My “proper” job is working in risk management for (usually) large banks around the world. Maths and statistics therefore interest me a lot, so for this piece, I thought it would be fun to apply some simple risk analysis to food and lifestyle-related issues.
The basis for one such type of analysis had been done a while ago. Around 1979, Ronald A. Howard of Stanford University invented a measure called the micromort which is a unit used to express the risk of a one in a million chance of dying due to engaging in some activity.
Micromorts change with age, so for example, a person aged 45 runs a risk of six micromorts (six in a million) of dying in bed while a 90-year old person has a daily risk of 463 micromorts of not waking up alive. Interestingly, a newborn baby runs a risk of 430 micromorts of not surviving the first day after birth, almost the same as a 90-year old person never getting up again.
The good news about micromorts is that they reset every risk period, which may be a day, a year, an event or after certain quantity thresholds. So if a person survived a day, then all that day’s daily micromorts would be reset to zero when he/she wakes up the next day.
Every activity people partake in, like swimming, carries a risk, which is calculated in micromorts. Photo: Carolyn Noble/Flickr
The bad news is that during the course of a risk period, micromorts are cumulative. Therefore, if someone rode a motorbike 60 miles (10 micromorts) to go for a swim (12 micromorts), then that person runs a total daily risk of 22 micromorts (assuming he/she does not do anything else risky). One might consider various activities as additions to a bucket of risk which one is obliged to carry around, and practically everything you do adds some (normally very small) amount of risk to the bucket.
Somewhat worryingly, micromorts are also transferable, often without you even knowing about it. In many cases, a person’s individual risk bucket has a profound effect on everyone relying on that person, or who may be in contact with that person.
For example, if Mr X is driving people around when inebriated, every passenger of Mr X will have their buckets of risk micromorts raised to be at least the same level of risk as his. And complete strangers on the same road who do not even know Mr X will also have their buckets of micromorts significantly increased.
How micromorts are calculated
The issue, of course, is how one can use micromorts in a helpful manner. This is already being done commercially, but first it helps to know how micromorts are calculated. A common example is based on the number of deaths resulting from the use of anaesthetics (but not the actual surgical procedure). This works out at one death per 100,000 applications of anaesthetics which therefore gives a risk of 10 micromorts (1,000,000 / 100,000).
As for commercial usage of micromorts, a prime example would be cars with added safety features, like extra air bags or reinforced roll bars. There is often a statistical trick applied, which uses relative differences; for example, the death risk in a car with five air bags in a 50 kph head-on collision may be 5,000 micromorts whereas the death risk in a car with only three air bags may be 10,000 micromorts.
This may mean the five-airbag car being advertised as being “twice as safe” as the three-airbag car, even the death risk is actually 0.5% vs 1%. So people will pay thousands more for a car with two more airbags which is only 0.5% safer than another car.
Horse-riding is less risky than walking. Photo: Pia Waugh/Flickr
As with risk management in banks, there are surprises when analysing actual micromorts. For example, many people might consider riding horses somewhat dangerous, but each ride on a horse is only rated at 0.5 micromorts while a long 17 mile walk is rated as twice as risky at one micromort. Skydiving is just as risky as riding a motorcycle for a distance of 60 miles – both are rated at 10 micromorts, and both activities are less risky than swimming, which is rated at 12 micromorts.
Regarding food, there are very low risks involved when measured using micromorts, mainly because it is difficult to establish a cause of death specifically due to one normal food episode (unless it is food poisoning). The risk of dying due to a steak dinner is rated at one micromort, but only after eating steak at least 100 times before. With bananas, the same risk of one micromort also applies, though only after eating 1,000 bananas earlier in your life. So in terms of food risk, micromorts are often too inexact to be of practical use and we therefore need to use another interesting statistical measure called microlives for food-related risks. Microlives will be covered in the next part.
To conclude the discussion about micromorts, it should be noted they can be helpful in other ways. For example, if one is forced to make a choice between swimming in a sea where sharks have been seen once in a while or running in a marathon, then despite what you might think, it is actually safer to do the swim because the chances of getting killed by a shark is only 0.125 micromort whereas a marathon has a risk of seven micromorts, which means that a marathon run is 56 times more likely to kill you.
