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Addition #23 - B1 - thiamine
This post has my checklist answers and some medical/psych/medicine and genetic history - which included B1, which the list, it turns out, needed.
Health care professionals need to remember "First, do no harm." Mental health patients are too often treated as if their bodies are not connected to their mind.
The problem with having a mental health problem, is that it can make thinking difficult. Once already not thinking well, it can be more difficult to care for oneself, or to understand advice and act on it, or to avoid advice that is potentially harmful if the details were really dug into. Informed consent too often in the medical system means minimal guidance with a glossing over of possible risks. True informed consent should also include a review of other treatment options including diet/exercise type options, and their risks and benefits. And also that of doing nothing, “Watch and wait”. Is the long-term prognosis varied? Is remission common? Or unusual? What are the long-term risks or benefits of the proposed treatment? Or are those unknown too? (…and you are being experimented upon.)
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Do-gooders can do the worst harm, while feeling good about it.
Quote by C. S. Lewis
“Of all tyrannies, a tyranny sincerely exercised for the good of its victims may be the most oppressive. It would be better to live under robber barons than under omnipotent moral busybodies. The robber baron’s cruelty may sometimes sleep, his cupidity may at some point be satiated; but those who torment us for our own good will torment us without end for they do so with the approval of their own conscience.” - C. S. Lewis
Having mental health symptoms in the current system is unpleasant and too frequently deadly for many patients. Withdrawal from meds may be leading to suicide because of the sudden change in serotonin or in the case of olanzapine, in cannabinoid levels. Other B vitamins and magnesium are also frequently depleted and can worsen mood problems or paranoia and anger. Psychiatric medications are prescribed too readily and often by a family doctor. They are also given to young children, and often to children in Foster Care who may not have adequate oversite by a concerned primary parent.
This Retinoid series has grown and isn’t done growing - Parkinson’s Disease may also have retinoid imbalance links. It and other work has been helpful to my own health, and the search for answers about my own health has taken me a lifetime. This feels like it is finally there at my fingertips. As a case example - patient number one - I will share which of the 23 variables I might be likely to have had during my worse years - all adding up to surreal, dissociated, anorexic and manic behavior.
Checklist style - I have added my own medical history answers.
Yes - Low vitamin D (can also be Yes - low magnesium or Yes - helped to cut it out, thoroughly, excess glyphosate) or Yes -gene differences in the Vitamin D Receptor (VDR). (47) VDR gene alleles are also seen in bipolar disorder. (48) Low vit D is a factor in Toxoplasmosis risk. (76)
Excess Retinoic Acid might affect Vit D Receptor transcription of proteins. (114)
Yes - Low iodine/hypothyroidism / excess fluoride, bromide and perchlorates. (55)
Yes - Excess Retinoic Acid might affect Thyroid Receptor function. (114)
Zinc finger transcription proteins are regulators of activated Retinoic Acid, so a deficiency of zinc may worsen an excess of RA, (114), as is seen in Fetal Alcohol Syndrome.
Yes - Excess copper in relation to a low zinc level - may be dietary or genetic - the copper/zinc transport protein dysbindin would be needed as a treatment if that was an underlying factor. (Dysbindin:56, 57, 58, 81),
Yes - (low selenium and zinc, probably elevated copper, marginal to okay iron) - Low trace minerals or excess, or imbalance - it is complex - some with individual impact: Zinc, Cobalt, Chromium, “Zn, Co and Cr”; or in combination with a group of minerals: Selenium, Lead, Phosphorus, Tellurium, Copper, and Thallium, “including Se, Pb, P, Te, Cu and Tl”, or a few that might affect it either individually or in a combination of minerals “such as Cs,” Cesium. Most were low or moderately low, a few were in excess (lead, iron). (83) Elevated iron is seen in chronic inflammation and adds to risk. Lead is a neurotoxin - avoid it.
