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

 

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.

 

 

Any benefits to ‘ancient’ grains?

Ancient grains are whole grains that are considered more… ancient… than some modern grains. If you ever visit health stores, than you probably had seen this marketing label multiple times – Ancient Grains Pasta! Ancient Grains Cereal! Ancient Grains Bread. Also now I see everywhere sprouted breads, sprouted cereals, sprouted oatmeal. There is even a brand that sells Ezekiel 4:9 bread with a verse from the Holy Scripture on the package. I suppose they were trying to emphasize how ancient the recipe is. Or holy.

In general I think dietitians would say that whole ancient grain breads, wraps, cereals, pastries, etc., are definitely healthier than same items made out of white flour. I also think they are healthier than similar gluten-free items. In those the main ingredient is usually tapioca starch or white rice flour. Take for example Glutino sandwich bread. I just Googled it and right away saw this description of their product by the company: “Did you know? Gluten comes from the Latin word for “glue”. So think of yourself as eating glue-free.” Yes, because the word gluten originates from some Latin word meaning ‘glue’, you should drop everything and switch to eating slices of white matter made out of modified tapioca starch, corn starch, potato starch, and baking soda. One slice of the Glutino bread contains 0g fiber, 0g protein, and I don’t see any other nutrients listed on the label.

In this conversation  I will not refer to people who have celiac disease. I understand that with celiac even one crumb of gluten would cause an autoimmune reaction. I’m referring here to all of us who did not test positive for celiac disease, but were told by naturopaths and other pseudo ‘doctors’ that gluten is causing their autoimmune disease, or thyroid disease, or depression, anxiety, autism, you name it. I don’t see any convincing evidence that whole grain gluten grains cause any of these diseases. To provide good evidence, I think a study would have to follow two randomized groups of patients for a while and restrict the diet of the test group to be gluten-free, group assignment of course would have to be unknown to the patients. The diets would have to be the same in other aspects, otherwise it’s not a fair comparison. Also the diet should be healthy , so the patients are receiving all the necessary nutrients, since we are interested in whether or not gluten has negative effects on health with an otherwise healthy diet. You would also have to do separate studies for each condition. Randomized test-control study for patients with schizophrenia, with depression, with autism, hypothyroidism, etc. If gluten negatively affects schizophrenia symptoms, it does not necessarily mean that  it also negatively effects patients with thyroid disease. For example high soy consumption is not recommended for those taking levothyroxine as it may interfere with medication absorption. On the other hand some research suggests that soy has antidepressant effects and therefore could help individuals with depression.

Is there some research in regards to gluten and neuropsychiatric and autoimmune diseases (except celiac)? Yes, there is. I just really don’t like the claims by naturopaths on their websites that it’s known that gluten causes schizophrenia, depression, and everything else. We definitely can’t claim causation, we don’t have such information at this point, and it doesn’t make sense to bundle up a dozen of diseases together. Schizophrenia is very different from hypothyroidism, and both are different from ADHD.

For schizophrenia: there is some renewed interest in regards to gluten-free diet. “Going gluten free shows a benefit for a subset of schizophrenia patients,… Those on the gluten-free diet also showed improvement in gastrointestinal symptoms and improvement in certain cognitive traits, such as attention and verbal learning.”

Interest renewed in targeting gluten in schizophrenia

Autism: The one review of research that I found indicated that evidence was inconclusive. “Studies evaluating gluten/casein-free diets reported some parent-rated improvements in communication and challenging behaviors; however, data were inadequate to make conclusions about the body of evidence (insufficient SOE). Studies of gluten- or casein-containing challenge foods reported no effects on behavior or gastrointestinal symptoms with challenge foods (insufficient SOE);”

Nutritional and Dietary Interventions for Autism Spectrum Disorder: A Systematic Review

Hypothyroidism: I could not find an actual systematic review on relationship between hypothyroidism and gluten research, therefore I am not sure if there is any evidence that gluten consumption negatively impact thyroid function. Clinical websites state that there is no such evidence. “Generally, there’s no hypothyroidism diet. Although claims about hypothyroidism diets abound, there’s no evidence that eating or avoiding certain foods will improve thyroid function in people with hypothyroidism.”

