In the footnotes of my previous post, I remarked that there appeared to be a correlation between starch consumption, salivary a-amylase activity, and stress responses in the human body. My thanks to Melchior, who passed on to me Pruimboom’s speculations regarding starch augmenting sympathetic nervous response.
Salivary a-amylase serves the purposes of predigesting starch in the human body, instigating its hydrolysis into more easily assimilated carbohydrate derivatives (the sugars maltose and glucose), where it is subsequently absorbed through the intestinal wall. As the caloric intake from starches increases, generally, so too does a-amylase activity.
Intriguingly, a number of studies in various disciplines have demonstrated a correlation between salivary a-amylase activity and stress, which by extension suggests that starch consumption augments sympathetic nervous response and engenders a state of fight-or-flight and hyperarousal. Nater et al. have documented increases in enzyme concentrations in participants who undergo physical and psychological stresses, such as being shown disturbing images of mutilation or accidents.[1] Similarly, Ljungberg et al. and Chatterton et al. have both recorded increases in SNS activity and a-amylase with physical exertion, along with engaging in dangerous or frightening activities (i.e.: skydiving).[2] These findings demonstrate a strong correlation between rises in norepinephrine and a-amylase activity in response to stress.[3] In addition, other studies have detailed elevations in both cortisol and a-amylase in reaction to stressful stimuli, finding a positive association between the two.[4]For an extensive review of the literature pertaining to salivary a-amylase as a biomarker for stress, please see Granger et al. 2007.[5]Ultimately, elevations in amylase appear to serve in the greater scheme of biological coping mechanisms to deal with states of acute stress.
In my previous post I discussed the significance of Perry et al.’s findings: that high-carbohydrate diets are strongly correlative with elevated salivary a-amylase expression, and that the human populations consuming them have more AMY1 copies than those consuming lower levels of starch.[6]It appears to be axiomatic that levels of a-amylase and expression are associated with the amount of starch in the diet. Extending this idea further, one could propose that lower a-amylase activity would temper the breakdown of starch into sugar, lessening the glycemic response and caloric availability.[7]
It appears likely that high-carbohydrate consumption engenders increases in SNS activation in the body, suppressing immunity, and augmenting the accumulation of fat. In fact, in 2007, Susman et al. found a positive association between elevated a-amylase activity and high BMI and in adolescents..[8]The evidence from evolutionary biology suggests that the adaptation and expression of the amylase gene in humans arose as a survival mechanism, resulting from the need to obtain energy from starches in famine situations. Since prehistory, the ingestion of starches has signalled an increase in salivary a-amylase activity,and a-amylase and cortisol have been shown to escalate during stress. Consequently, these findings support the hypothesis that the consumption of starches signal environmental food shortage and famine in the body, which commences energy conservation and fat accumulation accordingly.[9]
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EDIT: Additional material regarding amylase: Kataoka and Dimagno (1999) have documented how alpha-amylase inhibitors - which block the action of amylase - slow the rate of digestion and gastric emptying.
In addition, smoking appears to be associated with lower salivary a-amylase activity - Kitavans, anyone? The "highly acidic aldehydes in tobacco smoke in-activate the a-amylase enzyme". See:
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EDIT: Additional material regarding amylase: Kataoka and Dimagno (1999) have documented how alpha-amylase inhibitors - which block the action of amylase - slow the rate of digestion and gastric emptying.
In addition, smoking appears to be associated with lower salivary a-amylase activity - Kitavans, anyone? The "highly acidic aldehydes in tobacco smoke in-activate the a-amylase enzyme". See:
Nagler, R., Lischnisky, S. and Diamond, E. 2000. "Effect of cigarette smoke on salivary proteins and enzyme activities." Archives of Biochemistry and Biophysics 379:229-36. See also: Granger et al. 2007.
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I might also add that in speaking to my friend Woo on facebook the other night on this subject, she too had previously come to the conclusion that GI biota alter to favour fat storage in response to stress and nutrient depletion. I won’t say any more, but I look forward to future posts by Woo (over at itsthewooo.blogspot.com) regarding her greater insights on this matter.
[1] Nater et al. 2005; Nater et. al. 2006; Arhakis et al. 2013.
[2] Chatterton et al. 1997.
[3] Ljungberg et al. 1997; Chatterton et al. 1996.
[4] Granger et al. 2007; Granger et al. 2006.
[5] Granger et al. 2007.
[6] Perry et. al. 2007.
[7] Susman et al. 2007; Granger et al. 2007.
[9] See Spreadbury 2012; and Miki Ben-Dor over at the PaleoStyle blog.
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References
Ader, R., Cohen, N. and Felten, D. 1995. Psychoneuroimmunology. Academic Press. San Diego, CA.
Arhakis, A. Karagiannis, V., and Kalfas, S. 2013. “Salivary Alpha-Amylase Activity and Salivary Flow Rate in Young Adults,” The Open Dentistry Journal 7:7-15.
Chatterton, R. T., Vogelsong, K. M., Lu, Y. C, Ellma, A. B. and Hudgens, G. A. 1996. “Salivary Α-Amylase as a Measure of Endogenous Adrenergic Activity,” Clinical Physiology 16:433-448.
Chatterton, R.T., Vogelsong K. M., Lu, Y.C. and Hudgens, G. A. 1997. “Hormonal Responses to Psychological Stress in Men Preparing for Skydiving,” Journal of Clinical Endocrinology Metabolism 82:2503–2509.
Susman, E. J., Granger, D. A., Dockary, S., Baldes, K. T., Heaton, J., and Dorn, L. D. 2007. “A Longitudinal Perspective On Alpha-Amylase, Body Mass Index, And Timing Of Puberty: Interactive Processes In Adolescents,” The Biennial Meeting of the Society for Research on Child Development, Boston.
Granger D. A., Kivlighan, K.T., Blair, C., El-Sheikh, M., Mize, J., Lisonbee, J. A., 2006. Integrating the Measurement of Salivary A-Amylase into Studies of Child Health, Development, and Social Relationships. Journal of Social and Personal Relationships 23:267–90.
Granger, D.A., Kivlighan, K. T., El-Sheikh, M., Gordis, E.B. and Stroud, L.R., 2007. “Salivary Alpha-Amylase in Biobehavioral Research: Recent Developments and Applications,” Annals of New York Academy of Sciences 1098:288-311.
Ljungberg, G., Ericson, T., Ekblom, B, and Birkhed, D. 1997. Saliva and marathon running (Scandinavian Journal of Medicine and Science in Sports 7:214-219.
Nater, U. M., Rohleder, N., and Gaab, J. 2005. “Human Salivary Alpha-Amylase Reactivity in a Psychosocial Stress Paradigm,” International Journal of Psychophysiology 55:333-42.
Nater, U. M., LaMarca, R., Florin, L., Moses, A., Landhans, W. and Koller, M. M. “Stress-Induced Changes in Human Salivary Alpha-Amylase Activity—Associations with Adrenergic Activity,” Psychoneuroendocrinology 31:49–58.
Perry, G. H, Dominy, N. J, Claw, K. G, Lee, A. S. and Fiegler, H. 2007. “Diet and the Evolution of Human Amylase Gene Copy Number Variation,” Nature Genetics 39:1256–1260.
Spreadbury, I. 2012. “Comparison with Ancestral Diets Suggests Dense Acellular Carbohydrates Promote an Inflammatory Microbiota, and may be the Primary Dietary Cause of Leptin Resistance and Obesity,”Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 5:175–189.
