Developing a schedule for a healthier pregnancy

Pregnancy can be very difficult, especially if you already have chronic health problems. Personally, I felt very sick starting week three, and until around week 12 – 13. The sickness presented itself in terms of nausea, extreme fatigue, and increased anxiety. Only once I started to feel less nauseous, I was able to go back to my regular diet which limits refined carbs and continue with intermittent fasting again. I did then also start feeling worse in the third trimester, around after week 34. From my experience, these are the actions which have helped me to feel better:

  • Start taking folic acid as soon as possible, preferably before conception. Folic acid supplementation has been found to reduce neural tube defects, as well as congenital heart defects. Taking folic acid supplement every day can provide a positive feeling that you are doing the right thing for your baby’s health.
    From Health Canada: “Folic acid is vital to the normal growth of your baby’s spine, brain and skull. Taking a daily vitamin supplement that has folic acid can reduce the risk of your baby having a neural tube defect. The benefits of taking folic acid to reduce the risk of NTDs are highest in the very early weeks of pregnancy. At this stage, most women do not know they are pregnant. For this reason, taking folic acid before you become pregnant and in the early weeks of pregnancy is very important.”
    Recent studies have shown that high folate intake is associated with a reduced risk of birth defects other than NTDs. Higher maternal folate or periconceptional use of folic acid is associated with a lower risk of congenital heart defects (20-23) and oral clefts (24). A recent meta-analysis of 1 randomized controlled trial, 1 cohort study, and 16 case-control studies has shown that maternal folate supplementation is associated with a lowered CHD risk (RR =0.72, 95% CI: 0.63–0.82) (25). However, the results showed considerable heterogeneity, but after excluding the outliers the risk estimate was almost unchanged: the corresponding pooled RRs were not materially altered (RR =0.78, 95% CI: 0.69–0.89) (25).,and%20oral%20clefts%20(24).
  • Iron supplements – Iron deficiency is the most common nutritional deficiency during pregnancy. It happens most often during the third trimester. The iron in meat, fish and poultry is the easiest for our bodies to absorb and use. Foods rich in vitamin C help you absorb more iron. You can start taking an iron supplement during pregnancy in order to make sure you get enough and to prevent anemia. Low iron can lead to more fatigue, shortness of breath, weakness, headache, dizziness. All these symptoms in turn can make you more depressed. If low iron will lead to anemia, there will not be enough hemoglobin, and less oxygen will get to your cells. Cells won’t be functioning properly, and this can also contribute to depression and anxiety.
  • Prenatal vitamins – you can easily buy prenatal vitamins in a pharmacy or online. Nutritional yeast flakes also contain multiple vitamins. I’ve experienced more and more lethargy in the third trimester, and I started adding small doses of nutritional yeast flakes to smoothies. I have the Bob’s Red Mill brand, it is fortified inactive yeast, contains high doses of B vitamins – thiamine, riboflavin, niacin, B6, folate, and B12. It’s very cheap, given that the whole pack was around $8, and I consume less than a teaspoon a day, as the vitamin concentration is very high. I don’t see the need to take more than the needed daily value of B vitamins. I found that actually taking overly high doses of B vitamins for me can lead to panic attacks. Small doses of nutritional yeast do help me with energy during the third trimester, it can get me out of a very lethargic vegetative state to at least being able to wash the dishes, write in my blog, etc.
  • Sleep more – pregnancy can cause extreme fatigue. I found that instead of 7 – 8 hours, I currently need to sleep 9 hours. It helped me to start going to bed earlier, before 12am, then I am able to wake up for work before 9am. I also found that staying asleep became more difficult, I would wake up at around 4:30am, unable to fall back asleep. What helped me is eating the last meal four hours before bed, and the meal consisting mostly of non-refined starch, and not a lot of protein. The best sleep occurs for me if I eat short grain brown rice or potatoes (not fries) with something for dinner. Some studies mention that it is the prebiotic foods which can help sleep. “More commonly eaten foods that contain prebiotics include asparagus, onions, garlic, cashews, pistachios, and cooked and cooled grains and potatoes.” On the other hand, I found that eating cheese or red meat in the evening causes nightmares for me during the night, therefore I only eat those foods earlier on in the day.
  • Foods for anxiety – even though there is no recommendation to completely avoid coffee during pregnancy, I had to stop drinking any coffee as it would increase my anxiety more than before pregnancy. I also had to figure out which foods exacerbate acid reflux, which got worse. Ongoing acid reflux would make it uncomfortable for me to sit, lie down, sleep, and relax. It’s hard to calm down and do any breathing exercises, or just read a book, if your throat is burning, and you feel acid going up. I had to stop eating chocolate, spicy foods, coffee, black tea, lemon, soups, and meals containing a lot of tomatoes. I found oolong tea to be a good option. I also found helpful choosing complex carbs over refined carbs – making my own oat whole wheat pancakes, eating brown rice, potatoes, lentil pasta, plantains. Eat some protein with each meal.
    From the Mayo Clinic: “Carbohydrates are thought to increase the amount of serotonin in your brain, which has a calming effect. Eat foods rich in complex carbohydrates, such as whole grains — for example, oatmeal, quinoa, whole-grain breads and whole-grain cereals. Steer clear of foods that contain simple carbohydrates, such as sugary foods and drinks.
    I also had to stop consuming all dairy products, I noticed they were making my anxiety worse, as well as increasing brain fog. Again, from the Mayo Clinic:
    Pay attention to food sensitivities. In some people, certain foods or food additives can cause unpleasant physical reactions. In certain people, these physical reactions may lead to shifts in mood, including irritability or anxiety.
  • Food sensitivities – if you are avoiding any foods due to food sensitivities, make sure you get enough nutrients from other foods. I used to eat dark chocolate, which contains a lot of magnesium, but had to stop due to acid reflux. I made sure to eat other magnesium containing foods such as peanuts, bananas, and flax seeds. I also had to stop consuming any dairy, as I noticed that it was increasing my anxiety, rumination, and brain fog. I had to start consuming fortified soy milk, tofu, dairy-free yogurts, etc., in order to get calcium. I also took calcium supplements, and made my own supplement from egg shells.
  • Exercise – an important step with exercise, as with all pregnancy symptoms/issues in general, for me was acceptance. Acceptance that I could no longer do what I used to do several weeks ago. I used to dance for my mental health, because I enjoy reggaetón, and moving freely, and aerobic exercise is supposed to reduce depressive symptoms. I had to accept that I could no longer do that on most of the days due to nausea, fatigue, migraines. But still when I could, I tried to move – going for a walk near my house, going up and down the stairs (the house where I live has a staircase), doing a physical chose – washing the floor, vacuuming. Some movement is better than no movement at all, and I accepted that is it the situation right now, but it is also temporary.
  • Mindfulness – sometimes you cannot solve a problem. I have been feeling pretty lethargic throughout the whole pregnancy, especially in the third trimester. I was also not able to resolve the acid reflux issue and the stuffy nose, only reduce the symptoms somewhat. Mindfulness helps to observe your experiences from the side and accept that these are the current sensations/emotions/symptoms. I think observation can help realize how negative symptoms come in waves, so that you don’t end up generalizing or catastrophizing – “every day is terrible”, “I always feel awful”. I’m also mindful of the fact that I chose to be pregnant, as my goal is to have my own family, therefore this is something I have to go though in order to achieve my goal. I also remind myself that pregnancy is definitely a temporary condition, no one has stayed permanently pregnant.

It’s not always about some serotonin imbalance… let’s pay more attention to neurology

I get articles recommended by my Anroid phone, I assume based on an algorithm that performs some sort of machine learning model based on my browsing history. I actually like this feature, because I find the recommendations often actually interesting. So thumbs up for machine learning!

Today I came across an article about a woman with recurring severe depression, and in her case for many years no medical tests were performed, and her psychiatrist kept prescribing her different kinds of antidepressants, without considering any other potential causes or treatments. This reminds me of my own experience with autoimmune encephalitis, luckily I did get treated after two years from my first hospitalization in the psychiatric unit, not after more than a decade. In the case of this woman, eventually a brain tumour of a significant size was found, in 2019. She had recurring episodes of severe depression starting from 2002. As I understood, it’s not possible to find out at this point when the tumour actually originated, and whether it was the cause of depression, but it’s clear from the story that after the treatment of the tumour, the woman’s life significantly improved – she went back to her scientific career, finding a job as a scientist in a biotech firm. She got married, resumed activities she used to enjoy, and was weaned off antidepressants. Given these observations, it seems to me that the tumour and her depression were not just a correlation, but there is a causation here.

