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.

Available on Amazon
also on all local Amazon sites, just change .com for the local version (.co.uk, .jp, .nl, .de, .fr etc.)


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?’.

Available on Amazon
also on all local Amazon sites, just change .com for the local version (.co.uk, .jp, .nl, .de, .fr etc.)

Some science behind the scenes

Opioid receptors

Opioid receptors  are named from their opioid ligands. The endogenous (naturally occurring in the body) opioids are

Opiate receptors are widely distributed in the brain, and are found in the spinal cord,  digestive tract and on the skin in nerve endings.

There are four major subtypes of opioid receptors:

delta (δ) opioid receptors

also known as OP1s,  are found principally in the brain.  They have enkephalins as their endogenous ligands, but appear also to be stimulated by endorphins. Until comparatively recently, there were few pharmacological tools for the study of δ receptors. As a consequence, understanding of their function is much more limited than those of the other opioid receptors for which selective ligands have long been available.  Their function is thought to be to

  • provide pain relief - analgesia - although they provide less than that of mu-opioid agonists
  • antidepressant effects – ‘anti-anxiety’. 

There is also a suggestion that they may have some effect on ‘gastrointestinal motility’ as well as cardiovascular regulation.  There also appears to be some interaction with the GABAA receptors producing  GABAergic agonist and some Glycine inhibition. See neurotransmitters - GABAA

The following lists of agonist and antagonist chemicals are liable to change simply because this is an experimental area and also drugs come and go over time, but they are useful indicatively.  Those in italics were derived from the IUPHAR database. 

  • Agonists – include 7-Spiroindanyloxymorphone, ADL-5859 , Bremazocine, BU-48, BW373U86, Cyclazocine DADLE, Deltorphin, Dihydromorphine, Diprenorphine, DPDPE, DPI-221, DPI-287, DPI-3290, DSLET, Dynorphin, EKC, Endomorphin, Etonitazene, Etorphine, Fentanyl, Leu-enkephalin,  Met-enkephalin, Methadone, Morphine, Nalmefene , Nalorphine, Normorphine, Norbuprenorphine N-Phenethyl-14-ethoxymetopon, Pentazocine , RWJ-394,674, SNC-80, TAN-67, ; Mitragyna Speciosa(aka Kratom) Indole Agonists: Mitragynine, Mitragynine-pseudoindoxyl
  • Antagonists  - include Beta-FNA, BNTX, CTAP, Naltriben, Naltrindole, Naloxone, Naltrexon, nor-binaltorphimine, Quadazocine,  TIPPepsilon

kappa (κ) opioid receptor

also known as OP2.  This receptor binds the opioid peptide dynorphin as the primary endogenous ligand, but with some activity by enkephalin and endorphins.  These receptors are found in the brain, the spinal cord and ‘pain neurons’ in the skin.   The functions are fairly complex, acting both directly and indirectly:

  • Dysphoria - The anti-rewarding properties of κ-opioid agonists are well known and seem to work a number of ways.  These receptors  produce dysphoria (the opposite of euphoria) where the dysphoria differs between sexes.  Effects include nervousness, depression, restlessness and  crying.  In addition, the immediate effect of κ-opioid agonism leads to reduction of dopamine release, although the administration of a κ-opioid agonist  produces an increase in dopamine D2 receptors in the brain.  [Yuferov, V., Fussell, D., LaForge, K. S., Nielsen, D. A., Gordon, D., Ho, A., Leal, S. M., Ott, J. and Kreek, M. J.   (2004)  - Redefinition of the human kappa opioid receptor gene (OPRK1) structure and association of haplotypes with opiate addiction. Pharmacogenetics, 14: 793-804. [PMID: 15608558 ]
  • Pain relief - Stimulation of relief from abdominal pain and bloating this may be accompanied at high dose by cramps, dyspepsia, and a bitter taste
  • Nausea – and vomiting at higher doses
  • Diuretic - It also causes an increase in urine production because it inhibits the release of vasopressin. Vasopressin is an endogenous substance that assists in regulating fluid and electrolyte balance in the body and decreases the amount of water released into the urine.  In effect  we’ll want to wee more
  • Sedation  - sleepiness and at higher doses confusion
  • Interoceptive effects - depersonalising and derealising, psychotomimetic  - psychotomimetic actions mimic the symptoms of psychosis, including delusions and/or hallucinations.  Because the principal effects are that of dysphoria, these hallucinations are not pleasant and can include psychological symptoms such as feelings of unease and  paranoia
  • Cardiovascular – hypertension, increased cardiac load, or hypotension, bradycardia, tachycardia
  • Respiratory depression - at higher doses pulmonary edema occurs when the pressure in blood vessels in the lung is raised because of obstruction to remove blood via the pulmonary veins. Pulmonary edema produces shortness of breath. Pleural effusions may occur when fluid also accumulates in the pleural cavity
  • Visual distortions – possibly caused by the increase in blood pressure

