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

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

 

Improvement with lithium chloride supplement

I have extensive experience with psych meds, first prescription being abilify and seroquel in 2015, then mirtazapine, wellbutrin, risperidone, cymbalta, trazodone, and more. None of the meds worked for me. Last trial was of fluoxetine in November, which caused severe insomnia on only 10mg, and panic attacks. In March I also tried Zembrin which is a serotonin reuptake inhibitor (SRI). Zembrin also caused panic attacks for me and increased psychotic symptoms. I decided I don’t want to touch any additional SSRIs, SNRIs, nor SRIs.

I have also tried shrooms microdosing. I found that 1-4 gram occasional trips are better for me as microdosing makes me fatigued. While on shrooms though, a lot of thoughts came to me about reducing my caffeine intake and lithium. Lithium was mentioned to me several years ago by one consulting psychiatrist, but was never prescribed. I asked my current psych about it, but she refused to prescribe it.

While I was on Zembrin in March, by mid-month I started to get more paranoid and psychotic, as I was also in luteal phase of my cycle. A lot of women with mental illness experience PME – premenstrual exacerbation of symptoms. I unfortunately experience that as well. Mid-March I decided to stop Zembrin and any other supplements I was trying – mushroom coffee, rhodiola rosea, St. John’s Wort tea. I also stopped drinking coffee in general as I think it exacerbates my mood swings. I only continued with lithium orotate supplement that I purchased, but I stopped it as well as it seemed that it was causing more frequent urination. As I stopped these supplements and my period stabilized, my mental state somewhat stabilized to a point where I could better observe myself and think about what to do next. I decided that I still wanted to try lithium, but purchased a supplement which was in a different form – liquid which contains lithium chloride, instead of the lithium orotate tablets. I chose lithium chloride because there is more existing research on it than on lithium orotate. I also made homemade CBD oil from the Avidekel strain.

Well it has been over two months since mid-March and I’ve hard a lot more days which were just ‘alright’ instead of being a struggle with intrusive thoughts and depression. I’ve felt more calm and was able to read more throughout these two months, actually finished two books, on my third now. So in general a beneficial experience so far, will see how it goes.

Great psychiatry podcast. Impresionante podcast de psiquiatría.

Just wanted to post a link to a very interesting psychiatry podcast. For now I have specifically listened to the interviews with Dr. Cummings and I really enjoyed all the episodes. Dr. Cummings seems to be a very knowledgeable psychiatrist and provides a lot of information about areas of the brain, neurotransmitters, psychopharmacology. Currently I drive to work and back on a daily basis and I have been listening to the episodes in the car.

PSYCHIATRY & PSYCHOTHERAPY PODCAST

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Solo quería publicar un enlace a un podcast de psiquiatría muy interesante. Por ahora he escuchado específicamente las entrevistas con el Dr. Cummings y realmente disfruté todos los episodios. El Dr. Cummings parece ser un psiquiatra muy conocedor y comparte mucha información sobre áreas del cerebro, neurotransmisores, psicofarmacología. Actualmente conduzco diariamente al trabajo y de regreso y he estado escuchando los episodios en el auto.

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.

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

 

Dr. Roger McIntyre: Mood Disorders and Metabolic-Inflammatory Comorbidity

Very interesting lecture found on YouTube – Dr. Roger McIntyre is a quite important guy in psychiatry here in Toronto. He is a Professor of Psychiatry and Pharmacology at the University of Toronto and Head of the Mood Disorders Psychopharmacology at UHN. He is also the director of the first Ketamine Infusion Therapy Clinic for depression in the GTA.

So in this lecture, which was posted in 2016, he talked about how just elevated C-reactive protein, a sign of general inflamamtion in the body, leads to anhedonia (inability to feel pleasure), apathy, and destuction in the brain of dopamine neurons. I wish more psychiatrists would actually listen to his lectures as well. I got a feeling, from personal experience, that some psychiatrists weren’t aware about the link between inflammaion and anhedonia, because they easily prescribed antipsychotics that cause severe weight gain. Dr. McIntyre actually speaks in the lecture against easily prescribing antipsychotics for depression, as weight gain is known to increase inflammation and therefore actually cause anhedonia/dysphoria.
So basically when an antipsychotic is described for depression – the antipsychotic reduces dopamine, since that is its function, and then further you can have death of dopamine neurons through inflammation, so that can result in complete dysphoria.

Prospective studies revealed that the average weight gain during the first year of treatment was 11.7 to 13.9 lb for clozapine, 15 to 26 lb for olanzapine, 4.4 to 5.1 lb for risperidone, 6.1 to 13.3 lb for quetiapine, and less than 2 lb for aripiprazole and ziprasidone.

