Friday, December 23, 2011

The Blue Square Enigma

The diagram below (Figure 33.1) was sent to me by someone with an anagrammatic name. Knowing what nasties can emerge from Pandora’s cyber-box, I never open email attachments from unfamiliar sources. However, I know, also, what a rat smells like, so, for once, I felt confident in taking a risk.

Figure 33.1: The pieces fit, with or without the little blue square. How come?

Copyright unidentified. Fair Dealing asserted.

OK, what do we have? Two identical right-angled triangles, each 13 units by 5. ‘A’ contains four constituent shapes: two dissimilar right-angled triangles (red and dark green) and two L-shaped hexagons (orange and light green), all apparently comprising a precise geometric tessellation.

Now look at ‘B’. Within an identical space are the same four shapes along with an additional one, namely the blue, single-unit square. How can it possibly fit? Surely, the total area of any shape is equal to the sum of its parts. This cannot be true in both cases. Therein lies the rub; and it is, I admit, a pretty neat puzzle.

To find the solution, we must remember that the total area of ‘A’ is equal to that of ‘B’.

Area of a right-angled triangle = half the product of its perpendicular sides = ½(13 x 5) = 32½ units.

Next, we must calculate the area of each constituent shape.

Area of red triangle = ½(8 x 3) = 12 units

Area of dark-green triangle = ½(5 x 2) = 5 units

The hexagons are easy: we can just count the unit squares in each. Thus:

Area of orange hexagon = 7 units

Area of light-green hexagon = 8 units

Therefore, the area of the sum of the parts of ‘A’ is 32 (12 + 5 + 7 + 8) units. As for ‘B’, that of the sum of its parts equals 32 plus one, i.e. 33 units, taking into account the blue square.

Hence, neither in the case of ‘A’ nor ‘B’ does the total (32½ units) equal the sum of the parts. For ‘A’, the sum (32 units) amounts to half a unit less than its total, whereas for ‘B’, the sum (33 units) is half a unit more. In other words, the shapes of ‘A’ are slightly too small to fit the outer triangle, those of ‘B’ marginally too large. Neither represents an exact tessellation, despite appearing as such in the diagram. The truth is that a half-unit (1.5%) area discrepancy can be imperceptible to the human eye. It is, of course, an optical illusion.

My eyes light up at the sight of a puzzle (Figure 33.2). Family and close friends know that, which helped me to point the finger. Besides, my anonymous challenger, your anagram was clumsy. I know who you are. Nice try, though!

Figure 33.2: Feliz navidad a todos. Voy a estar en contacto pronto.

Copyright © 2011 Paul Spradbery

Copyright © 2011 Paul Spradbery

Sunday, December 11, 2011

An Edwardian Memoir


My great-grandfather was the first resident of Wrexham to own a motor car. Born in London in 1871, he had moved north at the age of 16, eventually becoming director of a large Liverpool-based brewery. At 38, he embarked on a two-week cycling holiday in the south of England. His six children, all under the age of nine, remained at home with their mother, who was six months pregnant with the seventh. (In order to absolve him of mindblowing selfishness, let us presume that he employed nannies.)

A summary of the adventure, which I copied verbatim from his original journal, provides a nostalgic view of Edwardian life by an upper-middle-class gentleman.


‘Left Wrexham, 7:12 a.m. train, with bicycle. Broke journey at Birmingham for an hour. Arrived at Warwick about noon. Walked around Warwick and saw castle from river. Weather turned misty, slight rain. Cycled to Leamington Spa, 3 miles. Lunched at hotel near station. Walked in gardens and took waters in Pump Rooms (Figure 32.1). Good roads and very clean town. Cycled to Banbury, saw the ‘Cross’ (Figure 32.2) and market and had tea at the Olde Cake Shop (Figure 32.3). Took 4:35 p.m. train to Oxford. Put up at Dodson’s Hotel (Temperance) near station. Music Hall in evening. Catholic church.’

Figure 32.1: The Royal Pump Rooms, Leamington Spa. At the turn of the 20th century, people would travel many miles to ‘take the waters’ in the belief that the perceived purity would act as a panacea for illness. Today, the building serves as a museum, art gallery, public library and café.

Copyright 1999-2011 The Francis Frith Collection

Reproduced by kind permission

Figure 32.2: Ride a cock horse to Banbury Cross, according to the 18th-century English rhyme

Copyright expired

Figure 32.3: A photograph of the Old Cake Shop, Banbury, Oxfordshire, taken in the 1960s.

Copyright 2004-2011 Banburyshire


‘Walked by river path and then to church 11 a.m. Cycled round city and to luncheon. Cycled in afternoon. Folly Bridge (Figure 32.4) etc.’

Figure 32.4: Oxford’s Folly Bridge is a two-part, stone construction, designed by London architect Ebenezer Perry, and built 1825-7.

Copyright expired


‘Left Oxford by steamer, Salter Brothers’ ‘Henley’ (Figure 32.5). Weather wet. Saw fishing contest 11 a.m. to 4 p.m. Met two Americans on board. Lunched at Wallingford The Lamb (Figure 32.6). Arrived at Henley and stayed at White Hart. Lovely scenery – house boats and riverside. Flowers in profusion.’

Figure 32.5: Salters steamer ‘Henley’, painted by British watercolourist William Matthison (1853–1926).

Copyright expired

Figure 32.6: The Lamb, Wallingford circa 1906. The building now houses an antiques arcade, café and Thai restaurant.

Copyright expired


‘Continued steamboat trip. Weather brighter. Lunched on board. Visited Windsor Castle and St George’s Chapel. Left steamer at Hampton Court and, after leaving bicycle at Parcels Office, caught train to Waterloo arriving about 7:30 p.m. Taxi to Strand Palace Hotel – opened today – full up for one month. Booked room at Faulkner’s Hotel (Figure 32.7), Villiers Street, Strand side of Charing Cross.’

Figure 32.7: Although Faulkner’s no longer graces Villiers Street, London, the building remains a hotel.

Copyright expired


‘Visited St Dunstan’s in the East Church. Person in charge of Registers, Mr W J Lang, was away. Next visited St Mary’s Parish Church, Rotherhithe – no trace of Grandpapa Spradbery’s first marriage. Lunched at Strand Palace Hotel. Spent two hours in Strangers’ Gallery at House of Commons. Just Land Bill discussion in the House. Went to cinematograph entertainment.’


‘Went by Bakerloo to Waterloo and caught train to Hampton Court. Cycled there via Staines, Henley, Windsor, Maidenhead (saw Woolley Hall), Reading where I lunched. Detained over an hour by heavy rain. Cycled via Chatham to Alton, Hants. Put up at Market Hotel (not over comfortable).’