One rather odd knock on effect is that kappa opiate receptor agonists increase the pituitary hormone prolactin [Source PMID: 3079599].  Prolactin has all sorts of effects:

  • Sexual depressant - It decreases the normal levels of sex hormones — estrogen in women and testosterone in men. It is this inhibition of sex steroids that is responsible for loss of the menstrual cycle in lactating women as well as lactation-associated osteoporosis.
  • Hair thinning - It seems to delay hair regrowth leading to balding
  • Brain neuron increase -  It “promotes neurogenesis”, neurogenesis is responsible for populating the growing brain with neurons.  This is why drugs in this class have sometimes been used to counteract the effects of drugs that cause permanent memory impairment.
  • It also stimulates growth hormones, whilst inhibiting the thyroid-stimulating hormones (TSHs).

One of the more interesting other knock on effects of the kappa opioid receptor is to inhibit the secretion of peripheral Oxytocin

The following lists of agonist and antagonist chemicals are liable to change simply because this is an experimental area and also drugs come and go over time, but they are useful indicatively.  Those in italics were derived from the IUPHAR database.  The natural agonist mentha is found in numerous species of mint, (including peppermint, spearmint, and watermint), the naturally-occurring compound, it is a weak k-opioid receptor agonist.

  • Agonists  - 2-EMSB, 2-MMSB, Alazocine, Asimadoline, Bremazocine, Butorphanol, BRL-52537, Cyclazocine, Cyprenorphine, DAMGO, Dextrallorphan, Dextromethorphan, Dezocine, Dihydromorphine, E2078, EKC, Enadoline, Etonitazene, Etorphine, Fentanyl, GR-89696- selective for κ2 subtype , Herkinorin, HZ-2, Ibogaine, ICI-204,448 - peripherally selective, ICI-199,441, Ketazocine, LPK-26 - highly selective, Menthol, Metazocine, Methadone, Morphine, Nalbuphine, Nalfurafine, Nalorphine, Naloxone benzoylhydrazone, Norbuprenorphine, Noribogaine, Normorphine, Oxycodone (disputed), Pentazocine, Phenazocine, Salvinorin A, Salvorin B, Spiradoline, Tifluadom, TRK820, U-50,488, U-62066, U-63,640, U-69,593
  • Antagonists – include 5'-Guanidinonaltrindole, Beta-FNA, BNTX, Binaltorphimine, Buprenorphine , Diprenorphine, GNTI, Naltriben, Nalmefene, Naloxone, Naltrindole, Natrexone, Quadazocine, Norbinaltorphimine, JDTic

Mu μ-opioid receptors (MOR) 

Mu μ-opioid receptors (MOR)  have high affinity for enkephalins and beta-endorphin but low affinity for dynorphins. They are also referred to as μ- opioid peptide (MOP) receptors. They can be found in the brain, the spinal cord, the olfactory bulb, the skin and nerve endings, and the intestinal tract.  The  more ‘physical’ functions they perform are generally suppressive in action:

  • inhibition of peristaltic action in the intestinal tract. This can cause constipation, a major side effect of μ- agonists.
  • Constriction of the pupil
  • Hypothermia – suppressing bodily  temperature
  • General pain relief [analgesia] – suppression of pain from wherever they are sited
  • ‘Locomotor sensitisation opposition’ – suppression of the need for physical activity - they slow you down physically, sedation, relaxation
  • Respiratory depression – at the higher doses

The less physical and more emotional functions that appear to be controlled by this receptor are:

  • Formation of attachments - There appear to be links between the mu opioid receptor and the formation of attachments between people – babies and mothers and adult with adult.  The babies  of μ receptor knockout mice “emit fewer ultrasonic vocalisations when removed from their mothers”. No attachments – so no distress at parting
  • Anxiety and curiosity  - μ opioid receptors may play a role in the modification of emotional responses to novelty, anxiety and depression. μ receptor knockout mice [no receptors so no effect] show “less anxiety in the elevated plus maze and emergence tests, reduced response to novel stimuli in the novelty test and less depressive-like behaviour in the forced swim test”.  No receptor so no drive [or motivational anxiety] and no curiosity. 
  • Anticipation - They also appear to control the function of ‘anticipation’ and ‘looking forward to good things’ [or bad I suppose].
  • Learning and memory - μ opioid receptor knockout mice show a significant spatial memory impairment compared to wild-type in the Morris water maze. They also exhibit an impairment in the ultimate level of spatial learning.  In effect  the μ-opioid receptor may play a role in learning and memory. No receptor, no ability to find your way around and remember where you’ve been.

Mu μ-opioid receptors are presynaptic, and inhibit neurotransmitter release; though through this mechanism, they can "disinhibit" presynaptic release of GABA meaning you get release of GABA – the calming neurotransmitter, and disinhibit the dopamine pathways, causing more dopamine to be released. By hijacking this process, exogenous opioids cause “inappropriate dopamine release” – which explains why they give us euphoria and pleasure.  As a knock on effect, over dose or high doses of any drug acting on this receptor can cause “excessive serum histamine levels” which causes intense itching.  Medically doctors treat these effects with antihistamines. The following list of agonists and antagonists comes from the IUPHAR database:

  • Agonists – buprenorphine, codeine, cyclazocine, DADLE, DAMGO, dihydromorphine, DSLET, endomorphine, etonitazene, EKC, etorphine, fentanyl, Leu-enkephalin, methadone, morphine, normorphine, pentazocine, PL017
  • Antagonists –, Beta-FNA, BNTX, , Bremazocine,  CTAP, CTOP, Diprenorphine,  Naltriben, Nalmefene, Nalorphine, Naloxone, Naloxone benzolhydrazone, Naltrindole, Naltrexone, Quadazocine, Norbinaltorphimine


The nociceptin receptor is a protein that in humans is encoded by the opioid receptor-like 1 gene, whose natural ligand is known as nociceptin.   This receptor is involved in “the regulation of numerous brain activities, particularly instinctive and emotional behaviours”.  This receptor appears to have inhibitory action – according to the IUPHAR database it stops or inhibits other activity.  In rat and mouse models it seemed to inhibit

  • muscle contraction in the vas deferens.
  • muscle contraction of the colon.
  • glutamate release.
  • dopamine release.
  • acetylcholine release.
  • noradrenaline release.
  • serotonin release.

It also appears to control

  • agonist-induced anxiolytic activity.
  • agonist-induced cardiovascular depression
  • water diuretic activity

There also seem to be other functions because ‘Knockout mice’ without the receptor don’t recover their hearing as well after sound exposure.