Hypothyroidism diet

Personally I did not achieve remission in depression or autoimmune disease with a gluten-free diet. In fact at first going gluten-free probably led to a worse diet for me, as I would eat two or three gluten-free bread cheese sandwiches a day, and as we can see this type of bread has no proteins, nor fiber, no other nutrients. So basically I was eating tapioca starch. I was also consuming gluten-free cookies, which are probably mostly sugar and again, tapioca starch, corn tortilla chips, and gluten-free subs (gluten-free Subway buns are a lot of cornstarch). I doubt there are any B vitamins in the above foods, nor any other nutrients. What about a healthy diet with gluten-free grains vs. the same diet, but also including gluten whole grains? It has been over a month for me since I started eating gluten again. I have not noticed so far any changes in my health. My health did not improve nor did it worsen. I don’t want to limit myself and keep falling victim to these restrictive diets promising to cure all your mental health problems. Gluten-free diet, alkaline diet, keto diet, AIP diet.. there will be claims found for each of these that this specific diet cures depression, autism, and schizophrenia. Well I have not found a cure for depression, so I do not have that answer. It’s important to eat healthy, but it doesn’t seem to me that a very restrictive diet is an answer.

Again, for myself I did not observe worsening of mental issues after introducing gluten whole grains to my diet. Also not obsessing over whether something was contaminated with gluten lessened my anxiety related to eating. I am still trying to avoid A1 cow dairy and yeast (based on my testing of my symptoms). I want to restrict as few foods as possible. Naturopaths telling people that a bite of gluten or a piece of corn will cause panic attacks for the next few months are the ones actually contributing to anxiety of people like me. By starting eating gluten again I made my life much easier – I don’t have to pay extra for gluten-free oats, I buy rotis, wraps, and samosas, which I can easily eat at work in the morning or as a snack. I’m eating cereal and getting the B vitamins. I can purchase good tasting spelt pasta for cheap, instead of buying very expensive chickpea pasta.

In regards to whole wheat vs. more ancient wheat related grains, I don’t think there is strong evidence that ancient grains are better, but there are some studies related to this. I buy and mix both types of flour – spelt and whole wheat. I noticed that using only spelt flour, the muffins or cookies don’t rise as well (even though I do add sodium bicarbonate or potassium bicarbonate).

There is some evidence in support of ancient grains consumption, I will review it below.

Grain composition is affected by both the environment and agronomy, particularly the type and amount of nitrogen fertilisation. Increased nitrogen application leads to higher protein content (Shewry et al., 2013), but this is accompanied by effects on protein composition, with high protein grain containing higher proportions of gluten storage proteins and of gliadin proteins within this fraction (Godfrey et al., 2010).

 compared data for ancient wheats with modern durum and bread wheats. However, to minimise effects of the environment they only considered studies in which modern and ancient wheats were grown together in field experiments. They concluded that ancient wheats differ little from modern wheat species in their contents of most bioactive components and may be lower in some components such as dietary fibre. However, there is clear agreement in the literature that einkorn, emmer and Khorasan (Kamut) wheat all have higher high contents of the carotenoid lutein than bread wheat, which is selected for white colour. Modern durum wheat is also rich in lutein due to selection for yellow colour.

Six trials reported comparisons of Kamut or related forms of Khorasan wheat with modern durum and/or bread wheats, measuring effects on parameters related to cardiovascular disease, glycaemic index, type 2 diabetes and irritable bowel syndrome. However, none of these studies compared Kamut wheat grown in identical conditions to the control wheats, presumably because the growth of Kamut is strictly controlled. As stated on the Kamut® web site (http://www.kamut.com/en/discover/the-trademark): “The KAMUT® trademark is a guarantee that the khorasan wheat bearing it is always the original, unmodified, unhybridized and non-GMO variety. KAMUT® khorasan wheat is also always grown certified organic and meets high purity, nutrition and quality standards”.