‘Cycled to Winchester, saw cathedral. Romsey (saw Priory) then thro’ New Forest, a delightful ride, beautiful scenery. Saw the ‘Rufus Stone’ (Figure 32.8) and on to Ringwood and Bournemouth, arriving about 7 p.m. Dunstan (brother) had secured rooms at Ferndale Middle Road, Westbourne, comfortable and very cheap. Enjoyed band on pier. Lovely gardens.’

Figure 32.8: The Rufus Stone, in the New Forest, marks the spot where King William II (c. 1056-1100) died during a hunting trip. He was given the name William Rufus because of his red-faced appearance.

Copyright expired


‘Took coach drive thro’ Rhododendron Drive to Cannock Rocks. Afternoon Winter Gardens. Evening church & pier.’


‘Church (a few doors off). Wait with Dunstan, Polly (sister-in-law) and Philippa (niece) to the shore – a lovely walk. Dined with Dunstan and Polly. Cycled to Poole – in morning to Boscombe in afternoon along the cliffs. A beautiful ride.’


‘Went for trip round Isle of Wight in Bournemouth, 2 miles most enjoyable and a beautiful day. Landed at Southsea.’


‘Said farewell to Dunstan and Polly. Cycled towards home via Wimborne, Cranborne, Salisbury (saw cathedral) over Salisbury Plain then Aylesbury up Avon to Hungerford. Put up in Three Arrows Hotel – very comfortable but expensive.’


‘Oxford (called for letters). Saw original picture ‘Light of the World’ (Figure 32.9) by Holman Hunt at Keble College. Banbury, had lunch. Leamington Spa – had a glass of the waters again – Warwick and on to Birmingham about 90 miles in all, arriving about 9 p.m. Put up at Waverley – read Belfast speech*, just delivered at Bingley Hall, before retiring.’

* On the 17th, prime minister Herbert Asquith had spoken on the subject of Irish Home Rule at Bingley Hall, Birmingham. The meeting was for men only. However, two suffragettes climbed on to an adjacent roof and threw slates at the PM’s car.

Figure 32.9: William Holman Hunt (1827-1910), a founder of the Pre-Raphaelite Brotherhood, painted Light of the World at night in a makeshift hut at Worcester Park Farm, Surrey. The original remains at Oxford’s Keble College, where my great-grandfather viewed it, 102 years ago.

Copyright expired


‘Thunderstorm at Birmingham. Delayed me 1½ hours. Had a vile ride from B’ham to Wolverhampton. Roads deplorable for about 15 miles, improving when W’hampton was left – Wellington – Shrewsbury (cycle carnival on) Ellesmere (took wrong road). Sheltered from rain and had wash and enjoyable tea at roadside public house near Ellesmere. Arrived Wrexham about 8 p.m. Machine and self very mud-stained.’

Madonna del Ghisallo would have been proud of him (Figure 32.10).

Figure 32.10: My great-grandfather (seated, left), photographed with his family circa 1946. He lived to the age of 82. (All that cycling ...)

Copyright 2011 Paul Spradbery

Copyright 2011 Paul Spradbery

Monday, December 05, 2011

Come, Eurogeddon, Come

What do former UK prime minister Margaret Thatcher, disgraced Canadian sprinter Ben Johnson and singer-songwriter Morrissey have in common? The link is both tenuous and personal, the date Saturday, 24th September, 1988.

The previous evening, I had arrived in the Scottish border town of Jedburgh and crashed at a friend’s place en route to Durham in northeast England. The Summer Olympics were in full swing, albeit 5,500 miles away in Seoul, South Korea. The nine-hour time difference meant that the Men’s 100m Final – all ten seconds of it – would take place at about 3:30 a.m. British time. We stayed up all night and watched a steroid-fuelled Johnson outrun reigning champion Carl Lewis (and future champion Linford Christie), smashing the world record in the process (Figure 31.1). Ethics apart, it was an unforgettable spectacle.

Figure 31.1: The infamous race in Seoul

Copyright 2007 The New York Times Company

After breakfast, I trudged, red-eyed, to the bus terminal and boarded a National Express coach. Past the stage of wanting to sleep, I spent three hours listening to my Sony Walkman – there were no iPods back then – and reading the Times. The song that always reminds me of the journey is Morrissey’s Everyday Is Like Sunday (Figure 31.2), a soulful 80s classic complete with plaintive melody and evocative lyrics. Who else but Morrissey could have written the words ‘Come, Armageddon, Come’?

Figure 31.2: Morrissey's obra maestra reached number 9 in the UK singles chart

Copyright 1988 EMI Group Ltd

In that day’s newspaper was the fallout from Mrs Thatcher’s seminal speech given to the College of Europe in Bruges the previous Monday (Figure 31.3) (see link below). Her words, which I read on the coach, still resonate:

‘To try to suppress nationhood and concentrate power at the centre of a European conglomerate would be highly damaging and would jeopardize the objectives we seek to achieve. Europe will be stronger precisely because it has France as France, Spain as Spain, Britain as Britain, each with its own traditions and identity. It would be folly to try to fit them into some sort of identikit European personality... We have not rolled back the frontiers of the state in Britain to see them re-imposed at a European level, with a European superstate exercising a new dominance from Brussels.’

Figure 31.3: Thatcher in Bruges – the birth of modern Euroscepticism

Copyright 2008 Bruges Group

Since I read those excerpts, 23 years ago, I have never doubted the wisdom of her warning. As I write, the markets are becoming convinced that the Euro currency is a failure. Many – I among them – would argue that it was ever thus. A few days ago, I decided to throw a firework under the table – or, more precisely, into an English-speaking German newspaper (see link below).

‘The Euro will collapse, possibly even before the end of 2011. Its creation was political and flew in the face of economic fundamentals. The UK learned a bitter lesson in 1992 when it was ejected from the Exchange Rate Mechanism of the European Monetary System. Prior to its de facto expulsion, interest rates had been kept cripplingly (and inappropriately) high in order to maintain an untenable exchange rate. Only when the pound was allowed to find its natural level, by devaluation, did the UK's economic recovery begin. As it was then, so it will be for the stricken Eurozone economies. Then, once the short-term shock subsides, each of the affected nations will, by means of an independent currency and floating exchange rate, be able to determine its own future, free from the Euro straitjacket.’

Then I waited, all of half an hour, for the predictable response.

‘The Euro is not a straightjacket [sic], but rather a part of a political project that has fostered peace and prosperity on the continent - a "guarantee for peace" as Kohl recently put it.’

