At the Grassland Research Institute, they pioneered the practices that now allow even a small part of England to grow all of the food needed to feed the whole country. They specialized in grass farming and were telling young farmers how much more efficient their farms would be if they took out most of their hedgerows. Hedgerows are made of woody plants entwined with brambles; they are natural fences festooned with natural barbed wire. They included all of the woodland trees: oaks, ash, beech as well as holly, blackthorn and hawthorn. It is said that in some places the age of a hedgerow can be guessed by counting the number of woody plants per thirty-yard run. Ten different species implied an age between one and two thousand years old. Hedgerows represent the most amazing symbiosis of human and woodland ecosystems, and they are places where birds can nest. They are the habitats of predatory insects—ichneumon flies, small wasps, and ladybirds—that are the natural means of keeping pests in check. Hedgerows evolved in the days when mass-produced farm machinery was non-existent. Horses were the power sources and small fields enclosed by hedgerows were the norm.
What we were doing at the Grassland Research Institute was providing essential information to the civil servants of the Ministry of Agriculture and Fisheries and the farmers. They then used it to plan their campaign to replace the old English countryside with an efficient agribusiness operation. We took the breath-taking beauty of our land as much for granted as would a peasant farmer that of his young wife, and we expected it to work for us, not realizing that a life of drudgery is incompatible with beauty. In the pursuit of agricultural efficiency we were concerned with choosing the breeds of sheep and cattle that most efficiently converted grass to meat, and Frank Raymond had the notion that the more placid an animal was the more weight it would gain during grazing and that unnecessary movement wasted energy. He had asked me—in my role as an inventor—if I would design and make a device that cattle could wear that would continuously monitor their movements. It would have to record how much time an animal spent walking, running, sitting down, chewing the cud, and so on. To meet this need I designed a small battery-operated radio transmitter that broadcast information on the animal’s movements as notes at different audio frequencies. The senior technician at Harvard Hospital, Ron Canaway, converted my rough breadboard design into a neat package that fitted on the back of a young bullock. I had brought the first model of this device with me for trials at Stratford-upon-Avon.
In the 1940s, unlicensed emissions of radio frequencies were forbidden and we needed a licence to operate our transmitter. Here we encountered an odd problem. The law required all transmitters to start and finish operation by sending their call sign in Morse code. How were we to train our bullocks to use a Morse key? When I explained our problem to the officials of the licensing authority, which was then the General Post Office, they laughed, relented and gave us a licence. I then went on to request a frequency of 175 megahertz for the transmitter. Higher frequencies would have been beyond the capacity of the simple devices then available and lower frequencies would have required an aerial (antenna) so long that the animals would have broken it off when they walked under trees. The civil servants at the General Post Office wisely saw that this was a genuine need, even though a peculiar one. They granted us a licence to transmit and waived the need to use our call sign, G9OO, which nevertheless they assigned. By present-day standards, the transmitter was heavy, bulky, and inefficient; the transistor had not yet been invented. For the technically minded, I used a DCC91 double triode as the output stage of the device. It was power hungry and batteries were much less long-lived than they are now, but it worked, and I played my small part in the destruction of the English countryside. The scientists, the farmers, the agribusiness men, and, most important, the civil servants who drafted the legislation that gave grants to farmers to take out their hedges, all of us were ignorant of the consequences. I am ashamed and now regard myself as part of the unconscious vandalism that has all but destroyed the beauty of my country.
4
The Mill Hill Institute
My boss at Harvard Hospital was a gentleman as well as a distinguished virologist; later he was knighted, but in the 1940s was just Christopher Andrewes. He was the co-discoverer of the influenza virus and a talented amateur entomologist. Often when he visited Harvard Hospital he would take me with him on expeditions to the New Forest where he collected specimens of his favourite insect, the sawfly. How different science was in those days. The two of us walked as companions enjoying the quiet delightful countryside and discussing our researches. Sometimes he would ask me to walk a few yards ahead on the path. It took me some time to discover that he was using me as bait for his beloved flies.
