Modernization Imperative

2006-12-27T14:42:00.000Z

Nobel prizes as a scientometric measure of revolutionary science

four 'in the press' editorials from Medical Hypotheses

by Bruce G Charlton.

PDF files of these articles are available on request from brucedot charltonat ncldot acdotuk

NOTE - I apologize for the bad formatting of the Tables

- but they can still be read, albeit with some effort...

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Editorial

Why there should be more science Nobel Prizes –

and why proportionate credit should be awarded to institutions

Charlton BG. Medical Hypotheses 2007; 68: 471-3 – doi:10.1016/j.mehy.2006.11.003

Abstract

The four science Nobel prizes (physics, chemistry, medicine/ physiology and economics) have performed extremely well as a method of recognizing the highest level of achievement. The prizes exist primarily to honour individuals but also have a very important function in science generally. In particular, the institutions and nations which have educated, nurtured or supported many laureates can be identified as elite in world science. However, the limited range of subjects and a maximum of 12 laureates per year means that many major scientific achievements remain un-recognized; and relatively few universities can gather sufficient Nobel-credits to enable a precise estimate of their different level of quality. I advocate that the Nobel committee should expand the number of Nobel laureates and Prize categories as a service to world science. 1. There is a large surplus of very high quality prize candidates deserving of recognition. 2. There has been a vast expansion of research with a proliferation of major sub-disciplines in the existing categories. 3. Especially, the massive growth of the bio-medical sciences has created a shortage of Nobel recognition in this area. 4. Whole new fields of major science have emerged. I therefore suggest that the maximum of three laureates per year in the categories of physics, chemistry and economics should always be awarded, even when these prizes are for diverse and un-related achievements; that the number of laureates in the ‘biology’ category of physiology or medicine should be increased to six or preferably nine per year; and two new Prize categories should be introduced to recognize achievements in mathematics and computing science. Together, these measures would increase the science laureates from a maximum of 12 to a minimum of 24, and increase their coverage. The Nobel Prize committee should also officially allocate proportionate credit to institutions for each laureate - both in retrospect for past prizes, and in the future.

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The Nobel prizes are more than 100 years old. They exist primarily to honour individuals, but the prizes also have a very important function in science generally, in particular providing a retrospective research quality evaluation for institutions and nations.

The four science Nobel prizes (physics, chemistry, medicine/ physiology, and since 1968 economics) have performed extremely well as a method of recognizing the highest level of achievement. (The literature and peace prizes, lacking objective and internationally-valid criteria for evaluation, have clearly failed to achieve the validity of the science prizes.) Although originally awarded to individuals, the science prizes are now awarded a maximum of once a year to a maximum of three laureates, which makes a maximum total of only 12 laureates annually. However this maximum number of laureates is not often reached due to the usual practice of awarding each year’s prize for achievements related to a single ‘theme’ of research – for which only one or two people may be responsible.

The science prizes serve not only to honour individuals retrospectively, but have also been used to evaluate the quality of universities and other research institutions by crediting the places that have been associated with the most ‘revolutionary’ science breakthroughs. For example, the Shanghai Jiao Tong academic rankings (http://ed.sjtu.edu.cn/rank/2006) uses 'alumni' data of the university where Nobel Laureates studied, and also the institution where laureates were working at the time of award. This generates a mostly-US world elite of universities containing the likes of Harvard, Chicago, Princeton, Colombia, MIT, Stanford, CalTech, Berkeley and Cambridge (UK).

But the maximum of only 12 science prizes per year means that many major scientific achievements remain un-recognized. Outside of the research super-elite, few universities can gather sufficient Nobel-credits to enable a precise estimate of their different level of quality. Such small numbers create considerable statistical noise, over-valuing a ‘lucky’ institution and undervaluing other places where Nobel-quality work was nurtured but un-rewarded.

I suggest that the massive expansion and specialization of world science since the foundation of the Nobel Prizes implies that the number of Nobel prizes should be at-least doubled. It would also be a very useful service to science if the prize committee would – in future and retrospectively – proportionately allocate an official share of institutional credit for each person’s prize.

Reasons why more Nobel prizes are justified

While it is understandable that the Nobel Committee and existing laureates would not want to 'inflate' the value of the award, given the number of unrewarded major scientists there seems to be no shortage of very high quality candidates for Nobels. So there should be no problem of increasing numbers reducing the quality of laureates.
The past century since the first Nobel Prize in 1901 has seen a vast, many-fold expansion of scientific research. Furthermore, there has been a continual process of specialization of research, as well as the generation of new hybrid categories (such as bio-chemistry). So, the meaning of a Nobel has changed. It is now appropriate that within a general category, several specialist prizes be awarded each year.
The relative importance of sciences have changed and for the several decades the bio-medical sciences have dominated in terms of size and achievements. This has created a shortage of Nobel recognition in the area of physiology and medicine. For example, many major therapeutic advances in drug discovery and innovative procedures have not been recognized by Nobel prizes.
New fields of science have merged and grown to maturity. Economics was recognized by a new Nobel Prize in 1968, but mathematics and computing science also seem worthy of new prizes. (The mathematic Fields Medal of the Royal Society only goes to candidates aged less than 40.)
An increase in the numbers of Nobel prizes would have great advantages for recognizing the scientific research institutions which have educated, nurtured and supported them. When there are so few prizes each individual prize carries a disproportionate weight in terms of institutional associations. Only a handful of universities have gathered enough prizes over sufficient years (eg. Harvard, Princeton, Cambridge, Chicago, MIT and CalTech) to eliminate chance effects. More prizes would mean that the contribution of institutions would be more precisely measurable, a wider range of scientific achievement would be rewarded, and also more up to date measures would become useable.
Related to this, it would be a great service to science if prizes were awarded not just to an individual, but if the official credit for each prize was also proportionately allocated between any institutions that were considered significantly to have supported the achievement - this process could also be retrospective.

In conclusion, I would advocate a progressive expansion of the number of science Nobel prizes. The exact mechanism by which this would be achieved in not critical, but here are some suggestions.

The maximum of three laureates per year in the physics, chemistry and economics categories should be awarded as a matter of routine; even when this means that prizes are being given for diverse and un-related achievements.
The number of laureates in the ‘biology’ category of physiology or medicine should be increased to six or preferably nine.
Consideration should be given to two new prizes to recognize achievements in mathematics and computing science.

A combination of these measures would ensure that the number of laureates per year would increase from the current maximum of 12 to a minimum of 21-24. The situation could be monitored to ensure that this change did not lead to any sign of incipient decline in quality of laureates, and consideration could be given to further expansion or adjustment of disciplinary categories in future.

While it is understandable and laudable that the Nobel committee should be cautious about the danger of devaluating the status of the award, in fact the real problem is exactly the opposite. By maintaining so few laureates when world science has expanded so much, there has been a deflationary extra-valuation of each award and an arbitrary element to the distribution of credit. As a service to world science, the Nobel Committee should seriously consider expanding the number of laureates to keep-up with the volume and quality of scientific activity.

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Editorial

Scientometric identification of elite ‘revolutionary science’ research institutions by analysis of trends in Nobel Prizes 1947-2006

Medical Hypotheses – do:10.1016/j.mehy.2006.12.006

Summary

Most research is ‘normal science’ using Thomas Kuhn’s term: checking, trial-and-error improvement and incremental extrapolation of already existing paradigms. By contrast, 'revolutionary science' changes the fundamental structures of science by making new theories, discoveries or technologies. Science Nobel prizes (in Physics, Chemistry, Physiology/Medicine and Economics) have the potential to be used as a new metric for measuring revolutionary science. Nobel laureates nations and research institutions were measured between 1947-2006 in 20 year segments. The minimum threshold for inclusion was 3 Nobel prizes. Credit was allocated to each laureate's institution and nation of residence at the time of award. Over 60 years, the USA has 19 institutions which won three-plus Nobel prizes in 20 years, the UK has 4, France has 2 and Sweden and USSR 1 each. Four US institutions won 3 or more prizes in all 20 year segments: Harvard, Stanford, Berkeley and CalTech. The most successful institution in the past 20 years was MIT, with 11 prizes followed by Stanford (9), Columbia and Chicago (7). But the Western United States has recently become the world dominant region for revolutionary science, generating a new generation of elite public universities: University of Colorado at Boulder; University of Washington at Seattle; and the University of California institutions of Santa Barbara, Irvine, UCSF, and UCLA; also the Fred Hutchinson CRC in Seattle. Since 1986 the USA has 16 institutions which have won 3 plus prizes, but elsewhere in the world only the College de France has achieved this. In UK's Cambridge University, Cambridge MRC unit, Oxford and Imperial College have declined from 17 prizes in 1967-86 to only 3 since then. Harvard has also declined as a revolutionary science university from being the top Nobel-prize-winning institution for 40 years, to currently joint sixth position. Although Nobel science prizes are sporadically won by numerous nations and institutions, it seems that long term national strength in revolutionary science is mainly a result of sustaining and newly-generating multi-Nobel-winning research centres. At present these elite institutions are found almost exclusively in the USA. The USA is apparently the only nation with a scientific research system that nurtures revolutionary science on a large scale.

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Most of scientific production can be categorized as ‘normal science’ using Thomas Kuhn’s term to describe research which constitutes the checking, trial-and-error improvement and incremental extrapolation of already existing paradigms [1]. Normal science can be measured and analyzed using standard scientometric research outputs such as number and share of publications and citations [2]. But a different method is need to detect and measure the much rarer, but potentially more-important, examples of paradigm-transforming Kuhnian ‘revolutionary science’ [3].

Revolutionary science changes the fundamental structures of a whole science (as achieved by Einstein, Newton or Darwin) or, more often, a significant sub-speciality of a major science [1]. For example science can be transformed or re-directed by new theories, discoveries or major technologies. Revolutionary science is therefore the cutting-edge which allows each science to continue to grow in rapid bursts, and to become qualitatively more accurate and useful in its predictions [3,4].

The problem of discriminating between revolutionary and normal science has become more difficult since the advent of Big Science [5]. Big Science comprises quasi-industrial forms of research organization, and arose initially in physics and chemistry but now characterizes biomedical research, which is currently the dominant world science. Big Science is almost inevitably a type of normal science (since it needs to be predictable) and tends to be ‘applied’ in its aims, and similar to industrial Research and Development in its methods [4,6]. Normal science now overwhelms revolutionary science in terms of quantity, so that revolutionary science has become almost invisible when research production is measured using standard scientometrics.

Science Nobel prizes have the potential to be used in detecting and measuring revolutionary science [3,7]. This may allow identification of those nations and institutions where revolutionary science has happened in the past, and help understand the conditions which could encourage revolutionary science in the future.

Nobel prizes as a measure of revolutionary science

The award of a Nobel prize in one of the four recognized sciences (Physics, Chemistry, Physiology/Medicine and Economics) seems to be the best current evidence of a significant achievement in revolutionary science. Although the small annual number of Nobel prize-winners (laureates) means that many significant achievements go unrecognized [7], nonetheless the perceived validity of these awards is high within the scientific community, and only a small proportion of awards are regarded as controversial or unjustified.

The number of science Nobel laureates in a nation and a research institution were measured between 1947 and 2006 in three 20 year segments of 1947-66, 1967-86 and 1987-2006 [8]. A maximum of three people can receive each prize, so there are a minimum of four and a maximum of twelve laureates per year (since 1969, when the economics prize was first awarded. Up to 1968 there were a minimum of three and a maximum of nine laureates).

A very large number of nations and institutions have won a single Nobel prize, but my interest was in those places which had won multiple prizes as evidence that they provided an environment conducive to revolutionary science. I set the threshold at three Nobel prizes during a 20 year period as the minimum number of laureates which counts as a significant national or institutional contribution to revolutionary science. (However, in 1965 the prize for Physiology/ Medicine went to Jacob, Monod and Lwoff of the Pasteur Institute, Paris, France; for the same topic.)

Official statistics are only available on Nobel laureates institutional affiliation at the time they receive the prize [8]. Clearly, this is not as valid a measure of revolutionary science as knowing laureates ' affiliations at the time prize-winning work was actually accomplished; however such information is not readily available. I therefore allocated credit to each laureate's institution and nation of residence at the time they received their award.

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Table 1 – Number of Nobel laureates by Nation – ten year segments from 1947-2006. A minimum of three prizes in one time segment is required for inclusion.

Nation - 1947-66 - 1967-86 - 1987-2006

USA -50 - 88 - 126

UK - 20 - 25 - 9

Germany - 8 - 7 - 9

Switzerland - 3 - 7 - 7

Sweden - 3 - 7 - 1

Japan - 2 - 1 - 3

USSR/Russia - 7 - 2 - 2

France - 4 - 3 - 5

Table 2 - Number of United States Nobel laureates by Institution – twenty year segments from 1947-2006. A minimum of three prizes in one time segment is required for inclusion.

Institution - 1947-66 - 1967-86 - 1987-2006

USA

Harvard - 9 - 13 - 5

Univ. California Berkeley - 7 - 3 - 4

Stanford - 4 - 5 - 9

Caltech - 4 - 4 - 5

Columbia - 4 - 1 - 7

Rockefeller Inst. & Univ. - 3 - 6 - 3

Chicago - 2 - 4 - 7

Princeton - 1 - 2 - 6

MIT - 1 - 5 - 11

Cornell - 1 - 4 - 2

UCLA - 1 - 0 - 3

Yale - 0 - 4 - 1

NIH - National Inst. Health - 0 - 4 - 0

Univ. Colorado, Boulder - 0 - 0 - 4

University of Washington - 0 - 0 - 3

Fred Hutchinson CRC, Seattle - 0 - 0 - 3

Univ. California, Santa Barbara - 0 - 0 - 3

UCSF (U Cal San Fransico) - 0 - 0 - 3

Univ. California, Irvine - 0 - 0 - 3

Table 3 - Number of Non-US Nobel laureates by Institution – twenty year segments from 1947-2006. A minimum of three prizes in one time segment is required for inclusion.