This is a tired, and quite ludicrous, argument. Peace in Europe does not depend upon the existence of a corrupt, anti-democratic supra-national authority with a one-size-fits-all currency. It never did. Indeed, cordiality between nations could go up in smoke if, for example, Germany succeeds in its attempt to determine fiscal policy in Greece and Italy (Figure 31.4). What right does it have? Besides, the fatal flaw inherent to the Euro was in removing the vital feedback mechanism of exchange rate fluctuation. Moreover, when it was introduced, there was no provision to allow any nation to leave. This was deliberate – and how very devious. It is a straitjacket, but its seams are about to give. ‘Eurogeddon’ is almost upon us, and it will certainly be painful in the short term. Nonetheless, I hope nothing stands in its way. A United States of Europe, the only alternative, would be anything but.

Figure 31.4: Not everyone views German chancellor Angela Merkel as an advocate of European harmony

Copyright 2011 Zeit Online

To paraphrase Morrissey: Come, Eurogeddon, come. I, for one, have waited long enough (Figure 31.5).

Figure 31.5: Crossing Durham's Elvet Bridge – a 22-year-old student with a head full of Margaret Thatcher, Ben Johnson and Morrissey

Acknowledgement: Malcolm Warne, Editor, Durham Times

Copyright 1988 Paul Spradbery

Friday, December 02, 2011

Emperor's New Paintings

One of my forebears, the celebrated Walter E. Spradbery (1889-1969) (Figure 30.1), was listed in Who’s Who in Art. An Official War Artist during WW2 (Figure 30.2), no one, regardless of personal taste, could view his works and deny his immense talent.

Figure 30.1: Walter E. Spradbery, DCM - a gifted artist

Copyright expired

Figure 30.2: Walter's iconic 1944 depiction of post-blitz St Paul's Cathedral, London

Copyright unidentified. Fair Dealing asserted.

In peacetime, Walter designed a number of classic posters for London Transport (Figure 30.3) (see link below). Whenever I am in London, I try to make time to visit the Transport Museum’s shop in Covent Garden, principally to see which of his posters have recently been reissued, but also to peruse other artists’ works. Almost all are skillfully created, some exceptional. My interest in London art is, therefore, more than casual.

Figure 30.3: One of Walter's many classic watercolours

Copyright unidentified. Fair Dealing asserted.

Next summer, London will host the 30th Olympiad. At a time of economic fragility throughout Europe, the event could become anything from a source of future national pride to an economic and cultural disaster. All the more reason, then, for the nation to portray itself artfully. Who could forget Walter Herz’s iconic poster design for the previous London Olympics, held in 1948 (Figure 30.4)?

Figure 30.4: Official poster for the 1948 London Summer Olympics

Copyright unidentified. Fair Dealing asserted.

This year, a variety of esteemed British artists were, according to the BBC, ‘asked to create a work that either celebrated the Games coming to London or embodied the values of the Olympics or Paralympics’. I have reproduced four of them in this article, alongside something my young sons painted (Figures 30.5, 30.6, 30.7, 30.8 and 30.9). In other words, four are by illustrious artists, the other by primary school kids with no discernible artistic talent. Which is which?

Figure 30.5

Figure 30.6

Figure 30.7

Figure 30.8

Figure 30.9

In case you cannot decide:

Figure 30.5: Martin Creed, a former Turner Prize winner, completed his work using only five brush strokes, one for each (apparently random) colour. He claims that it represents an extended podium. Creativity? Effort? Dexterity? Originality? Where? (Copyright 2011 Martin Creed)

Figure 30.6: The contributor, here, is Sir Howard Hodgkin CH, CBE. The BBC states: ‘in the darkest area ... a figure can just about be made out’. This is laughable. If I squint at my wardrobe door, I can make out a smiling face in the wood’s grain, but I would not credit the carpenter with anything other than good craftsmanship. Indeed, visualization of the human form in everyday objects is innate to us all. (Copyright 2011 Howard Hodgkin)

Figure 30.7: Bridget Riley CH, CBE uses parallel lines to indicate ‘the direction of the Olympic swimming lanes or athletic tracks. (She) began her career using only black and white patterns, started to experiment with colour in 1967, the same year she began painting stripes.’ With just a flicker of imagination, she might have included a bend in the ‘track’ or perhaps some demonstration of perspective. Have 44 years proved insufficient time to master such fine skills? (Copyright 2011 Bridget Riley)

Figure 30.8: ‘The large circle in the bottom of Gary Hume's poster represents the wheel of a wheelchair and the smaller circle represents a tennis ball.’ Really? Two dissimilar circles could represent almost anything. (Copyright 2011 Gary Hume)

Figure 30.9: This was produced by my sons, using a pack of felt-tips. It took them about five minutes, while they were watching television. (Copyright 2011 Paul Spradbery)

Perhaps the 2012 Olympic ‘artists’ are secretly laughing up their sleeves, having fooled at least some of their intended audience. At least I hope they are laughing. The alternative is that they, like the naked emperor in Hans Christian Andersen’s fable, are oblivious to their own pretentiousness, which would be mildly disturbing. What I find most depressing, though, is that these worthless daubs are to represent the best of British to the rest of humanity.

I wonder what my illustrious ancestor would think.

Copyright 2011 Paul Spradbery

Monday, November 28, 2011

Prostate Cancer: The Truth


For some of us, ‘Movember’ has been a hairy month (Figure 28.1). The Movember Foundation was set up, in 1999, to draw attention to men’s health problems. Throughout the world, men, including myself, stopped shaving on October 31st and let facial hair run riot. (A friend of mine claims to have grown a moustache in memory of his late grandmother, who, he insists, resembled Magnum PI.)

Figure 29.1: Check out 'No Shave November' at

Copyright 2011 Paul Spradbery

One of the foundation’s main concerns is prostate cancer (PCa), which is the second most common malignancy (after lung cancer) among men in Western Europe. In the USA, it is second to none. The current estimate is that there are more than 20,000 new diagnoses per year in the UK alone (Lane, Strefford & Oliver, 2006, pp. 3-5). Given its approximate population of 60,975,000 (Office for National Statistics, 2009), this level of occurrence implies that approximately 1 in 300 British men will be positively diagnosed within the next decade.

Such high incidence is a recent phenomenon. A three-fold (age-adjusted) increase has been observed over the past 20 years. Despite this, however, mortality rate has remained constant (Cancer Research UK, 2008). Several theories for the sudden increase have been postulated. These refer to both genetic and environmental factors (Ekman, 1999), in addition to changes in detection methods (Tannock, 2002).


Signs and symptoms of PCa are manifold, although the majority of sufferers are symptom-free when the initial diagnosis is made. As a consequence of the periurethral anatomy of the gland, the most common symptom is urethral obstruction, frequently resulting in impaired urinary flow and nocturia. If symptoms are severe, then it is likely that the tumour is well established. Associated spinal or pelvic pain is usually indicative of metastasis (Zisman, Twardowski, Liebovici & Figlin, 2008, pp. 320-322).


