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.

 

 

Depression and TSH levels

I continue to track my thyroid hormone levels and thyroid antibody levels. As my endocrinologist predicted, after a thyroid inflammation event (as indicated by ultrasound test results), and a state of hyperthyroidism, my thyroid hormone levels went the opposite way and now I am hypothyroid. I will say that for me personally the hyperthyroid state did not feel as bad as the current hypothyroid state, though I am hopeful that hypothyroidism can be treated with levothyroxine, which was recently prescribed to me. My antibody levels continue to be high and my endocrinologist stated that with Hashimoto’s autoimmune disease in general antibody levels stay chronically elevated. I might be receiving IVIG treatment soon, in April, and hopefully that will reduce the inflammation of the thyroid.

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In terms of emotions, during hyperthyroidism, I did feel jittery and very hungry, but I also experienced a roller coaster of more positive emotions such as more interest in men, infatuation, desire for adventure. I can’t say that my depression went away, but I do remember having moments of making plans to travel to Guatemala to attend a Spanish course, thinking of having an affair, wanting to perform in a band with my violin. Recently with hypothyroidism, as I described in a previous post, what I had been feeling is complete disinterest and grief. As if your life is somehow passing by, the world keeps going without you. There is a feeling of slowness in your movements and speech, a sense of painful emotional weight, inability to fully engage in an activity. Well if you have experienced hypothyroidism, you might know what I’m talking about. It’s feeling lonely and yet having no energy to call someone to make plans. Thinking that in theory I do enjoy playing violin, but today doing that would be just too difficult. Exercising definitely was becoming impossible, my legs have been feeling very heavy, and my whole body in general.

Today I started levothyroxine 0.025mg and I am hopeful that this will lower my TSH and therefore relieve all the symptoms that I am experiencing, at least I am very hopeful that levothyroxine in combination with IVIG will really help. I found an interesting study in which the authors seek a TSH threshold for depression. Two thirds of the study participants were female, as expected. There were 174 hypothyroid patients who were receiving levothyroxine treatment and were considered euthyroid. “Individuals who had developed euthyroid state under treatment with levothyroxine with TSH levels of 0.5–5 MIU/L with no need for dosage change were included in the study. After comprehensive history taking, laboratory tests including TSH, T4 and T3 were performed. Beck depression questionnaire was completed for all patients by trained interviewers. TSH cut-off values based on depression was determined by Roc Curve analysis.” Basically, as I understand, the researchers wanted to find out whether there is correlation between TSH levels and depression for patients who were diagnosed with hypothyroidism and are receiving levothyroxine.

Results were the following: “According to Roc curve analysis, the optimal cut- off value of TSH was 2.5 MIU/L with 89.66% sensitivity. The optimal TSH cut- off based on severe depression was 4 MIU/L. The present study suggests that a clinically helpful TSH cut-off value for hypothyroidism should be based on associated symptoms, not just in population studies. Based on the assessment of depression, our study concludes that a TSH cutofff value of 2.5 MIU/L is optimal.” I think what they are trying to say here is that based on large population studies there was a range for normal TSH levels determined, for example on my lab tests that range is stated as 0.32 – 4.00. Their study shows though that even though my individual TSH could be within this range, it doesn’t mean that I won’t be having any hypothyroidism symptoms, such as depression. Maybe for me personally TSH of 3.80 would be too high and my mood would be influenced and I would be better off at a level of levothyroxine that would bring my TSH below 2.5. Therefore it’s important to consider the symptoms of a specific patient and not just the determined ‘normal’ range.

TSH cut off point based on depression in hypothyroid patients

Also different countries and labs don’t state the same ‘normal’ ranges. In the study the TSH range is indicated as 0.5 – 5 MIU/L, while my lab states 0.32 – 4. So if I went to a doctor in another country, he could have said that my thyroid hormone levels are normal, but based on my lab’s range, my endocrinologist said that I might be becoming hypothyroid, since TSH is out of range, and therefore prescribed me levothyroxine. Also he did take into account the symptoms that I was experiencing, which is what the authors suggest – don’t just look at the TSH, how does the patient feel?

 

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.

Medication

Antidepressants

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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

Antipsychotics

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.

