Saturday 27 December 2008

Kealey on scientific motivations and incentives


Invisible colleges, private patronage and commercial profits versus public goods, government funding and ‘crowding-out’: Terence Kealey on the motivations and incentives driving science

Bruce G. Charlton

Medical Hypotheses. 2009; Volume 72, Pages 111-115



What kind of a thing is science and how does it work? [Kealey T. Sex, science and profits: In a recent book (Sex, science and profits: how people evolved to make money. London: William Heinemann; 2008) (p. 455)] Terence Kealey argues persuasively that the motivations driving science are widely misunderstood. Science is often assumed to be useful to the public but an economic loser for the scientist and his or her paymasters – in other words, science is supposed to be a ‘public good’. The public good argument is used to support large-scale government funding of science, on the basis that if government does not fund science it will not be funded adequately. But Kealey argues that most science is profitable to commercial organizations, and other types of worthwhile science will be supported by private patronage. Yet excessive government funding tends to ‘crowd-out’ potential private sources of funding – both by replacing and by deterring private investment. And scientists are not primarily motivated by money, but instead by striving for status within the ‘invisible college’ of active researchers in their field. Kealey’s take-home message is that overall and in the long-term, science neither requires nor benefits from government funding. Scientific research would be better-served by private funding from commercial organizations that are seeking profit, combined with patronage from charities and foundations that regard science as intrinsically valuable.


What kind of a thing is science and how does it work? In a recent book [1] – tightly packed with insights, evidence and jokes – Terence Kealey argues persuasively that the motivations driving science are widely misunderstood. Kealey suggests that the major motivation for scientists is to attain status within the ‘invisible college’ of active researchers in their field. So powerful is this motivation that scientists routinely subsidise their work from their own pockets.

Science is often assumed to be useful to the public but an economic loser for the scientist and his or her paymasters – in other words, science is supposed to be a ‘public good’. The public good argument is used to support large-scale government funding of science, on the basis that if government does not fund science it will not be funded adequately. But Kealey argues that most science is profitable to commercial organizations, and other worthwhile types of science will be supported by private patronage.

Yet excessive government funding tends to ‘crowd-out’ potential private sources of funding – both by replacing and by deterring private investment. Kealey’s take-home message is that science neither requires, nor benefits from, government funding; but that over the long-term science would be better-served by private funding by commercial organizations that are seeking profit combined with patronage by charities and foundations that regard science as intrinsically valuable.
Status motivates scientists

Although, like almost everyone else, scientists need income (and would prefer to have more of it), scientists are not ‘in it for the money’. Instead, scientists are ‘in it for the status’ – specifically the esteem of the peer group of scientists actively working in the same field.

The ‘sex’ element in the book’s title explains this, since it refers to sexual selection [2] and [3]. Sexual selection provides the ultimate evolutionary explanation as to the human motivation to seek status, because status is attractive – especially male status is attractive to females [4]. Science can be seen as one of many competitive social systems which harnesses and puts-to-good-use the human craving for prestige within a social group.

If scientists are primarily motivated by the desire for status rather than money, then this predicts that they will risk or sacrifice money to achieve scientific status. And this can often be observed – much scientific activity (e.g. computer, book and stationary purchases; journal subscriptions; conference attendance; media appearances; advice and consultancy; even postgraduate training) is funded to some extent from scientists’ own pockets or done in their private time.

In one of numerous witty and telling asides, Kealey comments that in economic terms virtually all science publishing is a type of ‘vanity publishing’ (a term usually reserved for the self-publication of slim volumes of verse) – since scientific papers are published at best with no monetary reward, and more often at significant monetary loss. Authors are prepared to pay when this helps to disseminate their research and scholarship: examples of ‘pay-to-publish’ journals are legion and include Proceedings of the National Academy of Sciences (PNAS), PLoS Medicine, and indeed Medical Hypotheses.

Tacit knowledge and the invisible college

The group within which a scientist seeks status is termed an ‘invisible college’ [5] Wikipedia. Invisible College. (accessed 12.09.08).[5] – ‘invisible’ in the sense that it is characterized by the exchange of information among dispersed peers rather than by co-residence in a specific physical building, and a ‘college’ in the sense that it is exclusive. Nowadays an invisible college is often international and may be sustained by electronic communications rather than face-to-face interactions. Nonetheless, Kealey emphasizes that personal relationships remains very important in science, as in many other areas of modern life, as evidenced by the phenomenon of ‘clustering’, in which rival niche businesses tend to locate near to each other. Clustering facilitates mutual evaluation of personal qualities and the build-up of networks of trust that allow information exchange. Conferences perform a similar function in science.

But the invisible college is not about giving-away information to all-and-sundry; the invisible college is specifically about trading information for mutual benefit. And the trading of knowledge is a matter of enlightened self-interest – in the long-term a group who share knowledge will out-perform those who do not share. However, the fact that an invisible college is based on trade means that participants must have something to trade which is valued by the other members of the college. Those with no useful knowledge to trade are excluded from the college.

One of the types of information which is traded in science is ‘tacit knowledge’ (the term comes from the philosopher and scientist Michael Polanyi [6]). In science tacit knowledge includes a great deal of unpublished, and probably un-publishable, knowledge about the skills and minutiae of doing science – the kind of thing that can only be learnt from direct personal apprenticeship – for example during a Ph.D. It is tacit knowledge which is learned by personal conversation, or lab visits, and by working alongside experts – for example in discovering and dealing-with raw data.

So, there is a substantial cost attached to membership of an invisible college. The cost involves attaining sufficient expertise to participate in college communications; and on top of that there is the effort required to generate new knowledge or skills which can be traded: i.e. the possession of knowledge or skills for which other scientists are willing to trade their own tacit knowledge.

The trading of knowledge depends on trust – the greater the level of trust the more extended and complex can be the networks of mutually-beneficial information exchange. But if trust is betrayed so that valid and useful information flows only one way, then the benefits of trade become merely one-sided and ultimately trade breaks-down [7]. And trust must be earned, which is another reason for the exclusivity of invisible colleges. Those who have not yet proved themselves trustworthy, or who have behaved in an untrustworthy manner, will not get access to tacit knowledge.

To what extent is copying a problem?

It is easy enough to acknowledge the workings of invisible colleges in non-commercial research, but Kealey emphasizes how exactly the same mechanisms support scientific research in the commercial, profit-seeking, sector. He argues that, far from being secretive, competitors in the private sector share their scientific knowledge – for the same self-interested reasons as in the non-profit sector: that those who share knowledge out-perform those who do not. However, private firms are selective concerning whom their knowledge is shared-with, and there must be trust in reciprocity. And most relevant and useful knowledge is either highly technical or tacit, and therefore, either incomprehensible or inaccessible to those outside the invisible college.

It is generally assumed that the major problem for commercial science is the danger of copying, whereby a commercial rival takes the benefits of innovation without paying the cost of development. Of course, in one sense, copying is the basis of human progress, the mechanism by which improvements spread from their originator. Unless there was copying there would be no general benefit. So, the real problem is attaining a balance between the public benefits of copying and the need for the originator to have an incentive to innovate. Copying is good, but there should also be the probability of a sufficient reward for the originator.

The question is what form this reward should take. Since scientists are primarily seeking status within the invisible college, they often welcome copying – so long as the innovator gets personal credit for having the original idea. In other words, since scientists are primarily motivated by status rather than money, it is logical that their rewards should primarily be in the currency of prestige rather than cash. From this ‘pure’ science perspective, plagiarism – i.e. copying without giving credit to the source – is a problem; but copying with credit is actually in itself a reward because it confers status.

But Kealey emphasizes that even in commercial business situations copying is not such a big problem as is sometimes imagined. The reason is that copying is usually costly: very costly. Copying takes both time and considerable money. Furthermore copying involves other scarce and valuable resources too, because a firm which is set-up to copy its rivals must support a high level of scientific expertise in order that they can detect and understand potentially-useful innovations as well as doing the actual copying and production.

In other words, although apparently ‘free’ and seldom kept secret, scientific knowledge is in fact comprehensible and usable by only a small and highly-trained elite group. Relevant tacit knowledge (without which explicit knowledge can seldom be exploited) is a kind of ‘secret ingredient’ that is extremely costly to acquire because it is usually only traded for equally valuable tacit knowledge – and this keeps it within the exclusive confines of the trust-based invisible college.

Kealey suggests that it is the intrinsic difficulty of copying, rather than ‘intellectual property rights’ such as patents, which are the significant factors in protecting the monopoly of innovators, allowing them to profit from their innovations and thereby providing the motivation for innovation.

If so, then the major commercial advantage of innovation is to gain the ‘first mover advantage’ in monopolizing a market niche: the temporary monopoly situation that exists before rivals are able to mobilize production, distribution and marketing of their copies. As a consequence Kealey suggests that patents are usually a bad thing all-round, both for the public and the patenter.

(There are exceptions in rare and specific circumstances where there is a long and expensive investment to generate a product which is relatively quick and cheap to copy – such as the pharmaceutical industry.)

An example of patents harming the public is James Watt’s steam engine patent, which held-back progress in the field for several decades. Furthermore patents can also distract innovators from the primary requirement rapidly to exploit their first mover advantage, and to continue seeking further innovations. An example of patents harming the patenter is the Wright brothers Wilbur and Orville, who invented the first functional aeroplane; but squandered prodigious time, energy and money in trying (and usually failing) to defend their patents.

If this is correct, and the argument seems plausible, then there needs to be a radical reappraisal of the current trend progressively to extend the scope and duration of intellectual property rights – especially copyright. If the aim is to benefit the public, probably we ought to be experimenting with narrowing the scope of patenting, and progressive shortening of the allowed duration of copyright and patents in most intellectual fields.

Government funding and ‘crowding-out’

By describing a range of powerful economic and personal motivations to do science, Kealey is arguing the falsity of the common conceptualization of science as a public good requiring government funding. His idea is that ‘self-interest’ of various types (individual and institutional) would ensure that enough science of the right kind was funded without need for government intervention.

Furthermore Kealey suggests that increasing government funding of science may not lead to greater funding overall, because state support ‘crowds out’ and deters private funding, leading to excess dependence on government funding and the damaging politicization of science.

