Corn Safety: Mycotoxins, Pellagra and the GMO Question

Corn is safe food, and the honest safety questions about it are not the ones that dominate the internet. The real risks are storage moulds — fumonisins and aflatoxins — which are a serious, documented, sometimes fatal problem in parts of the world where maize is stored badly and eaten in quantity, and a small residual issue everywhere else. The second real issue is niacin: a diet built on unprocessed maize with little else beside it causes pellagra, which is why the traditional alkaline processing matters. The third question people ask most loudly — whether genetically engineered corn is dangerous to eat — has been examined about as thoroughly as any food-safety question ever has, and the answer from the major scientific review bodies is consistent. That does not mean there is nothing to argue about; it means the arguments worth having are about herbicides, agronomy and market power, not about whether the kernel is toxic. This page takes all three in turn and tries not to campaign in either direction.

Table of Contents

  1. What Actually Grows on Corn
  2. Fumonisins: The Corn-Specific Toxin
  3. Fumonisins and Neural Tube Defects
  4. Aflatoxin and the Kenyan Outbreaks
  5. Who Is Actually at Risk
  6. How Mycotoxin Exposure Is Reduced
  7. The Niacin Problem, Restated Practically
  8. The GMO Question, Handled Factually
  9. What the Real GMO Debates Are About
  10. Other Concerns Worth a Straight Answer
  11. What to Do in Your Own Kitchen
  12. Key Research Papers
  13. Connections
  14. Featured Videos

What Actually Grows on Corn

Maize is a large, starchy seed that sits on a plant in a field for months and then in a bin for months more. Fungi find it. Two genera matter for human health, and they behave differently enough that it is worth keeping them apart in your head.

  1. Fusarium species — principally Fusarium verticillioides (formerly F. moniliforme) and F. proliferatum — are field fungi. They infect the growing plant, often entering through insect damage to the ear, and they produce fumonisins. Fumonisin contamination is largely decided before the crop is harvested, and it is worse in hot, dry, insect-pressured seasons. Fumonisins are essentially a maize problem: they are found in maize far more than in other cereals.
  2. Aspergillus flavus and A. parasiticus are field-and-storage fungi that produce aflatoxins, of which aflatoxin B1 is the most toxic and best studied. Aflatoxin risk rises sharply when grain is harvested at high moisture, dried too slowly, or stored damp and warm. Aflatoxins are not corn-specific — peanuts, tree nuts, cottonseed, dried figs and spices carry them too — but maize is one of the major dietary sources worldwide.

Both toxins are heat-stable. Ordinary cooking does not destroy them. Neither is destroyed by the temperatures used to bake, boil or fry. This is the point that surprises people most: you cannot cook mould toxins out of food the way you can kill bacteria. Prevention happens in the field, at drying, and in the bin.

Grain that is visibly mouldy should not be eaten, but the reverse does not hold — grain can carry meaningful toxin levels while looking and smelling normal, because the fungus can have grown and then died, leaving the toxin behind. This is why regulated food systems test rather than inspect.

Back to Table of Contents

Fumonisins: The Corn-Specific Toxin

Fumonisin B1 works by a strikingly specific mechanism. It is structurally similar to sphinganine, an intermediate in the body's synthesis of sphingolipids — a family of fats that are structural components of cell membranes and, in the nervous system, of myelin. Fumonisin inhibits the enzyme ceramide synthase, which blocks the pathway and causes sphinganine to accumulate while downstream sphingolipids fall. The sphinganine-to-sphingosine ratio in blood is used as a biomarker of exposure for exactly this reason.

The animal toxicology is dramatic and species-specific. In horses, fumonisin causes equine leukoencephalomalacia — liquefactive destruction of the white matter of the brain, a fatal condition long known to horse owners as "mouldy corn poisoning". In pigs it causes pulmonary oedema. In rodents it is hepatotoxic and nephrotoxic and, at high chronic doses, carcinogenic in liver and kidney. The International Agency for Research on Cancer classifies fumonisin B1 as possibly carcinogenic to humans (Group 2B).

The human epidemiology is more suggestive than conclusive but is not nothing. The earliest signal came from the former Transkei region of South Africa, where an area with unusually high rates of oesophageal cancer was found to have maize heavily contaminated with Fusarium moniliforme and fumonisins, at higher levels in the households growing the poorer-quality home-grown maize. Similar associations have been reported from parts of northern China and northern Iran. This is ecological evidence — comparing regions rather than individuals — and it cannot by itself prove causation, but it fits a coherent mechanism.