Unfortunately it seems rare that psychiatrists would order any medical tests even in the case of treatment resistant depression. I had to switch a few family doctors, and in the end went to one whom my mother knows for decades, and she agreed to order an MRI for me, and blood tests for thyroid hormones, infections, and antibodies. My psychiatrist never proposed to do any tests. Only after I received back the results, and some of them were abnormal, specifically the antibody levels, I was able to refer myself to neurology. Seems that we, psychiatric patients, have to often be very proactive in demanding medical testing. For this reason I think it is important to be aware of cases where depression was resistant to standard antidepressant treatments, but later on a specific medical cause was found.

Not ‘just depression.’ She seemed trapped in a downward mental health spiral.

  • Blaine’s first bout of depression occurred in 2002 when she was in her first year of a doctoral program in materials science at the University of California at Santa Barbara
  • She was prescribed Prozac, recovered and returned to California. Six months later she left school for good and found full-time work in a coffee shop
  • In 2005, Blaine began working as a research associate at a polymer film company
  • Her illness seemed to follow a pattern: after a few years the antidepressant inexplicably stopped working; her psychiatrist would prescribe a new drug and she would get better
  • In 2018 Blaine had lost her job of 10 years and she seemed trapped in a downward spiral
  • She left her job as a research scientist in 2018 and began working as a server at a variety of restaurants in Charlottesville
  • By late summer Blaine had developed what she assumed were frequent migraine headache, sometimes her balance was off and she complained that her vision had deteriorated and she needed new glasses, psychiatric medication was not effective
  • On Jan. 2 2019, a hospital psychiatrist doubled the dose of her antidepressant
  • Several days later Blaine suddenly collapsed and began vomiting, at the ER where she was diagnosed with a “vasovagal episode” — fainting that results from certain triggers including stress
  • Her sister and mother insisted doctors take a closer look, Blaine underwent an MRI scan of her brain
  • MRI findings showed a tumor the size of an orange had invaded the right frontal lobe of Blaine’s brain, there was evidence of herniation, a potentially fatal condition that occurs when the brain is squeezed out of position
  • During a 10-hour operation, University of Virginia neurosurgeon Ashok Asthagiri removed a grade 2 astrocytoma, a slow-growing malignancy that he said “could have been there for years.”
  • “especially in the setting of mental illness,” the neurosurgeon cautioned, “it is easy to disregard symptoms that maybe should be evaluated.” Doctors “need to be vigilant. Once [a patient] gets labeled, everything is viewed as a mental health problem.”
  • After recovering from surgery, Blaine underwent radiation and chemotherapy; she finished treatment in December 2019
  • Recently Blaine was hired as a scientist at a biotech firm. She has resumed the activities she previously enjoyed: rowing, cooking and walking her dogsHer psychological health has improved significantly and her new psychiatrist is weaning her off her antidepressant

More articles on this subject:

Why are women with brain tumours being dismissed as attention-seekers?

  • Women with serious medical conditions are more likely than men to have their symptoms attributed to depression and anxiety
  • Historically, women’s health has been viewed with a “bikini approach”, the primary focus being breasts and the reproductive system
  • One study drew data from 35,875 cardiac patients, 41% of them women, across nearly 400 US hospitals. It found that women faced a higher risk of dying in hospital, subsequent heart attacks, heart failure, and stroke. They were less likely to have an ECG within 10 minutes and to receive crucial medications. And women younger than 65 years old are more than twice as likely to die from a heart attack than men of the same age
  • A Bias Against Women in the Treatment of Pain, found that women were less likely to receive aggressive treatment when diagnosed, and were more likely to have their pain characterised as “emotional,” “psychogenic” and therefore “not real”

Woman misdiagnosed with anxiety actually had a brain tumour the size of a tennis ball

  • Laura Skerritt, 22, began suffering migraines, sickness and psychosis and was told her symptoms were caused by anxiety, depression – and even bi-polar disorder
  • She was prescribed anti-depressants but the medication had no effect on her condition which continued to deteriorate
  • By November 2018, the young swimming instructor, from Templecombe, Somerset, was struggling to walk and was having seizures.
  • A scan at Yeovil District Hospital revealed a tennis ball-sized brain tumour

Brain tumor revealed by treatment-resistant depression

  • The 54-year-old woman had been depressed for 6 months, but treatment with the antidepressant fluoxetine and the anti-anxiety medication bromazepam was discontinued after 5 months because these were not found to be effective
  • She had suicidal thoughts, admitted self-accusation due to ineffectiveness in her job, and lost interest in her usual past times
  • A neurological examination was normal. However, a brain CT scan and MRI revealed meningiomatosis with a giant meningioma–the most common primary benign brain tumour–in her left frontal lobe
  • The patient underwent emergency surgery, and made a recovery. The depressive symptoms disappeared within one month
  • Recommendation – brain scan should be performed if the patient presents a late onset of depressive syndrome after 50 years of age, if a diagnosis of treatment-resistant depression is made or if the patient is apathetic

1 gram of shrooms helped me realize that I have a caffeine addiction which negatively impacts my BPD symptoms

I recently did 1 gram of shrooms and even though it was not such a dose that I would see any visuals, it was a very useful experience for me.

I have been diagnosed with having borderline personality disorder traits, which then lead to depression and anxiety.

Caffeine definitely is not the cause of my BPD symptoms, but the recent shrooms experience helped me realize that I do have a caffeine addiction which negatively impacts my life. I think I have been denying it, saying to my self that – it’s just caffeine, it’s not like I do illegal stimulant drugs. Shrooms helped me accept that brain biochemistry doesn’t care about the legal status of caffeine. I had to accept that even though being completely legal and sold everywhere, I do get mood crashes from caffeine as I would from cocaine (which I tried a long time ago in high school). I can have a few cups of tea in a day, but I do like to drink several in a row, I also like coffee and yerba mate. I have been observing my symptoms for a while and I do notice that I get dysphoric later on in the day if I have coffee or yerba mate in the morning, especially on an empty stomach. I also get more paranoid about being alone, not having any friends (even though I do have several good friends), etc. I knew this for a while, just shrooms helped me accept that I really should do something about the caffeine addiction as it really negatively impacts my mood and sense of self.

I don’t think I need to completely give up tea, but I did have to quit coffee and yerba mate, which actually did help me to have a more even mood throughout the day. I also have been taking CBD oil that I made at home, I think that also helps with anxiety and mood swings. I will still have a few cups of black tea, which I love, but I need to limit myself at only three-four cups of tea per day, not very strong.

This realization might seem not very important, maybe some people expect some enlightenment or spiritual experiences from shrooms, but whenever I do shrooms I actually feel very logical and I am able to see myself from a side. I was able to analyze the correlation between my caffeine consumption and my BPD symptoms in a more unbiased way and this is actually an important realization for me, as BPD symptoms really worsen my quality of life, so if something like reducing caffeine can help – it’s not a breakthrough for humanity, but a big improvement for me. And also hoping to help anyone else reading it affected by BPD – I do believe caffeine might worsen psychiatric symptoms for some individuals.

Observations on calcium and PMS/PMDD symptoms. Observaciónes sobre calcio y síntomas de SPM/TDPM.

After several visits to the doctor, I finally received references for hormone blood tests. I definitely do not regret spending time on doctor visits and laboratory tests, because it was really interesting to observe hormonal fluctuations throughout the cycle. The results clearly showed that my progesterone level quickly rises during the luteal phase, close to 50 nmol/l. One day/several days before menstruation, my progesterone drops to 1.8 nmol / l. At the peak, my progesterone was close to the top threshold. The level was not exactly abnormal, but research indicates that some women react negatively to changes in hormone levels.

Premenstrual dysphoric disorder (PMDD)  – a much more severe form of premenstrual syndrome (PMS). It may affect women of childbearing age. The exact cause of PMDD is not known. It may be an abnormal reaction to normal hormone changes that happen with each menstrual cycle. The hormone changes can cause a serotonin deficiency.

What is premenstrual dysphoric disorder (PMDD)?

I also came across an article in the Journal of Clinical Endocrinology & Metabolism, which states that there may be cyclical changes in calcium metabolism during the menstrual cycle in women with PMDD. Interesting points from the article:

  • Irritability, anxiety, and mania have been associated with hypocalcemia, whereas increased calcium concentrations have been noted in some patients with depression.
  • Three separate investigations have demonstrated that the dysphoria, anxiety, depression, and somatic symptoms of PMS all respond favorably to either increased dietary calcium intake or daily calcium supplementation
  • Increased calcium intake proved to benefit significantly all four major categories of PMS symptoms (negative affective symptoms, water retention symptoms, food cravings, and pain symptoms).
  • When compared with asymptomatic women, women with PMS were shown to have exaggerated fluctuations of the calcium-regulating hormones across the menstrual cycle with evidence of vitamin D deficiency and secondary hyperparathyroidism.

