Anti-wheat fad diets undermine global food security efforts
by Julie Mollins / December 18, 2014
Roberto J. Peña, Hans J. Braun* and Julie Mollins
Global Wheat Program, CIMMYT
*Author for correspondence; Email: email@example.com
Hans Braun, CIMMYT. Global Wheat Program. Km 45 Carretera México-Veracruz, El Batán, Texococo, C.P. 56130, Estado de México, México.
This report discussion paper was prepared with support from Bimbo food company
Read Wheat Discussion Paper (463KB)
A recent review paper released by Britain’s University of Warwick in Coventry (Lillywhite and Sarrouy 2014) addresses two fundamental questions regarding wheat: “Are whole grain products good for health?”; and “What is behind the rise in popularity of gluten- and wheat-free diets?”
The paper was commissioned by cereal-maker Weetabix to address reports in the news media that wheat products are the cause of health problems, resulting in an increasing number of consumers switching to low-carbohydrate grain- and wheat-free diets. For many health professionals this is a worrying trend because wheat not only supplies 20 percent of the world’s food calories and protein, but has important benefits beyond nutrition, the authors state.
The Warwick paper provides a scientific assessment of the benefits of whole grain consumption, information that the authors note seems to have been lost in media headlines and the reporting of “pseudo-science.”
The paper concludes that whole grain products are good for human health, apart from the 1 percent of the population who suffer from celiac disease and another 1 percent who suffer from sensitivity to wheat. Eating whole-grain wheat products is positive, improves health and can help maintain a healthy body weight, the authors report.
Scientific evidence regarding wheat- and carbohydrate-free diets is thin and selectively used, they state, and a low cereal and carbohydrate diet “may cost more but deliver less.”
Additionally, an economically viable industry has developed around so-called “free-from” diets and may be persuading consumers to switch from staple foods to specialist foods created especially for those who need to avoid gluten, a protein found in wheat and other grains, they add.
This Wheat Discussion Paper serves as a foundation upon which the authors hope further conversation on this topic will develop. It aims to highlight unsubstantiated nutritional claims about wheat and shine a spotlight on the important role of wheat and fiber in human diets. It also seeks to encourage conversation about how non-scientific claims about wheat could affect poor consumers and global food security.
1.Wheat and fad diets
It is generally accepted among nutritionists that low-carbohydrate fad diets such as those detailed in such books as “Wheat Belly” (Rodale, 2011), written by cardiologist William Davis, and “Grain Brain”, written by neurologist David Perlmutter, (Little, Brown, 2013), which vilify wheat, can lead to rapid, but temporary weight loss.
Although low-carbohydrate diets show more rapid weight loss than other diet types in the first six months, they do not result in greater weight loss over time and lead to more dropouts than more balanced diets, which do not eliminate entire food groups, writes Julie Jones, a nutritionist and professor emeritus of food and nutrition at St. Catherine University in St. Paul, Minnesota (Jones 2012).
Not only do the authors of “Wheat Belly” and “Grain Brain” cast aside well-established medical and nutritional advice, they also disregard dietary guidelines and recommendations established by such reputable institutions as the World Health Organization (WHO), the U.N. Food and Agriculture Organization (FAO), the U.S. Department of Agriculture, the Whole Grains Council, the Whole Wheat Council, the American Dietetic Association, the American Diabetes Association and the American Heart Association.
To a large degree, their arguments are based on a view that imagines what dietary practices were like for early human hunter-gatherers before farmers began to domesticate wild grasses, creating wheat, which led to a more secure food supply and the capacity to develop sedentary societies.
Davis claims that wheat varieties grown today are unsuitable for human consumption because they haven’t been safety tested. He takes aim at the efforts of wheat breeders at the International Maize and Wheat Improvement Center (CIMMYT), who under the direction of Norman Borlaug in the 20th century developed dwarf wheat varieties.
CIMMYT is an intergovernmental research institute working with an international community of public and private partners to reduce worldwide poverty and hunger by sustainably increasing the productivity of maize and wheat.
CIMMYT, a non-profit organization, plays a key role in providing wheat germplasm – genetic material from wheat – to be tested and improved by government-run national agricultural research systems before its potential release to farmers. Additionally, CIMMYT provides smallholder farmer training and skills development on such topics as crop management and agricultural practices.
Borlaug, who died in 2009 at age 95, led efforts to develop semi-dwarf wheat varieties in the mid-20th century that helped save more than 1 billion lives in Pakistan, India and other areas of the developing world as global population expanded and land became more scarce.
He started work on wheat improvement in the mid-1940s in Mexico, where CIMMYT is headquartered near Mexico City. The country became self-sufficient in wheat production in the early 1960s due to the high-yielding, disease-resistant varieties developed by Borlaug and his colleagues.
Borlaug was awarded the Nobel Peace Prize in 1970 for his innovative, life-saving work, which became widely known as the Green Revolution. He used traditional plant-breeding techniques, still used worldwide for producing wheat and other food crops. Davis writes that 99 percent of wheat grown today is related to the dwarf varieties developed by Borlaug. Farmers prefer short-stalk wheat because it doesn’t fall over – or lodge – as easily as taller varieties, which means less grain is lost and harvests are bigger.
As the global population grows from more than 7 billion today to a projected 9.6 billion by 2050, wheat farmers continue to play a crucial role in food security.
Already, U.N. food agencies and the WHO estimate that at least 800 million people (WFP) do not get enough food and that more than 2 billion (FAO) suffer from micronutrient deficiency, or “hidden hunger.” Stunting affects more than 160 million children under age 5 and wasting affects more than 50 million children under age 5. Under-nutrition is linked to almost half of all child deaths under age 5, almost 3 million per year. On the other hand, about half a billion people are obese and three times as many are overweight (WHO).
Arguments posed in literature and the popular press regarding the dangers of consuming wheat and gluten overlook the key role that wheat plays in nutrition and ensuring global food security. In an effort to mitigate the impact of population growth, land scarcity and climate change, scientists at CIMMYT are developing wheat varieties with higher micronutrient content and reinforcing the capacity of wheat to withstand heat and drought caused by global warming.
Zinc supplementation can help reduce the duration and impact of diarrhea in children, and iron and vitamin A supplements can reduce the risk of anemia and blindness.
Fad-diet hyperbole over the supposed dangers of wheat consumption might cause worry and unnecessary health fears among all sectors of society, but it is the poor and low-waged that may suffer the most from these campaigns. Many families cannot afford such nutrient-rich foods as fresh fruit, vegetables, beans, meat and milk, and rely on bread, rice or maize and legumes – food staples – to supplement their diets.
Socioeconomic factors can make it impossible for many people to afford or even in some cases access specialty food items.
Rather than blaming wheat for humanity’s ailments, global health experts are addressing the key nutritional problem that foods high in fat, sugar and salt are relatively inexpensive and readily available, leading to both rich and poor people becoming overweight and obese.
In November, at the Second International Conference on Nutrition (ICN2) in Rome, the WHO, the FAO and 170 governments committed to fight malnutrition in all its forms, including hunger, micronutrient deficiencies and obesity. They laid out a framework for ending hunger, achieving food security and improving nutrition by 2025 (FAO/WHO).
Governments who signed onto the framework are tasked with encouraging a reduction in trans fats, saturated fats, sugar and salt, and to improve the nutrient content of foods through regulatory and voluntary instruments.
2. Healthy diets
A healthy diet helps prevent malnutrition as well as non-communicable diseases (NCDs) and conditions (FAO). However, increasing production of processed food, rapid urbanization and lifestyles have shifted dietary patterns, according to the WHO. Foods high in energy, saturated fats, trans fats, free sugars or salt are increasingly being consumed, while many people do not eat enough fruit, vegetables and such dietary fibre as whole grains.
