FORTY-EIGHT years ago, I had my first food culture shock. That was at the University of Nigeria, Nsukka (UNN). I was a fresh student and a Jonny Just Come (JJC) in Iboland. I could not eat well for about three months. The melon (egusi) soup got stuck in my throat, as did the okra soup, and the aroma of Abakaliki rice almost made me throw up. Back home in the West, we did not eat stock fish the way it was cooked in melon or okra soup in the East. Stock fish was cut and cooked in morsel sizes, which was the size of beef for the adult person or slightly bigger. So, in the West, we ate stock fish as we ate beef. At the UNN Margarette Ekpo Cafeteria, stockfish was chopped into chips of the block, so that every morsel of “garri” (eba) or fufu or whatever picked something like a magnet pulling up a piece of metal. The melon soup and its broken pieces of stockfish would soon teach me all over to chew my food, and not swallow it, as table manners educators had misinstructed us in High School. At school, we learned from table etiquette that the person who sat beside you at table should not hear the sounds of the movement of your mouth while you ate. It will take dietary life at UNN and nutrition education decades after to take all of that stuff out of my brain. What are teeth in the mouth for? I teach people today they are to use their teeth to micronise food for easy digestion in the stomach and in the intestine. They are also to allow saliva to mix well with complex carbohydrate in the mouth so that ptyalin, an enzyme in saliva, will reduce the complexe carbohydrate or polysaccharides to simpler ones called disaccharides. By this time, the taste of the food should have changed, signalling end of the first stage of digestion, and only then should it be swallowed. In doing this, how will my neighbour not hear the sound the teeth, the tongue and the saliva are producing in my mouth?
And the okra at UNN? Back home, it was micronised to the size of the white pods of the okra or smaller with the kitchen knife or the electric blender. Today, a kitchen grater does the job well as well. But in those days at the UNN, I was faced by an okra soup in which the okra had been cut to about four or fewer bits! As for Abakaliki rice, I traded my meal tickets for some other meal and went to town for a meal at a Yoruba food carteen beside the motor park. What a great discovery it was the day I discovered it was owned by the wife of one of my uncles who had left the village for Onitsha about 29 years before I came to Nsukka. Back home in the village, I always heard about an uncle nicknamed Millionaire Pikin. My grandma told me he went to the East and did not return home until during the 1967-70 Biafra war when he suddenly landed with about 18 children from three wives. After the war in 1970, he returned to the East. No one knew where he went. He was out of town in 1974 when I began to frequent this canteen, the owner unknown to me . When he returned and discovered I was a new regular customer, and asked where I came from and narrowed it to his village and compound, he put his hands on his head in lamentation that we should never throw a stone into a market crowd for it may land on the head of one of our relations. That was a great Yoruba proverb against evil doing. Soon, his children began to do my laundry and to bring me home cooking in my hostel room. Not only did his canteen become a dietary safe haven for me, it became as well a hiding place whenever the students union embarked on its Kodlinye Must Go rallies which may end in riots. Professor Kodlinye, the vice chancellor, was a UK-cultured man who, at the end of every budget year, returned unused funds to the government purse from which it had come, rather than hand them to his colleagues to butcher.
Happily, today, I now eat my melon soup the way UNN taught me to eat it. I also cannot eat okra soup without “something “in it. That “something “is not clumps of okra, though. From youth service among the Efiks in calabar, I learned to eat it with periwinkle. And, not too long ago, I enjoy it with what my Akwa Ibom friends call nkoriko. This is a specie of snail which does not grow beyond the young ones of other species before it dies. We found many of its carcases in the backyard garden and began to farm it in cages. You cannot crack the periwinkle with your teeth. A knife would have done that to let you suck out the tenant in the shell from the other end. But you can crack or crush nkoriko‘s bottom with your teeth and chew the shell for calcium, if you like. Both periwinkle and nkoriko make good dietary sense in okra soup cooked with ogbono (apon in yoruba) these days that Titus fish and beef are too expensive. My only concern is that the intestine of periwinkle and of nkoriko may be eaten along with their meat. I am unhappy anytime I test their poop in my mouth. For I know the faeces of all animals is a waste material which contains bacterial, fungi, etc. My friends from Akwa Ibom and Calabar do not appear to share my concern.