For the authors’ study – a total of 129 women completed the timed biochemical and hormone evaluation with 115 (68 PMDD and 47 controls) providing hormone data meeting criteria for analysis. Results – Although the screening baseline 24-h urine calcium was not found to be significantly different between the groups, the random urine calcium collections during hormonal sampling were significantly lower in the PMDD group compared with controls.

In the PMDD group, total serum calcium was found to be significantly lower at 3 points: at follicular phase 1 (menses) (9.17 ± 0.55 mg/dl, P < 0.001) compared with later phases 2, 3, and 4; at midcycle phase 3 (9.25 ± 0.55 mg/dl) compared with phase 2 (9.33 ± 0.58 mg/dl, P = 0.036); and during late luteal phase 5 (9.18 ± 0.73 mg/dl) compared with phase 4 (9.27 ± 0.55 mg/dl, P = 0.018). Ionized calcium did not fluctuate as dramatically as did total calcium, but a large difference was noted between early phases 1 and 2 of the menstrual cycle again with phase 1 having the lowest ionized calcium concentration (1.166 ± 0.072 vs. 1.175 ± 0.073 mmol/liter, P = 0.069). Intact PTH peaked in follicular phase 2 (56.9 ± 35.3 pg/ml) following the decline in serum calcium during phases 1 and 5. Follicular phase intact PTH was significantly higher than luteal phase concentrations and reached its nadir in luteal phase 4 (50.9 ± 34.4 pg/ml, P < 0.01). In conjunction with the follicular phase rise in intact PTH, serum pH was lower in the follicular phase 1 and 2 compared with midcycle phase 3 and luteal phase 4 (phase 1, 7.36 ± 0.004 vs. phase 3, 7.37 ± 0.023; P = 0.015; data not shown). The concentration of 1,25(OH)2D declined precipitously in luteal phase 4 and was significantly lower compared with all earlier phases (phase 4, 45.0 ± 27.5 vs. phase 3, 49.6 ± 27.5 pg/ml; P = 0.006). Urine calcium and 25OHD concentrations did not appear to vary between individual phases in the PMDD group.

Cyclical Changes in Calcium Metabolism across the Menstrual Cycle in Women with Premenstrual Dysphoric Disorder



Después varias visitas al doctor, finalmente recibí referencias para análisis de sangre de hormonas. Definitivamente no me arrepiento de pasar tiempo en las visitas al médico y las pruebas de laboratorio, porque fue realmente interesante observar las fluctuaciones hormonales a lo largo de ciclo. Los resultados mostraron claramente que mi nivel de progesterona sube rápidamente durante la fase lútea, cerca de 50 nmol / l. Un día/ varios días antes la menstruacion, mi progesterona baja a 1.8 nmol / l. En el pico, mi progesterona estaba cerca del umbral superior. El nivel no era exactamente anormal, pero la investigación indica que algunas mujeres reaccionan negativamente a los cambios en los niveles hormonales.

Trastorno disfórico premenstrual (TDPM): una forma mucho más grave de síndrome premenstrual (SPM). Puede afectar a mujeres en edad fértil. La causa exacta de TDPM no se conoce. Puede ser una reacción anormal a los cambios hormonales normales que ocurren con cada ciclo menstrual. Los cambios hormonales pueden causar una deficiencia de serotonina.

También me encontré con un artículo en el Journal of Clinical Endocrinology & Metabolism, que establece que puede haber cambios cíclicos en el metabolismo del calcio durante el ciclo menstrual en mujeres con TDPM. Puntos interesantes del artículo:

  • La irritabilidad, la ansiedad y la manía se han asociado con hipocalcemia, mientras que se han observado concentraciones elevadas de calcio en algunos pacientes con depresión.
  • Tres investigaciones separadas han demostrado que la disforia, la ansiedad, la depresión y los síntomas somáticos del síndrome premenstrual responden favorablemente al aumento de la ingesta de calcio en la dieta o a la suplementación diaria de calcio.
  • El aumento de la ingesta de calcio demostró beneficiar significativamente las cuatro categorías principales de síntomas de SPM (síntomas afectivos negativos, síntomas de retención de agua, antojos de alimentos y síntomas de dolor).
  • En comparación con las mujeres asintomáticas, las mujeres con síndrome premenstrual mostraron fluctuaciones exageradas de las hormonas reguladoras de calcio a lo largo del ciclo menstrual con evidencia de deficiencia de vitamina D e hiperparatiroidismo secundario.

Para el estudio de los autores, un total de 129 mujeres completaron la evaluación bioquímica y hormonal cronometrada con 115 (68 TDPM y 47 controles) que proporcionaron datos hormonales que cumplían los criterios para el análisis. Resultados: aunque no se encontró que el calcio basal en orina de 24 h para la detección sea significativamente diferente entre los grupos, las recolecciones aleatorias de calcio en orina durante el muestreo hormonal fueron significativamente más bajas en el grupo TDPM en comparación con los controles.

En el grupo TDPM, se encontró que el calcio sérico total era significativamente más bajo en 3 puntos: en la fase folicular 1 (menstruación) (9.17 ± 0.55 mg / dl, P <0.001) en comparación con las fases posteriores 2, 3 y 4; en la fase 3 del ciclo medio (9,25 ± 0,55 mg / dl) en comparación con la fase 2 (9,33 ± 0,58 mg / dl, P = 0,036); y durante la fase lútea tardía 5 (9,18 ± 0,73 mg / dl) en comparación con la fase 4 (9,27 ± 0,55 mg / dl, P = 0,018). El calcio ionizado no fluctuó tan dramáticamente como el calcio total, pero se observó una gran diferencia entre las fases tempranas 1 y 2 del ciclo menstrual nuevamente con la fase 1 con la concentración más baja de calcio ionizado (1.166 ± 0.072 vs. 1.175 ± 0.073 mmol / litro , P = 0,069). La PTH intacta alcanzó su punto máximo en la fase folicular 2 (56,9 ± 35,3 pg / ml) después de la disminución del calcio sérico durante las fases 1 y 5. La PTH intacta en la fase folicular fue significativamente mayor que las concentraciones de la fase lútea y alcanzó su punto más bajo en la fase lútea 4 (50,9 ± 34,4 pg / ml, P <0,01). Junto con el aumento de la fase folicular en la PTH intacta, el pH sérico fue menor en la fase folicular 1 y 2 en comparación con la fase 3 del ciclo medio y la fase lútea 4 (fase 1, 7.36 ± 0.004 vs. fase 3, 7.37 ± 0.023; P = 0.015 ; datos no mostrados). La concentración de 1,25 (OH) 2D disminuyó precipitadamente en la fase lútea 4 y fue significativamente menor en comparación con todas las fases anteriores (fase 4, 45.0 ± 27.5 vs. fase 3, 49.6 ± 27.5 pg / ml; P = 0.006). Las concentraciones de calcio en la orina y 25OHD no parecen variar entre las fases individuales en el grupo TDPM.

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 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 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.


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.



Caffeine experimentation

The take on caffeine is that it’s bad for anxiety and intrusive thoughts. Yet there is research indicating that coffee drinkers have a lower risk of depression. On the other hand caffeine could contribute to a panic attack? Evidence is therefore inconclusive – should you consume caffeine if you have mental problems, and how much?

I know there are diets such as the autoimmune protocol diet (AIP) that eliminate coffee, but I have not found much evidence contraindicating coffee consumption. AIP diet includes eliminating a lot of food groups, including nuts and coffee, but Harvard Health Publishing actually states and nuts and coffee are anti-inflammatory foods. I will trust Harvard on that (as the AIP diet blogs don’t provide any actual evidence that coffee and nuts are inflammatory). From Harvard Health – “studies have also associated nuts with reduced markers of inflammation and a lower risk of cardiovascular disease and diabetes. Coffee, which contains polyphenols and other anti-inflammatory compounds, may protect against inflammation, as well.” So here we go – one point for coffee.

The question is though – perhaps coffee drinking in the long-term reduces some inflammation, but what if in the short-run, it increases anxiety in a few hours. Is it really worth it? And does it actually increase anxiety? What do we know so far about what coffee does to the brain? “By blocking adenosine, caffeine actually increases activity in the brain and the release of other neurotransmitters like norepinephrine and dopamine. This reduces tiredness and makes us feel more alert. There are numerous studies showing that caffeine can lead to a short-term boost in brain function, including improved mood, reaction time and general cognitive function.” “Caffeine helps the brain release dopamine into the prefrontal cortex, a brain area important for mood regulation. Caffeine may also help storage of dopamine in the amygdala, another part of the brain important for anxiety regulation.

