Slap up Meal

Never eat an ugly fish

Casava Palaver

Curse of the lectins

No escape from aflatoxins

Never eat an ugly fish!

If you thought all fish was good for you, you might want to reconsider. Ever heard of fugu? It’s a traditional Japanese delicacy, a type of puffer fish (genus Takifugu), the only food the Japanese emperor is forbidden to indulge in. The taste of fugu is said to be quite bland, unless it’s been prepared in the “right” way, in which case the diner experiences a slight tingling sensation and subsequent numbness of the lips and tongue. The tingling is caused by tetrodotoxin (anhydrotetrodotoxin 4-epitetrodotoxin), a powerful nerve poison. The flesh of the fish is harmless – the poison is mainly stored in the liver, the reproductive organs, the intestines and the skin. One fish may contain enough tetrodotoxin to kill 30 people. Only licensed chefs are allowed to prepare and sell fugu to the public, and they train for about three years to learn how to avoid contaminating the edible parts of the fish with lethal amounts of poison. Still, accidents do happen, and there are an estimated 50-100 fatalities each year.

Death by tetrodotoxin poisoning is anything but a quick’n’easy way to exit, and there is no antidote. So, what would happen to you? The toxin disables your entire electrical signalling system by blocking your nerves’ sodium channels, inhibiting the propagation of action potentials. In other words, it shuts down your nervous system. First symptoms usually occur around 20 minutes after ingestion, but could take up to three hours to set in. The initial sensation of tingling and numbness spreads from your mouth over the rest of your face, working its way down your arms and legs. Headache, stomach pain, nausea and vomiting follow. Paralysis encroaches, you won’t be able to scream, never mind speak, and soon you will be unable to move. But don’t worry, you won’t miss a thing – you’ll remain fully conscious throughout. Breathing will become increasingly difficult, and once your respiratory system fails, you’ve pretty much had it. Not all fugu poisonings are fatal, of course, and if you make it through 24 hours, you will most likely recover completely. Occasionally stories surface in the Japanese press about fugu poisoning victims knocking from inside coffins minutes before their cremation.

As you’d expect, fugu is fairly expensive – sometimes over £100 for a full meal, although you can sample it as part of a less elaborate culinary affair for under £20. And to be fair, fugu poisoning is rare and mainly happens when untrained people catch and prepare the fish. So, next time you’ve in Japan, give it a try! Or maybe just have a burger instead.

Casava Palaver

Cassava, also called manioc, is a woody perennial shrub of the spurge family (Manihot esculenta), indigenous to tropical South America. Its fleshy, tapering roots have a high edible starch content of 30-35%, and crop yields can exceed 20 tons of roots per acre. These qualities make cassava a highly popular staple crop, and as many as 300 million people in the tropics and subtropics consume it daily. Cassava can be prepared in countless ways, e.g. boiled, baked, fried and made into flat breads. You may have eaten cassava yourself, it’s what tapioca pudding is made of, and health food shops sell bags of very tasty cassava chips.

The cassava products, which are imported into the UK, are made from sweet cassava. The poorer populations of tropical countries depend on bitter cassava for their sustenance. The bitter variety produces much higher yields than sweet cassava. There is one other crucial difference between the two: bitter cassava is laced with cyanide through and through (which is why it’s bitter). The cyanide occurs in the form of cyanogenic glucosides, mainly linamarin, and a tiny amount of lotaustralin (methyl linamarin). In the sweet variety, those cyanide compounds are mainly confined to the skin, which is easy to peel off. People who consume cassava as a staple have developed various ways of detoxifying the roots before consuming them. The most effective methods are grating and crushing, because the roots also contain the enzyme linamarase, which breaks down the linamarin and enables it to escape into the air as cyanide gas. Linamarase and linamarin are stored separately in the plant’s cells, so only by breaking down the cell structure can this process happen effectively.

Other methods are also used, such as boiling, sun drying and fermenting. The problem is that these aren’t always adequate. Some African regions, for example, are frequently afflicted by drought, which causes cassava to accumulate very high levels of cyanide. Grating and crushing are very labour intensive, and many cultures have not adopted this way of processing. A disease called konzo, prevalent in southern, eastern and central Africa, is thought to be a result of chronic cyanide poisoning caused by cassava consumption. Konzo causes sudden and irreversible paralysis of the legs, which mainly affects children and young women. TAN (tropical ataxic neuropathy), which can lead to blindness, deafness, and difficulty in walking, is found mainly in western Africa among older people, who have subsisted for a long time on a monotonous cassava diet. This is a case of cruel irony: the very food which many populations depend on to sustain life is also what debilitates and kills them – and what makes matters worse is that this unfortunate situation is entirely preventable.

Curse of the lectins

Less than half a dozen kidney beans (phaseolus vulgaris) can make you as sick as a parrot. Surprised? Well, you would be, seeing that you’ve probably had nearly as many chilli con carnes as you’ve had hot dinners with no ill effects … apart from maybe a bit of wind. But don’t be fooled – those innocent looking red beans harbour the potential for hours of torture. The evil force within them are lectins, also called phytohaemagglutinins, a type of protein found in many types of beans. Kidney beans have the highest concentration of lectins.

