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Rest in peace Dr. Zelenko
Zinc ionophores are very effective for latent intracellular pathogens, whether malaria or SARS-CoV-2 and possibly toxoplasmosis. Addition - or cancer and autoimmune conditions.
Rough times ahead. Trauma warning - this post includes a memorial for Dr. Zelenko who passed away on June 30, 2022 from an ongoing cancer concern. It also wanders into the topic of suicide or suicidal and self-harm urges relating to FAS, ADHD, alcoholism, major depression, and as drug side effects. Schizophrenia, Toxoplasmosis and lavender zinc nanoparticles as a treatment for Toxoplasmosis are also included.
This post did not get shorter - it can also be read in a tabbed document in which I’ve started to add the Retinoic Acid series written on this site.
Symptoms and common risks associated with Fetal Alcohol Syndrome and ADHD are described in more detail and self-harm and suicide may be a risk. Schizophrenia and Toxoplasmosis enter the discussion as excess histamine can resemble schizophrenia or be labeled bipolar disorder or other mental health diagnoses and can be a factor in suicidal urges; and Toxoplasmosis infection may be a risk factor for schizophrenia.
Carbohydrate toxicity, mitochondrial function, and the role astrocytes and cannabinoid receptors have to play in Alzheimer’s dementia and other hyperinflammatory conditions are discussed in later sections.
The nutrient deficiencies and imbalances that can be factors in schizophrenia are delved into in detail and the suggestion that since it can be a comorbid condition for so many other conditions and have so many nutrient related causal factors - that it might be better termed a symptom rather than a condition - a symptom of mitochondrial dysfunction and disrupted quantum biology.
Heads up for anyone with VAIDS or concerned about it - schizophrenia can also occur in later stages of HIV/AIDS. Knowing which nutrients are critically important may help prevent deficiency symptoms that may resemble schizophrenia. Related song: What’s the frequency Kenneth? - REM, (Youtube), reportedly a song written about two people who bothered Dan Rather and he reported on the incident and the phrase one of the men said to him. Later one of the men was identified and he was a patient with schizophrenia who thought the media were after him per his psychiatrist. He was arrested and served time. (Youtube) People with schizophrenia do seem to be tuned into another network - not always a pleasant one though.
What controls us? Our genes, or brain? Or our membranes, astrocytes and mitochondria? Evolutionary history is touched on briefly - better understanding of how things work can help us better understand when something is going wrong - for many different reasons.
Yesterday’s post: Sarah Hallberg - Low Carb, Higher Fat, was following a post, (June 28, 2022), about my ideal research scenario – well funded research scenario. The video by Sarah Hallberg, about Type 2 Diabetes and carbohydrate toxicity as the culprit in insulin resistance, supports the experimental diet ratio that my previous post had suggested is needed.
My basic research question: Is Retinoid Toxicity a factor in schizophrenia risk later in life for children with FAS or ADHD?
There may be a link between mitochondrial dysfunction and excess retinoic acid suggested by a retinal condition that can occur with Toxoplasmosis, but I am still reading.
Toxoplasmosis is a parasitic infection that can remain latent for a decade or more and eventually change from a cyst form into an active growing parasite. Good news though: Zinc ionophores, or zinc nanoparticles might help the infection, if tried, (14), the latent cyst stage is currently thought to be untreatable. (13)
Retina are one of the areas of the body with more mitochondria than average and they are also a target for Toxoplasmosis infections. Eyesight is at risk with Toxoplasmosis in an active phase (9, 13) and the keratic precipitates may involve autoimmune antibodies having formed against retinal tissue. (10) The retinal condition may also be autoimmune based, but is a frequent site of infection with T. gondii and can lead to vision loss.
Retinoid imbalance may be involved in some way. Treatment with cautious dosing or retinoid medications can be helpful for keratinization disorders, (11), however excess carotenoids may also be a factor. (33) Keratinization disorders include skin conditions with thickened growths that are often discolored patches or mole like in appearance. They may be precancerous but are often benign, just disfiguring. They may be autoimmune in nature and psoriasis is an example of a keratinization disorder. Keratic precipitates at the corneal endothelial layer seems to me like it would also be a keratinization disorder, but I’m still learning and medical terms can be used in different ways.
My research scenario simplified further:
The overarching question (This post: June 28, 2022) is whether an over-activation of vitamin A and carotenoids may be continuing for all of life after prenatal alcohol exposure (FAS or ADHS?); traditional vaccine injury; or a viral immune challenge such as Epstein-Barr Virus (EBV) (or possibly toxoplasmosis too, or a dysfunction of retinoic acid metabolism? 9, 10, 11, 12, 13, 14). The secondary question is whether Retinoid Toxicity (and the resulting histamine excess, and NMDA receptor overactivity from glutamate, would be factors) is also then playing a causal role in later diagnosis of Alzheimer’s dementia, other neurocognitive conditions, or kidney or liver disease.
Carbohydrate toxicity – a cause of Type 2 Diabetes and Cancer?
Adding more insulin and carbohydrates just worsens the underlying problem according to Dr. Hallberg, a clinician specializing in diabetes care – her patients are able to reverse their Type 2 diabetes – and she stresses that does not mean it is “cured” as it would return if they return to eating excessive carbohydrates again. The 55% ratio of carbohydrates that has been the standard of US dietary recommendations for many decades has not been proven to help control weight or prevent heart disease.
Cancer was linked to mitochondria dysfunction utilizing carbohydrates in 1931 and the work received a Nobel Award for Dr. Warburg. (31) Translational medicine is about getting the medical research findings into the doctor’s office with the patient who needs the help. 2022 minus 1931 = 71, a failure at Translational Medicine, which averages a lengthy 17 years to reach the patient. The “cure” for cancer was learned – stop eating excess carbohydrates and glutamate – and assure adequate magnesium, trace minerals, methyl B and other B vitamins and cofactors to support normal mitochondrial function.
“Mitochondrial Dysfunction and Cancer”
“Scientists point to mitochondrial dysfunction as the genesis of a number of diseases, including cancer. Mitochondrial changes and their relationship to cancer have been proven in a simple experiment. When scientists transfer the nucleus of a cell with cancer genes into a normal cell, the genes revert to normal genes—the cell does not become cancerous. However, when scientists do the reverse, transferring the nucleus of a normal cell to a cancer cell, the cell remains cancerous, suggesting that genes are not driving the cancer. Those engaged in this work have concluded that the driver of cancer is not genetic but dysfunctional mitochondria in cells.
Since food is consumed by mitochondria in the metabolic process, diet is an additional factor involved in mitochondrial dysfunction. Researchers have rediscovered the 1923 conclusions of scientist-physician Otto Warburg, who observed that cancer was caused by a metabolic change—a discovery for which he received a Nobel Prize in 1931. Warburg described how cancer cells stop using oxygen to make energy and shift to non-oxygenated, inefficient metabolism that uses fermentation to produce energy.
Fermentation metabolism causes mitochondria to produce only two ATPs per glucose molecule metabolized, [instead of 32-36 ATP], while also forming acidic byproducts. The cell nucleus then changes the gene code to support this impaired metabolism. The fact that the mitochondria change first—before any gene coding changes—undermines the “gene theory” premise of conventional cancer explanations. Most doctors are unaware that the build-up of lactic acid is a result of the cancer, not the originating cause, and so they try to de-acidify the cancer patient’s body by recommending that patients eat an alkaline diet.”* (31)
An effective treatment for the underlying cause of cancer was discovered in 1923 – lower carbohydrate diet – news to use! “Better late than never” is my own motto for tardiness, which led to “Done is better than perfect,” to help with perfectionistic procrastination.
*An acidifying diet would not be helpful either though. However, it is a valid point ~ Stop the cause, rather than addressing only the symptom. Correct the insulin resistance by reducing carb ratio in the diet and increasing ketone sources - coconut oil for the MCT content is a suggestion. Bitter tasting phytonutrients and adequate zinc would help and mitochondrial support nutrients and cofactors, and Nrf2 promoters to promote glutathione production. The link includes a list of things that may help promote AMPk. (31) More about AMPk and why it is helpful is included later.
Mitochondria are bacterial, and therefore also a large part of our microbiome – we are symbiotic.
Our mitochondria are part of our microbiome which is part of us. Being symbiotic means an organism is more than one species living in a mutually beneficial colony of sorts. We are the bigger visible part of the human symbiont colony and they are tiny but so numerous that their cells outnumber ours. Are we human or are we mitochondria? Or both?
Mitochondria are bacteria that evolved right along with other species, living within their cells, helping them by providing energy. Feeding mitochondria what they need will help us to have a good energy level and good clearance of cellular debris. Healthy mitochondrial support would also help prevent precancerous cells from becoming fully dysfunctional and cause mitochondria to have to burn sugar by fermentation, without oxygen or the other (missing) cofactors of the citric acid cycle. Function can’t happen without the necessary supplies.
To have healthy species growing in our intestines, or to support our bacteria-like mitochondria that are found in every cell of our body (averaging 500 per cell), - we need to feed them, provide them with the zinc that they need, and the other trace minerals, methyl B vitamins, and resistant starches and other fiber in our meals that supports growth of healthy species.
Mitochondria are involved in the regulation of autophagy - reuse of cellular debris; and apoptosis - controlled cell death and removal by white blood cells; and NLRP3 inflammasomes, (93), which also kill cells, hopefully pathogens instead of our own in autoimmune or hyperinflammatory conditions.
Low cholesterol, carotenoids & Vitamin A in Alzheimer’s dementia.
“The results showed that both Alzheimer's and multi-infarct dementia patients had significantly lower levels of vitamin E and beta-carotene than controls (vitamin E: 18.65 +/- 3.62 mumol/l in Alzheimer's disease and 15.80 +/- 6.93 mumol/l in multi-infarct dementia versus 30.03 +/- 12.03 mumol/l in controls; beta-carotene less than 0.13 to 0.42 mumol/l in Alzheimer's disease and less than 0.13 to 0.30 mumol/l in multi-infarct dementia versus 0.13 to 1.53 mumol/l in controls). Vitamin A was significantly reduced only in the Alzheimer's patients (1.56 +/- 0.78 mumol/l in Alzheimer's disease versus 2.13 +/- 0.86 mumol/l in controls).” (67)
Low levels of a nutrient might suggest a deficiency – unless there is an enzyme over-activation problem. Retinoic acid levels were not checked.
The active form of vitamin D is not checked as often as the inactive form that is found in larger amounts and is easier to measure – but in certain conditions there can be a “low” level of the inactive form, suggesting deficiency, and also an elevated level of the active form – showing a toxicity risk. An overactive enzyme problem is occurring due to parathyroid cancer or certain pathogen or autoimmune conditions. Giving that person vitamin D supplements for the “low” tested inactive 25-hydroxy D would just continue to be converted into the untested 1, 25 dihydroxy D form and the 25-D level might remain stubbornly low. The 1, 25-D might be getting more and more dangerously elevated. It is a secosteroid hormone and excess can cause severe anger – think Roid Rage – steroid drug abuse seen in the weight lifting or sports industries, also hypercalcemia and other risks.
It is important to figure out whether the low levels of carotenoids and vitamin A seen in Alzheimer’s patients are due to lack in the diet, or an excess conversion to Retinoic Acid.
Coconut oil in the diet could be beneficial to provide a cholesterol precursor with the medium chain triglyceride content of the oil. Coconut oil also acts as a ketone source which would be more usable by a brain with dysfunctional mitochondria, (32), - give them ketones instead of glutamate or glucose which would be inefficiently fermented without the citric acid cycle method of glycolysis. Dr. Warburg might be happy to see a reversal of mitochondrial fermentation.
Cholesterol sulfate is an agonist for a beneficial receptor, RORalpha. See: Standing on one leg – a life lengthening skill.