One recent study with some mice (don’t really know if that is applicable to humans), found that acute caffeine administration also reduced anxiety-related behaviors in mice without significantly altering locomotor activity. I think the researchers had only 12 mice, I guess they weren’t able to get a grant to afford more, so I wouldn’t take the study very seriously.

I have consumed caffeine since childhood, since in Russia black tea is a very common drink.  Coffee I started consuming regularly later on, when I was a teenager. I did quit coffee in 2016 as I was hoping that would help with panic attacks and also I started the AIP diet which eliminates coffee. Later on, in summer of 2017, I did go caffeine free for more than a week, but I noticed that my obsessive thoughts and aggressiveness were only exacerbated. I continued to consume black tea and this week I decided to try and  reintroduce coffee.

Caffeine is the quintessential mimic of a neurochemical called adenosine. While you’re awake, the neurons in your brain fire away and produce a compound called adenosine as a byproduct. Adenosine is constantly monitored by your nervous system through receptors. In the brain adenosine is an inhibitory neurotransmitter. This means, adenosine can act as a central nervous system depressant. In normal conditions, it promotes sleep and suppresses arousal. When awake the levels of adenosine in the brain rise each hour. Typically, when adenosine levels drop and hit a certain low level in your spinal cord and brain, your body will signal to you to start relaxing to prepare for sleep. Caffeine mimics adenosine’s shape and size, and enter the receptors without activating them. The receptors are then effectively blocked by caffeine (in clinical terms, caffeine is an antagonist of the A1 adenosine receptor). By blocking the receptors caffeine disrupts the nervous system’s monitoring of the adenosine tab. The neurotransmitters dopamine and glutamate, the brain’s own home-grown stimulants, are freer to do their stimulating work with the adenosine tab on hold. When a substantial amount of caffeine is ingested—such as the typical 100 to 200 milligrams from a strong, eight-ounce cup of coffee, caffeine tricks your body into thinking that it’s not yet time for sleep by acting like adenosine. Generally, caffeine lasts about five to six hours in the body before wearing off.

Research on depression, anxiety, and caffeine is still in its early stages. One study from the Journal of Alzheimer’s Disease links moderate caffeine intake (fewer than 6 cups of coffee each day) to a lower risk of suicide. Conversely, in rare cases high doses of caffeine can induce psychotic and manic symptoms, and more commonly, anxiety. Patients with panic disorder and performance social anxiety disorder seem to be particularly sensitive to the anxiogenic effects of caffeine, whereas preliminary evidence suggest that it may be effective for some patients with obsessive-compulsive disorder. In a small study, seven of twelve patients with OCD saw “immediate improvement” on 300 milligrams of coffee daily. The author suggests that caffeine may work better in one concentrated dose each morning than spaced out throughout the day, and reminds us that caffeine remains a “well-known anxiety producer in many people.”

If all of this research seems a bit contradictory, it is. Like almost anything in science, there’s no conclusive verdict about coffee.

Since my coffee reintroduction experiment starting this Monday, so far mu experiences are more positive than negative. During these past four days, it seems that I had a reduction in obsessive and anxious thoughts. A negative effect was yesterday night, I drank a decaf Americano around 11pm, and then woke up in the middle of the night from a nightmare in which I was kidnapped by a serial killer. Today I decided to have just two cups of coffee – in the morning and in the afternoon, and stop caffeine after 5pm. I don’t particularly enjoy participating in serial killer action dreams. I don’t know whether it was the decaf that lead to the nightmare, but there is one study in which Swiss scientists studying caffeine’s effects in a small group of people report markedly elevated blood pressure and increased nervous system activity when occasional coffee drinkers drank a triple espresso, regardless of whether or not it contained caffeine. The results suggest that some unknown ingredient or ingredients in coffee – not caffeine – is responsible for cardiovascular activation, he explains. Coffee contains several hundred different substances.

New Buzz On Coffee: It’s Not The Caffeine That Raises Blood Pressure

I have also come across an article discussing the best times to drink coffee. It states that The peak production of cortisol occurs between 8–9 am (under normal circumstances.) This means that at the time that many people are having their first cup of coffee on the way to work, their bodies are actually “naturally caffeinating” the most effectively.  Cortisol is considered a stress-related hormone and consumption of caffeine has been shown to increase the production of cortisol when timed at periods of peak cortisol levels. An increased tolerance for caffeine can therefore lead to heightened cortisol levels which can disturb circadian rhythms and have other deleterious effects on your health. The article suggests that the times of peak cortisol levels in most people are between 8-9 am, 12-1 pm and 5:30-6:30 pm. Therefore, timing your “coffee breaks” between 9:30am-11:30am and 1:30pm and 5:00pm takes advantage of the dips in your cortisol levels when you need a boost the most.


List of medications and supplements for depression and obsessive thoughts

Here I will list different medications, supplements, and  procedures that are used to treat depression, anxiety, and obsessive/suicidal thoughts. I am not suggesting that you go out and buy a bunch of antidepressants and try them one by one, I just want you to be aware of what exists out there so that you can discuss this with your doctor. Some things, such as a daylight lamp, or omega 3s, don’t require prescription. Since I have been dealing with autoimmune encephalitis for more than three years already,  I have tried most of these treatments in attempts to reduce my depressive symptoms, psychosis, and intrusive thoughts.

Many people do get better with antidepressants. I have to note though, that in my case, the most useful treatment was high-dose intravenous steroids (IV Solu-Medrol) for five days. I did have severe psychotic depression with suicidal tendencies, my neurologist and psychiatrist propose that this was due to autoimmune encephalitis (Hashimoto’s encephalitis) – brain inflammation. Many people have milder depression and do well after antidepressant treatment. My state has improved but it is not without moments of intrusive thoughts and for this reason I continue trying different methods.




How does your psychiatrist determine which antidepressant to try? It seems that in general this is not based on any specific medical tests, but is based on the discussion with you about your symptoms. I did get a genetic test done on my saliva. This was part of CAMH Impact Study in Toronto, the provided report is called GeneSight Psychotropic Test. The company states that their test “analyzes how your genes affect your response to psychotropic medications commonly prescribed to treat depression, anxiety, bipolar disorder, posttraumatic stress disorder (PTSD), obsessive compulsive disorder, schizophrenia and other behavioral health conditions. There are dozens of medications used to treat depression and other mental illnesses and selecting the right antidepressant medication or other medication can be a challenging and frustrating process. GeneSight Psychotropic’s genetic testing enables your clinician to identify and avoid depression, anxiety and/or other medications that are unlikely to work or may cause side effects.” This test was provided to me for free by CAMH in Toronto.

GeneSight Psychotropic Test link

New antidepressants: 

There are three new antidepressants that have become recently available in US and Canada – vortioxetine, levomilnacipran extended-release (ER), and vilazodone. Vortioxetine – may enhance serotogenic activity via reuptake inhibition of serotonin receptors. Levomilnacipran is a a serotonin norepinephrine reuptake inhibitor. Vilazodone is a serotonin reuptake inhibitor and partial serotonergic 5-HT1A receptor agonist.

The role of new antidepressants in clinical practice in Canada: a brief review of vortioxetine, levomilnacipran ER, and vilazodone


Sometimes antipsychotics are added to antidepressants during treatment. Usually antipsychotics are used to treat schizophrenia, why are they given to depressed patients? I think the reason is that many patients don’t achieve remission with antidepressants, so other medications/methods must be tried. In the large National Institute of Mental Health Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, only about 30% of patients achieved remission (virtual absence of depressive symptoms) after up to 12 weeks of first-line treatment with citalopram. Evidence of the usefulness of atypical antipsychotics in treating MDD goes back more than 7 years (statement from 2009). A controlled trial found that the combination of olanzapine and fluoxetine was more helpful in treating patients with MDD (without psychosis) than fluoxetine or olanzapine alone.2 The group that received combination therapy did significantly better than the others. In November 2007, the FDA approved aripiprazole as the first atypical antipsychotic to treat MDD. It is specifically for adjunctive treatment, along with an antidepressant, for the treatment of refractory MDD.

Atypical Antipsychotics for Treating Major Depression

Aripiprazole (Abilify) – was approved by FDA for major depressive disorder in 2007, for patients who had inadequate response to antidepressants. Aripiprazole is a partial agonist at dopamine D(2) and D(3) and serotonin 5-HT1A receptors, and is an antagonist at 5-HT(2A) receptors.