Scazzina et al (2008) obtained wholemeal Kamut and bread wheat flours from a local (Italian) supermarket and hence nothing is known about the growth conditions of the crops or the identity of the control wheat (although it would be expected to be a blend of commercial cultivars). Tortillas prepared with 60% flour had significantly higher fibre (6.7% compared with 3.5%) and lower starch (44.3% compared with 48.6%) when made from Kamut than from bread wheat, but did not differ in glycaemic index in an intervention trial.

Pasta made from the semi-whole wheat semolina fractions of Kamut and durum wheat and bread and crackers made from the semi-whole wheat flours from Kamut and bread wheats were compared in a randomised single blinded cross-over trial with 22 patients. The Kamut diet resulted in significant reductions in metabolic risk factors (total cholesterol, LDL cholesterol, blood glucose), improved redox status, increased serum potassium and magnesium and significant reductions in circulating levels of pro-inflammatory cytokines.

Do ancient types of wheat have health benefits compared with modern bread wheat?

Gluten, scary titles, and science

Last Friday during lunch I bought some spelt crackers and ate them, and nothing happened. Spelt is a type of grain that is strongly related to wheat. Why did I decide to try it? Well I have been trying to eat gluten-free since May 2016 when I was diagnosed with Hashimoto’s thyroiditis (and later on with Hashimoto’s encephalitis). I had been seeing a psychiatrist since October 2015 but I wasn’t responding to any of the prescribed psych meds, so my mom ordered the family doctor to refer me for autoimmune testing and high levels of anti-Tg and anti-TPO antibodies were found. I also tested positive for deamidated gliadin IgG, but negative for transglutaminase IgA antibodies. Total IgA was within normal range. Clinical websites state that if total IgA is normal and tissue transglutaminase (tTG)-IgA is negative, there is a low probability of the patient having celiac disease and a biopsy may not be necessary. My doctor did order a biopsy because of the elevated deamidated gliadin antibodies and the results indicated that there were no atrophic features identified (celiac disease causes persistent villous atrophy).

So what happened next? I think a rational doctor at this point should have said that I could go on with my bread eating, since the biopsy is the main test for celiac disease detection, and my results came back normal. But psychiatrically I was not well and my mom was very scared, she didn’t know what to do, since the psychiatrist was also out of ideas. When conventional medicine fails, people turn to alternative. Soon here we were, with my mom at a naturopath’s office. Consultation price per hour was around $250. The man in a white coat, pretending to be a doctor, asked me about my symptoms. He stated that I had to stop consuming gluten, dairy, needed to do a food sensitivities test, hair analysis test, should stop taking my antidepressant medication, and should buy $100 worth of supplements from him. He also mentioned eating cooked kale. In total this one consultation, after my mom also paid for all the tests he ordered, cost my mom around $2000 – $2500. That’s how you make money, ladies and gentlemen.

It’s very easy to come across articles online with scary titles about gluten. “Is Gluten Causing Your Depression?”, “The Surprising Link Between Gluten and Depression”, “Is gluten messing with your mind? Find out how.” One articles states that it could be actually FODMAPs (fermentable oligo di mono-saccharides and polyols) causing bowel inflammation and in turn depression. Wheat is high in FODMAPs and it’s effects could be misinterpreted as caused by gluten. This theory has some research to support it. Personally since I started eating gluten already a month ago, I did not experience abdominal pain from wheat products. I did notice bloating and pain after eating yeast containing products, such as bread, but no problem with eating wheat rotis, flatbread, etc. I am also using helminthic therapy, as I mentioned in previous posts, so this also could have helped with abdominal inflammation.