Cholesterol Sulfate - a ligand of RORα.
In Rheumatoid arthritis the alpha ROR down regulates inflammation, and the gamma upregulates it. Cholesterol sulfate or SR1078, a synthetic ligand for RORa were beneficial for RH arthritis. (24) The RORα are also anti-inflammatory in inflammatory bowel disease. (17)
“Retinoic acid receptor-related orphan receptor alpha (RORα) is a negative regulator of inflammatory responses, [down regulator] whereas RORγt, another member of the ROR family, is a Th17 lineage-specific transcription factor. [Th17 T helper cells are associated with autoimmune disease]
Here, we investigated the immunoregulatory potential of RORα in collagen-induced arthritis (CIA) mice, an experimental model of RA. Cholesterol sulfate (CS) or SR1078, a ligand of RORα, inhibited RORγt expression and Th17 differentiation in vitro. […] We found that RORα overexpression in CIA mice attenuated the clinical and histological severities of inflammatory arthritis. The anti-arthritic effect of RORα was associated with suppressed Th17 differentiation and attenuated mTOR-STAT3 signaling in T cells.” (24)
Epsom salt soaks, magnesium sulfate, are a good source of bioactive sulfate. Coconut oil would provide a vegan precursor for cholesterol. We can make our own. Vitamin D supplements are converted back to cholesterol by the body if there is already enough present. Vitamin D is a seco-steroid hormone made from cholesterol within our skin in the presence of sunlight, unlike other vitamins that we truly cannot make for ourselves.
Coconut: “Cocos nucifera”
“The hypoglucose metabolism that occurs in the brain is a major indicator of Alzheimer’s. The lack of glucose supplementation to the brain has to compensate by an external source to which coconut oil can be a potential candidate as it is rich with medium-chain fatty acids which can directly reach the hepatic system (Oboh et al., 2012). The lack of cholesterol level in AD brain is an indicator of the disease. Therefore, while devising a treatment and management plan, it is important to include sufficient levels of saturated fats to maintain the levels of high-density lipoproteins. The saturated fats in the coconut oil supplement the brain with medium-chain triglycerides which are further converted into ketone bodies during periods of starvation or fasting (Bhat et al., 2019). The glutamate levels in the hippocampal and prefrontal cortex cells were significantly reduced in the rats administered with virgin coconut oil (Chainoglou and Hadjipavlou-Litina, 2020). The virgin coconut oil exhibits anti-oxidant, anti-inflammatory, and neuroprotective properties (Zhang L. et al., 2021).” (32)
Other phytonutrients that may help reduce inflammation in Alzheimer’s or other inflammatory conditions include:
“A wide range of plant extracts and phytochemicals reported to possess the therapeutic potential to Alzheimer’s disease includes curcumin, resveratrol, epigallocatechin-3-gallate, morin, delphinidins, quercetin, luteolin, oleocanthal, and other phytochemicals such as huperzine A, limonoids, and azaphilones. Reported targets of these natural compounds include inhibition of acetylcholinesterase, amyloid senile plaques, oxidation products, inflammatory pathways, specific brain receptors, etc.” (32)
Many of those phytonutrients would promote Nrf2and inhibit NF-kB. Alzheimer’s is known to have an inflammatory basis but many attempts to directly reduce the amyloid beta accumulation with medications has not helped human patients. New approaches are needed and antioxidant, immunomodulating herbal based may be more effective at reducing the underlying hyperinflammation.
“Neuroinflammation has distinct traits based on fundamental reasons, such as its persistence, intensity and severity of occurrence, and duration time. Age-associated deterioration of anti-inflammatory pathways generates inflammation and develops mild clinical signs, such as neural inflammatory responses followed by severe brain damage, which can persevere for few years before its clinical presentation as AD (Hampel et al., 2018). Overexpression of microglial cells and astrocytes promotes prolonged and recurrent neuroinflammation by releasing proinflammatory cytokines such as interleukins, TNF-α, and γ-interferon, which influence the central nervous system are detected in AD patients. The γ-secretase activity cleaves APP to generate βA peptides, which are stimulated by reactive oxygen species (ROS). The anti-inflammatory methodologies are implemented to produce new compounds to address AD (Barage and Sonawane, 2015).” (32)
Why are the glial cells being over expressed though? We need to identify what in a person’s daily life is adding to inflammation and reduce the problem items: whether Retinoic acid overactivation causing a need to avoid vitamin A and carotenoid foods and histamine trigger foods, or diet sensitivity to over food allergens, molecular mimicry autoimmune antibody antigens*, lectins, oxalates, or TRP channel activator sensitivity; medication side effects; physical or emotional stress; other autoimmune antibodies; or low level infection. There can be overgrowth of candida yeast, helminths (worms), and negative species of bacteria all present in someone with an unhealthy microbiome. Intracellular infections like the chronic stages of Lyme’s disease, or cysts of Toxoplasmosis, can flair up at later times while being difficult to test for in the latent stages.
*Molecular mimicry autoimmune antibodies can form against proteins in the diet that are similar to a body protein, such as gluten and thyroid tissue causing autoimmune thyroid issues and albumin – found in egg white and most animal based foods, hemp kernels, ginger, and wheat, can lead to autoimmune antibodies against one’s own albumin too which can cause non-healing skin sores. Leaky bowel membranes along with low vitamin D can increase risk of autoimmune antibodies forming against proteins that are frequently eaten. I stopped eating animal products thinking it was an albumin problem, which hemp kernels confirmed as a blind challenge study – symptoms returned and I had to think about what I was eating that was different. I had been eating hemp kernels in small amounts for a while but had recently increased use to a full three tablespoon protein serving per day.
Health can be a challenge but is worth the detective work to figure out.
Inflammation for any cause will send signals that call for more white blood cells and also glial cells if it is in the area of nerve cells. (62) Therefore all causes of inflammation need to be identified and reduced if possible to aid in reducing oxidative stress and stopping hyperinflammation positive feedback loops, in any type of condition that involves inflammation, which includes most chronic conditions.
Nrf2 would help inhibit NF-Kb pathways which lead to TNFα.
“A recent discovery from our lab identified an endogenous inhibitor of Nrf2 known as retinoic X receptor alpha (RXRα). RXRα is a nuclear receptor, interacts with the Neh7 domain of Nrf2 (amino-acid residues 209–316) via its DNA-binding domain (DBD), and specifically inhibits Nrf2 activity in the nucleus. Moreover, other nuclear receptors such as peroxisome proliferator-activated receptor-γ, ERα, estrogen-related receptor-β, and glucocorticoid receptors have also been reported to be endogenous inhibitors of Nrf2 activity , .” (62)
Ah hem, we have found a clue. RXRα inhibits Nrf2 actions in the cell nucleus – and if retinoic acid is involved in that, then an overactivation of Retinoic Acid would be adding to inhibition of Nrf2 which could be adding to the positive feedback effect of hyperinflammation. I don’t know enough about retinoid metabolism and all it does.
Avoid Nocebo – negative messaging leading to lack of hope – leading to negative outcomes – a positive feedback loop of negativity.
“We don’t know” is better than “We don’t know the cause AND there is no cure.” How do they know? Nocebo, a negative close-ended thought: “Here is a label/diagnosis, but we don’t know the cause and there is no cure.” If they don’t know the cause then they can’t know whether there is or is not a cure. Now can they?
If there is a theme to this post it is that “more research really is needed” and that more solutions are known than mainstream medical admits or is aware of - so seek more information whenever you recognize a nocebo in front of you. “You have schizophrenia – we don’t really know what causes it or how to really help, but here are some drugs that cause seriously negative side effects potentially and you should take them, and may be forced to do so by a judge.” Reportedly patients with schizophrenia had a better quality of life one hundred years ago than they do today. Wholesome food type solutions were the basis of treatment at that time and there was less social stigma towards people with odd behavior.
The “cause” of schizophrenia may be a large number of nutrient deficiencies or imbalances that lead to a susceptibility for oxidative stress to accumulate to levels that damage mitochondrial and cellular DNA. Some of the common deficiencies or imbalances may be related to genetic differences that cause an increased need for a nutrient or CBD or a copper/zinc transport protein, which would mean genetic screening for the known problem genes would be needed. See subsection: Nutrients that may be an underlying causal factor of “schizophrenia”.
“We don’t know” or “I don’t know” are better, more open-ended responses and are stating the truth about an unknown instead of sticking on a label and an expectation that it is untreatable. Another more open ended and positive response would be: “We suspect such and such is involved and that might be an approach to look into further.” Even better: “Many people have a rough idea of what habits in their lives are more harmful than helpful, and may not want to admit it. Do you have any ideas about what makes you feel worse?”
Chemical imbalance – a discarded theory about mental illness that has a grain of truth.
“Chemical imbalance” as a theory for mental illness has gotten discredited, regarding serotonin/dopamine and serotonin reuptake inhibitors and other medications, however histamine excess is an imbalance. Too little 2-AG/CBD in ratio to anandamide/THC (CBD drops would help) is also an imbalance. Pure THC products in excess may be a cause of a shift in the ratio, or inflammatory health changes, or genetic differences, (more on THC/CBD imbalance is in the Nutrients & Schizophrenia section). Too little calming GABA, magnesium, or glycine; or too much excitatory histamine/Retinoic acid, glutamate or aspartate/aspartame; might also be factors that could lead to an imbalance in the inhibitors for the brain and anxiety or schizophrenia whirling thoughts might occur.
Providing a psychiatric drug is not restoring balance by providing Dimethylglycine, GABA or promoters for it, or magnesium glycinate, Mg threonate or Epsom salt soaks (Mg sulfate). Adequate cholesterol and vitamin D are also needed to protect against autoimmune risks and provide cholesterol sulfate (agonist for ROR alpha).
See the previous post: Standing on One Leg - a life lengthening skill?, for a list of the strategies that I would want to include in an experimental diet plan for reversing hyperinflammation.
Is any of this connected? All of it is. Life is complex and when it works, that is a miracle of complexity.
Balance and adequacy are the key to healthy function. Throw off the balance and we might get drunken-like stumbling or schizophrenia-like whirling irrational thoughts - or suicidal or self-harm urges. Hunger and fullness signaling can help us eat just the right Goldilocks amount that we need, if we have paid attention to what seems to help and what seems to cause symptoms of some sort – whether glutamate excitatory leading to over-eating the snack, or a good, “That really hit the spot” feeling. Think about how wonderful a cold glass of water is when you are feeling really hot and thirsty – feel that hot and thirsty again in the future and you will know that a cold glass of water is just the thing you need.
Bitter tasting phytonutrients help tell us we are full now, so it is good to include herbs and spices and produce with stronger flavors in our meals. Or finish a meal in the style of India – a small dish of fennel seeds is served as the ‘after dinner mint’. It freshens the breath and gives a satiating effect from the many strongly flavored (minty licorice) phytonutrients in the seeds.
Cannabinoid lack or imbalance can lead to binge overeating or anorexic* lack of appetite as they have some regulatory control over appetite signals. Cannabinoids and their receptors are discussed more later in relation to astrocytes and in schizophrenia and suicidal issues.
Lack of zinc can also cause a severe anorexic* lack of appetite. I have experienced zinc deficiency at a worse point of health. It/and or a combination of deficiencies at the time, caused an odd dryness in my throat that made swallowing a bite of food really difficult. It felt like being asked to swallow sawdust. I would make it through a couple bites and feel like that was as much as could be asked of me. Zinc deficiency when severe will be visible as little white spots on the fingernails – anywhere there was a bump on the nail bed might remain as a white spot on the pink of the rest of the fingernail. Supplementing with zinc since then has left me with only an occasional white spot instead of several on each nail.