Neoplasia occurs as a consequence of DNA mutation. The affected cell then fails to respond to normal stimuli and its progeny proliferate autonomously. Therefore, PCa is, by definition, a genetic disease (Raskó & Downes, 1995, p. 331). Hsing and Chokkalingam (2006) estimated that more than 40% of the associated risk was genetic, caused by genes of both high and low penetrance and, also, gene-gene interactions. Twin studies suggest that this figure is higher than those relating to tumours of the pancreas, stomach, breast and lung (Carpten & Trent, 2008, p. 54).

Some tumours have an inherited predisposition (Strachan & Reed, 2004, p. 488). They can be investigated by examining family histories. Carter (2007, p. 28) reported that the risk of PCa is doubled if an individual’s father or brother are similarly affected, and the probability of monozygotic twins contracting the disease (19-27%) is significantly higher than that for dizygotic twins. Similar conclusions were reached by Parnes, Hoque, Albanes, Taylor and Lippman (2006, p. 378).

Evidence does not, however, suggest that polymorphism at a single locus is responsible for PCa aetiology (Coughlin & Hall, 2002). Research into a variety of genetic markers, including single-nucleotide polymorphisms (SNPs), is ongoing. Most recently, Eeles et al. (2008), Kiermeney (2008) and Salinas et al. (2009) suggested that a combination of SNPs (at 8q24, 17q12 and 17q24.3) was highly significant, particularly when considered alongside family history. It is likely that additional markers will eventually be identified.

Perhaps the most well-researched locus is Hereditary Prostate Cancer I (HPCI) at 1q24-q25 (Klein, 2004, pp. 59-62). However, results regarding its significance are inconclusive (Carter, 2007, p. 28) and, furthermore, there is no evidence that the frequency of the crucial trimeric short tandem repeat (CAG) polymorphism has increased in recent years.

The proven existence of genetic aetiology does not imply that germline mutations have been responsible for recent statistics. (20 years represents barely a single reproductive cycle.) However, modulation of gene expression can result from environmental changes (Waghray et al., 2001) which take place more rapidly. Ornish et al. (2008) studied untreated, low-risk PCa sufferers and detected, using quantitative real-time polymerase chain reaction amplification, 48 up-regulated and 453 down-regulated transcripts following controlled environmental intervention.

Race is another causative factor (Tanagho, Smith & McAninch, 2007, p. 355). Incidence for white men is lower than for blacks but higher than for Asians (Carter, 2007, p. 29). In the UK, for example, net migration has been inward since the mid-1980s. In 2006, it was estimated that almost 20% of all foreign-born UK nationals were Asian, a greater percentage than any other racial group (Somerville, 2007, p. 2). Black Africans, too, have immigrated en masse (Kohnert, 2007, p. 37). Demographic changes of this magnitude could, therefore, have affected PCa incidence either positively or negatively. This factor alone, however, is unlikely to have caused a three-fold increase in such a short period.

PCa incidence rate increases with age. Most significantly, it increases five-fold from men’s late 50s to late 80s (Cancer Research UK, 2008). Moreover, it is higher than for many other sites of primary malignancy (Nelen, 2007, p. 6). As life expectancy in Western Europe increased by 11 years from 1950 to 2005 (World Health Organization, 2008, p. 24), it follows that longevity could be an additional determinant. If men continue to live longer, then the effect will be enhanced.


Many environmental causes of PCa have been postulated. The main categories are diet, lifestyle and pollution (Nelen, 2007, p. 6).

The effect of dietary animal fat dominates research findings. Japanese men consume only half as much of it as do American counterparts, and the former experience significantly less PCa (Carter, 2007, p. 30). However, correlation does not necessarily imply causation. In contrast, though, a diet in which vegetables predominate has been associated with a risk reduction (Chan, Lok & Woo, 2008), as has the inclusion of various vitamins, minerals and antioxidants (Carter, 2007, p. 31). Incidentally, chimpanzees, from which the lineage of Homo sapiens split only a few million years ago, eat mainly fruit and vegetables and do not experience PCa (Coffey, 2001). Again, though, sequence and consequence must not be confused.

Coffey (2001) implicated the recent shift in Western dietary patterns and stated that biological defence mechanisms would evolve too slowly to counteract the onslaught from such rapid change. This view would appear to have merit: the fast-food revolution was a late 20th-century phenomenon (Challem, 2003, pp. 46-47), and fat intake has increased substantially.

In spite of the conclusions of many dietary studies, Pruthi, Swords, Schultz, Carson and Wallen (2009) published current data which cast doubt on the impact of obesity and, hence, high fat intake.

The relationship between PCa and excessive alcohol consumption is contentious. Stanford et al. (1999) and Nelen (2007, p. 6) reported a weak positive association, whereas Lund Nilson, Johnsen and Vatten (2000) stated that there was no effect either way. Given its estimated hereditability of 50-60% (Dick & Bierut, 2006), it would seem improbable that alcohol dependence could produce such a marked increase in PCa incidence.

Carcinogenic effects of several environmental pollutants on PCa incidence have been investigated. For instance, exposure to the heavy metal cadmium has been linked (Timiras & Leary, 2007, p. 310). Sources include food and contaminated water (Agency for Toxic Substances and Disease Registry, 2008). Pesticides and other industrial waste have also been blamed (Puga & Wallace, 1999, p. 287). While it could be argued that industrial processes in Western Europe are more tightly regulated presently than previously, given that cadmium has a biological half-life of 20 years (Friberg, 1983), it would be reasonable to suggest that exposure when young might still have contributed to the development of disease during middle and old age.

Cigarette smoking has also been linked with PCa (Timiras & Leary, 2007, p. 310). However, its prevalence throughout Western Europe has declined within the last 20 years (British Heart Foundation, 2008). This would imply a negligible contribution, unless its effect is either delayed or cumulative — that is, smoking when young causes PCa when much older.

Epidemiological research on migrant populations has been useful when apportioning genetic and environmental contributions to disease incidence. Men from (low-risk) China and Japan, having immigrated to the (high-risk) USA, have been found to have increased rates (Tanagho et al., 2007; Zisman et al., 2008). Furthermore, first-generation migrants have had lower rates than those of subsequent generations (Greenberg, Daniels, Flanders & Eley, 2005, p. 179). These data would emphasize environmental, rather than genetic, causation.


PSA is a prostate-secreted serine protease and the most widely-used PCa marker (Balk, Ko & Bubley, 2003). Serum concentration is, generally, less than 4 ng/ml, but when the gland is either inflamed or cancerous, the value increases (Ellsworth, Wein, Heaney & Gill, 2008, pp. 2-10). This forms the basis for PSA screening.