Eating bananas carries some risk but only if you have eaten 1,000 bananas before. Photo: Filepic
But hopefully you would have noticed the statistical trick in that last statement, as in reality the chances of getting killed by a shark is 0.0000125% while the chances of dying during a marathon is 0.0007%.
Both are statistically extremely unlikely, but it has to be said that both are also possible, though death by shark is less probable.
Similarly, rock-climbing (three micromorts) is less risky than scuba-diving (five micromorts), travelling by train for 6,000 miles is as safe as flying in a jet for 1,000 miles or driving by car for 230 miles (all one micromort).
Curiously, one micromort of risk will also occur if you walk 17 miles, or cycle 20 miles, or ride a motorcycle for only 6 miles.
At this point, please understand that micromorts are based on statistics gathered from large populations and therefore not a measure of any individual’s personal risks when engaging in any activity.
The data used to derive micromorts will also vary from country to country. For example, the 0.5 micromort for horse riding is based on UK data where a safety helmet is normally required to ride a horse.
Horse-riding would therefore be more risky in countries where helmets are not mandatory. Murder risk is only 10 micromorts in the UK per year but 48 micromorts in the USA. Also it expresses only death rates, and ignores incidences such as serious injuries.
Micromorts also express risk generically. For example, swimming as an activity covers swimming in pools, lakes, rivers and oceans, but a high-level micromort for swimming does not necessarily express where deaths are more likely.
It is of course possible to calculate micromorts for specific situations; e.g. every attempt to climb Mount Everest has a risk of 37,932 micromorts.
Regardless of the above caveats, micromorts are a useful way to override our propensity to be irrational in our perception of risk. If data is available, it is extremely easy to calculate micromorts for any specific activity.
By providing a context for risk, micromorts allows us to be clear about the risks worth taking, thereby allowing us to balance what we enjoy doing with the risks associated with such activities. Micromorts also provide a basis to assess how much we are willing to pay to reduce/avoid risk in certain situations, and/or avoid getting into a car with a drunk driver and transferring his risks to you.
In the next part, we will discuss microlives and how they offer a thought-provoking framework for quantifying the risk in our diets and lifestyles.
We usually consume seedless fruits. Here in France, it is rare to get a supermarket lemon with seeds, or clementines/oranges with pips. Even many grapes do not have seeds. Seedless fruits are produced in huge volumes and now comprise the majority of fruit sold in the developed world, simply because people like the convenience of eating seedless fruits.
Seedless oranges are freaks
All fruits come from angiosperms, which are defined as flowering plants which spread or disperse via ovules (the seeds) developed within an encased ovary (the fruit).
However, due to genetic accidents, some angiosperms can end up losing its ability to produce seeds. In normal circumstances, such a mistake would end up with a dead plant that would have produced no offspring. Fortunately and oddly, this was how seedless oranges came about.
In the beginning of the 1900s, a clump of freak orange trees in Brazil were found to be producing seedless oranges and some of these trees were transported to the US where by using grafting techniques, these original trees were cloned/propagated via cuttings into the vast seedless navel orange orchards around the country.
It is much the same story with seedless grapes, except that their story happened even earlier. Grapes had traditionally been dried and stored for centuries as raisins but a problem was the dried seeds were very hard, making the original raisins difficult to eat. As such, techniques were developed to remove grape seeds before drying, but they all involved puncturing the skin to remove the seeds which then allowed the sweet juice to leak out. Drying such punctured fruits ended up with clumps of very sticky raisins which were messy to handle.
Seedless oranges only became commercially popular in the 1980s. Photo: Kabsik Park/Flickr
The problem was solved in the 1870s when a vineyard owner called William Thompson obtained some seedless grape cuttings from a company called Elwanger & Barry who may have obtained their stock from Constantinople in Turkey (though the history trail is not very clear). The original grape species was probably a sub-species called Lady deCoverly but Thompson renamed the grape as Thompson Seedless and to this day, it is the primary grape used for producing raisins and sultanas. Being seedless, the dried raisins were both easier to handle and much more palatable to eat.
Oddly, seedless grapes for the dinner table did not become commonplace until over a century later, in the 1980s, mainly because producers of seeded grapes held such a dominant share of the fresh grape market and did not want any new competition.