A healthy diet for adults includes fruit, vegetables, legumes, nuts and whole grains. Adults should eat at least 400 grams (14 ounces), or five portions, of fruit and vegetables daily, while less than 10 percent of total energy should come from free sugars and less than 30 percent of total energy from fat, according to the WHO. Unsaturated fats are better than saturated fats, the U.N. health agency reports. Additionally, it says that industrial trans fats in processed food, fast food, snack food, fried food, frozen pizza, pies, cookies, margarines and spreads are not considered part of a healthy diet, recommending that adults should consume less than the equivalent of one teaspoon of salt a day and use iodized salt.
For children, nutrition is vital to prevent the risk of death or developing non-communicable diseases and to ensure healthy growth and development. As well as taking into consideration the guidelines for adults, breastfeeding plays an important role in ensuring a nutritional beginning to life.
The WHO and FAO recommend that governments, public and private sector stakeholders must collaborate to help promote a healthy food environment, which allows people to adopt healthy dietary practices.
In practice, such activities include coordinating trade, food and agricultural policies with the protection and promotion of public health, encouraging consumer demand for healthy food and promoting nutrition in infants and young people.
3. Wheat and food security
For more than 10,000 years, wheat production and consumption has contributed to the socio-economic development of humankind (Salamini et al. 2002). Wheat is readily adaptable to a range of diverse environments, including marginal and extreme ecosystems. It is cultivated on about 220 million hectares (539 million acres) worldwide, which produce roughly 700 million metric tons a year. The grain provides on average a vital 20 percent of calories and protein for more than 4.5 billion people in 94 developing countries (Braun et al. 2010).
Over the next 35 years, wheat production must grow 60 percent to keep pace with demand as the population grows, according to FAO. However, climate change will have a profound impact on wheat production, affecting crops through such risk factors as increased levels of pests and disease, water shortages and nutrient depletion in soil, jeopardizing production levels. A short supply of wheat, particularly in developing countries, will result in serious nutritional problems and could lead to social unrest (CIMMYT 2011). Therefore, it is vital that the international community accelerate efforts to bolster the production of high-yielding wheat varieties to meet nutritional demands.
4. Health benefits of wheat
Wheat grain possesses several components that contribute to good nutrition (Bjork et al. 2012; Fardet et al. 2012; Flight and Clifton 2006; Shewry 2009). The dietary fiber it contains – comprised of polysaccharides, which pass undigested from the small intestine into the large intestine and colon – is a highly beneficial, fermentable prebiotic agent that promotes the growth of beneficial probiotic bacteria in the bowel.
The positive contribution of antioxidant agents and dietary fiber in wheat to good health is well documented (Bjork et al. 2012; Gibson et al. 2014). In addition, epidemiological studies conducted in various Ethiopian countries have associated the consumption of wheat whole grain with the prevention of obesity and such related chronic health problems as cardiovascular disease and Type 2 diabetes (Bjork et al. 2012).
In about 35 percent of countries fortification of milling flours with minerals and vitamins is mandatory. In these cases, the consumption of wheat-based foods helps reduce micronutrient deficiency, particularly in relation to iron, zinc, folic acid and vitamin A. Additionally, many wheat-based foods – bread used for sandwiches or wraps, for example — serve as “vehicles” for the consumption of complementary animal- and vegetable-based foods, contributing to balanced and healthy diets.
5. Wheat and chronic disease
“Grain Brain” and “Wheat Belly” both detail high levels of intolerance to wheat among the human population, although in actual fact, only 1 percent of people have celiac disease and 1 percent suffer from sensitivity to wheat (Lillywhite and Sarrouy 2014). Perlmutter, the author of “Grain Brain” claims that the gluten content in wheat causes inflammation leading to many different diseases, including Alzheimer’s, which he believes is Type 3 diabetes. Davis, the author of “Wheat Belly” claims that wheat not only causes many diseases, but that it is addictive and causes obesity.
People with celiac disease have a digestive condition which causes an adverse reaction to gluten resulting in diarrhea, bloating, flatulence, abdominal pain, weight loss and fatigue due to malnutrition. Celiac disease is an autoimmune condition, which means the immune system attacks healthy tissue, damaging the surface of the small bowel and preventing proper nutrient absorption.
“Grain Brain” and “Weeding Out Wheat” (CreateSpace 2013), an anti-wheat book written by Trisha and Luke Gilkerson, emphasize that cereal – in particular wheat – consumption contributes to degenerative diseases and such autoimmune neurological diseases as Alzheimer’s and Parkinson’s. The authors emphasize that they are writing for a U.S. audience – for all U.S. consumers they claim will benefit from diets without cereals and cereal products. They state that cereals in general are unhealthy due to their high carbohydrate content, and that wheat is particularly dangerous because of gluten.
Maize, wheat, and rice-based foods are inexpensive, satisfying culinary preferences as well as caloric and essential nutrient needs for billions of people on all continents who consume them as a major food staple. If it were correct that cereals were the cause of Alzheimer’s, arteriosclerosis, Parkinson’s, autism and loss of cognitive capacity and neurodevelopmental disorders, civilization would have been incapacitated and come to a halt many years ago.
Alarmingly, anti-wheat and cereals activism continues to gain momentum among consumers who hope to improve their health. However, wheat- and gluten-free diets can in fact be damaging to human health because they may not provide enough fiber and essential micronutrients (Biesiekierski et al. 2014; Lee et al. 2009). The recommended daily intake of dietary fiber is 38 grams (1.34 ounces) and 25 grams for adult men and women respectively, which is achievable by consuming a few servings of wheat foods or other cereals grains (Jones 2012). In contrast, fruits and vegetables supply only 2 to 4 grams per serving, which means an adult male on a wheat-free diet would have to consume approximately 12 to 13 servings of fruit and vegetables a day to get the same amount of dietary fiber (Jones, 2012). The exclusion of cereal grains would result in a fiber-intake deficit far below the recommended amount needed to maintain a healthy digestive system. 5.2 “Wheat Belly”
Davis emphasizes that his book is directed toward those who are overweight or obese.
Obesity in the United States is caused by excessive consumption of food – including protein, starch, sugar and fat – oftentimes the result of gorging on oversized meal portions and snacks at fast food outlets, restaurants and at home (Drewnowski and Darmon 2005; Ello-Martin et al. 2005).
Davis’ book does not present any nutritional information that is not already well known with regard to general causes of weight gain, obesity and related health problems. It is generally accepted by nutritionists that lowering daily caloric intake from more than 3,000 kilocalories to recommended levels of below 2,500 kilocalories will result in weight loss.
Davis claims that modern wheat has “new proteins,” which are different from those in the old wheat cultivars consumed some 60 to 70 years ago. He blames these “new proteins” for many present-day chronic diseases. This argument is not supported by recent research studies comparing historic and contemporary wheat varieties. Contemporary wheat is composed of the same constituents present in old wheat. A study by Caballero et al. (2008) shows that gluten-producing proteins in Mexican landrace varieties known as creole wheats, which were brought to Mexico by Spanish settlers nearly 500 years ago, are the same in many cases to those present in modern wheats grown in Mexico.
Most of the arguments presented by Davis’ have already been analyzed, discussed and often refuted on scientific grounds (Jones 2012, the National Wheat Improvement Committee of the United States in collaboration with several universities and research institutes from the United States and Europe, CIMMYT, the International Maize and Wheat Research Center (NWIC, 2013) and by several other scientific studies (Biesiekierski et al. 2013a; Brouns et al. 2013; Kasarda 2011; Shewry 2009).
The health problems described in “Wheat Belly” are in actual fact caused by many factors, including congenital immune deficiencies and overeating, in conjunction with the decrease in physical activity and lifestyle habits of inhabitants of the United States.
5.3 “Grain Brain”
“Grain Brain” is aimed at the U.S. population, and most of the reflections, testimonies, and recommendations – even those that appear to be supported by scientific results – cannot be generally applied to populations outside the country.