Ripseridone – risperidone has actions at several 5-HT (serotonin) receptor subtypes. A study showed that depression symptoms improved modestly but significantly more in the risperidone group compared with the placebo group, as measured by clinician-rated symptom response and patient-rated self-assessment. The 17-item Hamilton Rating Scale for Depression score improved more in the risperidone group versus the placebo group.

Quetiapine (Seroquel) – quetiapine is a dopamine, serotonin, and adrenergic antagonist, and a potent antihistamine with some anticholinergic properties. Quetiapine binds strongly to serotonin receptors; the drug acts as partial agonist at 5-HT1A receptors. One study involved more than 700 people who had suffered from depression for at least one month but less than one year. Patients were randomly assigned to take one of three doses of Seroquel or a placebo once a day for six weeks. Those taking Seroquel showed greater improvement in depression symptoms than those on placebo.


St. John’s Wort  – hypericum perforatum, it is a flowering plant. Sold in health stores/drug stores/online. A 2008 review of 29 international studies suggested that St. John’s wort may be better than a placebo and as effective as different standard prescription antidepressants for major depression of mild to moderate severity. A 2015 meta-analysis review concluded that it has superior efficacy to placebo in treating depression, is as effective as standard antidepressant pharmaceuticals for treating depression, and has fewer adverse effects than other antidepressants.[23] The authors concluded that it is difficult to assign a place for St. John’s wort in the treatment of depression owing to limitations in the available evidence base, including large variations in efficacy seen in trials performed in German-speaking relative to other countries. In Germany, St. John’s wort may be prescribed for mild to moderate depression, especially in children and adolescents.

Omega – 3 – omega-3 fatty acids are found in oily fish such as salmon. You can also purchase fish oil supplements in health stores/online. In general eating oily fish is considered to be a healthy choice. There is some evidence that omega-3s might help with depression, but this evidence is not very strong. From Cochrane review: “At present, we do not have enough high quality evidence to determine the effects of n-3PUFAs as a treatment for MDD. We found a small-to-modest positive effect of n-3PUFAs compared to placebo, but the size of this effect is unlikely to be meaningful to people with depression, and we considered the evidence to be of low or very low quality, with many differences between studies.

SAMe – S-adenosyl-L-methionine (SAMe) is a compound found naturally in the body. SAMe helps produce and regulate hormones and maintain cell membranes. A synthetic version of SAMe is available as a dietary supplement in the U.S. In Europe, SAMe is a prescription drug.  From Cochrane review: “We included eight studies involving 934 people in this review. There was no strong evidence of a difference in effectiveness between SAMe and imipramine or escitalopram when used alone. It was superior to placebo when used in combination with selective serotonin reuptake inhibitor antidepressants, but this evidence was of low quality. There was no significant difference in terms of effectiveness between SAMe and placebo alone, but again this evidence was of very low quality.

Folic acid – also known as vitamin B9. Foods that are naturally high in folate include leafy vegetables (such as spinach, broccoli, and lettuce), okra, asparagus, fruits (such as bananas, melons, and lemons) beans, yeast, mushrooms, meat (such as beef liver and kidney), orange juice, and tomato juice.

“The evidence for a link between depression and folate levels comes from various sources. Along with vitamins B6 and B12, folate helps break down the amino acid homocysteine. High blood levels of homocysteine are associated with Alzheimer’s disease and depression, although a cause-and-effect relationship hasn’t been proven. The breakdown of homocysteine generates SAMe, a major constituent of brain cells and, some think, a possible treatment for depression. Low levels of SAMe might explain any connection between folate and depression.”

Folate for depression

Probiotics – there is one combination of two bacterial strains that has shown some promise in treating mental health issues. Bifdobacterium longum R0175 and L. helveticus R0052 have been found to reduce symptoms of stress and anxiety. In Canada there are two brands with these strains – CalmBiotic and Jamieson Probiotic Sticks.

Clinical Guide to Probiotic Products Available in Canada

Other things to consider

  • Getting tested for hypo/hyperthyroidism – potential need for thyroid hormones

Treating an underactive thyroid gland may improve mood

  • Getting tested for anemia

Sometimes the first symptoms of iron deficiency are neurologic

  • Getting tested for coeliac disease – possible benefit from excluding gluten from diet

The Link between Celiac Disease and Depression

  • Autoimmune disease testing – includes coeliac disease, hashimoto’s thyroiditis, autoimmune encephalitis, lupus, type 1 diabetes, etc.

Infection, autoimmune disease linked to depression

  • Don’t forget to exercise and eat healthy! I really mean it, you just really need to do it, there is no other way…

Depression and anxiety: Exercise eases symptoms

Mediterranean diet tied to lower risk of depression

Are you sure your depression is in your brain?

I’m not. Actually I’m pretty sure that’s not where my depression started. I am quite positive that the encephalitis  – brain inflammation – had developed after several years of chronic gut inflammation. What if my irritable bowel/gastritis was stopped right after it started? What if I had known about celiac disease and stopped eating gluten not two, but ten years ago? My assumption is that I would not have developed brain inflammation then, I would not experience seeing the old women asking me to help them die, I would not feel the walls of my room closing in on me. There would be no primal fear, no encephalitis. Whatever has happened to me, happened, no point to dwell on the past, but I am writing for others, for whom such terrifying experiences may be prevented. It’s important to ask the question – are you sure your depression is only in your brain?


Above is my combination of the psychiatric meds that I was given by my first psychiatrist. She never questioned the origins of my depression – to her it was all a chemical imbalance in my brain, therefore she combined SSRIs, antipsychotics, benzodiazapines, and she failed at treating me. She started treating me in November 2015 and in May 2016 I bought hibachi grills and drove away into a forest with the two grills and a bag of charcoal, police had to track me. In June I could no longer work and became unemployed. Clearly I did not improve in the six months that I was her patient.

I did not improve because I don’t just have some serotonin imbalance, I have autoimmune encephalitis – brain inflammation. I also was diagnosed previously with irritable bowel syndrome (IBS) and chronic gastritis – gut inflammation. Did one lead to another? I believe so. I believe my depression started in the gut and there is research to support this theory.

“Recently, studies have emerged focusing on variations in the microbiome and the effect on various CNS disorders, including, but not limited to anxiety, depressive disorders, schizophrenia, and autism.2,8,9 Therapeutic interventions to treat dysbiosis, or disturbance in the gut, and mitigate its effects on the GBA (gut-brain axis) are only recently coming to the forefront as more is known about this unique relationship. As a result, research has been done on the use of probiotics in treatment of anxiety and depression both as standalone therapy and as adjunct to commonly prescribed medications.”

“When the human microbiome is challenged with changes in diet, stress, or antibiotics, the physiology of the normal microbiome undergoes change. A dysbiotic state leads to increased intestinal permeability and allows contents such as bacterial metabolites and molecules as well as bacteria themselves to leak through the submucosa and into the systemic circulation, a phenomenon aptly named leaky gut syndrome. … Increased intestinal permeability leads to detrimental effects on the host immune system, which have been demonstrated in diseases such as inflammatory bowel disease (IBD), diabetes, asthma, and psychiatric disorders including depression, anxiety, and autism.2,4,10,34,35

“Depressive disorders are characterized by both neuroplastic, organizational changes, and neurochemical dysfunction.42 Illness is thought to begin when there is deregulation of these systems and can largely be attributed to cytokine release secondary to an exaggerated systemic response to stressors.39,41 Endotoxin infusions to healthy subjects with no history of depressive disorders triggered cytokine release and subsequent emergence of classical depressive symptoms. The study established a direct correlation between increased levels of IL-6 and TNF-a with symptoms of depression and anxiety,43 indicating that pro-inflammatory cytokines play a role in the development of anxiety and depression. These effects correlated with a state of chronic inflammation and altered immune cells in the peripheral blood. However, TNF-a administered to healthy subjects resulted in no depressive symptoms,38 suggesting that toxin induced inflammation caused the mood disturbance.”

Gut microbiota’s effect on mental health: The gut-brain axis

There has also been found a link between IBS and depression and recent studies are indicating that probiotics may help with both issues.

“For the new research, scientists from McMaster University in Canada recruited 44 adults with IBS as well as mild to moderate anxiety or depression. They were followed for 10 weeks; half took a daily dose of the probiotic Bifidobacterium longum, and half took a placebo. The probiotics were manufactured and provided by Nestle, which also funded the study. (Nestle was not involved in collection, analysis or interpretation of study data.)

