Volume 31, Issue 2
Published by AEGIS Communications
Global Nutrition Transition Challenges Oral Health
Cyril O. Enwonwu, ScD, PhD, MDS, BDS
What is malnutrition? Thousands of miles across the ocean in an African village, Abubakar sits pensively in his dilapidated poorly ventilated hut, crying, squealing in pain, and grasping his abdomen. The hunger is too great. He had to share a small bowl of rice and legumes with his three siblings. That was the last time he ate a “full” meal in 2 days, even though he walks several kilometers to his village school daily. Here in the US, across town in East Baltimore, Bob is overindulging in his usual mix of television, chips, soda, and candy. Obese, with no nearby health food store, he ignores his stomach cramps and continues to overeat. He has not eaten a fresh fruit or vegetable in weeks, and unlike Abubakar, he enjoys the luxury of a daily free bus ride to school.
Although residing on separate continents an ocean apart, both are malnourished. Malnutrition (deviant nutritional status) includes both undernutrition (short stature) and malnutrition of affluence (overweight and obesity).1 Malnutrition is as much about what we eat as it is about what we do not—either a lack of food or an overabundance of the wrong kinds of food, impacting both oral and systemic health. Malnutrition impairs immune function, elicits heightened susceptibility to infections, promotes poor development of organs, and constitutes a starting point and stimulus for failure in most biologic systems.
Science of Nutrition: A Global Enterprise
At least 300 million adults in the world are clinically obese (body mass index equal to or greater than 30 kg/m2), with widespread global childhood obesity.2 In the US alone, about 39% of adults and 16% of children and adolescents are obese. Driving the global obesity epidemic is overconsumption of energy with decreased energy expenditure. Even in many resource-poor developing countries, severe obesity is prevalent among relatively affluent urban dwellers exposed to nutrition transition (readily available, calorie-sufficient diet and abandonment of traditional foods) with increased consumption of animal fat, protein, and refined sugars.2-4 Tumor necrosis factor-a, a proinflammatory cytokine that is overexpressed in adipose tissue, activates several signal transduction cascades.2 Thus, inflammation is a key feature of obesity, and the latter is a major risk factor for several nutrition-related chronic diseases (NRCDs), such as type 2 diabetes mellitus, hypertension, cardiovascular disease (CVD), and some cancers.4,5 The link between prolonged inflammation and NRCDs is strong.2,5 Like the undernourished, obese individuals may also be micronutrient deficient, readily susceptible to infections, and may be at increased risk of bacteremia and prolonged wound healing time.1
With the rapid global shift toward diets linked with noncommunicable diseases notwithstanding, African villages are still characterized by infectious diseases, often complicated by malnutrition (particularly micronutrient deficiencies), which constitute the major causes of mortality and morbidity.1,4,5 Malnutrition in these communities usually commences in utero as a consequence of maternal malnutrition and poor health, resulting in intrauterine growth retardation and low birth weight. About 90% of the 25 million babies born annually weighing less than 2.5 kg are in developing countries. The legacy of intrauterine stress includes poor development of some organs/systems (eg, tooth enamel, cell-mediated immune function, brain, and kidneys) and a higher risk of obesity and NRCDs in later adult life.4,6,7 Recent studies indicate that an isocaloric but protein-restricted diet fed to pregnant rats causes changes in vascular endothelial function of offspring.8 This suggests endothelial dysfunction that underlies CVD in humans may start in utero. The scope of complex interactions between nutrition, infection, and immunity is now extended to include roles of specific nutrients (eg, resolvins and protectins derived from essential lipids) in modulating inflammation.9
The global burden of oral diseases is now fairly well characterized.10 These diseases include dental caries, periodontal inflammation, enamel dysplasia in the primary dentition, oral mucosal lesions (including noma), oropharyngeal cancers, and oral lesions associated with human immunodeficiency virus and autoimmune deficiency syndrome. Underprivileged populations are affected disproportionately by oral diseases,7,10-12 with most of these conditions sharing common risk factors with nutrition-related chronic systemic diseases.2,9,13 Inflammatory mediators play a key role in the pathogeneses. Chronic marginal protein malnutrition in children, for example, elicits changes in serum cytokines characteristic of a low-grade systemic inflammation.14,15 This is consistent with the author’s reported observations 40 years ago that malnourished “Osegere children, in comparison with the (well-fed) optimal community from the same ethnic group in Nigeria, suffer more severe periodontal disease than can be attributed solely to poor oral hygiene.”16 At that time, it was virtually sacrilegious to ascribe the genesis of inflammatory periodontal disease to factors other than oral plaque. What was not widely appreciated then was the close, complex interaction of nutrition-related inflammatory effects on both oral and systemic health.17
Poverty and malnutrition are key global factors impacting various parameters of human health, including growth and development, host resistance to infections, and general lifestyles. To solve the global nutrition challenges related to human health, we must adopt a broad approach that recognizes malnutrition in its various forms.5 While pockets of undernutrition still exist, particularly in the developing world, there is an urgent need to appreciate the concept of nutrition transition, which relates to large, rapid global shifts in dietary habits and physical activity patterns.18 The latter is exemplified by the high prevalence of worldwide adult and pediatric obesity rates.18 The growth of multinational food companies has saturated both urban and rural communities in every country with junk food, increasing the high prevalence of noncommunicable chronic oral and systemic diseases.