Institution - 1947-66 - 1967-86 - 1987-2006

Cambridge, UK - 3 - 7 - 2

MRC Cambridge, UK - 3 - 3 - 1

Oxford, UK - 3 - 3 - 0

Imperial Coll. London, UK - 0 - 4 - 0

Pasteur Inst, Paris, France - 3 - 0 - 0

College de France, Paris - 0 - 0 - 3

PN Lebedez Institute, Moscow, USSR - 5 - 0 - 0

Karolinska Inst., Sweden - 0 - 4 - 0

CERN (multi-national) - 0 - 3 - 1

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By contrast with the general decline elsewhere in the world, the US system is increasingly successful in generating revolutionary science which leads to the award of a Nobel prize (Table 1). It can be seen that few countries have any research institutions which have earned three or more Nobel prizes over any of the defined 20 year time spans. Over 60 years, the USA has nineteen such institutions (Table 2), the UK has four, France has two, and Sweden and USSR one each (Table 3).

Table 2 shows that there are only four institutions which have won three or more Nobel prizes in all three 20 year periods, all from the USA - Harvard, Stanford, Berkeley and CalTech. The most successful institution in the past 20 years was MIT, with 11 prizes followed by Stanford (9), Chicago and Columbia (7). But the Western United States has become the world dominant region for revolutionary science – with Stanford, Berkeley and CalTech now being amplified by a new generation of elite public universities: University of Colorado at Boulder, University of Washington at Seattle, University of California at Santa Barbara, UCSF (University of California at San Fransisco), University of California at Irvine, UCLA (University of California at Los Angeles) - also the Fred Hutchinson Cancer Research Center at Seattle.

In the past 20 years, the USA has sixteen institutions which have won three or more prizes, but elsewhere in the world (Table 3) only the College de France has achieved three Nobel prizes. Since 1986 the previously Nobel-successful UK research institutions (University of Cambridge, the MRC Molecular Biology Unit at Cambridge, University of Oxford and Imperial College, London) have declined from seventeen prizes 67-86 to only three.

The USA demonstrates dynamic changes in ranking over the 60 year period (Table 2). New institutions have risen to prominence in the Western states. From one prize each in 1947-66, MIT and Princeton have both overtaken Harvard to become first and fifth among Nobel prize-winners. Columbia declined in the middle period, but recovered strongly to reach equal-third in the rankings. The NIH and Yale have significantly declined during the most recent 20 years.

Harvard is particularly interesting. In terms of conventional scientometric research measures, Harvard is currently by-far the top ranking university in the world. For example, Harvard has double the number of citations as Johns Hopkins (which is second) and about 65 percent more publications than UCLA (which is second) during 2000-2004 [9]. And Harvard has more elected Members of the US National Academy of Sciences than any other university (167 – Harvard; 129 – Berkeley; 128 – Stanford; 100 – MIT; 72 – Princeton; 71 – Cal Tech [10]). By a large margin, Harvard also tops the respected Shanghai Jiao Tong University world rankings [11].

Yet there are signs of a decline in revolutionary science at Harvard. From 47-86 Harvard was the top Nobel-prize-winning institution, but for the past 20 years it has been overtaken in prize numbers by MIT (11), Stanford (9), Columbia (7), Chicago (7) and Princeton (6) – all of which are considerably smaller. The implication may be that Harvard is evolving towards being a ‘normal science’ university – albeit unusually large and successful.

Conclusion

If this statistic of Nobel prizes is a valid measure of revolutionary science, then the main conclusion is that the USA has emerged to become the only nation that supports revolutionary science on a large scale. It seems that long-term strength in revolutionary science is mainly a product of a nation possessing numerous elite research institutions where revolutionary science thrives. A nation lacking such institutions will win relatively few Nobel prizes, and prizes will be spread around many institutions (eg. in Germany, the various Max Planck research institutions sometimes win a single Nobel prize, but no specific institute has ever won two prizes in 20 years).

Over the past 60 years, the UK has declined from being the only non-US focus of revolutionary science, to joining Switzerland and Germany (with nine prizes) as the kind of place where normal science has been thriving but revolutionary science is thinly-distributed and sporadic in occurrence. Presumably, recent US improvement has therefore been driven mainly by within-nation competition.

In contrast to the picture of long term decline in Nobel-prize-winning revolutionary science; UK and European scientific production (also that of Chinese science) is probably catching up with the USA in terms of scientometric measures such as numbers of publications and citations [12,13]. This difference between national performance in normal and revolutionary science seems to suggest that the research systems of revolutionary science and normal science are evolving towards separation [3]. Clearly, growth of the two types of science does not always go-together.

In future, it would probably be beneficial if this increasing separation between revolutionary and normal science were made explicit, with institutional self-definition and specialization, and differentiated funding streams and evaluation criteria for the small number of elite revolutionary science institutions [4]. Part of this process would be the development of a distinctive set of scientometric measures for revolutionary science. Counting Nobel laureates could be a first step in this direction.

Acknowledgement: thanks are due to Peter Andras, Andrew Oswald and Malcolm Young for comments and advice.

References

1. Kuhn TS. The structure of scientific revolutions. Chicago: Chicago Univesrity Press, 1970.

2. Garfield E. Essays of an information scientist. Philadelphia: ISI Press, 1977.

3. Charlton BG, Andras P. Evaluating universities using simple scientometric research output metrics: total citation counts per university for a retrospective seven year rolling sample. Minerva, in the press.

4. Charlton BG, Andras P. The future of 'pure' medical science: the need for a new specialist professional research system. Medical Hypotheses 2005; 65: 419-25

5. Price DJ de Solla. Little Science, Big Science and beyond. New York: Columbia Univesrity Press, 1986.

6. Ziman J. Real science. Cambridge, UK: Cambridge University Press, 2000.

7. Charlton BG. Why there should be more science Nobel prizes and laureates - And why proportionate credit should be awarded to institutions. Medical Hypotheses, in the press.

8. Nobel Foundation. Nobel prizes. http://nobelprize.org/nobel_prizes. Accessed: 7 December 2006.

9. Charlton B, Andras P. Oxford University's research performance (four articles published in Oxford Magazine during 2006). www.hedweb.com/bgcharlton/oxmagarts. Accessed 14 December 2006.

10. National Academy of Sciences. Members. www.nasonline.org/site/Dir?sid=1011&view=basic&pg=srch. Accessed 30 November 2006.

11. Shanghai Jiao Tong University: Institute of Higher Education. Academic Ranking of World Universities 2006. http://ed.sjtu.edu.cn/ranking. Accessed 14 December 2006.

12. Shelton, RD, Holdridge, GM. The EU-US race for leadership of science and technology: Qualitative and quantitative indicators. Scientometrics 2004; 60: 353-363.

13. Ping Z, Leydesdorff L The emergence of China as a leading nation in science, Research Policy 2006 35: 83-104.

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Editorial

Which are the best nations and institutions for revolutionary science 1987-2006? Analysis using a combined metric of Nobel prizes, Fields medals, Lasker awards and Turing awards (NFLT metric).

Medical Hypotheses – doi:10.1016/j.mehy.2006.12.007

Summary

I have previously suggested that Nobel prizes can be used as a scientometric measurement of ‘revolutionary science’; and that for this purpose it would be better if more Nobel prizes were awarded, especially in three new subjects of mathematics, medicine and computing science which have become major sciences over recent decades. In the following analysis of the last twenty years from 1987-2006, I use three prestigious prizes in mathematics (Fields medal), medicine (Lasker award for Clinical Medical Research) and computing science (A.M. Turing award) which are plausible surrogates for Nobel prizes. The combined Nobel-Fields-Lasker-Turing (NFLT) metric is strongly dominated by the USA. However the distribution implies that revolutionary science may be somewhat more broadly distributed than the pure Nobel metric suggests. The UK and France seem to be significant nations in some types of revolutionary science (although the UK has declined substantially as a centre of revolutionary science); and Germany, Switzerland, Japan, Russia, Denmark and Norway also feature. The top world institutions for revolutionary science according to NFLT are MIT, Stanford and Princeton - all in the USA - and the USA has nineteen institutions with at least three prize-winners. Second is France, with three institutions having three or more winners; the UK and Norway have one each. The NFLT metric confirms previous observations that many public universities in the Western USA have now become a major focus of revolutionary science; and that Harvard has declined from its previous status as the top world centre of revolutionary science to about seventh-place. This analysis confirms the potential value of increasing the number of Nobel prizes as a means of identifying and monitoring centres of excellence in revolutionary science.

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Revolutionary science is a term coined by Thomas Kuhn in his book The structure of Scientific Revolutions (Chicago University Press, 1970) to describe research which changes the fundamental structures of science by making new theories, discoveries or technologies (ie. new ‘paradigms’). But most research is ‘normal science’, comprising checking, trial-and-error improvement and the more gradual and incremental extrapolation of already-existing paradigms.

The choice of the Fields medal [4] as a near-Nobel equivalent was also made by the well-respected Shanghai Jiao Tong University rankings of the world’s best universities [5]. It is a highly prestigious prize awarded every four years (in batches of up to four winners – making the prize approximately annual) by the International Mathematical Union to a mathematician aged less than forty.

The approximately annual Lasker Award for Clinical Medical Research [6] recognizes from one to three scientists whose work pioneers a major improvement in clinical management or treatment. Unlike the Lasker award for Basic Medical Research, which frequently predicts a Nobel prize in Physiology/ Medicine, the Clinical Medical Research (CMR) award does not frequently overlap with the Nobel prize. Only one person in the last twenty years (Barry Marshall) has received both a Lasker award for CMR and also a Nobel prize, and this particular award was removed from the Lasker statistic in the following tabulations.

The A.M. Turing Award is given annually to one or two individuals by the Association for Computing Machinery for contributions of lasting and major importance to the computer field [7].

Having identified the winners of Fields, Lasker and Turing prizes for the past twenty years; I discovered their national and institutional affiliation at the time the prize was awarded - either from the official web pages of the prize-awarding institutions, or by wider internet searching for references to these awards (eg Wikipedia entries, press releases, references to the prizes in other publications etc.). Each prize-winner was therefore credited to a single nation and institution. The data from Fields, Lasker and Turing winners were then pooled with the data from Nobel prize-winners and tabulated.

Since the aim of this study was to identify the strongest nations and institutions in revolutionary science, there was a minimum threshold of three Nobel-Fields-Lasker-Turing winners before a nation or institution was included in the tables.

Table 1 – Number of Nobel-Fields-Lasker-Turing winners by nation 1987-2006. A minimum of three winners is required for inclusion.

Nation - Nobel prizes - Other awards - Total

USA - 126 - 45 - 171

UK - 9 - 10 - 19

France - 5 - 7 - 12

Germany - 9 - 0 - 9

Switzerland - 7 - 0 - 7

Japan - 3 - 1 - 4

Russia - 2 - 1 - 3

Denmark - 1 - 2 - 3

Norway - 1 - 2 - 3

Table 2 – Number of Nobel-Fields-Lasker-Turing winners by institution 1987-2006. A minimum of three winners is required for inclusion. IHES = Institut des Hautes Etudes Scientifiques.

US Institution - Nobel prizes - Other awards - Total

MIT - 11 - 2 - 13
Stanford - 9 - 2 - 11
Princeton - 6 - 4 - 10
Chicago - 7 - 1 - 8
Univ. California Berkeley - 4 - 3 - 7
Columbia - 7 - 0 - 7
Harvard - 5 - 1 - 6
Caltech - 5 - 0 - 5
UCSF (Univ. Calif. San Fransico) - 3 - 2 - 5
Cornell - 2 - 2 - 4
Rockefeller Inst. & Univ. - 3 - 1 - 4
UCLA - 3 - 1 - 4
Univ. Colorado, Boulder - 4 - 0 - 4
Univ. Pennsylvania - 2 - 2 - 4
University of Washington - 3 - 1 - 4
NIH - National Inst. Health - 0 - 3 - 3
Fred Hutchinson CRC, Seattle - 3 - 0 - 3
Univ. California, Santa Barbara - 3 - 0 - 3
Univ. California, Irvine - 3 - 0 - 3

Non-US Institution

Univ. Cambridge, UK - 2 - 3 - 5

College de France, Paris - 3 - 0 - 3

University of Paris-Sud - 0 - 3 - 3

IHES*, Paris, France - 0 - 3 - 3

University Oslo, Norway - 1 - 2 - 3

Results

The national Nobel-Fields-Lasker-Turing (NFLT) metric (Table 1) is strongly dominated by the USA, confirming the pattern demonstrated by the previous analysis of Nobel prizes [3]. But inclusion of Fields-Lasker-Turing winners implies that revolutionary science may be more broadly distributed than the pure Nobel metric suggests. The UK and France, in particular, seem to be more significant nations in revolutionary science than suggested by Nobels alone; and other nations are identified as significant which are missed by the purely Nobel prize analysis: Russia, Denmark and Norway.

The top world revolutionary science institutions identified by the NFLT metric (Table 2) are MIT, Stanford and Princeton in the USA; and the USA has nineteen institutions with at least three prize-winners. Harvard stays in seventh place for the combined Nobel-Fields-Lasker-Turing metric, which is the same as its Nobel prize-winning rank, tending to confirm my previous observation [3] that Harvard has indeed declined as a centre of revolutionary science – although it remains dominant in ‘normal science’ as measured by metrics such as numbers of publications and citations.

In second place to the USA as a home of revolutionary science institutions is France, which has three institutions having three or more Nobel-Fields-Lasker-Turing winners. This particularly reflects French strength in mathematical research, with six Fields medallists in the past 20 years. University of Cambridge (UK) and University of Oslo (Norway) also emerge as significant.

Interpretation

In general, this analysis demonstrates the potential value of increasing the number of Nobel prizes [2], since otherwise the significant strength of France - and its three elite institutions - would be missed. The analysis also confirms the results of the pure-Nobel metric in suggesting that a high level of national performance in revolutionary science is probably a consequence of having elite institutions that win three or more prizes in a twenty year period.