Seedless grapes, of course, cannot breed by themselves and are therefore cloned/propagated via planting cuttings in a sterile soil medium which usually contains the hormone auxin, found in the roots of plants.
A huge problem with such cloning practices is the loss of biodiversity; any disease which affects a plant is likely to spread and potentially destroy all similarly cloned plants.
Years ago in London, a friend introduced me to a neat trick where she basically stuck an opened bottle of vodka into a hole cut into a watermelon and left in the refrigerator overnight to soak in the vodka. From what I can recall, the resulting watermelon was fantastic. I repeated this trick last year and it was even better as, by chance, I had obtained a seedless watermelon.
I mention this because the development of seedless watermelons is an interesting story. Nowadays, the commercial way of propagating them is by grafting cuttings on various root stocks but there is another fascinating method which is still used, and it explains how we can actually buy seeds to grow seedless watermelons.
But first, a bit of background stuff.
Virgin fruits, gibberellins
Parthenocarpy is the production of fruit without seeds, and is derived from the Greek for “parthenos” which means virgin and “karpos” which means fruit. Curiously, parthenocarpy can sometimes occur naturally and classic examples are bananas and pineapples although the modern versions are those which have been selectively bred by humans. These modern plants can only be propagated via cuttings.
The story of gibberellins is mainly about a plant hormone called gibberellic acid-3 (GA3), and we know about it from a fungal disease called bakanae, which means “foolish seedling”. This fungus has been known for centuries by Japanese farmers to cause rice plants to grow much taller but without producing any rice seeds.
But it turns out that what is bad for Japanese rice farmers is great news for other farmers, for it was discovered that the bakanae fungus (officially gibberella fujikuroi) produces GA3, and GA3 is a very useful, potent plant hormone which is now widely used to promote the yields of commercial crops. For example, using GA3 with added fertiliser grows stronger, higher-yielding plants. GA3 can also be used to stimulate growth in smaller plants, such as courgettes while reducing seed production at the same time, and also help develop better rinds on citrus fruits.
And now, back to seedless watermelons.
Three distinct watermelons
Watermelons originated in Africa as small, tough, bitter fruits but centuries of selective breeding have resulted in the sweet melons we know today. The ingenious story behind the original seedless watermelons involve alterations to the plant genome itself via a process called mutation breeding, whereby plants were deliberately mutated by applying various chemicals.
Watermelons originate from Africa and were originally bitter. Photo: Steven Depolo/Flickr
In 1939, the use of the compound colchicine finally started scientists on the road to the seedless melon. It was not an easy, obvious route though.
Most normal cells are diploids, which mean each cell contains two copies of each chromosome. There are exceptions, such as haploids in mammals, but that is another story. In melons, colchicine interferes with structural proteins in cells causing the chromosomes to fail to separate properly during cell division, resulting in events called ploidy changes or variations in the number of chromosome sets in the new cells.
The original experiments in 1939 resulted in tetraploid watermelon plants; i.e. they had four copies of each chromosome in each cell. When these tetraploids were then bred with ordinary diploid melons, the resulting melon plants were triploids (cells with three sets of chromosomes) – and triploids cannot produce seeds because the reproductive cells require an even number of matching chromosome sets.
The story does not end there. Triploid melons still have to be triggered to bear fruit and this is achieved by pollinating female flowers from triploids with pollen from the male flowers of diploid melons.
So to produce a seedless watermelon, one first needs to create a tetraploid using colchicine, then mate the resulting tetraploid with a diploid (normal melon), and then the resulting triploid will have to be fertilised by a diploid before we achieve a seedless fruit. Therefore, every crop of seedless melons actually involves the participation of melons with three different genomes.
To increase the success rate, scientists have created diploid plants which do not produce female flowers thereby reducing the chances of two diploid melons producing seeded fruits. And the huge seedless watermelons now often seen in shops are probably due to the application of GA3 on the plant during growth.
One can buy seeds from triploid plants but the instructions will always mention a need to have the plant fertilised by another normal melon plant.
The last article about how our gastric acids kill pervasive clostridium botulinum bacteria in our environment raised an interesting question: How come such strong gastric acids do not cause the stomach to digest itself?
