Starch Correlation

The purpose of this lab was to assess any correlation between the AMY1 gene copy number and amylase concentration, as well as assess the relationship between amylase concentration and average starch consumption in ancestral diet. I had hypothesized that due to my South Asian descent I would have a moderate number of AMY1 gene copies and a moderate salivary amylase concentration. This hypothesis was based on the data presented by the Perry et al paper Diet and the evolution of the human amylase gene copy number variation, which claimed that ancestral starch diet influences the AMY1 gene copy number and that gene copy number and amylase concentration are strongly positively correlated. This is due to the gene evolution of the AMY1 gene being

The conclusion of the paper indicated a strong positive correlation between the number AMY1 gene copies, and amylase concentration, however, results from the lab resulted in an r value of 0.11 when looking at the gene copy number vs amylase concentration in the sample size of 24 reports from students, which indicates a weak positive correlation. The Perry et al. paper did cite some significant variance in their data, with an R2 value of 0.351. This is likely due to other factors influencing the gene expression, such as SNPs, or other external factors. Although the amylase concentration and the AMY1 gene copy number did not have a strong enough correlation to support the conclusions made by the Perry et al paper, figures 2 and 3 support the claim that those with more starch in their ancestral diet will have higher salivary amylase concentrations, although there were some outliers in the data. Generally, the average amylase concentration was highest for those who reported having high ancestral starch diets and lower for the moderate levels. Although only one data point was reported for low ancestral starch diet, it still followed the trend of a decreasing amylase concentration with decreased starch in the ancestral

First, the ancestral starch diet is largely self-reported and is based on assumptions of heritage and culture rather than population statistics or DNA analysis. Moreover, the methods used in this lab were prone to human error, such as inaccurate micro pipetting. In addition to this, my gene fragment volume from the PCR was extremely low. This could be due to a variety of factors, such as simple human errors, or primers binding to the wrong sequence (i.e binding with itself or binding with the second primer type). Regarding the conclusions drawn by Diet and the evolution of the human amylase gene copy number variation the sample size of L10 (n=24) was significantly smaller than that used by Perry et al. This small sample size does not accurately reflect the entire populations as external factors could influence the gene expression, such as SNPs, modified current diets, thirst levels, and stress levels (Perry et. al 2007). This could create outliers in the data, which is supported by the range error bars as seen in figure