A bad day at the lab for GM reserach

During this summer, I recall reading in the Sunday Times that the environmental NGOs are beginning to re-think their strategy on GM foods. I see some evidence that this is the case since I cannot find any mention of the following paper on any of their websites: Séralini et al (2012) “Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize”[1]. The publication of this paper has led to the greatest backlash by the scientific community that I have seen in 4 decades in this business. Essentially, Séralini published a paper showing that rats exposed to a GM food (maize) and a herbicide (which is used with the resistant GM crop) developed breast tumors significantly faster and to a greater extent than controls rats over 104 weeks (2 years). The most significant critic is the European Food Safety Authority (EFSA), which is the independent body charged with protecting consumer health in the EU and which is the judge, on the consumers’ behalf, of all scientific publications on food safety including those on GM technology.

The authors used Sprague-Dawley rats that will naturally develop tumors over their lifetime irrespective of any dietary or other treatment and the authors did not discuss the implications of this natural tendency to tumor development for their study. They also used 10 rats per treatment, which according to OECD protocols is adequate for standard 90-day toxicity studies. Monsanto’s submission to EFSA on the GM maize (NK603) used only 10 rats per treatment, but it was for a 90-day toxicity study. However, Séralini’s study was over a “lifetime” and the OECD guidelines recommend the numbers now be increased to 20 per treatment for chemical toxicity tests but that for carcinogenicity studies, this should be increased to 50 per treatment. In an article on this topic, Nature contacted Harlan Laboratories who supplied the rats and were told that for this strain of rat, only 33% of males and 50% of females live to 2 years. According to the OECD protocols, if a study is to last 104 weeks, then the survival rate should be 50% at least and that then 130 rats (half male half female) should be used per treatment.

The lead author apparently agrees that more rats per treatment would have boosted his statistical power but according to Nature[2], he argues that he did not design the study to find tumors.  If at this stage you are confused, then you’re normal!!!

Further criticism from EFSA includes the fact that no information is given on the composition of the rat diets and that no data is given on how much of the herbicide was consumed through its route, drinking water. No data are given on lesions that were found which were not tumors or dropout rates and reasons for dropouts. In addition, the EFSA working group state that the statistical techniques used were not “commonly-used statistical methods” and that the authors do not state whether the unusual statistical techniques they used were, in fact, the a priori choice and if so, why so? Finally EFSA requested the basic data from the authors to examine these shortcomings and they were refused access. Trust is hard won but easily lost. 

If all that wasn’t bad enough, Nature reports on a very sinister dimension to this saga, which has not received widespread attention. According to their correspondent, Declan Butler, the author orchestrated a very tight media offensive that included a film and his new book (Tous Cobayes: OGM, Pesticides, Produits Chimique: All Guinea Pigs, GMOs, pesticides and chemicals) on the work. A select group of journalists were invited (not from Nature) to preview the paper and were asked to sign a confidentiality agreement demanding total secrecy until formal publication. A breach of the terms of the confidentiality agreement would require, according to Nature, the following: “A refund of the cost of the study of several million euros would be considered damages if the premature disclosure questioned the release of the study”. I’m in the wrong business I believe!!!!

The Ethics Committee of one of France’s most august academic bodies Centre National de la Recherche Scientifique described the PR exercise as “inappropriate”.

Who’d like to be the first to write a review of his new book on Amazon[3]? Well although I would, it would be so slanderous that I could not ever afford the libel fee I’d have to pay.