One day in September 1951, on the way back from one of these expeditions to the New Forest, I voiced my doubts about continuing to work at the Common Cold Research Unit. Perhaps it was the slight pique of having been used as mere bait or, more likely, because I sensed that for me the virology chapter was due to come to a close. Andrewes was shocked to hear that I was thinking of resigning from his division but he was a good man and he promised to discuss my wish with the director of our parent Institute in London, Sir Charles Harington. He was true to his word, for within a day Sir Charles summoned me to London. He was a man who resembled the Prime Minister of that time, the Labour leader Clement Atlee, or, indeed, the US President, Truman. He was a small, perhaps shy man, with a limp caused by a tubercular infection of his hip as a child. His slight stature belied the strength of his character: they said he was descended from a line of judges. Whether or not this was true, he was one of those few people I have encountered in life whose presence was immediately and tangibly felt, who could exert authority even without speaking. Without preamble he said, ‘I am so glad you are coming back to the Institute. You have been much too long in the wilderness of Harvard Hospital. I have a problem for you and it is urgent. Can you start next week?’ He didn’t expect me to disagree. He was a man with an attention to detail that now you would think of as Japanese, and had already arranged that Helen and my family could stay at Harvard Hospital for as long as it took me to find somewhere for us all to live in London. He made a lab available for me on the first floor of the institute. It was like falling over a small waterfall, exhilarating but with the knowledge that there could be no going back, no indecision. The National Institute for Medical Research (NIMR) at Mill Hill in North London was an odd building. Its design reflected the chemical structure of a benzene ring. In the 1930s, so many drugs and important natural compounds had the hexagonal shaped benzene molecule as an important part of their structure that chemists and biochemists felt the need to recognize this fertile shape in the lab they hoped soon to occupy. In fact, it was not opened until 1950 and this was because during the war years, it was a barracks for women enrolled in the Navy and it took five post-war years to equip it as a medical research institute. By 1951 the hexagonal main building had four wings which made it more like the structure of the hydrocarbon durene (tetra methyl benzene). It was a wonderfully well-equipped institute with a first class library and a spacious lecture hall as well as having mechanical and electronic workshops and a vast animal house. In the spacious grounds was a small farm; the fields and woods of London’s Green Belt surrounded it. The whole of the administration occupied a few rooms on the first floor of the main building and only a few per cent of the annual budget of the Institute went for administration. This meant that often we had to type our own letters and papers but there was a great freedom from bureaucratic interference.
Soon I was living during the week with my beloved mother-in-law, Queeny Hyslop, in her flat at the foot of Highgate Hill near Parliament Hill Fields, in North London. I walked each day through the back streets to Archway Tube Station and took the tube from there to Mill Hill East and then a bus to the Institute, which was at the top of Mill Hill. I travelled by train to Harvard Hospital on Fridays and returned on Monday mornings.
On my first day back, they gave me a roomy perso
nal lab looking out over the front lawn of the Institute. It was in the experimental biology division, sited on the first floor. Here I met my colleagues, Alan Parkes, the divisional head; Audrey Smith, the Cambridge biologist; Chris Polge, a veterinarian; a visiting scientist from America, a haematologist, Henry Sloviter; and the senior technician of the department, Fred Crisp. Before long, the director summoned me and gave me my brief. ‘Lovelock,’ said Sir Charles, ‘Parkes and his colleagues are doing important work. Their successful freezing of a variety of cells and tissues will affect medical research and benefit it everywhere, but I’m concerned that these competent biologists are almost wholly ignorant of chemistry and physics. I doubt if they know one end of a thermometer from the other. Your job is to see that they do not make mistakes and bring discredit upon the Institute. Of course, you will want to do your own research so what are your plans?’ Fortunately for me, I had a clear idea of what I wanted to do because in the days before returning to London, I had thought of nothing except what could happen to cells during the process of freezing. I used my usual technique of empathy; that is, imagining myself to be a cell and wondering what would happen as I froze, and I had concluded that the worst thing that could happen would be an ever-increasing salinity as water was taken from the cell itself and from its medium to make ice. Ice always separates as a pure substance, and the dissolved solids are left behind concentrated in the remaining water. Interestingly, this meant, in effect, that freezing was the same as drying.
Everyone knows how easily lack of water kills plants and animals, but I knew that it was too soon to venture so odd an idea. The conventional wisdom was that freezing kills cells by literally spearing them with sharp ice crystals, and Audrey Smith herself had made a remarkable film of cells freezing on a microscope slide. She had travelled the world with this film and shown the growing ice crystals apparently penetrating the cells. I didn’t think it was appropriate for me to come out with a rival theory just at that moment so all I said was, ‘I have thought about it quite a bit and I have some ideas on what the mechanism of damage might be and how glycerol protects the cells against this damage. I’d like to try a few experiments before confirming these views and producing a research plan.’ He said, ‘Good, that’s fine by me.’ He was a good scientist and knew that I would have to do it that way. He then went on to the important things, to me, namely salary and finding a house for my family. In spite of his formidable air, he was a humane and kind man. He dismissed me, saying, ‘Well, if there’s anything you need or any support, just let me know.’
Unfortunately for me, some of his thoughts on the capacity of my biologist colleagues to handle the physical chemistry of freezing must have got back to them, and the first few months I spent at Mill Hill were rather strained; on bad days they saw me as a spy for the director. I worked mostly with Christopher Polge and Audrey Smith; Audrey resembled the actress Margaret Rutherford. She dressed in tweeds and sensible shoes and had a loud voice and bossy air. In other ways, Audrey was like my mother and, having grown up with one formidable lady I had no great difficulty discounting the externals and enjoyed working with the real and very able person that was underneath. I did not like the way my biological colleagues treated me as a useful technician and no more—one who could do wonders with thermocouples, diathermy and other physical devices but was, in their eyes, not a proper scientist. Like all specialists, they had disdain for the other disciplines of science. For them real science was biology. Chris Polge, although just as good a scientist, was easier company. He looked like a young farmer and, since he was in charge of the department’s livestock, which included twin bulls called Castor and Pollux, it seemed right that he should. The work he did was probably the most important. His pioneering success with a technique for preserving animal spermatozoa in the frozen state affected the conduct of farming worldwide. Rightly, the Royal Society elected him a Fellow in 1983 and he was awarded the Japan Prize in the 1990s.