Throughout the book, the author, David Perlmutter, hypothesizes possible metabolic mechanisms by which gluten or sugar may cause disease. He also interprets the results of several studies – in many cases related to celiac disease – to indicate that wheat and carbohydrates are the cause of many diseases affecting brain function. He says there is great risk from the negative effects of inflammation linked to the consumption of wheat, gluten and other cereals.
Grouping the key arguments in “Grain Brain”, which link wheat, gluten and carbohydrate consumption with chronic diseases allows analysis.
“Grain Brain” states the following:
- Claim 1: Modern wheat is different from historical wheat varieties and therefore is bad for human health.
- Claim 2: Gluten is poison for the human brain.
- Claim 3: The simple sugars and starch present in all cereal grains and some fruit are associated with Type 2 diabetes, cardiovascular diseases and such neurological dysfunctions as depression, Alzheimer’s (which Perlmutter refers to as Type 3 diabetes), schizophrenia, epilepsy and cognitive capacity.
- Claim 4: Gluten and sugars concomitantly promote inflammation, affecting structures and the function of beneficial components, finally causing chronic metabolism and diverse diseases.
- Claim 5: Fat and cholesterol is the “best friend” of your brain.
Claim 1. Modern wheat is different to old wheat and is damaging to health
Perlmutter, Davis and Gilkerson argue that modern wheat has very little resemblance with the grasses, known as wild relatives to wheat, consumed by our ancestors. Perlmutter also argues that due to hybridization and modern genetic technologies, the average 60 kilograms (132 pounds) of wheat Americans now consume per annum has no genetic or chemical similarity with the wheat our nomadic ancestors consumed. According to Perlmutter, today we are eating ingredients we were not genetically prepared to digest.
People first began eating grains about 75,000 years ago in western Asia (National Geographic 2014). These grains, including T. boeticum (an ancestor of einkorn) and wild emmer (diccocoides), were ancestors of today’s wheat. People harvested the grasses that grew naturally near their communities. They began cultivating, or growing, grain more recently and ancient people ate grains in much the same way we do today. Wheat grains were made into flour and used in breads.
Modern bread wheat is the most widely cultivated type of wheat today, making up more than 90 percent of global production. It is the product of natural hybridization among several grasses. One parent is Triticum urartu, a wild grass that still grows in the Middle East. Triticum urartu spontaneously hybridized with Aegilops speltoides and formed wild Emmer (Triticum dicoccocoides). The cultivated form (T. dicoccum) was consumed by the ancient Egyptians and Romans and is still consumed today in India. Durum wheat, derived from emmer (Triticum durum), is used today for pasta and semolina products. Around 10,000 years ago, emmer crossed naturally with goat grass (Aegilops tauschii (Peng et al. 2011) and formed the ancestor of modern bread wheat (T. aestivum). Wheat was wild at the outset until our ancestors started to cultivate and domesticate it.
Modern wheat (Triticum aestivum, or bread wheat, and Triticum durum, or pasta wheat), and other varieties such as Triticum spelt (spelt wheat) and Triticum turgidum subspp Turanicum, commercially known as Kamut wheat, has not changed in its fundamental genetic composition.
The nutritional and protein composition of durum and bread wheat eaten today varies very little from the wheat consumed 8,000 to 9,000 years ago. Ancient wheat had the same genetic base that wheat breeders still use today to generate improved wheat cultivars. The genes are the same, although recombined in diverse ways through cross-breeding (Cavanagh et al. 2013).
Alessio Fasano, an internationally recognized researcher of celiac disease pathology, immunology and related disorders at Massachusetts General Hospital, asserted in a seminar that modern wheat is no different from old wheat in its constitutional make up and grain composition (YouTube, 21 January 2014). In support of this, several biochemical genetic, and genomic studies (Akhunov et al. 2010; Cavanagh et al. 2013; Kasarda 2011; Naghavi et al. 2013; Peng et al. 2011; Shewry 2009) have shown that the cultivars of different varieties consumed today – including bread and durum wheat, emmer, spelt and kamut have their origin in the diploid and tetraploid ancestors (T. Urartu, Ae. tauschii, and wild emmer, among others.).
In addition, the gluten proteins found in modern wheat have their origin in the diploid species T. urartu, Ae. speltoides; and Ae. tauschii, i.e. also the diploid ancient wheats contain gluten (Dhanapal et al. 2010; Gutierrez et al., 2010; Molberg et al. 2005; NWIC, 2013; Salentijn et al., 2012). The protein content of wheat we eat today is similar to that consumed at least 100 years ago (Kasarda 2011). Some studies have found that the species T. monococcum (cultivated einkorn), and other landraces, or “old modern wheat”, of T. aestivum, T. compactum and T. spelta in which the wheat we eat today originated also contain gliadins (gluten proteins) similar to those in modern wheat that generate the gliadin peptides (epitopes) that provoke celiac disease (Colomba and Gregorini 2012; Molberg et al., 2005; van den Broek et al. 2010; Salentijn et al. 2012; Suligoj et al. 2012; Vaccino et al. 2009).
Claim 2. Gluten is poison for the human brain
Diverse gluten-induced conditions trigger the immune system in a range of ways via gliadin, which is one of two main protein fractions of the gluten protein complex. Sapone et al. (2012) propose a diagram and nomenclature for the spectrum of gluten-related disorders (Figure 3).
Gluten sensitivity is not an autoimmune condition as claimed by Davis and Perlmutter; it is believed to be innate or congenital.
Gluten Intolerance or Celiac Disease. A few decades ago it was confirmed that a small proportion of individuals (1 to 1.5 percent) are intolerant to gluten in the same way others are intolerant to lactose or other foods (Poole et al. 2006). This intolerance manifests itself as celiac disease, a genetic condition mediated by an immune response triggered mainly by small gliadin undigested peptides; among these, a unique 33-mer gliadin fragment is more immunogenic. This peptide is resistant to degradation by gastric, pancreatic and brush border peptidases (Sapone et al. 2012). On the surface of the small intestine, it is the main trigger of bowel inflammation, intestinal damage, up regulation of the 47-K Zinulin peptide, responsible for the opening of the intestine wall and entrance of the gliadin protein. The reaction (deamidation) of this gliadin peptide with tissue transglutaminasa (tTG) promotes recognition by HLA-DQ2/HLADQ8 antigen presenting cells and triggering the onset of celiac disease and related immune disorders (Fasano 2011; Jackson et al, 2012; Lundin 2014; Sapone 2012; Setty et al, 2008; Shan et al. 2002). This chronic enteropathy shows a wide range of manifestations of variable severity.
At present there is no cure or therapeutic actions that can be taken against celiac disease. Therefore, those suffering from the disease must eliminate gluten from their diets (Cummins and Roberts-Thomson 2009).
Perlmutter indicates that it is possible that some of the inflammatory processes provoked by the consumption of gluten may in some cases trigger the increase of inflammatory cytokines levels, which by attacking the brain could contribute to the onset of Alzheimer’s, Parkinson’s, multiple sclerosis and autism. In addition, Perlmutter speculates that the antigliadin antibodies (AGA) could combine with similar gliadin-like proteins in the brain, promoting even more production of cytokines, provoking more neuropathies. However, Sofi et al. (2014) indicate that pre- inflammatory cytokines are more related to irritable bowel syndrome (IBS).
Perlmutter’s arguments could hypothetically be possible metabolically. However, he does not present studies that demonstrate these processes actually occur. Fasano (YouTube, 21 January 2014) indicates that the potential relationship of gluten sensitivity to autism and schizophrenia is still very controversial, although there is a working hypothesis.