---

[1] Séralini GE, Clair E, Mesnage R, Gress S, Defarge N, Malatesta M, Hennequin D, de Vendômois JS. Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food Chem Toxicol. 2012 Nov;50(11):4221-31

[2] http://www.nature.com.eproxy.ucd.ie/news/hyped-gm-maize-study-faces-growing-scrutiny-1.11566

[3] http://www.amazon.co.uk/Tous-cobayes-pesticides-produits-chimiques/dp/2081262363/ref=sr_1_1?s=books&ie=UTF8&qid=1350944840&sr=1-1

Fat Englanders ~ 200 years ago

(Apologies for non-publication of some recent blogs but China still poses Internet challenges)

William Wadd, born in London in 1776. He was from a medical family and he followed in that tradition, becoming a Member of the Royal College of Surgeons of England in 1801. After a distinguished career in medicine, he was appointed one of the Surgeons Extraordinary to King George IV in 1820. Wadd wrote notes on his favourite topic, obesity and although he always proposed to tidy them up for into a book, they were in fact published in unedited form in1816. His book (still available on Amazon) bore the lengthy title: ”Cursory Remarks on Corpulence, Or, Obesity Considered As A Disease: With a Critical Examination Of Ancient And Modern Opinions, Relative To Its Causes and Cure.”  What is singularly important about this book is its comments on obesity and its prevalence, its perceived causes and consequences and on its social context all at the turn of the 18^th century. For those of us interested in obesity all of 2 plus centuries later it is worthwhile reflecting on some of the comments of Dr Wadd.

Epidemiology: Of the general epidemiology of obesity prevailing at the time he writes: ”If the increase of wealth and the refinement of modern times, have tended to banish plague and pestilence from our cities, they have probably introduced the whole train of nervous disorders, and increased frequency of corpulence”.  He goes on to argue that: ”It has been conjectures by some that for one fat person in France or Spain, there are an hundred in England.” These comments on the widespread prevalence of obesity 300 years ago is in direct conflict with a key assumption of Robert Kessler in his popular bestseller “An end of overeating” is that obesity is more or less a recent phenomenon…. A measure of opulence that surprises one at first but on reflection should not surprise us at all is the advent of chimneys. Wadd cheekily ponders the adornment of houses with chimneys but speculates that there is no associated record “…of the front of a house or the windows being taken away to let out, to an untimely grave, some unfortunate victim, too ponderous to be brought down the staircase”!

Genetics: “The predisposition to corpulency varies in different persons. In some it exists to such an extent, that a considerable secretion of fat will take place not withstanding strict attention to the habits of life and undeviating moderation in the gratification of appetite. Such a predisposition is often hereditary”. It is interesting to note that 300 years ago there was recognition that obesity had a genetic dimension, which modern research shows to be of the order of 75% in terms of heredity but which is still so hard to stomach for the high priests of health eating.

Social class and the obesogenic lifestyle: “Yet even such dispositions [hereditary] seem to require certain exciting causes to bring them to action. Of these, a free indulgence of the table is principal. For it must be admitted that the lower orders of society, the poor and the laborious are seldom thus encumbered and it is only among those who have the means of obtaining the comforts of life, without labour, that excessive corpulency is met with. You may see an army of forty thousand foot soldiers without a fat man. And I affirm, that by plenty, and rest, twenty of the forty shall grow fat.”

Comments on causes: ”The article of drink requires the utmost of attention. Corpulent persons generally indulge to excess; if this be allowed every endeavour to reduce them will be in vain”. Boo-hoo for the boozers! On sugar he wrote: ”Negroes in the West Indies get fat at the sugar season” and he also commented: “The following case, which occurred in my knowledge, seems to prove how readily the saccharine particles of vegetables contribute greatly to increase bulk”. He then goes to describe a case history of a brewer who got fat, not on the alcohol but on the “sweet wort” from which it was brewed.

Treatments: He describes very many treatments from vegetarianism (the most popular), the consumption of vinegar or soap, salivation, perspiration, exercise or bandaging. He concludes: ”These are the principal articles that have been resorted to in the treatment of this disease; and the person who depends solely on the benefit to be derived from the use of any of them, will find himself grievously disappointed”.

“How can a magic box of pills,

Syrup, or vegetable juice,

Eradicate at once those ills,

Which years of luxury produce”

200 hundred plus years and nothing much has changed!!

