Coming from New Zealand, it has been a fascinating experience to spend a week in Kansas, in America’s Mid-West.  Kansas is a big state geographically, right in the centre of the USA, but has only 2.5 million people. The economy is driven largely by agriculture, with the Boeing factory at Wichita being the other big industry.  Wichita is the biggest city, and Topeka the State Capital. Somewhat surprisingly, most of Kansas City is actually across the state boundary in Missouri.  There is a major army base at Fort Riley. The centre of agricultural activity is at the University town of Manhattan, where the Agricultural Faculty enrolments are booming. 

These are good times for agriculture in America’s mid West.

Corn is the big crop, with soybeans also of major importance, and then wheat a long way behind that. Cattle raising with cows and feeder calves on the Flint Hills and similar areas, and then feedlot finishing, is the major livestock industry.

Part of the grain storage for one large Kansas farm

The corn industry in particular is booming. Much of this is due to ethanol from the biofuel industry, which now takes about 40% of the corn crop. However, not all of that is lost to the food chain, as for every three kg of corn used for ethanol, there is a by-product of about one kg dry matter of distillers grain (DG). This DG is about 30% protein and makes up a valuable component of cattle feedlot rations, at up to about 25% of the total ration.

Prior to the white man arriving, most of Kansas was prairie grasslands on which vast herds of bison roamed. Initially cowboy country, the land was opened up in the 1850s by the development of the railways.  New settlers could take possession of 160 acres ( a ‘quarter section’), and after five years would be granted title.   Of course in the modern era, 160 acres is nowhere near sufficient for a living. Most farms are of several thousands of acres, typically a mix of owned and leased land. 

The trend to larger and larger farms is inexorable, as the best managed farms add more and more ‘quarters’ to their holdings. In the west, about a third of the land is irrigated from the Ogilala Aquifer from a depth of about 200 feet.  Unfortunately, this aquifer is gradually depleting, and in somewhere between 20 and 100 years, depending on who one talks to, irrigation will no longer be possible. Dryland yields of corn in Western Kansas are only about one third those of irrigated crops

Farming in the Mid West is both big and efficient. Nearly all of the corn and soybeans are genetically modified with Roundup-ready varieties that can be sprayed for weeds without harming the crop. Most of the land is farmed zero-till. This now productive land was once the dustbowl land of the 1930s.

Some of the farms also earn income from oil. The oil is at a depth of about 1500 metres, and oil rights go with the land title. The oil companies then lease rights to the oil, paying all expenses, and paying the land owner one eighth of the gross value. Most of the wells are small, and often only yield about 10 barrels (or about 1500 litres) per day. But it is a nice little income earner for those land owners lucky enough to be located over the oil-bearing formations.

Typical Kansas oil well

To an outsider like me from across the other side of the Pacific, there is much to admire about rural Kansas. The rural citizens of Kansas are hard working straight forward and friendly people. They farm under intense heat of over 40 degrees C in summer and under intense cold with snow in the winter. Many families can trace their forebears back about six generations to the original settlers who typically came from Germany or Scandinavia. The Kansas folk are patriotic, with soldiers in uniform treated with deference as esteemed citizens who risk all for the nation.  Kansas’s most famous citizen was General and later President Eisenhower, who is buried in his Kansas boyhood town of Abilene.  

Everything about Kansas is big. Big country, big farms, big cars, big people and big meals.  On our last night here, our group was dining at a small downtown restaurant and I got talking to our waiter, who it turned out was doing a turn at serving tables, but was actually the manager. I asked him what he paid his waiting staff. He said $2.13 per hour. Everything else comes from tips, with the norm being about 15%. I have never much liked the tipping system when I am travelling, because I am never sure, as an outsider, how much to pay in various circumstances. But it sure does lead to great service in the restaurants. In this restaurant, the waiting staff share tables and therefore share the tips – which can go onto the credit card payment.  At this restaurant, kitchen staff also get a share of these tips. Tips have to be declared for tax purposes, and the manager said that if, for example, the declared tips only totalled 10% then the tax authorities would probably pay him a less than friendly visit. On a quiet night the table staff might make $12-13 per hour, but on a busy night considerably more.

As for the Kansas cuisine, that predominantly comprises fried chicken, big steaks, french fries, mashed potatoes, beans, apple pie and ice cream.  For breakfast this morning I had a lovely plate of in-season fruit – strawberries, blueberries, blackberries and melon.  Cereal was on the menu but all varieties were sugar-laden. We still have to educate them about vegemite and marmite.

Gasoline, as they call it here, is about $3.30 per gallon. American gallons are just slightly less than 4 litres. After making adjustments for exchange rates, it means that fuel in Kansas in September 2011 is just over half the price that it is in New Zealand (where it is about $US6 per American  gallon), and well under half the price of fuel in countries like France (where it is about $US8 per American gallon). Most of the differences relate to taxes.

Typical leafy suburbs in Manhattan, Kansas

Today’s A2 article can be found at  http://www.heraldsun.com.au/news/milk-minus-mutants-boost-for-the-lactose-intolerant/story-e6frf7jo-1226096018913.