It is extremely important to be aware of, and to recognize, the possibility of crowding-out of private by state investment in science. Because those of us who live in the developed world are used to prodigious and rising levels of government funding for science – doubling in real terms about every 15 years for science overall [1] and with even more rapid growth (doubling about every decade) for medical science [7]. Kealey provides evidence that such expansion of government funding crowds out private funding in science. Crowding-out means that in practice (although not necessarily by intention) private funding usually declines as government funding increases until science becomes de facto almost a public monopoly.

Of course, most people assume that government funding will cause crowding-in to science – in other words they hope that the more money which government spends, the more private money will be attracted to the field. Kealey’s example of crowding-in occurs in road transportation when the government builts a new road with free usage, and private individuals then buy more cars to use the improved facility.

But the evidence suggests that increasing government funding of science usually crowds out private funding, leading – for instance – to reduced corporate investment in research and development (and Kealey emphasizes that R&D really is an investment, making a significant contribution to organizational profitability). The more that government funding increases, the more that private funding declines. Possible reasons for crowding-out the private sector include state money being used to substitute for private research funding, and the general reduction in competition between rival firms which is often explicitly encouraged by government policy.

Another factor in the phenomenon of government funding crowding-out private funding is, I suspect, probably related to science being a status-oriented activity. Where government provides the lion’s share of funding then government will take the lion’s share of status. Because status is a zero-sum game, if one party gets a larger share of prestige then this leaves less prestige for everyone else. There is little incentive for private patrons to engage in funding science if government then claims most of the credit for the achievements of science – so discriminating patrons will look elsewhere to gain prestige for allocating their support.

Creative destruction

Governments often believe that competition is harmful, in science as elsewhere, and they instead try to encourage cooperation. But Kealey agrees with Joseph Schumpeter’s general economic schema of capitalism as powered-by ‘creative destruction’ – an interpretation which emphasizes the value of competition in driving innovation, and innovation in promoting economic growth [8].

According to Schumpeter, the main driving force of capitalism is that companies compete to gain then retain monopoly. Entrepreneurs continuously pursue innovation and where this is successful the price of failure paid by commercial rivals may be extinction (i.e. destruction). Failure is intrinsic to the dynamic of success [9]. Incumbent monopolists are forced to seek innovation by the credible threat of rival entrepreneurs ‘snapping at their heels’ by generating innovations intended to take away their markets.

This destruction of commercial firms is termed ‘creative’ because in the long-term it allows better allocation of resources – innovation can only thrive at the expense of discarding the obsolete. A few hundred years ago some 90% of the UK population were engaged in growing food, now the proportion working in agriculture is less than 1%, and the other 89% of the ex-farm-labouring population have (forcibly) liberated to perform a multitude of other economic activities.

The destruction of agriculture as the dominant mode of employment was therefore, creative in the sense that it enabled a massive reallocation of manpower with an increase in productivity (economic output per person), and therefore, creative destruction of agriculture promoted economic growth. Failure in one area was necessary to success in another. Specific short-term suffering (e.g. reduced income among newly unemployed farm labourers) was intrinsic to the general long-term benefits (e.g. increased income spread among everyone, including the grandchildren of the unemployed farm labourers).

Creative destruction is, of course, also a feature of science: new theories displace the old and the destruction of old ideas is necessary in order to liberate resources to invest in new science. Karl Popper’s philosophy of science could, indeed, be regarded as an equivalent process to Schumpeter’s creative destruction in the economy [10]. Example are legion: the decline of astrology entailed by the creation of astronomy, the extinction of alchemy and the reallocation of effort into chemistry, the replacement of classical physics by relativity and quantum theory [11].

The progress of science generally and in the long-term is attainable only at the cost of specific and short-term destruction – e.g. of the reputations and livelihoods of scientists working in fields which have been superseded.

Political corruption of science by excessive government influence

Because expanding government support of science usually results in crowding-out of private support, the state tends to become a monopoly supplier of science. Government funding agencies then shape the direction of scientific research, and government thereby gains an unhealthy degree of control. Essentially, the systems of government and science fuse to form a single hybrid system of politicized science – i.e. science that promotes government interests.

At the end-point of decades of crowding-out, all kinds of pathologies of science have now emerged, although they are often taken for granted and hardly noticed. For example, in the UK, government-funded science is often regarded (especially by other government agencies) as having intrinsically higher prestige than privately-funded science. This principle has been formalized in some UK state-administered university research evaluation mechanisms (RAE – [12]) where extra credit was given to funding from government agencies (in my opinion credit should only have been given for scientific output, and not for input measures such as funding [13]).

Another almost inevitable effect of government funding is inefficiency [7]. As science becomes more like a monopolistic ‘nationalized industry’ there are the usual problems of excessive yet still-growing bureaucracy. Many economists recognize as a general principle that government provision is only about half as efficient (in terms of outputs per input, and controlling for quality) as the private sector [14].

Science funding may be used to pursue political, not scientific, goals. For example government may shift funding towards what are perceived as vote-winning causes that are likely to attract votes such as the ‘war on’ cancer, or special attention on AIDS, breast cancer or other diseases. The special government attention may or may not be scientifically or medically justifiable – but the reason for extra funding is primarily political. Or political parties may deploy large-scale research facilities to specific geographic regions as a reward for political support. Or parties may ‘buy’ the support of scientists by (in effect) bribing them with extra grants and salaries, or blackmailing scientists with the (credible) threat of bribe-withdrawal if the opposition party gets power.

And having crowded-out significant private funding from science, government may then shape the emphasis of science strategy so that they build-up science and scientific perspectives which bolster their political views while simultaneously starving-out science that is hostile to the governing ethos. The most notorious example of this was Stalin’s support of ‘Lysenkoism’ in the mid-twentieth century USSR and the persecution of biologists who adhered to Darwin’s theory of natural selection [15]. A similar phenomenon (usually minus the violence) can be seen in the way that IQ research has been marginalized by government policy in the US and UK [16].

Large-scale and long-term government funding of science creates economic and psychological dependence on the state. It is this pervasive dependency culture which makes Kealey’s message so alarming and unacceptable to most scientists.

A vision of diverse private science funding

Kealey’s ideal is a world in which government funding of science has dwindled to insignificant levels, and science is mainly funded by a mixture of private commerce and private patronage.

Commercial organizations would be motivated to do science by the bottom-line of profit; because pursuing continued innovation and supporting science is the only way they can have access to the invisible college of information (including tacit knowledge) upon which their continued competitiveness depends.

In the absence of crowding-out by government funding, substantial further science patronage would come from private research foundations and charities of many types, who would fund diverse branches of science simply because they value that science and like to support it – just as foundations and charities support the arts, sports, religions and numerous other good causes. This altruistic motivation is helped by the fact that supporting science is, in general, a prestigious thing to do.

Scientists are motivated to work mainly by the desire for enhanced status within their invisible college – which ensures competition; they are also motivated to trade their knowledge (i.e. cooperate) by the advantages this brings to their competitive pursuit of scientific knowledge. For these reasons scientists will spontaneously self-organize into exclusive and elite invisible colleges or communities of reciprocal trust for mutual benefit.

So, in a world of negligible state funding of science; competition and cooperation would work together at both individual and organizational levels to create a dynamic and self-regulating system orientated towards increased efficiency and growth of knowledge by means of creative destruction.

Modern science may be over-funded overall, and the pattern of funding sub-optimal

Kealey’s book provokes me to further speculation.

In Kealy’s world of mostly-private funding of science it seems possible, or likely, that the total quantity of private funding for science would differ significantly from the current level of state funding.

In other words, government might – according to circumstances – either be over-funding or under-funding science overall. Furthermore, it is likely that the pattern of state funding of science (i.e. the distribution of funding between specialties) would be different from the spontaneous outcome of a private system of funding.

Indeed, lacking a market, hence lacking ‘price’ signals, it may not be possible to know – even in principle – whether a system such as science was optimally-funded [17] and [18]. From a ‘systems theory’ perspective, it could be argued that a private (‘market’) system of funding would be able to reach a more efficient volume and distribution of funding for science than could centralized decision-making [19].

If science was under-funded by government, the spontaneous tendency would be for private funding to move-in to fill the gaps where needed. But science could be chronically under-funded if private companies and patrons were legislatively-prevented or financially-deterred from spending money on science. Or science may be blocked by political, religious or ethical considerations – especially in totalitarian societies. And even in liberal democracies, scientific research may become so hemmed-around with regulations, restrictions or potential legal pitfalls as to prevent, or at least deter, private spending.

Alternatively, or at the same time as there is chronic under-funding in some areas, other areas of science could be chronically over-funded by the government, especially if government spending was driven by political rather than scientific objectives, as described above. Indeed, my guess is that medical science is currently over-funded in the US, UK and Western Europe [7], because medical research is used as a way of government gathering voter support by spending public money to show that it ‘cares’.

And overall over-funding of scientific research may tend to be self-sustaining if it creates a bigger and more powerful interest group to lobby in favour of continued over-funding. This interest group would extend beyond scientific researchers to embrace universities and the science communications media.

If science was indeed over-funded by government, then there would be a decline in funding under private provision. Add to this the inevitable reallocation of funding between different branches of science which would result for any change in the funding mechanism, and these threats will mobilize interest groups to resist change – even when such change would be beneficial overall and in the long-term.

Of course, it is very likely that a private funding system would open-up many new areas of science that are currently starved of support; however, these areas of science (precisely because they have been starved!) currently lack any incumbents who might lobby for such policy changes.

So normal ‘interest politics’, politics as usual, will usually tend to prevent radical change to the scientific research funding allocation procedures – except when change benefits the most powerful incumbents.
Five (bad) reasons why Kealey’s analysis will be ignored (especially if correct)

I believe that Terence Kealey is generally correct in his analysis and arguments. However, I am pessimistic about the prospects for these ideas getting serious consideration.

There are at least five powerful aspects of mainstream scientific thinking which make it probable that the arguments will be ignored:

1. There is now a long-established dependency culture of science. Scientists find it hard even to imagine a world without quasi-monopolistic government funding of science.