Unknown - Low Cesium is also seen in Alzheimer’s. The research team speculate that it may chelate misfolded proteins. “The potential relationship between Cs and Schizophrenia may be due to its chelating proteins, such as amyloid-β (Aβ) and apolipoprotein (APOE) and adjusting oxidative status in the brain 27.” (83)
Yes - B vitamins – Yes - gene methylation difference and/or - Yes - pyroluria may be factors in chronic deficiency. Low methyl folate and methyl B12; possibly methylation gene differences. (55)
Yes - the pyroluria causes this for me. - Low B6, (82)
Yes - supplements help and are needed at least every other day or so or symptoms start returning. - B6, B8 (Inositol), and B12 supplementation helped. (85)
Yes - Low niacin – or a need for more than average for an unknown reason at this time. (45)
Yes - too low can cause easier bruising - Vitamin C supplementation helped, along with standard medication. (88)
Yes - I added that early in my Get Better Journey and have stuck with it - Cofactors: Alpha lipoic acid helped, “(100 mg/d) for 4 months” and standard med. (86)
Yes - I do find CoQ10 helpful too and have it used it for many years - CoQ10 supplementation found no difference – adherence taking the supplements may have dropped off. Blood levels of CoQ10 in the treatment group were raised at 3 months and not at 6 months compared to the control group. (87)
Adequate protein diet will provide enough cysteine for most people - N-acetylcysteine – an amino acid, used to form glutathione, along with glycine and glutamate. Doses of 600-1000 mg once or twice a day were used. (91) Also see NAC – N-acetylcysteine.
Yes - switching to vegan sources didn’t seem to help my skin, I use the fish oil and it doesn’t seem to affect any autoimmune symptoms. - Low DHA/EPA, omega 3 fatty acid: Supplementation helped most in early stages, fewer patients advancing to worse psychosis was observed, particularly helpful for adolescents with a baseline low DHA. Symptom improvement was seen for patients with a long-term diagnosis of schizophrenia. (43)
Yes - externally induced- high THC marijuana with no CBD for too long for my medical use - too much THC alone can worsen rationality - Low 2-AG (CBD equivalent) in relation to anandamide (THC equiv.). (49)
There is a genetic risk for low 2-AG (CBD equivalent) in relation to anandamide (THC equivalent). (49) Providing CBD may help particularly in early stages of the condition. (50) The genetic difference that might make someone more susceptible to developing schizophrenia may involve a gene difference in Cannabinoid Receptor Type 2. (75) CBD/2-AG is the main agonist for them. (51, 77) People with Cystic Fibrosis or a BHMT gene allele can’t make cannabinoids for different reasons, and both would be low in both 2-AG and anandamide. They also have an increased risk for social anxiety conditions later in life. The risk was reduced when treatment with cannabinoids was given in early infancy (animal-based study, cystic fibrosis model). (52)
Unknown - Glutathione levels were found to vary, with a wider range than the control, more elevated, and more low levels than in the non-schizophrenia group, but overall the average glutathione level was not significantly different in the schizophrenia group. (88)
Yes - excess - possibly congenital exposure via father, later chronic fatigue syndrome type symptoms following mononucleosis/EBV may have been worsened Retinoic acid levels. - Either deficiency of retinoids (Vitamin A and beta and some other carotenoids) or excess Retinoic acid can be a causal factor in symptoms of schizophrenia. (114, 116) See post #20.
Yes (Olanzapine for a few months - withdrawal caused strong suicidal urges, hard to resist - seriously - hard to handle this. I hid the knives and avoided high places and took Epsom salt baths every few days. Tapering very slowly, and Ibuprofen every 4 hours also helped. See post #21.) - Psych med use/withdrawal history and present use.
Yes - Psychosomatic symptom history and childhood ACEs or other trauma history. See post #22. *Additional Resource: How Your Past Trauma Really Works, Dr Gabor Maté, (Youtube). Dr Mate’ suggests early childhood caregiving methods may be leading to ADHD like changes in brain development. Screentime during infancy and early childhood, especially with rapid more strobe like imagery, is linked to ADHD risk in children.
23 Yes’s, 4 Unknown’s, 1 Adequate protein diets provide cysteine - but at my worst I was anorexic and lost a lot of weight and probably was low in cysteine too.
How did I get 28 answers about 22 variables? Because some of them are about several nutrients or reasons for a deficiency or imbalance, and a few of the B’s and trace minerals overlap and are listed in a few places. The numbered list is an initial draft. Starting at the beginning is always a good spot to start.
Recognition of a problem is the first step towards change. Recognition that old methods aren’t working well anymore, age, changing times, change in awareness that your norms aren’t that normal for other people - recognizing that norms for other people aren’t always all that normal or healthy. Truth hurts - through the pain is growth and possibly far better quality of life.