Calorie restriction for longevity ~ For mice, not man

Work in any field long enough and you get a “nose” for the job. It is an instinctive reaction to some new event or idea, built on decades of the passive accumulation of knowledge in ones chosen field. I’ve acquired such a nose an did so quite early on. Instinctively, I could spot a good, original and potentially new area of interest among a forest of dross. Equally, I could sniff a no-hoper, a line of research rapidly going nowhere. I first heard a lecture on calorie restriction over 15 years ago, appropriately at a hotel affiliated to the Orlando Disney Park. Rats, whose energy intake was restricted to 15 - 25% of caloric intake, lived longer than rats given as much as they liked to eat of standard rat chow. I neither like nor dislike rats but it remains that I really have no feelings for them of any substance. The fact that the caloric restriction made them live longer was really of no interest to me, other than to wonder how rats feel about longevity in a captive and restricted, if not slave-like existence. However, translating this to humans really made me titter. We live in an extraordinarily obesogenic environment with overweight and obesity abounding and growing in prevalence to every corner of the globe and with quack diets and trash books for every desirable attribute, including weight loss and aging, dominating the mass media. So, it appears from the rat handlers, that  we are to think about adding caloric restriction as an additional string to our public health nutrition bow to beat the grim reaper and steal a few more mortal years. As one of my teachers used to say in exasperation in class at daft responses: “Ye gods and little fishes.”

The effect of caloric restriction on longevity was first reported in 1935 and has now been studied in yeast, worms, flies and rodents and a 15-15% restriction in energy intake in the latter can increase longevity by up to 60%. Such is the wealth of data on these  diverse species that one must accept the literature that caloric restriction prolongs life expectancy. The big question is the translation of that concept to man. Relative to these species, we mature far more slowly and have a longer life span. People often talk about human equivalents of “dog years” but in absolute terms, we outlive dogs by at least 8 fold.

The Calorie Restriction Society^[1] boasts 7,000 members. One such member is described in a journalistic piece on the web site. This member is 48 years old, is fit as a fiddle, weighs 118 pounds which is 7 pounds less than the minimum recommended for his height, he confines his energy intake to 1,500 calories a day and although his energy expenditure is not described, he would appear to be very physically active. He first got interested in caloric restriction as a tool to longevity when he was faced with his first manifestation of aging, a receding hairline. Poor guy!!!

The whole are of calorie restriction took a hit recently when the National Institute on Aging published its long term study of energy restriction on longevity in rhesus monkeys, a species far closer to man than yeast, flies, worms and mice^[2].   A 20 year study examined the effects of caloric restriction introduced to rhesus monkeys at varying stages of life. No statistically significant differences were observed between control monkeys fed ad libitum and those calorie-restricted (10-40% restriction). The latter did achieve a longer life span than would normally be expected for this species but the authors point out that they lived a privileged life of good husbandry and veterinary care. The main causes of death did not differ between the two groups:cancer, cardiovascular disease and general organ deterioration. However, generally recognised beneficial biomarkers of health increased in the caloric restricted monkeys but this did not translate into a longer life. In fairness to the literature, another colony of monkeys elsewhere (different diet, management and breeds)  did respond but in the world of science, it only takes one black swan to demolish a theory. The recent Nature paper is that black swan.

From a practical point of view, I can see a few dedicated enthusiasts sharing the necessary skills via social networks to achieve successful caloric restriction but I fail to see how it would be dealt with the great majority of the people. Leaving aside the ever-present obesogenic food supply, how is the average person to know exactly what their energy requirements are and then how to pare that down by 20% or more of that to achieve the required level of calorie restriction? How, especially with increasing age, do we ensure that caloric restriction does not drift into malnutrition which in the older population is so strongly associated with increased admission to hospitals, increased complications hen there, longer stays and more frequent re-admissions. Professor James Hill of the University of Colorado in his excellent book “The Step Diet” ^[3], recommends 25,000 steps per day plus rejection of 25% of the food served at every meal, just to maintain weight loss. For the many fatties among us, moi included, there is (a) the need to shed pounds to an appropriate avoirdupois a la James Hill and (b) having done so, to then hit a 25% calories restriction.