2. This dependency culture of science has for decades been attracting into the profession a risk-averse and uncompetitive type of scientist who prefers the mediocre conditions and job-security of working under bureaucratic supervision to the freer and more meritocratic – but harsher and less predictable – world of ‘creative destruction’ associated with markets and private funding.

3. There is, I believe a covert suspicion among many scientists that science in the US, UK and Western Europe may be over-funded, and therefore, that any shift to a more efficient and effective mode of supporting science privately would lead (overall) to a significant cull of scientists and ‘down-sizing’ of scientific research organizations.

4. The current scientific leadership has evolved a cozy, collusive and mutually-beneficial relationship with government; and this would be threatened if there was a significant diminution of state support for science. For instance, in the UK the Royal Society gets more than two thirds of its income direct from the UK government. Senior personnel migrate back and forth between science and the civil service. A major change towards private funding would bring the potential for a major loss of power and prestige for many powerful figures in science administration.

5. Combining all the above points – if science funding was reformed, things would get worse before they got better. Creative destruction may be the way that the world improves; but, since destruction comes before creation, blame for early damage is almost inevitably allocated with greater surety than credit for later benefits. Those responsible for policies that trigger short-term harm to science and scientists will therefore, be subject to the certainty of immediate vilification and the possibility of an enduring negative reputation. These are major reasons for bad government everywhere and at all times.

In sum, sensible reform of science funding away from quasi-monopolistic government support and towards a multitude of private sources will probably have to wait until, eventually, some desperate crisis will force the appropriate action.


[1] T. Kealey, Sex, science and profits: how people evolved to make money, William Heinemann, London (2008) p. 455.

[2] H. Cronin, The ant and the peacock: altruism and sexual selection from Darwin to today, Cambridge University Press, New York, UK (1993).

[3] G. Miller, The mating mind: how sexual choice shaped the evolution of human nature, Heinemann, Oxford, UK (2000).

[4] D.M. Buss, The evolution of desire: strategies of human mating, Basic Books, New York (1994).

[5] Wikipedia. Invisible College. (accessed 12.09.08).

[6] R. Allen, Polanyi, Claridge Press, London (1990).

[7] B.G. Charlton, Boom or bubble? Is medical research thriving or about to crash?, Med Hypotheses 66 (2006), pp. 1–2.

[8] J.A. Schumpeter, Capitalism, socialism and democracy, Allen and Unwin, London (1954).

[9] P. Ormerod, Why most things fail: evolution, extinction and economics, Wiley, Hoboken, NJ, USA (2007).

[10] B. Magee, Popper, Collins, London (1973).

[11] J. Bronowski, The ascent of man, BBC, London (1983).

[12] Wikipedia. Research Assessment Exercise. (accessed 12.09.08).

[13] B.G. Charlton and P. Andras, Evaluating universities using simple scientometric research-output metrics: total citation counts per university for a retrospective seven-year rolling sample, Science and Public Policy 34 (2007), pp. 555–563.

[14] M. Friedman, Capitalism and freedom, University of Chicago Press, Chicago (1963).

[15] D. Joravsky, The Lysenko affair, Harvard University Press, Cambridge, MA, USA (1970).

[16] Charlton BG. Pioneering studies of IQ by G.H. Thomson and J.F. Duff – an example of established knowledge subsequently ‘hidden in plain sight’. Medical Hypotheses 2008;71:625-8.

[17] T. Sowell, Knowledge and decisions, Basic Books, New York (1980).

[18] F.A. von Hayek, The fatal conceit, Routledge, London (1988).

[19] B. Charlton and P. Andras, The modernization imperative, Imprint Academic, Exeter, UK (2003).

Sunday 30 November 2008

Sub-types of depression and self-treatment

A model for self-treatment of four sub-types of symptomatic ‘depression’ using non-prescription agents: Neuroticism (anxiety and emotional instability); malaise (fatigue and painful symptoms); demotivation (anhedonia) and seasonal affective disorder ‘SAD’

Bruce G. Charlton

Medical Hypotheses. 2009; 72: 1-7


This article will present a model for how ‘depression’ (i.e. depressive symptoms) can be divided into four self-diagnosed sub-types or causes which might then be self-treated using agents available without prescription. (Another, much rarer, cause of depressed symptoms is the classical illness of ‘melancholia’, which when severe cannot be self-treated and typically requires hospitalization.) A self-management option and alternative is now needed due to the an inappropriate emphasis of modern psychiatry on treatment of imprecise syndromal ‘disorders’ which may entail treating ‘depression’ at the cost of making the patient feel and function worse. By contrast, the basic theoretical stance of self-management is that depressed mood should be seen as a result of unpleasant symptoms – and it is the symptoms that require treatment, not the mood itself. Furthermore, drugs (or other interventions) need to be classified in terms of their potential therapeutic effects on these symptoms that may cause depressed mood. The four common causes of depressed mood considered here are the personality trait of Neuroticism; the state of malaise (fatigue, aching etc) which accompanies an illness with an activated immune system; demotivation due to lack of positive emotions (anhedonia); and the syndrome of seasonal affective disorder (SAD). Each of the four sub-types is then ‘matched’ with a first–line non-prescription agent. The ‘stabilizing’ agents such as St John’s Wort and the antihistamines chlorpheniramine and diphenhydramine are used for treatment of Neuroticism; analgesics/pain killers such as aspirin, ibuprofen, paracetamol/acetaminophen and the opiates are used to treat malaise; energizing agents such as caffeine and nicotine are used for the treatment of demotivation; and bright light used in the early morning to treat SAD. Self-treatments are intended to be used after research and experimentally, on a trial-and-error basis; with self-monitoring of beneficial and harmful effects, and a willingness to stop and switch treatments. The model of S-DTM (self-diagnosis, self-treatment and self–monitoring) is suggested as potentially applicable more widely within psychiatry and medicine.



‘Depressive disorder’ and ‘anti-depressant’ are categories that should be discarded
Imprecise diagnosis and treatment of depression
Self-diagnosis by introspection – the ‘phenomenological’ approach

The self-diagnosis, -treatment and- monitoring (S-DTM) model [4] treating depressed mood pharmacologically


‘Depressive disorder’ and ‘anti-depressant’ are categories that should be discarded
The gross imprecision of the diagnosis of ‘depression’ has become farcical in recent decades, when the supposed prevalence of ‘depression’ has risen from a fraction of a percent by about a hundred-fold to anything from ten to twenty-five percent [1] and [2]. Nowadays, any person suffering a persistent unpleasant emotional state may be officially diagnosable as depressed, and treated with drugs termed ‘anti-depressants’.

I have previously argued that the disease category of mood (affective) disorder called depression is neither coherent nor useful; and instead it would be preferable to regard ‘depressed mood’ as secondary to a variety of unpleasant emotional states [3]. In other words, depressed mood should be seen as caused by symptoms and emotions – for example anxiety, fatigue or lack of positive emotions (anhedonia) can all lead to depressed mood. Diagnosis and treatment of ‘depression’ should therefore be focused on the emotional states which cause depressed mood, and not upon treating a vaguely-defined – hence over-inclusive – syndrome termed ‘depressive disorder’. In principle there might be an unbounded number of causes of negative, depressed states of unhappiness – in practice, I will focus upon four which are apparently amenable to improvement by therapeutic intervention.

I have also argued that the term ‘anti-depressant’ should not be used, since there are no drugs which have a general action to alleviate depressed mood: what the effective drugs are really doing is to alleviate the causes of depressed mood [3]. There are a variety of different drugs types which can alleviate some symptoms that may lead to depressive symptoms in some people. For example, when anxiety is causing depressed mood then any drug which reduces anxiety (including alcohol, neuroleptics/antipsychotics, benzodiazepines or selective serotonin-reuptake inhibitors – SSRIs) may all (for a while) alleviate ’depression’. But when a person’s depressed mood is not caused by anxiety then these same drugs could be ineffective or may actually worsen the depressed mood.

I believe that a self-management option and alternative [4] is now urgently needed (at least in the UK and USA) due to the incorrect and counter-productive theoretical stance of modern psychiatry [3], the corruption of modern psychiatry by industrial and political influences [2], and the inappropriate emphasis of modern psychiatry on treatment of syndromal ‘disorders’ [3] and [4]. This focus on syndromes may lead modern psychiatrists to treat ‘depression’ at the cost of making the patient feel and function worse [5]

This is the rationale and justification for the following article, which represents a personal view – speculative and tentative – of a possible future for psychopharmacology in psychiatry, specifically in relation to negative symptoms of ‘depression’ such as sadness unhappiness, lack of motivation, long-term miserable anxiety, unpleasant mood swings and the inability to feel happiness. My hope is that these ideas are sufficiently accurate and valid to be useful and applicable – but also that they will stimulate discussion and serve as a basis for a process of evolution and improvement.

By extension, this general model of self-diagnosis, self-treatment and self-monitoring (S-DTM) could potentially be extended to other areas of psychiatry and medicine in which symptoms are the focus and where effective treatments are available without prescription. Indeed, as well as being used to alleviate negative states, the model is also applicable to lifestyle/quality of life enhancement [3] and [5].

Imprecise diagnosis and treatment of depression

I believe that, one the one hand, the treatment of depression can be more specific and effective than at present; but on the other hand it is also correct that the psychoactive drugs are all imprecise in their effects, and in particular tend to affect different people differently. This means that psychiatric treatment (whether self-treatment or treatment by professionals) is almost inevitably a trial-and-error matter, and should be embarked-upon in an experimental spirit.

Psychiatric drugs (and also some other psychiatric interventions such as electroconvulsive therapy and perhaps bright light) tend to be non-specific in relation to traditional diagnostic syndromes [3]. Different categories of drugs such as ‘antidepressants’ and the neuroleptics/antipsychotics often have over-lapping therapeutic effects, side effects and indications – mainly because many of the most-used drugs were chemically-developed from a relatively small number of coloured dyes which were initially made into antihistamines during the 1940s then further modified over the following decades to make the neuroleptic/antipsychotics, tricyclic and SSRI antidepressants [1], [6] and [7].

