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.

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.

CAMH ER Waiting Room

The room is in the building at College and Spadina. The room doesn’t have any windows,  but it does have a clock, so you can know what time of day it is. What you can’t know is when you will be let out (but to be fair, involuntarily hospitalization can be a maximum of 72 hours). There are armchairs along the perimeter of the area and in the middle. There are about six of us at the moment. Some will be released soon and new ones will arrive. None of us want to be waiting here, twisting on the pale green chairs. Also most don’t agree that they should be here. A young black woman is banging on the locked door of the staff room, a nurse comes out. The woman is nearly dressed with a designer purse and fur boots. She starts pacing back and forth. “If I knew what this place is like, – she yells at the nurse, – I would have never come here. Look at me, I don’t need to be here. I don’t cut myself and shit.” The nurse talks to her calmly, she tells her what she tells everyone – you have to wait to speak with the psychiatrist. The woman continues to yell that she is not like the rest of us. She complained to her family doctor about stress at work and the doctor referred her to this address,  told her that she could get a note for stress leave. She just wants a note,  she assures that she doesn’t cut herself.

As of that is what we all do. If only it was that simple – you either cut yourself and are insane, or you don’t,  and are not. I’ve never cut myself and yet I voluntarily checked myself into the CAMH ER. I also didn’t think that I needed to be in there, but there was no other way. I wanted to be set free from my inflamed brain, from the malfunctioning neuronal synapses. I wanted to be free to get lost in writings of other people’s ideas, to play Bach’s Gavotte, to be attracted and be attractive. I wanted to be released from the dark well inside my own mind. I wanted to suppress the hell, to get the intravenous immunoglobulin treatment. But how to convince them, how to make them understand that is what I needed?

After sometime the black woman was released. I was still waiting. There was renewed yelling,  coming from a different patient. Similar to the woman who just left,  she was yelling at the nurse that she didn’t need to be here. She was also getting extremely agitated,  I think if she had something to throw,  she would. The whole room now was aware that she was old enough to have ten children and that she didn’t want this visit on her record. Her sister couldn’t take care of her own kids and who would then be doing it if not her? But with a CAMH visit on the papers, maybe she wouldn’t be allowed to take the children in. The nurse tried to explain that visiting CAMH was not same as police record, but the woman already went into rage, reasoning does not work at that point.

So why do we all scream in fear – I shouldn’t be here, I am not like the rest of them? We must have evolved to have this fear of being declared insane. Insane means being banned from the tribe, starving alone in the savannah. It’s hard to let go of that basic fear of being abandoned by our tribe. Even in the isolated room at CAMH, where only the doctors and about five other strangers could hear you, we still don’t want to admit that something could be wrong. We could admit cancer, meningitis, infertility, but not that we are not mentally well. Most diseases are just affecting our body, but it is our mind that makes us who we are. And if there is something wrong with that, then what are we? Of course this is not what I think, this is an assumption of what goes on through people’s minds in this state of fear. There is no separation from mind and body, both are a combination of cells, proteins, amino acids. Signalling to each other, reproducing. And any part of the whole mechanism can malfunction.

I would say – learn to accept. You didn’t choose this body, you just sort of woke up in it. I would have chosen another model, if I could, but no choices were given. Well here I am, at CAMH ER, because some signals are malfunctioning, and it’s not my fault. This is the situation though, and I have to accept.