat kefir was ready. The day when I tried the first cup of kefir, I had continued sense of guilt and fear. I felt guilty for trying to feel well when such tragic things were going on in the world. I have already been through a lot of cognitive behavioural therapy by that point, so logically I understood that I was not obliged to feel unwell or be responsible for the world,  but the feeling was still there. This was more than a year ago, but I do remember feeling more calm the next day after starting goat kefir and letting go of some of the guilt. It wasn’t a complete relief, but I remember  no longer feeling overwhelmed and on the verge of tears.

Studies on probiotics and mental health are inconclusive. “A recent article in Annals of General Psychiatry reviewed the currently available medical literature on using probiotics to treat anxiety and depression. The doctors identified 10 studies that were well done (in other words blinded and placebo-controlled), and looked at each study in depth. All of these studies had relatively small numbers of patients, ranging as from as few as 42 to as many as 124. The results of these studies were mixed; some suggested that there may be mild benefits of taking probiotics if you have anxiety or depression while other studies showed no benefit. Overall, the authors concluded “the clinical effects of probiotics on mental health have yet to be studied comprehensively.” 

Can probiotics help treat depression and anxiety?

Probably just adding kefir to your diet will not cure mental issues, but I do enjoy drinking it, the sour yet creamy taste. It is also a source of calcium and protein. A glass of kefir has less sugar than a glass of milk since the bacteria and yeast from kefir grains break down the milk sugar lactose and convert it into lactic acid. “The only sugar naturally present is milk is lactose (is a sugar composed of galactose and glucose subunits). Most microorganisms lack the enzyme lactase which is required to break lactose into its two component sugars, namely, glucose and galactose. Lactic acid bacteria which do have lactase readily break down lactose and use glucose as an energy source. Lactic acid bacteria, therefore, have a competitive advantage in milk; that is, they are able to out grow other bacteria which are unable to obtain glucose from lactose. Further, some lactic acid bacteria are able to convert galactose to glucose.” Therefore when we drink kefir, the bacteria had already used up glucose and galactose for energy and therefore we don’t get glucose from the drink. When humans drink milk, it contains the sugar lactose. We have a protein named lactase that is produced in our small intestine. Lactose is then broken down by lactase into galactose and glucose, which is then absorbed into bloodstream. Therefore drinking non-fermented milk raises blood sugar more than kefir.

Is it safe to make kefir at home?

The good news is that fermentation of warm milk by lactic acid bacteria reduces milk pH to less than 4.0 and in turn makes the environment unlivable for pathogenic bacteria. Most organisms grow best at pH near physiological pH of 6.8, and not in acidic environments. I assume it would be great though for microbes from Yellowstone National Park acidic pools. these pools are usually of temperature ranging from 65 to 90 degrees Celsius and contain high sulfur contents, either as hydrogen sulfide (H2S(g)) emitted as a volcanic gas, or as elemental sulfur crystals. Who lives there – thermoacidophiles, a unique group of bacteria that are a combination of acidophiles and thermophiles. Thermoacidophiles are characterized by their exclusive ability to live in both highly acidic environments and also high temperatures. The typical conditions these thermoacidophiles live under include pH at around 2 with temperatures ranging from 80 to 90 degrees Celsius.

I am not sure if thermoacidophiles  are likely to contaminate homemade kefir, but I do sterilize my jars by pouring boiling water over them. Then I let the jar cool, place the kefir grains in, pour in milk, and cover with a coffee filter. I ferment my kefir at room temperature for 24 hours. Kefir is a versatile food as it can be drank on its own, used for smoothies, used to make tvorog (quark), syrniki (fried quark pancakes), and oladyi (fritters). Easy breakfast recipe – in the evening combine kefir, sorghum flour, ground oatmeal, egg, salt, and avocado oil in a bowl and let it stand overnight in the fridge. In the morning preheat a frying pan and then use the dough for fritters. Consume with honey and yougurt on top.

Who inhabits kefir?

