Gluten-free (wheat-free) diet have gained an enormous popularity lately. Most of the people in general fitness business (trainers, dietitians, and nutritionists) took for granted that it is wheat and the contain of gluten in particular, which causes symptoms of allergy, unpleasant side effects and is one of the main reasons for obesity amongst modern society. In this article, I’ll try to prove that it is not wheat in their nutrition plan and gluten itself, but rather something different – something much more evident and yet disregarded.
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Wheat is the most generally developed cereal grain worldwide, being grown in different temperate climates. It is third among the cereals, altogether worldwide generation, which was 704 million tons in 2011. The interest for wheat for human consumption is increasing globally, including the countries which are climatically unsuited for wheat production. Wheat is quite rich in nutrient. It consists minerals and B vitamins and supplies up to 20% of the energy intake of the global population (Cummins and Roberts-Thomson, 2009).
Most of the wheat that is grown and consumed globally is bread wheat (Triticum aestivum). Bread wheat is a relatively new species, having arisen in southeast Turkey about 9000 years ago (Feldman and Millet, 2001). However, small amounts of “primitive” wheat are also grown, mainly for specialist health foods: einkorn, emmer and spelt. The latter primarily differs from bread wheat in that the hull is not removed by threshing; resulting in a higher fiber content when consumed as whole grain.
Although wheat is a young species, it is immensely diverse, with forms adapted to a wide range of local environments and selected for different end uses.
The wheat grain contains many hundreds of individual proteins, which may have structural, metabolic, protective or storage functions (as reviewed by Shewry (2009)). They include the gluten proteins, which are the primary storage components and may account for up to 80% of the total grain protein (Wrigley, 1988). The protein composition of the grain is determined by the genotype, but also strongly influenced by the environment (climate and agronomy). For example, the contents of protective proteins may be greater when the plant is subjected to heat or drought stress while the total content of gluten proteins and the proportions of different gluten protein components are influenced by the availability of mineral nutrients (nitrogen and sulfur) (Shewry, 2011).
People claim that the current worldwide wheat production consists of “genetically modified” varieties, which contain new components that cause adverse health effects. In reality, the presence of such new components is not supported either by comparative studies of old and recently bred types of wheat (Ward, 2008) or by analyses of genomic sequences (Brenchley, 2012). Furthermore, data about harmful effects of wheat, consumed in extruded, baked, and other processed foods, are not accessible, and there are no grounds to advise the general public not to eat this common dietary staple. Only individuals with a genetic predisposition for celiac disease, or suffering from allergy or other forms of severe sensitivity to gluten and other wheat proteins, will benefit from excluding wheat and related cereals from their diet.
There are no accessible data to prove this suggestion.
The gluten storage proteins of wheat with a more extensive class of proteins with firmly related structures being available in strongly related species (rye and barley) and less tightly related structures in different (oats, millets, sorghum, corn and rice). Those proteins are additionally present in the “primitive” wheat species talked about above: einkorn, emmer and spelt.
Scientists isolate gluten proteins into two divisions, the gliadins which are available as monomers and the glutenins which are polymeric. Fragmented assimilation of gliadin has been appeared to discharge a peptide, called gliadorphin, that can prompt opiate-like effects, as demonstrated in laboratory tests. They injected rats the intact peptide (Sun and Cade, 2003). However, gliadorphin consists of seven amino acids and cannot be absorbed by the intestine. The reason for this is the gut peptide transporter PepT1 transports only di- and tripeptides (Gilbert, 2008). There is no classification of carriers for larger peptides. Gliadorphin is in this way not present in an in any human circulatory system and can’t reach and affect the cells of the central nervous system.
In this regard, people individuals extrapolate impacts seen on cells in a research center setting to the in vivo situation in humans. There are no reviews in which gliadorphin has been appeared to be caught up in an intact shape by the digestive system and no proof that gliadin either animates craving or instigates enslavement like withdrawal impacts. A study presented to support this argument did not include actual feeding of any food (Jones, 2012).
Giacco, (2011) and Koh-Banerjee (2004) concluded that regular consumption of whole grains was negatively correlated with weight gain. These authors described 14 cross-sectional research, in which higher intake of whole grains was associated with a lower body mass index (BMI). Also, they presented three studies in which a significantly lower waist circumference was noted. The argument that refraining from consumption of wheat in the diet induces weight loss should also be interpreted regarding the way that an incredibly set number of nourishments accessible in the market don’t contain wheat. Constrained accessibility of wheat-free foods may itself cause utilization dullness, prompting diminished general admission of sustenance and energy. The latter will result in weight loss, which will improve (type 2) insulin sensitivity and diabetic state, a dieting-related phenomenon which occurs during basically all famous eating regimen mediations.