Other Medical/Genetic Background:
I do not have a diagnosis of schizophrenia but did gain one for Bipolar Type 1 sometime after I was getting worse. Too often I was told that I must always have had these symptoms and I just hadn’t realized it. No. I worked as a manager and counselor at a busy job with crying children and worried parents and only had two serious complaints to the boss in 15 years. That is not bad for a customer-service type position.
I also have had social anxiety and nonspecific Personality Disorder - I have body language of a child was one of the symptoms observed for that diagnosis. I had early childhood trauma as a toddler which left a recurring nightmare. EMDR therapy as an adult helped breakthrough core negative messages I had learned at that time/believed from a toddler perspective. It helped get through some anxiety and the nightmares stopped but what I learned was that recognition doesn’t build new communication skills. Group role playing (real practice) and assertiveness training are recommended for early trauma survivors or others who need to learn healthy communication patterns.
I do have 11 gene differences of metabolic importance and four of them are double - no good copy, both alleles with dysfunction. Methylation differences, the overactive Vitamin D Receptor, and a BHMT enzyme involved in phosphorylation of cannabinoids and digestion of glycine and methionine. See: Methylation Cycle Defects – in me – genetic screening “for research purposes only”.
Pyroluria is in that land of We don’t talk about it in mainstream medical circles - but it can be screened for and treated by alternative practitioners. See: Pyroluria, anxiety, and deficiency of B6 and Zinc. People with congenital issues like Down’s syndrome are more likely than average to also have pyroluria as a genetic enzyme difference that leads to less recycling of B6 and zinc from its use in hemoglobin. Low B6 and zinc can lead to very poor stress tolerance, severe anxiety, and isolating is common - the poetry writing hermit. See: Pyroluria - when depression isn’t all in your head.
The severe zinc deficiency was the likely cause of anorexic appetite - hard to swallow, didn’t want to eat. It wasn’t about weight or calories or mood, except, lack of hunger as a non-mood. Around that time, I started B1 and improved with that addition. Low thiamine/B1 can also cause loss of appetite/anorexic appetite.
Vitamin B1 is very common in foods and deficiency is only seen in severe malnutrition such as with anorexia nervosa (a condition, rather than an adjective describing appetite) and chronic alcoholism. Deficiency can cause weak heart rate, lead to Beriberi heart disease, (2) and affect thinking and lead to delirium and eventually Korsakoff's psychosis. Chronic B1 deficiency may also lead to Wernicke's encephalopathy (WE) with mental and physical symptoms. (1)
“Severe thiamine deficiencies, such as Wernicke encephalopathy and Beriberi heart disease, are observed in patients with schizophrenia [12-15].” (2)
How could I forget B1? . . . #23
“Abstract: Objective: Review the relationship between thiamine and schizophrenia. Methods: Information was obtained from MEDLINE. Results: Nutritional status has been related to the development of schizophrenia. Genetic studies have identified numerous factors that link thiamine to schizophrenia, including the renin angiotensin system, heme oxygenase-1, advanced glycation end products, alpha-antitrypsin, coenzyme Q10, glycogen synthetase kinase-3, and the transcription factor p53. Thiamine has also been implicated in schizophrenia via its effects on matrix metalloproteinases, the Wnt/βcatenin signaling pathway, the mitogen-activated protein kinase pathways, the reduced form of nicotinamide adenine dinucleotide phosphate, prostaglandins, cyclooxygenase-2, reactive oxidative stress, and nitric oxide synthase. Conclusions: These data suggest a role of thiamine in patients with schizophrenia. Therefore, additional investigation of thiamine in schizophrenic patients is required.” (2)
Disclaimer: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.
Oudman E, Wijnia JW, Oey MJ, van Dam MJ, Postma A. Preventing Wernicke's encephalopathy in anorexia nervosa: A systematic review. Psychiatry Clin Neurosci. 2018 Oct;72(10):774-779. doi: 10.1111/pcn.12735. Epub 2018 Jul 31. PMID: 29984541. https://pubmed.ncbi.nlm.nih.gov/29984541/
Khanh vinh quốc Lương, Lan Thi Hoàng Nguyễn. The Role of Thiamine in Schizophrenia. American Journal of Psychiatry and Neuroscience. Vol. 1, No. 3, 2013, pp. 38-46. doi: 10.11648/j.ajpn.20130103.11 https://www.dropbox.com/s/l82rhpf4gpkerze/10.11648.j.ajpn.20130103.11.pdf?dl=0
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