In the USA, during the late 1980s, a national screening programme began. No such equivalent was introduced in the UK. Hence, cross-sectional transatlantic comparisons could subsequently be drawn. Within a decade, there had been an 80% rate increase among (white) Americans but a far less dramatic rise among Britons (Shibata, Ma and Whittemore, 1998). It was concluded that the sharp increase was caused solely by this new diagnostic test (Amling, 2006). Other populations in Western Europe yielded similar findings (Brewster, Fraser, Harris & Black, 2000).


In order to assess the efficacy of PSA testing, it must, firstly, be acknowledged that PCa progresses slowly and is largely symptomless (Tannock, 2002). Affected men, generally, die with it and not of it (Stamey, 2001).

The test’s sensitivity and specificity are of limited value (Marshall & Bangert, 2008, p. 351). Both false-positive and false-negative results are common (Breskin, 2009). There are multiple causes of elevated serum PSA concentration, including inflammation, benign neoplasms and infection (National Cancer Institute (NCI), 2009). It is also age- and race-dependent. Of further significance is that PCa is frequently detected among men whose serum PSA concentration is below 4 ng/ml (Thompson et al., 2004). Therefore, choice of diagnostic cut-off value has been highly consequential. The more sensitive the test, the greater is the number of false-positive diagnoses. Thus, another possible cause of increased incidence rate is identified.

To compound the sensitivity-specificity dilemma, serum PSA concentration fluctuates physiologically. Causes include sexual activity and, possibly, medical procedures such as cystoscopy and rectal examination (Ellsworth et al., 2008) which are, ironically, carried out to assess prostate pathology (El-Shirbiny, 1994, p. 108). Transurethral resection of the prostate (TURP) involves partial gland removal in order to ease urinary flow (Bupa, 2007). It is carried out frequently to treat benign conditions, and yet, increased treatment has been found to increase PCa incidence (Levy, Gibbons, Collins, Perkins & Mao, 1993; Brewster et al., 2000).

Etzioni, Gulait and Mariotto (2009, pp. 3-13) reported that the introduction of PSA testing has led to an increased detection rate in younger men and at earlier stages of the disease itself. These changes would have had a positive effect on PCa incidence rate.

All such findings have rendered PSA screening controversial. In Germany, Luboldt, Swoboda, Börgermann, Fornara and Rübben (2001) contended that it was ineffective. However, contradictory evidence from the USA has shown that PCa mortality rates have just begun to decline (Bryant & Hamdy, 2009, pp. 15-17). Nevertheless, it is debatable whether sufficient time has passed since the US programme began for it to have produced significant benefit.

Regardless of the intense argument and disputed findings, change in incidence rate depends on the level of uptake of PSA screening which is, in turn, determined by public awareness. In Ireland, Fitzpatrick, Corcoran and Fitzpatrick (1998) claimed that a social divide existed with regard to public understanding of PCa and readiness to undergo medical investigation. This conclusion was endorsed by Rowan (2007) who studied similar effects of social deprivation in England and Wales. It would be logical to suppose that incidence rates would be higher still if men among lower socio-economic classes were as motivated as those belonging to more affluent groups.


Circulatory PSA becomes bound by protease inhibitors. However, some remains unbound as ‘free PSA’ (Balk et al., 2003). A low ratio of free to bound PSA is indicative of PCa (NCI, 2009) and this discovery has been applied to clinical studies. Catalona et al. (1998) demonstrated increased specificity with a negligible reduction in sensitivity. The more this method is used, the more downward pressure on incidence rate might be exerted.

Another recent refinement is the measurement of rate of increase of PSA concentration with time, or ‘PSA velocity’ (Brosman, 2006). One study found that a velocity greater than 0.35 ng/ml/year increased significantly the likelihood of terminal PCa (Carter et al., 2006). However, these data would require confirmation by other studies, and are, in any case, too recent to have had any effect on incidence rates.


Environmental pressures will continue to change with time. Consequently, gene expression will be affected. If, as a result of media coverage, the public concludes that PCa screening is either worthless or potentially harmful, it is conceivable that fewer medical investigations will be carried out. Thus incidence rate might decline. It is clear, then, that increased reliability, of either PSA or a different marker, must be sought.


Substantial evidence has been put forward concerning both genetic and environmental contributions to the recent increase in PCa incidence throughout Western Europe. However, it would be difficult to provide a definitive explanation as to the relative importance of each factor. Probably the most significant change, though, has been the introduction of widespread medical screening. The irony of PSA testing is that it has, undoubtedly, increased the incidence of a disease which is, for the most part, both symptomless and harmless.

Much work remains to be done.

Happy shaving on December 1st.

Copyright 2011 Paul Spradbery


Agency for Toxic Substances and Disease Registry (ATSDR) (2008). Cadmium. Retrieved from the ATSDR Web site:

Amling, C.L. (2006). Prostate-specific antigen and detection of prostate cancer: What have we learned and what should we recommend for screening? Current Treatment Options in Oncology, 7(5), 337-345.

Balk, S.P., Ko, Y.J. & Bubley, G.J. (2003). Biology of prostate-specific antigen. Journal of Clinical Oncology, 21(2), 383-391.

Breskin, A. (2009). New prospects for early detection of prostate cancer by X-ray fluorescence. Retrieved from the Yale School of Engineering and Applied Science Web site:

Brewster, D.H., Fraser, L.A., Harris, V. & Black, R.J. (2000). Rising incidence of prostate cancer in Scotland: increased risk or increased detection? British Journal of Urology, 85(4), 463-472.

British Heart Foundation (BHF) (2008). Trends in smoking prevalence in Europe. Retrieved from the BHF Statistics Web site:

Brosman, S.A. (2006). Prostate-Specific Antigen. Retrieved from the emedicine® Web site:

Bryant, R. & Hamdy, F. (2009). Trends in Prostate Cancer Screening: Overview of the UK. In C.M. Tangen, D.P. Ankerst & I.M. Thompson (Ed.), Prostate Cancer Screening (2nd ed.). London: Springer.

Bupa (2007). Transurethral resection of the prostate (TURP). Retrieved from the Bupa Web site:

Cancer Research UK (2008). UK Prostate Cancer incidence statistics. Retrieved from the Cancer Research UK Web site:

Carpten, J.D. & Trent, J.M. (2008). Inherited Genetic Changes in Prostate Cancer. In R.G. Pestell, M.T. Nevalainen & M. Milken (Ed.), Prostate Cancer: Signaling Networks, Genetics, and New Treatment Strategies. London: Springer.

Carter, H.B. (2007). Prostate Disorders 2007. Baltimore: Johns Hopkins.

Carter, H.B., Ferrucci, L., Ketterman, A., Landis, P., Wright, E.J., Epstein, J.I., Trock, B.J. & Metter, J. (2006). Detection of life-threatening prostate cancer with prostate-specific antigen velocity during a window of curability. Journal of the National Cancer Institute, 98(21), 1521-1527.