When I was not helping them, I was able to pursue my own researches into the damage done to human red blood cells by freezing and how glycerol protected them, and it turned out to be exactly as I had imagined. My colleagues had developed a technique for freezing living cells that was quite slow and it took several minutes before the cells were frozen. At this slow rate of freezing, the water around the cells froze, but the cells themselves merely dried—and drying was the cause of their damage and death. I was able to show that glycerol and similar substances exerted their protective action by preventing this drying process from taking place. These solutes stopped it proceeding beyond what was a sharp critical point. This finding was published in two papers in the journal, Biochimica et Biophysica Acta, and has now become part of the conventional wisdom of cryobiology. Indeed, one of these papers ‘The mechanism of the protective action of glycerol against damage by freezing and thawing’ was the most cited paper in biological science for the year following its publication.
To confirm my ideas about the effects of freezing on cells I had to separate the mechanical effects of the ice crystals from the toxic effects of the concentrated salt solutions. The way I did it was to suspend cells in salt solutions of various strengths. I soon found that salinity greater than five per cent damaged almost all cells, whether from animals or plants. The strong salt caused lipid components like lecithin to leach from cell membranes. When this happened the membrane became fragile and it easily split when stressed. Freezing exposes cells to concentrated salt solution and thawing from the frozen state subjects them to stresses great enough to break open the salt-damaged cells. This knowledge stayed with me and when later the idea of Gaia, a self-regulating Earth, first came into my mind, I began to wonder how the salinity of the sea had always kept below five per cent. It has done so for over 3 billion years, otherwise marine life would not have survived. We still do not know what regulates salinity. Maybe the burial of salt goes on at just the right rate by chance. Much goes to form the lagoons of salt that exist on the shorelines of continents. These are the evaporite deposits and, when they are buried under sediments, become the ubiquitous salt beds of the Earth. I still do not know how ocean salinity stays below five per cent; it is one of the puzzles posed by the notion of Gaia.
In the first months back at Mill Hill I had to buy a house for the family to live in. Helen, who otherwise would have helped me, was in the last months of pregnancy and Andrew our third child was born in early November 1951 at Salisbury Infirmary. Alick Isaacs, a young virologist in Andrewes’s department gave me generous help in finding a house. He was a small, dark, mercurial man of about my own age and with a Scots accent. He knew Finchley well and he introduced me to estate agents and a solicitor and gave me wise advice about mortgages. I knew him a little from his visits to Harvard Hospital but soon we became close friends and I joined him on weekends in his search for flint implements and arrowheads in the quarries of Kent. Alick was the discoverer of Interferon; indeed, he named it and the name has lasted in spite of objections by purists who seem shocked by any new name. Sadly, he died before they successfully applied his discovery in medicine.
The road from Edgware to Mill Hill through north London was typical of suburban development. Graceless uniform shopping centres separated the ranks of semi-detached villas with tiny gardens; the shops and dwellings looked as if they had been factory-built to the plans of a council committee. They lacked the rich diversity of shops and houses of our older market towns. So dull was the journey that morning as I drove my old Rover car that I failed to notice I was speeding. The limit was 30 mph and I was travelling at over 40. Suddenly a police siren and flashing lights just behind me startled me. It shattered my deep thoughts of the experiments waiting to be done with the blood I had just collected from the Edgware blood bank. I pulled over, feeling that wretched guilt that comes with law breaking no matter how trivial. A young PC came to my open car window and said, ‘Can I see your licence sir?’ I handed him the small red book and awaited his admonition, but instead he looked at me, then
back to my licence and gazed at the litre bottle of blood sitting on the passenger seat. His manner changed from prefectorial to professional. ‘Sorry sir,’ he said, ‘I did not realize that you were on your way to an urgent case. Would you like us to escort you?’ I declined his offer as convincingly as I could. I feared the consequences of a high-speed drive back to the Mill Hill Institute with the sirens sounding. I took off decorously at just above the speed limit and was relieved to see the police car turn round and retreat down the road to Edgware. I had never thought that a PhD in medicine was such a powerful token. In fact, I was returning from my weekly visit to the blood bank not, as most do, to donate my blood, but to collect some for my experiments in the frozen state.
We donate our blood without charge in the UK. This generosity pre-dates the Health Service but is now an essential part of it. We need a constant supply of fresh blood to replace the losses that happen in accidents and in surgery and to maintain the stocks. The red cells that give blood its colour and capacity to carry oxygen to the tissues do not survive long in or out of the body. Even in their normal habitat, the life span of a red blood cell is only 100 days. After three weeks’ storage at refrigerator temperature they reach their use-by date. After this, only the plasma is used, and the red cells are discarded because blood cannot be stored in a deep freeze. The acts of freezing and thawing both cause the red cells to burst open. My colleague, Audrey Smith, had found empirically that after the addition of fifteen per cent glycerol, blood would keep for a year or more at –80° C. Unfortunately, blood containing fifteen per cent glycerol cannot be transfused. My job at the time was to try to find a way of removing the glycerol without harming the red cells.
Homage to Gaia Page 16