After six weeks, twice as many people who took the probiotic had decreased depression scores compared to those who took the placebo: 64% versus 32%. Results were similar after 10 weeks, as well. When people in the study were given functional MRI scans, the researchers found that improved depression scores were associated with changes in activity of several brain areas involved in mood regulation.”

How Probiotics May Help Depression

If you are suffering from treatment resistant depression – you are not improving with the SSRIs/SNRIs/TCAs/MAOIs/NASSAs/etc., it’s important to ask yourself whether you are also suffering from any other conditions. If I had previously known all the information about the gut-brain axis, inflammation, and autoimmune diseases, it would be more evident to me that the cause of my psychiatric issues was likely gut inflammation. My severe depression started in 2015 but other health problems were starting long before that. I experienced dry and peeling skin since I was 11 years old and after the age of 12 I developed severe acne. When I was 17 I started having strong abdominal pain in the evenings. Sometimes the pain was so severe that I found it difficult to sit up. I also remember difficulties with falling asleep because as I lay down I would feel my stomach grumble and I could not relax. Later on more symptoms were added such as facial swelling, gastric pain, rapid weight gain, and brain fog. Then the depression and psychosis came. A coincidence ? Just a chemical imbalance unrelated to the other health issues? Clearly not and these symptoms were all related. They developed together as I continued to have a diet, unknowingly, that was terrible for me – pasta, bread, pizza, cheesecakes, and the symptoms declined together as I changed my diet, got treated with steroids, and started consuming fermented foods.

Now that I am equipped with all of this information I hope that I will continue to improve. I no longer have a feeling that it will only get worse and worse. I hope this will be useful to you as well and I hope I can help you feel happier again. There is more and more research now on other possible treatments for depression in addition to existing antidepressants, so I am optimistic that something will work for you, there are many things to try, don’t give up!

Industrialization, autoimmune diseases, and depression

I used to think that I was in control of my own mind, but it’s clearly not the case. I don’t choose how to feel and how to emotionally respond to situations, just as I don’t choose when to feel hungry. I don’t choose my thoughts as well. I don’t know which thought is going to come next, it’s just going to pop up in my conscious mind and I will observe it, I will react to it. Someone recently told me that all the choice that we have in life is the direction of our view. We don’t choose our emotions, we don’t choose our thoughts, we don’t choose the environment around us, we can only turn our head and change the view, and observe.

That’s why doctors prescribe antidepressants – people don’t choose to be depressed and they can’t just “think their way out of it”. And sometimes antidepressants help, maybe for some people depression is just a lack of serotonin and SSRIs fix that imbalance. The chemical imbalance theory is not 100% confirmed, some scientists debate whether this is a cause of depression at all, perhaps antidepressants help some people not by increasing serotonin, but by decreasing inflammation. Autoimmune diseases are what can cause chronic inflammation.  This is when “the immune system prompts white blood cells to attack nearby healthy tissues and organs, setting up a chronic inflammatory process”. Turns out the brain can be affected by this process as well. “People who had been treated for a severe infection were 62% more likely to have developed a mood disorder than those who never had one. An autoimmune disease increased the risk by 45%. Multiple infections or the combination of severe infection and an autoimmune disease boosted the odds of developing depression, bipolar disorder, or another mood disorder even further.”

Infection, autoimmune disease linked to depression

Next I am going to speculate and talk about the possible causes of rising incidence of autoimmune disease. I am going to mention the idea that the lifestyle that we obtained through industrialization turned out to be pro-inflammatory. I am not proposing to go back to living in a village, but I want to propose making practical lifestyle changes that can help reduce chronic inflammation and in turn depression.

We are participating in less physical activity and are gaining higher body weight

One result of industrialization is we are eating more sugar, moving less, and weighting more. “How could carrying extra weight and sofa-sitting be connected to higher levels of inflammatory chemicals in the body and the development of diabetes?

Researchers discovered that excess body fat, especially in the abdomen, causes continuous (chronic), low levels of abnormal inflammation that alters insulin’s action and contributes to the disease.

The body becomes less sensitive to insulin and the resulting insulin resistance also leads to inflammation. A vicious cycle can result, with more inflammation causing more insulin resistance and vice versa. Blood sugar levels creep higher and higher, eventually resulting in type 2 diabetes.

Are Diabetes and Inflammation Connected?

We are eating high glycemic foods

We are eating more processed and high glycemic foods. The bread that people used to eat when they lived in villages was usually not the white bread from refined flour, it was sourdough, which has more nutrients, and a low glycemic index. I doubt anyone used to eat pasta, pizza, or fries often, if at all. I know that in peasant Russia there was fermented cabbage, sourdough rye bread, barley, and broth, sometimes meat and fish. Also fermented milk products. None of those foods have a high glycemic index.

According to Harvard researchers, healthy, middle-aged women who ate the meals with the lowest glycemic load had the lowest levels of C-reactive protein, a marker of inflammation in the body.

In overweight women who had greater levels of C-reactive protein to begin with, eating higher amounts of low glycemic index foods had an even greater impact on their inflammatory markers.

The Link between Glycemic Index, Diabetes, Inflammation and Heart Disease

We are eating fewer fermented foods

How often do you drink kefir or yougurt, eat kimchi or sauerkraut? Do you eat natto or fermented bean curd? Tempeh? Sourdough bread? Cassava fufu? If the answer is pretty often, I would say that’s good, but many people in US and Canada rarely eat fermented foods. Maybe sometimes yougurt, but it’s questionable whether store bought yougurt has live probiotics. Previously people ate fermented foods more often. They didn’t really have much choice since refrigerators weren’t available. Milk goes bad pretty quickly, so you need to make it into kefir or yougurt. In winter you don’t have fresh vegetables, you have fermented vegetables in jars that you prepared during the summer. Same with fruits. There have been several papers recently linking fermented foods to mental health, here is what is stated in one of them: “The extent to which traditional dietary items may mitigate inflammation and oxidative stress may be controlled, at least to some degree, by microbiota. It is our contention that properly controlled fermentation may often amplify the specific nutrient and phytochemical content of foods, the ultimate value of which may associated with mental health; furthermore, we also argue that the microbes (for example, Lactobacillus and Bifidobacteriaspecies) associated with fermented foods may also influence brain health via direct and indirect pathways.

Fermented foods, microbiota, and mental health: ancient practice meets nutritional psychiatry

We have lost our “old friends”

One of recent theories is that the rise in autoimmune disorders could be due to our gut microbiome depletion. With sanitary toilets, pasteurized milk, less time with animals (urban citizens rarely hang out with farm animals, neither do they milk cows, and now few even have pets due to smaller apartment sizes), we have lost many microbes and parasites that used to inhabit our gut. Turns out this might not be a good thing. It could be that because we as species cohabited with these organisms for so long, our immune system evolved to train on these parasites, and now we are lacking this training. “Diminished exposure to immunoregulation-inducing Old Friends in the perinatal period may enhance the consequences of psychosocial stressors, which induce increased levels of inflammatory mediators, modulate the microbiota and increase the risk for developing all known psychiatric conditions. In later life, the detrimental effects of psychosocial stressors may be exaggerated when the stress occurs against a background of reduced immunoregulation, so that more inflammation (and therefore more psychiatric symptoms) result from any given level of psychosocial stress. This interaction between immunoregulatory deficits and psychosocial stressors may lead to reduced stress resilience in modern urban communities.

Microbial ‘Old Friends’, immunoregulation and stress resilience

Do we need to move back to the village? Or to a cave?

Well I’m hopeful that I won’t have to, because my job is in downtown Toronto, and it would be hard to commute there from a remote village. I hope that given the recent research, we can use this information to improve our immune system function, while still living in a city. We can cook more food at home instead of buying processed food. I rarely buy anything at the food court during the work day, I bring everything from home. I am also making fermented foods – kefir, yougurt, sourdough bread, kombucha. I also purchased some at Asian grocery stores – they have fermented bean curd, natto, fermented Chinese cabbage.

In terms of moving around, I try not to sit at my desk at work for too long. I get up to make tea, go for a walk during lunch. Walk to the subway in the morning instead of taking the streetcar. Walk home after work with a friend. Gym I personally found very boring, but I do exercise at home with an aerobic step. Doctors suggest at least 30 minutes of aerobic exercise a day, heart rate needs to go up!

In terms of bringing back “old friends” – this can partly be done by consuming probiotic and prebiotic foods to increase gut microbiome diversity. There are also soil bacteria that are considered beneficial, we can obtain them by spending time near soil and breathing in the particles. Having a dog is stated to have beneficial effects on our gut microbiome. There is also experimental helminthic therapy – infecting yourself with parasites on purpose. I am planning on trying this therapy and I will write more on this topic later on.