So, drug recommendations for symptomatic treatment in psychiatry are mainly about suggesting which drug to try first. There needs to be an attitude of trial-and-error; with self-monitoring of the effects of treatment, willingness to change to stop treatment or change to another treatment if the first choice has undesirable side effects or is apparently ineffective.

With these cautions in place, I see no compelling reason why people should not self-treat for psychiatric symptoms using drugs which are available ‘over the counter’ and without prescription. After all, in a country such as the UK or the USA people in their tens of millions already self-treat for headaches and back pains, constipation and diarrhoea, runny noses and blocked noses, hay fever and eczema, high cholesterol, skin infections and duodenal ulcers. And in a world where it is common to assert that anything up to half the population have significant psychiatric symptoms of some sort (e.g. depression, anxiety states, various phobias and compulsions, insomnia) then self-treatment become a practical necessity.

Furthermore, I suggest that symptomatic self-treatment for ‘depression’, when done by careful and informed people, might well be superior to the average treatment on offer from psychiatric professionals. The main constraint is the limited range of drugs available without prescription (especially, see below, in the case of demotivated depression); but this restrictive public policy may change over time or be circumvented by the increased ease of purchasing pharmacological agents without prescription.

Self-diagnosis by introspection – the ‘phenomenological’ approach

The process by which self-diagnosis may be accomplished requires some elucidation. I have previously termed the sequence S-DTM – meaning Self-Diagnosis, self-Treatment and self–Monitoring. The aim is to introduce to self-management a helpful degree of thoroughness and formalization to make the process both safer and more effective than unstructured self-management.

The first step involves developing self-awareness of symptoms. The word ‘phenomenology’ refers to the process of introspection or inward-looking by which a person can become aware of their inner, subjective states – psychiatric symptoms are one of the body states which may be accessible to such introspection [3], [8] and [9]. To self-diagnose by introspection requires a skill which may be unfamiliar. For example, it is possible to be anxious but unaware of the anxiety [10] and [11]. To become aware of anxiety as a feeling, a person needs to be able to identify their own state of mental angst, muscular tension, rapidly beating heart, sweatiness, ‘butterflies in the stomach’ and so on.

Furthermore, inner states must be identified in terms of a system of classification – because body sensations tend to be experienced as formless and undividedly ’holistic’ unless there is a systematic classification which can describe them. Without some such analytic scheme, it may not be possible for someone to be aware of, and to express even to themselves, much more than a simple dichotomy of feeling either ‘good’ or ‘bad’. Self-treatment, however, requires that different types of ‘feeling bad’ can be distinguished and identified.

In terms of ‘depression’ – the process begins with recognition of a depressed mood, in other words a negative or unpleasant mood state which could be characterized by some kind of unhappiness. Then there is a further introspective process by which the sufferer tries to identify some inner physical, bodily state which may be the main cause of this unhappiness. The assumption is that if this causal symptom can be alleviated or eliminated then the person may become happier.

Happiness is not necessarily entailed by removing the cause of unhappiness, but it is easier and more probable that a currently-unhappy person will become happy if they are relieved of unpleasant symptoms. For example, it is hard to be happy when suffering a headache and relief of the headache may therefore cause a person to become happy who would otherwise have remained miserable.

More exactly, there is an attempt to match-up inner states against a pre-determined classification. Four body states which may cause unhappiness include emotional instability with anxiety (Neuroticism); fatigue and bodily aches and pains (malaise); lack of emotion – especially loss of the ability to anticipate future pleasures (demotivated depression); and sleepy, hungry, irritable mood specifically during the winter season (SAD).

Having identified a particular aversive body state as a probable cause of depressed mood, this symptom is then made the focus for self-treatment; and the symptom is monitored for its response to treatment. A treatment agent or mode is selected as being both safe and potentially able to alleviate the specific symptom, and a trial of this treatment is made. So, if the symptom underlying depressed mood is identified as anxiety and unstable emotions then stabilizing drug is chosen (such as St John’s Wort or chlorpheniramine – see below); and the symptom is monitored to see whether it responds to this treatment.
The self-diagnosis, -treatment and- monitoring (S-DTM) model [4] treating depressed mood pharmacologically

1. Recognition of a depressed, unhappy, low mood.

2. Introspective self–diagnosis of the sub-type of symptomatic and emotional cause of depressed mood.

3. Matching the symptoms and emotions to one of the four sub-types of ‘depression’.

4. Matching the sub-type of depression to the drug class which is most likely to alleviate those symptoms and emotions.

5. Researching the scientific literature on the effects, side effects and possible interactions of the drug class – and choose a (probably) safe first-line agent.


6. Begin trial of treatment.


7. Very careful monitoring for effects and side effects for the first 4 hours after taking the agent, and continued vigilance for several days. Keep a record. (e.g. Consider self-monitoring blood pressure when using psychostimulant type drugs.)

8. If immediate problems of side effects or feeling worse after taking a drug, consider stopping immediately – or continue with vigilant self-monitoring.

9. If no benefit at all after a few days consider increasing dose or stopping and trying another agent.

10. If side effects are bad, or there is concern over dependence, or if unsure about whether or not the drug is having benefit, or if wanting to stop taking the drug; consider stopping the drug and self-monitoring the result of stopping – then consider restarting and monitor the results of restarting.

11. Go through the process for each new drug tried. Avoid interactions between the drug stopped and a new one started, and between multiple agents.

Four sub-types of self-treatable depression

I will consider four sub-type causes of depressed mood (’depressive disorder’) which may be suitable for self-treatment: these are Neuroticism, Malaise, Demotivation and Seasonal Affective Disorder-SAD. I will also refer to a fifth type of depressive disorder - Melancholia - which was the original type of depression recognized for centuries, and is often too severe and debilitating to be self-treated and for which the best treatment (electroconvulsive therapy) cannot be self-administered.

This list of five sub-types is not exhaustive, and there almost certainly are other well-defined syndromes that are causes of depressed mood (or these four sub-types may fruitfully further be subdivided), and these might require different treatment, or treatments that are not available without prescription, but probably those sub-types described here are the commonest.

So, my suggestion is that sustained depressed mood (i.e. so – called depressive disorder) is ‘caused’ by least five more – specific sub-types. Naturally, each of these sub-types must have its own cause. Typically this cause is unknown or uncertain – and I will not consider the matter further here; because - whatever their cause may be – each sub-type has somewhat different symptoms and there are relatively specific treatments which have the potential to alleviate these symptoms.

I further suggest that there is no general purpose ’antidepressant’ action of a drug. Instead of there being ‘anti-depressants’, in actuality there are several types of intervention which alleviate different unpleasant symptoms and emotions, and which may as a result make people feel less depressed. A drug which alleviates depression in one person may actually cause depression in another person because the effect on depression is secondary to the effect on the symptoms or emotions. In what follows, drugs are classified according to their effect on symptoms; drug types considered here include stabilizing drugs; analgesics/pain killers and energizing drugs.

Melancholia – not self-treatable

Probably it is best to note and set-aside the ‘melancholia’ type of depression at this point. Melancholia is probably best described in textbooks from at least thirty years ago, before the diagnosis of depression became over-inclusive [12]. This is the classic, severe, debilitating form of ‘endogenous’ depression which may have psychotic features such as hallucinations, delusions, thought disorder, catatonia and psychomotor retardation.

Melancholia typically renders the sufferer incapable of work with severely-diminished or absent self-care and often suicidal tendencies. Subjectively, the mood state may be one of profound sadness, despair, emptiness, guilt, nothingness – speech and movement are slowed to near inertia, appetite may be absent, and death by starvation is a possibility.

Patients usually require admission to a hospital or similar institution for the treatment of melancholia – and they may require close supervision to prevent suicide. The episode of illness usually lasts for several months and the most effective treatment to improve symptoms is electroconvulsive therapy/electroshock therapy (ECT/ECS) [13] and [14].


Anxiety is a normal, evolved human emotion which functions to increase alertness and avoid harm. However, anxiety is almost certainly the most frequently-experienced psychiatric symptom, and anxiety and depression are major feature of the ‘neurotic’ personality type characterized by emotional instability.

Neuroticism is one of the ‘Big 5’ personality traits, and was derived from the work of Hans Eysenck [15] and [16]. Neuroticism is an underlying disposition which is substantially hereditary and tends to endure throughout life. The personality type extends from high Neuroticism with extreme unpleasant mood swings at one extreme, to emotional stability at the opposite extreme. Other aspects of high Neuroticism include guilt feelings, low-self esteem, irrationality, shyness, moodiness and emotionality. Low Neuroticism personalities are described as emotionally stable, and display the opposite traits: calmness, cheerfulness, confidence.

I regard Neuroticism as more-or-less the same entity as Nutt’s category of ‘depression with anxiety’ [17]; very similar to Neurotic Depression on the Newcastle Diagnostic Scale [12] and essentially the same entity as DSM IV dysthymic disorder [18]. Watson calls it ‘negative emotionality’ – the tendency to experience strong negative emotions [19].

Neuroticism is a kind of hypersensitivity to the environment, akin to feeling the hyper-vigilant state of being alone in an unfamiliar and threatening environment. The average level of Neuroticism is higher in women, and high Neuroticism may be commoner in modern mass societies [3].

Since it is a type of personality and not a disease, Neuroticism probably cannot be ‘cured’. But severity of symptoms related to Neuroticism tend to wax and wane, probably in response to life stresses and also factors such as age, illness, drug usage etc. Given the ineffectiveness of psychotherapy and counseling, the psychiatric treatment of Neuroticism is essentially a matter of using drugs either to blunt exacerbations or else to promote long-term stabilization of emotions.

Because Neuroticism is a dispositional trait, emotion blunting drugs – when they work – are perceived to have caused a change in personality – and such change in personality may be perceived either positively or negatively [20] and [21].
Stabilizing drugs for Neuroticism

The anxiety component of a personality high in Neuroticism can be treated using a variety of anti-anxiety agents (e.g. neuroleptics/antipsychotics, benzodiazepines, propranolol – and people may self-medicate with alcohol) but since the core problem is emotional instability then the more relevant classes of drugs seem to be those that stabilize by buffering or blunting emotions. I shall term these the class of ‘stabilizing’ drugs.