Some other articles outright claim that gluten causes “hundreds of symptoms”, also causing depression, psychosis, schizophrenia, and autism. To make extraordinary claims you have to provide extraordinary evidence. I have not been able to find strong evidence that gluten consumption causes any of the above conditions. There do exist several studies finding negative symptoms from gluten consumption, but I would not call this strong evidence. There are also other studies indicating negative impact of a gluten-free diet. I will list some of the studies below, covering both sides of the argument:

  1. Mood Disorders and Gluten: It’s Not All in Your Mind! A Systematic Review with Meta-Analysis. Meta-analyses with random-effects were performed. Three randomised-controlled trials and 10 longitudinal studies comprising 1139 participants fit the inclusion criteria. A gluten-free diet (GFD) significantly improved pooled depressive symptom scores in GFD-treated patients (Standardised Mean Difference (SMD) −0.37, 95% confidence interval (CI) −0.55 to −0.20; p < 0.0001), with no difference in mean scores between patients and healthy controls after one year (SMD 0.01, 95% CI −0.18 to 0.20, p = 0.94). There was a tendency towards worsening symptoms for non-coeliac gluten sensitive patients during a blinded gluten challenge vs. placebo (SMD 0.21, 95% CI −0.58 to 0.15; p = 0.25). Our review supports the association between mood disorders and gluten intake in susceptible individuals. The effects of a GFD on mood in subjects without gluten-related disorders should be considered in future research.
  2. Effects of a gluten-free diet on gut microbiota and immune function in healthy adult humans. The trial included 10 healthy subjects (30.3 years-old), which were submitted to a GFD over one month. Analysis of fecal microbiota and dietary intake indicated that numbers of healthy gut bacteria decreased, while numbers of unhealthy bacteria increased parallel to reductions in the intake of polysaccharides after following the GFD. Fecal samples of subjects under a GFD, which represent an altered microbiota, also exerted lower immune stimulatory effects on peripheral blood mononuclear cells than those of subjects on a regular gluten-containing diet.
  3. The Gluten-Free Diet: Fad or Necessity?

    Some evidence indicates that there are significant drawbacks to following the gluten-free diet. For example, gluten-free processed grain products (e.g., breads, cereals, and crackers) are often lower in fiber, iron, zinc, and potassium (29). The gluten-free diet also may increase the risks for nutritional deficiencies, especially in B vitamins, iron, and trace minerals (30). In addition, gluten-free products continue to be significantly more expensive. A 2015 study found that gluten-free bread and bakery products were on average 267% more expensive than gluten-containing breads, and gluten-free cereals were found to be 205% more expensive than gluten-containing cereals (29).

    Individuals following the gluten-free diet also may fail to adhere to recommendations regarding daily servings of grain products. One study found that 38% of patients with celiac disease included no grain or starch choice at meals; when patients did choose a grain product, 44% most frequently chose rice (31). In another survey of people with celiac disease, 80% were eating less than half of the recommended daily amount of grains, and only 1.1% ate the six recommended servings each day. Of those who did eat grain products, 61% most frequently chose rice and corn (32).

Personally I don’t see any strong evidence that a gluten-free diet would reduce depressive symptoms in persons with no celiac disease. In the first study, the authors state “anti-gliadin IgG antibodies disappeared in NCGS patients [34] and markers of systemic inflammation were reduced in IBS patients [36], as well as healthy mice [37] following initiation of a GFD.” I don’t see this applicable to me because I tested and I do not experience any IBS symptoms from consuming wheat or spelt. I do find myself having strong abdominal pain after consumption of regular cow milk products or yeast containing products, such as leavened bread. I have no problem with muffins prepared with baking soda, rotis, tortillas, or breakfast cereals. I see no reason to not eat these foods as they are healthy whole grains and contain B vitamins. In general I don’t want to have specific constrains for myself and feel guilty after eating once piece of pie. I know some naturopaths will say that even one piece of a cookie with gluten can make you depressed, but I see that as non-scientific nonsense. I have been gluten free, dairy free, on the autoimmune protocol diet, and I am still depressed. Depression can be caused by genetics, female hormones (such as premenstrual dysphoric disorder), epigenetics. One piece of pie isn’t going to make it or break it for me, but it does make that moment sweeter. I’m not going to be eating pie often and I do limit my sugar intake, but once a week at a friend’s house is no big deal.

