Schizophrenia – Keeping It Real
It’s sad when you realise how much is known about metabolic issues behind the symptoms of schizophrenia, whilst authority and profitability continue to influence the treatment approaches most commonly prescribed.
“…communication between the nervous, endocrine, and immune systems…plays an essential role in modulating the adequate response of the hypothalamic–pituitary–adrenal (HPA) axis to the stimulatory influence of cytokines and stress-related mediators…studies have shown that the interface between these complex systems is impaired in schizophrenia…”
No symptom is seen as definitive, although a so called ‘psychotic pathology’ of delusions, hallucinations or disorganized speech is still central to diagnosis. Cases are often assessed on the basis of arbitrary judgements regarding social or occupational ‘functioning’, expected levels of academic achievement as well as interpersonal relations and self-care.
Even so, it’s tempting for many to think of schizophrenia as a distinct and unique disease requiring specialized, specific treatment. From a more metabolic perspective however, symptoms can easily be observed to lie somewhere on a spectrum of stress and its effects upon brain function.
“…increased activity of cortisol metabolism in patients with bipolar disorder and schizophrenia compared to healthy controls…is involved in the pathophysiology and stress vulnerability in these severe mental disorders.”
Signs of schizophrenia are said to encompass: 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. Also included are: slow thinking; poor concentration and memory; difficulty understanding or expressing thoughts; and poor sleep.
Although official diagnosis requires ruling out that the illness results from ‘the direct physiological effects of a substance (e.g. a drug of abuse, a medication) or another medical condition’, the accumulating effects of ‘biological stress’ upon the progression of symptoms are rarely properly considered.
The more distinct ‘psychotic manifestations’ are also often identified based on vague, inconsistent judgements regarding what is and isn’t deemed ‘normal’ behaviour and thought, whilst ignoring many possible metabolic explanations for their existence.
Unfortunately, the impact of stress on thyroid metabolism and the beneficial effects of energy provision to support cellular function is largely ignored in the medical world.
“Abnormal thyroid hormonal status was observed in 29.3 per cent patients with schizophrenia-spectrum disorders in our study. This was comparable with that reported in a similar study in a hospital sample in South-East Asia which showed that 36.4 per cent of patients with schizophrenia had thyroid dysfunction.”
Generally speaking, looking for evidence of energy insufficiency in the face of increased requirements upon the body due to stress of any kind, can help to make sense of the progression of schizophrenia (and many seemingly unrelated symptoms).
This is likely to be a very important link between a variety of different approaches (and changing circumstances) which have been seen to lead to improvement in issues such as these.
There are a number of therapies which have shown promising results – promoting lasting reductions in symptoms of schizophrenia – via suppression of stress and corresponding improvements in thyroid function. Such approaches usually work by helping to correct biochemical imbalances commonly associated with hypo-metabolism, lowering systemic levels of inflammation and protecting against oxidative stress and cellular dysfunction.
“Oxidative stress is a part of the pathology in schizophrenia and appears as a promising field to develop new therapeutic strategies. Considerable attention has been focused on the determination of biomarkers of lipid peroxidation in schizophrenia. PUFAs peroxidation is a chain reaction with a large number of intermediates and end point molecules.”
An under active metabolism tends to go hand in hand with a sluggish, irritated and inflamed digestive system, and 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.
“Neuropsychiatric disorders (e.g., autism, schizophrenia) are partially characterized by social cognitive deficits, including impairments in the ability to perceive others’ emotional states…endotoxin-induced inflammation led to significant decreases in performance…”
Endotoxin stimulates the secretion of serotonin and nitric oxide and all of these can damage mitochondria, suppressing intestinal barrier capabilities and leading to an increase in absorption of toxins into the main system. This can then result in greater circulating levels of estrogen, cortisol and serotonin, worsening inflammation and further disruption of thyroid systems and organ function, including the brain.
“Because the considerable evidence base showing that alterations of activity of NO are active in pathogenesis of schizophrenia, recent attempts have been undertaken to develop the therapy correcting disturbances of the synthesis and release of nitric oxide. Minocycline, semisynthetic tetracycline of the second generation, inhibiting enzyme iNOS and preventing development of microglial inflammatory process has been quite well studied.”
Metabolic suppression resulting from stress, intensifies the bacteria promoting effects of hard to digest foods (like beans, grains, legumes, and other starches and fibrous things), increasing the quantity of poisonous substances which pass through the intestines, placing a greater toxic load upon the liver.