A second and more recent line of evidence concerns growth. A comprehensive review of dietary fumonisin and growth impairment in children and in animal models concluded that fumonisin exposure is associated with impaired growth, consistent across species, with plausible mechanisms involving both intestinal damage and disrupted sphingolipid signalling. In populations where maize is the dominant staple and stunting is common, this is a live public-health question rather than an academic one.

Back to Table of Contents

Fumonisins and Neural Tube Defects

The most-discussed human fumonisin finding concerns neural tube defects — spina bifida and anencephaly, birth defects arising when the embryonic neural tube fails to close in the first weeks of pregnancy.

The story begins with a cluster. In 1990–1991, an unusually high number of neural tube defects occurred among Mexican-American women along the Texas–Mexico border. That period coincided with a season of heavily fumonisin-contaminated maize in the region, and tortillas were a staple food in the affected community. Researchers followed this up with a case-control study measuring a biomarker of fumonisin exposure — the sphinganine-to-sphingosine ratio in maternal serum — and comparing it against reported tortilla consumption and neural-tube-defect status.

The published finding was an association between higher fumonisin exposure and neural tube defect risk, but with an important shape to it: risk rose with exposure across the low and moderate range and then fell at the very highest exposures. The authors' interpretation was that extremely high fumonisin exposure is embryolethal — the affected pregnancies are lost rather than carried to term with a defect — which would produce exactly that inverted curve. It is worth being careful here: this is one study in one population, the sample was not large, and the dose-response shape depends on an interpretation rather than being self-evident.

The mechanistic work is what gives the finding weight. Fumonisin's disruption of sphingolipid metabolism also interferes with folate transport: the folate receptor is anchored in the cell membrane in sphingolipid-rich domains, and disrupting sphingolipid synthesis reduces folate uptake. Folate deficiency is the single best-established nutritional cause of neural tube defects. Experimental work in embryo culture and in live animals showed that fumonisin exposure disrupts sphingolipid metabolism and folate transport and impairs neural tube development, and that folate supplementation can partially rescue the effect. So there is a mechanism that predicts the epidemiology, which is a stronger position than either would be alone.

The practical conclusion has been a regulatory one rather than an alarming one. Fumonisin limits in maize for human food are set by the US FDA (as guidance levels) and by the European Union (as binding maximum levels), with tighter limits for maize destined for infants and young children. The United States also authorised the addition of folic acid to corn masa flour in 2016, which addresses the folate side of the same equation for the population most likely to be eating maize as a staple.

Back to Table of Contents

Aflatoxin and the Kenyan Outbreaks

Aflatoxin is the more acutely dangerous of the two, and the clearest demonstration of that came from Kenya.

In 2004, an outbreak of acute aflatoxicosis struck the Eastern and Central provinces of Kenya. Patients presented with jaundice and rapidly progressive liver failure. Hundreds of cases were identified and the case-fatality rate was very high — roughly two in five of those who fell ill died. A case-control investigation compared households with and without cases and found that eating home-grown maize, and specifically maize stored while still damp, was strongly associated with illness; maize from affected households carried aflatoxin at concentrations orders of magnitude above regulatory limits. Follow-up mycological work identified the causal organism as an unusually toxigenic Aspergillus flavus strain group prevalent in the affected region.

The setting matters. This was subsistence maize, harvested in a wet season, stored in conditions that could not be kept dry, in households with no alternative food and no realistic option to discard the crop. It was not an industrial food-safety failure; it was a poverty and infrastructure failure. Kenya has had further aflatoxicosis episodes since, and comparable events have occurred elsewhere in East Africa and India.

The chronic risk is different and much larger in total burden. Aflatoxin B1 is a Group 1 human carcinogen — the highest IARC category, meaning the evidence in humans is sufficient. It causes hepatocellular carcinoma, and it interacts multiplicatively with chronic hepatitis B infection, so populations with both high aflatoxin exposure and high hepatitis B prevalence carry a strikingly elevated liver-cancer risk. A quantitative risk assessment estimated that aflatoxin exposure accounts for a substantial share of global hepatocellular carcinoma cases, overwhelmingly in sub-Saharan Africa, Southeast Asia and China.

A third effect, less dramatic but affecting far more children, is on growth. A cross-sectional study of young children in Benin and Togo measured aflatoxin-albumin adducts — a blood biomarker reflecting exposure over the preceding months — and found a strong inverse association with height-for-age and weight-for-age. Children with the highest exposure were substantially more stunted. The direction of causation cannot be settled by a cross-sectional design alone, but the finding has been reproduced in other African cohorts and dovetails with the fumonisin growth data.