The kefir grains initiating the fermentation consist of a symbiotic culture of lactic acid bacteria and yeasts embedded in a matrix of proteins, lipids, and polysaccharides. The matrix is formed by microbial activity, with color ranging from white to creamy yellow. Grains can include lactic acid bacteria, acetic acid bacteria, and yeasts. During fermentation, changes in the composition of ingredients occur. Lactose, the sugar present in milk, is broken down mostly to lactic acid (25%) by the lactic acid bacteria, which results in acidification of the product. Propionibacteria further break down some of the lactic acid into propionic acid. Other substances that contribute to the flavor of kefir are pyruvic acid, acetic acid, diacetyl and acetoin (both of which contribute a “buttery” flavor), citric acid, acetaldehyde, and amino acids resulting from protein breakdown. The slow-acting yeasts, late in the fermentation process, break lactose down into ethanol and carbon dioxide. Usually ethanol concentrations are 0.2–0.3%, so kefir is not much of an alcoholic beverage.

Probiotic bacteria found in kefir products include: Lactobacillus acidophilus, Bifidobacterium bifidum, Streptococcus thermophilus, Lactobacillus delbrueckii subsp. bulgaricus, Lactobacillus helveticus, Lactobacillus kefiranofaciens, Lactococcus lactis, and Leuconostoc species. Lactobacilli in kefir may exist in concentrations varying from approximately 1 million to 1 billion colony-forming units per milliliter, and are the bacteria responsible for the synthesis of the polysaccharide kefiran. In addition to bacteria, kefir often contains strains of yeast that can metabolize lactose, such as Kluyveromyces marxianus, Kluyveromyces lactis, and Saccharomyces fragilis, as well as strains of yeast that do not metabolize lactose, including Saccharomyces cerevisiae, Torulaspora delbrueckii, and Kazachstania unispora.

Kefir is made by adding kefir grains to milk typically at a proportion of 2-5% grains-to-milk. The mixture is then placed in a corrosion-resistant container, such as a glass jar, and stored preferably in the dark to prevent degradation of light-sensitive vitamins.

Hymenolepis diminuta observations and paper

As described in my previous posts, I have started HDC helminth therapy on June 4th. It has now been over a month. So far I have taken HDC three times – 10 on June 4th, 10 on June 9th, and 20 on June 25th. I have also updated my NA by adding three more on July 6th. It has now been over two weeks since my last HDC dose, helminth therapy wiki suggests dosing every two weeks and adult dosing is in range 30-60 HDC bi-weekly. I am waiting for my next order of 20, the delivery has been slow, and it’s expected to arrive on Friday. After that I plan to increase the dose to 30 as is advised, 20 may be not enough of a therapeutic dose for an adult.

One important observation is that during my period, which happened soon after the third dose of HDC, I did not have to take any pain relievers. I see this as not just a coincidence because last such occurrence happened almost a year ago in July 2018, after I started NA therapy. After that one time unfortunately pain levels during periods went back to usual unbearable and as usual I would take at least two Naproxen gels, sometimes also an ibuprofen. Several times I had to leave work early or work from home. Therefore I was quite surprised that when my period occurred in the end of June the pain began as usual but did not increase to unbearable levels. I went to work as usual, I always keep Naproxen in the drawer in the office and at home, but the pain never rose to the level where I would need a pain killer. I would say that just for this benefit HDC is already worth continuing as not being crippled by pain made me feel more free. Even though it’s not my fault, I often feel guilty leaving home early or asking to work from home every month. I am also not pleased with having to take Naproxen as for me it causes acid reflux and it makes me think that I am undoing the benefits of my efforts to heal the gut.

Another observation was recently increased heat tolerance.  In beginning of July temperatures rose to over 30 degrees Celsius and there is no central AC where I live. In order to cool down the house, I usually have to install two window air conditioner units. These units were taken down for the winter, so there were several days of temperatures around 30 degrees inside. I noticed that my sleep was not as disrupted as it previously would during heat. Also in general I was not as incapacitated by the temperature, I did feel lethargic, but did not have as severe indecisiveness nor mood swings exacerbation that often occur for me during summer heat.