Catalona, W.J., Partin, A.W., Slawin, K.M., Brawer, M.K., Flanigan, R.C., Patel, A., Richie, J.P., de Kernion, J.B., Walsh, P.C., Scardino, P.T., Lauge, P.H., Subong, E.N., Parson, R.E., Gasior, G.H., Loveland, K.G. & Southwick, P.C. (1998). Use of the percentage of free prostate-specific antigen to enhance differentiation of prostate cancer from benign prostatic disease: a prospective multicenter clinical trial. Journal of the American Medical Association, 279(19), 1542-1547.

Challem, J. (2003). The Inflammation Syndrome. Chichester: Wiley.

Chan, R., Lok, K. & Woo, J. (2008). Prostate cancer and vegetable consumption. Molecular Nutrition and Food Research, 53(2), 201-216.

Coffey, D.S. (2001). Similarities of Prostate and Breast Cancer: Evolution, Diet, and Estrogens. Urology, 57(Supplement 4A), 31-38.

Coughlin, S.S. & Hall, I.J. (2002). A Review of Genetic Polymorphisms and Prostate Cancer Risk. Annals of Epidemiology, 12(3), 182-196. doi:10.1016/S1047-2797(01)00310-6

Dick, D.M. & Bierut, L.J. (2006). The genetics of alcohol dependence. Current Psychiatry Reports, 8(2), 151-157.

Eeles, R.A., Kote-Jarai, Z., Giles, G.G., Al Olama, A.A., Guy, M., Jugurnauth, S.K., Mulholland, S., Leongamornlert, D.A., Edwards, S.M., Morrison, J., Field, H.I., Southey, M.C., Severi, G., Donovan, J.L., Hamdy, F.C., Dearnaley, D.P., Muir, K.R., Smith, C., Bagnato, M., Ardern-Jones, A.T., Hall, A.L., O’Brien, L.T., Gehr-Swain, B.N., Wilkinson, R.A., Cox, A., Lewis, S., Brown, P.M., Jhavar, S.G., Tymrakiewicz, M., Lophatananon, A., Bryant, S.L., The UK Genetic Prostate Cancer Study Collaborators, British Association of Urological Surgeons’ Section of Oncology, The UK ProtecT Study Collaborators, Horwich, A., Huddart, R.A., Khoo, V.S., Parker, C.C., Woodhouse, C.J., Thompson, A., Christmas, T., Ogden, C., Fisher, C., Jamieson, C., Cooper, C.S., English, D.R., Hopper, J.L., Neal, D.E. & Easton, D.F. (2008). Multiple newly identified loci associated with prostate cancer susceptibility. Nature Genetics, 40, 316-321. doi:10.1038/ng.90

Ekman, P. (1999). Genetic and Environmental Factors in Prostate Cancer Genesis: Identifying High-Risk Cohorts. European Urology, 35(5-6), 362-369.

Ellsworth, P., Wein, A.J., Heaney, J.A. & Gill, O. (2008). 100 Questions & Answers About Prostate Cancer (2nd ed.). London: Jones and Bartlett.

El-Shirbiny, A.M. (1994). Prostatic Specific Antigen. In H.E. Spiegel (Ed.), Advances in Clinical Chemistry. Oxford: Elsevier.

Etzioni, R., Gulait, R. & Mariotto, A. (2009). Overview of US Prostate Cancer Trends in the Era of PSA Screening. In C.M. Tangen, D.P. Ankerst & I.M. Thompson (Ed.), Prostate Cancer Screening (2nd ed.). London: Springer.

Fitzpatrick, P., Corcoran, N. & Fitzpatrick, J.M. (1998). Prostate cancer: how aware is the public? British Journal of Urology, 82(1), 43-48.

Friberg, L. (1983). Cadmium. Annual Review of Public Health, 4, 367-373.

Greenberg, R.S., Daniels, S.R., Flanders, W.D. & Eley, J.W. (2005). Medical Epidemiology (4th ed.). Maidenhead: McGraw-Hill.

Kiermeney, N. (2008). Identification of Prostate Cancer Susceptibility Loci. European Association of Urology, 23rd Annual Congress, Milan, Italy.

Klein, E.A. (2004). Management of Prostate Cancer (2nd ed.). London: Springer.

Kohnert, D. (2007). Crisis Region Western Africa: The Cradle of African Migration to Europe. In B. Gebrewold-Tochalo (Ed.), Africa and Fortress Europe: Threats and Opportunities. Farnham: Ashgate.

Lane, T., Strefford, J. & Oliver, T. (2006). An Update on Biotechnology in the Assessment of Prostate Cancer. In W. Bowsher & A. Carter (Ed.), Challenges in Prostate Cancer (2nd ed.). Chichester: Blackwell.

Luboldt, H.J., Swoboda, A., Börgermann, C., Fornara, P., Rübben, H. (2001). Early Detection Project Group of the German Society of Urology. Clinical usefulness of free PSA in early detection of prostate cancer. Onkologie, 24(1), 33-37.

Lund Nilson, T.I., Johnsen, R. & Vatten, L.J. (2000). Socio-economic and lifestyle factors associated with the risk of prostate cancer. British Journal of Cancer, 82(7), 1358-1363.

Marshall, W.J. & Bangert, S.K. (2008). Clinical Chemistry (6th ed.). Oxford: Elsevier.

National Cancer Institute (NCI) (2009). The Prostate-Specific Antigen (PSA) Test: Questions and Answers. Retrieved from the NCI Web site:

Nelen, V. (2007). Epidemiology of Prostate Cancer. In J. Ramon & L.J. Denis (Ed.), Prostate Cancer. London: Springer.

Office for National Statistics (ONS) (2009). Population Estimates. Retrieved from the ONS Web site:

Ornish, D., Magbanua, M.J.M., Weidner, G., Weinberg, V., Kemp, C., Green, C., Mattie, M.D., Marlin, R., Simko, J., Shinohara, K., Haqq, C.M. & Carroll, P.R. (2008). Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proceedings of the National Academy of Sciences of the United States of America, 105(24), 8369-8374.

Parnes, H., Hoque, A., Albanes, D., Taylor, P. & Lippman, S. (2006). Prostate Cancer. In D. Heber, G.L. Blackburn, V.L.W. Go & J. Milner (Ed.), Nutritional Oncology (2nd ed.). Oxford: Elsevier.

Pruthi, R.S., Swords, K., Schultz, H., Carson, C.C. & Wallen, E.M. (2009). The Impact of Obesity on the Diagnosis of Prostate Cancer Using a Modern Extended Biopsy Scheme. Journal of Urology, 181(2), 574-578.