Measured by the NFLT metric; outside of the USA (with its nineteen institutions of revolutionary science), only France seems to have succeeded in supporting more than one centre of revolutionary science over the past 20 years. Up until the mid-nineteen eighties, the UK was a long-term clear second to the USA in Nobel prizes [3]; but from 1987-2006 three of its major prize-winning institutions (ie. the University of Oxford, the Cambridge Molecular Biology MRC Unit, and Imperial College London) have declined as centres of revolutionary science, and now only the University of Cambridge achieves the three-winner NFLT threshold.

But the most significant result of this analysis is to demonstrate and confirm the massive US domination of revolutionary science [1,3], and the lack of any significant national competition for this status except in mathematics (France has six Fields medals to the USA’s eight). This contrasts with the general picture of European, East Asian and Chinese science ‘catching-up’ with the USA in terms of ‘normal science’ production (as measured by numbers of publications and citations [3,8]).

Looking into the long term, the lack of international competition in revolutionary science is somewhat worrying, since it means that world scientific progress may increasingly depend upon the US research system. In the US it is probably within-nation research competition between rival institutions that has so far maintained striving and standards in revolutionary science. But if US universities began to compete on the basis of ‘normal science’ instead of revolutionary science – as seems to have happened in the less-diverse, less competitive and more risk-averse Anglo-European research systems [9] - then we might expect to see a decline equivalent to that which has occurred over recent decades in mainland Europe and the UK [3].

The first signs of decline might be seen in previously-successful revolutionary science institutions which, like Harvard or Cambridge (UK), win progressively-fewer major research prizes [3] while maintaining a very high output of highly cited publications [1,10]. A more advanced state of decline might be harder to detect, since there would (presumably) continue to be Nobel-, Fields-, Lasker- and Turing-winners even in the absence of actual revolutionary science.

However, at present, the situation 1987-2006 looks healthy and competitive for revolutionary science in the USA, particularly in the elite of MIT, Stanford and Princeton and the recently-emerging Western US institutions [3] exemplified by UCSF with its three Nobels and two Lasker awards (Table 2).

Significance of the NFLT metric

The Nobel-Fields-Lasker-Turing metric only measures the tip of an iceberg of revolutionary science, and my assumption is that each successful example of revolutionary science which has led to a prize, medal or award must (on general theoretical principles [11]) have been supported by a very much larger and more complex system of revolutionary science comprising numerous people and institutions.

So, the NFLT metric will intrinsically register many ‘false negatives’ and systematically under-estimates the scale of revolutionary science. Despite this, the NFLT metric seems to have value, since these prizes apparently have a low false positive rate: impressionistically and anecdotally, the great majority of winners seem thoroughly to ‘deserve’ to win for their research, which has indeed been revolutionary in the sense of changing the direction of science.

It seems unlikely that scientists are frequently, primarily and specifically motivated to do high quality revolutionary science by the prospect of winning a Nobel prize or one of the other high medals and awards – although many would no doubt day-dream about the possibility. Indeed, there is vast variability in the personality types of scientists and their motivations. Rather, Nobels and the like can be seen as providing an after-the-fact identification of some of the clearest and best-validated examples of revolutionary science.

The NFLT metric can therefore be seen as analogous to a ‘top-down’ macroeconomic quantitative variable, such as national taxes and interest rates. Such a variable may have value for monitoring, evaluation and policy; but does not necessarily have a close relationship to individual motivations and behaviors [1]. The NFLT metric is suggestive, but its validity needs to be established by further empirical studies.

Acknowledgement: thanks to Jonathan Rees and Peter Andras for helpful comments.

References

1. Charlton BG, Andras P. Evaluating universities using simple scientometric research output metrics: total citation counts per university for a retrospective seven year rolling sample. Minerva, in the press.

2. Charlton BG. Why there should be more science Nobel prizes and laureates - And why proportionate credit should be awarded to institutions. Medical Hypotheses, in the press.

3. Charlton BG. Scientometric identification of elite ‘revolutionary science’ research institutions by analysis of trends in Nobel Prizes 1947-2006. Medical Hypotheses, in the press.

4. International Mathematical Union. Fields Medal. www.mathunion.org/Prizes/Fields Accessed 19 December 2006.

5. Shanghai Jiao Tong University: Institute of Higher Education. Academic Ranking of World Universities 2006. http://ed.sjtu.edu.cn/ranking. Accessed 14 December 2006.

6. Lasker Foundation. Former winners – Clinical Medical research. www.laskerfoundation.org/awards/all_clinical Accessed 19 December 2006.

7. Association for Computing Machinery. A. M. Turing Award. http://awards.acm.org/homepage.cfm?srt=all&awd=140. Accessed 19 December 2006.

8. Shelton, RD, Holdridge, GM. The EU-US race for leadership of science and technology: Qualitative and quantitative indicators. Scientometrics 2004; 60: 353-363.

9. Andras P, Charlton BG. European science must embrace modernization (Correspondence). Nature. 2004; 429: 699.

10. Charlton B, Andras P. Oxford University's research performance (four articles published in Oxford Magazine during 2006). www.hedweb.com/bgcharlton/oxmagarts. Accessed 14 December 2006.

11. Charlton B, Andras P. The modernization imperative. Exeter, UK: Imprint Academic, 2003.

Bruce G Charlton MD

Editor in Chief - Medical Hypotheses

Newcastle University

NE1 7RU

e-mail: bruce.charlton@ncl.ac.uk

***

Editorial – Medical Hypotheses - in the press

Measuring revolutionary biomedical science 1992-2006 using Nobel prizes, Lasker (clinical medicine) awards and Gairdner Awards (NLG metric)

doi: 10.1016/j.mehy.2007.01.001

Summary

The Nobel prize for medicine or physiology, the Lasker award for clinical medicine, and the Gairdner international award are given to individuals for their role in developing theories, technologies and discoveries which have changed the direction of biomedical science. These distinctions have been used to develop an NLG metric to measure research performance and trends in ‘revolutionary’ biomedical science with the aim of identifying the premier revolutionary science research institutions and nations from 1992-2006. I have previously argued that the number of Nobel laureates in the biomedical field should be expanded to at least about nine per year and the NLG metric attempts to predict the possible results of such an expansion. One hundred and nineteen NLG prizes and awards were made during the past fifteen years (about eight per year) when overlapping awards had been removed. Eighty-five were won by the USA, revealing a massive domination in revolutionary biomedical science by this nation; the UK was second with sixteen awards; Canada had five, Australia four and Germany three. The USA had twelve elite centres of revolutionary biomedical science, with University of Washington at Seattle and MIT in first position with six awards and prizes each; Rockefeller University and Caltech were jointly second placed with five. Surprisingly, Harvard University – which many people rank as the premier world research centre – failed to reach the threshold of three prizes and awards, and was not included in the elite list. The University of Oxford, UK, was the only institution outside of the USA which featured as a significant centre of revolutionary biomedical science. Long-term success at the highest level of revolutionary biomedical science (and probably other sciences) probably requires a sufficiently large number of individually-successful large institutions in open competition with one another – as in the USA. If this model cannot be replicated within smaller nations, then it implies that such arrangements need to be encouraged and facilitated in multi-national units.

***

I have previously argued that Nobel prizes (and other similar international awards and medals) may be used in scientometrics to measure research performance and trends in ‘revolutionary’ science [1]; with the aim of identifying the premier revolutionary science research institutions and nations [2].

Nobel prizes are typically awarded for theories, technologies and discoveries which have changed the direction of a science. By contrast, most successful scientific research is 'normal science' which represents a more incremental improvement on already existing work: normal science takes science further in an established direction rather than starting a new direction [1,2,3].

Biomedical research currently constitutes the dominant world science in terms of volume, funding and prestige. I have argued that the number of Nobel laureates in the biomedical field (ie. the prize in physiology or medicine, and sometimes chemistry) should therefore be expanded from the current maximum of three to a minimum of six, preferably nine, per year to recognize this dominance [2].

In the following analysis, I have attempted to predict the possible results of such expansion by creating a metric from Nobel prizes in physiology/ medicine [4] and adding two other prestigious awards: the Lasker award for clinical medical research and the Gairdner international award; over a fifteen year time span of 1992-2006 inclusive.

The NLG metric

I recorded the national and institutional affiliations of Nobel laureates who received the prize for medicine or physiology during the period 1992-2006, affiliations were allocated for the time laureates received the prize [4]. Lasker and Gairdner awards were likewise noted for that period.

The approximately-annual Lasker Award for clinical medical research recognizes up to three scientists whose work pioneers a major improvement in clinical management or treatment [5]. Unlike the Lasker award for basic medical research, which frequently predicts a Nobel prize in Physiology/ Medicine, the clinical medical research award does not frequently overlap with the Nobel prize. The Gairdner International award [6] is given to about six outstanding biomedical scientists per year, so the Gairdner award contributes about half the weight to this metric.

My impression is that early Gairdner awards considerably over-represented Canada (the award is administered from Toronto), and even now this probably still remains a small bias because Canada got five Gairdner awards (from the sixty-two included in this analysis) from 1992-2006, but no Nobels or Laskers. Therefore I restricted this analysis to the past 15 years when the Gairdner seems to have functioned as a more validly ‘international’ award for merit. I also considered including in the revolutionary science metric the one-winner-per-year Lasker award for basic medical research, but there were was such a high degree of overlap with the Gairdner award that this was omitted for the sake of simplicity and clarity.

Credit for the prize or award was given to the institution and nation to which the winner was affiliated at the time of the award (except where it was clear that the winner had moved in the past few months while awaiting the award). It would certainly be more valid to award credit to institutions and nations on the basis of where the prize- or award-winning research was actually accomplished, and I hope that future researchers will be able to do the investigative work needed to accomplish this.

Each individual scientist was counted only once, because a scientist who won more than one of these prizes and awards was credited for just one on the assumption that the Nobel is senior to the Lasker, and the Lasker is senior to the Gairdner. Credit for the prize or award was therefore given to the institution or nation to which the winner was affiliated at the time of the senior award or prize. Sometimes a Lasker or Gairdner award winner had also received a Nobel prize for chemistry (rather than medicine/ physiology) – such individuals affiliations were allocated for the time of winning either the Lasker or Gairdner.

This process created a pool of one hundred and nineteen winners, which (over fifteen years) represents an average of about eight winners per year – about the number of annual laureates I recommended for the Nobel prize in medicine. As in previous analyses [7,8] I set a minimum threshold of three prizes or awards before an institution or nation qualified as a centre of revolutionary science, on the basis that one or two might be luck or coincidence, but three prizes/ awards probably indicates systematic strength.

Measuring revolutionary science by counting such rare and highly-selective prizes and awards, and also of setting a minimum of three prizes and awards before a nation or institution registers as a significant centre, means that the NLG metric inevitably generates many false negatives. It must be presumed that many valuable centres of revolutionary science are not picked-up by this metric.

However, for the same reasons, the NLG metric is unlikely to generate many false positives; and the listed centres of revolutionary biomedical science can be assumed to deserve their elite status with a high degree of confidence - subject to the above caveats about the method of counting affiliations at the time of winning, rather than accomplishing the work which led-to winning.

Table 1 – Number of Nobel, Lasker, Gairdner (NLG) winners 1992-2005 by nation.

USA 85

UK 16

Canada 5

Australia 4

Germany 3

A minimum of three winners is required for inclusion as a centre of revolutionary biomedical science.

***

Table 2 - Number of Nobel, Lasker, Gairdner (NLG) winners 1992-2005 by institution (all institutions are in the USA, excepting Oxford).

MIT 6

University Washington, Seattle 6

Caltech 5

Rockefeller University 5

NIH 4

UCSF 4

University Pennsylvania 4

Yale 4

Columbia 3

Fred Hutchinson CRC, Seattle 3

Johns Hopkins 3

Washington University, St Louis 3

University of Oxford (UK) 3

A minimum of three winners is required for inclusion as a centre of revolutionary biomedical science. UCSF = University of California at San Francisco; CRC = Cancer Research Center.

NLG metric National and Institutional analysis

The NLG metric national distribution reveals a massive dominance of the USA in revolutionary biomedical science, confirming the previous results of US domination for revolutionary science generally, and provides further confirmation of a trend that this US domination may be increasing [7,8]. The UK is a clear second, with a number of prizes and awards that is broadly in proportion to the population difference between the UK and the US. Canada, Australia and Germany also feature (although I am suspicious that Canada only qualifies by winning the Canadian-administered Gairdner award).

The finding of overwhelming US domination is particularly interesting when contrasted with the probability that the ‘rest of the world’ is probably catching-up with the USA in terms of ‘normal science’ metrics (with these metrics presumably dominated by biomedical research) such as numbers of publications and citations. For instance, the European Union nations and China, and some smaller far eastern nations (eg. Taiwan, Souh Korea, Singapore), are probably increasing normal science production faster than the USA [9,10]. The implication is that only the USA has a research system which actively supports revolutionary science at the highest level [7,8].

The University of Washington at Seattle comes joint-top of the league table for revolutionary biomedical science (with MIT) which may surprise those observers who have failed to notice the rise to international prominence of this institution [7]. In a separate analysis of total Web of Science citations per US university, we also found that University of Washington was ranked fourth (after Harvard, Johns Hopkins and Stanford) [3]. So the clear implication is that University of Washington at Seattle should now be considered one of the truly elite research universities of the world, and that its pre-eminence is probably focused in biomedical science. Something similar also applies in relation to UCSF (University of California at San Francisco) [8]. It was also surprising to see the great strength of MIT in biomedical science, when this institution has traditionally been associated more with the physical sciences (and economics); and something similar applies to Caltech (joint second place) – which, unlike MIT, has no medical school.

Perhaps even more startling was the failure of Harvard to reach the threshold of three winners required in order to feature on this league table. During 1992-2006 Harvard achieved only two Gairdner awards and neither a Nobel prize for medicine nor a Lasker award. This confirms the relatively poor showing of Harvard in my previous analyses of performance in revolutionary science such as Nobel trends from 1947-2006 [7], and the analysis for the past 20 years which includes Fields medals, Lasker awards and Turing awards [8].