The new lab test results are also encouraging. Free T4 and T3 stayed at the same levels, within normal range. TSH went down to 2.0, which is below the previous value of 2.58. This is a positive result, since some research indicates that the optimal cut- off value of TSH is 2.5 MIU/L. Anti-TPO antibodies have also decreased.

TSH cut off point based on depression in hypothyroid patients

test_jul2019

On a side note, I found that someone wrote their undergrad honors thesis on Hymenolepis diminuta. “Impacts of Hymenolepis diminuta (benign helminth worm) colonization on chronic pain and the central nervous system in Sprague Dawley rats“. If I would go back in time, I would prefer to also study neuropsychology. Unfortunately in my undergrad I was calculating bond and option prices. Glad to hear whenever someone is doing research on treatments for autoimmune disorders, specifically the connection between neuropsychiatric problems and inflammation. “The results from this project partially support the tenets of the hygiene hypothesis. Though behavioral results following CCI surgeries were inconclusive, molecular investigation of cytokine levels in the hippocampus showed promotion of an anti-inflammatory cytokine milieu due to the upregulation of IL-10 and downregulation of its receptor. These promising results guide future research toward investigation of cytokine levels in other brain regions, such as the amygdala.“

Impacts of Hymenolepis diminuta (benign helminth worm) colonization on chronic pain and the central nervous system in Sprague Dawley rats

HDC Therapy for autoimmune disorders

HDC, hymenolepis diminuta cysticercoids, is a larvae stage of a nice and friendly rat tapeworm, an adult of this species can be 20-60cm long. You might have a thought now “what am I reading and why?”, but hold on. Humans are not the usual host of hymenolepis diminuta, rats are, and in humans this helminth does not develop into an adult. There have been very few cases documented of humans being infected with adult HD. For this reason the HD larvae, HDC, is one of the species chosen for helminthic therapy as it does not reproduce inside humans, stays in the gut, does not reach adult size, and yet modulates the immune system as it tries to survive.

HDC survive in humans only for about two weeks, therefore for continuous therapy, HDC would need to be ingested at these intervals. HDC will live in the small intestine and attach to the intestine wall. There are no reports in the scientific literature of H. diminuta mis-migrating to other organs in humans. In a scientific review of helminthic therapy from 2016, HDC was listed as one of the more popular helminths:

“Five physicians monitoring more than 700 self-treating patients were interviewed. The results strongly support previous indications that helminth therapy can effectively treat a wide range of allergies, autoimmune conditions and neuropsychiatric disorders, such as major depression and anxiety disorders. Approximately 57% of the self-treating patients observed by physicians in the study had autism. Physicians reported that the majority of patients with autism and inflammation-associated co-morbidities responded favourably to therapy with either of the two most popular organisms currently used by self-treaters, Hymenolepis diminuta and Trichuris suis. However, approximately 1% of paediatric patients experienced severe gastrointestinal pains with the use of H. diminuta, although the symptoms were resolved with an anti-helminthic drug. Further, exposure to helminths apparently did not affect the impaired comprehension of social situations that is the hallmark of autism. These observations point toward potential starting points for clinical trials, and provide further support for the importance of such trials and for concerted efforts aimed at probing the potential of helminths, and perhaps other biologicals, for therapeutic use.“

Practices and outcomes of self-treatment with helminths based on physicians’ observations

Here is another paper from 2017 reviewing HDC use by self-treating individuals. Unfortunately there are not many clinical trials with treatment and control groups, therefore we have to rely on information on experiences from people like me who are obtaining helminths and treating themselves. ” In this study, we describe the production and use of HDCs in a manner that is based on reports from individuals self-treating with helminths, individuals producing helminths for self-treatment, and physicians monitoring patients that are self-treating.” The authors from Duke University are quite optimistic about helminthic therapy: “Helminthic therapy, the use of helminths to treat disease, offers the best hope of decreasing inflammation via immunomodulation rather than immunosuppression, and probably also improves mucosal barrier function.”