For centuries, there have been populations who consume wheat-based bread and other wheat products as the primary source of their energy intake, without indices of causing weight gain. Moreover, the consumption of whole grain products, which in the U.S. and Europe are mainly based on wheat, has been shown to be associated with reduced risks of type 2 diabetes, cardiovascular sicknesses, certain kinds of cancer as well as a more favorable weight management (Ye, 2012).
Recently, Soares (2013) fed mice an ad libitum high-fat diet to induce obesity. The mice were divided into a control group, containing no gluten, and a group receiving 4.5% wheat gluten, for eight weeks. The high-fat diet was composed of 25%, 61% and 15% of the total energy from carbohydrate, fat, and protein, respectively. The eating regimen structure was not representative for the human diet, and there wasn’t any control group in which the added gluten was exchanged for another isolated protein type. It can’t be certain that effects observed were gluten effect in particular, instead of a general protein content impact. As a result, it seems to be premature to follow the conclusion that gluten exclusion helps in reducing body weight and that it can be a new dietary approach to prevent the development of obesity and related sickness in the general human population.
Statements on the adverse effects of gluten-containing wheat are diametrically opposite to the observations on consumption of whole grain and whole grain fiber. It significantly improves blood glucose control, improves cholesterol levels, reduces blood pressure and lowers the serum concentration of high-sensitivity C-reactive protein, a marker of low-grade inflammation (Gaskins, 2010; Jenkins, 2007; Masters, 2010; Qi, 2006; Raninen, 2011)
These observations all indicate improvement in overweight related metabolic dysregulation and have been attributed mainly to the fiber and phytochemicals that are concentrated in the aleurone layer of the bran (Brouns, 2011) as well as present in the wheat germ fraction. These compounds are thought to exert synergistic effects on specific health-related metabolic processes (Fardet, 2010).
Recently, Björck, (2011) summarized the findings of the HEALTHGRAIN project supported by the European Commission which included 26 academic research centers. They concluded that in well-controlled studies a negative correlation was observed between the circulating levels of short-chain fatty acids, resulting from grain fiber fermentation in the colon and improved insulin sensitivity and glucose homeostasis. As a consequence, insulin production at a particular carbohydrate load was favorably reduced. This points to important effects of components that are either not present, or only present in insignificant amounts in white wheat flour, but are present in whole wheat and whole grain flour.
In this matter, it is also noteworthy that the digestion and metabolism of whole grain goods induce significantly different effects on insulin-, incretin- and satiety hormone responses compared to the consumption of refined (white flour based) wheat bread (Juntunen, 2003).
Hauner (2012), summarized the evidence on carbohydrate intake and focused on the relation between wheat and nutrition-related diseases. The authors conclude that the evidence regarding the relevance of refined grain and whole-grain product intake for the risk of obesity is judged as insufficient. Moreover, they find that existing cohort studies show a possible relationship between whole-grain product intake and a reduced risk of obesity, a probable relationship with a lower risk of diabetes (see also: de Munter, 2007) and coronary heart disease, and a convincing relationship with a reduced level of LDL cholesterol. Also, Aune, (2011) concluded that the intake of dietary fiber from cereals and other whole grains are linked to a reduction in risk of colorectal cancer.
Although the studies discussed above indicate that whole grain consumption has health benefits, it should also be noted that part of the population cannot tolerate wheat or other cereals containing related proteins, particularly those suffering from celiac disease. CD is a genetically predisposed condition (Catassi and Fasano, 2008; Fasano and Catassi, 2001) and results from an autoimmune response initiated by the binding of modified gluten peptides to T-cells of the immune system. The described peptides are then recognized by specific CD4+ T cells which release inflammatory cytokines leading to damage of the gut villi. Individuals carrying HLA-DQ2 or HLA-DQ8 as a primary genetic predisposition are affected, representing ∼1% of the population. Rubio-Tapia (2009) concluded that the predominance of CD in the United States was 0.71% (1 in 141), like that found in several European countries (Mustalahti, 2010).
Very recently, gluten sensitivity has been defined as a new etiologically heterogeneous syndrome in which environmental factors may play a role in addition to that of food (Biesiekierski, 2011; Carroccio, 2012a; Di Sabatino, 2012; Pietzak, 2012). Other data shows that gluten sensitivity occurs in approximately 30% of the people suffering from irritable bowel syndrome (IBS). Given the prevalence of IBS in most countries, 10–15% (in some countries >30%) (Carroccio, 2012b; Verdu, 2009). This number is probably an underestimate because many sufferers are not diagnosed. Conservative estimate is that gluten sensitivity affects at least 5–10% of the population.