Pyroluria may be a genetic condition that causes a lifelong need for high dose supplements of zinc and vitamin B6 as an enzyme lack leads to loss of a hemoglobin metabolite that would normally be reused – the zinc and B6 would normally not be lost in the urine. Diet sources would not be adequate for the increased need for B6 and could be obtained with shellfish for the zinc but would be difficult with standard foods.
*Anorexic as a symptom descriptor rather than the diagnosis Anorexia nervosa, which generally involves perfectionistic emotional trauma too - a girl or boy too eager to please over-controlling parents or a sports coach may become even more controlled over her or his own body. What they eat and drink may be all that the young person has some control over.
As malnutrition worsens though, more severe zinc deficiency would then be adding physical symptoms of anorexia and possibly the difficulty I felt with swallowing a bite of food. Other nutrient deficiencies may have been involved in my case too though – deficiency of B1 and B6, and excess iodine were also present at the time. Excess iodine can cause swallowing symptoms too.
Zinc, Dr. Zelenko, and Toxoplasmosis
A great man passed away from cancer – Dr. Vladimir, ‘Zev,’ Zelenko - let us never forget his name, or his use of zinc and zinc ionophores for early and successful treatment of SARS-CoV-2 infections.
Zinc ionophores are effective for intracellular parasites and the use of zinc nanoparticles suggests that formulation can also enter infected cells somehow. Lipid nanoparticles may be attracted to and be absorbed directly into other bilayer lipid membranes – which encase cells.
*This post has wandered and was untitled – seeing the sad news about Dr. Zelenko’s passing immediately brought to mind the good news about zinc for toxoplasmosis and this post. Zinc nanoparticles were used successfully to end toxoplasmosis infections. (14) But the mainstream standard of care considers the latent cyst stage to be untreatable. (13) Toxoplasmosis is a comorbid issue with AIDS, so we may end up hearing about more cases in people with VAIDS.
Video message from his hospital before passing on June 30, 2022:
Via Grant Taylor @grantltaylor, Dr Zelenko’s Deathbed Message: Resist The WHO’s Fear Campaigns, Denounce The False gods Of Technology & Science, Turn Back To Our True Creator Rest in peace, June 30th 2022
It will take some work to keep his name and message from being suppressed. Twitter is not really free speech yet, don’t be fooled, Dr. Zev’s education group account was recently just suspended too. Realize that ALL effective treatments have been suppressed and fraudulent research published to make the treatments seem ineffective or dangerous. If you give an overdose of something - sure, then it will be dangerous. Lying about medical research is not only dangerous - it is criminal behavior.
Be aware, and wary, Twitter is likely a government controlled psy op site, and so is Facebook. Feeling free, while not being free, is the goal of the kid glove approach to authoritarian takeover - scare the people into thinking they will be rescued by the authoritarian increase in control - so they plead for it and vote for it and comply with the loss of freedom.
· Spartacus on what kind of mind control/gene altering biotech/nanotech may we realistically expect?: a review of tech and biotech research and medical trends. It looks grim for free will and non-GMO humans. The research exists for gene editing that could affect us whether we want or not. Being well nourished might help detox foreign particles before they are uploaded to a cell nucleus.
· Spartacus part 2, Revealing COVID-19’s Origins. Spartacus describes the illness and hypoxia effects of hyperinflammation and discusses modern diet and the Metabolic Syndrome risk factors. People of African ancestry are more at risk also because of an ethnic tendency towards less nitric oxide, made worse by the hypertension, obesity, or Type 2 diabetes of Metabolic Syndrome and modern life. He briefly recommends Nrf2 promoting foods or phytonutrients to help counteract the inflammation and hypoxia chemistry and mentions spinach, leafy greens and beets as Nitric oxide promoting.
Zinc Nanoparticles for Taxoplasmosis cysts – effective treatment.
Toxoplasmosis is considered treatable only in the active stages, (13) , and the medication would have side effects and leave the latent cysts in place for later emergence potentially. The parasites might become an infection early in life and remain in an inactive cyst stage for many years. Cat-box exposure with kittens or younger cats are the main risk factor, (74), or possibly intimate contact with someone else with an active infection.
The advantage of using nanoparticle formulations of substances is that the tiny size bypasses our body’s system for removal of foreign things – white blood cells look for larger foreign things and ignore nanoparticle sized material. Pomegranate peel is useful for the formulation of metallic nanoparticles of gold or silver in the tech industry or for medical use.
Returning to the Zinc nanoparticles for treatment of toxoplasmosis cysts - they were made with the leaves and/or flowers of a medicinal and fragrant herb, Lavendula augustifolia Vera - lavender - chosen in part for its antimicrobial benefits. An ethanol extract was made and then combined with zinc sulfate and microwaved to cause the nanoparticle formation.
“2.1. Preparation of biogenic ZnNPs
Aerial parts of L. angustifolia were was collected from the rural areas of Kerman, Iran during September 2019. The materials were extracted and prepared by means of a percolation system using 80% methanol for 72 h at the 21 °C. Preparation of biogenic ZnNPs performed based on the method explained elsewhere (Salari et al., 2017). In brief, 10 ml of L. angustifolia methanolic extract (LAME) at the concentration of 5 mg/ml was added to 40 ml of ZnSO4 solution (Merck Chemicals, Darmstadt, Germany). In the next step, this combination was exposed to microwave in a microwave oven (850 W, 60 s) to decrease the ions of metal; whereas the creation of a dark gray color indicated the production of Zn NPs.” (14)
The summary of how the zinc nanoparticles were made is brief and I can only guess that the ethanol extract contained phospholipids, which can spontaneously form nanoparticles. The combination must have changed the weight significantly because that high of a dose of elemental zinc would be too much.
“The results revealed that oral administration of Zn NPs at the doses of 32.5 (p < 0.001) and 75 mg/kg/day (p < 0.001) for 14 days significantly reduced the mean number of the brain tissue cysts in tested mice when compared with the control group (C2). The findings also exhibited that similar to a positive control (C3), no T. gondii tissue cyst was observed after oral administration of Zn NPs at the doses of 150 mg/kg for 14 days in mice of the tested group of Ex3.” (14)
I would like some lavender zinc nanoparticles. Pomegranate peel is helpful for forming nanoparticles because it is a good source of phospholipids which spontaneously form into bilayer lipid membrane nanoparticles when stirred in a watery or alcohol-based solution.
Zinc acts as a neurotransmitter too.
Zinc can act in neurotransmitter-like ways within the nervous system, influencing the actions of neurotransmitter receptors.
“ZnT3 (SLC30a3), a zinc transporter, packages zinc into glutamatergic synaptic vesicles, imparting the metal with potential neurotransmitter-like properties. In fact, zinc is released from nerve terminals in an activity-dependent fashion and interacts with neurotransmitter receptors, influencing their function. This is most notably the case for the NMDA receptor, where synaptically released zinc can effectively regulate ion channel function. Critically, synaptically released zinc also directly activates a receptor (mZnR/GPR39) whose primary ligand is the metal itself, regulating neuronal excitation. In essence, then, zinc is a neurotransmitter.” (27)
The impact of zinc regulation on NMDA receptors could help explain the role of zinc deficiency in schizophrenia - add glutamate or histamine and there would be even more NMDA activity.
“GPR39 G protein-coupled receptor 39 [ (human)]
This gene is a member of the ghrelin receptor family and encodes a rhodopsin-type G-protein-coupled receptor (GPCR). The encoded protein is involved in zinc-dependent signaling in epithelial tissue in intestines, prostate and salivary glands. The protein may also be involved in the pathophysiology of depression. [provided by RefSeq, Jun 2016]” (28)
Rhodopsin is a pigment with quantum energy potential found in some types of our eye’s light receptors. More about rhodopsin is included in a later section, Why go into so much detail about nutrients needed in schizophrenia?. Ghrelin is involved in appetite control. G-protein coupled receptors are a large group that can cross a membrane and sense the exterior and cause actions on the interior. The niacin/butyrate receptor, GP109, and cannabinoid receptors, CB1 and CB2, are also G-protein coupled receptors.
DHA, evolution and membrane control of life – sensation and response.
DHA is also a quantum chemical, and ancient, unchanged across species down to single celled. Life may have evolved around DHA omega 3 fatty acid and its unique energy characteristics rather than genes being first. They have had some changes over time. See: DHA – a quantum molecule.
The predominant theory about genes being the main control of biology has had to change as the original ideas did not prove to be true. Genes are not the control, they are the recipe box which other things have control over whether the recipe will be opened and transcribed or kept closed, (epigenetics and microRNA and actin are all involved). (64)
The cell membrane and all of its many receptors and surface marker proteins are really the main control of our life is an argument Brian Lipton makes in his work regarding membranes and quantum biology.
· Bruce Lipton, The Biology of Belief Full Lecture. (Youtube) this is a long video but is worth the time.
· See this post for quotes from the video, and anti-inflammatory diet and lifestyle information based on the Hyperinflammation series on Substack: Modern Life Syndrome – it’s not all in our heads, but that counts too! (peace-is-happy.org).
Astrocytes, support & regulatory cells for our brain and nerve cells.
Astrocytes are star shaped cells of the nervous system which act as support for the nerve cells that send signals. They may have more regulatory function than had been initially realized – rather than being primarily caretaker cells for nerve cells, they may be the operator.
Consider as a visual, the nerve cells and their connecting axons as a telephone network – the operator sends the calls or a person dialing a number, not the telephone itself (yes I am that old/ I am visualizing a rotary phone).
Astrocyte dysfunction is seen in Alzheimer’s
Dysfunction of astrocytes seems to be involved in Alzheimer’s dementia and with a positive feedback loop - amyloid beta protein can increase NF-kB too and may lead to more amyloid beta misfolding, leading to more NF-kB, and so on - a positive feedback loop. (29)
“Changes in astrocyte function have been observed in brains from individuals with AD, as well as in AD in vitro and in vivo animal models. The presence of amyloid beta (Aβ) has been shown to disrupt gliotransmission, neurotransmitter uptake, and alter calcium signaling in astrocytes. Furthermore, astrocytes express apolipoprotein E and are involved in the production, degradation and removal of Aβ. As well, changes in astrocytes that precede other pathological characteristics observed in AD, point to an early contribution of astroglia in this disease.
Astrocytes participate in the inflammatory/immune responses of the central nervous system. The presence of Aβ activates different cell receptors and intracellular signaling pathways, mainly the advanced glycation end products receptor/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, responsible for the transcription of pro-inflammatory cytokines and chemokines in astrocytes. The release of these pro-inflammatory agents may induce cellular damage or even stimulate the production of Aβ in astrocytes.
Additionally, Aβ induces the appearance of oxidative stress (OS) and production of reactive oxygen species and reactive nitrogen species in astrocytes, affecting among others, intracellular calcium levels, NADPH oxidase (NOX), NF-κB signaling, glutamate uptake (increasing the risk of excitotoxicity) and mitochondrial function. Excessive neuroinflammation and OS are observed in AD, and astrocytes seem to be involved in both. The Aβ/NF-κB interaction in astrocytes may play a central role in these inflammatory and OS changes present in AD.” (29)
An allele of apolipoprotein E is thought to increase risk for Alzheimer’s dementia. The protein is involved in lipid binding to membrane receptors and may have regulatory functions.
