Schizophrenia – Keeping It Real
“A spontaneous recovery from schizophrenia…is so rare…that when it occurs psychiatrists routinely question the validity of the original diagnosis” – A Beautiful Mind
It’s sad when you realize how much is actually known about the metabolic or biochemical issues behind the symptoms of schizophrenia, and how little of it ever makes its way into treatment. And it’s not like the standard approach has ever been that successful.
Officially, when it comes to diagnosing schizophrenia, no symptom is seen as definitive, and a so called ‘psychotic pathology’ of delusions, hallucinations or disorganized speech is considered central.
Cases get further assessed on the basis of arbitrary judgements, regarding social or occupational functioning, expected levels of academic achievement, interpersonal relations, and self-care.
Schizophrenia is popularly understood to be a distinct and unique, largely genetically driven disease, which relies upon a variety of ‘anti-psychotic’ medications for treatment, with limited improvement potential. It all sounds a bit contradictory, and not very promising.
From a metabolic perspective however, a potentially more practical and illuminating way to view the symptoms of schizophrenia, is to see them as existing somewhere along a spectrum of stress exposure, and the effects that stress can have upon brain and overall system function.
When you think about schizophrenia in terms of the function of metabolism (and the symptoms of interference which result from stress), just the mention of the HPA axis and high cortisol can be enough to make light bulbs go off in your head, inspiring a multitude of possible treatment ideas. But first you might need to do a little detective work.
Some of the signs of schizophrenia are said to include: an inability to enjoy regular activities; low energy; lack of motivation or interest in socializing; a flat voice; inability to make friends and social isolation in general; slow thinking; poor concentration and memory; difficulty understanding or expressing thoughts; and poor sleep. All potential symptoms of stress, and metabolic suppression.
The more distinct and extreme ‘psychotic manifestations’ associated with schizophrenia, are often identified based on vague, inconsistent judgements regarding what is and isn’t deemed ‘normal’ behavior and thought, with many possible metabolic explanations for their existence being ignored.
A good place to start is to look at the relationship between high stress and thyroid dysfunction. What if the provision of an abundance of energy in the face of stress, is able to support thyroid performance, enable proper cellular function, and protect against schizophrenia?
Insufficient energy availability when stress is high, impacts upon HPA axis function, increasing cortisol, and this can create conditions that are known to promote the things that interfere with thyroid energy metabolism, causing symptoms associated with schizophrenia.
The idea is to find the metabolic, biochemical links in the chain leading to worsening symptoms, and then use that information to build a holistic therapeutic response, so that you can work on improving overall function of metabolism from as many angles as possible.
Symptoms of schizophrenia can worsen a great deal (and fluctuate significantly) over time, so there is every reason to believe that an awareness of the different measures of metabolism connected to worsening symptoms (and knowledge regarding different stressors that have a negative impact) will be able to make a big difference in relation to disease progression.
Stress wastes glycogen stores leading to an increase in cortisol, and this promotes other biochemical changes associated with HPA axis dysfunction and schizophrenia. Rising levels of the stress substances are encouraged by a hypo-metabolic state, together with increased free fatty acid release, often polyunsaturated. These factors combined can cause a downward spiraling vicious circle of stress and metabolic suppression.
The breakdown products of the polyunsaturated fats (PUFAs) promote oxidative stress, inflammation and mitochondrial dysfunction, all of which are associated with thyroid energy production issues, and are known to be involved in the development of schizophrenia.
An under active metabolism resulting from stress, tends to go hand in hand with a sluggish, irritated and inflamed digestive system. Intestinal interference plays a significant part in the advancement of metabolic issues, including the disorders of the mind.
When digestion is slow, bacteria can grow in number and move further up the intestine promoting an increase in the release of bacterial toxins such as endotoxin. Endotoxin is involved in the promotion of inflammation and elevation of numerous stress substances associated with schizophrenia and other mood related issues.
Endotoxin promotes serotonin, estrogen and nitric oxide, and all of these things can interfere with mitochondria, reduce intestinal barrier function, and lead to an increase in absorption of toxins into the main system. This results in greater circulation of stress substances (including estrogen and cortisol), worsening inflammation, and further disruption of thyroid systems, impacting on the brain, encouraging symptoms of schizophrenia.
Metabolic suppression resulting from stress, intensifies the bacteria promoting effects of hard to digest foods (like beans, grains, legumes, and other starchy and fibrous things), increasing the quantity of inflammatory substances which pass through the intestine, placing a greater load upon the liver.
Stress has more impact upon metabolic function when the liver is damaged, and this can then suppress thyroid metabolism even further. The provision of enough protein, sugar and certain vitamins and minerals, play a crucial role in liver function, as well as protection from metabolic dysfunction and schizophrenia progression.
Continuously running down glycogen stores can mean that the stress substances become chronically high, and this is an important factor implicated in the progression of schizophrenia and other brain and mood related disorders and metabolic illness in general.
Chronic or acute stress and persistently low glycogen stores, lead to an increase in the release of the polyunsaturated free fatty acids, directly promoting inflammation, and impeding thyroid energy systems, promoting blood sugar dysregulation and insulin resistance. It is probably not a coincidence that schizophrenia and diabetes often go together.