Perlmutter indicates that Hadjivassiliou et al. (2010) reported a certain relationship between neuropathies and mainly celiac disease. But these authors actually show that only a small proportion (10 to 22.5 percent) of celiac disease patients have a neurological condition. They also indicate that there are differences in disease etiology in patients whose main manifestation occurs in the nervous system and those whose primary manifestation resides in the gastrointestinal system. At the same time, they indicate that it is unclear whether the central nervous system (CNS) pathology associated with gluten sensitivity (as they refer mainly to celiac disease) results from access of circulating antibodies that react with brain antigens after compromising the blood-brain barrier, or if it relates to a specific T-cell subset that is involved in immune surveillance of the brain. Why gluten presentation should specifically occur at a site distant to the digestive system (CNS, skin) is unclear. Finally (Hadjivassiliou et al. (2010) indicate that not all the patients presenting certain neuropathies claimed to be caused or related by celiac disease got better when excluding gluten from their diet.
Wheat allergic response
Wheat allergy is an adverse immunologic reaction where IgE antibodies intervene when there is exposure to wheat proteins (gluten but also other proteins), affecting the skin, gastrointestinal tract or respiratory tract, depending on the exposure and the site the immune response resides. Wheat allergy (WA) is a classic food allergy, which is wheat-dependent, producing exercise-induced anaphylaxis (WDEIA); baker’s asthma and rhinitis; and contact urticaria (Sapone et al. 2012). The incidence of people affected by WA is lower than that affected by celiac disease (Sapone et al. 2012).
Non-Celiac Gluten Sensitivity
Perlmutter indicates that there are individuals that do not suffer from celiac disease yet may have gut inflammation and other related conditions. He also suggests that this could be due to genetic immune deficiencies, or due to the lack of certain enzymes to digest gluten. This is true; it is now well known that besides celiac disease and wheat allergies, there are cases of gluten reactions in which neither allergic nor autoimmune mechanisms can be identified. However, gluten sensitivity is still an undefined syndrome, with several unsettled issues despite the increasing awareness of its existence. Only a few double blind, randomized placebo control (DBPC) studies have been performed, showing that in a variable proportion of patients classified as having gluten sensitivity, their symptoms could have been caused by a nocebo (a detrimental effect on health produced by psychological or psychosomatic factors such as negative expectations of treatment or prognosis effect) (Lundin 2014; van Buul and Brouns 2013; Volta et al. 2014).
Gluten sensitivity is an adverse reaction to gluten. Both gluten sensitivity and celiac disease involve an immune system response and may have similar symptoms, but the type of immune response is different (Sapone et al. 2012). People with gluten sensitivity do not develop severe intestinal damage like that seen in patients with celiac disease. These are generally defined as non-celiac gluten sensitivities (NCGS). The symptoms of NCGS are similar to those of patients with irritable bowel syndrome (IBS), including abdominal pain, bloating, gas, diarrhea, and constipation (Lundin, 2014). Sapone et al (2012) define NCGS patients as those patients in which celiac disease, wheat allergy and other clinically overlapping diseases (e.g., type-1 diabetes, inflammatory bowel diseases and Helicobacter pylori infection) have been ruled out. In NCGS patients, and in those suffering celiac disease, their symptoms are caused by gluten exposure and eased by gluten withdrawal.
NCGS is not accompanied by the concurrence of anti-tTG autoantibodies or other autoimmune comorbidities. The small intestine of gluten sensitive patients is usually normal (Sapone et al. 2012). Objective biomarkers to diagnose gluten sensitive condition are not available and may be difficult to develop. Gluten sensitivity may be caused by improper immune responses, intolerance to poorly digestible and fermentable substances in the wheat, or a combination of these.
Although the number of people suffering from NCGS has been estimated much higher than those suffering from celiac disease, some studies have demonstrated that the sensitivity of some of the patients who have been diagnosed with NCGS with inflammation and other gastrointestinal symptoms, were rather affected by the presence of fermentable, poorly absorbed oligo-, di-, monosaccharaides and polyols (FODMAPS) or other foods (Biesiekierski et al. 2013b; Biesiekierski et al. 2014; Carroccio et al. 2012; Lundin 2014; Halmos et al. 2014). Future research in the NCGS area should address how much gluten really is involved, using manageable, clinically acceptable, placebo-controlled investigation procedures.
For example, the study of Carroccio et al. (2012) shows a diagram of their clinical design and the response of 920 patients showing irritable bowel syndrome (IBS) symptoms and fulfilling the criteria for NCGS. Two groups of patients were identified. One group with 70 patients was suffering from no celiac wheat sensitivity alone and a second group with 206 patients suffering from multiple food hypersensitivity, including wheat sensitivity. Out of the total 920 patients, 644 did not suffer from wheat sensitivity and were excluded from the study (Carroccio et al. 2012).
A major limitation in studying NCGS is diagnosis, which remains highly presumptive. Therefore, at present a proportion of patients classified as suspected NCGS might improve after commencing a gluten-free diet (GFD) because of elimination of gluten or simply by a placebo effect (Volta et al., 2014). Although, according to Lundin (2014) there are no conclusive studies demonstrating the benefits of a GFD in NCGS patients.
Wheat is toxic for all. Fasano, in a seminar transmitted on YouTube (January 21, 2014) based mainly on a review article by Sapone et al. (2012) and by results and new findings reported during the second Meeting of Experts on Gluten Sensitivity (Catassi et al. 2013), explained his research group’s work of more than 15 years. Fasano indicated that three major elements are involved in CD and NCGS. The genetic factor (an individual’s genes), the environmental factor (food or intruder), and the one that allows gut permeability. In his discussion of the food factor, Fasano indicated rightly that humankind was not meant to eat wheat or gluten. During 2.5 million years of evolution man has been 99.99 percent gluten-free. Humankind started eating wheat only about 10,000 years ago. Therefore, gluten is toxic for everybody, but not everybody gets sick. Don’t get confused, he said, explaining that “the vast majority of people will clean up the fragments of gliadin and nothing happens. Only a very small percent of people lose this battle and the gluten fractions crossing the intestine will cause problems. The gluten fragments are taken as bacteria that can harm us. Some of the ones that lose the battle bear at least some of the factors that make them prone to acquire the disease.”
Is wheat or gluten the sole culprits of the disorders being attributed to wheat and gluten? No. Wheat and gluten are just some of the elements that could contribute to adverse health reactions, but wheat also has many positive contributions to human health too. It is inaccurate and dangerous to label wheat and gluten a wholesale danger for the human population—especially for the billions of people that need wheat to survive or to get their basic nutrients. The very, very small numbers of people that cannot tolerate gluten just have to embrace a gluten-free diet, and that will solve most of their health conditions and discomfort.
Inflammation, Zonulin and Tight Junction (TJ)
Gliadin peptides in the gut promote production of the protein zonulin, which opens the gut and increases permeability allowing the entry of undesirable peptides and other unwanted simple components. Hence gliadin is the trigger that activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to unwanted macromolecules (Drago et al. 2006).
Fasano (2001) developed an illustrative diagram showing the pathological and therapeutic implications of the passage of macromolecules through the tight junction. A “leaky gut” is a proposed condition some health practitioners say causes a range of long-term health problems, including chronic fatigue syndrome and multiple sclerosis. The human gut must be protected and for that it needs gut microbiota, which can protect against infectious bacteria, inflammation and gut permeability (Frazier et al. 2011) and contribute enzymatic complexes that help to completely digest food. Additionally, a Zonulin blocker drug has been developed to reduce or prevent gut permeability (Fasano, YouTube, 21 Jan 2014). The drug Larazotide Acetate consistently reduced gastrointestinal symptoms in three gluten-challenge clinical trials by preventing leaky gut.