Alternatively, a pdf is attched here:  Milk minus mutants boost for the lactose intolerant

Those of us that are interested in casomorphins and human health have known for a long time that bovine BCM5 is a more powerful opioid than bovine BCM7. One paper makes the comparison that whereas bovine BCM7 is similar in opioid strength to morphine, bovine BCM5 is ten times more powerful than either.(3) However, the accepted evidence has been that it is probably not released by digestion of cow milk in the human gut, whereas BCM7 was definitely released.(4, 5)

What the Polish work is indicating is that even if BCM5 is not normally found in the human gut (and there is a logic why that might be so, related to the DPP4 enzyme that is needed to break down BCM7 to BCM5 only being found within the gut on mesenteric cells, rather than circulating freely in the gut), BCM5 is getting formed from BCM7 in the sera (blood) (where DPP4 does circulate freely) or other tissues. From there it is getting transferred into human milk.  From there it gets into the stomachs and blood of babies. 

If all of this is true – and that is what this latest research is indicating – then the implications are huge.

So what did this Polish research actually report?

The study is reported as a case study of a child suffering bouts of apnoea immediately after breast feeding. But there is much more to it than that, and it is really a case-control with 10 normal babies as the controls.  I am actually more interested in the findings from the controls, but first the case itself.

The mother self diagnosed that the baby was suffering from the apnoea on those occasions when she (the mother) had been drinking large quantities of cow milk. Sure enough, on testing the baby’s blood, extremely high levels of bovine BCM5 were found. (For those that think quantitatively, 15,147 ng/mL.). Other possible causes of the apnoea were investigated but proven negative. So this in itself does not prove causation. But the association (which in science is not quite the same thing as ‘proof’) is a remarkable finding and points in only one direction.

So how does this level actually compare to the levels found in the normal babies?  In these babies it was much lower, ranging from 1 ng to 864 ng/mL. Accordingly, there is a remarkable contrast between the controls and the case, with the case being an extreme outlier.

However, my interest is in the fact that for seven out of eight of the controls (data for the other two is not presented, which is frustrating), considerable levels of BCM5 were found. For the eighth control which had only 1 ng/mL, the mother did not like cow milk and did not drink it, whereas all of the other mothers did. These babies were aged 7-14 weeks and all were exclusively breast-fed.  To reiterate, although much lower than for the case, the levels in these controls are still high.

So here we have evidence of considerable levels of BCM5 getting into babies blood via their mothers’ milk.  This is a remarkable finding, although highly consistent with other work of this group that showed BCM7 was getting through to babies via their mothers’ milk.(6)

Once again we can be confident that the mainstream dairy industry will denigrate this research. They will probably point out that it is only a case study (although actually it is a case-control). And they will point out that the authors themselves emphasise that further work is needed including measuring the BCM5 in the milk of the mothers, and taking blood readings at different times relative to feeding times.

However, what this research does do is throw light into a number of previously dark places.  BCM5 is now looking more important than previously, and this paper does provide confirmatory evidence that nasty peptides can get from cows’ milk to human babies via their mother’s’ milk.  What Mum eats and drinks is important for baby.  If Mum drinks milk containing A1 beta-casein, then it would seem that baby is gong to drink casomorphins.

REFERENCES

1.  Wasilewska J, Kaczmarski M, Kostyra E, Iwan M. Cow’s-milk-induced Infant Apnoea With Increased Serum Content of Bovine beta-Casomorphin-5. J Pediatric Gastroenterology and Nutrition. 2011 June; 52(6): 772-775  

2.  Woodford K. Devil in the Milk: Illness, Health and Politics: A1 and A2 Milk. Wellington New Zealand: Craig Potton Publishing 2007.

3.  Hedner J, Hedner T. beta-Casomorphins induce apnea and irregular breathing in adult rats and newborn rabbits. Life Sci. 1987 Nov 16;41(20):2303-12.

4.  De Noni I. Release of b-casomorphins 5 and 7 during simulated gastro-intestinal digestion of bovine b-casein variants and milk-based infant formulas. Food Chemistry 2008 110(4):897-903.

5.  Svedberg J, de Haas J, Leimenstoll G, Paul F, Teschemacher H. Demonstration of beta-casomorphin immunoreactive materials in in vitro digests of bovine milk and in small intestine contents after bovine milk ingestion in adult humans. Peptides. 1985 Sep-Oct;6(5):825-30.

6.  Wasilewska J, Sienkiewicz-Szlapka E, Kuzbida E, Jarmolowska B, Kaczmarski M, Kostyra E. The exogenous opioid peptides and DPPIV serum activity in infants with apnoea expressed as apparent life threatening events (ALTE). Neuropeptides. 2011 Jun;45(3):189-95.

Bovine BCM7 (beta-casomorphin7), which I call the ‘milk devil’, has long been suspected as a villain. This ‘milk devil’, which is an opioid derived from casein (and hence the name ‘caso’ from casein and ‘morphin’ from morphine), is only produced from digestion of A1 beta-casein (1, 2), which itself is only produced by some cows of European breeds. This A1 beta-casein is the consequence of a chance mutation in an ancestor some thousands of years ago (3). Unfortunately this mutated gene is now found in a considerable proportion of European cows.

Scientific evidence has linked bovine BCM7 to many health conditions such as Type 1 diabetes and heart disease (4, 5), child development and symptoms of autism (6, 7).  On the PUBMED database there are now more than 250 peer reviewed medical and scientific papers on casomorphins. However, the evidence that BCM7 might be a major villain for SIDS has, until now, been somewhat indirect.