Abakaliki rice
Excuse me, I am not a chef. Blessing Effiong, from Ikot Ekwere Itam in Akwa Ibom State set the stage for this column. She came to spend about two weeks with my household in Lagos. And one of her gifts for us was Abakaliki rice. The aroma fills the kitchen and the entire house. We are interchanging Abakaliki rice with local rice we bought from Mr. Sanni Eremosele who brings it to Lagos from Irua, near Auchi. Blessing also brought palm oil. We interchange also with palm oil from Irua. We are educated anew that we eat adulterated food in Lagos. Since the home grown rice revolution began under President Mohammadu Buhari, one of the silent achievements of his administration I dare say, my household has not eaten foreign rice. We are not only patriotic Nigerians, we care for our health as well. As you will find in the following article, white rice, which foreign rice is all about, destroys the lives of many people in Asia, particularly Japan, a little under 200 years ago. Many Africans, especially Nigerians, did not know about this, and, thus, go on instalmentally damaging their health and shortening their lives, whereas the rice grown on their own soil and untempered with can rebuild their health and prolong thier lives.
Acording to Anne Ewbank, writing in Google on February 22, 2018:
In 1877, Japan’s Meiji Emperor watched his aunt, the Princess Kazu, die of a common malady: kakke. If her condition was typical, her legs would have swollen, and her speech slowed. Numbness and paralysis might have come next, along with twitching and vomiting. Death often resulted from heart failure.
The emperor had suffered from this same ailment, on-and-off, his whole life. In response, he poured money into research on the illness. It was a matter of survival: for the emperor, his family, and Japan’s ruling class. While most diseases ravage the poor and vulnerable, kakke afflicted the wealthy and powerful, especially city dwellers. This curious fact gave kakke its other name: Edo wazurai, the affliction of Edo (Edo being the old name for Tokyo). But for centuries, the culprit of kakke went unnoticed: fine, polished, white rice.
Gleaming white rice was a status symbol—it was expensive and laborious to husk, hull, polish, and wash. In Japan, the poor ate brown rice, or other carbohydrates such as sweet potatoes or barley. The rich ate polished white rice, often to the exclusion of other foods.
This was a problem. Removing the outer layers of a grain of rice also removes one vital nutrient: thiamine, or vitamin B-1. Without thiamine, animals and humans develop kakke, now known in English as beriberi. But for too long, the cause of the condition remained unknown.
In his book Beriberi in Modern Japan: The making of a National Disease, Alexander R. Bay describes the efforts of Edo-era doctors to figure out the disease. A common suspect was dampness and damp ground. One doctor administered herbal medicines and a fasting regimen to a samurai, who died within months. Other doctors burned dried mugwort on patients’ bodies to stimulate qi and blood flow.
Some remedies did work—even if they didn’t come from a true understanding of the disease. Katsuki Gyuzan, an early, 18th-century doctor, believed Edo itself was the issue. Samurai, he wrote, would come to Edo and get kakke from the water and soil. Only samurai who went back to their provincial homes—going over the Hakone Pass—would be cured. Those who were seriously ill had to move quickly, “for the worst cases always result in death,” Katsuki cautioned. Since heavily processed white rice was less available outside Edo and in the countryside, this likely was a cure. Similarly, a number of physicians prescribed barley and red beans, which both contain thiamine.
According to Anne Ewbank, writing in Google on February 22 2018:
By 1877, Japan’s beriberi problem was getting really serious. When the princess Kazu died of kakke at 31, it was only a decade after her former husband, Japan’s shogun, had died, almost certainly from the mysterious disease. Machine-milling made polished rice available to the masses, and as the government invested in an army and navy, it fed soldiers with white rice. (White rice, as it happened, was less bulky and lasted longer than brown rice, which could go rancid in warm weather.) Inevitably, soldiers and sailors got beriberi.
No longer was this just a problem for the upper class, or even Japan. In his article British India and the “Beriberi Problem,” 1798–1942, David Arnold writes that by the time the emperor was funding research, beriberi was ravaging South and East Asia, especially “soldiers, sailors, plantation labourers, prisoners, and asylum inmates.”
Britannica.com
According to the Editors of encylopedia Britannica.com in an article last updated on October 10, 2022 and introduced as Beriberi, nutritional disorder caused by a deficiency of thiamin (vitamin b1) and characterised by impairment of the nerves and heart or Thiamine defficiency, vitamin B1 defficiency as alternative headline, it is reported:
“General symptoms include loss of appetite and overall lassitude, digestive irregularities, and a feeling of numbness and weakness in the limbs and extremities. (The term beriberi is derived from the Sinhalese word meaning “extreme weakness.”) In the form known as dry beriberi, there is a gradual degeneration of the long nerves, first of the legs and then of the arms, with associated atrophy of muscle and loss of reflexes. In wet beriberi, a more acute form, there is edema (overabundance of fluid in the tissues) resulting largely from cardiac failure and poor circulation. In infants breast-fed by mothers who are deficient in thiamin, beriberi may lead to rapidly progressive heart failure.