Autoimmune Encephalitis Story (part 2)

First part of the story:

Autoimmune Encephalitis Story (part 1)

Confusing summer continued

The confusing summer continued and it did not get better. I was allowed by the university to rewrite the exam that I failed and I had about two months to prepare for it. I continued working as a research assistant for a professor and I was supposed to be doing my own research since I was a graduate student but this task I found extremely difficult. I felt that a part of my mind which was responsible for creativity evaporated and I could not come up with any ideas myself, I could only follow clearly outlined instructions. I also became very indecisive and for anything that I was going to do, I required a confirmation from another person. Some part of my brain clearly started to malfunction because previously I was able to write academic papers, organize camping trips, participate in a band. Now I could not write even a paragraph about my research, I would just sit and stare at the screen, not able to extract any continuous thoughts from my mind. I was very uncertain of what I should be doing everyday and I would refer to my boyfriend for any decision – ‘what should I do in the evening?’, ‘should I continue with the graduate program?’, ‘should I call my friend to make plans?’.

My boyfriend and my parents could see that I was quite stressed about not having any ideas for research and not being able to decide whether to continue with grad school. Me and my boyfriend took some trips to national parks during the summer in order for me to de-stress, and usually I would really enjoy camping and hiking, but these times it was different. Trips became for me too emotionally overwhelming. A view of a lake from a lookout point would bring me to tears as I would think how meaningless the beauty of this was. We were just pieces of organic tissue clumped together, soon we would cease to exist and none of our experiences mattered. What was the point of having a camping experience if once you no longer exist you will have no memory of it? During the hike several times I had this dissociative experience where I would feel that the event is not happening right now but it was happened already in the past. As if you would watch an old video of your family or someone you know and maybe who was no longer alive. I could not enjoy the moment because I did not feel that I was in the current moment, I felt sadness and nostalgia for a time that had already passed.

All these psychological experiences were on top of the physical symptoms. Since I did not have courses during the summer I did not have to wake up early and there were many days where I could not get out of bed until 2 PM. I experienced extreme fatigue and muscle aches, my body felt very heavy and it was difficult to move around, I often had shortness of breath. My eyelids were swollen and I felt pressure at the top of my head, it was often difficult to look up or look straight. There were also frequent migraines and brain fog. It was as if I was getting detached from my body and my brain – I having difficulty controlling the movements of the body and processing thoughts. My consciousness was clouded and I could not get out of the fog.

I ended up leaving the graduate program as I could not see myself continuing with more courses, exams and a thesis. At the moment when I left I was not very upset about that because in my mind I had an explanation that my symptoms were sort of there as a message that I was not going the right way with my life. I guess my mind was looking for an easy solution or it was trying to make sense of the situation. It’s very difficult for a broken brain to realize its own sickness, especially if its the first time. After I already got diagnosed and connected with many other autoimmune encephalitis patients, I noticed that those who were diagnosed at an older age were more proactive about their health. Before the onset of the symptoms in my early twenties, I have probably visited a doctor only three times since I came to Canada. I saw a dermatologist once about my acne and later on I saw my family doctor twice when I needed some antibiotics. That was really it. I had no knowledge about existence of any diseases except most known ones such as cancer and heart disease, as well as some rare ones like leprosy and plague. The latter ones get mentioned in novels or movies a lot, that’s how I had any information about them. I had no idea that there was such a thing as autoimmune disease, and I had a lot of misconceptions such as thinking that only overweight people could have diabetes.

One evening in October, after I already left my graduate program, I was coming back home from downtown by subway. I was waiting for the train when I sensed oncoming fear. There were other people around me at the station, engaged in conversation, but no one was noticing my existence. I felt that I was not a full person and it became apparent to me that my life was very lonely and meaningless. I had no accomplishments, I failed to complete grad school, I didn’t have any children. It seemed to me that all the others around me could see at that moment that I was not a full individual, and in fact they were thinking that I should not exist at all. I heard the rumbling noise of the oncoming train and I had a sudden urge to jump onto the rails. I managed to get home and called my boyfriend. We agreed to go to ER the next day and to request psychiatric investigation.

Fun with psychiatry starts

Here is the fun part of the story where I tell you about all the psychotropic medications that I tried. You name one and I probably tried it.

The next day after my incident at the subway station I arrived at the ER. When the nurse at the intake asked me what was wrong I said that I was not sure and started crying. I tried to describe that I thought I was depressed and also my life was meaningless. I did not want to live because we were all going to die anyways and I was afraid that people that I knew were going to die before me. Also I described how I often felt dizzy, fatigued, had difficulty having my eyes open, and no one was helping me. All this time I continued crying and when a psychiatrist arrived to evaluate me he decided that I had to be involuntarily hospitalized.

I was given some antipsychotics, Abilify and Seroquel, in an effort to calm me down. The medication did not work as I had a severe panic attack after my boyfriend left. My cellphone was taken away by the nurses and I was sure that I would never be let out from the hospital. I started to think that my boyfriend placed me there on purpose in order to get rid of me, I was certain that he would never come back to get me and I was being institutionalized for life. These ideas do seem amusing now, after having more experience with the Canadian health care system. There are actually not enough beds now and many people are not able to obtain a hospital stay that they need. There are also not enough psychiatrists. Usually the maximum that they keep you if you are suicidal is three days. Well at that time my mind was in a state of total fear. I was placed in a room with another person who I thought was a man and probably a serial killer. Later on I realized it was an older woman who was very quiet and slept most of the time.

My predictions about institutionalization for life did not come true and I was released after two nights with a referral to a psychiatrist. Opposite to my fears at that time, I now consider myself pretty lucky that I was actually given a hospital stay and a quick referral. I’ve read that many patients in Ontario wait six or nine months for a psychiatrist, which is a very upsetting statistic.

Below I will describe my experiences with the psychiatric treatment, but remember that this is an experience of just one person. Antidepressants and antipsychotics did not work for me personally, but it does not mean that they don’t work for some other people. As I mentioned initially – I was later on diagnosed with Hashimoto’s Encephalitis and also Borderline Personality Disorder. Antidepressants and antipsychotics usually don’t work for these conditions but these diseases are different from depression and schizophrenia. I advise for thorough medical investigation in order to understand the causes of your psychiatric symptoms!


After the first visit, the psychiatrist diagnosed me with major depression and prescribed mirtazapine. My opinion is that she really overlooked all the physical symptoms for some reason and only focused on depression. At that time all that was known was that my TSH levels were normal, my fasting blood glucose levels were within range, and the regular blood test results were OK. As I mentioned, I was also previously diagnosed with chronic gastritis and IBS. No testing for autoimmune conditions was performed, free T3 and T4 levels were not checked, vitamin D levels were also not checked (later on it turned out that they were quite low). As I said, I had very little knowledge of medicine or disease, so I was not aware of medical tests that existed. When my psychiatrist told me that everything health related was verified and that nothing abnormal was found, I believed that they literally checked ‘everything’. Of course now I know that’s not possible because there are hundreds of tests and no doctor will order all of them for you because that is just economically implausible.

I started taking the medication daily and I think I had high hopes for it. I was expecting all my issues to be resolved. I did feel a bit better in the first few weeks and actually the brain fog cleared up a bit, my eyelids became less swollen. I am not a doctor but I think this could be related to the fact that mirtazapine is a strong antihistamine. In a few weeks though I was back at the psychiatrist’s office and Wellbutrin was added to the regimen. The day after I started this drug will be quite memorable for me. It was sort of like going to hell and coming back.

Pleading faces

On the second day of starting Wellbutrin I was a bit more energetic at work in the morning. I tried to do my job but by lunch anxiety started to creep in. This time it felt even more severe than before. Coworkers around me conversing with each other. How could they be smiling, easily speaking about some irrelevant topics such as reporting, when we were all going to die. Probably not at the given moment, but in general, it was going to happen, and how then could anything else matter? I also felt extreme fear of isolation – everyone was connected to each other but me. I could not engage in conversation, I had nothing to add, and my speech was paralyzed by anxiety. I couldn’t sit still, I felt agitated. I went down to the food court and that’s when I saw them. The old women. The food court area was filled with them. They were slowly dragging their bodies in uncertain directions, they had no where to go. I don’t know how for they had been there, but it could have been months. I know why they didn’t want to go home – at home, in the silence, it was ultimate loneliness. They came out, looking for humans, for someone to at least acknowledge their existence, but no one was noticing. They were looking at me with pleading gazes – ‘please, help us die’ – was their cry for help. They did not speak these words out loud, but I knew that is what they were asking for. I felt extreme emotional pain, I couldn’t stand looking at them. Why were people walking past them and not noticing them? They were being forced to exist here, in this underground concrete place, with no sunlight and no way out. I had to run back upstairs, I could not tolerate watching these women. It was better at my computer desk, the screen was familiar, there were windows around the floor. The fear lessened but still something was wrong. Awfully wrong. Why were all those women there, why had I never seen them before? Where was this emotional pain coming from?