Back to Table of Contents

Who Is Actually at Risk

It is important to scale this correctly, because the same facts support either "corn is dangerous" or "this is not your problem" depending on where you live and what you eat.

High risk. Households that grow, dry and store their own maize in hot, humid climates without adequate drying facilities, and eat maize as the dominant staple at every meal. This describes hundreds of millions of people, mostly in sub-Saharan Africa, parts of Central America, and parts of South and Southeast Asia. Here mycotoxin exposure is chronic, sometimes acute, and genuinely consequential for liver disease, child growth and possibly birth defects.

Moderate risk. Anyone eating maize from an unregulated supply chain — informal markets, home storage without moisture control, or a home-grown crop kept in a shed through a damp season. Also relevant to people feeding home-grown or salvaged maize to livestock, especially horses, which are exquisitely sensitive to fumonisin.

Low risk. Consumers in countries with enforced regulatory limits, buying commercially processed maize products. Testing occurs at multiple points in the chain, contaminated lots are diverted or rejected, and typical measured exposures fall well below the tolerable intakes those limits were set to protect. This is not zero risk — low-level exposure is common, and surveys do find products at or near limits — but it is a different order of magnitude from the situations above.

One group deserves a specific mention: infants and young children, who eat more food per kilogram of body weight than adults and, in maize-eating regions, are often weaned onto maize porridge. Both the EU limits and general public-health guidance set tighter thresholds for foods intended for this group, and diversifying a weaning diet beyond maize alone is the single most useful step available.

Back to Table of Contents

How Mycotoxin Exposure Is Reduced

The interventions that work are boringly practical, and they stack.

  1. Dry the grain fast and keep it dry. Aflatoxin production essentially stops below roughly 14% grain moisture. Rapid drying after harvest and moisture-proof storage are the highest-yield interventions anywhere in the chain. Simple improvements — drying on tarpaulins rather than bare ground, hermetic storage bags, raised cribs — measurably reduce contamination in smallholder settings.
  2. Sort and discard. Hand-sorting to remove damaged, discoloured, shrivelled and insect-bored kernels removes a disproportionate share of the toxin, because contamination is highly concentrated in a small fraction of kernels. This is a genuinely effective low-technology intervention.
  3. Control insects in the field. Ear-boring insects create the wounds through which Fusarium and Aspergillus enter. Anything that reduces insect damage reduces mycotoxin — and this is where the mycotoxin question and the GMO question intersect, discussed below.
  4. Nixtamalize. Alkaline cooking degrades a substantial fraction of fumonisins, and the steeping and washing steps carry more away in the discarded liquid. It also reduces aflatoxin, although the degradation is not complete and some reversal has been reported under acidic conditions. This is a real benefit of a technique that already had several others, described in full on the history page.
  5. Dry milling helps. Toxins concentrate in the germ and bran fractions, so degermed cornmeal and grits typically carry lower levels than whole-grain cornmeal from the same lot — one of the few genuine nutritional trade-offs in favour of the refined product, and one reason not to be absolutist about whole grain if your maize supply is unregulated.
  6. Diversify the diet. Toxin dose is the product of concentration and quantity. Eating maize as one grain among several halves or quarters the exposure without changing anything about the maize.

Back to Table of Contents

The Niacin Problem, Restated Practically

The full history is on the history page, and the clinical detail is on this site's Pellagra page. The practical residue is short.

Most of the niacin in maize is bound to complex carbohydrates as niacytin and is poorly absorbed. Maize is also low in tryptophan, from which the body makes niacin, and comparatively high in leucine, which interferes with that conversion. So a maize-dominant diet can deliver a niacin figure on paper and a deficiency in the body.

Three things independently prevent this, and you only need one:

  1. Alkaline processing. Masa, tortillas, tamales, pozole, arepas made from nixtamalised maize, and hominy and grits made from lye-treated corn all carry liberated, absorbable niacin. If you eat corn mainly in these forms, the problem does not arise.
  2. Fortification. Commercial cornmeal, grits, corn flour and corn-based cereals in the United States and many other countries are enriched with niacin. Check the label; "enriched" degermed cornmeal will list it.
  3. Anything else on the plate. Beans, eggs, fish, meat, poultry, mushrooms, peanuts, sunflower seeds and brown rice all supply niacin or tryptophan or both. The Three Sisters solved this agriculturally; a normal mixed diet solves it without anyone thinking about it.