Yet during the past three decades Harvard has massively dominated all other institutions in the world in terms of scientific research production such as numbers of papers published and number of citations earned ([3], and unpublished results from Web of Science by Peter Andras and Bruce G Charlton, Newcastle University, UK). Also Harvard has topped the authoritative Shanghai Jiao Tong university table of world universities by a large margin since its inception in 2003.

My interpretation of this overall picture is that, over recent decades, Harvard has failed to orientate its priorities towards the cutting-edge of the major dominant branch of world science. The institution has clearly been successful in maintaining massive productivity in very high quality ‘normal science’; but apparently has not encouraged the much riskier endeavours in the type of revolutionary biomedical science which wins major prizes, medals and awards.

Revolutionary biomedical science outside the USA

The University of Oxford is the only institution outside of the US which has won three prizes or awards in the past fifteen years and thereby ranks as a major centre of revolutionary biomedical science. This good performance of Oxford is in-line with that university’s increasingly emphasis on science (probably especially medical science) over recent decades, and its catching-up with its UK rival Cambridge and also with the US ‘Ivy League’ in terms of science production [11,12].

In the UK the other thirteen prizes and awards (outside of Oxford) are scattered across nine different institutions, so that less than twenty percent of UK NLGs were won by significant UK centres of revolutionary bioscience. This contrasts with the US picture where more than fifty percent of NLGs (fifty awards and prizes out of eightyfive) were won at major research institutions – representing a greater concentration of high level revolutionary science activity. This may well represent the evolutionary emergence of a separate research system of ‘pure medical science’, as we have previously advocated [13].

Due to the limitations of the Gairdner award more than fifteen years ago, I am unsure of the long-term UK trend in revolutionary biomedical science; but given that the UK seems to be declining as a centre of revolutionary science-in-general [7] it seems a plausible hypothesis that the US dominance in revolutionary science is a consequence of having revolutionary science concentrated in a relatively large number of individually significant and successful institutions. Furthermore these elite US institutions are apparently in competition as judged by the rise to prominence of the University of Washington at Seattle and UCSF, and the decline of Harvard. Moreover, this is apparently an open competition since it has enabled new entrants to this status as well as relegation from this status.

However, it must be remembered that the NLG only measures the visible and most fully-validated tip of an iceberg of revolutionary science. These prizes and awards credit successful revolutionary science which has changed the direction of a discipline in a big way, and where credit for this can be allocated to a single person or a few individuals. It is almost certain, on general theoretical grounds derived from complex systems theory [14], that the process of generating major breakthroughs in revolutionary science must be supported by a much larger submerged base of revolutionary science research which is harder to identify with confidence, and where credit for achievements is more diffused between individuals.

The possible lesson for countries outside the US may be that long-term success at the highest level of revolutionary biomedical science (and probably other sciences) may require a sufficiently large number of sufficiently large and individually-successful institutions in open competition with one another. If this model cannot be replicated within smaller nations, then it implies that such arrangements need to be encouraged and facilitated in multi-national units, such as the European Union.

Acknowledgement: Thanks are due to Peter Andras whose conversation and collaboration fuelled this work.

References

1. Kuhn TS. The structure of scientific revolutions. Chicago: Chicago University Press, 1970.

2. Charlton BG. Why there should be more science Nobel prizes and laureates - And why proportionate credit should be awarded to institutions. Medical Hypotheses, 2007; 68: 471-3.

4. Nobel Foundation. Nobel prizes. http://nobelprize.org/nobel_prizes. Accessed: 5 January 2007.

5. Lasker Foundation. Former winners – Clinical Medical research. www.laskerfoundation.org/awards/all_clinical. Accessed 5 January 2007.

6. Gairdner Foundation. Awardees. www.gairdner.org/winners. Accessed 5 January 2007.

7. Charlton BG. Scientometric identification of elite ‘revolutionary science’ research institutions by analysis of trends in Nobel Prizes 1947-2006. Medical Hypotheses, in the press. do:10.1016/j.mehy.2006.12.006

8. Charlton BG. Which are the best nations and institutions for revolutionary science 1987-2006? Analysis using a combined metric of Nobel prizes, Fields medals, Lasker awards and Turing awards (NFLT metric). Medical Hypotheses, In the press, doi:10.1016/j.mehy.2006.12.007

9. Shelton, RD, Holdridge, GM. The EU-US race for leadership of science and technology: Qualitative and quantitative indicators. Scientometrics 2004; 60: 353-363.

10. Ping Z, Leydesdorff L. The emergence of China as a leading nation in science. Research Policy 2006 35: 83-104.

11. Charlton B, Andras B. Oxbridge versus the ‘Ivy League’: 30 year citation trends. Oxford Magazine 2006: 255: 16-17. Available at: www.hedweb.com/bgcharlton/oxmagarts. Accessed 9 January 2007.

12. Charlton B, Andras P. Best in the arts, catching-up in science – what is the best future for Oxford? Oxford Magazine 2006; 256: 25-6. Available at: www.hedweb.com/bgcharlton/oxmagarts. Accessed 9 January 2007.

13. Charlton BG, Andras P. The future of 'pure' medical science: the need for a new specialist professional research system. Medical Hypotheses. 2005; 65: 419-25.

14. Charlton B, Andras P. The Modernization Imperative. Exeter, UK: Imprint Academic, 2003.

Bruce G Charlton MD

Editor-in-Chief – Medical Hypotheses

Newcastle University

NE1 7RU

2006-12-12T16:35:00.000Z

PSY 3007 - Abnormal Psychology and Psychiatry - complete lecture notes

Abnormal Psychology and Psychiatry – Lecture 1

Core texts:
- Psychiatric Drugs Explained – David Healy
- Psychiatry and the Human Condition – etc www.hedweb.com/bgcharlton
- Texts of psychiatry and abnormal psychology
- www.mentalhealth.com
- Google and PubMed
*****

Emotion
Lecture is a general model of an important psychological mechanism of psychiatric symptoms - and a powerful way of conceptualizing drug actions

My website
– Psych and the HC esp - Awareness, consciousness and language;
– Idea of Antonio Damasio

Problem of psychiatry – understanding how drugs interact with behavior. How can eating chemicals make you feel better, function better?

Basic model of cognitive psychology
Brain as information processing device - input/ process/ output.
Brain states many represent perceptions of external environment - eg vision, hearing, touch, smell, taste - so that (for eg.) patterns of nerve activation represent particular aspects of the visual scene. - outside the body.
But emotions represent body states. i.e. Emotions are patterns of nerve activation in the brain that represent the internal environment.
Emotions probably correspond to characteristic body states as they are sensed by the brain.
The brain senses the body by nervous and chemical means - the nerves of autonomic nervous system (the sympathetic and parasympathetic systems), and chemical information is obtained by specialized parts of the brain monitoring the concentration of hormones.
Brain is monitoring the body, continually updated picture of what is going on in the body, and can initiate appropriate behaviors in response to these body states.

What are the emotions?
The number and type of emotions corresponding to body states is not yet known. A good example to understand the cognitive nature of emotions.
One idea, by Ekman, is that emotions correspond to facial expressions - fear, anger, surprise, disgust, happiness/ joy, sadness/ distress. Discuss
But one of the emotions is almost certainly fear. This is relevant to the anxiety based forms of psychiatric illness - Generalized anxiety, phobias, panic disorder and obsessive-compulsive disorder.
Fear is a response mediated by the sympathetic nervous system, it prepares the body for action (fight or flight) - increased heartbeat, faster breathing, increased alertness, blood diverted to the muscles etc.
Fear can be conceptualized as a primary and a secondary emotion.

Primary emotion – Fear could occur in response to a perception, for example the primary emotion of fear in response to seeing a tiger.
Secondary emotion – Fear could occur in response to cognition, in other words thinking about a tiger - in response to modeling in one’s own mind the situation of being attacked by a tiger.
Secondary emotions probably only occur in humans and other animals capable of conscious thought - such as chimpanzees.
· The emotional state/ body state is the same for primary and secondary emotions - however primary emotions are triggered by perceptions while secondary emotions are triggered by cognitive modeling. This explains how emotions can occur even in the absence of stimulus.

Importance of emotions to psychiatry and abnormal psychology
1. Emotions link social behavior and emotions - we use emotions to judge social situations. Emotion and social symptoms are probably the commonest in psychiatric illnesses in general.
2. Emotions provide a model for psychiatric drug actions
Anything which changes the emotional body state, or the brains perception of body state, may affect emotions.
If a drug blocks the physical changes of anxiety, then body state change will be monitored by the brain and reduce the perception of anxiety. Eg diazepam/ Valium relaxes muscles, propranolol slows the heartbeat.

PSY3007-2 – BZs - Benzodiazepines and
SSRIs - Selective serotonin-reuptake inhibitors
· http://www.healyprozac.com/
· Sobo, S. Psychotherapy perspectives in medication management. http://www.psychiatrictimes.com/p990423.html
· My paper and book ‘… and the human condition’, ‘palliative’ also S-DTM paper.

As benzodiazepines were for the 70s and 80s, so the SSRIs are for the 90s and 00s – main class of drugs used to treat anxiety symptoms (and mild depression).
Among the most profitable medications of their era.
Similar trajectory from hyped wonder drug to villain.

Benzodiazepine Anxiolytics
Examples - diazepam (Valium), chlordiazepoxide (Librium) - long-acting; alprazolam (Xanax) - short-acting, clobazam (Frisium) – not-v-sedating.
Benzodiazepines introduced in 1960s as a substitute for the barbiturates: less sedative , less hangover, less addictive, safer in overdosage.

Mode of action
Act to modulate GABA neurotransmitter - major NT responsible for inhibition of neurons.
BENZ may be synthetic equivalent of natural brain chemicals called beta-carbolines.

Clinical Effects -
1. Subjective - soothing, relaxing like alcohol.
2. Anti-anxiety - especially when anxiety due to muscle tension
3. Muscle relaxation - diazepam is one of the best muscle relaxant drugs, used for spasm and spasticity.
4. Sedative - usually produces sleep in high enough doses - but variable between individuals. Some are not sedative - eg clobazam (Frisium).
5. Anti-convulsant - used in treatment of acute epilepsy and in withdrawal of alcohol or heroin
6. Control of violent behavior and acute psychosis - eg acute schizophrenia or mania. Usually lorazepam.

SIDE EFFECTS -
Rebound anxiety and insomnia. Quality of sleep is inferior to natural sleep.
Release of violent or antisocial behavior - like alcohol.
Dependence - probably a susceptible minority => < month.
Abuse - especially IV especially temazepam.
Now typically used for short periods, perhaps under-used given comparative safety and pleasantness.

SSRIs
Prozac - fluoxetine; Cipramil - citalopram; Seroxat/ Paxil – paroxetine, Lustral/ Zolofy – sertraline, Faverin/ Luvox – fluvoxamine, .
The only important group of psychy drugs to be discovered in ‘recent’ years (1970s).

Clinical use
Different from benzos - different kind of anxiolysis.
Used in outpatient depression, panic, social phobia and other generalized phobias, OCD, GAD.
Many people have had lives transformed for the better. Others unaffected, others worse.
Misunderstood to be ‘happy pills’ like barbiturates or cocaine - but do not make people euphoric (like BZs can) - almost the opposite.
More like a mild kind of emotional blunting – like a mild neuroleptic – as would be expected from their chemistry. May make people more ‘stable’, emotionally more robust/ less strongly emotional.
Therefore may make people more sociable, less shy, less prone to downward mood swings - but some people may also or instead feel that mood upswings are impaired.
Or, emotion-blunting, reducing extremes of emotion, hardening of personality – less caring and empathic.
Make some people more cool and sociable and confident; make other people cold, detached and indifferent. May cause break up of relationships – this may be a good or bad thing.
‘Serenic’ agent in some people - demotivating in other people

Addiction or dependence
Not classic ‘addictive’ euphoriant drug like heroin or cocaine.
But SSRIs may produce also dependence (eg paroxetine) – hard to stop taking without side effects.
Dependence may be hard to differentiate from original problem – need trials in normal volunteers. But dependence to SSRIs was noted in healthy volunteers during drug development.
Probably all psychotropic drugs have potential to induce dependence since they are alien substances which the brain and body need to ‘adapt’ to – when withdrawn the system needs to restore equilibrium. Withdrawal symptoms are mainly depression and anxiety.
Sometimes get ‘poop-out’ when drug seems to stop working – may respond to increased dose.

Unwanted side effects
Nausea and vomiting - usually wears off.
Akathisia – agitation and restlessness - rare but serious. Stop drug.
Rarely (< 1:1000) people feel acute mental turmoil, acutely suicidal with bizarre violent fantasies (eg about violent death) – may lead to suicide. Not used in children for this reason

Antidepressant, or anxiolytic
When launched, the benzodiazepines had become very unfashionable, vilified for their addictive and abuse potential. This worry spread to any anxiolytics.
The tendency was to diagnose what would have been anxiety as either depression or specific anxiety disorders such as panic, OCD, and phobias.
Move from early 90s to reduce suicide rates, main ideas was to treat undetected depression, mainly with antidepressants which had been shown to reduce suicide in tricyclic studies of rare moderate to severe hospital depression – the assumption was that this would transfer to common, mild, primary health care ‘depression’ treated with SSRIs.
In fact early, unpublished studies done by pharmaceutical companies tended to show increased rate of suicide on SSRIs – as is now known. Seems confirmed by retrospective analysis – severalfold increase in suicide on SSRIs. But tho’ flagged up more than 10 years ago, still no trials…

Issues raised by SSRIs
· Very widely prescribed but very poorly understood – eg. Why no suicide trial? Sheds light on interaction between marketing and science.
· Used by ‘normal’ people who experience psychiatric symptoms but who do not have a formal diagnosis. Response is very individual - may feel better, worse, or no effect.
· Raise question of ‘cosmetic’ or ‘palliative’ psychopharmacology - availability and mode of prescribing - eg analogies with oral contraceptive pill, or with analgesics.
· Self-treatment eg: Diphenhydramine, Chlorpheniramine, St John’s Wort.
***

PSY 3007-3 Generalized anxiety, Panic & Phobic disorders

REFERENCES
DSM-IV and ICD-10 - http://www.mentalhealth.com

Anxiety is a kind of fear, unpleasant increase in arousal - probably a universal experience - although magnitude is very variable.
A universal biological category, cross-cultural, once of the basic emotions an adaptive response – improves reproduction/ survival: increases arousal.