Inflammatory processes and gut permeability are the two major elements for the initiation of immune and autoimmune events. Triggers could involve such factors as peptides from wheat and other food, short chain carbohydrates, sugars, good and bad bacteria and a lack of certain hydrolyzing enzymes. They could also be due to innate predisposition or to variations during childbirth, diet in the early months, childhood and adulthood. Antibiotics and other medical drugs may also lead to a favorable predisposition for triggers resulting in a permeable gut. These factors may act on an individual or complementary basis to cause the problem (Fasano 2011; Halmos et al. 2014). Arthur Agatston and Natalie Geary, in their book. “The South Beach Diet Gluten Solution” (2013) explain in detail the signs of non-celiac gluten sensitivity and whether inherited or external factors made the person NCGS. They also emphasize that being NCGS does not necessarily mean you cannot eat gluten. They explain that you have to find out whether or not can eat gluten-containing foods and how much.
Microbiome. During the seminar presented on YouTube, Fasano stated: “What happened to these people that suddenly lose their capability to eat gluten?” What other factors must be considered? Perhaps, he suggests, the age at which a baby was introduced to gluten and, or, the changes of the microbiome composition as we age, or changes in our dietary habits, environment and lifestyle could have affected their ability to properly digest gluten.
It is important to consider that bacteria within the human body express 100 times more genes than we, as humans, do. Human beings are made up of genomes as well as microbiomes. The microbiome is inherited from the mother, which means babies delivered through the birth canal receive her microbiomes. Some have suggested that babies born by caesarean might have a higher risk of developing celiac disease or other diseases because they did not get all the microbiomes and microbiome-related enzymes present in the mother, which contribute to digestion of food in the small intestine.
Agatston and Geary (2013) also ask why those who are NCGS do not have the ability to digest gluten to a manageable point. There are other factors that could be related to the microbiome and immune system affecting capacity to perform better in the presence of gliadin or other protein or even bacteria. To list some:
•Not enough enzymes to digest excessive amount of ingested food.
•Excessive concentration of gluten in our food (gluten is added to some baking products, soups, dressings, sausages, etc.).
•Digestive track congestion with resulting inflammation from very low traffic and gut damage (and permeability).
•Abuse of pain relievers and anti-inflammatory drugs such as the non-steroidal anti-inflammatory medications (NSAID), including aspirin, naproxen, indomethacin and ibuprofen (30 billion doses of NSAIDs are taken in the United States each year). These drugs can damage both the stomach and small intestine, contributing to the capacity of gliadin peptides to leak through the intestinal lining causing diverse immune reactions.
•Abuse of antibiotics may also contribute to our gluten-related problems. Overuse and over-prescription of antibiotics is very high in the United States today. Medical doctors often unnecessarily prescribe antibiotics for bronchitis and flu, starting in childhood. Antibiotics kill both bad and good bacteria (our microbiome) in our intestine, reducing their ability to aid the digestion of gluten.
•We need good bacteria. Throughout our life good bacteria is affected by medications, diet, lifestyle and environment. A study (De Filippo et al. 2010) has shown that eating a high-fiber diet in rural Africa generates different gut flora than that found in western children who eat a low-fiber diet heavy in meat and starch. The gut flora of African children is protective against diarrhea and inflammatory disease, while the gut flora of Western children from industrialized countries is associated with a higher incidence of western diseases such as diabetes, allergies, inflammatory bowel disorder, and obesity (De Filippo et al. 2010).
General wheat avoidance
According to Agatston and Geary, in their book “The South Beach Diet Gluten Solution” (2013), the gluten phenomenon resembles the period of the low fat versus low carbohydrate debate during the 1980s and 1990s. At that time, experts recommended low fat and high carbohydrate diets. However dieters were frustrated because their weight loss was followed quickly by weight gain. Today, gluten debates are popular and many are becoming gluten phobic for no reason, but possibly related to gluten sensitivity mania, which considers that being gluten sensitive and going gluten free is “cool.” In any case, the sales of gluten-free foods have rocketed to approximately $6 billion annually (van Buul and Brouns 2013).
Claim 3. Carbohydrates are the main cause of obesity, diabetes and neuropathy
Perlmutter indicates that high carbohydrate foods are the main cause of brain dysfunction and diseases or conditions such as depression, epilepsy or anxiety, among others. Sugar levels close to the high limit tend to make the brain shrink, he argues. High glycemic index, refined flours, glucose, and fructose, all cause diabetes and inflammatory reactions affecting the brain and natural antioxidants; promote Alzheimer’s, atherosclerosis, and dementia; and reduce cognitive capacity.
Perlmutter takes his argument beyond the caloric load of wheat and includes all cereal grains (although he retracts arguments about rice in an interview with Dr. Oz on a popular TV show in the United States) as well as fruit with high starch and glucose concentration. In general, Perlmutter recommends consuming low carbohydrate foods, and the elimination from our diet of wheat, rye and barley because these contain gluten.
No doubt, the scientific and therapeutic community agree that excessive caloric intake is related with high glucose in blood, promoting Type-2 diabetes and obesity and cardiovascular diseases. We also know that it affects hormones and the capacity for the metabolism to operate normally.
Monash University in Melbourne, Australia has proven that a diet low in FODMAPS is an effective strategy for managing symptoms (diarrhea, bloating, abdominal pain, and flatus) of Irritable Bowel Syndrome (IBS) caused by poor absorption, osmotic activity, and rapid fermentation of short chain and simple sugars (Barrett 2013). Up to 86 percent of patients with IBS have achieved relief of overall gastrointestinal symptoms and, more specifically, bloating, flatus, abdominal pain, and altered bowel habit from the approach (Barrett 2013).
Although wheat is high in FODMAPS, hundreds of other foods are also high in FODMAPS. Therefore, a high FODMAPS diet does not exclude wheat. A balanced diet can regulate the amount of FODMAPS, avoiding inflammation and loss of cognitive capacity (Gómez-Pinilla 2008).
Excessive eating causes people to become overweight and even morbidly obese, which is associated with Type 2 diabetes and cardiovascular diseases. The solution to these problems is in the reduced caloric intake of a balanced diet with sufficient dietary fiber and good amount of antioxidants accompanied by physical exercise.
It is also known that changes in microbiota may also be a factor in becoming obese. Round and Mazmanian (2009) showed that the microbiome (gut flora) of overweight individuals was different from the microbiome of thin individuals.
On the other hand, Cho and Blaser (2012) in an experiment with mice, showed that excessive use of antibiotics affects our good microbiome, causing metabolic changes, possibly affecting the metabolism of fatty acids, increasing digestion of fat, enhancing caloric intake and an increase in accumulated fat of approximately 10-15 percent higher than the control mice. Trasande et al. (2013) postulated that microbes in our intestines may play a critical role in caloric intake from food. Exposure to antibiotics early in life may kill off healthy bacteria that influence the absorption of nutrients. In a study Trasande et al. (2013) found that administrating babies antibiotics before the age of 6 months increased the chance of being overweight by age three by 22 percent. These studies contribute to evidence of the effect of antibiotics on gut bacteria, contributing to obesity.
Contrary to what Perlmutter claims, people consuming three servings of whole grains throughout the day are less likely to acquire Type 2 diabetes (Venn and Mann, 2004) than those that consuming a smaller number of servings. In a survey on having or skipping breakfast by children and adolescents during the period 1999 to 2006, those who ate breakfast, which included wheat, maize, oats or rice, were associated with low saturated fat or cholesterol intake and high intake of carbohydrates, dietary fibre and various micronutrients, had a lower prevalence of obesity than those that did not eat cereal at breakfast or that skipped the meal altogether. Those who skipped breakfast showed higher body mass than those that had any of the two types of breakfast: ready-to-eat cereal (RTEC) and non RTEC breakfasts (Deshmukh-Taskar et al. 2010). Additionally, Rampersaud et al. (2005) in a similar study found that those children and adolescents that had breakfast including regular milk and cereal-based food showed better scholastic performance than those skipping breakfast.
Thus, a balanced breakfast should have a good, but balanced, load of cereal grains including wheat, milk and some polyunsaturated fat.