Production and Use of Hymenolepis diminuta Cysticercoids as Anti-Inflammatory Therapeutics

I was glad to read that I already have access to the most hopeful treatment for inflammation. I have to say that I tried a lot of supposedly anti-inflammatory treatments  and was quite disappointed with most. Turmeric lattes, green tea extract, probiotic capsules, licorice root tincture…  Personally, I don’t really want to buy any more supplements, except basic ones such as vitamin D, since I live in cold and dark Canada, and occasionally I take fish oil on days that I don’t eat seafood.

The idea behind helminthic therapy, on the other hand, is quite logical to me. It’s not a promotion of another one magical super inflammatory ingredient. The logic is that humans and certain helminths have evolved to co-exist in a symbiotic relationship and therefore our immune system has also evolved  to be modulated by molecules that helminths produce. Recent eradication of helminths in humans in developed countries could be resulting in a destruction of a beneficial symbiotic relationship and increase in rate of autoimmune diseases.

“Graph the data points, and the trend is unmistakable. Since the 1950s, rates of multiple sclerosis, Crohn’s disease, type 1 diabetes, and asthma have soared by 300% or more (1). Similar graphs depict concurrent spikes in hay fever and food allergies (2).”

“Prevalence of food allergy in preschool children is now as high as 10% in Western countries, but remains just 2% in areas like mainland China (). The number of new cases of type 1 diabetes (T1D) in Finland per year is 62.3 per every 100,000 children, compared with just 6.2 in Mexico and 0.5 in Pakistan (). Ulcerative colitis, a form of inflammatory bowel disease (IBD), is twofold higher in Western Europe than in Eastern Europe—6.5 per 100,000 people versus 3.1 per 100,000 ().”

In each of these disorders, either the immune system is overreacting to a trigger, such as pollen, peanuts, or pollution, or it’s attacking tissues it shouldn’t, such as beta cells in the pancreas in the case of T1D and in the intestines in IBD.”

News Feature: Cleaning up the hygiene hypothesis

 

Celiac disease, vitamin and mineral deficiencies, and a beef patty

I’ve done something today that I probably haven’t done for at least a year or more. I bought a beef patty. I felt very guilty because I don’t want to eat large mammals. Ideally I wouldn’t eat any birds or animals, but we have to make practical choices. From my experience, having celiac disease, I don’t absorb vitamins and minerals well. A chicken leg of 100 grams has approximately 6% daily value of cobalamin, 6% DV magnesium, 7% DV potassium, and 25% DV B-6. Without eating meat or fish, you could try to get vitamin B-6 from beans, also fortified cereals contain B-6. Here is the issue – with celiac you cannot eat most fortified cereals and breads since they are not gluten-free, also eating too many beans causes digestive problems. So I had to make a choice and about a year ago  I chose to eat seafood and poultry, but not mammals. My reasoning is that compared to chickens and turkeys, large mammals such as pigs and cows have more complex brains and nervous systems and therefore have more complex emotions and might suffer more during their short life in a cage at a factory farm. I have no proof of that, but I had to make a choice.

Unfortunately recently I had to make another choice to start eating red meat again. I was experiencing lethargy and noticed white bands on my nails. Some sources stated that white spots on nails could be a sign of zinc deficiency, while others indicated that there was no correlation. This did lead me to wondering whether I was getting enough zinc, selenium, and B vitamins from chicken and salmon. 100 grams of beef on average contain 43% DV (daily value) of B12, 20% DV of B6. Dietitians of Canada also list beef as top sources of zinc, 75 grams of beef containing 4.0 – 8.6 mg of the mineral (women need 8 mg per day).  Chicken is much lower in zinc, 1.3 – 2.2 mg per 75 grams. Salmon was not listed as it is not a good source of zinc, it contains about 0.64 mg per 100 grams. Some studies indicate that it’s harder to absorb zinc from a plant based diet, in addition to that my absorption may be worse due to gut inflammation caused by autoimmune disease.