Stress, blood sugar dysregulation and high levels of PUFA in the blood, promote further increases in cortisol and adrenalin, interfering with sleep, energy provision, cellular regeneration and optimal brain function.
Too much exposure to PUFA can feed a vicious circle of serotonin, estrogen and nitric oxide dominance, fueling systemic inflammation and exacerbating many symptoms which are biologically connected to the development of schizophrenia.
One thing impacts upon another, and so rising stress substance exposure, lack of sugar, and excessive circulation of PUFA, can promote dysregulation in almost every biological system, creating the potential for a gradually worsening degree of symptom seriousness, and yet the same information can be utilized for prevention or treatment.
Sugar avoidance in combination with stress, excess PUFA and exposure to endotoxin, interfere with pregnenolone production and can lead to an estrogen dominant (progesterone or testosterone deficient) state, similar to those seen post menopause as well as in breast cancer.
Although it is popular to suggest (as a means to explaining increased occurrence of schizophrenia in men) that estrogen is protective, this is contradicted by the fact that schizophrenia in women is associated with an increased risk of breast cancer and is more common post menopause, where tissue levels of estrogen are significantly increased, and progesterone is reduced. High testosterone has been shown to have protective effects against schizophrenia in men. Some other conditions which happen more regularly with schizophrenia, and are connected to estrogen dominance, include MS and epilepsy.
Another possible explanation for higher rates of schizophrenia in men, is the fact that women are better protected from iron accumulation pre-menopause. Interaction between accumulated iron, PUFAs and endotoxin has been shown to promote iron dysregulation, and iron issues are involved in inflammation and oxidative stress, and have been demonstrated to play a role in the development of diseases like cancer and diabetes, as well as brain disorders including schizophrenia.
If you look at changing levels of individual stress hormones, as well as inflammation or thyroid dysfunction, as though they were all unrelated (genetically predetermined) issues, it’s easy to think then, that there isn’t that much known about the development or potential treatment of schizophrenia, and often co-occurring diseases such as cancer and diabetes.
If you are unaware of the potential impact of excessive PUFA exposure and ongoing sugar restriction (and other nutritional factors) on all of the above conditions and on stress and metabolic function in general, it’s easy to disregard diet as a powerful causative or preventative element.
It’s not surprising that official dietary guidelines are unhelpful (at best), and sadly the ‘healthy diet’ paradigm is almost never questioned by practitioners, but rather it tends to be obediently and blindly recommended.
The ubiquitous nature of anti-sugar and salt, pro-PUFA propaganda means that the power of real nutrition as a means to fueling metabolism and protecting against stress, is no longer harnessed therapeutically.
Popularly prescribed anti-psychotic medications, whilst sometimes working at least for a while to suppress the so called ‘positive symptoms’ of schizophrenia, have been shown to gradually worsen metabolic function and lead to the progression of many symptoms often considered unrelated or irrelevant.
Some other known ‘side-effects’ of the anti-psychotic medications include movement disorders, heart problems, sexual dysfunction, suicidal depression and suicide. It has been suggested that failure to stay on these medications (because of their unpleasant effects) explains poor treatment success rates. Or it could be that they damage overall metabolic function, explaining lack of long term success.
I’m not a doctor or a scientist and I’m no expert on the subject of schizophrenia. I don’t believe that we have the power to fix every health issue, but it seems to me that there is a lot that is known that can help people who are suffering from schizophrenia, and if I know a bit about it, then what exactly am I missing here? Perhaps healing is not the priority.
The first generation anti-histamine cyproheptadine, is one example of a drug which has been shown over time to safely and effectively treat symptoms of schizophrenia. It has anti-serotonergic, anti-estrogenic, anti-cortisol, pro-metabolic effects, protects against the substances of stress and inflammation (including endotoxin, nitric oxide and PUFA) and is generally thyroid supportive and stress protective.
Other pro-metabolism, anti-stress things which have been shown to improve symptoms of schizophrenia include glycine, pregnenolone, progesterone, DHEA, thyroid hormone, the anti-histamine famotidine, aspirin, theanine, lysine, methylene blue and certain antibiotics.
“Pregnenolone and L-Theanine have shown ameliorative effects on various schizophrenia symptoms…”
The therapeutic application of red light, as well as techniques which look at the relationship between eye function, vestibular issues and nervous system performance, have potential in relation to brain function and mood issues.
A metabolism enhancing diet, removing PUFA and limiting difficult to digest starches and fibers, whilst including sufficient protein from milk, cheese and gelatin, and plenty of sugar from sweet ripe fruits, fruit juice and white sugar, is one possible approach to protecting against symptoms of schizophrenia.
Relapses into psychosis are commonly blamed on ‘genetics’, on brain defects or a failure to adhere to drug therapy regimens. What tends to be disregarded are the effects of changes in levels of exposure to biological stress in general (including dietary stress) and the cumulative damage from long-term exposure to numerous metabolically suppressive and harmful things.
See More Here
Glucose-insulin metabolism in chronic schizophrenia
Lipid peroxidation and antioxidant enzyme levels in patients with schizophrenia and bipolar disorder
Treating schizophrenia at the time of menopause.
