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Early Humans, Wheat Cultivation, and Your Health

February 8, 2013

Had I not been obsessed with training and nutrition, and not earned a Ph.D. in exercise physiology, I probably would have followed up on my undergraduate minor and pursued a career in archaeological anthropology. As a closet nerd I find early human anthropology fascinating: how did we as a species go from hunting and gathering in small clans to living packed in urbania with structures that reach for the stars? The answer is actually very simple: farming. The abundance of calories available from intense food production allowed humans to divide into craft specialization, develop complex (and often inhumane) social hierarchy, become more densely populated, and ultimately build what we now consider “civilization”.

Putting my feelings for city living aside, have you ever wondered what inspired one of our ancestors to take a grass seeds he/she gathered for food and instead bury it in the ground?

No doubt you have heard of the “Paleo Diet”; consuming the same foods our ancestors did prior to the cultivation of crops. According to the suggestions of Dr. Loren Cordain, founder of the popular “Paleo Diet”, humans should not eat grains because they were not consumed by early humans. While I tend to agree with some  of Dr. Cordain’s dietary suggestions (consume more whole foods, more fresh foods, less processed foods, eat more produce), his facts are not entirely accurate: paleolithic humans did indeed consume grains.  In fact, humans had been gathering and consuming wild cereal grains for at least 10-20,000 years prior to the advent of farming (8).  This week’s column deals specifically with the health and physiological ramifications that resulted not from consuming indigenous grains, but instead from the planting of that first seed: wheat.

To understand why wheat has received such a bad rap in the health and fitness media, we must first understand its history. Prior to cultivation wheat displayed two traits unique to the wild type: seed volume and seed dispersal (15). These traits posed a challenge for early foraging humans gathering wheat, in that the seeds were not only smaller, but they also shattered, or broke from the stalk and fell to the ground as they ripened. Thus, early humans had to gather a greater number of individual grains, and had only a finite period to gather them between near-maturity and shatter. It is most likely that an early human came upon a mutant wheat species that did not shatter, gathered the grains, and then accidently dispersed them near a camp site (5). As a result, a normally unviable trait was allowed to live, likely harvested the next season due to ease and proximity, and spread again ultimately leading to the discovery of cultivation.

Regardless of how this transition occurred, humans now had the ability to easily harvest grains, and more importantly, for the first time in history, had the ability to control specie traits to suit human needs. As a result, cereal grains have significantly evolved over the past 5-10,000 years. The average size of the domestic wheat grain, for example, grew immensely over a 1,000 year time period, as pictured below:

Wheat 1

Increased grain volume with cultivation was also accompanied by morphological changes. As the shape changed so did grain composition such that the endosperm comprised a significantly larger volume and proportion of the cultivated grain than the wild type (7). Shown below are comparisons between various species of wild and domestic wheat: ancestral wheat displayed a long, thin structure and had a lower mass to surface area ratio compared to modern wheat.

Wheat 2

The increase in grain volume and proportion of endosperm brings forth the crux of the wheat issue: gluten. Gluten is a protein that is deposited throughout the endosperm as the grain matures and endosperm cells die in order to form the continuous matrix of glucose polymers we know as starch (19). Gluten is also the protein that gives wheat dough its viscoelastic properties. As most bakers will tell you, the higher the gluten content the better the bread. Thus, the domestication and cultivation of larger wheat grains also resulted in proportionately greater gluten content.

Fast forward 10,000 years of selected genetic modifications and over the past four decades wheat has been genetically modified via crossing wheat with non-wheat grasses, and irradiation of wheat seeds and embryos with chemicals, gamma rays, and high-dose X-rays to produce more resilient plants with even larger seeds.  While these genetic variants have improved crop yield, they also dramatically altered wheat protein such that gluten and gliadin (a major wheat allergin) concentrations have increased significantly (21). This altered protein content in genetically modified wheat has been suggested to play a significant role in the increased prevalence of gluten intolerance document over the past decade (11).

The debilitating effects of consuming gluten proteins from wheat in individuals with a genetic predisposition to gluten intolerance (celiac disease) have been well documented and include: malabsorption (leading to diarrhea, flatulence, and bloating), inflammation, loss of intestinal villi and intestinal lesions, anemia, neuropathy, infertility, and fatigue (13).  Less clear are the effects of gluten in otherwise-healthy individuals, which are rumored by many “popular health bloggers” to cause GI distress, inflammation, weight gain, susceptibility to disease, eczema, and even impotence.

Are the internet nutrition “gurus” on to something?