“With reduced intake of meat and increased intake of phytate-containing legumes and whole grains, movement toward plant-based diets reduces dietary iron and zinc absorption.“

Moving Toward a Plant‐based Diet: Are Iron and Zinc at Risk?

zinc1

Why do we need zinc and what happens if there is a zinc deficiency? Zinc is found in cells throughout the body and is needed to make proteins and DNA. Zinc plays a role in cell division, cell growth, wound healing, and the breakdown of carbohydrates. It is important for the function of the immune system and also the senses of smell and taste.

zinc2

Zinc deficiency can cause appetite loss, poor immune system function, diarrhea, eye and skin lesions, feeling lethargic, strange taste sensations, hair loss, weight loss, poor wound healing. Individuals with chronic conditions and poor absorption are more likely to be zinc deficient.

Zinc performs its biochemical functions as a divalent cation (positively charged ion) primarily when bound to enzymes and other proteins. Zinc is essential as a catalytic, structural, and regulatory ion and is involved in homeostasis (the tendency to maintain a stable, relatively constant internal environment), immune responses, oxidative stress, apoptosis (the death of cells which occurs as a normal and controlled part of an organism’s growth or development), and aging. Zinc is recognized as being important for stabilizing DNA and appears to reside in the nucleus longer than any other cell compartment. Therefore, it is possible that as intracellular levels of zinc increase, more iron will be displaced from nucleoproteins and less OH-driven DNA damage will occur.

Biological consequences of zinc deficiency in the pathomechanisms of selected diseases

A study on zinc deficiency in relation to psychiatry:

“Zinc participation is essential for all physiological systems, including neural functioning, where it participates in a myriad of cellular processes. Converging clinical, molecular, and genetic discoveries illuminate key roles for zinc homeostasis in association with clinical depression and psychosis which are not yet well appreciated at the clinical interface. Intracellular deficiency may arise from low circulating zinc levels due to dietary insufficiency, or impaired absorption from aging or medical conditions, including alcoholism. A host of medications commonly administered to psychiatric patients, including anticonvulsants, oral medications for diabetes, hormones, antacids, anti-inflammatories and others also impact zinc absorption. Furthermore, inefficient genetic variants in zinc transporter molecules that transport the ion across cellular membranes impede its action even when circulating zinc concentrations is in the normal range. Well powered clinical studies have shown beneficial effects of supplemental zinc in depression and it important to pursue research using zinc as a potential therapeutic option for psychosis as well. Meta-analyses support the adjunctive use of zinc in major depression and a single study now supports zinc for psychotic symptoms.”

The Emerging Role for Zinc in Depression and Psychosis

From my own experiment with N=1, I did feel better after eating a beef patty. This could be a coincidence, a placebo effect, or an actual effect of the minerals/vitamins in beef on my mood. I also thought of a substitute for beef that is not a mammal – mussels and clams. A 3-ounce serving of cooked mussels contains about 15% of daily value of zinc. The same amount of moist-cooked clams also provides 15% of the daily value for zinc. Clams and mussels contain high amounts of vitamin B12, selenium, and iron, as well as omega-3 fats. I think therefore it’s possible for me to continue avoiding beef if I include chicken, fish, mussels, and clams.

Green tea vs. infliximab and tracking thyroid antibodies

I continue to track my thyroid antibodies and I will post my results here in case this information will be useful for anyone. Trust me, I know how fluctuating thyroid hormones suck and what it means for you in terms of your mood, energy, sleep. Today is a work day and since my work place is quite formal, I should be there by 9am. Nine to five, the usual. Well I couldn’t fall asleep until 1am and woke up at 6am. I felt cold shivers and my palms were sweaty. I lay in bed for a while but it was no use, I could not fall back asleep. I did get to work slightly after 9, not very late, sat down in my cubicle, turned on my screens and stared at the code. What was I supposed to be doing today? I had forgotten. My hands continued to sweat and I had chills. Emotionally I felt as if a train had run over me. I couldn’t remember on what task I stopped at on Friday. I sensed such fatigue that I was finding it difficult to sit up straight.