By law, in Canada white wheat flour has to be enriched, therefore by eating flour products you obtain several B vitamins.  “The mandatory enrichment of white flour with B vitamins, iron and folic acid is a cornerstone of Canada’s fortification program aimed at helping to prevent nutrient deficiencies and maintain or improve the nutritional quality of the food supply.

Section B.13.001 (Food and Drug Regulations):

[S] Flour, White Flour, Enriched Flour or Enriched White Flour

(d)shall contain in 100 grams of flour

  1. 0.64 milligrams of thiamine
  2. 0.40 milligrams of riboflavin
  3. 5.30 milligrams of niacin or niacinamide
  4. 0.15 milligrams of folic acid, and
  5. 4.4 milligrams of iron

(e) may contain

(xv) in 100 grams of flour

  1. 0.31 milligrams of vitamin B6
  2. 1.3 milligrams of d-pantothenic acid, and
  3. 190 milligrams of magnesium

(f) may contain calcium carbonate, edible bone meal, chalk (B.P.), ground limestone or calcium sulphate in an amount that will provide in 100 grams of flour 140 milligrams of calcium.

All white flour and foods containing white flour that are sold or intended for sale in Canada, both imported and domestically produced, are expected to be in compliance with the enrichment requirements for white flour.

White flour is processed and has high glycemic index, so it’s not advised to eat it often, but I am no longer trying to completely avoid it. Whole grain gluten flours such as whole wheat, splet, and kamut, also contain B vitamins. I am also glad to eat fortified cereal again, as they are cheap, convenient, and in one bowl you get a lot of B vitamins, plus magnesium, zinc, and iron. For example, I bought a giant box of bran flakes for $5 at Drug Mart and only 3/4 of a cup contains 30% DV iron, 45% DV thiamine, 10% DV B6, 8% DV folate, 10% DV zinc. It’s pretty hard to get that nutrition from consuming gluten-free corn cereal or puffed rice. Also it tastes better, so why not eat it? Unless someone provides strong and clear scientific evidence to do otherwise.

 

Clams and coffee for a good morning

I like B vitamins and caffeine, that is a good combinations. And a bit of carbs. Coffee, clams, and oatmeal bar with dates makes a good breakfast. I don’t know the mechanism, but I am finding that coffee helps me to be more present in the moment with fewer anxious thoughts about the future. Going back to coffee was not a random idea, there are several studies in regards to the use of caffeine for treatment resistant OCD. By the way, OCD is not just about washing your hands multiple times or checking five times that you locked the door. The worst aspect of if it is how your mind is affected by unwanted and intrusive thoughts. There are infinite types of OCD, it can impact on any thought, on any subject, on any person, on any fear, and frequently fixates on what’s important in a person’s life. For example, if religion is important to someone, OCD fixates on unwanted intrusive thoughts around religion, perhaps making the sufferer believe their actions/thoughts will offend their god. Another example is if someone begins a new relationship, OCD can make a person question that relationship, their feelings, their sexuality resulting in almost constant rumination, perhaps with the sufferer worrying that they may be misleading their partner.

Obsessive thoughts are what happens when you just want to go for a walk in the forest. It’s a warm day, finally summer, you are surrounded by colourful moss on intriguing rocks. You want to wander around observing the details of nature, but your mind is fixated on the thought that there is no point. There is no god, therefore our lives are meaningless, and there is no point of this wandering. Or the thought is – I don’t have a child, so I need to work on getting a family. And then you feel that because you haven’t achieved this goal, you will be punished for wandering around the forest. You should be punished for any enjoyment as those are not focused on the goal. You need to solve the problem at hand, you need to act now, you need to think through the plan. And it goes on.