Back in the 1990s, beta-casomorphins were found in the brainstems of SIDS babies (8). But comparing this with the brainstems of healthy children was obviously not possible. Also, in young rabbits and rats (9) it had been shown that injecting BCM7 into the blood leads to apnoea (depressed and irregular breathing). But obviously these sorts of trials cannot be done with humans. Also, it is only recently that detection kits have become readily available for testing BCM7 in blood.  A further complication has been that in all likelihood some babies are more susceptible than others, but there has been no way to identify the genetic aspect of risk.  In my book ‘Devil in the Milk’ (p152), first published in 2007 (10), I introduced the latest evidence relating to SIDS (11), but at that time there was nothing conclusive.

However, recent work in Poland led by Dr Elzbieta Kostyra, and published by leading scientific and medical publisher Elsevier in the April 2011 issue of the journal Neuropeptides, has provided answers to the major questions (12). There can now be little doubt that BCM7 is a risk factor for SIDS.  Also, it is now clear that the babies most at risk are those who have low levels in their blood of an enzyme called DPP4 (dipeptidyl peptidase 4). This is the only enzyme in humans that can break down BCM7 (13-15).

The Polish work is based on studying babies who have had life threatening events from apnoea, but whom the parents and/ or doctors managed to save. Blood samples from these babies were then compared to healthy babies. Key findings were that the ‘at-risk’ babies had three times the level of bovine BCM7 in their blood as the healthy babies. Also, these at-risk babies had 42% less DPP4 than the healthy babies. Both of these results were statistically significant at p< 0.001.  In other words, the chance of getting a result like this due to random factors, rather than being causatively linked either to each other or a common third factor, is less than one in one thousand.

Analysis of the healthy babies showed that variation of BCM7 within this group was positively associated with more DPP4 activity. In other words, in healthy children the body naturally increases DPP4 activity when BCM7 is high.  But in the at-risk babies the DPP4 level was actually much lower rather than higher. This demonstrates that the at-risk babies are deficient in their ability to quickly respond to high BCM7 by producing sufficient quantities of the only enzyme that can break it down.

The babies were fed on three types of diet, determined by their mothers. Not surprisingly, those fed milk formula that was high in casein had much higher BCM levels than those fed infant formula that was predominantly (but not exclusively) whey. This was to be expected given that BCM7 can only come from casein and not from whey.  However, somewhat intriguingly, babies aged 1-4 months who were apparently being exclusively breastfed also had bovine BCM7 in their blood. How did this get there? The Polish researchers and other scientists have been investigating for quite some time how protein fragments, such as but not only bovine BCM, can get from the mother’s stomach into breast milk. It could be that the BCM7 is being transferred through the blood (16, 17), but it is looking increasingly likely that it might also be via other mechanisms, perhaps including the lymph system.  Regardless of how is it is occurring, there seems little doubt that bovine BCM7 can get into human breast milk, and that it can cause life threatening events in babies. So the evidence indicates that it is not only the babies, but also the lactating mothers, who need to be on cows’ milk that is free of A1 beta-casein.

The Polish work led by Dr Kostyra dovetails very nicely with work by Russian scientists that was published in another international journal, Peptides, in late 2009 (6) . That work showed that babies fed infant formula not only had high levels of bovine BCM7in their blood, but that a proportion of these babies were much slower than other babies to metabolise and eliminate the BCM7. These slow eliminators were at high risk of delayed psychomotor development. The Russian scientists did not investigate the reason why some babies were slow BCM7 eliminators, but an obvious hypothesis would be that they had low DPP4 in the blood.  This latest Polish work now provides strong confirmatory evidence for this hypothesis.

The implications of this work would seem obvious. If infants are to be fed milk formula then it needs to be free of A1 beta-casein. In other words, it needs to come from cows that are what we call ‘A2 cows’ and which produce ‘A2 milk’. Also, lactating mothers would be well advised to not drink milk containing A1 beta-casein. 

My assumption is that the mainstream dairy industry will try and denigrate this research. For example, Dairy Australia has a standard response to any new research on A1 beta-casein along the lines that ‘all milk is the same’.  Of course all milk is not the same and such a statement is scientific nonsense.  So how will they denigrate this research? Detractors might say that it is ‘just one study’.  This was a typical response to the Russian work (6) published in 2009.   They might also refer to the European Food Safety Authority (EFSA) report of January 2009 (1), which claimed there was no proof that BCM7 was getting through from the digestive system to the blood.  Back in 2009 that statement might have been defensible, in that arguably there was strong evidence (which EFSA failed to acknowledge) but not final proof. But now in 2011 that position is no longer tenable.  They may also argue – as was said with the Russian research, which like this Polish research came out of leading scientific institutions – that we do not know enough about their research standards. Well, in that case it is time they went and found out. These are leading scientific institutions. In any case, both the Russian and Polish work is published in highly ranked international  journals following international peer review.

Major elements of the mainstream dairy industry, at least in Australia and New Zealand, have known about BCM7 and the apparent links to a range of health conditions for more than a decade. They hoped that those apparent links might disappear. And for a while it seemed that this might happen. Now, there is no chance that this will happen.

So what can the industry do about it? Well, one thing they could do is breed A2 cows. This is easy to do, using semen that carries the A2 variant of the beta-casein gene. Most New Zealand and Australian bulls already have their A1/A2 status known and recorded. In ten years time the national herds could be close to pure A2, with only inconsequential levels of A1 beta-casein remaining. Then we would have all of our dairy herds the way nature originally intended!  The irony is that we could already be in that position if we had only acted when evidence first emerged.   But because only a minority of farmers have been converting their herds, the industry will now have to work out how to sell ‘A1 milk’ for the next 10 years. That might be a challenge, and hence there will be a continuing industry fightback (‘we must not say anything negative about milk’, or ‘nothing is proven’). There will still be plenty of people who will drink the ‘ordinary milk’ despite the risks, and indeed many of those people may not be susceptible to the BCM7. So ordinary milk will still sell while the change is being made.