Pellagra in a modern setting is not caused by eating corn. It is caused by eating almost only unprocessed, unfortified corn — or by alcoholism, malabsorptive disease, anorexia nervosa, certain medications such as isoniazid, carcinoid syndrome, or the inherited transport disorder Hartnup disease, all of which can produce it on any diet. If you eat polenta or cornbread as part of a varied diet, this section is history, not advice.

Back to Table of Contents

The GMO Question, Handled Factually

Most field corn grown in the United States, Brazil, Argentina and several other large producers is genetically engineered. Two traits account for nearly all of it:

  1. Bt corn carries one or more genes from the soil bacterium Bacillus thuringiensis encoding crystalline (Cry) proteins that are toxic to specific insect larvae — European corn borer, corn rootworm, fall armyworm. The proteins require an alkaline gut and specific receptors found in those insects to become active; the mammalian stomach is acidic and lacks the receptors, and the proteins are digested like other dietary proteins. The same Bacillus thuringiensis preparations have been used as a sprayed insecticide in organic agriculture for decades.
  2. Herbicide-tolerant corn carries a gene making the plant insensitive to a broad-spectrum herbicide, most commonly glyphosate, so the field can be sprayed after emergence without killing the crop.

On the question people actually ask — is eating this food harmful — the assessments from the major independent review bodies converge. The US National Academies of Sciences, Engineering, and Medicine conducted a comprehensive two-year review published in 2016, examining over 900 publications and hearing from a wide range of stakeholders including critics. It found no substantiated evidence of a difference in risk to human health between currently commercialised genetically engineered crops and their conventional counterparts, while being notably careful about the limits of that conclusion and explicit that each new product warrants its own assessment. A separate systematic overview of a decade of genetically engineered crop safety research reached a similar conclusion after screening the published literature. Comparable positions have been stated by the World Health Organization, the European Commission's summary of its own funded research programmes, and the major national science academies.

A field-data meta-analysis of 21 years of genetically engineered maize trials is worth knowing about because it looked at the food-quality question directly rather than only at feeding trials. Pooling agronomic, environmental and toxicological outcomes, it reported higher grain yields and — the relevant part here — lower concentrations of mycotoxins in Bt maize than in comparable non-Bt maize, with the largest reductions in fumonisins. The mechanism is straightforward and is the intersection flagged earlier: insect damage to the ear is the entry route for Fusarium, so reducing borer damage reduces fungal infection and therefore reduces fumonisin. An earlier review comparing Bt and non-Bt isogenic maize had reported the same direction of effect. Whatever one thinks of the technology overall, this particular consequence is a food-safety improvement, and it deserves to be stated as plainly as the risks are.

The most famous contrary study should be named because people encounter it. A 2012 rat-feeding study by Séralini and colleagues reported tumours in rats fed genetically engineered maize and glyphosate. It was retracted by the journal in 2013 after sustained criticism of its design — particularly the small group sizes and the use of a rat strain with a high spontaneous tumour rate, which together made the tumour findings uninterpretable. It was subsequently republished in a different journal without new data. It is cited in the reference list below and labelled as retracted, because pretending it does not exist is not honest either.

Back to Table of Contents

What the Real GMO Debates Are About

Saying the food is safe to eat is not the same as saying there is nothing to argue about, and it would be dishonest to leave the impression that the question is closed on every front. The substantive debates are elsewhere, and they are worth understanding on their own terms.

  1. Herbicide use. Herbicide-tolerant crops were adopted precisely because they make herbicide application easier, and total glyphosate use rose enormously alongside them. Glyphosate's own toxicology is contested: IARC classified it as probably carcinogenic to humans in 2015, while the EPA, EFSA and several other regulatory agencies concluded it is not likely to be carcinogenic at expected exposures. Those bodies were partly asking different questions — hazard versus risk at realistic dose — but the disagreement is real. This site covers it separately on the glyphosate page. The point for the present page is that this is a herbicide question, not a question about the corn protein.
  2. Resistance. Continuous use of one herbicide selects for herbicide-resistant weeds, and continuous exposure to one Bt protein selects for resistant insects. Both have happened; both were predicted; both are managed with refuges, trait stacking and rotation, with mixed compliance. This is an agronomic sustainability problem, and it is the strongest technical criticism of how the technology has been deployed.
  3. Market concentration. Seed with patented traits is sold under licences that restrict saving seed, and the seed and agrochemical industries have consolidated into a handful of firms. Concerns about farmer autonomy, seed prices and corporate power are political and economic questions. They are legitimate and they are not settled by any amount of toxicology.
  4. Gene flow and landraces. Cross-pollination between engineered maize and traditional landraces, particularly in Mexico where the crop's genetic diversity lives, has been a persistent and genuinely contentious topic in conservation policy.
  5. Labelling and choice. Whether consumers should be told is a question about transparency and consent, not about hazard. People can reasonably want to know what they are buying regardless of whether it can hurt them.