“A major function of apoE is to mediate the binding of lipoproteins or lipid complexes in the plasma or interstitial fluids to specific cell-surface receptors. These receptors internalize apoE-containing lipoprotein particles; thus, apoE participates in the distribution/redistribution of lipids among various tissues and cells of the body. In addition, intracellular apoE may modulate various cellular processes physiologically or pathophysiologically, including cytoskeletal assembly and stability, mitochondrial integrity and function, and dendritic morphology and function.” (30)
Cytoskeletal assembly involves some of the types of proteins that can misfold, dendrites support nerve cells, and mitochondrial function is critical for energy and are involved in removal of cellular debris along with AMPk. This reference has a list of herbals or medications that may help promote AMPk. (31)
The NMDA receptors in the hippocampus modify with stages of development. A more active form is present at younger years, allowing more calcium flow which might lead to more learning/memory formation in the hippocampus. In later life low level chronic calcium seems to lead to more forgetfulness. (41)
“Recent work suggests that redox regulation of NMDA receptor function contributes to schizophrenia (Steullet et al., 2016), stressor-induced depressive-like behavior (Ibi et al., 2017), and synaptic plasticity during development . […] In contrast to younger animals, little or no effect of oxidizing agents was observed for older animals, suggesting that cells were already in an oxidized state. In contrast, reducing conditions enhanced NMDA receptor mediated synaptic responses in hippocampus of aged animals [53, 55, 56, 112–114]. Recent results provide evidence for a link between the redox-mediated decline in NMDA receptor function and the emergence of an age-related cognitive phenotype with impairment in the rapid acquisition and retention of novel spatial information [55, 56]. These results demonstrate that the age-related decrease in NMDA receptor-mediated synaptic responses at CA3-CA1 hippocampal synapses with advanced age is related to redox state such that the reducing agent, dithiothreitol (DTT) significantly enhanced the NMDA receptor component of the synaptic response to a greater extent in cognitively impaired animals relative to unimpaired animals  (Fig 2).” (41)
*Reducing agents donate an electron which would stop an oxidizing agent from taking an electron from other molecules and causing a rust like oxidation of other tissue.
“Examples of oxidizing agents include halogens, [fluorine, bromine], potassium nitrate, and nitric acid, [also oxygen and hydrogen peroxide]. A reducing agent, or reductant, loses electrons and is oxidized in a chemical reaction. A reducing agent is typically in one of its lower possible oxidation states, and is known as the electron donor.” (42)
Astrocytes, Cannabinoid Receptors and Nerve Plasticity – learning and forgetting.
Astrocytes may do more than supply nutrients and remove toxins however. They may also help regulate which nerve pathways are maintained and which are removed - plasticity - the reshaping of our memories is aided by adequate cannabinoid function. Learning and forgetting is called neuroplasticity – the connecting networks between nerve cells can be assembled or disassembled by the supporting glial cells.
The glial cells, astrocytes and others, have both CB1 and CB2 receptors to aid in regulating the cell’s differentiation, functions, and health. (19) Cannabinoid receptors are involved in plasticity. Forgetting trauma is difficult and Post Traumatic Stress Disorder (PTSD) is associated with endocannabinoid deficiency.
“CB1 and CB2 receptors are activated by a plethora of cannabinoid compounds, be they endogenously-produced, plant-derived or synthetic. These receptors are expressed by microglia, astrocytes and astrocytomas, and their activation regulates these cells' differentiation, functions and viability.” (19)
We need cannabinoids to help learn, and build new nerve networks, and we also need them to remove unneeded pathways - the old apartment address or a PTSD trauma memory. Lack of cannabinoids is associated with PTSD and phantom limb pain/memory - when a stump is still seeming to indicate a whole limb is still present. Providing an external source of balanced cannabinoids can help patients with those and other conditions related to inability to produce the molecules.
Lack of cannabinoids is also associated with cancer. Also linked to cancer is a lack of magnesium, which would add to the switch seen within mitochondria to fermentation of glucose or glutamate prior to cancer – suggesting a temporally causal link and worth a Nobel Prize. Fermentation does not use ATP or the citric acid cycle and its many nutrients. The mitochondria need the whole group of nutrients and cofactors to be able to use the citric acid cycle for energy production from glycolysis of glucose. The dysfunction seems fairly clear. Cancer may be better termed trace nutrient deficiency syndrome. The cure may be less carbohydrates, more produce, fatty fish and/or other better food choices and targeted supplements after a genetic screening or other deficiencies were identified.
Having more of ATP2A2 gene expression was associated with better prognosis for astrocytic tumor patients. (17) The gene transcribes an enzyme, ATPase2, which is involved in Endoplasmic reticulum membrane control and autophagosome formation.
The enzyme ATPase2 needs magnesium to function. It responds to starvation, extended hunger, with increased autophagy and it controls autophagosome formation at the Endoplasmic reticulum (ER) membrane. It also controls ER contact with lipid droplets, mitochondria and endosomes. This makes it very important for controlling what is happening at the main site of misfolding protein identification and removal - and emphasizes the importance of magnesium for cancer removal.
Autophagy is the cellular recycling of unneeded proteins for use as other nutrients - being hungry long enough is necessary for that to happen, which is why it is better for health to not eat much in the later hours of your evening. During sleep is when our body ideally has the time and need to focus on cleaning up and reusing cellular debris, or infected, aged, or precancerous cells.
The enzyme ATPase2:
Involved in autophagy in response to starvation.
Upon interaction with VMP1 and activation, controls ER-isolation membrane contacts for autophagosome formation (PubMed:28890335).
The CB2 receptor is more prevalent throughout the body than in the brain, where there are more CB1 receptors in ratio. The CB2 receptors are likely involved in regulating immune function and mice without the gene are more likely to have an over-active inflammatory response.
“The CB2 receptor is the peripheral receptor for cannabinoids. It is mainly expressed in immune tissues, highlighting the possibility that the endocannabinoid system has an immunomodulatory role. In this respect, the CB2 receptor was shown to modulate immune cell functions, both in cellulo and in animal models of inflammatory diseases. In this regard, numerous studies have reported that mice lacking the CB2 receptor have an exacerbated inflammatory phenotype.” (20)
Astrocytes utilize release of calcium from endoplasmic reticulum as a regulatory signal. Increased calcium intracellularly can cause various actions to occur. Lack of magnesium may make excessive calcium signaling to occur - and make stress coping function less effective. Instead of being able to calm, reactive responses may be likely - letting the temper or tears leak instead of letting it go and moving on with your day.
Nerve cells send signals, astrocytes may tell them which signals to send.
“Astrocytes generate robust intracellular Ca 2+ signals that are assumed to be key regulators of astrocytic function. Among various Ca 2+ mobilization mechanisms, Ca 2+ release from the endoplasmic reticulum (ER) via the inositol 1,4,5-trisphosphate receptor (IP 3 R) has attracted attention as a major component of astrocytic Ca 2+ signaling.” (21)
*Note that if we want our astrocytes to work or our mitochondria, or our endoplasmic reticulum, that we need inositol, a B vitamin, and the ability to phosphorylate probably too (BHMT gene and probably others, redundancy is frequently the secret to life). Inositol 1, 4, 5-trisphosphate (IP3) is the main agonist for the IP 3 R receptors. They are found in all cells of the body. (22)
Inositol Food Sources (more about inositol later also).
Inositol is found in whole grains, beans, sprouted seeds, beans, or grains, artichoke heart, okra, eggplant, bell pepper, broccoli and green leafy vegetables, prunes, cantaloupe, citrus, peaches, pears, - many produce items. Do not overcook or use excess water that is thrown away - the B vitamins and C are water soluble and heat sensitive. (Foods high in Inositol, 23)
Phospholipids are in membranes and are part of endocannabinoid molecules, (a fatty acid is the other half of the molecule). Seeds, whole grains, beans are also good sources. The inner germ of corn or wheat is rich and cardamom, coriander or cumin powder, mustard seed, fennel or pomegranate seeds. Phosphatidylserine is available as a supplement. See: Clinical Endocannabinoid Deficiency, (CED), and phospholipids. (transcendingsquare.com)
Arachidonic Acid - an omega 6 fatty acid used in some endocannabinoids. This omega 6 fatty acid may add to inflammation from dietary sources or from inflammation. Inflammatory signals cause endocannabinoids to be freed from the cell membrane and arachidonic acid is part of some types of endocannabinoids. When the endocannabinoid is further broken down, the arachidonic acid may then be changed into another type of signaling chemical, eicosanoids. (24). Omega 3 fatty acids can also be formed into endocannabinoids which have an anti-inflammatory effect.
CB1 receptors can inhibit calcium channel activity which would be protective against inflammatory signaling.
“Earlier studies demonstrated how neurotransmission could be modulated by CB1 receptors through the inhibition of calcium channels independently of cAMP, suggesting direct G protein-dependent mechanisms (Mackie and Hille, 1992; Twitchell et al, 1997).”
“Briefly, CB1 receptors can inhibit N- and P/Q-type Ca2+ channels, activate different types of K+ channels and promote phosphorylation of extracellularly regulated kinases (ERKs). More recently, experiments on retinal ganglion cell revealed that CB1 receptor activation can lead to the AMP-activated kinase-dependent inhibition of the Na-K-Cl co-transporter (NKCC1) activity, eventually reducing intracellular levels of Cl− (Miraucourt et al, 2016).” (26)
CB1 receptors are expressed inside of cells and at mitochondrial membranes where they effect oxygen consumption by cannabinoids.
“However, in 2012, electron microscopic immunogold experiments accompanied by controlled functional assays revealed that a small but significant proportion of hippocampal CB1 receptors are localized at mitochondrial membranes (called mtCB1), where they mediate reduction of O2 consumption by exogenous and endogenous cannabinoids (Benard et al, 2012). Interestingly, similar mitochondrial localization of CB1 receptors has been also shown in peripheral tissues, such as sperm cells (Aquila et al, 2010) and muscles, where the proportion of mtCB1 receptors appears to be higher than in the brain (Mendizabal-Zubiaga et al, 2016).” (26)
A possible explanation - Mitochondria and cannabinoids play a role in sperm motility. Mitochondria produce energy for us and store it. They even vibrate or pulse with the ionic energy field. There are more mitochondria located in the heart and other muscles and in the flagellum of sperm – the moving tail. (p46, 40)
“Mitochondrial genes regulate the molecular frequency of ATPsynthase. In a sense mitochondria oscillate and three ATP are produced per revolution. This is why mitochondria are close to contractile muscles and the heart. Also, this is why they are wrapped tightly in the motile flagellum of sperm for its arduous and rather random flight for impregnating an ovum.” – Triveni P. Shukla, The Immortal Mitochondria (p46, 40)
If more males knew that sperm cell mitochondria use endocannabinoids – and that both are needed for movement – motility of the flagellum - then maybe marijuana would be changed from “No medical value” within the U.S. legal system. **The sperm need a lot of energy to swim where they need to go. Endocannabinoid deficiency is linked to sperm motility issues. Chocolate is the richest source of cannabinoids among commonly used foods but has little in comparison to marijuana or hemp kernels. News to use.
More news to use
“It is clear that the machinery required for the production of eCBs is located at synapses. This means that eCBs release occurs at, or very close to, synaptic sites. For example, at hippocampal glutamate synapses, the 2-AG synthesizing enzyme, DGL-α, is highly accumulated in nanodomains in the perisynapse region (Katona et al, 2006).” (26)
In summary: The non-euphoric CBD equivalent endocannabinoids are present near the hippocampal glutamate synapses, which would be NMDA receptors. The 2-AG would play a role in protecting the hippocampus from inflammatory damage and excess NMDA receptor activity.
Schizophrenia can have many underlying causal factors and may occur along with other mental health conditions, or HIV/AIDS.
Schizophrenia may be a co-diagnosis later in life for people with FAS as a primary diagnosis. Temporal lobe differences from birth can be a factor in schizophrenia and are discussed in a case study of a girl with FAS who developed schizophrenia as an adolescent. See Figure 2: The temporal lobe of our FAS case (B) is compared to that of an adult control (A), (34) Later effects or changes that occur into adulthood for people born with Fetal Alcohol Syndrome are not well studied. (34) Mental illnesses and addictions are common co-conditions with FAS, but another author also stated a need for study and surveyed 25 people with FAS and 18 had other conditions. One had schizoaffective disorder and a few with other psychosis related diagnoses. (35) ADHD can also be a comorbid condition with schizophrenia. (36) Schizophrenia may also be a symptom/co-condition with more severe HIV/AIDS, (39) so our current times may see an increase of VAIDS related mental illness symptoms.