The most powerful emotion stabilizing drugs are the neuroleptics/antipsychotics; but these tend to blunt emotions to the point of blank inertia [7]. Indeed, the neuroleptic core effect is to induce Parkinsonism as a method of non-sedating behavior control – as implied by the name which means ’nervous system-seizing’ (i.e. seizing and holding the nervous system, so it does not react) [22] and [23].

So assuming that people do not wish to suffer from self-inflicted Parkinson’s disease, neuroleptic/antipsychotics should be avoided and instead the most appropriate class of drugs for treating emotional instability are probably those which have serotonin-reuptake-inhibiting properties of which the class of selective serotonin-reuptake inhibitors (SSRIs) are the best-known and most widely-prescribed examples. These can buffer or blunt the strength of emotions [3] (Healy has termed them ‘serenic’ in their effect [2]) but without necessarily demotivating the individual. Indeed, the emotional stability induced by SSRIs might provide previously-Neurotic people with better focus and direction.

‘Over the counter’ versions of the SSRIs that are available without prescription include at least two of the drugs sold as ‘antihistamines’ [4]. These antihistamines were used as the basic molecules from which SSRIs drugs were manufactured [6], [7], [24], [25] and [26]. (They were also the base molecules for the tricyclic antidepressants such as imipramine, and the earliest neuroleptics/antipsychotics such as chlorpromazine – consequently there are overlapping therapeutic effects and side effects among these drug classes [7].)

Diphenhydramine was the base molecule for synthesizing fluoxetine (‘Prozac’) which was the first SSRI to reach market [6]. Diphenhydramine is marketed as a sedative cough suppressant; and is probably an SSRI in terms of blocking reuptake of serotonin more potently than noradrenaline [24] (this is the pharmacological definition of an SSRI).

Chlorpheniramine was the base molecule for the synthesis of zimelidine; which was the first SSRI to be made but which never reached market due to its side effects [25] and [26]. Chlorpheniramine is sold as an anti allergy/anti-hay fever medication and is regarded as very safe; even being used in pregnancy for the treatment of nausea [27]. Chlorpheniramine blocks the reuptake of serotonin and also of noradrenaline [24], so is probably best regarded as a Serotonin and Noradrenalin Re-uptake Inhibitor (SNRI) resembling venlafaxine [26].

To support the use of these antihistamines in treating depressive symptom exacerbations due to Neuroticism there is the above strong theoretical argument plus a small literature of the beneficial effects of chlorpheniramine as an anti-anxiety drug and probably stabilizing agent (e.g. [28], [29] and [30]) – evidence for the benefits of diphehydramine is at present more theoretical and anecdotal. However, with a self-treatment approach using safe and non-prescription drugs, the evidence of effectiveness comes from personal experience – it is relatively easy to discover whether the drug ‘works for you’ since typically the benefits (and side effects) on the core symptom of emotional instability can be felt (or not felt) as soon as the drug is absorbed – i.e. within an hour or two. However, drug effects on mood are much more indirect and more variable, and mood improvement may take days or weeks to emerge [3].

However, probably the best drug for producing emotional stabilization is the herb St John’s Wort/Hypericum. The evidence concerning the usage and value of this drug is conveniently gathered in an excellent Wikipedia survey [31]. According to the preponderance of randomized trials, St John’s Wort (SJW) seems to be the equal or superior of the SSRIs; in terms of equal or better therapeutic effectiveness, fewer unwanted side effects and greater drug safety. St John’s Wort has mainly been evaluated as an anxiolytic and/or ‘anti-depressant’; but my inference is that SJW is essentially an emotion stabilizing drug akin to SSRIs. SJW is available in measured doses without prescription from pharmacists and supermarkets, usually being sold as a food supplement alongside vitamins, minerals and other herbs.

In conclusion, an exacerbation of ‘depression’ due to Neuroticism may imply a first-line self-treatment with St John’s Wort, chlorpheniramine or diphenhydramine. Since Neuroticism is a personality trait, when stabilizing drugs are effective they produce a change in personality, and potentially may make the neurotic individual feel more positive than ever before – they may seem to themselves and others as if they are ‘better than well’ [20]. Alternatively, stabilizing drugs such as SSRIs in another individual, or too high a dose, might cause a ‘hardening’ of personality (making the person more indifferent to things which ought to be of concern) and this may cause a reduction in motivation and a reduced inability to enjoy life (anhedonia) [21].

Very rarely SSRIs (and other psychoactive drugs, such a neuroleptics) can provoke extreme unpleasant states of inner turmoil or suicidal feelings in predisposed individuals [2] – and this may be a feature of the chemical structure of stabilizing drugs [7].


Malaise is a term I suggested in 2000 for a sub-type of depression which is underpinned by that state of exhaustion which is familiar as the effect (and persisting after – effect) of infectious disorders such as influenza or glandular fever [3] and [32]. Since this description, some of the main features of the Malaise theory of depression have been confirmed by further studies (e.g. [33], [34], [35], [36], [37] and [38]).

The main symptoms of malaise are fatigue, feeling physically ‘TAT’ (tired all the time – and by ‘tired’ is meant physically-exhausted rather than sleepy), a washed-out or drained sensation in the body and limbs, heaviness in the head or limbs, aching, headaches and low-grade pain or tenderness in trunk and limbs. Malaise corresponds to Kurt Schneider’s ‘vital’ symptoms of depression, which he regarded as being of primary diagnostic significance [39].

Depressed mood is the response to this state of malaise, so that malaise depression is primarily a problem of the body, and not necessarily the brain. The idea of malaise comes from a general recognition of ‘sickness behavior’ as the general behavior which is characteristic of a sick mammal (summarized in [32]). Sickness behavior is regarded as an evolved adaptation to acute infectious disease – a behavioral state that is energy-conserving, risk-minimizing and immune-enhancing to allow an all-out (but temporary) attack on invading micro-organism.

So, malaise is caused by activation of the immune system, and is associated with increased blood levels of immune chemicals called cytokines – eg interferons, interleukins, Tumor Necrosis Factors (TNFs) and dozens more types. There is considerable evidence of raised levels of cytokines in depression (e.g. [32], [36] and [39]). But blood cytokines are typically also increased in autoimmune diseases (such as rheumatoid arthritis) and disseminated cancer – and these types of disease are also associated with ‘sickness behavior’ and malaise which can lead to depressed mood [3].

From anecdotal observation and general reading, I believe that sleep disruption is probably a common cause of malaise. Potentially there can be neurotransmitter and/or hormone changes triggered by sleep deprivation or sleep disruption. For example, malaise often follows sleepless nights, shift working or as an aspect of ’jet lag’ due to crossing several time zones; or post-operative states with catabolism triggered by tissue destruction and sleep disruption; or following childbirth (with a combination of major hormonal and phychological changes, tissue damage and sleep disruption).

Since malaise is characterized by unpleasant, pain-like physical states, it follows that an appropriate treatment for malaise is with analgesic or pain killer drugs [32]. For example, painkillers often alleviate (to some extent) the aching and exhausted physical state associated with influenza or its aftermath.

Analgesics/pain killers for malaise

There is considerable anecdotal and indirect evidence to suggest that analgesics are effective in treating some types of depression. I am aware of one formal trial designed partially to test this hypothesis – which confirmed it [38].

However, the effectiveness of the traditional ‘tricyclic’ antidepressants (TCAs) in ’major depressive disorder’ (which includes malaise symptoms in its definition) may be interpreted as being due the drugs’ analgesic properties [40]. Especially this applies to the effectiveness of amitriptyline, which has been the most widely-prescribed TCA for depression [1]; and which is also currently used in the treatment of cancer pain in terminal/palliative care, migraine etc. Furthermore, opiates (which are analgesics) have, at various times throughout history - most recently during the 1980s – been apparently successfully used in the treatment of depressive symptoms [3], [32] and [41]. (By contrast, SSRIs probably do not have significant analgesic properties [3] and [40].)

When depressed mood is associated with a malaise state, there could be a trial of the various simple analgesics available without prescriptions: aspirin, ibuprofen, paracetamol/acetaminophen and the mild opiates such as codeine or dihydrocodeine. Either aspirin or ibuprofen can also be combined with paracetamol and/or an opiate. Individual responsiveness to these analgesics is variable, and so are the experienced side effects – so there may need to be a period of trial-and-error before concluding that analgesics are ineffective.

As when treating Neuroticism with stabilizing drugs; the analgesics/pain killers would be expected to have a rapid effect in alleviating malaise symptoms as soon as the drug has been absorbed – i.e. in just a few hours [3]. But because mood is not directly related to malaise symptoms, it may take days or weeks before a reduction in malaise symptoms leads to an improvement in mood. So even when malaise is alleviated with treatment, the mood may remain depressed for other reasons – perhaps due to other unpleasant emotions, or to circumstances or habit [3], [9] and [32].

Demotivated depression

Demotivated depression is characterized by reduced positive emotions; and it is this inability or impaired ability to experience pleasure (i.e. anhedonia) that is the cause of demotivation.

Motivation is at root a product of the ability to feel current pleasure in anticipation of future situations – it is this pleasurable anticipation of future positive states of emotion which provides the immediate motivation needed for present action [3] and [10]. If one cannot experience pleasure, and if nothing seems likely to induce pleasure, then there will be a generalized loss of interest in life and its opportunities, and this will be experienced as a lack of vitality and drive (including reduced sexual drive).

Life usually involves a trade off between present and future pleasure and pains – normal people will often do something which is worse in the here-and-now, if this leads to the prospect of something better in the future. Something as simple as making the effort to visit a friend is done in the expectation that the here-and-now inconvenience of walking or catching a bus will be compensated by the future pleasure of conversation. But if the thought of having a conversation with a friend does not lead to a here-and-now sense of pleasure (pleasurable anticipation), then the deterrent effect of the unpleasant aspects of walking or catching a bus will weaken the motivation to visit the friend.

