Diet-Related Diseases

The Modern Epidemic

Stephen Seely, David L. J. Freed, Gerald A. Silverstone, Vicky Rippere

• Publisher: Routledge
• Year: 2022
• ISBN:
  9781000577952
• Edition: 1
• Topic: Medicine
• Subtopic: Nutrition, Dietics & Bariatrics

Originally published in 1985, and authored by an epidemiologists, a medical immunologist, a chemist and a clinical psychologist, this books shows that unravelling the links between diet and disease is a very complex task, and while the evidence is strong in many cases, in others if is of doubtful validity. Many of the diseases prevalent in developed countries are discussed here: cancer, arterial heart disease, food allergies and intolerances as well as the impact of diet on mental health.

1 Diseases Known to be Caused by the Diet

D.L.J. Freed and S. Seely

Probably every disease known to mankind has some connection with the diet, at least in the sense that nutritional deficiencies weaken the natural defence mechanism of the body. A serious metabolic disturbance, like diabetes, even if corrected by the administration of insulin, predisposes to unrelated diseases, like coronary disease, presumably because neither the quantity, nor the timing of the dosage is as good as the regulatory effect of the healthy pancreas. However, this book is not concerned with distant connections with diet. Nor does it discuss an obviously diet-related disease: malnutrition. Its subject is the connection between various diseases and a hygienically prepared, adequate Western diet. Such a diet, in spite of all precautions, still plays a part in the pathogenesis of some diseases, presumably because some foods are in fact mildly toxic and their cumulative effect can be pathogenic. Such mildly toxic substances in the diet can be immensely difficult to detect.

Once a dietary pathogen has been identified, the disease it causes tends to fade into insignificance. Diseases which, at one time, were the scourges of mankind, tend to yield to ridiculously simple measures once the cause is known. Bovine tuberculosis for example, was still an important disease at the beginning of the century. It was transmitted to humans mainly in cow’s milk, and the comparatively simple remedial measure of heating milk to about 70° C – pasteurisation – was sufficient to cause a dramatic reduction in its prevalence.

Most diseases which are known to be diet-related, are therefore only of historical interest. Nevertheless, we are giving a few examples, mainly to show the work of medical detection that went into the discovery of the pathogenic agent. The object is not only to give credit to the many unsung scientists whose work saved countless people from premature death but also because the examples serve as good omens for the future. Successes in this field are soon forgotten, the failures are still with us. Recounting the successes gives some indication of the difficulties that had to be overcome and justifies the hope that what was possible in the past, can be repeated in the future.

Dietary toxins, in the usual sense, mean substances which are toxic to a normal person. However, metabolic defects which make harmless foods pathogenic to a minority population group constitute a confusing factor and appear as added difficulties. Some examples will be cited to illustrate the point.

Contaminants and Food Additives

The Sacred Flame

In the year 994 a terrible epidemic struck in the South of France. The first sign of the unknown disease was pain in the extremities, first the toes and fingers, then the feet and hands turned blue and gradually black. Ultimately gangrene set in and the victim died, slowly and painfully, of the general sepsis that followed. The epidemic is mentioned in several chronicles, one of which estimates that it caused 40,000 deaths. What there was of medical practice at the time was largely in the hands of the priests, whom the epidemic took as much by surprise as anyone else. They were quite helpless to resist its progress and named it ‘ignis sacer’, declaring it to be a visitation for the sins of mankind. This was probably the best explanation at the time, but it could hardly have given much succour to the ill and dying.