However, for parents of young children in particular, the time has come for them to be made aware of the emerging evidence: BCM7, and hence milk that contains A1 beta-casein, is an evidence-based risk factor for a range of childhood health conditions.  SIDS has now moved up that list of conditions. There are options to reduce those risks.

 *******

UPDATE: (14 April 2011)

It has been suggested to me that this is all a bit scary. Perhaps it is even scaremongering. The first (i.e. it is scary) I disagree with, and the second (scaremongering) I refute even more strongly. It is SIDS and not this story that is scary. This is a story of hope and moving forwards with solutions. But I do agree that perhaps a little more guidance might be helpful. Some time in the future, and hopefully the near future, it will be possible to purchase infant formula made from the milk of A2 cows. In the meantime the ‘no-cost’ or ‘low-cost’ options to reduce risk are:
1) breast-milk
2) whey-based infant formula (although most of these formulas will still contain some casein).
It seems that mothers who are breast-feeding can further reduce their risk by themselves drinking A2 milk; i.e.milk that is free of A1 beta-casein .  And once the babies are weaned from the breast or from infant formula, then the milk they drink can also be from A2 cows, at least in countries like Australia and New Zealand where A2 milk is commercially available.
Of course for specific advice parents should consult a professional dietitian.

Update: This version was updated 25 April 2011.

*********************** 

Note: the full reference for the SIDS paper is:

Wasilewska J, Sienkiewicz-Szlapka E, Kuzbida E, Jarmolowska B, Kaczmarski M, Kostyra E. The exogenous opioid peptides and DPPIV serum activity in infants with apnoea expressed as apparent life threatening events (ALTE). Neuropeptides. 2011 DOI: 10.1016/j.npep.2011.01.005  ( This is a corrected proof, peer reviewed, and able to be cited, available online to subscribers to the journal, with hard copy and page numbers still to be assigned.)

Other References

1.      Scientific Report of EFSA prepared by a DATEX Working Group on the potential health impact of β-casomorphins and related peptides. EFSA Scientific Report (2009) 231, 1-107.

2       De Noni I,  Release of b-casomorphins 5 and 7 during simulated gastro-intestinal digestion of bovine b-casein variants and milk-based infant formulas. Food Chemistry 2008; 110:897-903

3.     Ng-Kwai-Hang KF, Grosclaude F. Genetic polymorphism of milk proteins. In: Fox PFaM, P.L.H editor. Advanced Dairy Chemistry: Volume 1: Proteins, Parts A&B. New York: Kluwer Academic/Plenum Publishers; 2002. p. 739-816.

4.     Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE. Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia. 1999 Mar;42(3):292-6.

5.     Laugesen M, Elliott R. Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein. N Z Med J. 2003 Jan 24;116(1168):U295.

6.     Kost NV, Sokolov OY, Kurasova OB, Dmitriev AD, Tarakanova JN, Gabaeva MV, et al. Beta-casomorphins-7 in infants on different type of feeding and different levels of psychomotor development. Peptides. 2009 Oct;30(10):1854-60.

7.     Cade JR, Privette MR, Fregly M, Rowland N, Sun Z, Zele V, et al. Autism and Schizophrenia: Intestinal Disorders. Nutr Neurosci. 2000;3:57-72.

8.     Pasi A, Mahler H, Lansel N, Bernasconi C, Messiha FS. beta-Casomorphin-immunoreactivity in the brain stem of the human infant. Res Commun Chem Pathol Pharmacol. 1993 Jun;80(3):305-22.

9.     Hedner J, Hedner T. beta-Casomorphins induce apnea and irregular breathing in adult rats and newborn rabbits. Life Sci. 1987 Nov 16;41(20):2303-12.

10     Woodford, K. ‘Devil in the Milk.  Craig Potton Publishing 2007. (Updated Edition 2010, American Edition published by Chelsea Green 2009)

11      Sun, Z., Zhang, Z., Wang, X., Cade, R., Elmer, Z., Fregly, M., Relation of betacasomorphin to apnea in sudden infant death syndrome.   Peptides.  2003;  24,:937–943

12.   Wasilewska J, Sienkiewicz-Szlapka E, Kuzbida E, Jarmolowska B, Kaczmarski M, Kostyra E. The exogenous opioid peptides and DPPIV serum activity in infants with apnoea expressed as apparent life threatening events (ALTE). Neuropeptides. 2011.

13.   Nausch I, Mentlein R, Heymann E. The degradation of bioactive peptides and proteins by dipeptidyl peptidase IV from human placenta. Biol Chem Hoppe Seyler. 1990 Nov;371(11):1113-8.

14.   Kreil G, Umbach M, Brantl V, Teschemacher H. Studies on the enzymatic degradation of beta-casomorphins. Life Sci. 1983;33 Suppl 1:137-40.

15.   Tiruppathi C, Miyamoto Y, Ganapathy V, Roesel RA, Whitford GM, Leibach FH. Hydrolysis and transport of proline-containing peptides in renal brush-border membrane vesicles from dipeptidyl peptidase IV-positive and dipeptidyl peptidase IV-negative rat strains. J Biol Chem. 1990 Jan 25;265(3):1476-83.