Hypophobia
? Maladaptive if LACK of anxiety - increase accidents etc. “Hypophobia”, Isaac Marks. Absence of fear of heights in children associated with more serious falls – and instead of developing a fear of heights they are still less afraid of heights as adults.

Evolved fears
Many fears are non-associative/ evolved eg. fear of the dark, of being alone, of strangers – we do not learn these fears – on the contrary we learn to overcome them.
Anxiety disorders may be more a failure to learn to overcome fears, rather than learning of fears.
RG Menzies and JC Clarke evolved fears:
1. danger to species
2. avoidance increases reproductive success
3. under genetic influence

Psychological symptoms - mental anxiety: dread, worry, irritability/ sensitivity, restless, poor concentration. Maybe intrusive and distressing thoughts or impulses
Physical symptoms and signs - Tension - from suppression of action: essentially muscular tension.GI, heart, RS, GU, Neural - ie. Sympathetic nervous system over-activity including adrenal gland hypersecretion.

GENERALIZED ANXIETY DISORDER (GAD)
Used to be termed just Anxiety
Chronic unrealistic or excessive anxiety (about 2 or more themes) - for most of the time and for several months at least. NOT phobic, obsessive, hypochondriac or panic.
The person may have good reason to be anxious, but the anxiety has become maladaptive, prevents them doing anything constructive. Or else the causal problems may be intractable.
Epidemiology - not known ?maybe 5%-ish. Depends on definition - no clear division between those with and those without. Many people self-medicated.

Treatment:
1. Relaxation - especially self-hypnosis, learned muscle relaxation; and Supportive discussion, explanation, advice
2. Cognitive-behavioral - difficult, no specific entry point.
3. Drugs :
· Alcohol (self-medication) - far more dangerous than most of the drugs. Impairs cognitive function and many aspects of performance, causes violence and accidents.
· Benzodiazepines – muscle relaxation, tranquillizing/ calming
· SSRIs - emotional buffering
· Beta-blockers - eg propranolol - peripheral effects, reduce feedback to brain. Unpleasant in high doses.

PANIC DISORDER
Disabling anxiety

Rapid build-up of anxiety
Physical symptoms prominent - palpitations, shaking, nausea
Fear of a catastrophic outcome - heart attack, fit, collapse
?Unpredictable precipitant
Hyperventilation common - feel breathless

Epidemiology- ?c 1.5% prevalence in one year men; 3% in women.

Evolutionary Significance
? Triggering of suffocation-avoidance response
?? Separation anxiety - project with Sarah Matthews - not to avoid danger, but signal for assistance (from family group) like a child.

Treatment
Re-breathing of CO2 (although some claim this is ‘occupational therapy’)
Cognitive therapy - implications of attack (eg. MI, epilepsy) - induce symptoms
Tricyclic antidepressants - usually imipramine (advocated by discoverer of panic disorder - Donald Klein).
SSRIs, Benzodiazepines - eg. alprazolam spec marketed. Promoted along with panic disorder, and to distance from other benz - got licensed for this.

PHOBIC ANXIETY
Anxiety in relation to particular circumstances
Avoids situation
Anticipatory anxiety

Specific/ Simple phobia
eg: spiders, snakes, heights, dentists, flying.
General phobia
· Agoraphobia
· Social phobia

Simple
Treatment - Behavioral Therapy. Utilize habituation by seeking out exposure to stressor, block avoidance activities.
Eg. exposure therapy, graded exposure. Sometimes antidepressants, esp SSRI
Agoraphobia - long lasting may have poor prognosis - nip in bud.

Evolutionary significance
Nature of phobia - fear is best if switched-on at need. Costs and benefits of XS fear. (eg. timid guppies survive in double the numbers as bold ones). Avoidance may be best policy.
But fear that is on average adaptive in ancestral environment may be maladaptive under modern conditions - often understandable in this light. Eg fear of snakes or spiders and social phobia would have been legit under ancestral condits. .
Social Phobia. DSM IV
1. Fear of social or performance situations in which the person is exposed to unfamiliar people/ scrutiny by others. Fears that will act in a way (or show anxiety symptoms) humiliating or embarrassing.
2. May take form of a situationally-bound Panic Attack.
3. The feared situations are avoided or intense anxiety.
4. Avoidance or distress interferes significantly with normal life.
5. Duration is at least 6 months.

Treatment
Probably CBT is treatment of choice
The cognitive component - For example, a person with social phobia might be helped to overcome the belief that others are continually watching and harshly judging him.
The behavioural component of CBT seeks to help people become less anxious in the situations that frighten them. Key element is exposure, in which people confront the things they fear.
The exposure process generally involves three stages. First, a person is introduced to the feared situation. The second step is to increase the risk for disapproval in that situation so a person can build confidence that she can handle rejection or criticism. The third step involves teaching a person techniques for coping with disapproval.
In this stage, one is asked to imagine his worst fear and is encouraged to develop constructive responses to his fear and perceived disapproval.
These stages are often accompanied by anxiety management training -- for example, teaching people techniques such as deep breathing to control their anxiety.
But SSRIs probably commonest (quicker, cheaper) – especially associated with Paroxetine (Paxil/ Seroxat) who got a licence for SP a few years ago and marketed the disease.

PSY 3007 – 4 OCD - Obsessive Compulsive Disorder and PTSD Post-Traumatic Stress Disorder

OCD
Obsessions – cognitive
Subjective unwanted/ distressing/ inappropriate thoughts (alien but recognized as personal)

Compulsions – behavioural
Objective actions - quasi-rituals, performed unwillingly, with anxiety and inner struggles, to get relief from…
Indecisive, cannot take action
Mood state - usually anxious, may be depressed

Obsessions -
1. Thoughts - words, phrases, rhymes
2. Images - eg violent, disgusting
3. Impulses - eg violent, shameful
A fear that they will act on these obsessions

Compulsions - rituals, maybe specific number of repetitions

Epidemiology - c2% population prevalence and 2% chance of having it in lifetime – (unusually) same prevalence in men and women. Same sex incidence implies that it is not a classic ‘anxiety disorder’. Some degree of intrusive thoughts almost universal.

Aetiology (cause)
Unknown, small (5% parents) tendency to run in families
?genetic; some abnormality of serotonergic system of brain.
Prognosis (outlook) - 2/3 improve in a year - but may persist for decades.

Treatments
1. Explanation, reassurance, support…
2. Cognitive-Behavior therapy
Can treat objective compulsions effectively eg rituals by Exposure and response/ritual prevention – eg a patient who fears germy things and washes hands must be exposed to germy things and not wash hands until anxiety subsides. Often relate to invisible (technological) things like germs, gas, minute quantities of poison etc. Learn that feared outcome does not happen.
Less effective for obsessive thoughts. Cognitive therapy (CT), which may be added to E/RP, addresses such things as faulty estimation of danger or the exaggerated sense of personal responsibility often seen in OCD patients.
Thought experiment – patients encouraged to try and do (with mind) the thing they fear (eg harm someone).
Thought stopping – distraction. Think about the intrusive thought in relaxed environment then therapist unexpectedly shouts STOP! – moves to thinking about pre-prepared image. Aim to espablish a connection.
3. Drugs - SSRIs (? Because work serotonin neurotransmitter systems) - clomipramine (tricyclic) also serotonergic. MAOI – eg. phenelzine.

PTSD – Post-traumatic Stress Disorder
Introduced in 1980 DSM III, following return of veterans from Vietnam War. Main similarity is with ‘combat fatigue/ shell shock’.

Diagnosis
1. Delayed/ protracted response to severely stressful or traumatic event (war, disaster, torture, violence, RTA most frequent) – latency of weeks/ months < 6 months
2. Intrusive memories/ flashbacks - Symptoms of re-living (feel real, maybe partial – or images like a movie, maybe when recovering) nightmares
3. Distress at reminding cues
4. Avoidance of possible cues
5. High arousal, hyper-vigilance, low startle threshold, insomnia +/- background of numbness/ emotional blunting

Now NIMH estimate of 4% of adult population at any one time with PTSD (but can occur in all ages).
Twice as many women as men (in line with most anxiety disorders – women have a lower threshold for fear in relation to physical violence/ harm, related to their evolved concern with physical self-preservation).
Higher than population rates of PTSD-like syndromes in combat troops – maybe two or more fold greater – but depends on casualty rate, nature of fighting, duration of fighting, training, leadership
But always a certain percentage of psychological casualties – range between 2 percent and 50 percent.

Conceptualizing cause
Evolutionary perspective Secondary Emotion - Memory for events is laid down with memory of emotions experienced at the time (state-related).
When events are recalled, emotion is re-experienced, re-enacted
When body is in the same emotional state, event-recall may be triggered.

Treatment
Similar to other kinds of specific anxiety -SSRIs,
Mood stabilizers (eg sodium valproate – anti-epileptic) anti-irritability/ anger

Psychotherapy
1. Relaxation training
2. Cognitive therapy: helping to modify unrealistic assumptions, beliefs, and automatic thoughts that lead to disturbing emotions and impaired functioning. For example, trauma victims often have unrealistic guilt related to the trauma
3. Exposure therapy: learning to confront specific situations, people, objects, memories, or emotions associated with stressor
· Imaginal exposure: the repeated emotional recounting of the traumatic memories until they no longer evoke high levels of distress.
· In vivo exposure: repeated confrontation with situations that are now safe, but which the person avoids because they have become associated with the trauma and trigger strong fear (e.g., driving a car again after being involved in an accident) Person learns that the feared situation is no longer dangerous

Evolutionary similarity of OCD and PTSD – learning to avoid harmful situations, and remembering of emotions as well as information. Recall of emotions (secondary emotions) causes emotions to be replayed in the body, re-live the body state of the event remembered. Therefore - Prob OCD and PTSD are extreme and maladaptive versions of normal psychological mechanisms.

PSY 3007 - Lecture 5 Depression, SAD

Listening to Prozac by Peter Kramer
My book and papers on website - www.hedweb.com/bgcharlton esp Malaise Theory of depression

Kraepelin - c 100 years ago divided the functional psychoses between Schizophrenia and the ‘affective’ psychoses, or mood disorders.
Idea that mood is the core abnormality - depression = ‘low’ mood.
Core status of mood is not sustainable. What is mood? - hard to define precisely. Something like average emotional state. The same mood can be produced by many causes - like pain.

Depression
Syndrome – DSM IV Major Depressive Disorder (or Depressive Illness or Melancholia)
Diagnostic Criteria
At least one of the following three abnormal moods which significantly interfered with the person's life:
1. Abnormal depressed mood most of the day, nearly every day, for at least 2 weeks.
2. Abnormal loss of all interest and pleasure most of the day, nearly every day, for at least 2 weeks.
3. If 18 or younger, abnormal irritable mood most of the day, nearly every day, for at least 2 weeks.
At least five of the following symptoms have been present during the same 2 week depressed period.
1. Abnormal depressed mood (or irritable mood if a child or adolescent) [as defined in criterion A].
2. Abnormal loss of all interest and pleasure [as defined in criterion A2].
3. Appetite or weight disturbance, either:
i. Abnormal weight loss (when not dieting) or decrease in appetite.
ii. Abnormal weight gain or increase in appetite.
4. Sleep disturbance, either abnormal insomnia or abnormal hypersomnia.
5. Activity disturbance, either abnormal agitation or abnormal slowing (observable by others).
6. Abnormal fatigue or loss of energy.
7. Abnormal self-reproach or inappropriate guilt.
8. Abnormal poor concentration or indecisiveness.
Also physical symptoms - Patients ‘feel ill’, ‘malaise’ (like flu) fatigue, ‘TAT’ (tired all the time), washed-out, heaviness, aching, headaches and pain in trunk and limbs.
When depression is severe (c 1% diagnosed depression) and associated with sleep deprivation - may develop psychotic features.
Delusions of worthlessness, guilt, sickness, poverty, ‘nihilism’.
Hallucinations - voices of a derogatory, accusatory nature.
Severe slowing of speaking and moving.
Stupor, dehydration, starvation - potentially fatal.

Epidemiology
Prevalence MDD – 5-10 percent – more than 100 fold increase since 1950s
If untreated - cases psychiatrists see usually spontaneously recover within several months, majority have a relapse within 10 years.
Around 10% patients who have serious depression (psychiatric contact) will commit suicide - but suicide rate probably not elevated in primary health care depression.

Aetiology
No single cause, probably many causes and sub-types.
Main theory is some kind of brain deficiency in amines – dopamine, noradrenaline and/ or serotonin.
Life events
Malaise due to immune system activation

Treatments
Supportive psychotherapy/ counselling
Psychological therapies - esp CBT
Drugs - antidepressants – Tricyclics; SSRIs; Monoamine oxidase inhibitors (MAOIs) – phenelzine; other drugs not in these classes - eg trazodone, venlafaxine (effexor); St John’s Wort - Hypericum
SSRIs for milder, outpatient depression/ anxiety - tricyclics for moderate to severe hospital depression.
ECT for severe depression especially with psychotic features or danger of suicide or starvation/ dehydration.

Mechanism
Nowadays more general ‘amine hypothesis’ - 5-HT is the most fashionable cause. Idea of brain deficiency of amine NT, corrected by drugs.
Both tricyclics and SSRIs are amine re-uptake blockers, MAOIs block enzyme that breaks down amines.

