A high percentage of psychiatric patients actually have some advanced biotoxic disease based on haplotype HLA for mold or very high inflammation, accompanied by elevated levels of cytokines. Neurological inflammations in which there are a number of mechanisms that cause mental disorders are very widely documented in psychiatric literature. Infections that are associated with depression and anxiety are in the majority of cases, Lyme disease, streptococci and moldswhich, if not properly treated, can lead to obsessive-compulsive disorder, also known as PANDAS syndrome.

Some coinfections of Lyme disease get into the spinal cord causing symptoms of psychiatric diseases. For example, toxoplasmosis is associated with an increase in the number of suicides and is involved in the seeds of schizophrenia. Toxoplasmosis changes the personality of the patient. It has long been a practice among the medical community that if a patient complains about many somatic symptoms at the same time and the doctor cannot find any physical basis for his ailments, he diagnoses depression and administers a psychotropic drug. The medical world does not look at cytokines, does not remove inflammatory states of the brain, thus does not remove the cause, treats symptomatically and condemns the patient to ineffective, drug-resistant, endless treatment.


Drug-resistant depression is always associated with cytokines, which in fact have a tendency to reduce the expression and function of serotonin. Serotonin is one of the neurotransmitters that is commonly associated with depression but is probably not the cause of it. The drug-resistant depression has its origin always in the hypothalamus-pituitary axis, where the infection carries out the first damage. This, in turn, leads to a decrease in hormones, often we see a decrease in androgens and cortisol levels. Sometimes, however, one can observe a temporary increase in the level of cortisol, which is the last desperate step of the body to attempt to correct the errors of homeostasis. It’s a matter of time and the adrenal glands will hang out the white flag sooner or later. Whenever cortisol falls, a cascade of events occurs in the brain. Inflammation in the body leads to excitotoxicity, which reduces the number of neurotransmitters and causes depression and anxiety attacks. Cytokines destroy tryptophan, which is a precursor to serotonin, a neurotransmitter associated with depression, which works with all SSRIs. Destroyed tryptophan turns into quinolinic acid, which is highly inflammable and is well-studied as the cause of inflammation leading to neuropsychiatric symptoms. This type of inflammation leads to suicide, and is present in Alzheimer’s, Parkinson’s and Huntington’s disease. The breakdown of tryptophan in Lyme disease is often caused by the so called “leaking brain”.


One common thing in Lyme disease is that cytokines reduce the conversion of T4 to T3. Even large doses of T4 will not convert it to T3 if cytokines are in the way. Active thyroid hormone T3 is responsible for the mood and mental state. Today, standard treatment in psychiatry often involves the direct application of active T3 hormone, which clearly improves the condition of a patient suffering from drug-resistant depression. Unfortunately, this technique is currently inaccessible in Poland. In Poland, SSRIs are administered at the spot, although people with refractory depression may have the type of neurological inflammation that does not properly transform thyroid hormones, and the addition of T3 may be all they need to eliminate psychiatric symptoms and depression.


There is strong evidence that schizophrenia is associated with some infectious factors and inflammation. NIH is continuing research till this very day and is seeing hypersensitivity to gluten in schizophrenics. Hypersensitivity to gluten in Lyme disease is very common.


Aspergillosis is an active infection with Aspergillus fungus and is often an obstacle to the treatment of Lyme disease. Ochratoxin associated with Aspergillus, actually depletes dopamine in the striatum (part of the forebrain). This is closely related to mood disorders as well as movement disorders such as Parkinson’s disease. It also depletes the hippocampus, which largely concerns our memory. There is much evidence that ochratoxin is damaging parts of the brain, disrupting mood and movement. Another mold-associated neurotoxin is fumonisin, which causes degeneration of neurons in the cerebral cortex, disrupting executive functions. Research on mildew shows that patients with this form of toxin lose their executive control. The executive functions of the brain analyse all incoming information. For people who lose their executive control, it often happens that they say exactly what they think, which may give the impression of being somewhat irritable and mad at the whole wide world. These people ask questions over and over again. Questions are asked and received, and five minutes later the very same question appears. The brain exposed to molds shows damage caused by elevated levels of TGF-beta and MMP9. This causes swelling of the frontal lobes, hippocampus and cerebellum, and contraction of the caudate nucleus.


Another issue is unusual reactions to drugs. Patients using SSRIs may feel even worse, which may indicate the role of biotoxins in mental illness. Often in medicine, people who have unusual reactions to drugs can be marked as histrionic, somatic or hypochondriac. Reactions that are marked as crazy are actually a hint to look at something else and something extraordinary.


(1) Benros ME, Waltoft BL, Nordentoft M, Ostergaard SD, Eaton WW, Krogh J, Mortensen PB. Autoimmune diseases and acute infections as risk factors for mood disorders

(2) Shenassa ED, Daskalakis C, Liebhaber A, Braubach M, Brown M.Dampness and Mold in the Home and Depression: An Examination of Mold-Related Illness and Perceived Control of One’s Home as Possible Depression Pathways

(3) Arnett SV, Clark IA. Inflammatory disease and sickness behaviour

(4) Gardner A, Boles RG. Beyond the serotonin hypothesis: mitochondria, inflammation and neurodegeneration in major depression and affective spectrum disorders.


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