In the northern Italian town of Ferrara hangs a little-known painting by Giuseppe Mentessi (1857-1931). Surrounded by a field of maize, a woman carries her exhausted child in her arms, her eyes downcast with suffering. Behind this painting lies a story of medicine, food, economics, and culture – the story of pellagra, perhaps one of the greatest tragedies of malnutrition known to the Western world.
Exhibited at the Venice Biennale in 1895, Mentessi’s image of a cornfield depicts what once was a common sight throughout the region. Maize or corn was first domesticated as a cereal crop in the Americas, making its way to Europe via traders in the sixteenth century. This new foodstuff proved to be a lifeline for Italian agricultural workers who labored under the pressures of wheat shortages and insecure employment. With its low cost and high yield, cornmeal or polenta was quickly established as the staple food of the poor. Landowners were eager to profit from maize production, and eventually forests, vineyards and pastures across the Veneto and Lombardy were replaced by fields of this single crop. It was fitting that Mentessi named his picture “Our Daily Bread” – for by the 1800s, northern Italian peasants were living on a diet made up almost exclusively of corn.
At the same time, increasing numbers of them were falling victims to a new disease. Characterised by a flaking rash on the sun-exposed skin of the arms and neck, they named it pellagra (from pelle agra, loosely translated as “rough skin”). Symptoms included confusion, mania, lethargy, and eventual death. While the link between pellagra and maize dependence was quickly recognized by scientists at the time, the mechanism remained a mystery. Today, we know that pellagra is a disease of severe niacin (vitamin B3 or nicotinic acid) deficiency. Niacin is the precursor of two essential coenzymes of cellular activity – nicotinamide adenine dinucleotide (NAD) and NAD-phosphate (NADP) – both involved in DNA repair, cell signalling, and metabolism. Tissues with high energy requirements and high cell turnover are particularly vulnerable to their deficiency. Without sufficient dietary niacin – or tryptophan, the amino acid used in its biosynthesis – a systemic disease occurs affecting the skin, gastrointestinal tract, and nervous system. The resulting clinical features have been famously described as the 4 D’s: dermatitis, diarrhea, dementia, and death.
The unvarying cornmeal diet that poor Italians relied on in the lean winter months, without the addition of vegetables, dairy products, or meat, was severely deficient in both niacin and tryptophan. An epidemic of pellagra resulted, with thousands of deaths attributed to the illness – particularly in women, who had increased nutritional needs because of pregnancy and breastfeeding, and whose inferior social position meant that they tended to have less food then the men in their family. So common did the neuropsychiatric effects of the illness become, that mental asylums such as Venice’s San Servolo and San Clemente were full of victims of what was then termed “pellagrous insanity.” For almost two centuries, pellagra was endemic in the agricultural lands of the Po valley across northern Italy.
It was this widespread suffering which Giuseppe Mentessi sought to depict in his painting. Born into poverty in Ferrara, Mentessi went on to have a successful career as an art teacher and professor at the Accademia di Brera in Milan. Nevertheless, his work maintained a deep affinity with his humble origins and he often used his art to highlight the social issues of the day. In “Our Daily Bread,” he shows the misery of the Italian rural poor, with the woman’s sickly countenance a mark of the effects of pellagra. What he depicted in paint, the writer Goethe described in words in his ‘Italian Journey:’ “Of the (Italian) inhabitants, I have little to say and that unfavourable … (the) sallow complexion of the women spoke of misery and their children looked just as pitiful … I believe that their unhealthy condition is due to their constant diet of yellow polenta …”
It was not the diet of cornmeal alone which gave rise to pellagra in southern Europe, but also the method of preparation. While maize had been a staple food of central America for thousands of years, the indigenous peoples were accustomed to soaking the dried corn kernels in alkaline lye or quicklime before cooking. This process, known as “nixtamalization,” increased the bioavailability of bound niacin in the corn by converting it into the water-soluble free compound, allowing it to be absorbed by the gut. As a result of their traditional cultural methods of preparation, the native people of the Americas did not suffer from pellagra.
When corn was brought across the Atlantic to Europe, the tradition was lost. Furthermore, pellagra was then introduced to the Americas, where European colonizers grew and ate corn without realizing the benefit of nixtamalization or the importance of a varied diet. Particularly in the Southern states, in the economic downturn following the American Civil War, the daily fare for poor people consisted almost entirely of corn-based products such as cornbread and grits. Rural sharecroppers and populations lacking access to fresh produce – in prisons, coal-mining camps, and cotton-mill towns – were particularly vulnerable to niacin deficiency. The devastation occurred on a grand scale; across the United States from 1906 to 1940 approximately 3 million cases and 100,000 deaths were attributed to pellagra.
It was a US public health physician, Joseph Goldberger, who determined that pellagra was a nutritional deficiency and not (as was commonly supposed) an infectious epidemic. In 1915, he carried out a series of experiments in Mississippi prisoners which demonstrated that symptoms of pellagra appeared after six months of eating only corn-based foods; when fresh, varied produce was introduced, the illness resolved. He concluded that “no pellagra develops in those who consume a mixed, well-balanced diet,” yet struggled to convince the political establishment that poor social conditions might be responsible for the disease. It took several more decades of research – including the isolation of niacin itself from liver tissue by Conrad Elvehjem in 1937 – before federal recommendations to fortify flour supplies with vitamins led to the eradication of the condition in the United States by 1945.