Demotivated depression is therefore a concept derived from and almost identical with Nutt’s ‘Depression with loss of interest and energy’ [17] and Watson’s state of low positive emotionality [19]. Causally, demotivated depression may be an exacerbation of the personality trait of introversion (asocial, quiet, submissive, timid, avoidant) [15] and [16] or a sub-clinical state of early Parkinsonism [42]. Demotivation may be a consequence of taking certain types of drug – especially drugs that lead to a reduction in dopaminergic – or noradrenergic/norepinephric – activity in brain; agents such as the neuroleptic/antipsychotic drugs which block dopaminergic receptors [7] and [23]. The motivational system seems to involve mainly the dopaminergic neurotransmitter system, and this seems to interact with noradrenergic, serotonergic and cholinergic systems – among others [43].

It is important to recognize that demotivated depression would probably be made worse by stabilizing drugs which tend to blunt emotions – since stabilizers would blunt the positive emotions which are already deficient in demotivated depression.
Energizing drugs for demotivated depression

The suggested treatment of demotivated depression is with energizing drugs which enhance dopamine or norepinephrine actions – either directly or indirectly [44]. The classic examples of such drugs include the psychostimulants such as dexamphetamine or methylphenidate (‘Ritalin’). Other energizing drugs include bupropion, monoamine-oxidase inhibitors such as phenelzine or moclobemide, amineptine, reboxetine, and the tricyclic desimipramine [17] and [44]. However, these drugs are only available with a prescription.

There are few energizing drugs which are available without prescription (probably due to fears of inducing addiction or dependence). The best-known and by far the most widely used energizers are caffeine and nicotine.

Caffeine [45] is found in coffee and tea and available in tablet form without prescription. It is a weak psychostimulant which increases alertness. Caffeine probably has properties as an analgesic or painkiller; and probably also has beneficial effects in preventing and perhaps treating Parkinson’s disease (suggesting that caffeine acts like a dopamine agonist) [46] and [47].

Nicotine [48] is found in tobacco but is also available as a non-prescription drug (for example as lozenges, chewing gum, or skin patches). While nicotine works directly upon the cholinergic neurotransmitter system, it appears to have indirect effects as a ‘dopaminergic’ psychostimulant – it often increases energy and alertness and like caffeine (but with stronger evidence) seems to have both a preventive and therapeutic effect on Parkinson’s disease [47], [48], [49] and [50].

In conclusion, the range of possibilities for self-treatment of demotivated depression with non-prescription drugs are at present both limited and somewhat speculative.

Seasonal Affective Disorder – SAD

Seasonal Affective Disorder (SAD) is winter depression or winter blues: low mood that occurs with greater frequency at more extreme latitudes (north or south) almost certainly due to the short daylight hours during winter months [51]. It is treated, not with drugs, but with bright artificial light, usually administered in the early morning [52] and [53].

The typical symptoms of SAD include excessive sleeping (hypersomnia) i.e. still tired when waking in the morning and sleepy throughout the day; increased appetite with carbohydrate craving and weight gain; irritability; fatigue; reduced motivation and sociability. In other words, while sleepiness and carbohydrate craving with weight gain are somewhat distinctive to SAD; many of the symptoms of SAD overlap with the three other sub-types of depression (i.e. irritability overlaps with Neuroticism, fatigue overlaps with malaise, and reduced motivation and sociability overlap with demotivated depression).

It is therefore the seasonal pattern of depressed mood and the characteristic behaviors which are crucial for the diagnosis rather than the specific subjective symptoms being experienced. Another diagnostic factor is the rapid and profound improvement of these symptoms in response to exposure to bright early morning light – which makes the response to light treatment something of a ‘diagnostic test’ for SAD.

SAD needs to be distinguished from the increased seasonal incidence of malaise symptoms which would be expected during winter months due to the increased prevalence of infectious diseases in many parts of the world (especially upper respiratory tract infections such as colds and influenza). Indeed, discriminating SAD from malaise could be tricky, since in the first place the main symptom of malaise is physical tiredness or ‘fatigue’ while the main symptom of SAD is mental tiredness or ‘sleepiness’. In the second place there is no reason why a person should not simultaneously suffer from both malaise and SAD, therefore from ‘tiredness’ due to both fatigue and sleepiness.

Indeed, it is plausible that the circadian hormone disruptions which are plausibly associated with SAD might themselves lead to immune activation as a secondary consequence – so that SAD might precipitate malaise.
Bright light therapy for the treatment of SAD

Bright artificial light usually administered early in the early morning seems a very effective treatment for SAD [51], [52] and [53] – this requires no prescription but only the purchase of a device delivering suitably bright light.

Especially-bright artificial light is needed to treat or prevent SAD because the aim is to simulate the kind of brightness that is provided by natural outdoor light. Normal indoor house lighting in a kitchen is only about 400 lux (there is even less light in bedrooms), while outdoors, even on a cloudy day, there is about 10 times greater intensity of light – 4000 lux.

Specialized ‘light boxes’ generate about 10000 lux of suitable-wavelength light at close range. This should be sufficient to cure SAD if administered for 30 minutes - however the subject must usually be sedentary and near to the light. A ‘light visor’ shines the light from much closer to the eye for about the same length of time, while allowing the subject to be mobile. ’Dawn simulators’ are like an alarm clock that brightens up to about 400 lux over a period of about an hour – apparently these also seem to work for some people.

If a person has SAD, then bright early morning light will probably produce a marked improvement in their symptoms within just a few days and continued use of bright light therapy would probably prevent a return of SAD symptoms.
SAD is a syndrome

SAD therefore is an example of diagnosing and treating a syndrome; rather than the symptom based-management model as recommended for Neuroticism, malaise and demotivation.

The delineation of SAD is actually a tremendous success story of psychiatry within the past few decades. And interestingly, (although perhaps not surprisingly) this process of definition and development of treatments happened largely outside of the professional structures of modern psychiatry, presumably because bright light treatment is non-pharmacological and not patentable.

It is a significant paradox (and one which supports the need for self-management in psychiatry) that probably the most valid and most effectively-treatable of recently-defined psychiatric syndromes arose mostly outwith the ‘official’ field of heavily-funded psychiatric research.


The main benefits of the S-DTM approach to self-management of psychiatric symptoms using non-prescription drugs (Table 1) is that it allows people to avoid contact with modern psychiatry and to maintain control of their own therapy and tailor treatment to their own needs. The main limitations are those of limited (or inaccurate) knowledge, difficulties of introspection and self-monitoring, and the restricted range of treatments available without prescription.

Table 1.

Four sub-types of ‘depression’ and first-line agents for their treatment
Sub-type Emotions Treatment
Neuroticism Anxiety, unstable emotions Stabilizing drugs
Malaise Fatigue, pains Analgesics/pain killers
Demotivated Anhedonia – lack positive emotions Energizing drugs
SAD Winter seasonal symptoms Bright morning light

One major advantage of a more specific approach to diagnosing and treating sub-types of ‘depression’ in a symptomatic fashion is that of avoid the damaging consequences of treating demotivated depression with stabilizing drugs. Under the currently prevailing standard model of depressive disorder, it is quite likely that any person with a depressed mood would first be tried-out with the stabilizing and emotion blunting SSRIs; and any observed worsening of mood would probably be blamed on the ‘disease’ of depression instead of the drug. But since demotivated people lack strong positive emotions, SSRIs would probably make them feel worse by blunting their emotions still further. (i.e. if your problem is insufficient pleasurable experience, the last thing you need is to be made even less responsive to pleasurable stimuli.)

The five sub-types of ‘depression’ (including melancholia) are not mutually exclusive. An individual might suffer from two or more of these syndromes simultaneously. Various combinations are possible. For example, a person with depressed mood due to a neurotic and unstable personality might well in addition suffer from seasonal affective disorder during the winters, or from malaise following influenza. Or a person with lack of drive due to a chronic demotivated depression might in addition experience malaise secondary to a chronic infection or autoimmune disease, or SAD. Such subjects might perhaps, rarely, go on to develop severe melancholia.

In such situations of several simultaneous diagnoses, alleviation of one type of symptom could fail to improve mood due the persistence of other types of symptom. More than one type of treatment may be required simultaneously, as in any situation characterized by multiple causal pathologies.

In terms of the treatments available without prescription, the biggest problem is that there is only a limited number of energizing drug treatments available without prescription; and the premier energizing drugs all require prescription at present. On the other hand, St Johns Wort is quite possibly the best all-round stabilizing drug (better than SSRIs), bright light therapy is certainly the best treatment for SAD (short of moving to live in a latitude nearer the equator and with sunnier weather); and there is a reasonable range of effective analgesics available ’over the counter’ for treating malaise – stronger opiates and stronger NSAIDs being the main categories of pain killers currently requiring a prescription.

In sum, the ability of individuals to self-manage ’depression’ is already powerful, and the future looks promising. I hope the above ideas will be useful and will also stimulate debate. And, looking beyond depression, it is possible that the general S-DTM model might be more widely-applicable within psychiatry and medicine, and for enhancement of the quality of life.


[1] D. Healy, The antidepressant era, Harvard University Press, Cambridge, MA (1998).

[2] D. Healy, Let them eat Prozac, New York University Press, NY, USA (2004).

[3] B. Charlton, Psychiatry and the human condition, Radcliffe Medical Press, Oxford, UK (2000).

[4] B.G. Charlton, Self-management of psychiatric symptoms using over-the-counter (OTC) psychopharmacology: the S-DTM therapeutic model - self-diagnosis, self-treatment, self-monitoring, Med Hypotheses 65 (2005), pp. 823–828.

[5] B.G. Charlton, Palliative psychopharmacology: a putative speciality to optimise the subjective quality of life, QJM 96 (2003), pp. 375–378.

[6] E.F. Domino, History of modern psychopharmacology: a personal view with an emphasis on antidepressants, Psychosom Med 61 (1999), pp. 591–598.

[7] D. Healy, The creation of psychopharmacology, Harvard University Press, Cambridge, MA, USA (2002).

[8] A. Sims, Symptoms in the mind, WB Saunders, London (1987).

[9] D. Healy, The suspended revolution, Faber, London (1990).

[10] A.R. Damasio, Descartes error: Emotion, Reason and the Human Brain, Putnam, New York (1994).

[11] A.R. Damasio, The feeling of what happens: body, emotion and the making of consciousness, William Heinemann, London (1999).

[12] W. Mayer-Gross, E. Slater and M. Roth, Clinical psychiatry (third ed.), Bailliere, Tindall & Cassell, London (1969).