Seasonal Affective Disorder – SAD

Eagles JM, British Journal of Psychiatry. 2003; 182: 174-6
Lam RW. Primary Care Psychiatry. 1998; 4: 63-74
www.mentalhealth.com under Cyclothymic Disorder

Winter depression/ blues, linked with treatment with bright light therapy given in the mornings.
Increased incidence of depressive symptoms/ major depressive disorder during winter months (although ‘seasonal’ does allow for other times of the year).

Typical clinical picture varies in severity in a continuum, with symptoms such as:
1. Fatigue & Reduced motivation
2. Excessive sleeping (hypersomnia)
3. Increased appetite (carbohydrate craving) and weight gain
4. Irritable mood
5. Reduced sociability

Some doubt about the validity of this disorder in some quarters, since depressive symptoms are common and by chance could occur in winter. Some people regard it as hypochondriacal. It seems to be completely accepted professionally and socially in high latitude countries such as Scandinavia and Canada/ Alaska.
But SAD has a high level of biological plausibility given the profound effects of light and seasons on animal behaviour and evolution.

Humans evolved in Africa between c30 degrees north and south
Eg. Texas 30 degrees North, Naples 40, Canada 40-50, Newcastle 54, Iceland 65 Arctic Circle 66.5.

Pathology
Main theory is that people with SAD are unable to adapt to shorter photo-period in winter.
Circadian phase shift – daily hormonal and neurotransmitter rhythm gets delayed by late rising and insufficient light.
Some people think this is related to the hormone melatonin XS melatonin (usually suppressed by light).
Other theories relate to serotonin dysregulation – has seasonal variation in normal metabolism.

Epidemiology
Some inconsistencies in literature – often use Seasonal Pattern Assessment Questionnaire (SPAQ) which probably gives false positives.
Prevalence varies from 0-10 percent – worse in winter.
Commoner in women, especially in childbearing years

Latitude
SAD prevalence seems to be associated with latitude.
But relationship between SAD and latitude may plausibly have a threshold, and need not be a straight-line relationship (this seems not to have been taken into account in studies).
Rosen at al (1990) demonstrated a gradient in SAD going up the east coast of the USA from Florida to New Hampshire (27-43 degrees North).
Evidence of acclimatization in individuals and SAD seems worse for people who migrate to extreme latitudes.
Also evidence of longer-term adaptation of populations who have been at extreme latitude for many generations (eg Iceland) – seem to have lower prevalence than otherwise expected for latitude (eg Icelandic Winnepegians versus non-Icelandic. ie. SAD seems to vary by ‘ethnicity’.
This implies some genetic element – and SAD probably heritable.

Treatment
A proportion of people get better with time – c. one third?

Light therapy
Seems very effective, although it is hard to compare with placebo
Indoor lighting c 100-400 lux (evening at home - office)
Outdoor cloudy winter day – 4000 lux
Outdoor bright sun – 40 000 lux plus
Treatment with ‘light boxes’ usually (in trials) 2500 lux for 2 hours/ 10 000 lux for 30 mins.
‘Light visor’ efficacy seems not to benefit from high intensity light - ? close proximity of light source
Dawn simulators go from darkness to c 400 lux.

Administered in the morning – tends to support the idea of circadian rhythm abnormality, since bright light would cause ‘phase advance’ – make circadian rhythm occur earlier in the 24 hour cycle.
Dawn simulation alarm clocks also seem to work (while the person sleeps) – easier to integrate with a normal life (esp with hyper-somnia as a symptom)
Problem of funding trials of non-pharmacological treatments, and blinded controls.
Antidepressants - SSRIS are widely used and may be effective
Or can ‘go south’ for the winter – that works within a few days, but only for as long as you stay, relapse about a week after return…

Normal SAD sufferers
Would expect a continuum, and for this to be shifted by latitude (interacting with other factors such as age and weather).
Leading to ideas for combating this in extreme latitudes – eg brighter lighting in hospitals and workplaces
Outdoor/ bright light exercise is another factor

PSY 3007- Lecture 6 - Tricyclic antidepressants and ECT

Tricyclic antidepressants (name refers to chemical structure).

Imipramine, amitriptyline, clomipramine (mainly serotonin effect), desipramine (mainly norepinephrine effect), lofepramine is probably current favourite due to safety.

Psychological action
Poorly understood, apart from Prozac, drugs are not even well known
Considered generally to be ‘mood normalizers’.
Not tranquillizers, not addictive, not abused, not significantly mood elevating/ euphoriant/ activating.
Supposedly do not significantly affect mood of non-depressed.
Many patients aware only of side effects (sedation, dry mouth, nausea), not the therapeutic effect which is slow and gradual
Perhaps their core action is to treat physical symptoms of depression, not the psychological symptoms - ie affect body primarily, rather than brain (my theory).
Threshold dose in order to be effective, and tricyclics and MAOIs dangerous in overdose

Mechanism
Catecholamine hypothesis 1965 Schildkraut - emphasized deficiency of norepinephrine action.
Nowadays more general ‘amine hypothesis’ – includes 5-HT is the most fashionable cause, or possibly dopamine.
Idea of brain imbalance of NT, corrected by drugs. That certain types of NT are responsible for certain aspects of behavior.
Antidep.s act (but weakly) on receptors in brain.
In many people depression, is a chronic illness, and drugs do not cure it but alleviate symptoms - so drugs may need to continue. Also prone to relapse.

Positive and Negative Affect (ideas of David Watson, U of Iowa)
Positive Affect: Happiness, Interest, Motivation, Alertness, Self-confidence
Negative Affect: Subjective distress, fear, anxiety, irritability, loneliness, guilt, disgust, hostility.

Two kinds of depression:
Both exhibit low mood/ sadness
Depression with loss of energy and motivation, and anhedonia.
Depression with anxiety, guilt, irritability and fear.

Depression with loss of energy best treated with drugs that increase synaptic dopamine/ NE – ie MAOIs such as phenelzine or moclobemide, tricyclics such as desipramine, or other unusual drugs such as reboxetine or more ‘psychostimulant’ drugs such amineptine.
Depression with anxiety best treated with drugs that increase synaptic serotonin – ie. SSRIs

General clinical effect -
Act rapidly on physical symptoms
- improve sleep and appetite reliably,
- analgesic effect
- – treats some unpleasant feelings such as fatigue (‘run down’ ‘tired all the time’), heaviness, dullness, aches.
Act slowly to improve mood - 2-6 weeks.
Tricyclic side effects
- weight gain
- dry mouth, constipation,
- sedation,
- impotence or difficult orgasm
- Dangerous in overdose (not lofepramine).

ECT – electroconvulsive therapy or ECS – electroshock therapy

The History of ECT - Edward Shorter - Psychiatric Times. February 2004
ECT – textbooks
http://www.americanscientist.org search site for ‘fink’
hedweb.com/bgcharlton - delirium and psychotic… anti-delirium theory…

Use of electrical current passed through the brain to induce a ‘grand mal’ general epileptic seizure.

Describe procedure
General anaesthetic – patient asleep
Muscle relaxant – patient ventilated
Application of electrical current via moistened electrodes on scalp
Epileptic seizure usu. tens of seconds
Anaesthetic and muscle relaxant wears off – patient wakes, goes to rest and recover

Describe therapeutic aspect
Is benefit from:
1. epileptic seizure - seizure ‘re-sets’ brain?
2. passage of electrical current - current ‘re-sets’ the brain.
3. Both

Indications
1. psychotic depression
2. mania
3. acute schizophrenia
4. delirium
5. Parkinson’s disease.

Side effects
For about an hour immediately after awakening – ‘acute confusional state’ of disorientation, transient memory loss, and headache. Laying-down of new memory is impaired. Longer term memory problems – but memory problems due to the reason for which ECT is given – eg severe depression, mania etc.
Severity of memory problems is greater with more treatments and less if only one side of the brain is treated (usually R – non-language function).
Learning new information is impaired affected for c. several weeks after ECT course, then returns to normal.
Some patients report subjective LT impairment in memory function especially for events that before ECT (retrograde amnesia) – as if recently laid-down memories were ‘wiped’ by ECT.

Mechanism of action – some theories
Not known – and no accepted theory (not even a false one) – this limits confidence in use.
NT, amine imbalance in some subtle way – or receptor changes?
Hormones – Max Fink suggests hypothalamus releases mixture of hormones
ECT alleviates delirium caused by sleep disruption.
ECT-induced fit may promote natural sleep. Plus electrical current may suppress abnormal brain waves, and allow normal ones to be re-established – analogous to cardioversion.

PSY 3007 Session 7 - Psychological treatments - behavioral and cognitive therapies

References - Textbooks of Clinical Psychology

Many types of psychological treatment for psychiatric illness - including psychoanalysis/ psychodynamic psychotherapy, many forms of ‘counselling’. Often very ambitious, aiming at a profound transformation of personality.
But most of these appear to be elaborate placebos, in that they have no measurable specific effect related to the background theory or training of therapists.
With regard to effectiveness, a professional and trained psychoanalyst, psychotherapist or counselor is no better at treating eg. depression than a randomly selected person.
But also ‘Psychological therapies’ which are distinctive in having underpinning in psychological theories, and evidence for specific effectiveness in specific conditions
These therapies produce, on average, better results than T,D or H when used appropriately.
They tend to be short-term, focused, goal-oriented – not transformative.
The most important are Behavioral Therapy, and Cognitive Therapy - and their combination - CBT.

Behavioral Model and Behavioral Therapy
Theory - Abnormal behaviors are learned via standard learning processes
eg. Classical conditioning, Operant conditioning, Modelling.
Treatment of abnormal behaviors involves replacing them with new behaviors learned by the same mechanisms
In simple words, in BT a person practices doing the kind of things that they fear doing or try to avoid.

· eg Snake phobia - Analyzed in terms of Exposure to stimulus, and response to stimulus.
· Someone sees a snake, becomes anxious, runs away, anxiety is reduced - behavior is reinforced, phobia is maintained.
Behavioral therapy, the idea is that the client learns new behavior, breaks a vicious cycle of maladaptive learning. eg.
Control exposure to stimulus, graded hierarchy of exposure to snakes - systematic desensitization. At each stage in exposure, wait for anxiety level to diminish ‘extinguish’, then move on to next level.
Control response to stimulus - do not run away, wait for anxiety level to subside ‘extinguish’.
Plan of treatment - highly focused, agreed. Agree on exposure hierarchy - think about snake, picture of snake, toy snake, video of snakes, look at tiny snakes, handle tiny snakes…
Exposure in therapy sessions, ‘homework’ (carry pictures, toys of snakes).
Can continue therapy intermittently to maintain gains.

Cognitive Model and Cognitive Therapy
People are regarded as information-processors, as with cognitive psychology.
Emotions and behaviors are a consequence of information processing (perceptions-processing-behavior)
Changing the way you process information can change emotions and behaviors.

CAUSE of symptom: Abnormality is due to maladaptive ways of processing information - misinterpretations.
eg. If I have a headache, then I have a brain tumor.
Negative beliefs schemas - about oneself, about other people, the world.
Schemas are general patterns of interpretations about ‘how things work’.
‘I start well but then fail’,
‘people like me at first then realize I am boring’.

Treatment
· ‘Collaborative empiricism’ - collaborative, worked out between therapist and client, empiricism - things are tried out in sequence to see if they are effective.
· Try to establish the key errors in information processing that lead to low mood. Identification of eg: negative thoughts, triggers, emotions.
· Generate plausible alternative explanations - the client should generate these in a hypothetical spirit.
· Identify and challenge maladaptive processes - rules, assumptions, beliefs.
· Behavioral experiments and monitoring for behavioral change often as homework.

In other words, with CT the therapist rationally discusses patterns of thinking and emotions, and elicits suggestions of alternative plausible more adaptive patterns.

Beck’s Cognitive Therapy for depression (really CBT)
Depression is caused by negative thinking - negative cognitive triad:
1. about oneself,
2. the world and
3. the future .

Unclear how this kind of cognitive abnormality or bias arises – tends to be accepted as the starting point of therapy.
Therapist looks for thinking ‘errors’ (maladaptive habits) –
eg.
· Over-generalization,
· dichotomous thinking,
· mind-reading.
Challenges these errors, usually by asking for justification or critique.
Generates alternatives, usually by asking client to do so, perhaps in a formal way.

Conclusions
CBT - good evidence from treatment trials of effectiveness in depression and other focused conditions (eg delusions).
When it works probably has long-term benefits – claimed to be ‘cognitive re-structuring’, or at least change of habitual style of thinking.
Indeed, Cognitive Therapy is a kind of indirect persuasion or ‘soft sell’ as it is termed in advertising. Guide the client to believe they have reached pre-determined conclusions for themselves, which is more convincing.
But research patients highly selected and relationship between theory, practice and mechanisms of change are not clear - eg cognitive changes occur with antidepressants.

PSY 3007-8 Mania
Muzina DJ et al 2002. Epilepsy Research 50: 195-202

MANIA
Bipolar disorder, manic-depressive disorder.
A long term illness in which person has periods (weeks/ months) being ‘high’/manic and periods being low/depressed
Bipolar refers to these two ‘extremes’

Case history - young adult man or woman, episode in which feels more energy, increased activity, several days without sleep, goes completely crazy and scary, but no insight. Ends up heavily sedated in psychiatric hospital - usually rapid recovery and complete return to normal (though without always getting insight).

Not a concept in common use - nearest would be John Cleese as Basil Fawlty, Robin Williams in Good Morning Vietnam, or Eddy Izzard in full flow.

Manic mood: ‘high’ - elated, irritable, hostile
Core Features of Hypomania (less than mania)
1. Increased energy/ activity - decreased desire for sleep
2. Hyperactivity including over-talkative, racing speech
3. Poor Concentration or Attention
4. Inflated Self-Esteem or Grandiosity
5. Reckless or Impulsive Behavior

Associated: uncharacteristic behaviours
- Economic Problems, impulsivity, novel illegal or criminal behaviour, promiscuity or sexual aggressiveness, physical violence, alcohol/ drug abuse.
React badly to thwarting (humor the manic!)