Stress depletes glycogen stores at a faster rate, especially when liver function is interfered with and thyroid is sub-optimal. The provision of enough protein, sugar and particular vitamins and minerals can play a crucial role in protection from metabolic downturn.
Continuously running down glycogen stores can mean that stress and the substances which rise under such conditions become chronically high and this is an important factor implicated in the progression of schizophrenia and other brain disorders and metabolic illnesses.
Low glycogen levels spur the release of fat out of storage as free fatty acids, and particularly when polyunsaturated, this can cause serious damage to thyroid systems and lead to chronic disruption of blood sugar regulation, as well as insulin dysfunction. Studies have shown a connection between schizophrenia and diabetes related conditions.
“…our study ultimately illustrates a potential molecular mechanism to link disparate genetic and environmental factors (i.e. obesity/diabetes/insulin resistance) to dysfunction in a putative “final common pathway” of schizophrenia…”
Insufficient glycogen stores, blood sugar disregulation and high levels of fat in the blood promote further increases in cortisol and adrenalin, interfering with sleep, energy provision, regeneration and optimal brain function.
“It has been reported in the earlier literature that many patients with psychoses had abnormalities in glucose metabolism as revealed by glucose tolerance testing…the schizophrenic population appears to have…a 2–3-fold increased risk for…diabetes…Because glucose is essential for energy metabolism in neurons, any change in…levels in brain…may have significant clinical implications.”
Together this 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.
Whether these stress symptoms are recognized as part of the progression of schizophrenia or not, the hormonal, biochemical and nervous system effects which can result from following popular dietary recommendations are rarely taken seriously by professionals.
“High levels of pro-inflammatory substances such as cytokines have been described in the blood and cerebrospinal fluid of schizophrenia patients…stress may increase pro-inflammatory cytokines and even contribute to a lasting pro-inflammatory state…Further support for the inflammatory hypothesis comes from the therapeutic benefit of anti-inflammatory medication.”
A lack of positive results from the application of official dietary guidelines in the treatment and prevention of schizophrenia symptoms is more likely to lead to encouragement of a more stringent observance of ‘the rules’. The ‘healthy diet’ paradigm is almost never questioned, missing the opportunity for the effective use of powerful experimentally validated nutritional information.
The ubiquitous nature of anti-sugar, anti-salt fear mongering and propaganda means that their metabolism enhancing, stress limiting effects are 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, gradually worsen metabolic function and lead to the progression of many other 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. This shows little understanding of (or regard for) scientifically well demonstrated metabolic explanations for degeneration and disease progression.
The 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 and pro-metabolic effects and helps protect against the substances of stress and inflammation (including endotoxin, cortisol, estrogen and nitric oxide) which suppress thyroid systems.
“We conclude that cyproheptadine 16 mg/day is as effective as propranolol for the treatment of acute NIA [neuroleptic-induced akathisia]. The antiakathisic effect of cyproheptadine may be mostly attributable to its serotonin antagonistic activity.”
Other substances which have been shown to improve symptoms of schizophrenia include glycine, pregnenolone, progesterone and DHEA, the anti-histamine famotidine, aspirin, theanine, lysine, methylene blue and certain antibiotics. All of these things protect against stress and promote improvements in metabolic function.
“Treatment with…pregnenolone significantly decreased negative symptoms in patients with schizophrenia or schizoaffective disorder…and elevations in pregnenolone…post-treatment…were correlated with cognitive improvements.”
The therapeutic application of red light as well as techniques which look at the relationship between things like eye function and vestibular issues (in order to dramatically improve nervous system performance) have enormous potential in relation to brain dysfunction.
“The brain suffers from many different disorders…traumatic events…degenerative diseases…and psychiatric disorders…There is some evidence that all these seemingly diverse conditions can be beneficially affected by applying light to the head.”
“…visual abnormalities in children in the general population are more strongly associated with the later development of schizophrenia than any other form of sensory impairment…Given this, and the fact that vision is the most studied and best understood function in neuroscience, why is vision such an understudied area in schizophrenia research?”
An understanding of the potential usefulness of these things in combination with a metabolism enhancing diet – removing polyunsaturated fats, limiting difficult to digest starches and fibers, 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 stress in general (including dietary stress) and the cumulative damage from long-term exposure to metabolically suppressive and harmful treatments.
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Image: Thorazine advertisement, 1973