Biesiekierski et al. (1) investigated the effects of gluten consumption on gastrointestinal symptoms in inflammatory bowel disease patients without celiac disease.  Subjects were screened for celiac disease, followed a gluten-free diet, and only those whose symptoms improved with gluten exclusion were included in the study.  Subjects were then randomly placed into two groups, one of which received gluten-free bakery items and another whose bakery items were spiked with 16g gluten for 6 weeks.  The gluten-spiked diet group experienced a significant increase in symptoms including pain, bloating, and diarrhea.  The largest difference in symptoms between groups was fatigue. Because there were no changes in colonic inflammation, Biesiekierski suggested that gluten may have caused fatigue by acting systemically, possibly by inducing small intestinal low-grade inflammation.

Wheat 3

Non-celiac gluten-sensitive patients display a unique immune response to wheat compared with celiac patients. In particular, the consumption of gluten results in the release of IgG/IgA antigliadin antibodies (22).  The activation of intestinal immune cells and their subsequent secretion of inflammatory cytokines stimulate both the enteric nervous system (14) and interact with the central nervous system (3), and gut inflammation has been linked with chronic fatigue (9).  Evidence from in vitro research lends support to the hypothesis that gluten induced inflammation may increase fatigue in non-celiac patients.  Gliadin has been shown to induce apoptosis (6), increase oxidative stress (16), and induce inflammation (10) in isolated human intestinal epithelial cells via the NF-kappaB/TNF-α pathway.  Because gliadin increases epithelial permeability (17), gut leakage of large pro-inflammatory polypeptides may occur (4), leading to autonomic dysfunction via vagal nerve afferents (12), and possibly resulting in the increased fatigue seen with wheat consumption in self-diagnoses gluten sensitive individuals (as pictured below). Whether this happens in vitro and what dosages of gluten or gliadin are required to induce observable interactions with vagal afferents is still unknown.

Image 3

And what about weight gain?

Soares et al. (20) investigated the effects of a hypercaloric high-fat diet with or without gluten consumption in mice. Food intake was not different between groups; however, the fat mass and fat distribution was increased with gluten consumption. Increases in adiposity with gluten consumption were accompanied by alterations in hormone concentrations and gene expression. In particular, the consumption of gluten elevated adipose tissue inflammation leading to increased resistin and reduced adiponectin concentrations, which ultimately resulted in decreased insulin sensitivity and fatty acid oxidation.

Gluten has been shown the expression of PPAR-α/γ. PPAR-α activation increases fatty acid uptake and oxidation myocardiocytes (2). PPAR-γ is localized to subcutaneous adipose tissue, and its activation increases adiponectin expression and adipocyte glucose uptake. While activation of PPAR-γ may not be optimal for body composition purposes, it plays an important role in glucose homeostasis, especially in diabetics or during a hyper-caloric diet in preventing the accumulation of more metabolically active, pathological visceral adipose tissue (18). Again, whether these changes occur in skeletal muscle, and whether moderate consumption of wheat provides enough gluten/gliadin to cause these changes is also unknown.

Perhaps what the internet gurus like to harp upon most are the effects of gluten consumption on the expression of lipolytic and lipogenic genes. Gluten consumption reduced the expression of LPL, HSL, and CPT, while increasing ACC expression.  LPL and HSL are involved with breaking down and extracting lipids from lipoproteins and CPT-1 transfers lipids across the mitochondrial membrane for beta-oxidation. On the other hand, ACC is highly expressed in adipose tissue and a rate limiting step in adipocyte lipid synthesis (fat accumulation). Taken collectively, the results from Soares et al. suggest that the exclusion of gluten from the diet may have a positive effect on nutrient partitioning – at least in mice. Whether a similar relative dose of gluten causes these changes in humans is still unknown. More importantly, and also unknown is whether typical daily intakes of gluten cause similar changes in lipolytic and lipogenic gene expression.

Should you avoid gluten?

The most accurate way to determine if you are gluten sensitive is to get serologically tested for the IgA/G antigliadin antibodies; however, that would require an intestinal biopsy, which likely would not be fun. A more practical way to determine gluten sensitivity has been described by Biesiekierski (1): cease the consumption of gluten for 6 weeks; note symptoms of bloating, GI distress, and pain; then add wheat back into the diet for a few weeks and observe how you react.  If symptoms of bloat and GI distress appear then exclude wheat or slowly introduce it back into your diet until you find your point of tolerance.

As an anecdotal reference, I stopped eating wheat approximately three years ago. Prior to that time I struggled with maintaining my bowels through class and knew where every public restroom was on my 30 minute commute to graduate school.  Removing wheat gave me greater control over my bowels – and that was it: no improvements in energy, recovery, or body composition (as all the internet gurus claim).

What we need to look at most in the case of this recommendation is the ratio of harm to benefit. Consider the following questions:

  1. Will giving up wheat products in exchange for other grains or starch sources negatively affect health or performance? Not likely.
  2. Will it improve performance or body composition? The answer to that is ambiguous.
  3. Will giving up gluten and not replacing those starches affect performance or body composition? Most likely, and the changes could swing positively or negatively depending upon sport and caloric intake.
  4. Will giving up wheat products in exchange for highly processed, preserved, and expensive “gluten-free” varieties affect health?  Maybe. Will they affect your wallet? Absolutely.

