Linear enamel hypoplasia and nutritional status

I just wanted to take down a note about this paper from last year, along with a couple of older studies of linear enamel hypoplasia:

Brief Communication: Linear enamel hypoplasia and the shift from irregular to regular provisioning in Cayo Santiago rhesus monkeys (Macaca mulatta)
Debbie Guatelli-Steinberg, Zeynep Benderlioglu
This study investigates changes in the prevalence of linear enamel hypoplasia (LEH) before and after the shift from irregular to regular provisioning in the Cayo Santiago rhesus monkey population. Prior to 1956, monkeys on this island colony did not receive consistent provisions, and were reported to be in poor health (Rawlins and Kessler [1986] The Cayo Santiago Macaques; Albany: State University of New York Press). A regular provisioning program, instituted in August 1956, resulted in the improved health of individuals and the growth of the population (Rawlins and Kessler [1986] The Cayo Santiago Macaques; Albany: State University of New York Press). LEH, a developmental defect of enamel, is a sensitive indicator of systemic physiological stress (Goodman and Rose [1990] Yrbk. Phys. Anthropol. 33:59-110). It was therefore hypothesized that the prevalence of LEH would be higher in monkeys who were irregularly provisioned than in monkeys who experienced regular provisioning. To test this hypothesis, teeth were examined for LEH in a sample of 181 female rhesus monkeys. The results support the hypothesis: the mean number of defects was statistically significantly higher in the preprovisioned group than it was in the postprovisioned one. When LEH prevalence was assessed using only defects occurring on antimeric pairs, the preprovisioned group again had a higher prevalence than the postprovisioned one, although the difference was not statistically significant, most likely because of the reduced sample size. The results of this study indicate that changes in LEH prevalence, at least in this population of rhesus monkeys, are associated with changes in nutritional status.

Other studies have shown a relationship between LEH prevalence and malnutrition among human populations. The unique aspects of this study are that it shows the same relationship in another primate species, and that it shows the response to a change in nutritional levels.

This response was shown in a human context by Alan Goodman and colleagues in 1991:

Nutritional supplementation and the development of linear enamel hypoplasias in children from Tezonteopan, Mexico
AH Goodman, C Martinez and A Chavez
The purpose of this study was to compare the effect of nutritional intake during tooth-crown formation on the subsequent development of linear enamel hypoplasias (LEHs) in Mexican nonsupplemented (control) adolescents (n = 42) and adolescents who had received daily nutritional supplements since birth (n = 42). The proportion of individuals with LEHs was nearly two-fold greater (74.4%; 95% CI 64.7-84.1%) in the control than in the supplemented group (39.5%; 95% CI 28.6-50.4%; chi 2 = 9.44; P = 0.001). Although the estimated peak age at formation, approximately 2-2.5 y, is similar in both groups, the proportion of early (before 1.5 y) and late (after 3.0 y) LEHs was greater in the control group. LEH was also more common in females and was associated with an increase in illness days and a decrease in growth velocity. Results of this study suggest that mild to moderate undernutrition during enamel formation is causally linked to the formation of LEHs.

The distribution shows that the two samples actually are very similar in the incidence of LEH at the modal age of between 1.5 and 2.5 years. Plausibly, this is not only attributable to disease, but also stress associated with weaning; some degree of LEH incidence may be more resistant to change by nutritional supplementation. Goodman et al. (1991:780) wrote:

The greatest relative difference in freuqency of LEH between supplemented and control groups occurs before 1.5 y and after 3.0 y, or before and after weaning and the time of greatest illness. It is as if all children are at great risk of LEH immediately after weaning, but the supplemented individuals are afforded greater protection before and after weaning. These data also support the hypothesis that common respiratory and gastrointestinal illnesses are an immediate cause of LEH, especially in individuals with compromised nutritional status.

Richard May, Alan Goodman and Richard Meindl conducted similar observations in Guatemala, reported in 1993:

Response of bone and enamel formation to nutritional supplementation and morbidity among malnourished Guatemalan children
Richard L. May, Alan H. Goodman, Richard S. Meindl
Enamel matrix secretion responded positively to increased supplementation. Children who received less than 34.25 kcal/day in supplement had more LEH than those who received more supplement. No differences in ossification status were found between supplementation groups. These data suggest that enamel formation may be more sensitive to changes in nutritional status than is bone mineralization. Disruptions of bone and enamel formation were both associated with frequent illness. Children who were ill more than 3.6% of the time had more LEH and fewer ossified hand-wrist centers than children who were less frequently ill. Conclusions regarding relative environmental sensitivity must take into account the specific aspects of dental and skeletal development examined.

This last part is an observation that different teeth seem to be more or less resistant to enamel formation disruptions.

References:

Guatelli-Steinberg D, Benderlioglu Z. 2006. Linear enamel hypoplasia and the shift from irregular to regular provisioning in Cayo Santiago rhesus monkeys (Macaca mulatta). Am J Phys Anthropol 131:416-419. doi:10.1002/ajpa.20434

Goodman AH, Martinez C, Chavez A. 1991. Nutritional supplementation and the development of linear enamel hypoplasias in children from Tezonteopan, Mexico. Am J Clin Nutr 53:773-781.

May RL, Goodman AH, Meindl RS. 1993. Response of bone and enamel formation to nutritional supplementation and morbidity among malnourished Guatemalan children. Am J Phys Anthropol 92:37-51. doi:10.1002/ajpa.1330920104