Encyclopedia of Evolutionary Psychological Science

Living Edition
| Editors: Todd K. Shackelford, Viviana A. Weekes-Shackelford


  • Christine LalondeEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-16999-6_731-1



A medical condition in which arterial blood pressure remains abnormally elevated, classically >140/90 mmHg.


The development of a maladaptive health disorder may seem counterintuitive to the evolution and fitness of a species; however, pathologies such as hypertension are the result of a biological response to inadequate environments that may have been in favor of survival for previous generations.

Blood Pressure

All organ systems within the body receive energy and oxygen via blood transportation; in larger animals and humans, this transportation requires a significant vascular system to deliver these nutrients to the furthest organs and tissues (Weder 2007). The strength of the blood pressing against arterial walls is defined as blood pressure, and this pressure rises and falls with the heart’s synchronous pumping as it is forced through the cardiovascular system. Blood pressure is measured at its maximum, during contraction of the heart (systolic), and at its minimum, the resting state between two heartbeats (diastolic), and is presented as a ratio measured in units of millimeters of mercury (mmHg). Normotensive or normal blood pressure is defined as 120/80 mmHg or lower (Hypertension Canada 2015; Whelton et al. 2018). The volume of the blood being pumped through this system affects the blood pressure, with increased volume forcing excess cardiac output. Two salts, sodium and potassium, are required in a balanced state to stimulate the kidneys to remove excess water from the body; when sodium is present in excess, the ability of the kidneys to remove water is inhibited and plasma volume increases, forcing blood pressure to increase, which may develop into the health disorder, hypertension.


Hypertension develops in response to extended periods of stress, whereby the body attempts to adapt through increased energy consumption or, the other way around, stress comes in the form of excess energy input and the body has an incapacity to utilize the abundant resources. Stress can be defined as anything that poses a threat to the health or survival of an organism, such as bacterial infections, inadequate nutrient intake, injury, or even mental trauma. Many organisms, including humans, are often driven to increase available energy to fuel the metabolic demand of dealing with a stressful event (Pettit and DeBarr 2011; Torres and Nowson 2007). Chronic stress can lead to increased stores of glucose and/or sodium, increasing risk of a number of disorders, including hypertension. The classical diagnosis of hypertension is repeated measures of blood pressure greater than 140/90 mmHg; however, some medical professionals are treating patients with measurements greater than 130/80 mmHg (Daskalopoulou et al. 2018). Short-term high blood pressure can be harmless; however, chronically it has been linked to a cascade of health issues such as cardiovascular diseases, stroke, vision loss, dementia, and metabolic syndrome.

Thrifty Gene and Salt Hypotheses

A promising concept was developed in 1962 by James Neel, named the thrifty gene hypothesis, which predicted diabetes and obesity were diseases that have developed as a survival adaptation, a remnant of the early evolution of the human species. Early humans were faced with famine, immune threats, and disease. The thrifty gene hypothesis argues that for early ancestors who were able to retain the most out of consumed nutrients, a blood pressure sensitivity would increase their chances of survival by maintaining normotension during low-sodium conditions. These ancestors would pass along their genotype to their offspring, propagating a line of humans suited for conservation of nutrients in times of deficit. As noted, sodium consumption plays a significant role in blood pressure regulation, and Gleibermann (1973) proposed a sodium hypothesis that describes a drive by our ancestors who lived in hot, arid climates, to consume salt to replenish loss from sweat. The readily available, abundant, and nutrient-rich foods in industrialized nations render these proposed evolutionary genotypes maladaptive, rather than efficient, leading to the development of hypertension and other metabolic disorders (Weder 2007).

These theories have been met with criticism over the past few decades, predominantly over genotypes and population studies. Gosling et al. (2015) argues that, during times of nutritional abundance and deficit, these theories do not hold true for Pacific Island populations, noted to be the exemplary model for the thrifty gene hypothesis. A lack of genetic markers linking diseases to metabolic disorders, Gosling continues that the hypothesis has failed to provide sufficient evidence in its current definition. Different conceptions of the thrifty gene hypothesis, however, are presently driving research in the growing field of epigenetics and fetal programming.

Barker Hypothesis

In 1992, Hales and Barker devised the thrifty phenotype or Barker hypothesis which stipulates that stress in the prenatal environment correlates to the expression or inhibition of genes linked the metabolic consumption. This influences the physiology and metabolism of the fetus through permanent changes in transcription factors, a process termed fetal programming. During significant acute or chronic stress, steroidal hormones called glucocorticoids are released into the circulatory system from the mother, in high concentrations, and are able to overcome an enzymatic placental barrier that usually suppresses the passage of hormones to the fetus (Seckl and Holmes 2007). Infection, injury, or lack of adequate nutrition during pregnancy all present either acute or chronic stress states that can lead to increased levels of circulatory hormones during critical and sensitive periods of fetal growth. Glucocorticoids can inactivate or silence genes that are sensitive to metabolism, predisposing offspring to hypertension when faced with nutrient abundance or stress of their own. Research involving both humans, such as Holocaust survivors, and nonhuman animals currently supports this hypothesis providing evidence of links between early-life stress, glucocorticoids, and hypertension (Keinan-Boker et al. 2015; Nguyen et al. 2015).