Jason Cholewa, Ph.D., CSCS

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References

1. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, Gibson PR: Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. The American journal of gastroenterology 2011, 106:508–14; quiz 515.

2. Brandt JM, Djouadi F, Kelly DP: Fatty acids activate transcription of the muscle carnitine palmitoyltransferase I gene in cardiac myocytes via the peroxisome proliferator-activated receptor alpha. The Journal of biological chemistry 1998, 273:23786–92.

3. Collins SM, Bercik P: The relationship between intestinal microbiota and the central nervous system in normal gastrointestinal function and disease. Gastroenterology 2009, 136:2003–14.

4. Davin JC, Forget P, Mahieu PR: Increased intestinal permeability to (51 Cr) EDTA is correlated with IgA immune complex-plasma levels in children with IgA-associated nephropathies. Acta paediatrica Scandinavica 1988, 77:118–24.

5. Fuller D, Allaby R: Seed dispersal and crop domestication: shattering, germination and seasonality in evolution under cultivation more. academia.edu 2009, 38:238–295.

6. Giovannini C, Sanchez M, Straface E, Scazzocchio B, Silano M, De Vincenzi M: Induction of apoptosis in caco-2 cells by wheat gliadin peptides. Toxicology 2000, 145:63–71.

7. Hands P, Kourmpetli S, Sharples D, Harris RG, Drea S: Analysis of grain characters in temperate grasses reveals distinctive patterns of endosperm organization associated with grain shape. Journal of experimental botany 2012, 63:6253–66.

8. Kislev M, Nadel D, Cami I: Epipalaeolithic cereal and fruit diet at Ohalu II, Sea of Galilee, Israel. Rev. Palaeobot. Palyn. 1992, 73:161–166.

9. Lakhan SE, Kirchgessner A: Gut inflammation in chronic fatigue syndrome. Nutrition & metabolism 2010, 7:79.

10. Laparra Llopis JM, Sanz Herranz Y: Gliadins induce TNFalpha production through cAMP-dependent protein kinase A activation in intestinal cells (Caco-2). Journal of physiology and biochemistry 2010, 66:153–9.

11. Lohi S, Mustalahti K, Kaukinen K, Laurila K, Collin P, Rissanen H, Lohi O, Bravi E, Gasparin M, Reunanen A, Mäki M: Increasing prevalence of coeliac disease over time. Alimentary pharmacology & therapeutics 2007, 26:1217–25.

12. Morris G, Maes M: A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Metabolic brain disease 2012.

13. Mubarak A, Houwen RHJ, Wolters VM: Celiac disease: an overview from pathophysiology to treatment. Minerva pediatrica 2012, 64:271–87.

14. Ohman L, Isaksson S, Lindmark A-C, Posserud I, Stotzer P-O, Strid H, Sjövall H, Simrén M: T-cell activation in patients with irritable bowel syndrome. The American journal of gastroenterology 2009, 104:1205–12.

15. Purugganan MD, Fuller DQ: The nature of selection during plant domestication. Nature 2009, 457:843–8.

16. Rivabene R, Mancini E, De Vincenzi M: In vitro cytotoxic effect of wheat gliadin-derived peptides on the Caco-2 intestinal cell line is associated with intracellular oxidative imbalance: implications for coeliac disease. Biochimica et biophysica acta 1999, 1453:152–60.

17. Sander GR, Cummins AG, Henshall T, Powell BC: Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins. FEBS letters 2005, 579:4851–5.

18. Semple RK, Chatterjee VKK, O’Rahilly S: PPAR gamma and human metabolic disease. The Journal of clinical investigation 2006, 116:581–9.

19. Shewry PR: Wheat. Journal of experimental botany 2009, 60:1537–53.

20. Soares FLP, de Oliveira Matoso R, Teixeira LG, Menezes Z, Pereira SS, Alves AC, Batista NV, de Faria AMC, Cara DC, Ferreira AVM, Alvarez-Leite JI: Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression. The Journal of nutritional biochemistry 2012:2–8.

21. van den Broeck HC, de Jong HC, Salentijn EMJ, Dekking L, Bosch D, Hamer RJ, Gilissen LJWJ, van der Meer IM, Smulders MJM: Presence of celiac disease epitopes in modern and old hexaploid wheat varieties: wheat breeding may have contributed to increased prevalence of celiac disease. TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik 2010, 121:1527–39.

22. Volta U, Tovoli F, Cicola R, Parisi C, Fabbri A, Piscaglia M, Fiorini E, Caio G: Serological tests in gluten sensitivity (nonceliac gluten intolerance). Journal of clinical gastroenterology 2012, 46:680–5.

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