16.   Iwan M, Jarmolowska B, Bielikowicz K, Kostyra E, Kostyra H, Kaczmarski M. Transport of micro-opioid receptor agonists and antagonist peptides across Caco-2 monolayer. Peptides. 2008 Jun;29(6):1042-7.

17.   Shimizu M, Tsunogai M, Arai S. Transepithelial transport of oligopeptides in the human intestinal cell, Caco-2. Peptides. 1997;18(5):681-7.

The first map (above) shows the three major fault systems in New Zealand: the North Island System, the Marlborough System and the Alpine Fault. What is also highlighted in this picture is that the North Island System actually separates the main Indo-Australian Plate (in this diagram more simply called the Australian Plate) from a ‘rootless fragment’ of this same plate. This Indo-Australian fragment has detached and is now taking a ride on top of the Pacific Plate. The real surface boundary of the Indo-Australian Plate is the Hikurangi Trough (also called a trench) to the east, where the Pacific Plate is being pushed under. The main NZ tsunami risk comes from an undersea earthquake in this trough. The figures printed within this map of 38, 39, and 41 are the average annual movement in millimetres along these parts of the trough. Elsewhere, I have seen GNS data (reported in earlier posts) indicating that the Alpine Fault moves at a similar rate to this, but that the two segments of the Indo-Australian trench are moving relative to each other at only 5-10 mm per annum. This recognition that movement between the two Indo-Australian fragments might be less than previously thought has led to suggestions that the risk to Wellington might also be less than  previously thought. Basically, the smaller annual movement leads to longer return intervals between big earthquakes. (However, the earthquakes that Wellington feels are not only those between the two parts of the Indo Australian Plate, as the Pacific Plate does reach under Wellington at a depth of 30-40km. More on Wellington later.)

The picture above shows where the major shallow earthquakes have been in the last 160+ plus years.  It is shallow earthquakes that do the most damage. There are two big swathes of the country where no big damaging earthquakes have occurred. One of these is all of the North Island to the east of the North Island faults. This is not unexpected, as it is generally an area of only moderate risk for shallow earthquakes (but not for volcanoes). The second is the area adjacent to (i.e. both west and east) of the Alpine Fault. This is not so reassuring, as it indicates that pressure is building up. (The Magnitude 7.1 Arthur’s Pass earthquake of 1929 was on the Poulter Fault which is one of several faults, this one relatively minor but others considerably larger, branching off the northern extremity of the Alpine Fault.)  The earthquakes in Fiordland are associated with the Puysegur Trench where the Indo-Australian plate is subducting (diving beneath) the Pacific Plate.

 The third map (above) shows all of the shallow earthquakes of more than Magnitude 3 over a ten year period. Most likely, this is up to the end of 2009, or perhaps even earlier, as the Magnitude 7.1 Darfield (Canterbury) earthquake of 4 September 2010 is not shown. Essentially, this map confirms how we really are the Shakey Isles but with the shallow earthquakes largely along the faults, and overlapping on this map as a splodge of red.

This last map (above) provides key information of several things. First, it shows how in the North Island the Pacific Plate is descending beneath the main part of the Indo-Australian Plate. The increasing depth going from east to west across the North Island gives a strong indication of the slope at which the Pacific Plate is descending. The second point is how there have been no earthquakes at depth  along the Alpine Fault. Once again, this is indicative of pressure building up. The two plates are in a stalemate, but the pressure is continually building, and with nowhere else to go the fault must eventually unzip. The eastern side including the peaks of the Main Divide will move south. The western side will move North.

So what does all of this mean? My own interpretations are multiple. The first is that the GNS data reinforces the notion that the Alpine Fault, which last unzipped in a major way in about 1717, is a major menace. The greatest risk, because of proximity to the Fault, is on the West Coast. (See earlier posts.) 

My second interpretation is that the Hikurangi Trough provides our greatest risk for a tsunami. I would like to learn more about that. I know that the Gisborne earthquake of 6.8 in December 2007 was at 40km depth within this trough.  However, although this earthquake did considerable damage to Gisborne, it was too deep and of insufficient magnitude to create a tsunami. Apparently, the risk of tsunami  from the Hikurangi Trough is enhanced by the possibility of major sediment deposits, deposited by the sea currents, being shaken off the sides as a landslide.  It seems that the risk of sediment landslides is strongest at the southern end of the Hikurangi Trough. This is of particular concern for those living along the Kaikoura Coast in the South Island. However, for anyone who lives in low-lying areas along the east coast of both islands, from East Cape in the north to Christchurch in the south, this Hikurangi Trough seems far too close for comfort. 

I indicated earlier that I would say more about Wellington. Despite some indications that they have already had their big one (officially known as the 1855 Wairarapa earthquake of magnitude 8.2, the biggest recorded in New Zealand since European settlement), and that the return intervals are longer than  previously thought, there is still great scope for massive earthquakes. There are also some low-lying parts of Wellington that are susceptible both to liquefaction and tsunami. Similarly, cities like Blenheim, Nelson, Hastings, Napier, Gisborne and Tauranga, together with many smaller towns, would all seem to have significant risk from tsunami. All we can do is plan and prepare, and then get on with living.

http://www.youtube.com/watch?v=NkTy6ogLDX8

In this post I report in summary terms what I learned from these plus many other reports and websites. Hopefully, other lay people will find this useful in understanding something of the ‘big picture’, and it is on this basis that I share my learnings.   What I did learn  along the  way is that there is general agreement about that big picture, but the details can be debated, even by the so-called experts.  Despite all the modern tools of science, it is not easy to see everything that is going on deep beneath the earth.