Cognitive functioning, cortisol release, and symptom severity in patients with schizophrenia.
Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited
Stress and the hypothalamic pituitary adrenal axis in the developmental course of schizophrenia.
The relationship of sex hormones and cortisol with cognitive functioning in Schizophrenia.
Potential metabolite markers of schizophrenia
The stress cascade and schizophrenia: etiology and onset.
Secondary psychosis induced by metabolic disorders
Antipsychotic Response Worsens With Postmenopausal Duration in Women With Schizophrenia.
Meta-Analysis of Oxidative Stress in Schizophrenia
Cerebral glucose metabolism in childhood onset schizophrenia.
Recurrent Psychosis Associated with Liver Disease and Elevated Blood Ammonia
Schizophrenia-like psychosis and epilepsy: the status of the association.
The varieties of psychosis in multiple sclerosis: A systematic review of cases.
Serum thyroxine levels in schizophrenic and affective disorder diagnostic subgroups.
Cyproheptadine in treatment of chronic schizophrenia: a double-blind, placebo-controlled study.
Pregnenolone Rescues Schizophrenia-Like Behavior in Dopamine Transporter Knockout Mice
The role of estradiol in schizophrenia diagnosis and symptoms in postmenopausal women.
Progesterone reduces hyperactivity of female and male dopamine transporter knockout mice
Cancer mortality in patients with schizophrenia: systematic review and meta-analysis.
Testosterone Is Inversely Related to Brain Activity during Emotional Inhibition in Schizophrenia
Serum fatty acid patterns in patients with schizophrenia: a targeted metabonomics study
Association of Schizophrenia With the Risk of Breast Cancer Incidence: A Meta-analysis.
Thyroid Hormone Levels in Chronic Schizophrenic Patients: Association with Psychopathology.
Mitochondrial dysfunction in schizophrenia: pathways, mechanisms and implications.
Thyroid dysfunction in major psychiatric disorders in a hospital based sample
Schizophrenia and type 2 diabetes mellitus.
Dose-Dependent Effects of Endotoxin on Neurobehavioral Functions in Humans
Schizophrenia and breast cancer incidence: a systematic review of clinical studies.
Revisiting Thyroid Hormones in Schizophrenia
Morning cortisol levels in schizophrenia and bipolar disorder: a meta-analysis.
A serotonin hypothesis of schizophrenia.
Sources of estrogen and their importance.
Genomics of schizophrenia: time to consider the gut microbiome?
Mitochondrial function in individuals at clinical high risk for psychosis
The metabolic syndrome in schizophrenia: is inflammation a contributing cause?
Vision in schizophrenia: why it matters
Acute psychosis as an initial manifestation of hypothyroidism: a case report
Inflammation impairs social cognitive processing: a randomized controlled trial of endotoxin
Glycine treatment of the risk syndrome for psychosis: Report of two pilot studies✩
Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia.
A role for bioenergetic abnormalities in the pathophysiology of schizophrenia
Shining light on the head: Photobiomodulation for brain disorders
Executive functioning and diabetes: The role of anxious arousal and inflammation
Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia
Glucose Metabolism in Relation to Schizophrenia and Antipsychotic Drug Treatment
Near-Infrared Transcranial Radiation for Major Depressive Disorder: Proof of Concept Study
Clonidine Normalizes Levels of P50 Gating in Patients With Schizophrenia on Stable Medication
Effect of clonidine on plasma ACTH, cortisol and melatonin in children.
Oxidative metabolism may be associated with negative symptoms in schizophrenia
Pregnenolone Rescues Schizophrenia-Like Behavior in Dopamine Transporter Knockout Mice
Levothyroxine Augmentation in Clozapine Resistant Schizophrenia: A Case Report and Review
Role of mitochondria and energy metabolism in schizophrenia and psychotic disorders.
Association Between Vitamin D Status and Schizophrenia: A First Psychotic Episode Study.
Brain metabolic abnormalities in schizophrenia patients
The “selfish brain” hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia
GABA and brain abnormalities in schizophrenia.
Metabolic changes in schizophrenia and human brain evolution
A randomized clinical trial of histamine 2 receptor antagonism in treatment-resistant schizophrenia.
Profile of minocycline and its potential in the treatment of schizophrenia
Exploring the link between inflammation and mental disorders
Inflammation in Schizophrenia: Pathogenetic Aspects and Therapeutic Considerations.
Altered brain arginine metabolism in schizophrenia
The role of inflammation in schizophrenia
Microhemodynamics and energy metabolism in schizophrenia patients.
Oxidative Stress in Schizophrenia
GABA and schizophrenia: a review of basic science and clinical studies.
Inflammation in schizophrenia: A question of balance.
Stress, schizophrenia and bipolar disorder.
Acetylsalicylic acid (aspirin) for schizophrenia
Oxidative Stress in Schizophrenia: An Integrated Approach
Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization
GABA and glutamate in schizophrenia: A 7 T 1H-MRS study
#serotoninsorrow
#sugarsaves
#raypeat
Image: Thorazine advertisement, 1973