It ain’t going to happen. My nose was right!

Finally, apologies for the late post of this blog but that happens. Also next two mondays are in Asia and a lot of teaching at China Agricultural University in Beijing and Honk Kong University so I’ ll try but please be understanding!

---

^[1] http://www.crsociety.org/

^[2] Mattison JA et al (2012) Nature, 489 (7415), 318-321

^[3] http://tinyurl.com/9pbpbh3

Genes, memes and obesity

I have blogged several times about the uniqueness of obesity to the human race. Notwithstanding the fact that we share 98% of our genes with our nearest biological relatives, the chimpanzees, we alone get fat. It therefore follows that our obesity has origins in the basic biology of energy metabolism and storage but that it also has origins in the society we have constructed. For hard-nosed reductionist biologists, sniffing around the causes of obesity outside the laboratory is most unattractive because it brings us into the world of psychology, of human behaviour and of social organisation and these are all seen as “soft sciences”. If this view persists, then the so-called ‘hard sciences” of genetics and its associated disciplines, will wane in importance. Consider the brouhaha that greeted the discovery of cafeteria feeding of rats to induce obesity, the discovery of genetically obese rodent models, the incredible discovery of the appetite regulating plasma protein leptin and now, the flavour of the month, the gut microbiota. All have hit the front covers of Nature and Science and all have been the flavour of the months at key scientific conferences. But when all of these are added up, the best they can do is explain bits and pieces of the “how” of obesity. They cannot some of the “why” such as genetic predisposition but they cannot explain the “why” of individual obesity and overweight.

What makes humans so different from other species is that we alone have mastered the ability to learn from one another by imitation. This imitation can be vertical such as what we learn from our parents. It can be horizontal such as what we see others doing. Of course, we actually don’t have to see others doing something to imitate it. A third party can describe what he or she saw and we can have a shot at it, maybe getting it right first time, maybe having to go back for another look at the person who has mastered this act and eventually, we will be able to do it. These acts of imitation spread through society at a rate vastly greater than that of natural selection of genetic potential. To the biological scientist, this is interesting but seriously wooly. It is poorly defined, poorly characterised, impossible to measure and impossible to attribute origins of imitated acts.

In 1976, Richard Dawkins wrote a book which to this day remains a best seller entitled the ‘Selfish Gene’. Dawkins did not mean that there was a gene for selfishness but rather that all genes were utterly selfish in competing with other genes to be included in the blue print of the next generation, the one after that and so on. The human body is the vehicle and the gene is the “replicator”. But Dawkins stepped boldly out of biology in coining the term ‘meme” to explain the basic unit that is involved in the vertical and horizontal transmission of human knowledge. The exact quote is thus: “ We need a name for a new replicator, a noun that conveys the idea of a unit of cultural transmission, or a unit of imitation. ‘Mimeme’ comes from a suitable Greek root, but I want  a monosyllable that sounds a bit like ‘gene’. I hope my classicist friends will forgive me if I abbreviate mimeme to meme^[1]”.

A meme is any concept or idea that is replicated by imitation. It can be verbal (rote, word-of-mouth, sung or chanted), written (prose, verse or music) and it can be an action (the Maori Haka, the handshake, the Christian blessing). The private thoughts and fantasies you have lying in bed or day dreaming on the bus to work are not memes since there is no expectation of transmission to others. Dawkins saw memes as being identical to genes in their characteristics with the three prerequisites of the latter: replication, variation and selection. Memes compete with one another for retention within our brains and there are far more meme than there is storage space in our brains  for them so the memes that win out to to be transmitted  vertically are no different from the genes that win out for retention in the next generation.