It should be noted in this respect that gluten sensitivity is not the same as wheat allergy (Battais, 2008), which occurs in about 0.3–3.0% in adults and children. Wheat grain proteins are involved in the three routes of sensitization: inhalation, contact, and ingestion. Depending on the route of allergen exposure and the underlying immunologic mechanisms, wheat grain allergy can appear as occupational asthma and rhinitis, contact urticaria or classic food allergy affecting the skin, gut and/or respiratory tract. Allergy may also appear as exercise-induced anaphylaxis. Apart from gliadin and glutenin protein fractions, wheat allergy can be caused by a large number of other grain components (Battais, 2008; Tatham and Shewry, 2008).
A recent study (Sapone, 2011) evaluated possible mechanisms underlying gluten sensitivity. Patients who were not suffering from a coeliac disease (proved by gut tissue biopsy analysis) but were sensitive to gluten were exposed to a supervised 4-month gluten or non-gluten diet. The main gastrointestinal symptoms of the gluten-sensitive individuals were gas production, diarrhea, weight loss, and abdominal pain. In this study, the gluten-sensitive individuals did, however, show decreased intestinal permeability.
In the only available double-blind, randomized, placebo-controlled study addressing wheat gluten sensitivity (Biesiekierski, 2010), a re-challenge trial was undertaken in people suffering from irritable bowel syndrome in whom celiac disease was excluded and who were closely controlled on a gluten-free diet. Participants received either gluten or placebo in the form of two bread slices plus one muffin per day with a gluten-free diet for up to 6 weeks. Symptoms were evaluated using a visual analog scale and markers of intestinal inflammation, injury, and immune activation was monitored. Although more intestinal distress symptoms were reported in those consuming wheat gluten, there were no changes in levels of celiac antibodies and other crucial determinants.
This highly controlled study (Biesiekierski, 2010) disproves the suggestion that gluten protein in wheat and/or wheat germ agglutinin cause adverse effects in individuals without celiac disease, thus giving no reason to discourage the general population to consume wheat containing products.
However, some gluten-containing products also contain relatively rapidly fermentable carbohydrates, such as oligofructose and arabinoxylan. Lack of these and other fermentable carbohydrates; (also referred to as “FODMAPs”) from the diet, has been reported to reduce intestinal distress to similar extents as gluten free foods (Barrett and Gibson, 2012). It is therefore still unclear whether gluten proteins or other factors are involved in the etiology of gluten sensitivity in non-celiac patients (Biesiekierski, 2011).
The very recent studies of Schuppan (2012) and Junker (2012) on “cereal triggers of innate immune activation” describe the role of wheat amylase-trypsin inhibitors (ATIs), which probably confer defense against pests and parasites by inhibiting their digestive enzymes. The authors state that, based on the review of Ryan (1990), the breeding of high yielding and highly pest-resistant varieties of wheat has automatically lead to the selection of types that have a high content of ATIs. According to Altenbach (2011), the ATIs are accumulated to sufficiently high levels in the grain to also function as storage proteins. These ATIs appear to mostly resist intestinal degradation in humans and stimulate mucosal cytokine release after feeding in vivo.
Preliminary studies showed that neither gliadin which had been digested in vitro with trypsin and pepsin nor the celiac-active peptide elicited innate immune responses in intestinal epithelial cells. The pepsin-trypsin digested gliadin did strongly activate inflammatory responses, but this activity was due to the presence of contaminating ATIs.
These findings identify cereal ATIs as novel contributors to celiac disease.
Moreover, the authors suggest that ATIs may fuel inflammation and immune reactions in other intestinal and even non-intestinal immune disorders (Junker, 2012). This warrants further research to unravel oral tolerance and gut disease-related mechanisms. However, the existence of many anecdotal patient reports should not be ignored due to lack of scientific data and evidence, but used as a basis for well-designed studies and with more accurate biomarkers.
As a result, some medical doctors advise those who suffer from physical complaints that cannot be explained by routine medical testing (no physical cause can be established) to request a gluten sensitivity test and/or to refrain for several weeks from consuming gluten-containing foods. Then they advise observing whether their symptoms (such as sensitive intestinal system, gastrointestinal distress, bloating, rumbling, colic, chronic fatigue, poor concentration, ADHD, frequent headache, migraine, repeating episodes of loose stools of diarrhea and arthritis) disappear.
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