If you prefer to avoid genetically engineered corn, the practical routes are certified organic products, which exclude it by standard, and products carrying a verified non-GMO seal. Note also that sweet corn and popcorn sold for direct human consumption are far less likely to be engineered varieties than the field corn that dominates the acreage statistics.

Back to Table of Contents

Other Concerns Worth a Straight Answer

Is corn inflammatory? Whole corn is a fibre-containing whole grain, and the large prospective and interventional literature on whole grains points toward lower, not higher, inflammatory markers. Refined corn derivatives — syrups, starches and the ultra-processed foods built from them — are a different matter, and the objection to those is about refinement and added sugar rather than about maize.

Does corn contain gluten? No. Corn does not contain the gliadin and glutenin proteins that cause coeliac disease, and corn is a staple of gluten-free diets. Corn does contain its own storage proteins, the zeins, sometimes loosely called "corn gluten" in industrial contexts — the name is a processing term, not a coeliac-relevant one. A small number of people with coeliac disease report symptoms with corn; the evidence base for a genuine zein reaction is thin, and cross-contamination in shared milling facilities is a more common explanation. Buy certified gluten-free cornmeal if that applies to you.

Do whole kernels pass through undigested? The visible fragments are the pericarp — the outer seed coat, made largely of cellulose, which humans cannot digest. The starch, protein, fat and micronutrients inside are digested normally. Seeing corn in the stool means the hull survived, not that the meal was wasted. Chewing thoroughly, or eating corn as masa, cornmeal or polenta, avoids the phenomenon entirely.

Does popcorn cause diverticulitis? This was standard medical advice for decades — avoid nuts, seeds, corn and popcorn if you have diverticulosis, on the theory that fragments lodge in the diverticula. A large prospective cohort study following men over 18 years tested it directly and found no increased risk; if anything, nut and popcorn consumption was inversely associated with diverticulitis. The old advice does not have evidence behind it, and guidelines have largely moved on.

Is corn allergy common? True IgE-mediated corn allergy exists but is uncommon compared with the major allergens. It is not a mainstream reason to avoid corn.

Is corn "just sugar"? Sweet corn eaten fresh has a moderate glycemic index, lower than many people expect, and whole corn products carry fibre and resistant starch that slow the response further — the subject of the resistant starch deep-dive. Corn syrup is sugar. These are not the same food and the confusion between them does most of the work in the claim.

Back to Table of Contents

What to Do in Your Own Kitchen

  1. Buy from a regulated supply chain and store dry. Cornmeal and corn flour contain the germ's oil and go rancid; whole-grain cornmeal in particular keeps best refrigerated or frozen, and that also suppresses mould growth.
  2. Discard visibly mouldy or musty grain without trying to salvage it, and never feed suspect maize to horses.
  3. Do not buy in bulk beyond what you will use. A year's supply of cornmeal in a warm cupboard is the storage problem in miniature.
  4. Eat corn in its whole and traditional forms — corn on the cob, whole-grain cornmeal polenta, masa tortillas, hominy, plain popcorn — rather than as syrup, starch and snack extrusions.
  5. Vary the grains. Rotating corn with brown rice, oats, barley and quinoa reduces every exposure discussed on this page and improves the amino-acid profile of the week at the same time.
  6. Pair corn with beans. Nine thousand years of Mesoamerican practice, one line of nutritional logic, and it also happens to taste right.