B vitamins are essential for creating dopamine, epinephrine, serotonin, and myelin. They also help the mind focus, help hemoglobin hold oxygen and lower cholesterol. Vitamin B is essential to good health. It is also used for energy production in the human cells. B vitamins help convert food often consumed as carbohydrates into fuel. They also help the nervous system function properly. B vitamins are water-soluble, which means that they are easily dissolvable in water and easily excreted out of the body via urine output. As a result of this type of vitamin that can be dissolved in water, individuals cannot overdose on them because all excess will simply be excreted.

Solubility – Solubility is defined as the maximum quantity of a substance that may be dissolved in another. How a solute dissolves depends on the types of chemical bonds in the solute and solvent. For example, when ethanol dissolves in water, it maintains its molecular identity as ethanol, but new hydrogen bonds form between ethanol and water molecules. For this reason, mixing ethanol and water produces a solution with a smaller volume than you would get from adding together the starting volumes of ethanol and water.

When sodium chloride (NaCl) or other ionic compound dissolves in water, the compound dissociates into its ions. The ions become solvated or surrounded by a layer of water molecules.

Thiamin is vitamin B1, it is essential in carbohydrate metabolism and neural function. It is water soluble and is absorbed through both active transport and passive diffusion. Not being endogenously synthesized, the only available source of thiamine is dietary (beef, poultry, cereals, nuts, and beans). In the human body, thiamine-rich tissues are skeletal muscles, heart, liver, kidney, and brain. Thiamine serves as a cofactor for a series of enzymes in different metabolic pathways and is required for the production of ATP, ribose, NAD, and DNA. Thiamin plays a key role in the maintenance of brain function. Thiamin diphosphate is cofactor for several enzymes involved in glucose metabolism whereas thiamin triphosphate has distinct properties at the neuronal membrane.

Thiamin metabolism in the brain is compartmented between neurons and neighbouring glial cells. Thiamin deficiency is commonly encountered in severe malnutrition associated with chronic alcoholism, HIV-AIDS and gastrointestinal disease where it frequently results in Wernicke’s encephalopathy (the Wernicke-Korsakoff syndrome).

In developed countries, the predominant use of industrial food processing often depletes thiamine content along with other vitamins and nutrients. An increased consumption of processed food in the form of simple carbohydrates, not supplemented with adequate levels of thiamine, has been named “high calorie malnutrition”. As thiamine is a key factor in the metabolism of glucose, an increased carbohydrate intake will proportionally increase thiamine’s dietary demand. Heavy consumption of tannin-containing or food rich in caffeine, theobromine, and theophylline (such as those present in coffee, chocolate, and tea, respectively) can inactivate thiamine, thereby compromising the thiamine status. Other risk factors that increase the likelihood of insufficient thiamine intake include aging, economic status, eating disorders, medical conditions affecting the gastrointestinal tract, subjects receiving parental nutrition, bariatric surgery, diabetes, and alcohol abuse.

Thiamine deficiency might cause brain tissue injury by inhibiting brain energy utilization given the critical role of thiamine-dependent enzymes associated within glucose utilization. This is supported by the significant rate of thiamine uptake by the blood–brain barrier emphasizing the high brain demand for thiamine and the need for its supply to sustain adequate brain functions.

Throughout the digestive tract, dietary proteins get hydrolyzed, releasing thiamine. In the intestinal lumen, alkaline phosphatases catalyze the hydrolysis of thiamine-phosphorylated derivatives into free thiamine.

There are cases of psychosis resulting from thiamine deficiency.

Case 1 – a 63-year-old woman with thiamine deficiency who showed auditory hallucinations, a delusion of persecution, catatonic stupor, and catalepsy but no neurological symptoms including oculomotor or gait disturbance. Her thiamine concentration was 19 ng/mL, only slightly less than the reference range of 20-50 ng/mL. Her psychosis was unresponsive to antipsychotics or electroconvulsive therapy, but was ameliorated by repetitive intravenous thiamine administrations at 100-200 mg per day. However, one month after completing intravenous treatment, her psychosis recurred, even though she was given 150 mg of thiamine per day orally and her blood concentration of thiamine was maintained at far higher than the reference range. Again, intravenous thiamine administration was necessary to ameliorate her symptoms. The present patient indicates that the possibility of thiamine deficiency should be considered in cases of psychosis without neurological disturbance and high-intensity T2 MRI lesions. Also, this case suggests that a high blood thiamine concentration does not necessarily correspond to sufficient thiamine levels in the brain. Based on this, we must reconsider the importance of a high dose of thiamine administration as a therapy for thiamine deficiency.