Adaptation to novel environments promotes the survival of a species; however, total adaption can produce complications when environmental conditions change (Weder 2007). Humans have adapted to environments deficient (or at least lower) in nutritional support and, as such, are now faced with current health challenges linked to abundant resources. The correlation between the availability of nutrients and the presence of early-life stress suggests that the fetus is provided with information about its probable environment; the Barker hypothesis claims maternal nutrition and the presence of hormones adjust the phenotype through silencing or activation of genes to enhance the fetus’ ability for survival. If the fetus were born in a nutrient-deficient environment, the sensitivity to dietary sodium and other nutrients would enhance available energy and cardiovascular circulation required to deal with stress; conversely, this phenotype may lead to the development of a number of health disorders, such as hypertension.



  1. Daskalopoulou, S. S., Rabi, D. M., Schiffrin, E. L., Feldman, R. D., Padwal, R. S., Tremblay, G., & Khan, N. A. (2018). Hypertension guidelines in the United States and Canada: Are we getting closer? Hypertension, 71(6), 976–978.CrossRefGoogle Scholar
  2. Gleibermann, L. (1973). Blood pressure and dietary salt in human populations. Ecology of food and nutrition, 2(2), 143–156.CrossRefGoogle Scholar
  3. Gosling, A. L., Buckley, H. R., Matisoo-Smith, E., & Merriman, T. R. (2015). Pacific Populations, Metabolic Disease and ‘Just-So Stories’: A Critique of the ‘Thrifty Genotype’ Hypothesis in Oceania. Annals of human genetics, 79(6), 470–480.CrossRefGoogle Scholar
  4. Hales, C. N., & Barker, D. J. (1992). Type 2 (non-insulin-dependent) diabetes mellitus: The thrifty phenotype hypothesis. Diabetologia, 35(7), 595–601.CrossRefGoogle Scholar
  5. Hypertension Canada. (2015). Hypertension Canada guidelines. http://guidelines.hypertension.ca. Accessed 09 July 2018.
  6. Keinan-Boker, L., Shasha-Lavsky, H., Eilat-Zanani, S., Edri-Shur, A., & Shasha, S. M. (2015). Chronic health conditions in Jewish Holocaust survivors born during World War II. The Israel Medical Association Journal: IMAJ, 17(4), 206–212.PubMedGoogle Scholar
  7. Neel, J. V. (1962). Diabetes mellitus: A “thrifty” genotype rendered detrimental by “progress”? American Journal of Human Genetics, 14(4), 353.PubMedPubMedCentralGoogle Scholar
  8. Nguyen, P., Khurana, S., Peltsch, H., Grandbois, J., Eibl, J., Crispo, J., … Tai, T. C. (2015). Prenatal glucocorticoid exposure programs adrenal PNMT expression and adult hypertension. Journal of Endocrinology, 227(2), 117–127.CrossRefGoogle Scholar
  9. Pettit, M. L., & DeBarr, K. A. (2011). Perceived stress, energy drink consumption, and academic performance among college students. Journal of American College Health, 59(5), 335–341.CrossRefGoogle Scholar
  10. Seckl, J. R., & Holmes, M. C. (2007). Mechanisms of disease: Glucocorticoids, their placental metabolism and fetal ‘programming’ of adult pathophysiology. Nature Clinical Practice Endocrinology & Metabolism, 3(6), 479–488.CrossRefGoogle Scholar
  11. Torres, S. J., & Nowson, C. A. (2007). Relationship between stress, eating behavior, and obesity. Nutrition, 23(11–12), 887–894.CrossRefGoogle Scholar
  12. Weder, A. B. (2007). Evolution and hypertension. Hypertension, 49, 260–265.CrossRefGoogle Scholar
  13. Whelton, P. K., Carey, R. M., Aronow, W. S., Casey, D. E., Collins, K. J., Himmelfarb, C. D., … MacLaughlin, E. J. (2018). 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology, 71(19), e127–e248.Google Scholar

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© Springer Nature Switzerland AG 2018

Authors and Affiliations

  1. 1.Laurentian UniversitySudburyCanada

Section editors and affiliations

  • Steven Arnocky
    • 1
  1. 1.Department of Psychology, Faculty of Arts and SciencesNipissing UniversityNorth BayCanada