Puga, A. & Wallace, K.B. (1999). Molecular Biology of the Toxic Response. London: CRC Press.

Raskó, I. & Downes, C.S. (1995). Genes in Medicine: Molecular Biology and Human Genetic Disorders. London: Springer.

Rowan, S. (2007). Trends in cancer incidence by deprivation, England and Wales, 1990-2002. Health Statistics Quarterly, 36. Retrieved from:

Salinas, C.A., Koopmeiners, J.S., Kwon, E.M., FitzGerald, L., Lin, D.W., Ostrander, E.A., Feng, Z. & Stanford, J.L. (2009). Clinical utility of five genetic variants for predicting prostate cancer risk and mortality. The Prostate, 69, 363-372.

Shibata, A., Ma, J. & Whittemore, A.S. (1998). Prostate Cancer Incidence and Mortality in the United States and the United Kingdom. Journal of the National Cancer Institute, 90(16), 1230-1231.

Somerville, W. (2007). Immigration Under New Labour. Bristol: Policy Press.

Stamey, T.A. (2001). Preoperative serum prostate-specific antigen (PSA) below 10 microg/l predicts neither the presence of prostate cancer nor the rate of postoperative PSA failure. Clinical Chemistry, 47(4), 631-634.

Stanford, J.L., Stephenson, R.A., Coyle, L.M., Cerhan, J., Correa, R., Eley, J.W., Gilliland F, Hankey, B., Kolonel, L.N., Kosary, C., Ross, R., Severson, R. & West, D. (1999). Prostate Cancer Trends 1973-1995. Bethesda, Maryland: National Cancer Institute.

Strachan, T. & Reed, A.P. (2004). Human Molecular Genetics (3rd ed.). Abingdon: Taylor & Francis.

Tanagho, E.A., Smith, D.R. & McAninch, J.W. (2007). Smith’s General Urology (17th ed.). Maidenhead: McGraw-Hill.

Tannock, I.F. (2002). Eradication of a disease: how we cured symptomless prostate cancer. The Lancet, 359(9314), 1341-1342.

Thompson, I.M., Pauler, D.K., Goodman, P.J., Tangen, C.M., Lucia, M.S., Parnes, H.L., Minasian, L.M., Ford, L.G., Lippman, S.M., Crawford, E.D., Crowley, J.J. & Coltman, C.A. Jr. (2004). Prevalence of prostate cancer among men with a prostate-specific antigen level < or =4.0 ng per milliliter. New England Journal of Medicine, 350(22), 2239-2246.

Timiras, P.S. & Leary, J. (2007). The Kidney, Lower Urinary Tract, Body Fluids, and the Prostate. In P.S. Timiras (Ed.), Physiological Basis of Aging and Geriatrics (4th ed.). London: CRC Press.

Waghray, A., Schober, M., Feroze, F., Yao, F., Virgin, J. & Chen, Y.Q. (2001). Identification of Differentially Expressed Genes by Serial Analysis of Gene Expression in Human Prostate Cancer. Cancer Research, 61(10), 4283-4286.

World Health Organization (2008). World Health Statistics 2008. Geneva, Switzerland: World Health Organization.

Zisman, A., Twardowski, P., Liebovici, D. & Figlin, R.A. (2008). Urinary Tract Cancers. In D.A. Casciato & M.C. Territo (Ed.), Manual of Clinical Oncology: Spiral Manual Series (6th ed.). London: Lippincott Williams & Wilkins.

Monday, November 21, 2011

Mobberley's HedgeHopper

The chocolate-box English village of Tarporley has four pubs along its High Street. For that reason alone, it seemed well worth a visit. I came across an article in Cheshire Life (see link below) outlining a 5-mile walk around the surrounding countryside (Figure 28.1), so my partner and I decided to spend a day getting some outdoor exercise before the inevitable watering-hole finale.

Figure 28.1: Route around Tarporley

Copyright 2011 Google Maps

Clutching a copy of the article, along with a makeshift map, we set off along Park Road from the High Street at 11 a.m. Only at that point did I notice that the piece had been published last year. Plenty of time, I thought, for part of the route to have been altered or disrupted. On we walked regardless. It was a blissful autumn morning. The low November sun filtered through semi-naked tree branches, while red and golden leaves fluttered to the ground.

Everything was going to plan until we crossed our first grassy field, leading to Winterford Farm. As we prepared to negotiate a (non-barbed) wire cordon stretched between us and Winterford Lane, we noticed a black battery pack semi-hidden in the long grass. Just as well we did. Straddling a 20,000-volt electric fence has never been on my bucket list. The only alternative to testicular electrocution was to climb a double wooden fence, clearly not meant to be breached, leading to a field full of bulls.

The bovine gauntlet, positioned between ourselves and the lane, was about fifty yards long. We dismounted from the fence and every pair of eyes turned to stare. We took a few tentative steps towards the bulls; they moved the same distance towards us. It was risk assessment time, and we decided to go for it. In the middle of the field, past the point of no return, the daddy bull emerged from a pond and took exception to our presence. The choice was either to run, and risk spooking every one of them, or to continue walking steadily with fingers crossed and buttocks clenched.

The leap of faith paid off. We made it safely to the lane, but still the bulls stared. I referred to the article again. It advised us to turn right and proceed along the lane until we crossed a brook. Fortunately, the brook was flowing rapidly enough to make a noise; the water itself was completely obscured by undergrowth.

At a gap in the hedge, we hopped over another stile leading to some crop fields. Unfortunately, a designated cross-field path was nowhere in sight – so often the case – and the article was equally unhelpful as to the necessary direction. No matter. The midday sun being due south, we headed west, back toward the village, through a long, upward stretch of mud and puddles.

Back on solid ground, we wandered along a narrow lane (Figure 28.2) to Rhuddal Heath. Not a single vehicle passed by, just a solitary woman on horseback with all the time that most people these days do not have.

Figure 28.2: The tranquil lane leading to Rhuddal Heath

Copyright 2011 Paul Spradbery

We reached Tarporley High Street two-and-a-half hours after we had set off. The only remaining decision to make was to select a pub. Herself chose wisely: The Swan Inn (Figure 28.3) (see link below), a former coach house serving a variety of cask-conditioned ales in warm, elegant comfort.

Figure 28.3: The Swan Inn, captured neatly by France-based photograher Stephen Nunney (see link below)

Copyright 2011 Stephen Nunney

Reproduced by kind permission

One of the beers seemed to fit the occasion: Mobberley’s HedgeHopper, brewed at Kell House Farm in the nearby village of Mobberley. With its malty, hoppy – and not too bitter – taste, this was as pleasant as anything I have come across. I would recommend it without reservation to anyone who wants something different from the mass-produced, watered-down stuff served in Identikit pubs the length and breadth of the country.