Case 2 – Mr A, a 40-year-old man, was transferred to our drug and alcohol dependency clinic after admission to the emergency department of a general hospital. He had a 25-year history of regular alcohol consumption (2 bottles of wine and 3–4 bottles of beer per day recently). Notably, he gradually increased his alcohol intake. His family stated that for the last 2 years he started his mornings with his usual “eye opener,” and he had not been eating enough or regularly. They also described periods of alcohol withdrawal, which resulted in delirium tremens symptoms such as confusion and auditory and visual hallucinations. He presented to the emergency room with forgetfulness, difficulty walking, falling down, urinary incontinence, losing his belongings, and not being able to recognize where he was or the current date. His family also reported that he had been telling incongruent stories that never seemed to have happened.

Mr A was diagnosed with Wernicke-Korsakoff syndrome according to DSM-IV diagnostic criteria, and diazepam detoxification, rehydration, and thiamine repletion therapy were started. He had no signs of alcohol withdrawal in the clinical follow-up. He was administered intravenous (IV) 2,000 cm3 of 5% dextrose and 1,000 mg thiamine hydrochloride. This regimen was administered until the fifth day of treatment since gait ataxia and restriction of eye movements were no longer prominently present. On the sixth day of treatment, the IV thiamine was replaced with 100 mg oral thiamine. Within the third week of the treatment regimen, his gait and postural ataxia improved and his orientation to time, place, and person was intact. By the fourth week of treatment, he was able to find his way around the city and back home when he was on home leave for 2 days. However, it was observed that it took him longer to remember his past experiences when questioned. He was discharged 41 days after his hospitalization. He had no significant mental symptoms apart from a minimally longer reaction time and minimal impairments in current memory, although he still had difficulty in tandem walk and a minimal nystagmus in his neurologic examination at discharge.

Neuropathology of Wernicke-Korsakoff syndrome is characterized by gliosis and microhemorrhages specifically in the periaqueductal and paraventricular gray matter, atrophy in the mammillary bodies and thalamus, and volume deficits in the hippocampus, cerebellar hemispheres, pons, and anterior superior vermis; however, anterior thalamus, mammillary bodies, and the mammillo-thalamic tract are reported to be related with later memory impairment and Korsakoff syndrome.

Active transport – the movement of molecules across a membrane from a region of their lower concentration to a region of their higher concentration—against the concentration gradient or other obstructing factor.

Passive diffusion – is a movement of ions and other atomic or molecular substances across cell membranes without need of energy input. Unlike active transport, it does not require an input of cellular energy because it is instead driven by the tendency of the system to grow in entropy.

Hyrdolysis – any chemical reaction in which a molecule of water ruptures one or more chemical bonds.

Alkaline phosphatase – an enzyme that liberates phosphate under alkaline conditions and is made in liver, bone, and other tissues.

Gliosis – is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). The glial cells surround neurons and provide support for and insulation between them. Glial cells are the most abundant cell types in the central nervous system. The four main functions of glial cells are: to surround neurons and hold them in place, to supply nutrients and oxygen to neurons, to insulate one neuron from another, and to destroy and remove the carcasses of dead neurons (clean up).

Microhemorrhages – cerebral microhemorrhages, best visualized by MRI, result from rupture of small blood vessels in basal ganglia or subcortical white matter.

Mammillary bodies – the mammillary bodies are part of the diencephalon, which is a collection of structures found between the brainstem and cerebrum. The mammillary bodies are best known for their role in memory, although in the last couple of decades the mammillary bodies have started to be recognized as being involved in other functions like maintaining a sense of direction.