An essay written by nutritionist Jones appeared in April 2014 on the CIMMYT website. Jones refers to statements made in the book “Wheat Belly” (Davis 2013). Davis indicates that the increase in obesity and diabetes in the United States directly correlates with the increase in the sales of wheat-based products. But, wheat is not the real culprit. Jones indicates it is the caloric imbalance, because in the United States caloric intake has increased while physical activity has decreased. The increase in calories does not come from a single food or food group, Jones indicated.
“Food available for consumption increased in all major food categories from 1970 to 2008. The number of average daily calories per person in the marketplace increased approximately 600 calories”, according to the President’s Council on Fitness, Sports and Nutrition and statistics from the U.S. Census Bureau .
Weight-loss diets that advocate the elimination of an entire food group such as wheat may cause initial weight loss, but,like many fad diets, rarely show long-term maintenance of weight loss.
In fact, studies confirm that the easiest diets to maintain are those that deviate least from normal eating patterns. They are also much more likely to be associated with long-term weight loss and maintenance of the loss. Further, diets that include a balance of foods and do not have “forbidden” or excluded foods are associated with the greatest success in sustaining the weight loss.
Elimination of wheat and gluten can result in problems because wheat is a major contributor to dietary fiber, B vitamins and other nutrients.
Claim 4. High fat diet is good for your brain
Perlmutter indicates that fat is a best friend to the human brain. They indicate that “the story does not end with gluten. This is just one piece of the puzzle”.
But Perlmutter says that we have to understand why cholesterol is one of the best foods for our brain. Citing research by Elias et al. (2005) the authors report that a low cholesterol diet is associated with low cognitive capacity. He also states that there are more and more studies demonstrating that high cholesterol reduces the risk of developing neuropathies while increasing longevity, but he provides no references.
Perlmutter defends low density lipoprotein (LDL) as a danger for cardiovascular disease (CVD), saying that the problem with LDL results from oxidized LDL, which is modified by glucose rendering it useless for its function in the brain while increasing the level of free radicals.
The other big problem, Perlmutter indicates, is the prescription of statins to lower the cholesterol levels in post-menopausal women. He cites an unnamed study, which he says resulted in 48 percent higher risk of developing diabetes, while this latter condition doubled the risk of getting Alzheimer’s.
However, it has been found that saturated fat is a culprit in the reduction in cognitive capacity (Solfrizzi et al. 2011), while, on the contrary, diets rich in polyunsaturated fatty acids such as Omega 3, contribute positively to achieve effective cognitive capacity (Gomez-Pinilla 2008; Solfrizzi et al. 2011). In addition, saturated fat contributes to weight gain and obesity (Gomez-Pinilla 2008). The American Pediatrics Academy recommends a caloric intake from fat in women and children of not more than 30 percent of the total calorie intake to avoid becoming overweight and obese. This claim has been reviewed and documented by Lee and Birch (2002).
Wheat and other cereals should always be part of a healthy and nutritious balanced diet for most of the population. Its consumption is highly recommended to ensure an appropriate intake of dietary fiber, minerals, vitamins, and other beneficial bio-compounds present in the wheat grain. The approximately 1 percent of the population suffering from congenital immunological CD incapacity should not consume wheat products or any product containing gluten. However, these groups should be aware that the gluten-free food they are going to consume has a composition that will not necessarily positively affect their health, starting with the calorie intake coming from carbohydrates and sugar. For those with a gluten sensitivity, it is important to be aware if they are truly gluten sensitive and, if so, to what degree, to determine whether they should eat gluten-containing foods.
The media hype around the supposed “dangers of wheat” enumerated by Davis, Perlmutter and others is detrimental to the important and ongoing research agenda to sustainably increase wheat production for nutritional needs of the global population.
Agatston, A. and N. Geary. 2013. The South Beach Diet Gluten Solution: The Delicious, Doctor-Designed, Gluten-Aware Plan for Losing Weight and Feeling Great – Fast! New York: Rodale Books.
Akhunov, E.D., A.R. Akhunova, O.D. Anderson, J.A. Anderson, N. Blake, M.T. Clegg, D. Coleman-Derr, E.J. Conley, C.C. Crossman, K.R. Deal, J. Dubcovsky, B.S. Gill, Y.Q. Gu, J. Hadam, H. Heo, N. Huo, G.R. Lazo, M.C. Luo, Y.Q. Ma, D.E. Matthews, P.E. McGuire, P.L. Morrell, C.O. Qualset, J. Renfro, D. Tabanao, L.E. Talbert, C. Tian, D.M. Toleno, M.L. Warburton, F.M. You, W. Zhang, J. Dvorak. 2010. Nucleotide diversity maps reveal variation in diversity among wheat genomes and chromosomes. BMC Genomics 11:702.
Barrett, J. S. 2013. Extending Our Knowledge of Fermentable, Short-Chain Carbohydrates for Managing Gastrointestinal Symptoms. Nutrition in Clinical Practice 28: 300–306.
Biesiekierski, J.R., J.G. Muir, and P.R. Gibson. 2013a. Is gluten a cause of gastrointestinal symptoms in people without celiac disease? Current Allergy and Asthma Reports. DOI 10.1007/s11882-013-0386-4.
Biesiekierski, J.R., S.L. Peters, E.D. Newnham, O. Rosella, J.G. Muir, and P.R. Gibson. 2013b. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology 145:320-328.
Biesiekierski, J. R., E.D. Newnham, S.J. Shepherd, J.G. Muir, and P.R. Gibson. 2014. Characterization of Adults with a Self-Diagnosis of Nonceliac Gluten Sensitivity. Nutrition in Clinical Practice 29: 504–509.
Bjork, I., E. Ostman, M. Kritensen, N.M. Anson, R.K. Price, G.R.M.M. Haenen, R. Havenaar, K.E.B. Knudsen, A. Frid, H. Mykkanen, R.W. Welch, and G. Riccardi. 2012. Cereal grains for nutrition and health benefits: Overview of results from in vitro animal and human studies in the HEALTHGRAIN project. Trends in Food Science & Technology 25:87-100.
Braun, H.J., G. Atlin, and T. Payne. 2010. Multilocation testing as a tool to identify plant response to global climate change. In: Reynolds, CRP. (ed.). Climate Change and Crop Production, CABI, London, UK.
Brouns, F.J.P.H., V.J. van Buul, and P.R. Shewry. 2013. Does wheat makes us fat and sick? J Cereal Science 58: 209-2015.
Caballero, L., R.J. Peña, L.M. Martin, and J.B. Alvarez. 2008. Characterization of Mexican Creole wheat landraces in relation to morphological characteristics and HMW glutenin subunit composition. Genet Resour Crop Evol 57:657–665.
Carroccio, A., P. Mansueto, G. Iacono, M. Soresi, A. D’ Alcamo, F. Cavataio, I. Brusca, A. M. Florena, G. Ambrosiano, A. Seidita, G. Pirrone and G. Battista Rini. 2012. Non-Celiac Wheat Sensitivity Diagnosed by Double-Blind Placebo-Controlled Challenge: Exploring a New Clinical Entity. Am J Gastroenterol 2012, 107:1898–1906.
Catassi, C., J. C. Bai, B. Bonaz, G. Bouma, A. Calabrò, A. Carroccio, G. Castillejo, C. Ciacci, F. Cristofori, J. Dolinsek, R. Francavilla, L. Elli, P. Green, W. Holtmeier, P. Koehler, S. Koletzko, C. Meinhold, D. Sanders, M. Schumann, D. Schuppan, R. Ullrich, A. Vécsei, U. Volta, V. Zevallos, A. Sapone, and A. Fasano. 2013. Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders. A Review. Nutrients 5: 3839-3853.