Several days without any sleep may precede exacerbation to more severe variant of Mania.
Mania is a psychotic illness
Delusions & Hallucinations, (mood congruent)
Grossly disorganized speech or behaviour
Overactivity without treatment (olden days) may lead to exhaustion, collapse, even death.

Prognosis
90 percent chance of further episodes – usually few years between them
c10 episodes in life
Usually full recovery between episodes
But in 5 years maybe 5 percent have died, suicide is common.
Tend to become more frequent with age (rapid cycling)

Treatment
Lithium carbonate
Mood stabilizers – carbamazepine, sodium valproate/ valproic acid
Neuroleptics
Benzodiazepines
BUT – most patients are ‘non-compliant’ - do not take their treatment
Pateints may need supervising/ watching to prevent a breakdown building
NB- antidepressants, especially tricyclics, sometimes seem to provoke mania.

Epidemiology
c1 percent lifetime prevalence – c 10 percent or more in first degree relatives.
Same in both sexes

Cause - probably genetic predisposition (plus acute stress), often runs strongly in families eg Amish, other migrant groups.
c40 percent concordance in MZ twins (but not 100%), c5 percent in DZ twins.
May be some advantages in slight hypomania, commoner in creative types and emigrants.

Insight
Manic patients usually lack insight. Do not feel ill, react angrily to suggestions that they are, will not take treatment, usually require compulsory admission and treatment.
May never admit they have been ill – explain it all as a mistake, a misunderstanding
Usually reluctant to take preventive treatment
Therefore an almost unique disorder in that it is diagnosed on the basis of abnormal behavior as defined by other people
Why such poor insight? Because manic patients often feel good, more energetic, higher self esteem – all subjectively interpreted as a consequence of good health, not of illness.

Treatments of mania
1. Lithium
And a group of anti-epileptic / anti-convulsant drugs
2. Carbemazepine
3. Sodium Valproate/ Semi-sodium valproate / Divalproex sodium/ Valproic Acid
4. Neuroleptics

Lithium
One of the most important psychiatric drugs
An ion, prescribed as a salt - lithium carbonate.
Initially recognized as a calming, or tranquilizing drug - used as a sedative in acute mania. Discovered 19th century lithium water (naturally occurring, eg Perrier, Vichy - used as treatment for gout
Then again discovered mid 20th as sodium substitute in salt-free diets – but caused some deaths so withdrawn.
Cade (Australia) working on urine of manic patients in guinea pigs, found that lithium seemed to protect against toxicity and sedate the GPs. But still problems of toxicity.
Re-launched in 1960s esp by Dane called Schou – with blood level monitoring.

1. Now lithium is used mainly as prophylactic (preventive) for manic depressive illness - prevents recurrences of both mania and depression.
2. Unknown mode of action.
3. Narrow therapeutic range. Ineffective in low doses, toxic in high doses – must monitor blood levels.
4. Dangerous in overdose, toxic to fetus.
5. Often bad side effects - tremor, dry mouth (thirst), weight gain. Seems to make people feel dulled and unresponsive - or they may miss the excitement of mania.
6. Probably, lithium maintenance significantly reduces suicide rate, but withdrawal significantly increases it.
Therefore in 1980s psychiatrists began trying out different type of drugs – the anti-epileptic ‘mood stabilizers’.

Mood Stabilizers
So-called ‘mood stabilizers’ are anti-epileptic drugs used for two purposes. But anti-epileptics don’t help MDD as a class, only certain types - and these seem to operate in different ways.

1. Treatment of manic episodes
2. Prevention of mania +/- Depression in bipolar disorder
3. Reduction of mood swings/ aggression/ irritability

Carbamazepine
Used in controlling aggression and some types of pain syndrome – trigeminal neuralgia.
Mainly effective in controlling mania – probably works as a kind of tranquillizer.
Rare nasty blood side effects
An anti-irritability anti-manic agent – alternative to neuroleptics.

Sodium Valproate/ Valproex/ Valproic Acid
Used in children as anti-epileptic.
Sedative action, useful at controlling and preventing mania – but not depression.
But side effects include XS sedation, fatigue, weight gain, hair loss
A sedative anti-manic agent.

Neuroleptics
Given to control agitated behaviour in acute mania. May also be given to prevent MD episodes, especially mania. Sometimes given by long-acting injections. Increasingly used in children who are increasingly diagnosed as bipolar.

Probably carb, valp and lithium are not truly preventive, but actually acute symptomatic treatments. They are like continuous acute treatment. Analogy: taking paracetamol every day does not prevent paid, but continuously treats pain (if present).
But the sedative action may promote sleep, and prevent the positive feedback cycle that leads from a high mood to full blown manic episodes

PSY 3007-9 - Schizophrenia and Psychotic Symptoms

Sims A, Symptoms in the mind
My book chapter- theory of mind delusions and bizarre delusions

Schizophrenia
The classic form of ‘madness’
Almost certainly not one ‘disease’ with one cause - a collection of diseases that produce broadly characteristic symptoms.
Nature of such diseases may have changed over time – eg. at various points and places in past hundred years mania, delirium from various ‘malnutrition’ diseases, and late-stage syphilis may all have been diagnosed as schizophrenia.

Clinical features
1. Hallucinations - hearing voices, eg. running commentary, voices discussing third person, spoken thoughts
2. Delusions - bizarre false beliefs
3. Thought-disorder - weird illogical, interrupted speech
4. Catatonia - illogical, strange movements
5. Supposedly - Negative symptoms - asocial, lack of drive, blunted emotions. However, these are also side effects of neuroleptic drugs used for treatment – probably negative symptoms are usually iatrogenic.

Epidemiology: c 1 percent of population, usually insidious onset late teens early twenties, both sexes equivalent. Some people say this is similar is all societies, but actually varies several-fold and has different prognosis at different times in history and in different countries today – maybe different mixes of diseases, and different effects of treatment.

Give case history
Chronic, usually progressive with relapses and remissions
May slide down social scale, seldom sociable or creative
Evidence that the prognosis has become worse over recent decades, and is worse in developed countries. This could be caused by changes in the nature of patients diagnosed as schizophrenia (eg that the causes in the past differ from causes nowadays).
Also linked to the increased usage of neuroleptic drugs, and withdrawal from these drugs – both of which may also lead to increased suicide rate in this group.

Treatment –
Acute – as for mania – sedation using benzodiazepines (lorazepam, midazolam) or antihistamines such as promethazine; and neuroleptics/ antipsychotics such as haloperidol or droperidol.

Chronic – Social
Role of CPN.
Hospitalisation, Rehabilitation, Day Hospitals, Supervised Housing.
Neuroleptic drugs (next week). Probably prevents relapse in some people; but stopping them causes relapse in most people.

Causes
Not known, probably because many diseases and many causes
Usually considered to be a brain disease. Suggestion that dopamine activity may be excessive (related to action of neuroleptic drugs and amphetamine psychosis).
Some evidence for genetic transmission, although there is reduced fertility. Maybe a spontaneous genetic mutation or a range of mutations that affect brain in general way.
Some cases may be due to viral infection or trauma when brain is developing.
Some cases may be a dementia-like process.
Almost certainly, schizophrenia is not one thing nor does it have one cause, but is a variety of causes and disease processes with some common features.
Psychotic symptoms
Madness - qualitatively abnormal behavior (either for group, or for that individual).
Disorganised and agitated behaviour without insight.
Reality judgment (‘reality testing’) is significantly disturbed (eg. bizarre/ impossible delusions).
Not understandable from personality and circumstances.
Refers to symptoms such as hallucinations, delusions - also incoherent speech/ thought-disorder.

Hallucinations
Sensory perception when there is no real object to perceive - a false perception (NOT a distortion of a real perception or a misinterpretation). Appears to the patient as a normal sensory experience, indistinguishable from real.
Any sensory modality - hearing, vision, touch, taste, smell.
Occur in schizophrenia, mania, depression, chronic alcoholism, delirium, dementia, also hypnagogic hallucinations.
Depression and mania – auditory, mood congruent themes.
Bodily sensations (heat or cold, touching, fluid inside, tingling, formication). Can be linked to delusions of control - hallucinatory experience and a false belief - sex with both Kennedy brothers all the time.
Delusions of smell or taste - eg smell a poisonous gas or taste a poison, or depressive (rotting, disgusting smell etc).
Delusions
False, unshakeable and dominating idea, out of keeping with personal and cultural background.
Feels indistinguishable from a true belief - only recognized by other people.
Some delusions are primary, apparently not derived from other symptoms.
Others are secondary - ie false beliefs to ‘explain’ hallucinations, or mood changes.
Some delusions are bizarre, others are plausible but untrue.
Some delusions are associated-with, or based-on, illogical reasoning, others occur in context of normal reasoning.
Schizophrenia - delusions typically of ‘self-reference’, usually persecutory, may be bizarre and illogical (budgie).
Depression and Mania delusions are mood-congruent

Causes?
Unknown – some ideas…
1. Dopamine hypothesis - symptoms may be improved by neuroleptics. But this may instead merely suppress behaviour in response to symptom; change attitudes to hallucination – indifferent to them.
2. Auditory hallucinations: Sub-audible vocalizations (whispering). Sometimes can record with throat microphone.
3. Auditory hallucinations (Despite definition) may involve misinterpretation of environmental sounds (eg TRESS repeated) - May be suppressed by other noise (Walkman) or earplugs.
4. Delusional disorder - delusions of persecution, jealous delusions of sexual infidelity - Charlton ‘theory of mind’ delusions - mistaken inference about the intentions of others plus vulnerable personality - eg low self-esteem and jealousy. Implies treatment by rational persuasion – CBT etc.
5. Charlton & Kavanau - hallucinations and delusions caused by delirium secondary to sleep disturbance - ie all hallucinations may be ‘hypnagogic’ - like ‘waking dreams’. May be treated with sedation to allow sleep, perhaps ECT for severe cases.
6. Bentall - that hallucinations caused by faulty judgement of the origin of perceptions. Meta-cognitive ability to discriminate self generated from external sources of information.
7. Bentall has suggested that in patients with persecutory delusions there may be faults in reasoning - eg. tendency to jump to conclusions based on insufficient evidence. Fits with fact that some delusions can be improved by cognitive-behavioral therapy.

PSY 3007 - 10 Neuroleptics

Whitaker R. The case against anti-psychotic drugs. Medical Hypotheses 2004; 62: 5-13.
Charlton BG – book and neuroleptics papers.

Neuroleptics - major tranquillizers, anti-psychotics
eg chlorpromazine (first), haloperidol (strongest), clozapine (atypical)
Used mainly to suppress psychotic, aggressive or in some way socially inappropriate behaviour.
Most associated with treatment of schizophrenia, both acute treatment of breakdowns, and chronically in order to prevent further breakdowns.

Behavioural control
Before neuroleptics behaviour was controlled – in psychosis and otherwise – using sedative drugs such as bromide, barbiturates, paraldehyde, and antihistamines.
These made patients sleepy – less motivated to be violent etc. Aslo, sleep may have a therapeutic role, especially if sleep deprivation has been a causal factor in producing the symptoms.
Sedatives may induce dependence, barbiturates were addictive.
Related sedative anti-histamines available OTC for anti-emetic, anti-allergy, cough suppressant, or as hypnotics or anti-histamine eg. promethazine/ Phenergan, trimeprazine/ Vallergan, diphenhydramine / Nytol & Benylin.
Neuroleptics discovered – some were sedative, but they controlled behaviour even when the sedation had worn off, and some were not sedative but still apparently ‘calmed’ agitation.
Sedation still remains a very important mode of controlling behaviour – most acute patients continue to receive eg benzodiazepines or sedative anti-histamines, or modern very sedative ‘atypical’ neuroleptics.
But the discovery of neuroleptics brought something new to behavioural control

Discovery of neuroleptics
Manufactured from antihistamines – promazine modified with addition of a chlorine to make chlorpromazine – the first neuroleptic.
Discoverers were French: Delay, Deniker, Laborit - generally consider major therapeutic breakthrough, but no Nobel, mainly due to disputes between discoverers.
Synth 1950, given to humans 1952.
Rapidly spread to be vastly prescribed and profitable – sometimes every patient in a massive hospital would be tried on it/.
‘Neuroleptic’ means ‘nerve-seizing’ – seizes and holds the nervous system in a constant state, ie. blunts emotions

Major therapeutic effect of neuroleptics
1. Induces state of psychic indifference (tranquillization) by blunting of emotion (neuroleptic).
2. Anti-agitation - not getting worked up (rather than getting sedated-down towards sleep)

But not truly ‘Anti-psychotic’, when used for treatment of hallucinations, delusions, thought-disorder. Usually stops people responding to psychotic symptoms, making them ‘indifferent’ to symptoms, rather than actually alleviating the psychotic symptoms.

Clinical uses
Used in schizophrenia, mania, psychotic major depressive disorder, agitation from any cause, and to suppress undesired behavior in demented and deliriuous old people – eg elderly homes, and in non-psychotic violent people eg. in prisons.
May be given as a long-acting depot injection. Various formulations – some work for c 3 days others for about a month.
In very high doses – produce immobilization – ‘chemical straitjacket’ (but inner turmoil).

General view - neuroleptics suppress symptoms, do not cure disease.
Patients who take the drugs ‘cleverly’ (as required) feel better and do not suffer any more hospital admissions.

Side effects
Dysphoric – make people ‘feel bad’, patients hate taking them – not abused. Negative symptoms - demotivation, loss of enjoyment, lack of energy and drive.

Akathisia – inner turmoil, restlessness and agitation
Generate abnormal movements – Parkinson’s disease or Parkinsonism – tremor, difficulty in moving etc. Behavioural control effect is dose related and related to dopamine blocking potency. Cannot get benefits without side effects.
Indeed, essentially neuroleptics control behaviour by inducing Parkinsonism which includes emotional blunting and indifference. By inducing indifference people are less motivated to behave, general reduction in motivation and drive affects both pathological psychotic symptoms and normal human motivations.
Long term high dose use may create a permanent kind of Parkinson’s disease termed Tardive Dyskinesia may be permanent – presumably due to toxic effect on nerve cells.
Dependence with long term usage, so that it may be difficult to stop taking the drug without provoking an agitated psychotic breakdown. More prone to relapse than if hadn’t taken them in the first place – probably major factor in worse outcome of ‘schizophrenia’ in modern societies – neuroleptic damage and dependence.