I have since been back to that food court several times, since it is close to my new work location. I can tell you that it’s quite rare to see an older person there because the food court is located under the office buildings in the financial districts. It’s mostly bank employees there. But that is what our mind is capable of, painting such horrifying images.


I called my psychiatrist after the food court event and was told to stop Wellbutrin. I also scheduled an appointment with her and during my visit I told her in more details about the day with the old women. The old women that were in the food court, in dozens, silently asking me to help them die. On the way back from work that say day I also found apartment buildings with no balconies terrifying. Those apartments must have also had old women trapped in them. They could see the world and life pass them by only through the window. There were no balconies there on purpose, it was so that they could not jump. The society was forcing them to exist, not live but exist, in this abandoned state, they were being mentally tortured.

At this point the psychiatrist saw that this was not just major depression but a psychotic episode. I heard the words schizophrenia, schizoaffective disorder. She said it is common to have an onset in your early twenties. I was exhibiting paranoid symptoms, delusional thoughts. All the symptoms matched. There is no medical test do diagnose schizophrenia though, the diagnosis is based on a psychiatric evaluation. I was taken off Wellbutrin and risperidone, which is an antipsychotic, was added to mirtazapine. I do forgive the psychiatrist for this misdiagnosis, but more investigation should have been done after it had become clear that I did not improve on antipsychotics. I also mentioned multiple times my physical symptoms which I have already described – brain fog, eye inflammation, migraines, fatigue, abdominal pain, etc. All these physical symptoms were regarded as separate by the psychiatrist, and not related to the psychiatric symptoms.

Unfortunately a misdiagnosis of schizophrenia or psychotic disorder is a common one for patients with autoimmune encephalitis. I hope me telling this story will bring more awareness of this disease and that autoimmune testing will be considered for psychiatric patients.

As I said, I did not improve with risperidone. Risperidone was then switched to olanzapine and trazadone was added for insomnia. I was still on mirtazapine, now on increased dose. Lorazepam was added for anxiety. Four psychotropic medications in total but I was not doing better. I continued to have panic attacks, mostly they would occur if my boyfriend or my parents did not pick up the phone. Even if it was for five minutes, I would feel completely abandoned and the instant thought was that they are in danger or already dead. There were many times when I arrived at my boyfriend’s office looking for him, making up excuses to the security guards about a relative in the hospital. I would blame him for torturing me and causing me these emotions by not picking up his cell phone and I would become violent. Many times 911 had to be called.

My brain was in constant fear mode and I would say that from reading about and speaking to other people with autoimmune encephalitis, fear is one of the key symptoms. I also continued to have what my psychiatrist called ‘ideas of reference’ – anything that I saw or heard was somehow related to my being, my current life or my future. Hearing some one mentioned their cousin would bring me great emotional pain as I was instantly reminded that my cousin lived in Russia and we were separated by an ocean. The word ‘cousin’ itself would be emotionally painful. A picture of a family on a poster ad would seem to be laughing at me and telling me that I did not deserve to be with other people, I was bound to be alone. There was emotional pain in everything that I saw and heard. I could no longer go into Starbucks because they always had music on and I could not tolerate the sounds. One evening for distraction I tried to watch a movie, ‘A Streetcar Named Desire’, but I had to stop because the story of Blanche making me more paranoid. I became certain that the movie was about me and there was a message in it specifically for me – the message was that I was not willing to accept that I had gone insane but everyone else around me already knew it and soon I would be locked up in a mental institution.

I continued to work full-time but it was becoming extremely difficult. I was having a hard time waking up. My body felt heavy and my eyelids swollen, I felt that the eyelids were being pushed down and I had to put effort into keeping my eyes open. I would often be overcome with panic at my work desk. My hands would become sweaty and breath uneven. I would have an urge to run out to the stairwell as I believed that everyone was observing and judging my emotional state. Olanzapine had also made my thoughts slower and I was not able to code, which was required for my job. It would take me twenty minutes to write a simple loop because I could not retrieve the necessary thinking process. I knew that this task was something that I had done before many times but  a link was missing between my memory and actual implementation. I started missing a lot of work because some nights I did not sleep at all or because I was left too exhausted after  a panic attack. I had no sick days since I was on a contract, therefore had no benefits, and soon I was let go. The psychiatrist still insisted on further antipsychotic treatment even though I was only getting worse and olanzapine was replaced with latuda.

At that point I saw in front of me only a dark narrowing tunnel and non-existence started to seem more and more appealing. I contacted the euthanasia clinic in Switzerland, Dignitas, and I started to research suicide methods. I ended up buying hibachi grills and a bag of charcoal as from my understanding that is a reliable and practical method, frequently used in Asia. I did once go out in my car in the evening with this equipment and sat for a while in an empty dark parking lot beside a park. My parents and my boyfriend called the police and I was again involuntarily hospitalized. The hospital stay was not very useful as  I ended up being there only for one night and all they did was prescribe me clonazepam and told me to see my psychiatrist. The next time I went my mom came with me. With all the antipsychotics and my symptoms worsening I was not very active during my visits, I also did not have any ideas of what I could ask for. My mom on the other hand was much more proactive (makes sense, considering that I was trying to commit suicide), and she demanded MRI tests. She was also frustrated with continuous antipsychotic treatment since I was only becoming more suicidal, and started to do her own research online. By research I mean googling. We are lucky that we can do that nowadays. As an efficient googler and being a mother, so having more interest in my well-being than my psychiatrist, she put all my symptoms together into a more coherent picture. I had weight gain, fatigue and bad skin – those could be symptoms of thyroid disease. I also had abdominal pain and bloating – celiac disease and gluten intolerance came up a lot for those symptoms in google search. My thyroid hormone levels were normal though, we already knew that. Something else came up though – hypothyroid mom website, where many women told their stories of having normal thyroid hormone levels and yet felling awful and depressed. All these women wrote that they had elevated thyroid antibodies, Anti-Tg and Anti-TPO, and were given a diagnosis of autoimmune disease.

I now probably read at least one article on autoimmune disease a day but in 2016 I had no idea that such a condition existed. I thought there was cancer, heart attacks, diabetes and dementia. Well also schizophrenia and depression. Of course also tropical diseases but I was in Canada, so those were irrelevant. I had never heard of a disease where your own immune system produced antibodies that attacked your organs. From what the psychiatrist whom I saw seeing told me – you either had low serotonin levels and were depressed or you have hyperactive dopamine signalling and you have schizophrenia. In her opinion I had both and that’s why I was on antidepressants and antipsychotics. She did say though that there is a 30-30-30 rule in regards to antidepressants – about 30% of patients get out of the depression with medication, 30% improve and then relapse, another 30% don’t notice any positive effects. (Actually it should be 30.3333% for each, should add up to 100, to be exact).

The dopamine hypothesis has not actually been proven – how do we know that everyone who was diagnosed with schizophrenia has too much dopamine? Do we measure it? No. Schizophrenia is diagnosed by a psychiatrist based on a verbal  consultation with the patient about their symptoms. Some researchers thing that schizophrenia is actually a number of disease, just the symptoms are similar. There is also a hypothesis that a significant percentage of patients with schizophrenia are cases of autoimmune disease.

Autoimmune attack behind some cases of schizophrenia

So in June 2016 I went for a blood test and results came back positive. I had high levels of Anti-Tg and Anti-TPO antibodies. I had now a diagnosis of autoimmune disease, Hashimoto’s thyroiditis at that point, and was undiagnosed with schizophrenia. Yes, that can happen, you can be undiagnosed. My psychiatrist said that autoimmune diagnosis changes everything and I was taken off most of the medications, I only kept Sertraline, until October. I also had an appointment with an endocrinologist and he prescribed me Cytomel, which is the manmade version of the thyroid hormone T3. It was prescribed not because I had issues with thyroid hormone levels, my hormones were normal, but it was added in hope to help with fatigue and depression.

T3 augmentation of SSRI resistant depression

From this point on I spent many hours reading about autoimmune diseases and trying to figure out what happened to me. I continue with my story in part 3 and describe how I came to be diagnosed with autoimmune encephalitis.

Autoimmune Encephalitis Story (part 3)