Tectonics

Here in New Zealand, we lie at the interface of the Pacific Plate and the Indo-Australian tectonic plates.  These  plates have been grinding against each other for millions of years.  However, the outcome of the collisions has three different outcomes which vary according to the location within New Zealand.  

In the North Island, and the top of the South Island including Marlborough, the relatively light Indo-Australian Plate is riding-up over the denser Pacific Plate at a rate of between 10 and 40mm per year.  Multiple fault lines extend north across Marlborough, then cross the Cook Strait, then up through Wellington and the Wairarapa, eventually exiting through Hawkes Bay, Gisborne and the Bay of Plenty. Most of these faults fracture at intervals between 500 and 2500 years. The  Wellington Fault, which extends up through the Hutt Valley, is widely considered the most likely one of these to fracture in  the next hundred or so years. But it could be another fault either adjacent to Wellington (such as the Ohariu Fault) that fractures first, and it could either be in the near future or not for several hundreds of years. Or it could be one of the  faults in the northern part of the South Island that is the next fracture.

Although Wellington is actually on fragments of the Indo-Australian Plate, the Pacific Plate lies only about 30km below. So when earthquakes occur some of these are likely to be at this depth, which is sufficient to cushion some of the shaking. Wellington’s recent Magnitude 4.7   earthquake on 4 March 2011 was actually on the Pacific Plate lying underneath the Indo-Australian Plate at about 30 km depth. A slightly smaller earthquake three days previous was at about 40km.  All major North island earthquakes – such as the Napier earthquake of 1931 and the Wairarapa earthquake of 1855 – lead to the land being uplifted by what  is known as ‘subduction’ of the Pacific Plate, which gets squeezed beneath  the Indo-Australian Plate.   Eventually, the leading edge of the Pacific Plate gets forced down to depths of about 600 km where it melts into magma.

To the west of the main North Island faults, fissures develop in the Indo-Australian Plate.  In effect, the plate cracks as it is  forced up over the Pacific Plate. These cracks provide a means for magma to escape, and hence we have the North Island volcanoes.  In contrast, on the eastern side of the major fault we have the Hikurangi Trench and the Kermadec Trench. These are caused by the Pacific Plate being forced downward, with some of that having occurred nany millions of years ago.

In Fiordland, at the southern end of the country, the reverse is occurring. Here, the Indo-Australian Plate is being subducted under the Pacific Plate. In contrast to the subduction in the North Island which involves a relatively shallow dive, in Fiordland the Indo-Australian Plate is taking a steep dive. In Fiordland it is common to get big earthquakes, but many of them tend to be at considerable depths (because of  the steep dive), and hence their effects on the surface are  less.

The Alpine Fault

In between these two zones lies the Alpine fault, which extends south from about Greymouth, and disappears into the Ocean about 12km north of Milford.  In this zone, and for a distance of between 450 and 600km, there is a stalemate between  the Pacific and Indo-Australian Plates, with neither being able to ride up over the other. Along this Alpine Fault – which actually lies some distance from the high mountain peaks  and well down on the West Coast side of the Southern Alps – the stalemate leads to a relative  absence of small earthquakes. Instead, the two plates lock together, building up pressure causing the rocks at depth to melt, until there is a cataclysmic release. The West Coast side slips north, and east of the fault the land slips south. Typically, each major earthquake on the Alpine Fault is of Magnitude 8 or greater. Horizontal slippage is 8-10 metres. There is also uplift of about 4 metres along the edge of both plates .  Over many millions of years the uplift has totalled about 20,000 metres, but  erosion has limited the mountain tops to less than  4000 metres.

 During the last 1000 years, the Alpine Fault has fractured four times, at intervals of about 150-350 years. The last fracture is widely believed to have been  in 1717.  So the maths is not comforting. According to the GNS website, there is a strong likelihood of a Magnitude 8 earthquake on this fault within the next 40 years.  The greatest destruction would likely be along the aWest Coast. Towns such as Greymouth, Hokitika, Ross, Harihari and Whataroa, plus the Glacier Towns of Franz Josef and Fox, would probably take the greatest hits.  The effect in Christchurch from a Magnitude 8 earthquake on the Alpine Fault would likely be similar to the Canterbury 7.1 earthquake of September 2010, but hopefully much less than the 6.3 eathquake of 22 February 2011, which was almost underneath the city and at very shallow depth. An 8.5 or even greater earthquake, which is defintely possible,  hardly bears thinking about. But even then, our recent experience seems to say that genuinely modern buildings built on firm ground, and to the latest building code, are incredibly robust.

Christchurch

So how does the Alpine Fault explain the Christchurch earthquake of February 2011?  In a direct sense, it does not, in that neither the September 2010 or the February 2011 earthquake involved fracture of the Alpine Fault. But these earthquakes were related to the pressure exerted between the two great plates, of which the Alpine Fault is the most explicit sign. Instead of fracturing at the boundary, these recent earthquakes involved fractures within fragments of the Pacific Plate on which Canterbury lies.  In other words, they were ‘within-plate ‘ earthquakes but caused by tension between the plates.  There is also speculation that the North island subduction zone is slowly (over many millenia) shifting southwards and this could be part of the story.

If we go back some millions of years, there is evidence that at one time the Pacific Plate was actually climbing over the Indo-Australian Plate along much of the length of the South Island. This is the most likely explanation for the Banks Peninsula volcanoes. This would also explain the extinct volcano of the Dunedin Peninsula in Otago, and the volcanic origins of Mt Somers in the Canterbury foothills. But those events were all many millions of years ago.