“The frequency of the first psychotic episodes in HIV-positive individuals ranges from 1 to 15% [41,42]. For psychoses arising in HIV-infected patients, hallucinations, affective disorders, cognitive impairments, and dementia are common [43,44]. Moreover, the risk of schizophrenia and acute psychosis in people infected with HIV during the first year after infection is quite high, with an incidence rate of 8.24 and 12.7, respectively . Moreover, an increased risk of developing schizophrenia persists for more than 5 years after the diagnosis of an HIV infection, at which point the majority of PLWH receive antiretroviral therapy (ART), leading to suppression of viral replication and of opportunistic infections .” (39)
People with mental disorders are more at risk for becoming HIV positive, it is thought that hypersexuality and increased risk for victimization may be factors in the increased risk. Impaired social skills or intelligence can leave someone more at risk for being coerced or easily manipulated. The person may be gullible socially or emotionally neglected and starved for love. (39)
“Additionally, as a result of impaired cognitive abilities, evaluation, and judgment, people with mental disorders are much more likely to be at risk of coerced sex [13,14,15,16,17,18]. The frequency of forced sexual intercourse among this group of individuals is 10–38% [14,19,20]. Many patients with mental illnesses such as schizophrenia and bipolar disorder have been found to have experienced sexual abuse in childhood [17,19,21]. The traumatic experience is later reproduced in life and such persons repeatedly become victims of sexual violence; they are characterized by sexually promiscuous and risky sexual behavior in adulthood [17,22].” (39)
The hyperexcitability of histamine excess also includes an increased sex drive – hypersexuality – which may make the person an active participant in seeking frequent sexual encounters, potentially risky for sexually transmitted pathogens, pregnancy, or new autoimmune conditions occurring if low in vitamin D.
Schizophrenia, being a comorbid condition with so many other conditions, and being related to a number of nutrient deficiencies or imbalances, might suggest that it is a symptom rather than a stand alone condition. Schizoaffective disorders may be the label used more commonly now.
The “voices” heard in schizophrenia, are likely the person’s own sub-vocal speech.
The “voices” that people with schizophrenia reportedly hear turn out to likely be their own thoughts. With brain activity at hyper speed, the memory of the thought may not form, and if spoken sub-vocally, it may seem as if someone or something else is speaking. A sensitive microphone was used to record a person with schizophrenia and it picked up subvocal speech at a time that the person didn’t realize they were speaking. (68)
The over-active brain of a someone with schizophrenia may no longer recognize the voices of self-talk, or those of voices in memories or in imagined conversations, as being internally self-generated and instead probably tend to make up some explanation for whatever or whoever they think might be doing the talking that they heard - hearing voices.
Our internal chatter can get busy and sometimes can be quite mean - shaming, threatening, devaluing. It would be scary to not realize that it is just yourself repeating things that you had heard elsewhere possibly, or from childhood, or more current concerns that the hyper-excited brain won’t stop ruminating over. Put the cow out to pasture and try an Epsom salt bath or Dimethylglycine and/or inositol powder in water (~half teaspoon of DMG) instead. Pomegranate juice or fruit or peel extract might also help if histamine excess is part of the problem, or quercetin or luteolin supplements.
Dosing for inositol, a B vitamin, varies with the condition; two grams twice a day is mentioned for Metabolic Syndrome. (77) Up to 12-18 grams per day for panic or obsessive-compulsive disorders are mentioned on rXlist.com. It also states that inositol may be ‘possibly ineffective’ for autism, Alzheimer’s or schizophrenia. (78) I would caution that any B vitamin in mega doses without the rest of the B complex being provided may cause more problems than benefits as they work in a team within mitochondria and in other ways. Excess of one may lead to deficiencies of others. Inositol may also be helpful for treatment of epileptic seizures, (myo-inositol, animal- based study). (79)
Nutrients that may be an underlying causal factor of “schizophrenia”.
Multiple nutrient deficiencies and imbalances are related to schizophrenia, and several may have genetic metabolic differences as the chronic issue. Genetic screening and targeted treatment would be needed then. Enzyme dysfunction may cause an increased need for a nutrient above levels available in food or a mineral transport protein may be dysfunctional and providing it would restore function. (56)
Doing a research study focused on only one of the many potential nutrient issues could show minimal benefit because there might be many other nutrient issues left unresolved and still causing symptoms.
The following excerpt from an Abstract about iodine deficiency and thyroid conditions in schizophrenia – explains a lot of the problem in four sentences – nice job review team. Inflammatory signals related to nutrient deficiencies lead to oxidative stress and mitochondrial damage, which leads to apoptosis of astrocytes and thryocytes – death of the support cells for our nervous system and thyroid cells which are essential for our energy level.
“Schizophrenia is associated with a deficiency of dietary antioxidants like vitamin B6, B9, and B12 resulting in defective methylation leading to hyperhomocysteinemia. Hyperhomocysteinemia causes mitochondrial DNA damage, oxidative stress, vascular damage, and lipid peroxidation. Oxidative stress and increase in reactive oxygen species result in 8-oxodG production which induces apoptosis of both astrocytes and thyrocytes thus predisposing them to thyroid dysfunction and neurodegeneration. Furthermore, the presence of excessive free radicals increases thyroid thermogenesis causing hyperthyroidism or its excess may cause hypothyroidism by inhibiting iodide uptake.” (55)
Vitamin D deficiency, or VDR gene differences, and Toxoplasmosis risk.
Low vitamin D: Vitamin D deficiency is associated with more severe schizophrenia symptoms suggesting a causal link. Genetic differences in the Vitamin D Receptor may be a factor (47) or a factor in toxoplasmosis risk (76) and low magnesium will limit the effectiveness of vitamin D supplements
More research into optimal dosing is needed …
“However, we recommended that patients with schizophrenia who are in long-term care in rehabilitation psychiatric units should be assessed with regard to their vitamin D levels. According to their vitamin D levels, these patients should have appropriate exposure to sunlight, activity and dietary adjustments to normalize vitamin D levels. Vitamin D containing foods are very few in nature. Fatty fish (such as tuna, salmon and mackerel) and fish liver oils are the best sources [Ross et al. 2011]. Beef liver, cheese, egg yolks and mushrooms are other vitamin D sources [Cranney et al. 2007]. Fortified foods such as milk and breakfast cereals often contain added vitamin D, as do some brands of orange juice, yogurt, margarine and other food products.” (47)
And/or an underlying infection with Toxoplasma gondii may be present, and a genetic difference in the Vitamin D Receptor or vitamin D metabolism may increase risk for infection with T gondii (cat box litter of a young cat is a risk factor for T gondii infection).
Vitamin D Receptor or D metabolism gene alleles are also seen with Bipolar Disorder. (48) The VDR receptor was upregulated on average. “Expression of VDR was up-regulated in total cases compared with controls (Posterior beta = 0.683, P value = 0.001).” (48) I may have one of these, VDR/Fok1 – may cause increased risk for mood swings. (Post, my gene alleles in common with autism.) Too much vitamin D or sunshine makes me feel worse.
Low iodine, thyroid conditions, excess halides (fluoride, bromide, perchlorates), low Nrf2.
Low iodine/hypothyroidism – oxidative stress increases risk to thyroid tissue and may reduce iodine uptake. (55) Low iodine prenatally and/or low zinc prenatally, may increase risk for schizophrenia later in life.
Lack of Nrf2 leading to less glutathione production would lead to less conversion of thyroid hormone T4 to the T3 form as the enzymes for the conversion requires glutathione. Antioxidant enzymes also need glutathione. Blood plasma levels of antioxidants such as Vit E and CoQ10 and the thyroid hormones tend to be similar – all low or all good, which suggests that the glutathione level is either low or good.
“Reduced glutathione (GSH) is an important cofactor of both antioxidant enzymes and deiodinases, the enzymes responsible for the conversion of thyroxine (T4) to triiodothyronine (T3). Moreover, plasma levels of small antioxidant molecules, such as Vitamin E and CoQ10, and thyroid hormones are closely related to each other [2, 17].” (55)
Excess fluoride, bromide and perchlorates may be a factor in the hypothyroidism;
Pyroluria may be a factor in chronically low zinc and vitamin B6 – high dose supplements for life are needed to correct the lack of an enzyme involved in hemoglobin breakdown for reuse;
Zinc & Copper – gene differences potentially, dysbindin for copper transport, pyroluria for chronic low zinc and B6.
Zinc deficiency prenatally or later in life. Zinc deficiency prenatally seems a risk for schizophrenia later in life. (69, 70, 71, 72) It also worsens FAS and is seen with dyslexia, thought to worsen the ability to cope with stress and to increase risk of zinc deficiency throughout life. “Zinc is the commonest deficiency before conception, during foetal development, in children and in adults of all ages. Zinc deficiency in early foetal life reduces the production of foetal steroid hormones but also, in animals and humans in my experience of dyslexic individuals, causes a reduced ability to cope with stress and a predisposition for zinc deficiency throughout life.” - Ellen C G Grant, physician, UK (73)
Excess copper in relation to a low zinc level; a genetic dysfunction in copper transport may be involved as copper binding agents cause schizophrenia like symptoms. Plasma levels of copper would be elevated, and probably causing varied problems, but the brain regions needing copper wouldn’t be receiving it. (81) The copper transport protein dysbindin (58) or isoforms can be given as a treatment when this gene issue is identified. (56) Dietary imbalance of excess copper and low zinc is not uncommon in the modern diet, even with normal genetics. That finding does add clarity or confuses prior beliefs – copper excess may not be causing the schizophrenia symptoms, copper deficiency might be though.
If a copper transport protein issue is causing functional copper deficiency, then providing the transport protein is the needed solution – in addition to assessing the o diet for excessive copper sources and limiting those as the overall elevated blood plasma level of copper would be affecting zinc transport proteins – which include dysbindin. (57)
Other Trace Minerals – they share transport proteins frequently.
Low manganese and iron were found along with elevated copper in patients with schizophrenia. In that study the zinc and selenium levels were not significantly different from the control group’s levels. (80) If dysbindin was dysfunctional due to a gene difference, (56, 58, 81), than it would show elevated copper and symptoms of copper deficiency in the brain – zinc levels might also seem good while not being as available to cells. Protein transport carriers for trace minerals can be shared and dietary excess of one might compete with others for the shared transport proteins. (57)
Low trace minerals – it’s complicated. A team noticed the many mineral deficiencies can be involved in schizophrenia and measured a population of Han Chinese with schizophrenia, and a control group. They make the point that cause and effect can not be established with this study. Metabolic imbalance due to schizophrenia may lead to some of the other imbalances – an unknown without more study.
The deficiency patterns or adequacy of 35 trace elements were further analyzed and grouped into minerals that seem to affect schizophrenia individually: 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. (83)
*Chromium and Lead were elevated in the schizophrenia cohort compared to the control group; iron was elevated for the test group of the schizophrenia cohort. (83, *Supplementary data) Elevated iron is seen in inflammation and iron chelating herbs (forgeable plantain for example, 84) or medications can help.
Zinc, cesium and selenium were low on average in this Asian group of people with schizophrenia. Low zinc has not been seen as often in studies with European participants. Diet differences are suggested to be a factor. (83) More meat in a population’s average diet would be likely to have more zinc than a diet with more beans or soy.