Cavanagh, C.R., S. Chao, S. Wang, B.E. Huang, S. Stephen, S. Kiani, K. Forrest, C. Saintenac, G.L. Brown-Guedira, A. Akhunova, D. See, G. Bai, M. Pumphrey, L. Tomar, D. Wong, S. Kong, M. Reynolds, M.L. da Silva, H. Bockelman, L. Talbert, J.A. Anderson, S. Dreisigacker, S. Baenziger, A. Carter, V. Korzun, P.L. Morrell, J. Dubcovsky, M.K. Morell, M.E. Sorrells, M.J. Hayden, and E. Akhunov. 2013. Genome-wide comparative diversity uncovers multiple targets of selection for improvement in hexaploid wheat landraces and cultivars. Proc Natl Acad Sci 110: 8057-8062.
CIMMYT Int. 2011. Wheat Global Alliance for improving food security and livelihoods of the resource poor in the developing world. Pp. 189 www.cimmyt.org
Charalampopoulos, D., R. Wang, S.S. Paniella, and C. Webb. 2002. Application of cereals and cereal components in functional foods. A review. Int J Food Mictrobiology 79:131-141.
Cho, I. and M. Blaser. 2012. The human microbiome: at the interface of health and disease. Nature Reviews Genetics 13: 260-270.
Colomba, M.S. and A. Gregorini. 2012. Are Ancient Durum Wheats Less Toxic to Celiac Patients? A Study of α-Gliadin from Graziella Ra and Kamut. The ScientificWorld Journal 2012.
Cummins, A.G. and C. Roberts-Thomson. 2009. Prevalence of celiac disease in the Asia-Pacific region. J Gastroenterology and Hepatology 24: 1347-1351.
Davis, W. 2011. Wheat Belly. New York: Rodale Books.
De Filippo, C., D. Cavalieri, M. Di Paola, M. Ramazzotti, J.B. Poullet, S. Massart, S. Collini, G. Pieraccini, and P. Lionetti. 2010. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe. Proc Natl Acad Sci 107: 14691–14696.
de Punder, K., and L. Pruimboom. 2013. The Dietary Intake of Wheat and other Cereal Grains and Their Role in Inflammation. Nutrients 5: 771-787.
Deshmukh-Taskar, P.R., T.A. Nicklas, C.O. O’Neil, D.R. Keast, J.D. Radcliffe, and S. Cho. 2010. The relationship of breakfast skipping and type of breakfast consumption with nutrient intake and weight status in children and adolescents: The National Health and Nutrition Examination Survey 1999-2006. American Dietetic Association 110: 869-878.
Dhanapal, A. P., M. Ciaffi, E. Porceddu and E. d’Aloisio. 2011. Protein disulphide isomerase promoter sequence analysis of Triticum urartu, Aegilops speltoides and Aegilops tauschii. Plant Genetic Resources: Characterization and Utilization 9: 338–341.
Dickey, W. and N. Kearney. 2006. Overweight in celiac disease: prevalence, clinical characteristics, and effect of a gluten free diet. Am. J. Gastroenterol 101: 2356–2359.
Drago, S., R. El Asmar, M. R. Di Pierro, M. G. Clemente, A. Tripathi, A. Sapone, M. Thakari, G. Iacono, A. Carroccio, C. DÁgate, T. Not, L. Zampini, C. Catassi and A. Fasano. 2006. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scandinavian Journal of Gastroenterology 41:408-419.
Drewnowski, A. and N. Darmon. 2005. The economics of obesity: dietary energy density and energy cost. Am J Clin Nutr 282(suppl): 265S–273S.
Ello-Martin, J. A., J. H. Ledikwe and B.J. Rolls. 2005. The influence of food portion size and energy density on energy intake: implications for weight management. Am J Clin Nutr 282(suppl):236S-241S.
Elias, P.K., M.F. Elias, D’Agostino, L.M. Sullivan, and P.A. Wolf. 2005. Serum Cholesterol and Cognitive Performance in the Framingham Heart Study. Psychosomatic Medicine 67: 24–30.
Food and Agriculture Organization of the United Nations. Statistics. www.fao.org/statistics/en/ (15 December 2014).
Food and Agriculture Organization of the United Nations (FAO). “Food-Based Dietary Guidelines. (15 December 2014)
Food and Agriculture Organization of the United Nations and World Health Organization (FAO/WHO). “Second International Conference on Nutrition. Conference Outcome Document: Framework for Action.” (November 2013) (15 December 2014).
Food and Agriculture Organization of the United Nations. “Magnitude Causes and Consequences of Micronutrient Malnutrition.” http://www.fao.org/docrep/x0245e/x0245e01.htm (15 December 2014).
Fardet, A., E. Rock and C. Rémésy. 2008. Is the in vitro antioxidant potential of whole-grain cereals and cereal products well reflected in vivo? Review. Journal of Cereal Science 48: 258-276.
Fasano, A. 2001. Pathological and therapeutic implications of macromolecules passage through the tight junction. In: Cereijido M, Anderson J (eds.) Tight Junctions. CRC Press: 697-722.
Fasano, A. 2011. Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer. Physiol Rev 91: 151–175.
Fasano, A. 2012. Novel Therapeutic/Integrative Approaches for Celiac Disease and Dermatitis Herpetiformis. Clinical and Developmental Immunology Volume 2012, Article ID 959061, 7 pages doi:10.1155/2012/959061.
Flight, I. and P. Clifton. 2006. Cereal Grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature. European Journal of Clinical Nutrition 60: 1145-1159.
Frazier, T. H., J. K. DiBaise and C. J. McClain. 2011 Gut Microbiota, Intestinal Permeability, Obesity-Induced Inflammation, and Liver Injury. J Parenter Enteral Nutr 35: 14S-20S.
Gibson, S., M. Ashwell, J.W. van der Kamp. 2013. New results and science-based nutrition guideline (HEALTHGRAIN Forum). Event report. Symposium in the 20th International Nutrition Congress, 18th September, 2013 Granada, Spain. Complete Nutrition Vol.13 No.6 Dec 2013/Jan 2014, p. 26-28.
Gilkerson, L. and T. 2013. Weeding out wheat: A simple scientific faith-based guide. http://intoxicatedonlife.com
Gomez-Pinilla, F. 2008. Brain foods: the effects of nutrients on brain function. National Reviews in Neuroscience 9: 568-578.
Gutierrez, M. V., C. Guzman, L.M. Martin and J. B. Alvarez. 2011.Molecular characterization of the Glu-Ay gene from Triticum urartu for its potential use in quality wheat breeding. Plant Genetic Resources: Characterization and Utilization (2011) 9(2); 334–337
Hadjivassiliou, M., D. S. Sanders, R. A. Grünewald, N. Woodroofe, S. Boscolo and D. Aeschlimann. 2010. Gluten sensitivity: from gut to brain. Lancet 9.
Halmos, E. P., V. A. Power, S. J. Shepherd, P. R. Gibson, and J. G. Muir. 2014. A Diet Low in FODMAPs Reduces Symptoms of Irritable Bowel Syndrome. Gastroenterology 146: 67–75.
Jackson, J.R., W.W. Eaton, N.G. Cascella, A. Fasano and D.L. Kelly. 2012. Neurologic and Psychiatric Manifestations of Celiac Disease and Gluten Sensitivity. Psychiatr Q 83: 91–102.
Jones, J. 2012. Wheat Belly: An Analysis of selected statements and basic theses from the book. Cereal Foods World 57: 177-189.
Junhua, H., J.H. Peng, D. Sun, and E. Nevo. 2011. Domestication evolution, genetics and genomics in wheat. A Review. Mol Breeding 28:281–301.
Kasarda, D.D. 2011. Can an increase in Celiac Disease be attributed to an increase in the gluten content of wheat as a consequence of wheat breeding? J Agricultural and Food Chemistry 61: 1155-1159.