Similar outbreaks, sporadic and capricious in occurrence, plagued Europe for a thousand years. Besides France the main sufferers were Germany, Austria, Poland, Finland, the Balkans and Russia. There was at least one major outbreak in every century, small outbreaks considerably more often. Another bad epidemic occurred in the South of France in 1777, causing 8,000 deaths. Probably the only European country which never suffered any fatalities was England, though some people were taken ill in a minor outbreak at Wattisham, near Bury St. Edmunds, in 1762. In Norway there was only one outbreak in recorded history, while in Finland there were two as late as the nineteenth century, in 1840 and 1862, with a death toll of about 300. There were four outbreaks in the nineteenth century in France and a serious epidemic in 1857 in Hungary. The last major outbreak occurred in 1926 in Russia. More than 10,000 people were ill, 1,600 seriously, 93 died. The last small outbreak occurred in 1951 in the small French town of Pont St. Esprit where 150 people were taken ill, and four died.

It took something like 500 years after the epidemic of 994 to discover that the disease was caused by the rye fungus ergot (Claviceps purpurea), the overwintering fructification (the sclerotium) of which mixes with rye grain, and if ground up with it, makes the rye flour toxic with its alkaloids (Figure 1.1). Thus in the sixteenth century in Germany sieves were used to separate the sclerotia of ergot from the grain. In other cases a flotation process was used for the separation, as the sclerotia, which are lighter than the rye grains and lighter than water, float to the surface when the mixture is immersed in water. In spite of these techniques, epidemics continued unabated, mainly because of the sporadic nature of the outbreaks. Like lightning, they seldom struck in the same place twice, and if a locality did not experience an outbreak for a century or more, farmers were invariably taken by surprise when an outbreak did occur.

Figure 1.1: Ergot-infested Grass

The explanation of the sporadic nature of the epidemics is in the life cycle of ergot. This differs from other parasitic fungi. Instead of dispersing a multitude of individual spores, ergot produces an overwintering stage, the sclerotium. This contains a store of nutrients as well as a number of toxic alkaloids, protected by a chitinous cover. In the spring 30–40 small mushroom-like plants grow out of the sclerotium, which altogether produce about a million spores. These, unlike the spores of other parasitic fungi, like rust or mildew, which can establish themselves on the leaves of the host plant, must find their way to the stigma of a grass flower; they cannot establish themselves in any other position. There they germinate and find their way to the ovary. The fungus sequestrates the nutrients the plant produces for its seedling and the sclerotium develops in its place.

Ergot can parasitise a number of grasses, but its main hosts are rye and its wild counterparts, the rye grasses. The reason is that rye and rye grasses depend on cross fertilisation, while many other grasses are either exclusively or mainly self-pollinators. In wheat, notably, self-pollination takes place within unopened florets, so the stigma is inaccessible to fungal spores. Wheat and rye represent the two extremes, other cereals, like oats and barley are between the two, but rely mainly on self-pollination.

The ergot infestation of rye in most years is slight. One of us did some fieldwork on the subject and found that ergoted plants were not easy to find in a rye field in normal years, one had to search for them. However, rye plants growing in isolation, like self-sown plants at the roadside or among other crops, were usually heavily ergoted. The reason is that the fungal spores have to compete with the pollen of the host plant. A single floret of rye produces about 50,000 pollen grains, an ear of rye nearly as many as the spores of a sclerotium. When rye plants are growing in close proximity to each other, the competition is highly unequal in favour of the pollen. As soon as the floret is fertilised, it closes, making its stigma inaccessible to spores. The florets of isolated plants have to stay open longer, so the chance of infestation is correspondingly increased. This normal sequence of events is probably upset if heavy and prolonged rain falls at the critical time when rye pollen is released. Many pollen grains are probably beaten to the ground and washed away. The florets remaining unfertilised for longer than usual, are vulnerable to fungal spores. Such freak conditions are needed to give rise to the rare outbreaks of heavy ergot infestation.

Ergoted grass growing among other cereals, their seeds mixing with the grain, can give rise to minor outbreaks. Thus there were a few minor outbreaks in the last century in Sweden, though little if any rye is grown there. The small outbreak at Wattisham may have been caused in this manner, though ergot infestation of oats or barley might have been the possible cause. Cattle can also be affected by ergoted grass.