A chemical dance
And the answer is a sophisticated dance of chemicals, involving hydrochloric acid and a vigorous enzyme called pepsin. The way this chemical tango works involves precise timing and ingenious co-ordination involving the secretion of other compounds – any tiny misstep would be severely injurious to our digestive system.
The main gastric acid is hydrochloric acid, an acid potent enough to pickle steel, and powerful enough to destroy most of the strains of bacteria and fungi that we are constantly inadvertently ingesting in our food, including clostridium botulinum.
The initial pH of hydrochloric acid emitted into the stomach can be 10 times the acidity of pure lemon juice. — Rob Bertholf/Flickr
Depending on concentration, the initial pH of hydrochloric acid (HCl) discharged into the stomach cavity (or lumen) can be less than pH 1, more than 10 times the acidity of pure lemon juice. However, this pH is usually diluted by the presence of food and other ingested fluids.
The parietal cells in the inner layer of the stomach (the mucosa) are responsible for secreting HCl into the lumen. How this works is ingenious. One function of the parietal cell involves a “proton pump” mechanism where potassium ions (K+), are recycled by hydrogen ions (H+) directly in the lumen – this involves the cell combining carbon dioxide with water to form carbonic acid which is then catalysed by an enzyme called carbonic anhydrase into H+ and bicarbonate (HCO3-) – the H+ then swaps out the K+ ions originally output from the parietal cell.
This function is complemented by another chloride ion “exchanger” in the parietal cell which picks up chloride ions (Cl-) from blood by exchanging them with bicarbonate ions from the previous function. The resulting free H+ and Cl- ions then combine as HCl outside of the parietal cells, in the lumen. This avoids damage to the parietal cells themselves.
During the secretion of HCl, an additional protective layer of mucus is also secreted by goblet cells in the mucosa to further shield other parts of the inner stomach from HCl.
Despite the extreme acidity of gastric HCl, there is a famous species of bacteria that can survive and breed in the harsh environment in our stomachs. The bacteria is called Helicobacter pylori, and is believed to be the cause of chronic gastritis and gastric ulcers.
Curiously, over 80% of humans are infected with Helicobacter pylori and do not display any symptoms, so a theory suggests that this bacteria may form part of the stomach’s bacterial fauna and becomes problematic only under certain (currently unknown) circumstances.
The dance with HCl continues with a large molecule called pepsinogen which is secreted by gastric chief cells in the mucosa. By itself, pepsinogen is inert because it is a zymogen, which is a precursor to a potent enzyme called pepsin.
Production of pepsinogen is stimulated by a hormone called gastrin which is produced as a response to signals from the stomach, such as distension or the detection of proteins in the lumen. Gastric chief cells also produce pepsinogen due to other signals received from the vagus nerve, usually as a result of emotional or other types of stress.
On contact with HCl, pepsinogen unwraps itself, losing 44 amino acids in the process from the molecule, which results in a new pepsin enzyme molecule. Pepsin molecules then initiate a chain reaction as they also act as catalysts to cleave away the same 44 amino acids from other pepsinogen molecules without the need for further HCl, resulting in more pepsin.
Pepsin is a one of the earliest known enzymes to be isolated from stomach tissue. This was done in 1836 by a German physician called Theodor Schwann, who found that pepsin can break down proteins in egg albumin into shorter peptides chains. Basically, Schwann discovered that pepsin is a digestive enzyme which targets proteins. Such protein digestive enzymes are now known as proteases.
Pepsin is a potent protease, and particular good at cleaving away many types of peptide bonds holding together peptides (chains of amino acids) that make up proteins. It works efficiently in strongly acidic environments where the acid also helps to unfurl proteins by denaturing them.
There are two other proteases in the human stomach, chymotrypsin and trypsin and between these three proteases, the stomach is able to pre-process all the types of digestible proteins in our diets, ensuring that they are ready for absorption later by the intestines. Pepin is most efficient at cleaving peptide bonds between hydrophobic (water-resistant) amino acids as well as amino acid chains containing phenylalanine, tryptophan, and tyrosine molecules.