Lee, Y., and L.L. Birch. 2002. Diet quality, nutrient intake, weight status, and feeding environments of girls meeting or exceeding the American Academy of Pediatrics recommendation for total dietary fat. Minerva Pediatrics 54: 179-186.
Lee, A. R., D. L. Ng, E. Dave, E. J. Ciaccio and P. H. R. Green. 2009. The effect of substituting alternative grains in the diet on the nutritional profile of the gluten-free diet. J Hum Nutr Diet 22: 359–363.
Lillywhite, R.D., and C. Sarrouy. 2014. “A Review of the Dietary, Health and Environmental Status of Whole Grain Cereals.” University of Warwick.
Lundin, K. E. A. 2014. Non-celiac gluten sensitivity – why worry? BMC Medicine 12: 86.
Molberg, O., A. K. Uhlen, T. Jensen, N. S. Flaete, B. Fleckenstein, H. Arentz-Hansen, M. Raki, K.A. Lundin and L. M. Sollid. 2005. Mapping of Gluten T-Cell Epitopes in the Bread Wheat Ancestors: Implications for Celiac Disease. Gastroenterology 128: 393–401.
Naghavi, M. R., S. Ahmadi, A-A. Shanejat-Boushehri, G. Komaei and P.C. Struik 2013. Characterization of low-molecular-weight-glutenin subunit genes from the D-genome of Triticum aestivum, Aegilops crassa, Ae. cylindrica and Ae. Tauschii. Biochemical Systematics and Ecology 50: 23–29.
National Geographic, 2014. http://education.nationalgeographic.com/ education/encyclopedia/grain/?ar_a=1
National Wheat Improvement Committee. 2013. Wheat Improvement: The Truth Unveiled. http://www.wheatworld.org/research.
Nijeboer, P., H. J. Bontkes, C. J. J. Mulder and G. Bouma. 2013. Non-celiac Gluten Sensitivity. Is it in the Gluten or the Grain? J Gastrointestin Liver Dis 22: 435-440.
Perlmutter, D. and C. Loberg. 2014. Cerebro de Pan. La devastadora verdad sobre los efectos del trigo, el azúcar y los carbohidratos en el cerebro (y un plan de 30 días para remediarlo). (traducción: Molinari-Tato, A.). Pp. 382. Editorial Grijalbo. Original title: Grain Brain: The Surprising Truth about Wheat, Carbs, and Sugar—Your Brain’s Silent Killers.
Poole, J.A., K. Barriga, D.Y.M. Leung, M. Hoffman, G.S. Eisenbarth, M. Rewers and J.M. Norris. 2006. Timing of initial exposure to cereal grains and the risk of wheat allergy. Pediatrics 117: 2175–2182.
Poutanen, K. 2012. Past and future of cereal grains as food for health. Trends in Food Science & Technology 25: 58-62.
Rampersaud, G.C., M.A. Pereira, B.L. Girard, J. Adams and J.D. Metzl. 2005. Breakfast habits, nutritional status, body weight, and academic performance in children and adolescents. Journal of the American Dietetic Association 105: 743-760.
Round, J. L. and S. K. Mazmanian. 2009. The gut microbiota shapes intestinal immune responses during health and disease. Nature Reviews Immunology 9: 313-323.
Salamini, F., H. Ozkan, A. Brandolini, R. Schafer-Pregl and W. Martin. 2002. Genetics and geography of wild cereal domestication in the near east. Nature Reviews 3: 429-441.
Salentijn, E. M. J., D. C. Mitea, S. V. Goryunova, I. M. van der Meer, I. Padioleau, L.J.W.J. Gilissen, F. Koning and M.J.M. Smulders. 2012. Celiac disease T-cell epitopes from gammagliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation. BMC Genomics, 13: 277.
Shan, L., Ø. Molberg, I. Parrot, F. Hausch, F. Filiz, G. M. Gray, L. M. Sollid and C. Khosla. 2002. Structural Basis for Gluten Intolerance in Celiac Sprue. Science 297: 2275-2279
Sapone, A., K. M. Lammers, V. Casolaro, M. Cammarota, M. T. Giuliano, M. De Rosa, R. Stefanile, G. Mazzarella, C. Tolone, M. I. Russo, P. Esposito, F. Ferraraccio, M. Cartenì, G. Riegler, L. de Magistris and A. Fasano. 2011. Divergence of gut permeability and mucosal immune gene expression in two gluten associated conditions: celiac disease and gluten sensitivity. BMC Medicine 9:23.
Sapone A., J. C. Bai, C. Ciacci, J. Dolinsek, P. H.R. Green, M. Hadjivassiliou, K. Kaukinen, K. Rostami, D. S. Sanders, M. Schumann, R. Ullrich, D. Villalta, U. Volta, C. Catassi and A. Fasano. 2012. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Medicine 10: 1-13.
Shewry, P.R. 2009. Wheat Review. J Experimental Botany 60: 1537-1553.
Setty, M., L. Hormaza and S. Guandalini. 2008. Celiac Disease Risk Assessment, Diagnosis, and Monitoring. Mol Diag Ther 12: 289-298.
Sofi, F., A. Whittaker, A. M. Gori, F. Cesari, E. Surrenti, R. Abbate, G. F. Gensini, S. Benedettelli and A. Casini. 2014. Effect of Triticum turgidum subsp. turanicum wheat on irritable bowel syndrome: a double-blinded randomised dietary intervention trial. British Journal of Nutrition 111:1992–1999.
Solfrizzi, V., F. Panza, V. Frisardi, D. Seripa, G. Logroscino, B. P. Imbimbo and A. Pilotto. 2011. Diet and Alzheimer’s Disease Risk Factors or Prevention. Expert Rev Neurother 11:677-708.
Specter, M. 2014: Against the Grain. Should you go gluten-free? http://www.newyorker.com/ magazine/2014/11/03/grain
Suligoj, T., A. Gregorini, M. H. Colomba, J. Ellis and P. Ciclitira. 2013. Evaluation of the safety of ancient strains of wheat in coeliac disease reveals heterogeneous small intestinal T cell responses suggestive of coeliac toxicity. Clinical Nutrition 32: 1043-1049.
Trasande, L., J. Blustein, M. Liu, E. Corwin, L.M. Cox, and M.J. Blasé. 2013. Infant antibiotic exposures and early-life body mass. International Journal of Obesity 37: 16–23.
van Buul, V. and F. Brouns. 2013. Tackling Wheat Sensitivity. The World of Food Ingredients April-May 2013: 49-50.
van den Broeck, H.C., H. C. de Jong, E. M. J. Salentijn, L. Dekking, D. Bosch, R. J. Hamer, L. J. W. J. Gilissen, I. M. van der Meer and· M. J. M. Smulders. 2010. Presence of celiac disease epitopes in modern and old hexaploid wheat varieties: wheat breeding may have contributed to increased prevalence of celiac disease. Theor Appl Genet 121: 1527–1539.
Venn, B.J. and J.I. Mann. 2004. Review: Cereal grains, legumes and diabetes. European Journal of Clinical Nutrition 58: 1443-1461.
World Food Program (WFP). Hunger Statistics. https://www.wfp.org/hunger/stats (15 December 2014).
World Health Organization (WHO). “Healthy Diet Factsheet.” (September 2014). http://www.who.int/mediacentre/factsheets/fs394/en/ (15 December 2014).
World Health Organization (WHO). “Countries vow to combat malnutrition through firm policies and actions” (November 2014). http://www.who.int/mediacentre/news/releases/2014/icn2-nutrition/en/ (15 December 2014).
World Health Organization (WHO). “WHA Global Nutrition Targets 2025: Policy brief series.” (November 2014).
http://www.who.int/nutrition/en/ (15 December 2014)
September 19, 2018
September 17, 2018
September 14, 2018
September 13, 2018
September 13, 2018MORE