The most important toxic constituents of ergot are two alkaloids, ergotamine and lysergic acid diethylamide (LSD). In small quantities ergotamine is a contractor of smooth muscle. Its action on the pregnant uterus causes powerful contractions, accelerating childbirth. On the muscular layer of blood vessels it acts as a vasoconstrictor. In large doses the vasoconstrictor effect can be powerful enough to shut down peripheral circulation, causing blood-starved tissues to die of ischaemia. The other alkaloid, LSD, is a hallucinogen, a small dose of which can cause vivid visual sensations. A large, but sublethal dose, can cause epileptiform convulsions, an even larger dose is fatal.

The main reason for the disappearance of ergot epidemics is not so much that the fungus has been brought under control, but that rye, as a food plant, has largely been displaced by other foods. The cultivation of rye in Europe considerably decreased with the introduction of potatoes, and the advent of artificial fertilisers made wheat growing possible on poor soils previously suitable only for the more undemanding rye.

Butter Yellow

Coming nearer to our times, there was a serious outbreak of liver cancer in the early 1930s in the Far East. The Japanese scientist R. Kinosita,¹ investigating the outbreak, came to suspect a yellow aniline dye used to colour butter and margarine, introduced some years before in that area. Though the use of the dye was beginning to spread in Europe, it was still restricted mainly to the East when Kinosita started his investigations. He demonstrated the powerful carcinogenic effect of the dye, subsequently named butter yellow, in experiments on rats. The use of the dye was discontinued and the epidemic gradually petered out. Apart from the Far East, the timely discovery also saved Europe from a similar experience.

Pink Disease (acrodynia)^{1, 2, 3, 4, 5 and 6}

Although the culprit agent of pink disease was not strictly a food, the story of its discovery and eradication is nicely illustrative of this kind of detective work.

Pink disease⁶ was a chronic and unpleasant, occasionally fatal, illness of babies and young children that first became apparent in the late nineteenth century in Australia and soon spread to the rest of the English-speaking world and (albeit in older children) to continental Europe. By the 1940s it was quite common; most family doctors had three or four cases in their practices (especially in industrial towns) and pink disease accounted for 3-4 per cent of all paediatric hospital admissions in some cities. Within a decade, following the pinpointing of the cause, it had virtually disappeared.⁵ Today’s doctors have never seen a case and are not taught about it; a new epidemic of pink disease would probably catch us as unprepared as were our fathers.

Breast-fed and bottle-fed babies were equally susceptible. The child became restless and listless, unable to play, occasionally irritated by light. The arms and legs hung passively, and children who had been old enough to walk before the disease, stopped walking, although there was no true paralysis. The fingers and toes, then the palms and the soles, became swollen, cold and clammy, and assumed the dusky red colour that gave the disease its name. The cheeks and nose were often bright red. The hair fell out. The teeth loosened in inflamed gums, and there was even patchy erosion of the jawbone in some. The child lost interest in food, although it salivated excessively and was often thirsty. Most wearing of all was the dreadful insomnia, which kept child and parents awake, night after night after night. The mortality was about 10 per cent, and we can assume that some of that was due to battering, by overtired parents driven beyond breaking point.

There was no shortage of theories to explain this disease, varying from primary emotional disorder and neurosis through to endocrine or electrolyte disturbance, photosensitivity, allergy, virus infection, ergotism (see above) and arsenic or thallium poisoning. There was also no shortage of reported cures. Tonsillectomy, liver powder, vitamin supplements, hormone injections, and electrolyte adjustments all enjoyed transient popularity as first glowing claims, then negative counter-claims, appeared in the medical and lay press. Controlled clinical trials were still in their infancy, and many hopes were raised time after time, only to be cruelly dashed as the uselessness of the touted cure became obvious. Disease states similar to pink disease were induced in laboratory rats by depriving them of pyridoxine, but this vitamin proved another disappointment when tried in patients.

Then in 1945 a severely affected ...