The development of obesity is a passive event over time since nobody really sets out to gain weight. But once we gain weight, we access memes that are implanted in our brains: “Fat isn’t pretty”; “Being fat is bad for health”. But when it comes down to the decision to “do something”, what is the behaviour we imitate? For some, especially among young professionals, the imitated behaviour fights the passive gain in weight, a life-time commitment of watching and weighing, of eating carefully and of exercising diligently. This behaviour is also true for some who lost weight and who want to imitate that behaviour that retains weight loss. For others, and it is a fact of life that it is the majority, the imitated behaviour is to do nothing. The meme to do something about overweight has to compete with memes that govern other activities in daily life and the modeled meme is one of the status quo. Fat people don’t die on the streets. They grow old. They are no sadder and no happier, no poorer and no richer and no more loved or feared than lean people.

The future of cell biology will reside in the cell since the latter is the raison d'être of cell biology. Human obesity can be studied by the geneticists and the memeticists on different planets as is presently the case. Those who bring these disciplines together will be the future. Memes are neither angels nor demons, which flit around some unique ethereal space entering our head for good or bad. Memes are ultimately connected to a neuronal network in the brain, unique to that meme. Thus they do have a biological base but not a genetic base. The biological base must connect to the phenotype. I wish I could sing like the late Luciano Pavarotti or swing my golf club like Tiger woods but I cant. Why not? I can cut the grass and I’m good at figuring out complex scientific concepts and at designing experiments to test these theories. Why so? Is our phenotype where our genotype meets our ‘memotype’? Complex questions indeed but valid complex questions.

---

^[1] For those of you who would like a quick tour of memes, try the review by McNamara in Frontiers of Evolutionary Neuroscience May 2011 (volume 3): “Can we measure memes”. For a truly fantastic introduction to memes, buy Susan Blackmore’s book “the Meme Machine”, Oxford University Press.

Media reporting of food related health claims

In 2009, the World Cancer Research Fund (WCRF)^[1] conducted a survey of 2,400 UK subjects to ascertain their views as to the evidence linking diet and physical activity to cancer. WCRF argue that the advice linking diet and physical activity to cancer is both robust and relatively unchanged in the last decade. However, what they found was that in the 55+ group, 60% felt that scientists were always changing their mind and that 30% thought that the best advice was to avoid health advice and eat what you want. The figure for the sample as a whole were marginally lower. A group of London scientists decided to follow this up with a survey of material appearing in the UK press in one week covering food and health and to examine this the media representation to determine the accuracy or otherwise of the coverage. Their paper was published in the journal “Public Understanding of Science”^[2].The lead authors were Professor Tom Sanders, a world authority on diet and cardiovascular function and Dr Ben Goldacre, best known for his book “Bad Science”, but he is also a research fellow at the London School of Hygiene and tropical medicine. They were joined by Ben Cooper a medical student and William Lee an MRC Training Fellow in Psychiatry.

Overall, the top 10 best selling newspapers in the UK are read daily by about 10 million people so print media has a very big audience. The study was carried out in the first week of November and the focus was on articles that recorded an actual health claim to a food in some way. Stories about GM or about waste or other issues were excluded - the story had to involve a health claim as defined by the European Food Standards Agency. A total of 111 such stories were reported in the week. The next stage was to subject the reported new story to two grading systems specifically designed to grade scientific evidence. The first of these is called the Scottish Intercollegiate Guidelines Network (SIGN)^[3] and that of the WCRF. As the authors point out, each might have its flaws but “..taken together, these tools represent robust and widely recognised measures of relative evidence of quality”.

I have averaged the scores of the two grading systems since they were generally similar. The single most important figure was that only 10% fell into the category “convincing”. All the rest fell into shades of doubt such as 15% “probable and 7% “possible” or 4% “unclassifiable”. By far the biggest figure of 64% is for “insufficient” evidence. In effect the general take home message is that 1 in 10 media stories involving linking some aspect of diet to health is true. For two thirds, the evidence is non-existent and the rest fall in between. Where does the blame lie?

 Journalists rely quite a lot on press releases and the nature of press releases is that the releasing body, be it a company, an NGO, a university or a trade organisation want the media to take up the press release. Ideally, the journalist should use the press release as the starting point to make contact with the researcher and to develop the story from there. But quite often, it is the press release alone which makes it to the print edition. One of the main culprits in this communication change in my view are university communications units. They are constantly looking for press coverage in an ever increasing academic environment and they have a captive audience of academics who enjoy their moment of glory in the media. 