[13] M. Fink, Electroshock: healing mental illness, Oxford University Press, NY, USA (1999).

[14] E. Shorter and D. Healy, Shock therapy: a history of electroconvulsive therapy in mental illness, Rutgers University Press, New Jersey, USA (2007).

[15] G. Matthews, I.J. Deary and M.C. Whiteman, Personality traits (second ed.), Cambridge University Press, Cambridge, UK (2003).

[16] D. Nettle, Personality: what makes you the way you are, Oxford University Press, Oxford, UK (2007).

[17] D. Nutt, K. Demyttenaere, Z. Janka, T. Aarre, M. Bourin and P.L. Canonico et al., The other face of depression, reduced positive affect: the role of catecholamines in causation and cure, J Psychopharmacol 21 (2007), pp. 461–471.

[18] American Psychiatric Association. Diagnostic and statistical manual of mental disorders, vol. IV. Dysthymic disorder. Accessed 7 August 2008.

[19] D. Watson, L.A. Clark and G. Carey, Positive and negative affectivity and their relation to anxiety and depressive disorders, J Abnorm Psych 97 (1988), pp. 346–353.

[20] Sobo S. Psychotherapy perspectives in medication management. Psychiatric times. Accessed 10 August 2008.

[21] P. Kramer, Listening to prozac, Fourth Estate, London (1994).

[22] B.G. Charlton, If ’atypical’ neuroleptics did not exist, it wouldn’t be necessary to invent them: perverse incentives in drug development, research, marketing and clinical practice, Med Hypotheses 6 (2005), pp. 1005–1009.

[23] B.G. Charlton, Why are doctors still prescribing neuroleptics?, QJM 99 (2006), pp. 417–420.

[24] A. Carlsson and M. Lindqvist, Central and peripheral monoaminergic membrane-pump blockade by some addictive analgesics and antihistamines, J Pharm Pharmacol 21 (1969), pp. 460–464.

[25] A. Carlsson and D.T. Wong, A note on the discovery of selective serotonin reuptake blockers, Life Sci 61 (1997), p. 1203.

[26] E. Hellborn, Chlorpheniramine, selective serotonin-reuptake inhibitors (SSRIs) and over-the-counter (OTC) treatment, Med Hypotheses 66 (2006), pp. 689–690.

[27] B.G. Charlton, Self-management interventions for panic, phobia and other anxiety-disorders might include over-the-counter (OTC) ‘SSRI’ antihistamines such as diphenhydramine and chlorpheniramine - Correspondence, Acta Psych Scand 112 (2005), pp. 323–324.

[28] M. Humble and E. Hellbom, Dex-chlorpheniramine treatment of panic disorder, Nord J Psychiat 52 (1998), pp. 440–441.

[29] E. Hellbom, M. Humble and M. Larsson, Antihistamines, selective serotonin reuptake inhibitors, and panic disorder, Nord J Psychiat 53 (1999), p. 100.

[30] E. Hellbom and M. Humble, Panic disorder treated with the antihistamine chlorpheniramine, Ann Allergy Asthma Immunol 90 (2003), p. 361.

[31] Wikipedia. St John’s Wort.’s_Wort. Accessed 6 August 2008.

[32] B.G. Charlton, The malaise theory of depression: major depressive disorder is sickness behavior and antidepressants are analgesic, Med Hypotheses 54 (2000), pp. 126–130.

[33] M.P. Szuba, B.H. Guze and L.R. Baxter, Electroconvulsive therapy increases circadian amplitude and lowers core body temperature in depressed subjects, Biol Psychiat 42 (1997), pp. 1130–1137.

[34] J.L. Rausch, M. Johnson, Y. Fei, J. Li, N. Shendarkar and H.M. Hobby et al., Depressed outpatients have elevated temperatures, Biol Psychiat 47 (2000), p. 93S.

[35] M. Maes, The depressogenic effects of cytokines: implications for the psychological and organic aetiology and treatment of depression, Int J Neuropsychopharmacol 5 (2002), pp. 329–331.

[36] U. Vollmer-Conna, C. Fazou, B. Cameron, H. Li, C. Brennan and L. Luck, Production of pro-inflammatory cytokines correlates with the symptoms of acute sickness behaviour in humans, Psychol Med 34 (2004), pp. 1289–1297.

[37] M.C. Whichers, G.H. Koek, G. Robaeys, A.J. Praamstra and M. Maes, Early increase in vegetative symptoms predicts IFN-[alpha]-induced cognitive depressive changes, Psychol Med 35 (2005), pp. 433–441.

[38] J. Mendelwicz, P. Kriwin, P. Oswald, D. Souery, S. Alboni and N. Brunello, Shortened onset of antidepressants in major depression using acetylsalicylic acid augmentation: a pilot open-label study, Int Clin Psychopharmacol 21 (2006), pp. 227–231.

[39] K. Schneider, Clinical psychopathology, translated by Hamilton MW and Anderson EW, Grune and Stratton, New York (1959) pp. 135–7.

[40] M.E. Lynch, Antidepressants as analgesics: a review of randomized controlled trials, J Psychiat Neuroscience 26 (2001), pp. 30–36.

[41] In: K. Vereby, Editor, Opioids in mental illness: theories, clinical observations and treatment possibilities, New York Academy of Science, New York (1982).

[42] J. Knoll, The psychopharmacology of life and death. In: D. Healy, Editor, The psychopharmacologists vol. III, Arnold, London (2000).

[43] Pearce D. Wirehead Hedonism versus paradise engineering Accessed 7 August 2008.

[44] Pearce D. The responsible parent’s guide to healthy mood-boosters for all the family. BLTC Good Drug Guide. Accessed 7 August 2008.

[45] Wikipedia. Caffeine. Accessed 7 August 2008.

[46] A. Aschero, S.M. Zhang, M.A. Hernan, I. Kawachi, G.A. Colditz and F.E. Speizer et al., Prospective study of caffeine consumption and risk of Parkinson’s disease in men and women, Ann Neurology 50 (2001), pp. 56–63.

[47] M.A. Hernan, B. Takkouche, F. Caamano-Isorna and J.J. Gestal-Otero, A meta-analysis of coffee-drinking, cigarette smoking and the risk of Parkinson’s disease, Ann Neurology 52 (2002), pp. 276–284.

[48] Wikipedia. Accessed 7 August 2008.

[49] M. Quik, Smoking, nicotine and Parkinson’s disease, Trends in Neurosci 27 (2004), pp. 561–568.

[50] G. Villafane, P. Cesaro, A. Rialland, S. Baloul, S. Azimi and C. Bourdet et al., Chronic high dose transdermal nicotine in Parkinson’s disease: an open trial, Eur. J Neurology 14 (2007), pp. 1313–1316.

[51] N.E. Rosenthal, D.A. Sack, J.C. Gillin, A.J. Lewy, F.K. Goodwin and Y. Davenport et al., Seasonal affective disorder: A description of the syndrome and preliminary findings with light therapy, Arch Gen Psychiat 41 (1984), pp. 72–80.

[52] R.W. Lam, Seasonal affective disorder: diagnosis and management, Primary Care Psychiat 4 (1998), pp. 63–74.

[53] J.M. Eagles, Seasonal affective disorder, Brit J Psychiat 182 (2003), pp. 174–176.

Wednesday 22 October 2008


*Since writing this piece my understanding has changed and I now believe it contains fundamental flaws. Anyone who would like further clarification is welcome to e-mail me at hklaxnessat-*

Genospirituality: Genetic engineering for spiritual and religious enhancement

Bruce G. Charlton

Medical Hypotheses. 2008; Volume 71: 825-828


The most frequently discussed role for genetic engineering is in relation to medicine, and a second area which provokes discussion is the use of genetic engineering as an enhancement technology. But one neglected area is the potential use of genetic engineering to increase human spiritual and religious experience – or genospirituality. If technologies are devised which can conveniently and safely engineer genes causal of spiritual and religious behaviours, then people may become able to choose their degree of religiosity or spiritual sensitivity. For instance, it may become possible to increase the likelihood of direct religious experience – i.e. ‘revelation’: the subjective experience of communication from the deity. Or, people may be able to engineer ‘animistic’ thinking, a mode of cognition in which the significant features of the world – such as large animals, trees, distinctive landscape features – are regarded as sentient and intentional beings; so that the individual experiences a personal relationship with the world. Another potentially popular spiritual ability would probably be shamanism; in which states of altered consciousness (e.g. trances, delirium or dreams) are induced and the shaman may undergo the experience of transformations, ‘soul journeys’ and contact with a spirit realm. Ideally, shamanistic consciousness could be modulated such that trances were self-induced only when wanted and when it was safe and convenient; and then switched-off again completely when full alertness and concentration are necessary. It seems likely that there will be trade-offs for increased spirituality; such as people becoming less ‘driven’ to seek status and monetary rewards – as a result of being more spiritually fulfilled people might work less hard and take more leisure. On the other hand, it is also possible that highly moral, altruistic, peaceable and principled behaviours might become more prevalent; and the energy and joyousness of the best churches might spread and be strengthened. Overall, genospirituality would probably be used by people who were unable to have the kind of spiritual or religious experiences which they wanted (or perhaps even needed) in order to lead the kind of life to which they aspired.


The genetic engineering imperative

The future continuation of modernizing societies (characterized by growth and progress in science, technology and the economy [1]) may depend upon rapid progress in, and widespread usage of, genetic engineering, since there are numerous processes of natural selection at work in advanced societies which are likely to have been increasing the proportion of deleterious genes and reducing the proportion of socially-useful genes over several generations – at least in developed nations [2], [3] and [4].

Because these demographic trends seem to be so strong – yet unacknowledged and therefore socio-politically irreversible – one probable implication is that the development of genetic engineering (including gene therapy and related stem cell and embryonic biotechnologies, etc.) should be regarded as a social imperative, and pursued as rapidly as possible [5] and [6].

It is widely – although not universally – appreciated that genetic engineering might potentially be very useful. The most frequently discussed role for genetic engineering is in relation to medicine, where deleterious and disease-causing genes could potentially be corrected. Assuming genetic engineering were safe, available and affordable; many people would be pleased to utilize medical genetic engineering.