In Italy, economic growth helped end the pellagra epidemic during the 1950s, but not before the illness had provoked widespread debate about the impact of social injustice and deprivation on human health, with commentators such as Flarer (1849) referring to pellagra as “malattia del padrone” – “illness due to the landlord.” Today, we understand more than ever the impact of socio-economic factors on our health, with recognition that the West’s adoption of a highly-processed, energy-dense diet has contributed to our modern epidemics of obesity and diabetes. Such “malnutrition in the midst of plenty” has echoes of Mentessi’s work. It is said that he had the idea for his painting when he was taking an afternoon walk through a field of corn and was struck by the contrast between the bountiful crop and the sickly peasant woman with her child: “misery, perhaps hunger, in the middle of that insolent and healthy wealth!” In both Europe and the United States, it is still the poorest sections of society who suffer the most from their dependence on an abundance of cheap calories. While it may have been largely forgotten, the story of pellagra ought to be a lasting lesson in how social structures, globalization, and economic change once conspired to cause thousands of deaths from an entirely preventable disease.
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MEERA LADWA, MBBS, BSc qualified in medicine in 2008 and works as a clinical research fellow in London. Her interests include diabetes and metabolism, particularly the impact of the environment on human health and physiology. Currently, she is studying for a PhD in diabetes and nutritional sciences.
I believe the correct answer would be yes. As in yes to both options…8-/
This review will summarize current information on bacterial skin flora including Staphylococcus, Corynebacterium, Propioni-bacterium, Streptococcus and Pseudomonas. Specifically, the review will discuss our current understanding of the cutaneous microbiota as well as shifting paradigms in the interpretation of the roles microbes play in skin health and disease.
Through an analysis of the limited current literature, we highlight a new hypothesis that suggests skin microbes directly benefit the host and only rarely exhibit pathogenicity. In this model, the delicate balance of the skin barrier and innate immunity combine to maintain healthy skin, and disturbance of this balance can predispose the host to a number of cutaneous infectious and inflammatory conditions.
Unlike the intestine, the role of microbes on the skin surface has not been well studied. An incomplete understanding of the fundamental biology of cutaneous microflora is the result of the limited research efforts to date…In light of symbiotic relationships of microbial mutualism and commensalism demonstrated as critical to human health in studies of gut microbiota, a need exists to expand this research in skin.
The typical vector for Brugia malayi filariasis are mosquito species from the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound.
Some of you are aware that I have been fighting a long battle back to health. What I originally thought was an allergy to gluten back in 2012 ended up being a form of lymphoma. Accurate diagnosis didn’t happen till November 2018. My stubborn self and dislike of anything hospital was partially at play but also cutaneous t-cell lymphoma is one that goes misdiagnosed for some time with most. I was lucky enough to be informed by someone I was giving a ride to who had been diagnosed with the same thing and in treatment for many years before we met.
To add lucky duck icing on top of that good news I was fortunate enough to have a friend of the family that is an oncologist who’s specialty is lymphoma and leukemia. What luck to say the least.
Now here is the interesting twist. I had been through diet, supplementation and Dr. Google been addressing what I thought was something systemic but by no means did I really think that I had cancer. I had my primary Dr. do all of my blood tests to make sure that everything internal that I couldn’t see was functioning properly and continued on my path to recovery. I still am not sure I agree with the diagnosis but I have accepted it and respect it, however I reserve my right to remain a skeptic. Have I made all of the right decisions for treatment along the way? I don’t know. We will see.
Back to the diagnosis and oncologist. Though he recommended that I have further tests done, I chose not to. Many of the neoplasia(tumors) had already resolved or reduced in size significantly. In other words my immune system was doing its job and my skin was fixing itself and expressing all of the diseased tissues gradually over time. REEEEEALLY GROSS. On the other hand, no nasty scarring. Just a prolonged recovery and a lot of self care.
Cutaneous T-Cell Lymphoma which was originally called Mycosis fungoides was first described in 1806 by French dermatologist Jean-Louis-Marc Alibert. The name mycosis fungoides is very misleading—it loosely means “mushroom-like fungal disease”. The disease, however, is not a fungal infection but rather a type of non-Hodgkin’s lymphoma. It was so named because Alibert described the skin tumors of a severe case as having a mushroom-like appearance. Which is exactly why I had no clue that it was cancer. I frankly thought I was just a sick ass dirty bird that drank way too much and ended up with a really bad fungal infection that was paying the piper.
All this to say…I identify with Legion…LoL. I swear this guy had the same thing as me. Him and Job. Too much fun.
Now if I could just figure out how to write a book. How to publish. Because I have an amazing story to tell about my recovery from a disease I didn’t know I had. And how my recovery and principles learned in A.A. helped my mentally remain strong through my return to health.
I also want to help people. I want to help people not have to go through what I did. And here is why…
When all this started back in September of 2017 I made some drastic lifestyle changes and dedicated myself to learning how to optimize health and existence. Along the way I have explored many different diet trends and tried many a different thing eventually arriving where I am at today almost fully recovered.
I still have a little ways to go, but I expect that the full recovery process will take about 42 months or 3.5 years. I’ve been documenting some of it at https://3.5tolife.com
And the best part is my body looks and feels significantly younger and I don’t think it is anything magic that I have done. Just followed some basic ideas and rules.
What if cancer, dementia, diabetes and cardio vascular issues were all simply the process of aging taking its course? I imagine that would mean that all we have to do is figure out what it means to be simply younger and go there.