I would go further back in the communication chain to the actual research process and bemoan the growth and dominance of unchallenged data on food and health. Fine, I understand that certain associations between diet and health are not readily amenable to testing in intervention studies. But these are few and far between. What is exasperating is the rush to publicise the relationship observed between serum whatever and some wonderful health attribute in some cross sectional study without any direct evidence from human intervention studies that the relationship stands up to this test. One area which is without doubt the most culpable these days is the great news that “scientists have discovered a link between some nutrient intake profile, a relevant common genetic variation and some disease”. These triangular links of diet, phenotype and disease (e.g. the gene for some lipoprotein, high blood cholesterol and olive oil intake) are ten-a-penny and each worth more or less nothing without some verification with an intervention study. So rapid is the expansion of this unholy triangle that the funding to establish an intervention study is never likely to be extensive. Which of the putative claims do you spend your money on?

An exception is the work done by scientists at the University of Ulster and Trinity College Dublin who showed that if low riboflavin status was corrected in persons on medication for hypertension, those with a common (ca 30%) genetic variation showed a dramatic reduction in blood pressure^[4]. So they set out to recruit equal numbers of the three genetic classes (the less common genetic variation being absent or inherited from one parent or both) and they carried out an intervention study (riboflavin supplement versus placebo) which proved that those with the less common genetic variation responded very positively with dramatically reduced blood pressure. They went back then four years later and those that had been randomized to the placebo were now given the riboflavin and vice versa and again they proved the association. This is darn hard work but it is what is needed to take an “association” to a “verification”. Sadly, the moment of glory in the media seems to satisfy most scientists and most universities. It is easy to be critical of journalists for not following press releases in more depth getting a second and their opinion but those in glass houses......

---

^[1] http:www.wcrf-uk.org/audience/media/press_release.php?recid=63

^[2] Cooper BEJ et al (2011) The quality of the evidence for dietary advice given in UK national newspapers. Public Understanding of Science, May, 1-10

^[3] http://www.sign.ac.uk

^[4] Wilson et al (2012) Riboflavin offers a targeted strategy for managing hypertension in patients with the MTHFR 677TT genotype: a 4-y follow-up. Am J Clin Nutr.  Mar; 95(3):766-72. Epub 2012 Jan 25.

The fridge and the human food chain

I grew up in a house without a fridge but then again I grew up in Ireland which suffers neither extreme cold in winter or extreme heat in summer, thanks to the gulf stream. In summer, we had a cold box which was kept in a shed and was used to store milk and butter. Today, it is impossible to imaging a fridge free house in any developed country. The advent of mass use of refrigeration totally transformed the human food chain. Ice has of course long been a means of preserving perishable food but it was not until the start of the 19th century that the concept of the mass use of ice began to be developed. Frederic Tudor, also known as the “Ice king”, effectively started what was to become a big industry, the harvesting of large quantities of ice from naturally frozen waters and shipping it across long distances^[1].  As the demand for ice grew, the technology for harvesting it also grew and one of Tudor’s suppliers invented a horse drawn ice plough that cut cut large uniform blocks of ice. Between 1827 and 1830, the price of ice fell from five cents to as low as half a cent. Like all natural resources, mother nature could help or hinder by way of winter temperatures, which meant that the price of ice fluctuated quite considerably. In the suburbs of Boston, ice was delivered daily to homes in blocks of fifteen pounds by the ice man with his horse drawn carriage. Between 1843 and 1856, Boston’s consumption of ice grew from 6,000 to 85,000 tons. The ice was placed in an ice box to preserve meats, milk and vegetables. Ice was also beginning to be used for the transport of food and in 1851 the first refrigerated rail car shipped butter from Boston to New York. In contrast to the US, ice was not widely used in Europe. In contrast to the US, European housewives shopped daily for their food. US consulates were asked about the likelihood of Europeans adopting ice boxes and the French consul replied thus: “In the great cities of Marseilles and Bordeaux butchering is done every day in winter and twice a day in summer, and the meat is cooked within a few hours of killing”. Indeed, in the great Parisian market, Les Hallles, it was generally forbidden for traders to keep stocks of one day’s foods to be sold the next day.