Pepsin & acid reflux
From understanding how proteases work, you should now be wondering how come pepsin does not attack and digest the inner lining of the stomach, which is made of protein-based muscle tissues. The answer is two-fold. The mucus layer secreted by the goblet cells in the mucosa also helps to prevent pepsin reaching the inner stomach lining. Additionally, pepsin is only released when pepsinogen is unbundled by HCl, and this happens inside the lumen, away from the stomach wall.
However, when there is some malfunction in the stomach, then pepsin can digest away the stomach lining, resulting in potentially dangerous stomach ulcers.
An example of how potent pepsin and HCL are is the raw, burning feeling in the throat whenever one vomits or there is any reflux from the stomach going back up the oesophagus. That tingly, painful, extremely sour/acidic sensation in the throat is actually due to HCl and pepsin denaturing and pre-digesting the oesophagus.
Most bacteria are unlikely to survive the harsh conditions in the human stomach. In most cases, the extreme acidity would denature the cell walls of bacteria, causing holes in the cell membranes into which HCl can flow in and destroy the bacteria.
Food has to be cooked properly before consumption. Hillary V/Flickr
But we can get ill because of toxins already produced by bacteria in food before we eat such contaminated food. Toxins are chemicals which are not affected by digestive systems, so never ingest food that has been left out for too long.
However, there are other bacteria other than Helicobacter pylori which can also survive the conditions in human stomachs. They include strains of salmonella, Escherichia coli (commonly known as E. coli) and shigella.
Their methods of evading the effects of our digestive tracts vary. Salmonella can hide and shield itself behind peptides that have been cleaved by pepsin, and then flow into the calmer intestinal tract where they can breed and cause severe illnesses. E. coli and shigella have evolved resistance to strong acids and can breed once in the intestinal tract.
Other types of bacteria disperse via spores which are unaffected by gastric acid. Two such examples of bacterial spores are Clostridium perfringens and Clostridium difficile which will activate only once they are in the intestinal tract.
Temperature, kinetic energy & tasteHeat can also kill bacteria. The latest UK food safety guidelines state that the danger zone for bacterial growth is between 8°C and 63°C, and recommend that food be cooked to reach an internal temperature of 75°C before serving. However, using temperature alone as a guideline to cooking usually means some meats would be overdone as temperature alone does not take into account the use of kinetic energy for cooking.
By this, I mean that one can cook and kill all bacteria if food is cooked to reach an internal temperature of 60°C (or more) and then left at that temperature for a longer cooking time – kinetic energy can also kill bacteria, not just temperature. This technique is used in sous vide cookers and can preserve taste better. More on this can be found in my previous article, The temperature of heat.
EVERYBODY is now probably aware that for some time, we have been living with strains of bacteria which are immune to many common antibiotics. This is not unexpected as it is one of the logical (and short-sighted) consequences of adding vast quantities of antibiotics into animal/poultry feeds. In fact, over 80% of the antibiotics produced worldwide are used in the food industry. Antibiotic resistance is simply a predictable outcome of the quest for profits in the meat and dairy industry.
So a recent study from Brazilian researchers was interesting as it attempted to analyse how certain bacteria acquire this resistance to antibiotics. Foodborne diseases have affected hundreds of thousands of people in Brazil in the last two decades, and many cases were linked to bacteria in the genus Salmonella. This is particularly intriguing as a friend in London had contracted salmonella poisoning around 20 years ago, and it was so severe he was hospitalised for six weeks. Fortunately, the antibiotics he was given eventually worked but it was sobering and traumatic to see him so ill for so long. Imagine what would have happened had it been a strain of salmonella immune to antibiotics.
Men were not made to hunt for meat but vegan diets are slow to gain acceptance. – AFP
More about salmonella
The Brazilian study investigated 90 serovars (sub-strains) of salmonella typhimurium (ST), a sub-species of salmonella enterica, which is the species of salmonella most involved in human food poisoning (normally resulting in gastroenteritis). Testing serovars of ST with common classes of antibiotics revealed that 72.2% were immune to sulphonamides, 48.9% were resistant to streptomycin, 30% are tetracycline resistant, 23.3% were unaffected by gentamicin, etc. In addition, a previous study had reported that 46 serovars of ST were also resistant to nalidixic acid (and also to flouroquinolones). It was grim reading, especially as it was also noted that streptomycin and tetracycline are still common additives in animal feeds.