Supplements

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

Following the MIND diet for autoimmune encephalitis and depression

So there has been the MIND diet going around. Some research indicates that it can reduce the risk of developing Alzheimer’s/dementia. The MIND diet is very similar to the Mediterranean diet. As most people know, that means eating a lot of oily fish, whole grains, vegetables, nuts, and beans/legumes. The MIND diet is a bit more specific – it recommends green leafy vegetables every day, berries (especially blueberries), whole grains three! times a day, nuts every day. You can see the list below:

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Dietitians provide some information on how this diet might work: “A diet that supports vascular health is certainly protective against vascular dementia, but certain foods and food components have been directly linked to improved neurological function or reduced AD biomarkers in the brain.1,8 “MIND diet foods reflect nutrients shown to slow cognitive decline, lower risk of AD, decrease amyloid in the brain or neuron loss in animal studies, or decrease oxidative stress and inflammation”.

Food for Thought: The MIND Diet — Fighting Dementia With Food

Well since my brain seems to be screwed up, anything that might fight inflammation while improving neurological function sounds good to me! It’s also a lot less restrictive than the AIP diet or ketogenic diet. Definitely much easier than intermittent fasting. I see myself being able to follow this diet long-term. I want to eat my grains, I also haven’t found much evidence that excluding grains helps with depression or inflammation. I like to eat my quail eggs and goat yougurt, so I don’t want to be excluding eggs or dairy (AIP excludes these foods). I don’t think the strict AIP diet should be followed for a long time, neither the ketogenic diet. I am not even sure whether keto diet can help with inflammation and depression, it includes tons of saturated fat. The MIND diet researchers actually recommend limiting saturated fat.

So how do you follow the MIND diet list in practice? Green leafy vegetables every day, berries, olive oil, nuts… how do you fit all of that into one day? And what if you don’t like looking or don’t have time? What if you are not one of those people who post on their vlog about avocado toast? I came up with some quick recipes, here I will post my breakfast idea. The breakfast consists of onions (vegetable √ ), kale (green leafy vegetable √ ), cooked with olive oil √, yougurt with blueberries (berries √), also you can add some toast (I don’t eat gluten, but I make gluten-free sourdough buns  – whole grain flour √), or you can easily make a lot of brown rice pudding – also whole grain √.

I want to make this simple. This is for actual practical eating, now a decorative meal. I prepare several items in the evening so that in the morning I can cook my breakfast in several minutes. I start work at 9 am and I try to wake up as late as possible, I don’t want to be cooking for even fifteen minutes in the morning.

Ingredients to buy:

  • Buy some frozen chopped onions, chopped kale, olive oil, eggs. Yougurt, frozen blueberries, nuts/seeds. Bread/sourdough bread. I don’t consume cow milk, so I buy goat/sheep yougurt, I also make soy yougurt. I also eat gluten-free, so I make sourdough buns at home. I make a lot of buns and a liter yougurt at once, so I don’t have to do this every day.
  • Why frozen vegetables? Because they are chopped and I don’t like chopping. Also they don’t go rotting in my fridge if I forget about them. Also you don’t need to wash frozen vegetables. So many benefits!

Evening preparation:

  • Get a frying pan. I hope you have one in your house. You do need at least one frying pan for this MIND diet project. If you don’t have one – go to the Dollar Store and get one please. Place the pan on your your counter. 20 seconds
  • Take out frozen kale and frozen onions out of the freezer. 10 seconds20181101_213108           20181101_213148 
  • Place some kale and onions into the frying pan. Add salt, pepper, and olive oil. 30 seconds

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  • Place the pan in the fridge. The vegetables will defrost overnight. 10 seconds

Morning cooking:

  • Take out some eggs from the fridge, take out the pan

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  • Turn on the burner, place frying pan on the burner, leave it on medium-high for about five minutes. And don’t just stand there those five minutes, go brush your teeth, or something!
  • After five minutes crack the eggs onto the pan, mix everything together with a spatula
  • Fry for another three- four minutes
  • Place in a container and take to work, if you work in an office using a computer – you can easily enjoy eating while pretending to work
  • Take a jar of yougurt with you, add frozen blueberries – another item checked off from the MIND list

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  • Don’t forget toast/sourdough bread – because they say whole grains three times a day. Can be gluten-free. Eating toast should be easy, not like eating a bunch of kale. Toast is good!