Back to Table of Contents

Key Research Papers

  1. Missmer SA, Suarez L, Felkner M, et al. Exposure to fumonisins and the occurrence of neural tube defects along the Texas–Mexico border. Environmental Health Perspectives. 2006;114(2):237-241. — doi:10.1289/ehp.8221
  2. Marasas WFO, Riley RT, Hendricks KA, et al. Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo: a potential risk factor for human neural tube defects among populations consuming fumonisin-contaminated maize. Journal of Nutrition. 2004;134(4):711-716. — doi:10.1093/jn/134.4.711
  3. Rheeder JP, Marasas WFO, Thiel PG, Sydenham EW, Shephard GS, van Schalkwyk DJ. Fusarium moniliforme and fumonisins in corn in relation to human esophageal cancer in Transkei. Phytopathology. 1992;82(3):353-357. — doi:10.1094/Phyto-82-353
  4. Chen C, Riley RT, Wu F. Dietary fumonisin and growth impairment in children and animals: a review. Comprehensive Reviews in Food Science and Food Safety. 2018;17(6):1448-1464. — doi:10.1111/1541-4337.12392
  5. Azziz-Baumgartner E, Lindblade K, Gieseker K, et al. Case-control study of an acute aflatoxicosis outbreak, Kenya, 2004. Environmental Health Perspectives. 2005;113(12):1779-1783. — doi:10.1289/ehp.8384
  6. Probst C, Njapau H, Cotty PJ. Outbreak of an acute aflatoxicosis in Kenya in 2004: identification of the causal agent. Applied and Environmental Microbiology. 2007;73(8):2762-2764. — doi:10.1128/AEM.02370-06
  7. Liu Y, Wu F. Global burden of aflatoxin-induced hepatocellular carcinoma: a risk assessment. Environmental Health Perspectives. 2010;118(6):818-824. — doi:10.1289/ehp.0901388
  8. Gong YY, Cardwell K, Hounsa A, et al. Dietary aflatoxin exposure and impaired growth in young children from Benin and Togo: cross sectional study. BMJ. 2002;325(7354):20-21. — doi:10.1136/bmj.325.7354.20
  9. Ostry V, Ovesna J, Skarkova J, Pouchova V, Ruprich J. A review on comparative data concerning Fusarium mycotoxins in Bt maize and non-Bt isogenic maize. Mycotoxin Research. 2010;26(3):141-145. — doi:10.1007/s12550-010-0056-5
  10. National Academies of Sciences, Engineering, and Medicine. Genetically Engineered Crops: Experiences and Prospects. Washington DC: The National Academies Press; 2016. — doi:10.17226/23395
  11. Nicolia A, Manzo A, Veronesi F, Rosellini D. An overview of the last 10 years of genetically engineered crop safety research. Critical Reviews in Biotechnology. 2014;34(1):77-88. — doi:10.3109/07388551.2013.823595
  12. Pellegrino E, Bedini S, Nuti M, Ercoli L. Impact of genetically engineered maize on agronomic, environmental and toxicological traits: a meta-analysis of 21 years of field data. Scientific Reports. 2018;8:3113. — doi:10.1038/s41598-018-21284-2
  13. Klümper W, Qaim M. A meta-analysis of the impacts of genetically modified crops. PLoS ONE. 2014;9(11):e111629. — doi:10.1371/journal.pone.0111629
  14. RETRACTED — Séralini GE, Clair E, Mesnage R, et al. Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology. 2012;50(11):4221-4231. This paper was retracted by the journal in 2013 and is listed here only because it is frequently cited; it should not be treated as evidence. — doi:10.1016/j.fct.2012.08.005
  15. Strate LL, Liu YL, Syngal S, Aldoori WH, Giovannucci EL. Nut, corn, and popcorn consumption and the incidence of diverticular disease. JAMA. 2008;300(8):907-914. — doi:10.1001/jama.300.8.907
  16. Nuss ET, Tanumihardjo SA. Maize: a paramount staple crop in the context of global nutrition. Comprehensive Reviews in Food Science and Food Safety. 2010;9(4):417-436. — doi:10.1111/j.1541-4337.2010.00117.x
  17. Gwirtz JA, Garcia-Casal MN. Processing maize flour and corn meal food products. Annals of the New York Academy of Sciences. 2014;1312:66-75. — doi:10.1111/nyas.12299
  18. Carter EG, Carpenter KJ. The bioavailability for humans of bound niacin from wheat bran. American Journal of Clinical Nutrition. 1982;36(5):855-861. — doi:10.1093/ajcn/36.5.855

Live PubMed Searches

  1. PubMed: fumonisin and human health
  2. PubMed: aflatoxin outbreaks and storage
  3. PubMed: nixtamalization and mycotoxin reduction
  4. PubMed: Bt maize and mycotoxins
  5. PubMed: GE crop food-safety reviews
  6. PubMed: corn, zein and coeliac disease

External Resources

Back to Table of Contents

Connections

Back to Table of Contents