Logically I knew the cause, it all happened as my endocrinologist said it would. After a period of hyperthyroidism, my TSH went to almost non-existent level and now instead of being too high, my thyroid hormones were quickly dropping. Lab test on February 1st showed that free T4 and total T3 were near their lower threshold and TSH was also low. Since TSH continues to be low, and it is the thyroid-stimulating hormone, it was not stimulating the thyroid enough to produce T3 and T4. Therefore it’s likely that today hormone levels were even lower and I went into hypothyroid state.

test_feb2019

So this is what’s going on with my thyroid. I think the hypothyroidism symptoms are definitely starts as I have been getting chills, freezing even when my thermostat is at 24 degrees, not having the energy to talk to people even though I did not want to stay home on a Friday night. In theory, according to my endocrinologist, after an acute hyperthyroidism again, there will be not enough thyroid hormones stores in the thyroid gland, and therefore levels will fall. After sometime function should restore to normal, but hypothyroid state could last 8 months. I will be waiting for this normalization and in the meantime I will keep trying to reduce inflammation, because what else is there left to do.

Recently I came across a paper on green tea and exercise intervention for arthritis patients. “One-hundred and twenty subjects who had a mean age of (60.7 ± 2.53 years) and had been diagnosed with rheumatoid arthritis at least ten years previously were randomly included in this study. Patients were treated with infliximab, green tea, or a supervised exercise program for six months. Disease activity markers as well as antioxidant activity of green tea extracts were estimated before supplementation using in vitro assays. [Results] Rheumatoid arthritis patients treated with green tea for 6 months alone or in combination with infliximab or an exercise program showed significant improvement in disease activity parameters, including C-reactive protein, and erythrocyte sedimentation rate, swollen and tender joints counts, and modified Stanford Health Assessment Questionnaire score, along with an increase in serum levels of bone resorption markers, i.e., deoxypyridinoline, amino-terminal telopeptide of type 1 collagen, and bone alkaline phosphatase, at 6 months of after initial treatment. The European League Against Rheumatism and American College of Rheumatology scores revealed more clinical improvement in the disease activity of rheumatoid arthritis patients treated with green tea along with exercise compared with rheumatoid arthritis patients treated with infliximab or exercise combinations.”

Green tea and exercise interventions as nondrug remedies in geriatric patients with rheumatoid arthritis

I know this is just one study and we should take the results with a grain of salt, but I see no harm in including green tea and exercise in your day. I want to note that I am not looking for only ‘natural’ treatments neither am I trying to prove that they are better. I am only looking for something that I can implement. When I was referred for IV corticosteroids treatment, I was happy to receive it and did see improvements. Since then I have not been prescribed any treatment even though I did ask for it. It’s possible that something like infliximab would work for me, but I have no access to it. I have Hashimoto’s thyroiditis, celiac disease, and autoimmune encephalopathy, but inflixiamab is a medication that is prescribed for rheumatoid arthritis.

Infliximab is a monoclonal antibody that suppresses some parts of the immune system. Infliximab is a lab made molecule that binds to a specific cytokine TNF-α (chemical messenger), which is one of the causes of autoimmune reaction. TNF-α is tumor necrosis factor aplha, a cell signaling protein involved in system inflammation. Wiki states that Dysregulation of TNF production has been implicated in a variety of human diseases including Alzheimer’s disease, cancer, major depression, psoriasis and inflammatory bowel disease (IBD). Though controversial, studies of depression and IBD are currently being linked to TNF levels.

Infliximab has to be given as IV and cannot be taken orally as it would be destroyed by the digestive system. In the US the cost is about $19,000 per month and is mainly prescribed to arthritis patients who have not responded to other therapy. No one is going to prescribe it to me here in Canada.

Therefore, given that I have not been prescribed any meds at this point, and my psych and neuro keep debating whether to place me on IVIG or not, for now I have to do things on my own. Also trying green tea and exercise of course doesn’t cancel out any other treatment that I might get. I continue with helminthic therapy and hopefully I will get an IVIG trial (intravenous immunoglobulin therapy).