So there, in one breakfast – kale – green leafy vegetable √ , onion – a vegetable , good enough! √, olive oil √, toast/sourdough – whole grains √

What else did they say… nuts? just add them to yougurt √ add blueberries √ don’t add oily fish to your yougurt… Χ

Wine? Well I think you can have that any time 😉

Sniffing soil for depression and PMS

I have been sniffing soil and I think it did me some good. And by soil I mean regular soil, it’s not some kind of code name for a street drug. I started sniffing soil and eating unwashed parsley this summer, after I came across an article about antidepressant effects of a bacteria mycobacterium vaccae, which lives in the soil. Since none of the standard antidepressants worked for me, I am very open to new research. Also soil from the backyard or pots seems pretty harmless. I am currently renting in a first floor of a house and my landlord is a very nice lady, she let me plant stuff at the back, where she also grows kale and tomatoes. I purchased stems of parsley and leek and usually I eat them right from the ground, unwashed. I have also placed a fork in my slot in the backyard and each morning I try to remember to stop by and inhale some soil that I pick up using the fork.

About m. vaccae  “In 2004, Mary O’Brien, an oncologist at the Royal Marsden Hospital in London, published a paper with unexpected results: She injected lung cancer patients with a common, harmless soil bacteria, Mycobacterium vaccae, to see if it could prolong their life. M. vaccae had some success in earlier trials where it was tested for its abilities to fight drug-resistant pulmonary tuberculosis and boost immune system response. O’Brien thought maybe the bacteria could help her patients’ immune systems beat back the cancer in their lungs. It failed.

Only, it succeeded elsewhere: the bacteria injection “significantly improved patient quality of life,” O’Brien wrote in the paper detailing the findings. Her patients were happier, expressed more vitality, and better cognitive functioning—in short, it reduced the emotional toll of advanced cancer.”

Dirt has a microbiome, and it may double as an antidepressant

I am a one person sample and I cannot construct a test and control group using just myself, but I can still provide some observation. Friday was a day three days before my period. I did not know it then because I am never aware of when my period will start. I do know from multiple observations that days -3, 1, 2, and 3 in regards to period start are when I have more severe mood swings. So it was day -3 and I started to get more depressed already after lunch. Like a crushing feeling coming on, everything becomes more bleak, it becomes painful to speak. It’s a real sense of dysphoria, as if from opiate withdrawal. I held it in, but started to cry on my way home. At the back of my mind I still had a thought of hope that there were still interventions I could try and hopefully not go into a very dark hole.

I had plans to meet with my friend at a noodle place near my house after work and I was starting to be concerned that I wouldn’t be able to do it. You could say – why not? Wouldn’t it be better in any case if you do see your friend? Yes, yes, it would, but a severe depressive episode is not just being sad, it can be such extreme emotional pain that you are just unable to speak. What’s also interesting, is that the closer you are to such a state, the less likely you are to try an intervention. You have to keep reminding yourself about the time you said to yourself that you will try. You could write it down in your phone, put an alarm clock. I had to say to my brain – I don’t care about your opinion at this moment, I don’t care that you say no treatment will work. So I stopped in the backyard and ate a lot of parsley from the garden bed. I lifted up soil crumbles to my nose and I inhaled.

An hour and a half later I made it to the noodle place and I was able to talk and laugh. Maybe it was m. vaccae, or placebo effect, it could have been also just the natural course of my symptoms that day. Therefore I have no concrete proof, but still wanted to share this observation, especially considering that there is research out there indicating antidepressant effects of soil bacteria. From Friday on, I continued sniffing soil each morning and I can definitely say this period was less emotionally eventful. No running out to the staircase during work to sob. Also it has been the first time in many months that I did not take any naproxen or ibuprofen. I believe this is an indication that there is a reduction in inflammation. As I have written previously,  I am on a specific Mediterranean diet with extra exclusions such as gluten. I have also been consuming goat kefir and kombucha daily, and infected myself with therapeutic helminths six weeks ago. Which one of these treatments has reduced my PMS pain I am not sure, but I sure am glad that one of them or all of them are showing some positive results.

I suggest you consider getting dirty and maybe eat some herbs straight from the ground. Just make sure to read about parasites in your area, we don’t have any serious pathogenic parasites in Ontario soil, therefore I am not concerned about eating unwashed herbs/vegetables here. I hope some m. vaccae will provide you with a better day.

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?

meds

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!

Yes, I am using this self-made incubator instead of Zoloft to treat depression

Here is my self-made incubator. It was constructed at home from several cheap and available components – a nice big Styrofoam cooler, a light bulb, a light bulb socket, a temperature controller, and some tape. That’s all, very simple. The cooler I got from Canadian Tire for about $14, light bulb, socket, and tape also from Canadian Tire. The temperature controller I purchased on Amazon for $35. What does the incubator do? The light bulb goes inside the cooler, so does the sensor from the controller. You close the lid and choose the desired temperature. The controller keeps the light bulb on until the chosen temperature is reached, then it turns it off. If the temperature drops, the light bulb is turned back on.