Low selenium in combination with polyunsaturated fats had additional risks of oxidation with likely impact on mitochondrial oxidative stress. Selenium is an antioxidant, unless reduced, at which point it is an oxidant. It is needed for the enzyme glutathione peroxidase which helps with the protective effects of the mitochondrial antioxidant glutathione. (83)
“Schizophrenia has been reported to be more prevalent in areas where the soil contains very low Se 22. The element Se, an essential component of glutathione peroxidase, plays a key role in the glutathione peroxidase anti-oxidant system and has an important role in anti-oxidative protection against free radical damage to cell membranes, lipoproteins and nucleic acids 23,24. Reduced Se may cause oxidative stress, which may in turn increase the risk for Schizophrenia. Furthermore, we have also found a significant correlation between Se and long chain fatty acids (correlation r of −0.2 to −0.1, P = < 0.05), including hexadecanoic acid, tetradecanoic acid, oleic acid, octadecanoic acid and eicosanoic acid (data not shown; manuscript in preparation). Fatty acids have been reported as potential markers for Schizophrenia 25; here, beta-oxidation of long-chain fatty acids regulated by Se are suggested to have important roles in Schizophrenia since the glutathione peroxidase metabolizes hydroperoxide formed from polyunsaturated fatty acids.” (83)
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 brain27.” (83)
B vitamins – gene methylation difference and/or pyroluria may be factors in chronic deficiency.
Low methyl folate and methyl B12, methylation gene differences may be a factor. (55)
Low B6, 35% of a group of people with schizophrenia had low B6 levels. Animal based research found that vitamin B6 deficient animals displayed schizophrenia like behaviors and “…that the behavioral deficits shown in VB6(−) mice are caused by enhancement of the noradrenergic (NAergic) system.”” Dosing guidelines for humans with schizophrenia need to be established after further study. (82)
*High dose B6 dosing example (too much may be an issue for some people): for my suspected pyroluria condition I try to take a 250 mg B6 in the morning and a 100 mg Pyridoxal 5' phosphate (P5P), a more bioactive form, in the evening and a 50 mg zinc with a meal. Pyroluria is not screened for or treated by mainstream medical but it can be fairly common among populations with congenital genetic conditions such as Down’s Syndrome.
B6, B8 (Inositol), and B12 supplementation helped in schizophrenia treatment in a review study. (85)
Low niacin – or a need for more than average for an unknown reason at this time: 1000 mg of niacin taken three times a day was very effective for treatment of schizophrenia – in 1971 research by Dr. Hoffer. (45) NADH and NAD+ are involved in ATP production and can be formed from niacin. Cell types and animals that use more energy for active movement have more NADH present than average cell types. (40, pp 55-56) The high dose niacin protocol can give a sense of more energy and clear headedness, in my personal experience.
High Dose Niacin protocol recommended by Dr. Kats and earlier, in 1971 by Dr Hoffer for schizophrenia treatment. (45);
How-To’s and Cautions about it with my experiences as an example: Niacin & Early Treatment…is sensible….
Better late than never for people who read! But another translational medicine fail – high dose niacin treatment is still not being used as a standard of care for patients with schizophrenia. 2022 -1971 = 51 years, more than the 17 year Translational Medicine average.
Vit C, Cofactors, Essential omega 3 fatty acid DHA/EPA and endocannabinoids.
Vitamin C supplementation helped, along with a patient’s standard medication. (88)
Alpha lipoic acid supplementation helped, “(100 mg/d) for 4 months” along with the patient’s standard medication. (86)
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)
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. The meta-analysis team suggest further study following patients longer to see if there is an increase during active psychosis phases as a response to increased glutamate activity, followed by a drop in glutathione to below average. (88)
N-acetylcysteine – an amino acid, used to form glutathione, along with glycine and glutamate. Doses of 600-1000 mg once or twice a day has consistently seemed to help reduce negative symptoms but not make much difference for cognitive improvement or positive symptoms. (91) Also see NAC – N-acetylcysteine.
Low DHA/EPA, omega 3 fatty acid: Supplementation can help. It helped more in earlier stages, preventing worsening to psychosis. Some symptom benefits were seen in chronic stages of schizophrenia. Adolescents with a low baseline for polyunsaturated fatty acids, DHA in particular, were most responsive to supplementation. Symptom improvement and prevention of worsening to psychosis was seen in the younger participants. (43)
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 cannot make cannabinoids and 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)
Cannabinoids help us forget trauma and to learn new things, see: Astrocytes, CBRs & Nerve plasticity.
Excess THC only strains of marijuana or concentrated THC products may cause schizophrenia like symptoms – and the products may not be recognized as the cause of the mental changes. Instead of starting psychiatric medications there would simply be a need to stop using the THC only products, moderate use, and/or justuse CBD too. THCV as a reverse agonist or antagonist for the CB1 receptors may be a beneficial cannabinoid found in a few strains. (44) THCV strains or products are not widely available yet.
· Self medicating with strains of marijuana that are high THC with no CBD would likely worsen the schizoaffective symptoms.
· THCV is another cannabinoid found in some strains of marijuana in a lower ratio to THC. It also needs heat to be converted from a precursor found in the green bud. (44) – “THCV acts as a neutral CB1 antagonist / reverse agonist. It may also serve as an agonist or antagonist at the CB2 receptors depending on the dose.” (44)
For comparison - Cofactors needed in the Citric Acid Cycle
We need the whole baseball team of nutrients and cofactors for mitochondria to be able to perform the Citric Acid Cycle. Adequate protein is also needed to help support the assembly line like steps of the cycle. The nutrients we need daily include niacin and many other B vitamins, trace minerals, antioxidants and amino acids:
Amino acids: Carnitine (derived from lysine), Cysteine,
Antioxidants: CoQ10, Glutathione, Alpha-Lipoic Acid (ALA).
The Citric Acid Cycle Cofactor List is based on a graphic of the Citric Acid Cycle showing the chemicals involved, by Dmitry Kats, PhD.:
available in a post on transcendingsquare.com: Niacin and Migraines.
The list of Citric Acid Cycle cofactors looks familiar, don’t they? Many were included in the preceding list of nutrients that may be related to schizophrenia risk.
Many or all of the deficiencies and imbalances listed for schizophrenia are also related to mitochondrial function or are needed for the citric acid cycle. Nrf2 promotion would help promote glutathione and other anti-inflammatory changes that would help with oxidative stress that leads to mitochondrial dysfunction, and which seems an underlying condition of ‘schizophrenia’ – the name for a larger group of individual variations of causal factors. (59, 60)
N-acetylcysteine (NAC) an amino acid that we need it to make glutathione.
Whey protein is an equivalent to NAC, ½ teaspoon per day of why protein might be an equivalent serving of cysteine and provide about 3 grams of total protein. Excess use, as a protein bulking agent to add by scoopfuls, might add too much glutamate for NMDA risks and overexcitation of the brain. Over supplementation with NAC is not recommended for healthy people, 600 mg once a day as a preventative might be used. Increasing that to twice or several times a day would be typical use during an infection or for chronic inflammation.
N-acetylcysteine is a precursor amino acid for glutathione, glycine and glutamate are also needed. When oxidative stress increases Nrf2 then promotes more glutathione production and other enzymes that help reduce the oxidative chemicals. Treating neuropsychiatric illness with Nrf2 promoting NAC, CoQ10, and melatonin is discussed in the following Abstract. (60)
“Abstract: Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor encoded by NFE2L2. Under oxidative stress, Nrf2 does not undergo its normal cytoplasmic degradation but instead travels to the nucleus, where it binds to a DNA promoter and initiates transcription of anti-oxidative genes. Nrf2 upregulation is associated with increased cellular levels of glutathione disulfide, glutathione peroxidase, glutathione transferases, thioredoxin and thioredoxin reductase.
Given its key role in governing the cellular antioxidant response, upregulation of Nrf2 has been suggested as a common therapeutic target in neuropsychiatric illnesses such as major depressive disorder, bipolar disorder and schizophrenia, which are associated with chronic oxidative and nitrosative stress, characterised by elevated levels of reactive oxygen species, nitric oxide and peroxynitrite. These processes lead to extensive lipid peroxidation, protein oxidation and carbonylation, and oxidative damage to nuclear and mitochondrial DNA.
Intake of N-acetylcysteine, coenzyme Q10 and melatonin is accompanied by increased Nrf2 activity.
- N-acetylcysteine intake is associated with improved cerebral mitochondrial function, decreased central oxidative and nitrosative stress, reduced neuroinflammation, alleviation of endoplasmic reticular stress and suppression of the unfolded protein response.
- Coenzyme Q10, which acts as a superoxide scavenger in neuroglial mitochondria, instigates mitohormesis, ameliorates lipid peroxidation in the inner mitochondrial membrane, activates uncoupling proteins, promotes mitochondrial biogenesis and has positive effects on the plasma membrane redox system.
- Melatonin, which scavenges mitochondrial free radicals, inhibits mitochondrial nitric oxide synthase, restores mitochondrial calcium homeostasis, deacetylates and activates mitochondrial SIRT3, ameliorates increased permeability of the blood-brain barrier and intestine and counters neuroinflammation and glutamate excitotoxicity.” (60)
Having adequate cysteine, and glutathione, is very important for preventing death of cells from excess free radicals – oxidizing iron – picture rust throughout our bodies causing cell death, ferroptosis. The glutathione is an antioxidant that prevents the rust reaction. Lack of cysteine leads to ferroptosis and cell death likely due to the lack of protective glutathione.
“Deficiency of cellular cysteine induces a unique cell death program known as ferroptosis, a peroxidation-driven and iron-catalyzed form of non-apoptotic cell death17. It has been proposed that deficiency of intracellular cysteine induces ferroptosis primarily due to failure to synthesize GSH, which protects cells against ROS and lipid peroxidation18. Consistently, inhibition of cellular cysteine uptake by using erastin (an inhibitor of system xc−) depleted GSH and induced ferroptosis19. Depletion of cellular GSH by using buthionine sulfoxamine (BSO), which inhibits glutamate–cysteine ligase (the rate-limiting enzyme for GSH synthesis) is sufficient to induce ferroptosis due to impaired cellular antioxidant capacity18. Given that ROS that drive ferroptosis is reduced by GSH, the effect of cystine limitation on ferroptosis is mainly ascribed to the loss of antioxidant capacity.” (90)
We need to make glutathione (GSH) for ourselves, as supplements are broken down in digestion. Liposomal forms do seem to be effective. However, many important changes occur with our normal circadian cycle epigenetic changes, hundreds of genes are activated or deactivated each night/day – unless we are stuck in a permanently inflamed day mode of too much stress or modern living.
Modern life has many factors that lead to not switching to the healing night mode when Nrf2 is active more than the inflammatory action-oriented NF-kB pathways. We need Nrf2 for more than promotion of glutathione production. It promotes DNA repair and immune function.
Why go into so much detail about nutrients needed in schizophrenia?
Schizophrenia seems to be a catch-all term for a condition that is mitochondrial dysfunction and disrupted quantum biology. DHA (See DHA – a quantum molecule) and iodine are both involved in quantum field effects, and mitochondria and cannabinoid receptors are also, and not-misfolded proteins. The straight structural proteins act like antennae and help direct and stabilize our energy fields. (Quantum biology/earth-ocean.info) The structural proteins also help guide cell division, needed for new cells or a new baby. (Meiosis/earth-ocean.info)
Rhodopsin is a light absorbing pigment that is found in the human eye and single celled organisms. (Rhodopsin/earth-ocean.info) It works with quantum effects too. Rhodopsin can convert a signal perceived as light in the eye into a nerve signal which will then be interpreted by other areas of the brain as to shape or color or movement of the light signal – pixels that may include directional light information.