Agonists – Buprenone, Norbuprenorphine,  NNC 63-0532, Ro64-6198, Ro65-6570

SCH-221,510,  SR-16435 (mixed mu / nociceptin partial agonist), UFP-102[3H]N/OFQ,     [(pF)Phe4]N/OFQ(1-13)NH2,       N/OFQ-NH2,       N/OFQ(1-13)NH2 ,   Ac-RYYRWK-NH2, ,   N/OFQ   [Arg14Lys15]N/OFQ,    [F/G]N/OFQ(1-13)NH2,        AC-RYYRIK-NH2

Antagonists - JTC-801,  J-113,397, SB-612,111,   SR-16430 ,  [Nphe1]N/OFQ(1-13)NH2    UFP-101   peptide III-BTD

There are theories of more opioid receptors.  The ε opioid receptor is but one whose  existence was hypothesised  after the endogenous beta-endorphin was shown to produce additional actions that did not seem to be mediated through any of the known opioid receptors.  This  receptor – if it exists [it is not on the IUPHAR database] would provide strong analgesia.  But I will concentrate on the four confirmed ones.

What would help a spiritual experience?


  • provide pain relief - - delta, ,mu, kappa
  • antidepressant effects – delta
  • Interoceptive effects - kappa
  •  Sedation, relaxation – mu and kappa
  • euphoria pleasure - mu


  • Dysphoria – kappa
  • Nausea  and vomiting  - kappa
  • Cardiovascular – kappa
  • Respiratory depression -  kappa and mu
  • Visual distortions – kappa
  • Sexual depression and impotence - kappa.
  • Hair thinning - kappa
  • Constipation - mu
  • Hypothermia – mu
  • Learning and memory - mu opioid receptor.
  • Learning and memory for non human facts and figures would be much improved , but there would also be an inability to remember human faces, or names and a lack of social skills and the ability to work with social cues - kappa
  • Itching – mu
  • Discontent,  anxiety, insecurity, ‘jitteriness’ – kappa
  • Inability to love or bond or even care about anybody - kappa
  • Suspiciousness, paranoia, control freakery, fear, distrust – kappa
  • Lack of empathy - kappa


  • Diuretic - kappa
  • Brain neuron increase -  kappa.
  • GH stimulation – kappa
  • TSH inhibition – kappa
  • Constriction of the pupil – mu
  • Curiosity - mu
  • Anticipation – mu
  • Female reproduction system disruption – kappa
  • Meanness and stinginess - kappa

We have a hugely complex picture here which produces no clear cut set of rules.  In the chart above I have tried to summarise the actions under the general headings of helpful and not helpful as well as neutral.

What might help is the pain relief and numbing of sensation which would help in sensory deprivation.  This is provided by:

  • delta (δ)opiod receptors agonists
  • μ-opioid receptors (MOR)  agonists

Next we need to have ways of limiting locomotor activity and promoting  relaxation, sedation and general sensory deprivation.  This might be provided by

  • kappa (κ) opiod receptor agonists
  • μ-opioid receptors (MOR)  agonists
  • delta (δ)opiod receptors agonists

Finally we need a way of stilling the reasoning function and memory .  This might be provided by

  • kappa (κ) opiod receptor antagonists

As we can see from the list, however, the last thing we want is a kappa agonist, although kappa antagonism might be helpful.  Kappa agonists clearly have a role in nature in balancing the effects of the mu and delta receptors, but as a means of obtaining any form of spiritual experience it is a no-goer.  The only thing it has in its favour is the supposed hallucinogenic effects – but I suspect these are caused by hypoxia.

In contrast there is a synergy between the Mu and Delta receptors. There appears to be some evidence that the delta agonists act to counter some of the respiratory depression induced by the mu agonists.

But, again we have a dilemma because the μ-opioid receptors (MOR)  agonists appear to help in learning and memory.

It would almost seem that the best solution is a substance that is

  • a delta (δ)opiod receptors agonist
  • a μ-opioid receptors (MOR)  agonist
  • has NO kappa (κ) opiod receptor activity
  • has NO NOP opiod receptor activity

which can be teamed with a substance that does temporarily inhibit memory and learning or alternatively a technique that does the same.