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How is any of this relevant to depression treatment? Well turns out that it is, and this incubator has been helping me a lot more than my previous trials of anti-depressants. I use the incubator to make fermented foods and research shows that eating probiotic foods can reduce chronic inflammation in the body and this in turn can reduce symptoms of depression. I have been making goat kefir, goat yougurt, sourdough, fermented fruits. I have also ordered a tempeh starter – spores of a specific mold, Rhizopus, that is used to ferment soy beans. I have also been buying natto (another type of fermented soy beans) in a Japanese store and eating it for breakfast.

It has been a bit more than a month since I started all this fermented food consumption and I think it has definitely improved my brain function in many ways. Correlation doesn’t mean causation, but I have noticed improvement in the way I think, the way I react to stressful events, my ability to sit down and spend time on meditation. I have rediscovered my interest in violin playing and my interest in the opposite sex. Last week I found my headphones because I wanted to listen to David Guetta in the subway on my way to work. Maybe that doesn’t sound like much, but if you’ve experienced severe depression and if you’ve seriously considered suicide, I think you would understand that this means progress. If you have experienced a state of mind in which your only desire was finding a way to end your life, then you know that going to a state where you have a desire for something else, anything else, is definitely an improvement.

I think therefore that constructing this incubator was the best decision this year so far. Last year the best decision that I made was pursuing immunosuppressant with intravenous steroids. I was treated with IV Solu-Medrol for five days in December and after that I saw my mind opening up. No, my depression did not vanish, but I started to have ideas, to be more proactive. Participating. I through of sharing my experience with autoimmune encephalitis, so I started a blog. I took the psychiatrist’s advice to do aerobic exercise in order to reduce brain inflammation. I researched further anti-inflammatory treatments and decided to build an incubator. I also became interested in helminthic therapy, so I learned how to use bitcoin and purchased some helminth larvae in order to infect myself. I don’t think this is all a coincidence, I think the steroids treatment did reduce inflammation that was there in my brain and some neural pathways opened up, more ideas started coming in. My tunnel vision became broader, the world became less black and white.

You can read my previous post about fermented foods and depression treatment here:

Bacteria, yeast, stinky tofu, desire?

My case of severe depression and improvement after immunotherapy is another piece of evidence supporting the idea that depression and suicidal thoughts are not always just caused by imbalance of serotonin, but inflammation can also play an important role.

Recently researchers at the University of Manchester conducted a study measuring level of inflammation in the brains of patients with clinical depression. “Dr. Talbot and colleagues measured the levels of translocator protein (TSPO) in the brains of people diagnosed with major depressive disorder. TSPO generally plays a role in the immune response system and cell death.

In the brain, elevated TSPO levels activate the microglia, which are immune cells specific to this organ. Microglial activation indicates brain inflammation, so this is what the scientists targeted.

People with depression who were experiencing suicidal thoughts were found to exhibit significantly higher levels of TSPO, associated with microglial activation and indicating inflammation of the brain.

Depression: Is brain inflammation tied to suicidal thoughts?

I was suffering from treatment resistant depression, but now I believe that it is not resistant, the treatment was just incorrect. I was put on mirtazapine, bupropion, risperidone, sertraline, multiple combinations of antidepressants and antipsychotics were tried. Well none of those combinations worked, but today I am still alive. I cannot thank my psychiatrist who continued to treat me with the same medications just in different doses and mixes, but I am thankful to all the researchers, journalists, and bloggers, who have written on the topic of the link between inflammation, suicidality, and depression. I am very thankful for Susannah Cahalan for her book “Brain on Fire: My Month of Madness” about her terrifying experience with anti-NMDA receptor encephalitis. I think, maybe not in the average psychiatrist’s office, but in general there has been progress in understanding the impact of our diet, lifestyle, and chronic inflammatory conditions, on mental health. Diet matters, exercising matters, so does our gut microbiome, blood glucose levels, inflammatory markers. All of this cannot be fixed by just taking Zoloft or Prozac and I believe that is why many people don’t get better on antidepressants. They are not treatment resistant, the right treatment is available, it just hasn’t been applied.