The idea of producing “winter-free” ice took off in the mid nineteenth century. Ice harvested from ponds was by no means pure and could be contaminated by debris, insects and dirt. Moreover. as the concept of food hygiene took off, the possibility that harvested ice might be contaminated by sewage was a worry. In addition the ice-man who delivered the daily block of ice was described as a national joke - uncouth and dirty. While mechanical refrigeration was developed in the mid 1850s, they units were very large, very noisy and quite dangerous, particularly in relation to fire hazards. The first domestic fridges were so large that they were installed in basements with the coolant piped up into the iceless box in the kitchen. By the turn of the twentieth century, the big manufacturing companies began to take an interest in domestic refrigeration: General Electric, Frigidaire (subsequently bought by General Motors) and Kelvinator (founded by ex-GM executives). The big switch was to move from a gas driven system to an electric system. In 1927, GE released its first compact domestic fridge, the Monitor Top. The market however still had to compete with the traditional ice box with harvested ice and they were not about to give up. The ice-man was given a uniform, ice boxes insulation was improved and external portals were developed so that ice could be delivered into the home with no one present. A marketing war broke out between harvested ice and the fridge. The fridge manufacturers hit back and produced booklets with recipes and emphasised the value of refrigeration for summer fruits.

In 1930, a Frigidaire engineer developed a new gas, freon, which was non-toxic, non-inflammable and required less pressure to achieve colder temperatures leading to even smaller motors and thus bigger space for food storage. The ice-man vanished. By 1940, half of all US homes owned a fridge and today, a home without a fridge in the developed world is unthinkable. Refrigeration transformed the human food chain allowing foods to be transported great distances to everyone’s economic gain. It transformed shops and shopping and with that it transformed lifestyles, liberating people from frequent and nearby shopping. Freshness became the expectation of the consumer with respect to food. All of this is exactly what the locavore movement would want to see reversed but as is sung in the famous Irish song, Galway Bay: “They might as well go chasing after moonbeams or light a penny candle from a star”.

Ironically, the gas that came to transform refrigeration was to be targeted as the main cause of the loss the earths ozone layer and thus alternatives to freon and other CFCs had to be developed. The Montreal Protocol was the international treaty that all countries signed up to  to eliminate CFC gases and it has been hailed as the most successful collaborative effort in relation to the environment.

The fridge lives on and is taken for granted in today’s food chain.

---

^[1] Based on a chapter in “Freshness: a perishable history” by Susanne Freidberg, published by Harvard University Press 

The obesity epidemic re-visited

When we measure the prevalence of obesity, it is usually by way of a survey over a defined period. Thus the National Adult Nutrition Survey (NANS) here in Ireland was conducted over a 12 month period in 2009-2010.  This gives us a single measure in time but it tells us nothing about the dynamics of obesity. In other words, any individual selected at random from within the NANS database, might have acquired any excess weight at any time prior to being measured and even a subject within a normal weight range might have been fat at some previous time. Thus, there is a growing literature in the use of birth cohorts to gain a more accurate picture of the dynamics of the present obesity epidemic. Such studies seek to examine the separate effects of age, period and cohort (APC studies). We know that as we get older, our body fat rises and our lean body mass falls. The question is, does this happen at an equal rate independent of year of birth or period of life. Birth cohorts are groups of subjects born the same year or over a small number of years. They grow old together and they experience major period effects (war, depression, economic boom, technological innovation etc) at the same age. the period effect is the consequences of some event which effects all ages when it occurs. Thus the advent of the internet is a period, in this sense, which all ages encounter at a given time.