  • provide pain relief - delta, mu
  • antidepressant effects – delta
  •  Sedation, relaxation – mu
  • euphoria pleasure -  mu


  • Respiratory depression -  mu
  • Constipation - mu.
  • Hypothermia – mu
  • Addiction – mu
  • Itching - mu

There are no pharmaceuticals that I could find that have this combination of opioids with memory inhibitors, but  this combination can be found ‘naturally’ in plants and animals.

 In other words, the sedative relaxing and analgesic power of the delta and mu opioids are combined with other chemicals acting on other receptors that knock out the learning capability.


One of the very unfortunate aspects of opioid products is that we can very quickly build up a tolerance to them.  The chemistry behind this is hugely complex and frankly not well explained in most scientific literature.  But simply put, if we fill our system full of a chemical that binds naturally to a receptor and this chemical is at high sustained levels, the body adjusts and reduces the number of receptors.

The technical name for this is Tachyphylaxis  -  a medical term describing “a rapid decrease in the response to a drug due to previous long term exposure to that drug such that increasing the dose of the drug will not increase the pharmacological response”. Tachyphylaxis is characterised by the “rate sensitivity: the response of the system depends on the rate with which a stimulus is presented. Specifically, a high intensity prolonged stimulus or often repeated stimulus brings about a diminished response”.  This is also often referred to as ‘desensitisation’.  And opioids are some of the worst drugs around for desensitisation.

If you ignore the advice to only use these products very infrequently, you will build up a tolerance to them and eventually you will get no effects at all and sink into a kappa state – which is frankly dreadful.  Furthermore, if you decide to cut back and reduce the frequency of dose or the dose itself you will get withdrawal symptoms, after having built up the tolerance all you will get is a kappa like world of paranoia, awful hallucinations, distrust, lack of love, anxiety, fear, dysphoria, acute depression and an aching, aching longing to be back where you were.  A truly aching longing.

You will feel strange or overwhelmed coping with daily activities, uneasy, restless, full of the jitters, unable to find peace or calm, you will suffer from mood swings and  amnesia (forgetfulness), you may end up with low self-esteem.  Along with these mental feelings you are also likely to get a number of very unpleasant physical withdrawal symptoms too.

  • muscle cramps, muscle twitches and spasms, involuntary leg movements( from which we get the expression "kicking the habit"), aching muscles, aching bones, severe pains in the bones and muscles of the back and extremities,
  • dreadful fatigue, yawning
  • perspiration and profuse sweating, hot flashes, flushing  and then chills or cold flashes.  There can also be  goose bumps (again from which we get the expression "going cold turkey")
  • excessive uncontrollable crying and runny nose
  • dilated pupils (midriasis), floaters, difficulty seeing
  • appetite loss with considerable subsequent weight loss, after some time there can be  problems with weight control in either direction
  • intestinal cramps; diarrhoea or loose stools, in extreme cases of too regular use you can get free and frequent liquid diarrhea
  • elevation of blood pressure, hypertension, tachycardia (elevated pulse).  In acute cases, both systolic and diastolic blood pressure increases, usually beyond the level it was before you took the drugs, and heart rate increases,which has the potential to cause a heart attack, blood clot, or stroke.
  • increase in the frequency of breathing and tidal volume
  •  insomnia
  • nausea and  vomiting
  • involuntary ejaculation, which is often painful
  • increased sensitivity to pain – this can be really dreadful, even the slightest wound can be agonisingly painful and anything more serious can be almost unbearable

In time the withdrawal symptoms may [may being the operative word] disappear, but the craving won’t. The craving never really goes.

There may be people reading this tut tutting about drug users and how they have only got themselves to blame, but we should never forget that within our system we have endorphins and endorphins are nature's own feel good drug – a drug which is released when we are in love and make love, or when we go on exciting fairground rides or – well - get excited about anything! 

People who have been really really in love and lost their partner for whatever reason can experience all the symptoms above  - for months and even years.

We can literally die of a broken heart.