Looking back over the last 150 years – a mere instant in geological time – there have been several earthquakes in Canterbury of about Magnitude 7. Given the particular geology of Canterbury, and the associated risk of liquefaction,  the damage would seem to have been higher than would normally be expected with this magnitude of earthquake. It would seem reasonable to expect more of these earthquakes over time, although where in Canterbury they will be is probably impossible to predict. There may be a greater likelihood  for these to occur in North Canterbury and along the Kaikoura Coast than in South Canterbury.

Christchurch versus Wellington

When I was young, and indeed until recently,  the conventional wisdom was that Wellington was the region of New Zealand with the highest earthquake risk. This assessment was based on the known effects of the 1855 Wellington /Wairarapa earthquake, plus the high visibility of major fault lines.  In Canterbury, where the fault lines are buried beneath the shingle, and where there has never been a Magnitude 8 earthquake within recorded history, the risk was assessed much lower. But that has now changed. An increasing knowledge of the tectonics of the Alpine Plate has created an understanding that the likelihood of a Magnitude 8 or greater earthquake on the Alpine Fault is very high. And the two recent earthquakes on fragments of the Pacific Plate that lie beneath the Canterbury Plains have provided new understandings of how the tectonic forces are occurring. Over time, there is considerable potential for further ‘within-plate’ earthquakes of Magnitude 6 or 7, and for these to occur at very shallow depths.

Personally, I am happy to stick with Canterbury as my home. However I am one of the lucky ones who has a house that is largely undamaged. I might see things differently if I were a young person with a destroyed house.  What I do  now  know is that in Canterbury we are all truly  part of the Shakey Isles. Whether the risk going forward is actually more in Christchurch than in Wellington I do not know. At least here in Christchurch we are 100km from the Alpine Fault, whereas Wellington sits right on top of major faults. Of course one could go and live in Auckland. There the risk of earthquakes is much less, although they too are still part of the Shakey Isles. However,  Auckland has the additional risk of volcanoes, as do most parts of the North Island lying west of the plate boundary.   Those  Auckland volcanoes are only sleeping, as is Mt Taranaki and many others. At least there are no Aussie snakes anywhere in the Shakey Isles!

There are many puzzles as to why some of Christchurch’s  buildings have survived the 6.3  earthquake of February 2011, and others have not. However,  a combination of observations plus document-searching does provide some answers.  In terms of magnitude, this was just a moderate earthquake, but the local effects on  Christchurch have been huge because of its proximity and shallowness. Even within Christchurch, location was of huge importance, but there is more to it than that.

It seems that we do indeed have very stringent building codes in New Zealand. Not only are the codes stringent, but they are enforced. However, in Christchurch we also have many old buildings which predate these regulations. The original building codes go back to 1935, but earthquake design really only started in 1965. The codes were further strengthened in 1976 with the concept of ‘controlled failure’, and strengthened again in 1984 and 1992. The codes focus on the standards that have to be met, rather than specifying precise building procedures. This is to encourage new and innovative building methods that can meet the required standards.

Having planned the building of a new house both in Australia (in the 1980s) and in New Zealand ( in 2001), I know that the building code is a lot stronger here in  New Zealand than in Australia. Our Queensland house was built on a hill-top and had a special cyclone rating, but I doubt very much whether it would have withstood the shaking that our New Zealand house has withstood. The Christchurch building inspectors made multiple visits at key times to our New Zealand home, particularly when the foundations were being laid. It is the stringent New Zealand building codes that make house building so expensive in this country. I have also looked with wonder at the simplicity of house construction in Uruguay, where earthquakes are essentially unknown.

The messages from the 7.1 ‘dress rehearsal’  earthquake on September 2010 seemed reasonably straightforward. Old houses and commercial buildings constructed in the early 20th century, or in some cases in the 19th century, and which relied on single or double brick for their structural integrity, disintegrated rapidly. Also, houses built on a concrete pad in areas adjacent to streams and waterways, were found to be susceptible to cracking of the pad linked to liquefaction of the soils.  

Unfortunately, a house with a concrete pad that has cracked and split is history. Each day over the last five months, as I have driven to work, I have looked with wonder at a multi-million-dollar modern home owned by a well-known sporting identity, which looks normal from the road but is going to be pulled down for exactly this reason. 

The conventional view on liquefaction seems to be that the damage is caused by subsidence of the buildings into the soil, but I don’t think it has to be this way. At least over my side of town (Halswell),  I saw evidence in the 7.1 September earthquake of a powerful wave. I liken it to an undergound tsunami, that travelled through the aquifer from the epicentre, and then burst upwards as it hit the underlying rocks of the Port Hills. Anywhere adjacent to a current or former spring was at risk. Even the underground fuel tanks at my local service station, filled with fuel just the day before, were thrust upwards by this force. Across the suburb, the silt and sand laden water continued to flow from some of the boils for several hours afterwards. In contrast, in parts of the low-lying Eastern suburbs I assume that the liquefaction damage was indeed through subsidence, as I have no evidence to argue otherwise. 

Liquefaction on Kilmore St ( Asher Trafford)

Liquefaction in park off Colombo St (Asher Trafford)

There is a somewhat historical  (probably about 1999) but generally informative assessment of the liquefaction risks in Christchurch at http://ecan.govt.nz/publications/General/solid-facts-christchurch-liquefaction.pdf  However, I think that if they were to write this document again it would say some things differently.  One small but perhaps important point is that at least in some places the water and sand continued to bubble up for hours after the earthquake and not just during the earthquake. Also, both  in September 2010 and again in February 2011, there has been some liquefaction in areas previously identified as low risk. Some places that escaped liquefaction last time have received it this time, and vice versa. It seems to me that we still have much to learn about liquefaction.