All studies show that as we age, there is a gradual rise in our level of body-fat. It rises gradually from late teens up to mid-fifties and then it begins to decline. So age effects obesity. Looking at data from 1976 to 2000^[1], there is a rise in the prevalence in obesity. Thus the prevalence was about 12% in 1976. Some 8 years later in 1984, it had increased to just 15%. A further 8 years saw the obesity prevalence rise to 22% and by 2000 it was 28%. So period has an effect.  The key question is whether every birth cohort experiences the same effect of age in the development of obesity. The Reither paper shows that for birth cohorts starting in 1895, there was a gradual but constant rise in the % of the population that were obese, reaching a peak in the late 1920s.  Then the rate of obesity declined until the late 1950s when it took off again. Clearly, this paper shows that each birth cohort or in lay terms, each generation, experiences the age related gain in weight in a different manner. A second paper ^[2] also looked at US birth cohorts and also found a similar effect. This second paper presented data in a novel manner such that we can look at what the authors call iso-BMI lines. This is like looking at a map and examining the contours of mountainous regions where specific heights appear on a continuous line. The closer the lines get, the steeper is the climb. Thus we can look at birth year on one axis and age on another axis and see the manner in which iso-BMI contours change. Those born in 1900, could expect to have a BMI of 21 by age 40.  However, for those born ten years later, that BMI of 21was achieved at 30 years of age. A decade later, it was achieved at 20 years of age. If we look at a BMI of 25, this was achieved by 20 in 1980, by 30 in 1950, by 40 in 1940, by 50 in 1920 and by about 65 in 1900. The paper of Komlos & Brabec also shows that the rise in obesity came in waves. There was a surge between 1900 and 1920 and then a decline with a second surge in the late 1940s. This pattern of surges differed according to both race and sex with African American women showing the highest level of obesity at all times and the highest post WW2 surge.

These data tell us quite a lot about the dynamics of the obesity epidemic. Firstly, more recent generations experience greater levels of obesity and at an earlier age the older generations. One could argue that this is a period effect. There is greater sedentary leisure time and a more abundant obesogenic environment. However, one could also look at a biological explanation and argue that uterine programming is involved and that as each generation experiences obesity, it somehow enhance the likelihood of even greater obesity in the next generation. In my recent book, I called my chapter on obesity “A tsunami of lard” citing other data from the US and Europe on the cyclical growth of obesity which began well over a century ago. In fact, data from pooled US and Canadian actuarial data involving 34 insurance companies examined health related risks of obesity for 163,000 policyholders were deemed overweight. Of the overweight men, those whose body fat was distributed around their abdomen had a higher risk of death than other overweight men. Among the severely overweight men, those with abdominal obesity had a 52 percent increased risk of death, whereas those without abdominal obesity had only a 35 percent greater risk compared to the general population^[3].

So when the likes of David Kessler writes in his book “The end of overeating” that the incidence of obesity soared from the late 1980s, he is ignoring an indisputable fact that obesity more or less tracked the industrial revolution. This is of huge importance. If Kessler chooses to ignore the early origins of obesity, then he can be comfortable blaming the advent of foods high in salt, sugar and fat^[4]. Others can comfortably blame the advent of high fructose corn syrup, fast food, sugar sweetened beverages. Well consider Lucius Columella in his great work De Re Rustica (On Agriculture) in the year of 65 AD. when he wrote: "The consequence is that ill health attends so slothful a manner of living; for the bodies of our young men are so flabby and enervated that death seems likely to make no change to them." It is a simple fact of  life that obesity is one of the drawbacks of affluence where food is abundant and where labour saving devices (and slave labour) are accessible. This is not for one iota to play down the health consequences of obesity. It is to simply of enormous importance in understanding the causes of obesity.

---

^[1] Reither EN et al (2009) Soc Sci Med November;69 (10) 1439-1448

^[2] Komlos J & Brabec M (2010) Am J Hum Biol;22, 631-638

^[3] Kahn HS & Williamson DE (1995) Int J Obes Relat Meat Disord; 18 (10) 686-691

^[4] That will be the subject of a future and highly critical blog on Kessler’s book.