Dr. Roger McIntyre: Mood Disorders and Metabolic-Inflammatory Comorbidity

 

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

 

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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.

Vitamins before antidepressants . Vitaminas antes de los antidepresivos.

Texto en español a continuación.

This post will not be against antidepressants. I only want to share my experiences, in case they might help someone. I found out the hard way that eating healthy and obtaining all the basic vitamins is necessary (but not sufficient) for mood stability and emotional regulation. Unfortunately not all doctors or psychiatrists check for vitamin and mineral deficiencies before prescribing antidepressants. There is a lot of research indicating that many vitamins and minerals are important for the functioning of neurotransmitters. So I am not stating ‘always vitamins instead of antidepressant’, but in my opinion as a patient, diet should always be reviewed first. Especially if you have any gastrointestinal problems, family history of gastrointestinal issues, or you live in a northern country. Also if you are vegan, vegetarian, or have any other food restrictions.

I have written in my previous posts about getting a diagnosis of autoimmune encephalitis, but let’s set that aside for now. I did end up being referred to a neurologist, but in this post I want to focus on my experience with psychiatrists. When I was referred to a psychiatrist by the emergency department, several blood tests were performed. Blood glucose level, iron level, thyroid stimulating hormone (TSH) test results were sent to the psychiatrist. Since these test results came back normal, right away the psychiatrist prescribed me mirtazapine.

Mirtazapine did not help my mood and I only gained weight on it and had trouble waking up in the morning. Therefore, my dissatisfaction with this approach is that several important blood tests were not prescribed. For example, I live in a northern country, therefore it is possible to be deficient in vitamin D. They also didn’t ask me about my diet, but a spicy diet can lead to deficiencies in B vitamins and omega 3 fatty acids. Additional point – my blood glucose was checked only once, it was not proven how I react to eating carbohydrates.

Later I discovered that I was deficient in vitamin D, that my blood sugar level would jump too high after eating refined carbohydrates, and I was not getting enough folic acid and calcium. By not performing the necessary laboratory tests, the doctor lost a lot of time and delayed my treatment. I was also taking unnecessary high doses of antidepressants, which were not helping.

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Esta publicación no será contra los antidepresivos. Solo quiero compartir mis experiencias, en caso de que puedan ayudar a alguien. Descubrí por las malas que comer sano y obtener todas las vitaminas básicas es necesario (pero no suficiente) para la estabilidad del estado de ánimo y la regulación emocional. Desafortunadamente, no todos los médicos o psiquiatras verifican las deficiencias de vitaminas y minerales antes de recetar antidepresivos. Hay mucha investigación que indica que muchas vitaminas y minerales son importantes para el funcionamiento de los neurotransmisores. Por lo tanto, no estoy diciendo “siempre vitaminas en lugar de antidepresivos”, pero en mi opinión como paciente, la dieta siempre debe revisarse primero. Especialmente si tiene problemas gastrointestinales, antecedentes familiares de problemas gastrointestinales o si vive en un país del norte. Además, si eres vegano, vegetariano o tienes otras restricciones alimenticias.

He escrito en mis publicaciones anteriores sobre el diagnóstico de encefalitis autoinmune, pero dejemos eso de lado por ahora. Terminé siendo referido a un neurólogo, pero en esta publicación quiero centrarme en mi experiencia con los psiquiatras. Cuando el departamento de emergencias me remitió a un psiquiatra, me realizaron varios análisis de sangre. Los resultados de las pruebas de nivel de glucosa en sangre, nivel de hierro y hormona estimulante de la tiroides (TSH) se enviaron al psiquiatra. Como los resultados de estas pruebas mostraron ser normales, de inmediato el psiquiatra me recetó mirtazapina.

Mirtazapine no ayudó mi humor y solo subí de peso, y tuve dificultad para despertar en las mañanas. Entonces, mi insatisfacción con este enfoque está que varios análisis de sangre importantes no fueron prescritas. Por example, vivo en un país del norte, por lo tanto está posible estar deficiente en vitamina D. También no me preguntaron sobre mi dieta, pero una dieta espicifica puede conducir a las deficiencias en vitaminas B y ácidos grasos omega 3.  Punto adicional – mi glucemia se comprobó solo una vez, no fue probado cómo reacciono al comer carbohidratos.

Mas tarde descubrí que era deficiente en vitamina D, que mi nivel de azúcar en la sangre saltaria demasiado alto después de comer carbohidratos refinados, además no estaba recibiendo suficiente ácido fólico y calcio. Al no realizar las pruebas de laboratorio necesarias, el doctor perdió mucho tiempo y retrasó mi tratamiento. Además estaba tomando dosis altas innecesarias de antidepresivos, que no estaban ayudando.

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.