The second area which provokes discussion is the use of genetic engineering as an enhancement technology. For example, biotechnology will probably be able to increase intelligence, to improve happiness, and to boost physical skills or specific abilities such as music or mathematics. This is more controversial than the medical deployment of genetic engineering – nonetheless it seems probable that safe and effective genetic enhancements would be used by many people if they were given the choice.

But one neglected area of enhancement technology is the potential use of genetic engineering to increase human spiritual and religious experience – genospirituality or genospiritual engineering. I suggest that if, or when, such technologies become a potential choice – then genospiritual engineering will find plenty of takers.

Who would want to use genospiritual technologies?

Genospirituality would not be of interest to everyone, indeed I would expect there might be hostility to the idea both from convinced atheists who regard religious and spiritual matters as false, nonsensical and probably harmful; and from some traditionally religious people who would be suspicious of such apparently un-spontaneous and artificial religiosity.

However, other people will take the view that spirituality and religious experiences are real and definable subjective psychological states or human experiences. Leaving aside the question of whether these real psychological states and experiences refer to anything external, objective or supernatural; it could be argued that spiritual and religious subjective states may be regarded as valuable, desirable and/or biologically adaptive for at least some people in some circumstances.

So, whatever the cause of religiousness and spirituality, even if the cause is not accepted to be supernatural, it is at least plausible that significant numbers of people would choose to have such experiences if they could.

What benefits might be obtained from enhanced religiousness or spirituality?
The quest for a ‘meaningful’ life is of obvious and compelling importance for many people. Of course, there are plenty of people who find life meaningful and significant without the inclusion of any spiritual or religious elements. They are content to live their lives without either spirituality or religion.

But other people – probably the majority of the population in most countries – look for something more, or something else. They may find what they need from one (or more) of the major world religions, or from other churches, or from New Age type spiritual movements.

But a large proportion of the population of most countries apparently do not find what they are looking for in these social structures. These are the people sometimes termed ‘seekers’ [7] whose life is spent searching for ‘meaning’ – this may take the form of trying-out many churches and spiritual movements, exploring art and culture, trying psychopharmacology (either from prescribed drugs or using self-medication with drugs such as alcohol), or sampling from the many types of counselling, psychotherapy and psychoanalysis.

However, despite this multiplicity of possible sources of potential assistance, there are people who feel that their life or the world itself is lacking in meaning, they feel alienated and cut-off from experience, they do not feel properly alive [8]. These are the people who may in future seek a solution to their insoluble problems in changing themselves by means of genetic engineering so that they can enhance their spiritual and/or religious capacity.

Other people who practice organized religion may nonetheless wish for more powerful experience, or for the potential to shape their own behaviours in a direction in-line with their hopes and beliefs. They are already religious, but wish to become more so.

Some potential uses of genospiritual engineering

It seems likely that soon the genes associated with an increased religiousness or capacity to have spiritual experiences will become known by genome mapping methods (which link variations in the genome with traits and behaviours) becoming ever-cheaper, more sensitive and reliable, and more powerful. Some of the discovered gene-behaviour associations will on further investigation then turn-out to be causal – and this would potentially enable genetic engineering (and therapy) to modify the behaviours.

If technologies are devised which can conveniently and safely engineer these genes causal of spiritual and religious behaviours, then people may become able to choose their degree of religiosity or spiritual sensitivity. In other words genospirituality may emerge with the potential to become a popular option among spiritual seekers and those engaged in a religious quest.

In order to clarify what might be the uses, I will describe a few sample spiritual or religious experiences that might be enhanced by genospiritual engineering.

It may become possible to increase the likelihood of direct religious experience – i.e. ‘revelation’, or the subjective experience of communication from the deity/deities [9]. In the past it was unusual to experience direct communication with God/s, but perhaps this could be changed, and revelation might become accessible to a much greater number of people.

As another possible option, people may be able to engineer themselves to experience ‘animistic’ thinking – a mode of cognition in which the significant features of the world (such as large animals, trees, distinctive landscape features, or even some types of complex organization or technology) are regarded as sentient and intentional beings [10]. Animistic thinking is typical of early childhood in all societies, and is also believed to be universal among those hunter-gatherers who were the ancestors of modern humans.

One advantage of such changes could be that an animistic person has a personal relationship with the world, because the world is seen as composed of active agents. By contrast, the more typical modern mode of thinking sees the world as an abstract system of passive objects moved by impersonal forces – and this can create feelings of alienation, loneliness and pointlessness.

Another spiritual experience which would likely be popular is shamanism [11] and [12]. Shaman is the term used for the healers and ‘medicine men’ (or women) of many societies who may also do divination and make important decisions for the tribe – and characteristically their work is done by means of states of altered consciousness (e.g. trances, delirium or dreams) in which they may undergo transformations, ‘soul journeys’ and contact a spirit realm.

In modern societies, it seems that only a minority of people are able to enter shamanistic trances without some kind of technological assistance. Some artists and other creative people (including scientists) apparently do important work (for example experience inspiration, or gain sudden insight) in states of somewhat-altered consciousness [8] and [10]. These mental states need not be regarded as supernatural; but may simply offer a different, more associative, way of thinking.

Shamanistic trance states can be difficult or impossible for people to achieve spontaneously and safely, and they may require the use of fairly extreme-measures such as prolonged dancing, drumming in groups, use of mind-impairing hallucinogenic agents or other technologies. Indeed, the measures necessary for modern individuals to induce a trance state at minimum time consuming and at the extreme are dangerous. It may also be several hours or more before the side-effects of a trance, or the method used to induce a trance, wears off, so that the person would be mentally unable to do responsible tasks such as child-care, driving a car, or operating equipment.

However, in principle, it may be possible to make genetic changes such that such trance states might be spontaneously attainable at will. Ideally, shamanistic consciousness could be modulated such that trances could self-induced only when wanted and when it is safe and convenient; and then switched-off again completely when full alertness and concentration are necessary.

Trade-offs and priorities

It seems likely that spirituality and religiousness will not be found to be under the control of single genes or even just a few genes, but rather caused by the combination of suites of alleles, each of which exerts a relatively small effect. Furthermore, some of these genes will probably be pleiotropic or multi-functional – such that altering spirituality will have side-effects in terms of altering other functions or behaviours.

Indeed, except where genospiritual engineering is merely correcting deleterious single mutations; it seems likely that there will be trade-offs (as there are likely to be trade-offs for most conceivable forms of enhancement technology). For example, higher IQ is predictive of longer life expectancy and greater wealth and social status in modern societies – yet increasing IQ may (at least above a certain point) also be associated in modern cultures with impairments from an increased tendency for short-sightedness to reduced fertility rates [13] and [14].

So we should anticipate trade-offs for increased spirituality. One possible example could be the possibility that increasing spiritual fulfilment might make people less ‘driven’ to seek status and monetary rewards. Greater contentment might benefit the individual but perhaps may not benefit society as a whole – if as a result of being more spiritually fulfilled more people worked less hard and took more leisure.

While greater religiousness may be associated with greater happiness, more altruistic behaviours and higher fertility [9], and these may turn-out to be significantly causal – it is possible that genetically-enhanced religiousness might lead to other problems. Perhaps churches would get too powerful and attempt to control science, technology and the economy with disastrous effects. Or perhaps church members might become fanatically loyal and too easily manipulated into dangerous behaviours.

On the other hand, it is also possible that highly moral, altruistic, peaceable and principled behaviours might become more prevalent; and the energy and joyousness of the best churches might spread and be strengthened.


In considering the desirability of genospiritual engineering, it is possible to take an ‘agnostic’ stance over whether or not spiritual and religious experience refers to an external and objective supernatural world. It might be agreed that, whatever the underlying objective facts might be, some types of religiousness and spirituality are plausibly associated with some good outcomes both in terms of subjective states of mind (making people feel better) and in terms of objectively observable social behaviours (making people behave better). There are also some disadvantages of spirituality and religiousness – so the outcome is likely to vary between individuals, according to the extremity of spirituality or religiousness, between religions and spiritualities, and between societies.

Whatever the answer in a specific instance, genospirituality would probably – if available – be used by people who were unable to have the kind of spiritual or religious experiences which they wanted (or perhaps even needed) in order to lead the kind of life to which they aspired.


[1] B. Charlton and P. Andras, The modernization imperative, Imprint Academic, Exeter, UK (2003).

[2] R.A. Fisher, The genetical theory of natural selection, Clarendon Press, Oxford, UK (1930).

[3] W.D. Hamilton, The narrow roads of Gene Land vol. 2, Oxford University Press, Oxford, UK (2002).

[4] R. Lynn and J. Harvey, The decline of the world’s IQ, Intelligence 36 (2008), pp. 112–120.

[5] D. Pearce, The Hedonistic Imperative. [Accessed 10.6.2008].

[6] R. Baschetti, Evolutionary biological origins of morality: Implications for research with human embryonic stem cells, Stem Cells Develop 14 (2005), pp. 239–247.

[7] W.C. Roof, Spiritual Marketplace: baby boomers and the remaking of American religion, Princeton University Press, Princeton, USA (1999).

[8] B.G. Charlton, Alienation, recovered animism and altered states of consciousness, Med Hypotheses 68 (2007), pp. 727–731.

[9] R. Stark, Discovering God: the origins of the great religions and the evolution of belief, HarperOne, London (2007).

[10] B.G. Charlton, Scientific discovery, peak experiences and the col-oh-nell flastratus! phenomenon, Med Hypotheses 69 (2007), pp. 475–477.

[11] D.C. Noel, The soul of shamanism, Continuum, New York (1998).

[12] R. Hutton, Shamans: Siberian spirituality and the Western Imagination, Hambledon and London, London, UK (2007).

[13] W. Mak, M. Kwan, T. Cheng, K. Chan, R. Cheung and S. Ho, Myopia as a latent phenotype of a pleiotropic gene positively selected for facilitating neurocognitive development, and the effects of environmental factors, Med Hypotheses 66 (2006), pp. 1209–1215.

[14] R. Lynn and M. Van Court, New evidence for dysgenic fertility for intelligence in the United States, Intelligence 32 (2004), pp. 193–201