Atypical Neuroleptics
Fewer Parkinsonian effects, weaker neuroleptics
Weight gain – diabetes and similar disorders
Sedation
Increased death rates from variety of causes including diabetes

Mechanism of action
Dopamine blocking by neuroleptics – reduces drive and emotional responsiveness - libido.
Act on basal ganglia – control of emotions and fine muscular coordination
Atypical neuroleptics clozapine, reserpine, olanzepine.
Different chemical mode of action - also act on blocking serotonin - 5-HT2 receptors - esp clozapine and the atypical neuroleptics. Serotonin receptor blockade seems to be related to sedation and weight gain.

Future?
For many decades have been regarded as one of the major therapeutic breakthroughs ever. But arguably neuroleptics overall do much more harm than good.
The behavioural control effect seems to be achieved by making patients Parkinsonian, indifferent and demotivated. Achieves its social goal, but for the individual emotional blunting and dysphoria may profoundly reduce the quality of life. If patients then become dependent then the situation may be permanent.

Conclusion - ?
Minimize neuroleptic prescription except as a last resort.
Use sedatives and seek alternative substitutes.

2006-08-08T08:40:00.000+01:00

The loneliness of the highly-educated, high-status career woman in the 21^st century

A recent series of articles in the New York Times has been documenting some aspects of what they term ‘The Gender Divide’. For example, they find that women are outperforming men on average throughout the educational system, some men who lack college degrees are unable to marry, and other men prefer to be unemployed rather than take a low status job. Another aspect is that successful career women are less likely to get married, more likely to marry late, and less likely to have children.

These journalistic observations are highly interesting and relevant, but the socio-cultural explanations offered typically ignore basic evolutionary psychology. The main root of these profound social trends among men and women is quite clear and simple. It is the increasing success of women in the economy acting upon evolved biological sexual preferences. The change in women’s status is primary, and personal problems of both women and men are secondary to this.

In brief, women are mostly attracted by men of higher status than themselves, so high status women are much choosier about who they marry. This generates are two groups who are less likely to marry: high status women and low status men.

Because it is based on evolved preferences, the problem of increasing numbers of lonely, unfulfilled career women and unmarried, unemployed, uneducated men are likely to increase – unless people can understand why this is happening and make rational adjustments to their preferences and behaviour.

***

Women’s economic success and women’s sexual preferences

It is a striking aspect of modern economies that women are being recruited to the workforce in ever increasing numbers. And women increasingly outperform men in modern educational systems. As modern economies value educational skills more than strength, women are occupying ever more high status positions.

This has profound effects on marriage and in the sexual arena generally, because when it comes to sexual attraction, men and women are different. The key difference is that men most value beauty, while women relatively value high status. In a nutshell, the most attractive sexual partners are rich and successful men, and healthy young women. By contrast the least attractive partners are low status men and old, sick-looking women.

The gender differences in sexual attraction are well established by decades of work in evolutionary psychology, originating from researchers such as Don Symons and David M Buss. These preferences are based on fundamental evolutionary considerations – male preferences are for women with the greatest reproductive potential (young and healthy looking women); and female preferences on the advantages of high status partners (eg. good genes, good brains, good immune systems etc.). These preferences have been supported in dozens of empirical studies and found in dozens of culture around the world. Presumably, men genetically-attracted to post-menopausal women and women who deliberately married losers both left behind fewer children, and their genes (and preferences) became extinct.

As the research of Robert Trivers showed more than 30 years ago: in a biological sense, women are the shortage sex. Men compete and women choose.

In traditional societies, only men worked in the economy, and almost all men had a job. In some societies, therefore, almost all men were higher in status than almost all women – so most women would have found almost all men somewhat attractive – even those who had failed in the competition for status. Almost all men could find a women who would marry them.

But in modern societies, women have entered the economy in large numbers, and by now have probably achieved a level of status higher than the average status of men. As women continue to increase in status, fuelled by their educational and economic success, this will automatically reduce the status of most men relative to women, and make men as a whole less attractive. The ‘awfulness’ of modern men is another standard media topic in columns, comedies and drams – this is an accurate reflection of the perspective of the modern career woman. She perceives herself as surrounded by men who are ‘losers’, ‘wimps’ and idiots.

Effects of the increasing status of women

Generally, women will only look for a marriage (or sexual) partner among men of at least the same status as themselves (preferably higher), and as a woman increases in status, there will be fewer and fewer such men around her.

But, as a woman goes through life gathering advanced educational qualifications and then climbing the career ladder, two things are happening – first she is getting older, and second she is attracted to fewer and fewer men (because only the men equal or higher in status attract her). The longer she delays marriage, and the older she gets, the choosier but less attractive she will become.

So, the first major social trend is the loneliness of the successful career women. Increasing status (in effect) reduces her choice of partners. It is not that high status is unattractive in a woman, more than she high status makes her pickier. Of course, if she is very attractive and retains her youthful looks, the career woman may be able to ‘have it all’ in the sense of a stellar career and a husband of high status (there are some famous examples). But if the career woman is less attractive, or gets too old before marrying, she may find herself without much prospect of marriage to someone she herself finds attractive. Her choice is then to stay alone, or to marry ‘beneath’ her, socially.

This is not a problem for the career man, because his increasing status will make him more attractive even though he gets older. Indeed, as a man increases in status, his choice of marriage partners increases – just the opposite to a career women. A 45 year old highly successful man might even be able to marry a 20 year old beauty – indeed this happens quite frequently. But a near-menopausal 45 year old successful career woman is unlikely to be able to marry a 45 year old successful man – because she is in competition with women who are anything up to 25 years younger.

Therefore, in modern society the people left-out of the mating and marriage game tend to be the high status women and the low status men. The low status men might well be pleased to marry the high status women, even if the women are older, because men are less choosy and someone is better than no-one– but usually a successful career woman is simply not attracted by men whom she considers ‘losers’.

Any solutions? It is up-to the career women.

It is possible that current trends will continue. High status women may marry less often, later, and be childless more often – or have very small families. And this may lead to loneliness and frustration. Low status men will suffer similar problems without the consolation of career fulfilment, but with increased possibilities of entertainment and creative activity via cheap communications media such as e-mail mobile phones, and the internet.

One way that career women might diminish their loneliness would be banding together in colonies, rather like women’s residential colleges. These could be places where like-minded women would live in a private by semi-communal life – perhaps easting and socializing together. This might even lead to elective lesbian partnerships.

Alternatively, observation and rational analysis may lead some intelligent women to forgo their potential for education and careers, or delay advanced education and career-building, and instead marry younger and have children. This would be a loss to the national economy, but lead to a gain in personal satisfaction.

In contrast, while women might opt to be less educated, the incentive for low status men is to get as much education as possible – even though they may lack the aptitude or find education unappealing. New ways of educating this low-motivation, low-ability group might be devised.

It is also interesting to speculate as to the extent which understanding their own sexual preferences can lead to women rationally modifying their own sexual preferences. The ideal solution would be if those who are currently left-out of the marriage market could pair-off voluntarily – for the career women to hitch-up with the lower status men.

For example, if high status career women who don’t happen to be unusually beautiful can understand why they have difficulty in finding their ‘ideal’ high status partner, maybe they can compromise and seek a partner among lower status men who display other characteristics that they admire: for example a kind and steady ‘house husband’, a physically-attractive ‘toy boy’, or a man who shares the career woman’s religious or political convictions, hobbies or pastimes.

The key players in this are the career women, because men compete and women choose. Highly educated, high status women are faced with the challenge of career success leading indirectly to lack of personal fulfilment. The first step for them is to understand why this has happened, the second step is to decide what to do about it.

2006-07-11T10:35:00.002+01:00

Why is nobody interested in how the British Empire abolished slavery worldwide?

The (virtual) abolition of slavery was perhaps the greatest moral achievement of humankind, so far. At any rate, I can't think of any superior achievement, and there would be very few people who would openly defend slavery nowadays. Until about the mid 18th century it was universally accepted as an institution, all major civilizations had slaves, and was found in all historically-recorded societies (except simple hunter gatherers). At that point the British Empire was probably the largest slave trading nation (although there was also a huge amont of slave trading in North Africa, magnitude uncertain).

The simplest answer is because most people do not know much about the abolition of world slavery - as I didn't until a few weeks ago when I was reading Thomas Sowell (Black Rednecks and White Liberals). I have since been reading widely to confirm Sowell's arguments and facts - as usual with this scholar, they seem to be correct.

If people do know anything about the abolition of world slavery it is restricted to William Wilberforce and the parliamentary acts in the UK, or black slavery in the USA.

The steps by which slavery was abolished seem quite well established.

1. Around the mid 18th century, English Quakers (Society of Friends) first began to question slavery and decided it was an evil that required abolition. The British were not exceptional in being slave owners and traders - that was universal - what was unique was that the British first decided that slavery was an evil.

2. Late 18th century a group of evangelical protestants in London (The Clapham sect - William Wilberforce being the most famous) began to organize to abolish slavery - initially the tactic was to abolish the slave trade in the British Empire but the goal was universal.

3. Over the next few decades the moral conviction that slavery was wrong spread throughout Britain and became a mass moral movement (a mass pressure-group) leading to a series of pieces of legislation which banned the Slave Trade in the British Empire (1807), then slavery in the British Empire (1833).

4. But that was just the beginning. Making laws does not make it so. The British Empire then embarked upon many decades of of unrelenting pressure to abolish slavery throughout the world - by whatever means necessary: moral persuasion, diplomacy and treaties, and by military force - especially by the Royal Navy.

These decades of effort consumed a great deal of money, and many lives of British sailors, soldiers, missionaries and explorers - as well as slave traders and - tragically - slaves themselves (who were for instance sometimes thrown overboard to drown when slaver's ships were stopped by the Royal Navy - to hide the evidence). But the crusade had massive and sustained support among the British population.

Eventually, the goal was (almost) achieved, and slavery was universally condemned - and (almost) universally abolished.

Why is this successful, heroic and admirable story so little known?

Probably because abolition was initiated by evangelical ('born again') Christians - and these people are not popular among the liberal and leftish commentators who are most-often concerned with issues of slavery nowadays. And - although legislation and treaties were important, and although many abolitionists and abolition societies were pacifists (eg. Quakers) - in practice, world slavery was abolished by coercive force deployed my a major world power. This is an uncomfortable fact for moral activists to swallow.

Probably, the lesson of the abolition of world slavery is one which only relatively tough-minded people wish to take on board. To rid the world of a great evil required a sustained and single-minded moral crusade of a kind which many intellectuals find simplistic and narrow. Maybe slavery could have been abolished without this kind of 'fanaticism' - but in fact slavery was abolished by a kind of moral fanaticism.

To rid the world of slavery also involved military imposition of the will of the British Empire on the rulers of societies who resisted abolition, and who saw nothing wrong in the institution of slavery. Abolishing slavery involved the death and extra suffering of many people of many types. Maybe slavery could have been abolished with less death and suffering, but in fact it was abolished by a kind of 'the means justifies the end' moral reasoning.

Slavery was (mostly, but of course not entirely) abolished as a consequence of the moral conviction of the dominant world power - the British Empire. Critics of other nations, who wished to retain slavery, claimed that the British were hypocritical (in ignoring other major problems of their own - such as the horrendous povery and deprivation caused by indistrialization) and that the British were using abolition as an excuse to pursue their own economic and political interets.

No doubt all of these accusations were true to a varying extent in different times and situations - the British were (like everyone else) hypocrites, and they did turn abolition to their advantage in some ways or even perhaps wherever possible. Nonetheless, it was the British who for more than 100 years kept up the pressure to abolish slavery worldwide, and poured resources into the task until it was all-but accomplished.

The conclusions that I draw from this are:

1. That abolishing a great evil may require a sustained and single minded dedication in mass popular movements that many intellectuals find narrow and simplistic.

2. Abolishing a great evil may require many methods, including the use of coercive force and short/ medium-term sacrifices (including even sacrifice of the group that it is intended to help) to attain long-term goals. Uncomfortable though it is, and open to abuse, we have to accept that the end substanially justifies the means - or else we will probably not attain the end.

3. Abolishing a great evil involves being accused of hypocrisy - and these accusations may be correct. But achieving the primary goal involves sacrifices in secondary goals. It is no doubt desirable that people be morally consistent - but there are worse sins than moral inconsistency. Abolishing a great evil involves focusing on remedying the great evil, but even when the mission is successful it does not abolish all evil. What followed the abolition of slavery was often very bad for the ex-slaves and/or others. Nonetheless, abolishing slavery was a great good.

4. In a nutshell, morality in great things may therefore entail immorality in smaller things. Abolishing world slavery entailed death and suffering of many slaves, and other innocent parties. It also involved the British Empire forcibly imposing its own moral values and laws on other cultures. This is a high risk tactic, it is an argument that can be misused - but it is probably true.

The persistence or resurgence of of slavery in modern life is focused in societies which are isolated from communication with the modernizing world, and the lack of a modern equivalent of the desire, willingness and ability of the British Empire to use whatever means are necessary to abolish slavery wherever it is found.

The lessons of the successful abolition of slavery may apply more generally in the modernization process. For example with respect to abolishing dictatorships and replacing them with democracy. The parallels between the British crusade to abolish slavery and the post 9/11 and emerging US crusade to abolish dictatorships, seem to me very striking. The parallels extend to the kind of people involved in the crusade and their methods, and the people againstof the crusade and their criticisms.

If the similarity with abolition is genuine, this parallel also implies something of the probable nature and duration of the US mission to abolish dictatorships wherever they are found.