The author would like to thank Dionne Dougall-Bass and Carol Schadelbauer of Burness Communications in the development of this report.
1. Solomons NW. Malnutrition and infections: an update. Br J Nutr. 2007;98(suppl 1):S5-S10.
2. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860-867.
3. Jenkins DJ, Kendall CW, Marchie A, et al. Too much sugar, too much carbohydrate, or just too much. Am J Clin Nutr. 2004;79(5):711-712.
4. Caballero B. A nutrition paradox—underweight and obesity in developing countries. N Engl J Med. 2005;352(15):1514-1516.
5. Uauy R, Corvalan C, Dangour AD. Conference on “Multidisciplinary approaches to nutritional problems.” Rank Prize Lecture. Global nutrition challenges for optimal health and well-being. Proc Nutr Soc. 2009;68(1): 34-42.
6. Ingelfinger JR. Prematurity and the legacy of intrauterine stress. N Engl J Med. 2007;356(20):2093-2095.
7. Enwonwu CO. Influence of socio-economic conditions on dental development in Nigerian children. Arch Oral Biol. 1973;18(1): 95-107.
8. Rodford JL, Torrens C, Siow RCM, et al. Endothelial dysfunction and reduced antioxidant protection in an animal model of the developmental origins of cardiovascular disease. J Physiol. 2008;586(pt 19):4709-4720.
9. Van Dyke TE. The management of inflammation in periodontal disease. J Periodontol. 2008;79(suppl 8):1601-1608.
10. Petersen PE, Bourgeois D, Ogawa H, et al. The global burden of oral diseases and risks to oral health. Bull World Health Organ. 2005;83(9):661-669.
11. Enwonwu CO. Noma—the ulcer of extreme poverty. N Engl J Med. 2006;354(3):221-224.
12. Enwonwu CO, Phillips RS, Ferrell CD. Temporal relationship between the occurrence of fresh noma and the timing of linear growth retardation in Nigerian children. Trop Med Int Health. 2005;10(1):65-73.
13. Enwonwu CO, Ritchie CS. Nutrition and inflammatory markers. J Am Dent Assoc. 2007;138(1): 70-73.
14. Sauerwein RW, Mulder JA, Mulder L, et al. Inflammatory mediators in children with protein-energy malnutrition. Am J Clin Nutr. 1997;65(5): 1534-1539.
15. Enwonwu CO, Phillips RS, Savage KO. Inflammatory cytokine profile and circulating cortisol levels in malnourished children with necrotizing ulcerative gingivitis. Eur Cytokine Netw. 2005;16(3):240-248.
16. Enwonwu CO, Edozien JC. Epidemiology of periodontal disease in Western Nigerians in relation to socio-economic status. Arch Oral Biol. 1970;15(12): 1231-1244.
17. Johnson NW, Glick M, Mbuguye TN. (A2) Oral health and general health. Adv Dent Res. 2006;19(1):118-121.
18. Popkin BM. Global nutrition dynamics: the world is shifting rapidly toward a diet linked with noncommunicable diseases. Am J Clin Nutr. 2006;84(2): 289-298.
About the Author
Cyril O. Enwonwu, ScD, PhD, MDS, BDS
Paul G. Rogers Ambassador for Global Health Research
Microbial Pathogenesis and Oncology and Diagnostic Sciences
School of Dentistry
University of Maryland
Adjunct Professor of Biochemistry and Molecular Biology
School of Medicine
University of Maryland