“The cardiac symptoms, in both infants and adults, generally respond promptly and dramatically to the administration of thiamin. When neurological involvement is present, the response to thiamin is much more gradual; in severe cases, the structural lesions of the nerve cells may be irreversible”.
“Thiamin normally plays an essential role as a coenzyme in the metabolism of carbohydrates; in its absence, pyruvic acid and lactic acid (products of carbohydrate digestion) accumulate in the tissues, where they are believed to be responsible for most of the neurological and cardiac manifestations.
Thiamin occurs widely in food but may be lost in the course of processing, particularly in the milling of grains. In East Asian countries, where polished white rice is a dietary staple, beriberi has been a long-standing problem. The history of the recognition, the cause, and the cure of beriberi is dramatic and is well documented in medical literature. In the 1880s the Japanese navy reported that beriberi had been eradicated among its sailors as a result of adding extra meat, fish, and vegetables to their regular diet. Before that time, almost half of the sailors were likely to develop beriberi, and many died of it. In 1897 Christiaan Eijkman, working in the Dutch East Indies (now Indonesia), found that a beriberi-like disease could be produced in chickens by feeding them a diet of polished rice. British researchers William Fletcher, Henry Fraser, and A.T. Stanton later confirmed that beriberi in humans was also related to the consumption of polished white rice. In 1912, Casimir Funk demonstrated that beriberi-like symptoms induced in pigeons could be cured by feeding them with white rice that was supplemented with a concentrate made from rice polishings. Following this discovery he proposed that this, as well as several other conditions, were due to diets that were deficient in specific factors that he called “vitamines,” later called vitamins.
The prevention of beriberi is accomplished by eating a well-balanced diet, since thiamin is present in most raw and untreated foods. The incidence of beriberi in Asia has markedly decreased because an improved standard of living has allowed a more varied diet and partly because of the gradual popular acceptance of partially dehusked, parboiled, and enriched rice—forms that contain higher concentrations of thiamin. In Western countries, thiamin deficiency is encountered almost solely in cases of chronic alcoholism”.
Port of Maha Chai
According to Pawinee Doung-ngem, ( Ministry of Public health Thailand), S Kesomsukhom, J Kanlayanaphotpom, S Wanadurongwan, Sriwatana Songchitsomboon (Mahidol University), writing in the Southeast Asian Journal of Tropical Medicine and Public Health:
“In April 2005, The Tahi Bureau of Epidemiology investigated a reported outbreak of beriberi among commercial fishermen in Maha Chai, a port city in the Gulf of Thailand. The objective of this study was to verify the diagnosis of beriberi in affected individuals, describe the possible outbreak, ascertain risk factors, and provide prevention and control measures. We interviewed ill persons and treating doctors, and reviewed medical records to conduct a descriptive study. A probable case was defined as a crewmember of Ship A with one of the following: leg edema scrotal edema or ascites, dyspnea, chest discomfort, chest pain, extremity numbness, or extremity weakness. Confirmed cases were those with clinical criteria and laboratory findings consistent with thiamine deficiency. The outbreak started in early March, 2005 and continued until March 31, 2005. Ship A had 28 crewmembers (four Thai, 24 Myanmar). Overall, there were 15 probable cases (attack rate 53.6%, with three confirmed and 12 probable cases). Only three were tested for Vitamin B1 deficiency. All cases were male, with a median age of 28 years (range 20-45). Fourteen of the 15 cases were Myanmar and one Thai. Due to limited resources, the crew ate only seafood and polished rice for almost two months prior to symptoms. Symptoms included edema (60%), chest discomfort (54%), and dyspnea (27%). Two persons died while on board the ship (case fatality 13%). The total time at sea for Ship A was 18 months, including a five-month delay in docking due to licensing problems”.
Thailand
Thailand must be a wicked country. It knows about the dangers of eating white rice, yet it kept pumping white rice into Nigeria irrespective of the ban on foreign rice. Nigerians must be an ignorance or a stupid people to prefer Thai’s white rice to their own nutrious rice thereby enriching Thailand, creating jobs in Thailand impoverishing their country, depending on another country to feed them, creating no jobs in their own country and cursing and fighting their government from trying to save them from food colonisation by another country.