Whole genome sequencing (WGS) was used to analyse how this resistance developed in the ST serovars – this is a non-trivial task as the ST genome contains 4.7 million base pairs. The results were interesting. The research detected different types of mutations in the gyrA, gyrB, parC and parE genes, and only one mutation point in one of these genes was observed. Resistant ST serovars also have additional activated genes, which may be one or more of the qnr, qepA, oqxAB and aac(6’)-Ib-cr genes. It appears that antibiotic resistance in ST serovars is conferred by single point mutations in certain genes in conjunction with the activation of other specific genes.
There are two other curious findings in this paper. One is the antibiotic/antimicrobial resistance of ST serovars have been declining since the 1990s. This may be due to the rise of a more aggressive salmonella enterica sub-species called salmonella enteritidis which caused a worldwide pandemic in the 1990s and has been prevalent ever since. Salmonella enteritidis is the very dangerous pathogen (disease-causing agent) associated with eating undercooked contaminated eggs.
The other odd finding is that resistance to certain antibiotics developed even without any exposure to such antibiotic compounds in the feed or anywhere else. It appears that mutations arising from other antibiotics may be sufficient to promote resistance to unrelated (but somewhat similar) categories of antimicrobials.
As salmonella usually breeds in the intestinal tracts of animals and poultry, I am safe from any possibility of contracting gastroenteritis, at least for a while. This is because I am in the middle of a vegan challenge with my daughter until the end of the month.
The author had to drive 40km to another town to find his vegan meal. – CHRIS CHAN
Being vegan here in France is not as easy as in Berlin where I was last month. I quickly grew tired of my own vegetable stews and curries and decided to get some different vegan meals at the small supermarket in the next village. When I could not find any chilled vegan foods after a search, I eventually asked an assistant about them. He looked incredulously at me as if I was mad before shaking his head sadly. “Désolé, nous n’avons pas de truc végétalien.” (Sorry, we do not have any vegan stuff).
I finally found some tasty vegan foods in a large supermarket in a town about 40km away. The labelling of vegan items in France is heavily influenced by the meat industry here – for example, it is not allowed to label food as burgers or sausages if they are made with non-meat products. But it seems they had forgotten to ban vegetarian “steaks” and “cordon bleu” dishes, which is what I got.
There are several reasons for my vegan challenge. One is curiosity, another is not adding on excessive weight now that the cold season has started – but the main reason is to confront my own denialism about meat production. Denialism is a mechanism used to alter how we think about things so that we can function better or, at least feel better. Sometimes we fool ourselves but very often, we are fooled by other people/things. You can read more on https://www.star2.com/food/2018/09/09/curious-cook-a-quiet-month-of-denialism/
Having access to thousands of research papers provides an in-depth insight into meat production, its consequences, health impacts and development over time. If you think about it, we should not be eating so much meat – not because meat is necessarily unhealthy, but because humans are physically not good predators. Lions are better adapted to be at the top of the food chain in the wild, not humans.
Our brains, again
However, our brains have allowed us to overcome our physical limitations, initially by crafting tools/weapons which enhanced our ability to hunt. Then around 13,000 years ago, humans began domesticating animals for food. In normal evolution, lions required hundreds of thousands of years to evolve their speed, claws and teeth, but human intelligence allowed us to short-cut our way to the top of the food chain and a practically limitless supply of meat.
The speed of change is staggering: the first chicken super-farm was devised in 1926 but before the end of the last century, Concentrated Animal Feeding Operations (CAFO) and industrial meat farms were already supplying chicken, pork and beef to billions of people, without any consumer making any more effort than picking up a pack of meat and paying for it.
In France, you can’t label a food item a sausage unless it’s made of meat. — AFP
The only way to achieve such prodigious productivity in meat is to invent artificial solutions and ignore the existing natural order of things. This disregard for natural circumstances has profound consequences: deforestation, desertification, antimicrobial resistance, global warming, pollution, etc, and includes the creation of animal and bird hybrids which would be considered mutants in the wild. The world now also plants more food for meat production than for humans.