The brewery, Mobberley Fine Ales, was established only this year, by Phil Roberts and Ray Britland.

‘Our first brew was produced in mid July and to ensure we had a product of the highest quality, we invited just over 80 villagers to come and taste the beer, at a specially arranged “tasting evening” at our brewery.’

Pity I was elsewhere. Anyhow, Cheshire pubs are quickly realizing its potential. So, look out for the pheasant-in-a-propeller-plane logo (Figure 28.4). More importantly, if ever you fancy rambling around the fields and lanes of this Midsomer Murders-style village, look out, also, for the bulls who will be looking out for you.

Figure 28.4: The eponymous ale

Copyright 2011 Mobberley Fine Ales

Copyright 2011 Paul Spradbery

Wednesday, November 16, 2011

Adventure Of The Seas

My daughter thoroughly enjoyed sailing from Málaga, through the Strait of Gibraltar, to the Canary Islands. As autumn school holidays go, this one surpassed all others. No wonder. MS Adventure of the Seas (Figure 27.1) (see link below), owned by Royal Caribbean International, is one of the largest cruise ships in the world, costing a cool half-billion (US) dollars to construct.

Figure 27.1: MS Adventure of the Seas was built by Kvaerner Masa-Yards (KMY), the largest shipbuilder in Finland, and made its maiden voyage exactly 10 years ago.

Copyright 2011 Royal Caribbean International

Compare her general characteristics with those of the legendary Titanic:

The word ‘impressive’ has rarely been so inadequate. Currently, the Adventure spends the summer months in and around Spanish waters, departing for the Southern Caribbean when winter begins.

The ship’s leisure facilities cater for everyone, regardless of energy levels. They include a circumferential running track, basketball court, fitness centre and climbing wall (Figure 27.2). There is also a spectacular theatre and various restaurants (Figures 27.3 and 27.4), including a 1950s-style diner which was my daughter’s favourite. For sun-worshippers, there is even – believe it or not – a beach. Only the terminally dissatisfied would have found cause for complaint.

Figure 27.2: Climbing a moving cliff face

Copyright 2011 Phoebe Spradbery

Figure 27.3: On-board shops and restaurants

Copyright 2011 Phoebe Spradbery

Figure 27.4: Some of the catering staff

Copyright 2011 Phoebe Spradbery

Unlike the Titanic exactly a century ago, and much to my relief, the Adventure of the Seas docked safely at its subtropical destination. After a 900-mile voyage around the Moroccan coast, she reached los Islas Canarias (Figure 27.5) on schedule. Long may she sail (Figure 27.6).

Figure 27.5: The view from Deck 8

Copyright 2011 Phoebe Spradbery

Figure 27.6: Dressed for the occasion

Copyright 2011 Royal Caribbean International

Copyright 2011 Paul Spradbery

Friday, November 04, 2011

The Three Disgraces

Liverpool’s Pier Head is a UNESCO World Heritage Site. This accolade was bestowed upon the city in 2004, mainly in recognition of what are known locally as ‘The Three Graces’. These are three supremely elegant buildings which have graced the waterfront on the east bank of the River Mersey for a hundred years (Figure 26.1). Each has its own unique architectural features, many of them intricate, and all are loved by Liverpudlians and visitors alike.

Figure 26.1: (Left to right) The Royal Liver Building, Cunard Building and Port of Liverpool Building, a.k.a. 'The Three Graces'

Copyright 2005 Chris Howells

In 1992, I bought a two-storey apartment situated directly across the mile-wide river. I loved it purely because of the view. At all times of day, I would stand on the roof terrace and gaze in silent admiration upon one of the world’s most beautiful waterfronts. I sold the place at the turn of the millennium. A decade on, the view has been spoiled – and in a way I could never have imagined.

A while ago, I took my family to the recently-opened Museum of Liverpool. Our opinions of its exhibits differed considerably, as you might expect, but we were unanimous in our verdict of the edifice itself (Figure 26.2). What a sight. My eyes are still smarting. The phrase ‘in keeping with its surroundings’ seems to have been made unceremoniously redundant. There, among the Baroque, Byzantine and Italian Renaissance influences of the Three Graces, now stands the proverbial sore thumb.

Figure 26.2: The Museum of Liverpool, in all its 'splendour'

Copyright 2011 Paul Spradbery

Sadly, on our way out, there was no escape from the visual assault. Mann Island, opposite the museum’s main entrance, is now home to three monstrous chunks of granite-and-glass (Figure 26.3), which obscure the view of the Three Graces from the ever-popular Albert Dock. Worse still, they are black – the only non-white buildings at the Pier Head. In terms of aesthetics, fine architectural detail and respect for surroundings, my sons’ Lego constructions are arguably superior.

Figure 26.3: Mann Island monstrosities

Copyright 2011 MonkeyFish Marketing Ltd.

La guinda del pastel, however, is the new Ferry Terminal (Figure 26.4). This is truly awful. Having such a ludicrous block of wonky masonry dumped directly in front of the (Grade 1 listed) Royal Liver Building is akin to seeing the image of George W. Bush carved into Mount Rushmore.

Figure 26.4: The new Ferry Terminal, beyond a wide expanse of concrete with not a single tree or shrub in sight.

Copyright 2011 Paul Spradbery

There is, of course, no accounting for taste. This leads to a more fundamental point. Architecture, as with art and literature, is vulnerable to acute subjectivity. Was Gaudi a better architect than Frank Lloyd Wright? Were Bach’s works ‘better’ than those of Mozart? Is an unmade bed a ‘better’ art exhibit than Constable’s Hay Wain? Some arguments cannot be settled, and this is the very reason why charlatans and bullshitters are so prevalent among arty types. Anyone who believes Liverpool’s new buildings are hideous could be dismissed as a Philistine who ‘just doesn’t get it’. The world of science is different. Its rational and empirical nature ensures that pretentiousness and ignorance are swiftly, and brutally, exposed and condemned.

If the architects are damned by their own creations, then, what about those who sanctioned the planning applications in the first place? Liverpool Council’s decision-makers were ultimately responsible for desecrating the Pier Head. I have already heard some cynics suggest that ‘the kickbacks must have been substantial’. Of course, libel laws being as they are, I would never publish a conclusion without evidence, however logical it might be to draw.

All the unlovely buildings (Figures 26.5, 26.6 and 26.7) – where do they all come from?

Figure 26.5: The Port of Liverpool Building is now overshadowed by the black blocks of Mann Island

Copyright 2011 Paul Spradbery

Figure 26.6: The new museum (right) makes this shot even less appealing than the previous one.

Copyright 2011 Paul Spradbery

Figure 26.7: Laugh or cry?

Copyright 2011 Paul Spradbery

Copyright 2011 Paul Spradbery