One of the key messages from the September quake seemed to be that as long as a building was away from the streams, rivers, or low-lying land with a high water table, then it could withstand the shock as long as it was of modern construction. Where the shaking or ground movement was severe, then houses on piles seemed to fare  somewhat better than those on concrete pads. Houses with modern timber structural framing  also stood up particularly well.  As for the brick chimneys on the older wooden houses, well they descended ungracefully to the ground.

With the February earthquake there now seem many more lessons to learn.  The devastation in  the CBD includes modern buildings built from the 1960s to the 1990s that were untouched by the larger but not so close 7.1 September dress rehearsal. At least up until the mid 1980s, the designs were non-ductile. In other words , they were built for strength, but with rigidity rather than the flexibility needed to  absorb the energy of a huge quake.  Modern design is not supposed to mean there will be no damage, but it is meant to prevent catastrophic failure that causes death.

Grand Chancellor Hotel with earthquake damage and tilting at 2 degrees

The story behind the failure of the 26 (some reports say 27) level Grand Chancellor Hotel, constructed in 1995, will take some time to emerge. Presumably it was built to the latest codes so as to absorb the energy without suffering structural failure. It is in Cashel St, several hundred metres from the Avon River. Clearly it suffered immediate damage, but it was only some hours later that it began to tilt. Perhaps the ground acceleration went beyond the design capacity, as there is no doubt the ground acceleration was extreme. Maybe the wonder is that more modern buildings have not collapsed, and perhaps we should give due credit for that.  A big unknown is how many of the modern buildings that apparently survived will still have to be pulled down. Semi official reports coming through are suggesting more than  500 buildings in the CBD will have to go.

Before and after shots of  the PGC building (see below) tell a story of a modern-looking building, although built in about 1963. That means it pre-dated the first earthquake design requirements of the 1965 code. Originally this was known as the ‘Drainage Board Building’. Eventually the Drainage Board morphed into Environment Canterbury. Whether or not PGC were actually the building owners in 2011, or simply the major tenants with naming rights, is not clear to me. [Update: The buildng was sold to private investors in 2009.] What is clear is that people on the upper floors had the best chance of escape, with many of those on the lower floors being crushed by the collapse of heavy concrete floors. This building is adjacent to the Avon River in  Cambridge Terrace.

Before and after shots (below) of the seven storey CTV building (built in the 1980s) show another  modern-looking building. [Update of 1 March: there are conflicting reports as to the date of construction. It may have been 1979.]  This building looks heavy but with light structural support in the corners. [Update of 1 March: There are reports that the structural strength was supposed to come from the 'core' built into the rear of the building. This core is still visible in the 'after' photo. The rest of the building was in effect suspended from this core with only light support in the corners.] The building is many hundreds of metres from the Avon River on the corner of Cashel and Madras Streets. It was built nearly ten years after the 1976 regulations [see update above] which  introduced the principles of  ’controlled failure’ and may also have been subject to the 1984 regulations. Either way, there are questions to be answered as to why the failure was so catastrophic. This is the building where most of the deaths occurred, perhaps as many as a hundred or even more, including most of the foreign deaths at the Kings Language School. It would seem that some were killed by the ensuing fire after being trapped.

CTV building before and after

Christchurch Cathedral

 

The collapse of the cathedral is less surprising. In Christchurch we have been very attached to our heritage buildings, but now it is time to move forward and rebuild from the ground up. 

Christchurch Cathedral

Over on the eastern hills of Sumner, Redcliffs, and Mt Pleasant ,  it seems the shaking of the ground was so extreme that no practical building code could have saved many of the houses. However, on the western hills, where I live, the form of cladding seems relevant. Most of the houses have timber framing and this has stood up well. But whereas plaster cladding has survived, some of the brick veneer homes are looking a little naked, with timber and building paper now visible. As to whether they have retained their structural integrity underneath, that will require an engineer’s report.

As for the low-lying eastern suburbs, here too it won’t be until the engineers’ reports are available that the real picture will emerge. The liquefaction on these soils is much greater than  in September, and initial reports are of up to 150,000 tonnes of sand and silt needing to be removed, compared to about 30,000 tonnes last September. [Update: By early March some 180,000 tonnes had been trucked out.] A lot will depend on whether the concrete pads have shifted, cracked, and tilted.

What we do know for sure is that thousands of homes cannot be brought back to being livable.  And a lot of those that may be livable in the short-term, are still incapable of being permanently repaired.

As each day goes by, the task of rebuilding Christchurch city and suburbs seems to grow.  Yet only a few km away there is no damage. Earlier today I was out at Lincoln Uni, only 20 km from the city centre, and there the damage is minimal. In my Uni office, and in sharp contrast to the September earthquake, there is not one paper or book that has moved. This provides a reminder that the Christchurch earthquake really was a local event: short, sharp and vicious. Although Lincoln Uni does remain closed, that is because many staff and students live in the city. In any case, the Uni itself is being used as a base for rescue personnel.

(Photo credits: The first three photos in this post come from Asher Trafford. These are just three of many photos taken by Asher, who jumped on his bike and took some amazing photos around the city in the immediate aftermath. Other photos are sourced from Google and are currently uncredited.)