Does heaven exist? With well over 100,000 plus recorded and described spiritual experiences collected over 15 years, to base the answer on, science can now categorically say yes. Furthermore, you can see the evidence for free on the website allaboutheaven.org.

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This book, which covers Visions and hallucinations, explains what causes them and summarises how many hallucinations have been caused by each event or activity. It also provides specific help with questions people have asked us, such as ‘Is my medication giving me hallucinations?’.

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Observations placeholder




Type of Spiritual Experience


Number of hallucinations: 24


A description of the experience

Rimifon  , Laniazid, Nydrazid, Isoniazid  is used to treat tuberculosis – mycobacterium tuberculosis. 

On Jan, 12, 2017 9,998 people reported to have side effects when taking Isoniazid.
Among them, 17 people (0.17%) have Hallucination

On Jan, 19, 2017 658 people reported to have side effects when taking Rimifon.
Among them, 6 people (0.91%) have Hallucination, Visual

On Jan, 19, 2017 658 people reported to have side effects when taking Rimifon.
Among them, 1 person (0.15%) has Hallucinations, Mixed

The way it works is highly complex, I will quote…

Isoniazid is a prodrug and must be activated by a bacterial catalase-peroxidase enzyme that in M. tuberculosis is called KatG.KatG couples the isonicotinic acyl with NADH to form isonicotinic acyl-NADH complex. This complex binds tightly to the enoyl-acyl carrier protein reductase known as InhA, thereby blocking the natural enoyl-AcpM substrate and the action of fatty acid synthase. This process inhibits the synthesis of mycolic acid, required for the mycobacterial cell wall. A range of radicals are produced by KatG activation of Isoniazid, including nitric oxide,  which has also been shown to be important in the action of another antimycobacterial prodrug PA-824.  Isoniazid inhibits the P450 system

From our point of view, however, it is what causes the hallucinations that is of interest and it appears that like all the other antibacterials it can be toxic to some people and causes liver damage.

Severe isoniazid-associated liver injuries among persons being treated for latent tuberculosis infection - United States, 2004-2008.  Centers for Disease Control and Prevention (CDC).
Since the 1960s, 6 to 9 months of isoniazid (INH) has been the mainstay of treatment for latent tuberculosis infection (LTBI), but its application has been limited by concerns about the toxicity of INH and the long duration of treatment.
To quantify the frequency of severe adverse events (SAEs) associated with LTBI treatment and to characterize the clinical features of affected patients, in January 2004 CDC began a national project to monitor SAEs associated with treatment for LTBI. State health departments were encouraged to report SAEs associated with any LTBI treatment regimen to a passive surveillance system.
This report summarizes the results for 2004-2008, when 17 SAEs in 15 adults and two children (aged 11 and 14 years) were reported. All patients had received INH therapy and had experienced severe liver injury. Five patients, including one child, underwent liver transplantation. Five adults died, including one liver transplant recipient. These findings underscore the risk for an idiosyncratic drug-induced reaction in patients of any age treated with INH, including those with or without a putative predictor for INH-associated liver injury.
Patients receiving INH for LTBI therapy should be monitored according to American Thoracic Society (ATS)/CDC recommendations because of the risk for drug-induced hepatoxicity. Providers should counsel patients to terminate INH therapy promptly and seek medical attention if they experience signs and symptoms of illness.

The known adverse reactions include rash,  hepatitis, sideroblastic anaemia, high anion gap metabolic acidosis, peripheral neuropathy, and central nervous system (CNS) effects.  Where anaemia is present then hallucinations may be being caused by lack of oxygen – hypoxia [see hypoxia]

The drug is acetylised by the liver.  Slow acetylation may lead to higher blood concentrations with chronic administration of the drug, with an increased risk of toxicity. Fast acetylation leads to higher blood levels of the toxic metabolite acetylisoniazid and thus to an increase in toxic reactions and  hepatitis which is 250 times more common than in slow acetylators.  The rate of acetylation is genetically determined. Approximately 50% of blacks and Caucasians are slow inactivators; the majority of Inuit and Asians are rapid inactivators. The half-life in fast acetylators is 1 to 2 hours, while in slow acetylators it is 2 to 5 hours.

The source of the experience


Concepts, symbols and science items



Science Items

Activities and commonsteps