Simply breathing calmly at a steady pace can help us calm our energy and then maybe our mood will also be improved. Listening to certain tones with a heartbeat like rhythm can also help reset our ‘nerves’ to a calmer vibration. (Breathing/earth-ocean.info)
However, simply trying to think happier thoughts cannot really help the whirling odd thoughts of hyperexcitability of histamine, which is sometimes diagnosed as schizophrenia and in later stages may be called Alzheimer’s dementia. I did find that I could try to substitute different phrases or repeat a mantra instead of the more negative repetitive thoughts as the meltdowns kept continuing for several years with no clear cause. I got worried that I might have some permanent brain condition causing it and am glad that diet changes were able to make a big improvement for me. I rarely have mood meltdowns now and are less severe when some symptoms occur.
Oddly, flickering lights, strobe light effect can cause histamine release from mast cells – and trigger one of my mood meltdowns – tested as an after effect from a neurology exam for ruling out epilepsy – I didn’t have a seizure during the strobe light part of the screening, but I did have a two hour meltdown afterwards, the worst and longest ever. Action movies or concerts with light shows gave me migraines the next day – it was a histamine reaction. I learned to wear sunglasses for strobe light effects which can occur when driving through winter treescapes in bright sunshine.
It turns out that we need the blackout curtains at night because our skin uses rhodopsin and other opsins to sense light. (92) Cover up for modesty? Or because it helps us grow and repair while we sleep? (Both is okay.)
If schizophrenia can be a comorbid condition for FAS, ADHD, and HIV/AIDS and be caused by so many varied nutrient deficiencies or imbalance, then is it really a stand-alone condition? … a label that goes along with a ‘One condition – one cure’ expectation?
Or is it a symptom that can be caused by varied reasons? And needs varied treatments?
Not everyone would need the same diet changes or supplements, but many might benefit from many of the same ones that help support mitochondria and energy functions of our body.
In which case to effectively treat it, each individual patient would need to have genetic screening and a detailed nutrition analysis with lab testing to help correct their personal varied reasons for developing that severe a level of cognitive change. The BIGGER point is that with that level of individual screening, the symptom can likely be changed back to clear headed and not have a brain that is overactive and whirling with so many thoughts they may be perceived as other voices.
Effective treatment is the goal to aim for, rather than a lofty “cure” for a “condition”. Many conditions are multifactorial – many causes, all of which would need to be addressed for a true “recovery” – recovery of normal function is the goal and improved quality of life.
With allergies, the allergen needs to be avoided, or a rotation diet sometimes helps reduce food sensitivity by limiting frequency of moderate problem foods. It depends on the type of food allergy with anaphylactic shock risk or sensitivity causing other less risky symptoms.
With autoimmune conditions: the antigen does need to be avoided for life in the case of autoimmune disease. Memory cells are for life and the antigen re-exposure causes a flair up in antibodies and then more attacking or your own cells, of whatever type involved, and that means cell death and inflammation and fibrotic scarring and misfolded proteins and a disrupted energy field.
Methylation Diet – methyl donors and mitochondrial support.
A methylation promoting diet is recommended by Triveni P. Shukla in the book The Immortal Mitochondria, Our Electronic Life, Longevity, and Health. Menu examples and a recipe section is included for a whole-food based diet rich in colorful phytonutrients, trace minerals, B vitamins, and omega 3 fatty acid. (40)
The methyl donors are methyl folate and methyl or hydroxycobalamin (B12 that is not cyanocobalamin), and choline. Avoid BPA to help as it takes methyl groups and can affect epigenetics – DNA changes that are like an on/off switch.
“Methylation diet is the key to maintaining DNA stability, both nuclear and mitochondrial. Well designed methylation diet should provide all necessary nutrients (magnesium manganese, zinc, iron, vitamin C, CoQ10, Vitamin K, Vitamin C, E, and beta-carotene, pyrroquinoline quinone, alpha lipoic acid, and even antioxidant carnosine from poultry, fish and beef). N-acetyl cysteine and curcumine from turmeric are necessary for antioxidant glutathione, and pantothenic acid (B5) is necessary for enzyme cofactor Co Enzyme A. Ubiquinol acts very much like vitamin C and beta-carotene.” (40)
Why does methylation matter? The epigenetic control of our genes requires methyl groups – the on/off switch as to whether the gene may be transcribed into an RNA and then a protein. The presence of methyl groups is an off switch – the cap is on the tube of toothpaste. We need lots of methyl donors to provide methyl groups on a daily/nightly basis. (89)
The circadian cycle is a phrase representing night and day – and all the epigenetic changes that occur when the body switches from night mode to day mode and then back again. Blackout curtain darkness at night and dim twilight or reddish light in the pre sleep hours is helpful to make the transition to sleep mode. Full spectrum light in the early morning hours helps with switching to an alert active mode. Alarm clocks that have a sunrise, slow increase in light, may also be helpful with encouraging a natural awakening into day mode epigenetics. Hundreds of genes are switched from on to off and back again with each 24 hour cycle – which requires many methyl groups.
“Moreover, neuronal activity can modulate their pattern of DNA methylation in response to physiological and environmental stimuli. The precise regulation of DNA methylation is essential for normal cognitive function. Indeed, when DNA methylation is altered as a result of developmental mutations or environmental risk factors, such as drug exposure and neural injury, mental impairment is a common side effect.
The investigation into DNA methylation continues to show a rich and complex picture about epigenetic gene regulation in the central nervous system and provides possible therapeutic targets for the treatment of neuropsychiatric disorders.” (89)
Why else does methylation matter? Epigenetic changes are not the same as a mutation in the DNA nucleotides, but they can be shared with offspring – the next generation. Prenatal malnutrition can lead to epigenetic changes that leave the child more conserving of energy – and in a modern high calorie world – at greater risk for obesity. The child would have had an improved survival chance if the malnutrition was due to an ongoing famine and food was plentiful for the growing person. Their body would be conserving the limited calories that were available.
DNA changes in the cell nucleus can lead to cancer and in the mitochondrial DNA can lead to Parkinson’s Disease and other chronic conditions. The DNA in the mitochondria is more susceptible to changes and is in an oxidative environment. The glutathione and alpha lipoic acid and other antioxidants are necessary to maintain the balance of life – we need the energy, so we must clean up the smoldering coals that are left after the fire. Basic facts of life, nothing is for free.
FAS effects, likely diagnosed as ADHD, can be caused by the alcohol use habits of a Father-to-be prior to the fetal conception.
Alcohol use by a father-to-be in the ~ 74 days prior to conception of a baby, may cause ADHD or other changes in the fetus that are related to FAS but not as severe as when the pregnant woman is drinking too much alcohol.
The No-more-than guidance for a pregnant woman is zero alcohol prenatally ideally, but one serving per week use is likely not going to cause FAS– unless also zinc deficient possible. One serving once at a special celebration will likely not harm a fetus. One serving is one shot of hard liquor, one 6 oz wine glass, one beer - not one Long Island Ice Tea (mixed drink with 4-5 shots of liquor) – and a petite woman would be more effected by a single serving than a taller woman – use common sense is the best strategy and try not to worry too much. Stress isn’t good for mom or baby either.
Alcohol use at least weekly by the fathers-to-be prior to conception, as surveyed by their pregnant wives, was associated with more behavior and health symptoms in the children later in life, screened at periodic times during preschool ages. In previous animal research more excessive alcohol exposure for the males did lead to ADHD like and other symptoms in their offspring. (38)
“Spermatogenesis is estimated to take approximately 74 days, which is considered to be a process susceptible to exogenous disturbance4,5. The preconceptional period is thus increasingly recognized as a highly sensitive window6. Evidence from animal studies has also shown that preconceptional paternal alcohol consumption can induce genetic and epigenetic alterations in sperm that may increase the risks of adverse neurodevelopment in offspring, including attention deficit hyperactivity disorder-like behaviors, anxiety and depression-like behaviors, and cognitive impairment7–11. In humans, previous studies about the effects of paternal alcohol consumption on adverse neurodevelopment of the offspring were mainly focused on fathers with alcohol dependence, which indicated the crucial role of genetic transmission in their associations12,13.” (38)
Coincidentally … or causally, I also have ADHD and smaller than average temporal lobes. I have had a SPECT brain scan at rest and after 15 minutes doing a concentration exercise. The scan showed a slowdown in electrical activity in the prefrontal cortex and the cerebellum/movement area of the brain after the concentration exercise (watch for a certain letter in a stream of symbols and type a button for the correct one). The scan also showed slightly smaller than average temporal lobes, you take what you get in life and run with it.
Coincidentally … or causally, zinc deficiency worsens FAS, as zinc is needed for the enzyme that breakdowns alcohol (37) and zinc deficiency is associated with schizophrenia.
FAS & ADHD - Similarities, Differences? Frequently co-diagnoses.
The following excerpt was written by Robert More, an adoptive father of three children with FAS and ADHD, who fortunately also has twenty years of experience as a Special Ed teacher. The article has concrete guidance for positive parenting tactics to help cope with the special needs of a child with learning and behavioral issues.
“We learned that FASD is a permanent brain injury where the connections within the brain are essentially missing. Different impairments arise depending on when and how much alcohol is consumed during the fetus’s brain development. Common challenges associated with FASD can include executive functioning issues, learning disabilities, neuromotor difficulties, and sensory concerns.
People impacted by FASD often experience a wide range of physical conditions and mental health challenges, which is why researchers now describe it as a whole-body disorder. A 2016 report from CanFASD lists attention deficit hyperactivity disorder, reactive attachment disorder, oppositional defiant disorder, trauma, stress, addictions, self-harm, and suicide as particular areas of concern.” (1)
ADHD can lead to poor concentration and decision making, poor impulse control problems and reckless behavior or talking, and stress or fatigue make it worse. Trying harder makes the poor concentration worse, less brain electrical activity occurs instead of more. Physically klutzy may also be a problem. Cerebellum damage during childhood can have lasting effects on coordination and is seen in ADHD, autism and dyslexia, and likely other congenital disorders. (61)
FAS may have more obvious physical differences and also have decision making or other learning disabilities. Neuromotor difficulties might mean poor coordination for catching or throwing a ball or writing with neat penmanship or being able to chop vegetables without chopping fingertips too. The Standing on One Leg test would involve “balance, coordination, agility, gait, and proprioception,” (3), and is included in example exercises for improving neuromotor skill. (Neuromotor Exercise Training) (3)
Proprioception is the ability to sense where your body is in relation to the world around you and involves the vestibular system of the inner ear. The vestibular system is more specific to the position of your head in relation to the world. Vision is also involved in balance. We are more likely to stumble or bump into things in a familiar location when it is dark - even though we know the arrangement of the furnishings.
People can have proprioception difficulties without also having vestibular dysfunction, and autism is a possible condition. Propioception requires “healthy functioning of the dorsal columns of the spinal cord.” (4) Some people might have had a birth malformation of the spinal cord affecting their ability to balance on one leg.
Other problems that are frequent concerns with FAS would also make parenting or self-care as an independent adult difficult: “reactive attachment disorder, oppositional defiant disorder, trauma, stress, addictions, self-harm, and suicide.” (1)
Reactive attachment disorder can occur when an infant or toddler isn’t receiving interactive nurturing care but can also occur in infants who don’t interact and bond with their caregiver.
Oppositional defiant disorder is used to describe individuals who can not take direction well, even if it is beneficial for them, an order will be defied - the opposite action may be done. Parenting may end needing to rephrase things so the oppositional defiant person can make their own choices. Suggest a choice - red shirt or green shirt today? There is a choice to be made - control of the situation for the child or adult (but a shirt will be put on hopefully).
Trauma and stress can be more of a problem for anyone who has metabolic gene differences that affect detoxification or production of antioxidants or other enzymes that are needed for energy production, growth or repair. Methylation differences would be an issue as methyl donors help protect our genes and are needed for the breakdown of formaldehyde or homocysteine.