There are health consequences for humans too. The ubiquity of meat means that most humans have little regard for the sources of animal proteins, practically treating animals like insentient plant crops. Ignoring the disturbingly cruel realities of industrial meat production means that many people now unknowingly ingest meats contaminated with pesticides, herbicides, antibiotics, growth hormones, chemicals such as preservatives, flavourings, etc. Crop-treatment compounds are present in meat because animal feed need not meet human safety standards but these compounds can accumulate in animal flesh and offal, sometimes to problematic levels.
In summary, people generally do not know as much as they should about animal proteins, and our denialism conspires to keep us ignorant. There is also something wrong when humans can use their intelligence to satisfy our lust for meat but cannot apply the same intelligence to more important issues like our environment. The only difference appears to be the quest for profits, as discussed earlier about the rise of antibiotics-resistant bacteria.
The irony is humans need only tiny amounts of daily protein (animal or non-animal is immaterial): only 0.8 grams per kilo of body weight. So, a quarter-pounder burger fulfills the protein requirement for someone who weighs over 141 kilos. If people cannot wean themselves off meat, then limiting consumption to only the protein amount they actually need would be both healthy and responsible.
In time, the survival of humans will inevitably require overcoming, among other things, our genetic disposition for preferring meat, just as we overcame our genetic limitation of being lousy predators. And this probably starts with overcoming our denialism.
Curious Cook appears on the second and fourth Sunday of the month.
The Hidden France tour
A few weeks ago, I was walking my dog in the evening when a coach stopped outside the hotel in the village centre and started disgorging a gaggle of Chinese tourists. They saw us and started talking to me excitedly in Mandarin, a dialect which I do not understand – so I responded in Cantonese which agitated them even more. Eventually I found out from their tour guide that the group was doing a tour of “Hidden France” (or something like that), visiting places which are way off the usual tourist routes. Hence their surprise at meeting a Chinese man walking a pug in a remote French village at one of their first stops.
From a description of their itinerary around the village the next day, I doubt they will ever come back. The plan was a visit to some local minor historical sites, then a cheese farm which I know to be extraordinarily odorous, so much so even French people gag when visiting. That was then to be followed by a typical local lunch at the farm restaurant – this would usually be a starter plate of various pates and terrines, then a dish called “truffade” comprising of cooked cheeses with potatoes, bacon and locally-cured dark ham, followed by a selection of regional cheeses and a cream-based dessert.
Considering that statistics show around 90% of Chinese are genetically lactose-intolerant, this does not bode well for their “Hidden France” plans for the rest of the day after lunch. Presumably, the group would also be plied with strong wines as per the local custom for lunches – this again would not help the statistical 30+% of the group unable to digest alcohol efficiently. If you are curious why, please read this story.
Chinese dairy industry
For fun, I looked into China’s statistics for dairy production, and found some surprising facts. The country is now the world’s largest importer of fresh/liquid milk – and on top of that, China is also the third largest producer of milk globally at around 36 million tonnes a year. By comparison, France produces less than 24 million tonnes, and is ranked seventh. However, the tolerance of lactose within the country has not increased, so 90% of China’s population will feel some negative effects when consuming dairy products past their bodies’ sufferance levels. This anomalous behaviour appears to be linked to dairy foods being perceived as a sign of affluence and “fashionable” as it is very much a Western tradition. And curiously, increasing nationwide dairy consumption has been part of Chinese government policy since 2007.
And in case you are wondering, no, I do not understand it either – maybe the Chinese really like ice cream, pizza or something like that.
Is this even worse?
However, despite the likely discomfort that would be suffered by some of the intrepid Chinese tourists in the village, their woes might pale compared to people eating another type of food.
The nutritional content label on a bag of rice.
The nutritional label pictured above is from a packet of basmati rice bought in Kuala Lumpur by a friend and sent to me here. If the label is correct, then it is curious and alarming to see both potassium and lead paired together as an item in the nutritional list. For one, the potassium content of basmati rice hovers at around a maximum of 55mg per 100g, which means that the lead content cannot be much less than 96.5mg per 100g. For another, lead is not a nutritional metal by any definition: it is in fact a toxic metal linked to several dangerous conditions, including brain damage in young children, cardiovascular problems and kidney damage in adults.