Why are lectins so terrible? For two main reasons: they bind to intestinal cells preventing nutrient absorption and, when they enter the blood stream, they also bind to red blood cells. This causes the red blood cells to clump together, a process referred to as “agglutination”, rendering them useless. Symptoms of “red kidney bean poisoning” occur 1-3 hours after consumption, entailing extreme nausea, severe vomiting, followed by diarrhoea and abdominal pain. Recovery is usually rapid, and sets in after 3-4 hours.

You’re probably still wondering why this has never happened to you. The answer is simple: lectins are inactivated during cooking. Tinned kidney beans are always cooked, and when buying them dried, they are soaked and boiled before eating. It takes only four to five raw kidney beans to trigger symptoms – and, paradoxically, undercooked beans are worse than raw beans. You should, for example, never use dried or raw beans in a slow cooker, which cooks foods at low temperatures over extended time periods. Heating kidney beans to only 80°C (i.e. below boiling point) can turn them five times more toxic. To be on the safe side, you should soak dried kidney beans in water for at least 5 hours, pour away the water, and then boil them for at least one hour in fresh water. Raw beans need to be boiled for a minimum of ten minutes. Even green beans, such as French or runner beans, contain a small amount of lectins and should not be eaten raw.

The good news is that there is some interesting research going on in trying to find medical applications for lectins. Two promising areas are HIV and cancer, for which the selective toxicity of lectins may be harnessed.

“E” for Emulsifier

Emulsification is one of the great marvels of kitchen science - it’s how you get oil and water to mix.  Without it, your bowl of deliciously smooth chocolate ice cream would turn into globules of oil bobbing about in a murky liquid. An emulsifier is a molecule with one hydrophilic (water friendly) and one lipophilic (oil friendly) end, and this is what keeps the two opposing substances floating blissfully in a dreamy, creamy suspension.

Many natural substances can act as emulsifiers: phospholipids (combinations of lipophilic fatty acids and hydrophilic phosphate groups), proteins and complex carbohydrates. Milk, for example, is an emulsion, stabilised by its own protein content. One of the most powerful natural emulsifiers is the phospholipid lecithin, and you’ll find it on the ingredients labels of many foods as “E322”.  Egg yolks are rich in natural lecithin, and this is why they are a chief constituent of mayonnaise, the poster child of all emulsions. For industrial purposes, lecithin is often extracted from soybeans or peanuts.

Other common emulsifiers are found in the E400 range. Some are synthetically produced mono- and diglycerides of fatty acids (e.g. E471), but many do come from natural sources. You may be surprised to discover that you have consumed several bucket and spadefuls of seaweed over the years. Seaweed constituents have unique emulsifying, stabilising, gelling and thickening properties, which the food industry cannot do without. Alginates (E400-E405), as the name suggests, are made from the cell walls of brown algae. Carrageenan (E407) and agar (E406) are obtained from red seaweeds. These E-numbers are typically found in desserts, yoghurt, sweets and sauces.

No escape from aflatoxins

‘Did you know that many of the foods you eat are laced with a highly toxic contaminant? Forget E-numbers, aflatoxins constitute a much more serious threat to food safety. These substances are mycotoxins produced by two types of fungus (moulds), called Aspergillus flavus and Aspergillus parasiticus, and they affect a multitude of food crops around the world, such as peanuts, tree nuts (e.g. almonds, brazil nuts), corn, wheat, oil seeds (e.g. cotton seed), and some spices.

Milk, dairy products, meat and eggs can also be affected, because this is where aflatoxins in contaminated animal feed end up. This can be a serious problem, especially in developing countries, where there may be a lack of control and in addition to environmental factors which help the aflatoxin to form.

There are two types of aflatoxin poisoning – acute aflatoxicosis and chronic aflatoxicosis. The acute form, which can cause death, particularly in young children, is caused by ingesting large doses of aflatoxin (in excess of 6000mg). This is thankfully very rare in developed countries, due to screening of crops and sophisticated storage facilities. Chronic aflatoxicosis, a result of frequent, low-level consumption of contaminated foodstuffs, may on the other hand be quite common, possibly even in developed countries, although it’s rarely diagnosed because there are no specific symptoms. Sufferers are afflicted by impaired nutrient absorption, slow growth and also cancer - aflatoxins are known to be carcinogenic.

You may be wondering why aflatoxins aren’t headline news every night on tv. The reason is that they’re considered unavoidable contaminants, and in developed countries such as the UK, testing procedures are routine and strict. Any products with excessive aflatoxin levels are detected and stopped.

The latest aflatoxin contamination alert was issued by the UK Food Standards Agency (FSA) on 3 February 2006, involving a kebab powder made in Ghana. Such alerts happen frequently, and the affected products are then recalled from shops. Large supermarkets react very quickly to withdraw such products from their shelves, but if you were to trail round several small corner shops with a list of recalled products, chances are, you’d find some of them still sitting on their shelves. Go check out the FSA’s food alert page and see what you can find!

http://www.food.gov.uk/enforcement/alerts/

<< Go Back