Addictions are tricky because they may indicate the person has a metabolic need for something and they are self-medicating with a substitute. Cannabinoid deficiencies may lead to binge overeating, alcoholism, opiate addictions, and possibly nicotine abuse, in addition to use of marijuana. However, cocaine addictions do not seem to involve the endocannabinoid system. If a person does have a genetic need for an external source of cannabinoids - then it would be genetic discrimination to withhold the best source. Cardamom, pomegranate seeds, and some other membrane rich seeds or plants do provide a little cannabinoids or phospholipids to our diet, but not enough if a person can’t make them normally.
Self harm and suicidal urges may have to do with secondary hyperparathyroidism which can be caused by chronically low calcium or vitamin D. The problem of eye gouging urges and low calcium has been noted in the autism community. Eye gouging can also be a symptom of secondary hyperparathyroidism - and the treatment is to provide adequate calcium supplementation or foods for life, and/or vitamin D which may mean correcting low magnesium levels too. Calcium and potassium levels may be kept abnormally low by the body when magnesium is deficient.
Suicidal urges can also be related to histamine and/or Retinoic acid excess. Retinoic acid excess may be a factor in FAS and also ADHD, if that condition is related to FAS prenatally, but is a less severe presentation of the prenatal complication. Suicide rate among teens, adolescents and grade school children has been increasing. Young black males with family strife and ADHD are more common risk factors among the increase. (94) Organophosphate pesticide exposure can also increase risk of suicide, seen in rural areas compared to urban. (95)
Medications (psychiatric and others) or withdrawal from meds can cause odd physical symptoms (Extrapyramidal Symptoms, EPS, 2) and/or suicidal urges. The problem is known as akathisia among sufferers and the cause or effective treatment is not really known. Medications may be changed, reduced, and others added. (2)
“The flat facial expression, psychomotor slowing, and low energy level in akathisia may mimic the negative symptoms of schizophrenia. In addition, restlessness in akathisia may also appear similar to anxiety and psychotic agitation. ” (2)
Physically restless legs may jiggle endlessly, visibly, but that may be an outer representation of thought processes that are also endlessly repeating in anxious, shaming, devaluing, or other negative self-talk. When the histamine hyperexcitability gets severe the repetitive cycle of thought becomes so fast that memory formation is patchy (personal experience of histamine hyperexcitability - mood meltdowns is my name for it). A diagnosis of schizophrenia may be given instead of histamine excess and a modified diet.
Akathisia treatment includes 5HT2A (Serotonin 2A) antagonists:
“For the management of akathisia, there was adequate evidence to allow recommendations regarding antipsychotic dose reduction, antipsychotic polypharmacy, switching antipsychotic medication, and the use of adjuvant medications including beta-blockers, anticholinergics, 5HT2A antagonists, benzodiazepines, and vitamin B6.” (5)
Olanzapine potent for increasing appetite and weight (animal-based study). It also had an intial down regulation on expression of 5-HT2A receptor mRNA, at 2 hours, and there was a rebound by 48 hours after the last dose. (96) Munchies - the drug also reduces breakdown of cannabinoids and causes the appetite changes of increased cannabinoids. The company was fined due to diabetes risk as a side effect that patients were not warned about (2005, $690 million), (98); and for promoting it for anxiety, dementia and sleep disorders between 1999-2005 - off label use unapproved by the FDA (1.4 billion fine, $515 million of it criminal). (99)
Olanzapine caused akathisia and suicidal urges for me. It prevents breakdown of cannabinoids so there is more than normal while using it - then withdrawal can cause suicidal urges as the previously overactivated cannabinoid receptors in the prefrontal cortex suddenly have a deficit of cannabinoids to activate them. (Ibuprofen every four hours during the three days or so of withdrawal helped me, and initially cutting them into ever tinier pieces to wean off slowly first.) The rebound in mRNA for 5-HT2A receptors also suggests a withdrawal effect of some sort would be likely with a large change in serotonin receptors.
CBD – the non-euphoric cannabinoid may help depression or schizophrenia.
Cannabinoids can help the body cope with the effects of stress and the receptors are upregulated in females, but down regulated in males (animal-based study). Providing an external source of cannabinoids helped depressive symptoms in females (animal based study).
“For instance, chronic stress significantly downregulates CB1 receptor levels in the hippocampus of male rats, while it upregulates these receptors in the dorsal hippocampus of female rats (90, 91).” (6)
Women are diagnosed with Major Depressive Disorder more frequently than men and low levels of cannabinoids have been found during life and at autopsy. The level of the non-euphoric 2-AG levels were found to correlate negatively with duration of major depression - the longer the problem, the lower the level of 2-AG. (6) The euphoric THC equivalent is anandamide and it is found lower in concentration during normal health than the non-euphoric CBD equivalent, 2-AG. The CB1 receptor is more activated by the anandamide and moderated by 2-AG (CBD equivalent).
“In women with major depression, serum 2-AG levels correlated with the duration of the depressive episode: the longer the duration of the depression, the lower the 2-AG levels.” (6)
In the case of olanzapine, less breakdown of cannabinoids might lead to a better mood, until you run out of cannabinoids suddenly and the brain is now used to having a whole lot.
CBD/2-AG helps calm the THC/anandamide activity. Eventually a CBD/2-AG similar cannabinoid did help me - beta caryophyllene from copaiba oil, a food grade essential oil used as flavoring. At the time of worsened symptoms, I was using a THC only medical marijuana and sensed that something was wrong with it, but I had no access to other strains at the time. THC alone, in excess, can cause schizophrenia like symptoms. Lack of 2-AG seems to be part of the condition, but it can have varied nutrient related causal factors, deficiency or imbalance and a history of toxoplasmosis may also be a causal factor of schizophrenia.
Suicide risk in alcoholism is a little different than in other suicide cases, downregulation of CB1 receptors instead of upregulation, (8), severe alcoholism impairs zinc levels and that affects the gut and may be causally related in severity of FAS. Zinc deficiency in combination with alcohol during fetal development can cause more severe physical deformities. (25)
“These findings suggest that alcohol dependence is associated with the downregulation of the CB1 receptors, while suicide is linked to the upregulation of these receptors in the ventral striatum. Alteration in the activity of FAAH enzyme that regulates the anandamide (AEA) content might in turn explain differences in the CB1 receptor function in alcohol dependence and suicide.” (8)
Correcting some of these problems would require a change in diet (or stopping alcohol use and eating shellfish or pumpkin seeds instead) rather than talk therapy about addictions or mystery aches and pains that might be psychosomatic or might be nutrient deficiencies or Retinoic Acid/histamine excess. Talking about problems on a weekly basis may be a nice way to vent, but otherwise it is just paying someone to listen to you vent and may still lead to suicide if the underlying physical issues are never addressed and function restored or improved.
Enjoying every moment is not really possible while the brain is over excited and when that is daily it can become easy to forget what normal had been. It may be easy to give up and believe you are just crazy or worthless. Being present for the little things can help ground us and calm our over excited energy, or stimulate a low energy feeling. Being around nature can help reduce stress and be healing. Literally taking off shoes and socks and standing on a safe patch of sand or soil for about 15-30 minutes can be calming and seem restorative. We may be retuning our inner vibration to that of the planet.
People with daily thoughts of suicide learn to not share them because it can be used as emotional manipulation and therefore might be taken that way or already had been taken that way. Or it may lead to a commitment to a facility with help that already hadn’t been very helpful. It is nicer to have rational return to the mind, and for the whirling odd repetitive thoughts or conversations to stop.
The disturbing increase in suicide among grade school and adolescent children with ADHD as a more frequent risk factor (94) suggests that more needs to be done to help those kids sooner. Talking about why you want to gouge yourself everyday may distract momentarily, but it would not make hyperparathyroidism due to low calcium or low vitamin D levels any better - so the daily horrific feelings would continue, as long as the real problem was left unidentified. Others might feel better by cutting out fermented foods, tomatoes, and other histamine triggers.
Schizophrenia may become more common with VAIDS increasing in all age groups, as HIV/AIDS patients may have schizophrenia as a comorbid condition at more severe stages of AIDS. If it is primarily multiple trace nutrient and cofactor deficiency or imbalance - then wouldn’t that be nice to know?
Reducing inflammation in the life and diet may be needed for many people, and many youngsters. Adding mitochondrial support nutrients, omega 3 fatty acids, and even cholesterol rich foods or coconut oil may be beneficial.
For more on lifestyle and diet changes that may be needed, see: Standing on one leg – research plan for a list, and Hyperinflammation - ER stress & misfolded proteins for more detail.
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.
Thanks for reading deNutrients - News to Use! Subscribe for free to receive new posts and support my work.
In appreciation for all he has done for Covid care and his community - Dr. Vladimir ‘Zev’ Zelenko - let us never forget his name, or his use of zinc and zinc ionophores for early and successful treatment of SARS-CoV-2 infections. Zinc ionophores are effective for intracellular parasites and the use of zinc nanoparticles for toxoplasmosis suggests that formulation can also enter infected cells somehow. Lipid nanoparticles are attracted to other lipid membranes and can dissolve through.
Video message from his hospital before passing on June 30, 2022:
It will take some work to keep his name and his healing message from being suppressed.
For more about the anti-inflammatory diet and lifestyle changes that may help a variety of chronic conditions or help prevent infection, see the previous post: Standing on One Leg - a life lengthening skill?
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.
Robert More, ADHD and FAS - Making Sense of the Connections, bcadoption.com, https://www.bcadoption.com/resources/articles/adhd-and-fasd-making-sense-connections *written by an adoptive father of three children with FAS and ADHD who fortunately also has twenty years of experience as a Special Ed teacher. The article has concrete guidance for positive parenting of a child with learning and behavioral issues.
Extrapyramidal Symptoms - STATPearls - NCBI.nlm.nih.gov, https://www.ncbi.nlm.nih.gov/books/NBK534115/
Neuromotor Exercise Training, CMSFitnessCourses.co.uk, https://www.cmsfitnesscourses.co.uk/blog/neuromotor-exercise-training/
Romberg’s test, Wikipedia.org, https://en.wikipedia.org/wiki/Romberg%27s_test
Pringsheim T, Gardner D, Addington D, Martino D, Morgante F, Ricciardi L, Poole N, Remington G, Edwards M, Carson A, Barnes TRE. The Assessment and Treatment of Antipsychotic-Induced Akathisia. Can J Psychiatry. 2018 Nov;63(11):719-729. doi: 10.1177/0706743718760288. Epub 2018 Apr 23. PMID: 29685069; PMCID: PMC6299189. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6299189/
Mannekote Thippaiah S, Iyengar SS, Vinod KY. Exo- and Endo-cannabinoids in Depressive and Suicidal Behaviors. Front Psychiatry. 2021 Apr 23;12:636228. doi: 10.3389/fpsyt.2021.636228. PMID: 33967855; PMCID: PMC8102729. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8102729/
Underwood, M.D., Kassir, S.A., Bakalian, M.J. et al. Serotonin receptors and suicide, major depression, alcohol use disorder and reported early life adversity. Transl Psychiatry 8, 279 (2018). https://doi.org/10.1038/s41398-018-0309-1 https://www.nature.com/articles/s41398-018-0309-1 *whatever is happening in alcoholism is a little different than in major depression and suicide.
Vinod KY, Kassir SA, Hungund BL, Cooper TB, Mann JJ, Arango V. Selective alterations of the CB1 receptors and the fatty acid amide hydrolase in the ventral striatum of alcoholics and suicides. J Psychiatr Res. 2010 Jul;44(9):591-7. doi: 10.1016/j.jpsychires.2009.11.013. Epub 2009 Dec 16. PMID: 20015515; PMCID: PMC2878847. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878847/ “These findings suggest that alcohol dependence is associated with the downregulation of the CB1 receptors, while suicide is linked to the upregulation of these receptors in the ventral striatum. Alteration in the activity of FAAH enzyme that regulates the anandamide (AEA) content might in turn explain differences in the CB1 receptor function in alcohol dependence and suicide.” (8)
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