Finally, 96.5mg of lead per 100g is a staggering amount, considering that the EU Food Safety Authority and the Codex Alimentarius Commission (jointly run by the UN Food and Agriculture Organization and the World Health Organization) both established a maximum of 0.02mg per 100g of rice. This rice would be banned in the EU, and should not be consumed anywhere else.
After double-checking the data, I immediately advised my friend to throw away the rice, preferably without touching the grains.
Out of curiosity, I did some research on the available options to treat lead poisoning, and the main technique is the use of various compounds to remove the lead from body tissues, particularly blood. This involves a chemical process called “chelation”, which is defined as the binding of chelating compounds to various metal ions, forming less harmful chelates which can then be excreted from the body. Chelation can only remove from the body a proportion of the targeted metal – it does not repair any damage that had already been done. An interesting 2016 paper from the American College of Cardiology on the results of the TACT (Trial to Assess Chelation Therapy) study on 1,708 people found that test subjects exposed to lead increased the excretion of body lead up to 3,830% using the chelating agent edetate disodium. Perhaps more significantly, the TACT study indicated that major cardiac events were reduced by 18% in normal subjects and a remarkable 52% in subjects with diabetes (a disease associated with a higher risk of cardiac problems) by chelation therapy using edetate disodium.
Other claimed chelating agents are 2,3 Dimercaptosuccinic Acid (DMSA), Racemic-2,3-dimercapto-1-propanesulfonic acid (DMPS) and B-dimethylcysteine (penicillamine) though there is not much data about their effectiveness and some of them have notable adverse side effects. There is also a quack industry based around chelation therapy which tries to obscure the facts behind various chelation agents. I hope you are careful about what you ingest and never have to undergo chelation therapy.
Autumn is the season for gathering wild mushrooms in the French countryside, a fun hobby for me but probably very dangerous if it is not done with expert knowledge as it can lead to a fatal dose of mycetism (mushroom poisoning). In any case, I try not to overdo it due to the complex nature of toxins found even in edible wild mushrooms – more on this later.
Mushroom hunting is known as “la chasse aux champignons” or “la cueillette de champignons” and is one of the national hobbies of France, with people grinning with anticipation when embarking on early morning trips to their secret locations. Despite their enthusiasm (or probably because of it), over a thousand cases of wild mushroom poisoning are treated each year with several deaths reported. Some severe cases also require liver transplants, so it is a hobby fraught with significant risks – there are several thousand species of mushrooms but only a handful are edible. In many ways, wild mushrooms are to the French what fugu fish is to the Japanese.
- Rouge (left) and cèpe des pins de montagne are two mushrooms that are safe to eat.
A poisonous mushroom.
In the forests, I very often come across the seriously toxic amanita phalloides (commonly called “death caps”), hallucinogenic amanita muscaria, blood coagulating clavulinopsis fusiformis, stomach cramp-inducing entoloma sinuatum, etc. But I only forage for two types specific to the region: a species known locally as “rouges” even though it is not red in colour (clitocybe nuda), and “cèpe des pins de montagne” (boletus pinicola).
Even though I often gather the two types of mushrooms together, I do not mix them when cooking – and they usually do need long cooking to denature some of the compounds inherent within them. There is no scientific reason why I do not mix them – it is a personal preference as each mushroom will have a group of denatured compounds after cooking and I feel it is not necessary to mix the two groups together.
The poisons found in deadly mushrooms are known as mycotoxins and no amount of cooking will destroy these compounds. The most dangerous mycotoxin is probably alpha-amadin which is found in death caps. This toxin will destroy the liver within three days of ingestion, often sooner.
Other deadly mycotoxins are orellanine (kidney failure), muscarine (neuromuscular disorder), monomethylhydrazine (brain damage), ibotenic acid (nerve cell damage) and ergotamine (cardiovascular failure).
Despite the sobering dangers of mycotoxins, good wild mushrooms are still delicious cooked with butter, onions, garlic, eggs and sprinkled over with chopped chives. Just do not ever pick up wild mushrooms if you are not sure.
Curious Cook appears on the second and fourth Sunday of the month.