Diet-induced Stress: It’s well known that excessive stress can be detrimental to our health. As a result, we hear about the importance of stress reduction as an essential component of overall wellness. But certain types of stress are beneficial and can even lead to positive adaptations in the body. The key is to understand the body’s response to stress. With this knowledge, we can use stress to our advantage but also recognize when too much can have negative consequences.
Diet-induced Stress: What is stress?
When discussing stress, most people automatically think of external stressors. External stressors can be caused by anything that disrupts a person’s sense of well-being or challenges homeostasis in the body[1]. The body responds with a biological reaction known as “fight or flight.” This reaction is hardwired into our physiology. In fight or flight, the body releases stress hormones so that it is primed to react to a perceived threat. Through biological adaptations such as an increase in blood flow, heart rate, and blood sugar, the body is ready to respond – even if the danger isn’t really there. Physiological stress can be caused by three main stressors: environmental, intrinsic, and aging[2].
While long-term or chronic stress can be bad for us, we can use short-term physiological stress to our benefit through dietary changes.
How can we use stress to benefit our health?
It’s known that some stress is good for us as it can increase our focus and productivity. As shown in a bell-shaped curve known as Yerkes–Dodson Law, too little stress can cause us to be lethargic and underperform, while too much stress can lead to burnout and poor health[3]. It is diet-induced stress that falls right in the middle that can improve our performance and our health.
The body is smart and will work hard to return to a state of homeostasis whenever possible. This is illustrated with the health benefits seen for both keto and fasting lifestyles. When nutrients are removed from the diet, certain hormonal adaptations will occur that we can use to our benefit. The reduction in cellular inflammation that is seen as a result of following these diets is simply a response to stress when the body moves into survival mechanisms[4]. Autophagy, a significant benefit behind both fasting and ketosis, is a stress response. When the body believes it does not have the nutrients needed to turn on pathways for growth, it instead focuses on cellular clean up and repair[5].
Autophagy is closely linked to another adaptation to stress known as the mTOR pathway. The mTOR pathway signals for cellular growth and division and is upregulated during times of nutrient availability[6]. When nutrients are scarce, as with fasting, the pathway is inhibited, allowing for autophagy and fat breakdown to occur. Similarly, ketosis is another physiological adaptation to stress. When the body is not taking in carbohydrates that are easily converted to glucose, it switches to the utilization of fat for energy to maintain cellular homeostasis. And this process, as we know, has significant health benefits.
Diet-induced Stress: How much physiological stress is too much?
Despite all of these benefits, prolonged stress of any kind can damage our health. Over time chronic stress can lead to literal “wear and tear” on the body. As a response to the constant release of stress hormones, the body can experience such adverse health outcomes as heart disease, diabetes, cognitive dysfunction, and more[7].
The same negative adaptations can occur when the body is in a state of physiological stress response for too long due to a restricted diet. While the body is brilliant at adapting to maintain homeostasis, prolonged stress can counteract any primary health benefits. To protect itself, the body will respond with survival adaptations if the stress goes on too long. In the case of dietary changes (as with fasting or ketosis), people can start to experience negative health outcomes after initial positive changes. The body becomes concerned about missing out on nutrients.
For example, while the health benefits of following a keto diet are numerous, some people can experience increases in fatigue or micronutrient deficiencies when strictly followed long-term[8]. While this can happen with both sexes, women are especially sensitive to dietary stress due to the complex nature of female sex hormones[9]. In one study comparing keto in male and female mice, the males continued to lose weight over time, but the women started to gain[10]. The stress hormone cortisol can also lead the body to store fat and disrupt normal hormone signaling[11]. The metabolic rate can also decrease while hunger cues can increase as the body attempts to signal the perceived threat of caloric deprivation.
Diet-induced Stress: How to balance the impact of stress on the body
Stress management techniques are taught to support stress resilience or the ability to minimize the adverse effects of stress. The same can be said for creating resilience in the body’s metabolic adaptations. Specific dietary strategies can help the body to feel “safe,” so it can decrease the signaling of certain survival mechanisms. This can be accomplished by cycling through fasting, keto, and periods of increased carbohydrates, or what I call diet variation.
This process of diet variation helps the body move out of fight or flight mode by reducing the perceived risk of starvation. Diet variation not only helps to support the continuation of the favorable metabolic adaptations from fasting and keto but also helps achieve weight loss. Cycling with planned periods of fasting and increased carbohydrates (from appropriate sources) can help you obtain benefits while keeping the body feeling “safe.”
In summary, while stress is usually associated with harmful health outcomes, some types of stress can be beneficial. The positive biological responses associated with fasting or following the keto diet are a result of the body’s adaptation to stress. While these survival mechanisms can improve our health initially, the body may perceive prolonged restriction of nutrients as a threat of starvation. As a result, cycling through periods of varying intake of nutrients can counteract the potential of any negative health risks.
References:
[1] Yaribeygi, Habib, Yunes Panahi, Hedayat Sahraei, Thomas P. Johnston, and Amirhossein Sahebkar. “The Impact of Stress on Body Function: A Review.” EXCLI Journal 16 (July 21, 2017): 1057–72. https://doi.org/10.17179/excli2017-480.
[2] Kagias, Konstantinos et al. “Neuronal responses to physiological stress.” Frontiers in genetics vol. 3 222. 26 Oct. 2012, doi:10.3389/fgene.2012.00222
[3]Cohen, Ronald A. “Yerkes–Dodson Law.” In Encyclopedia of Clinical Neuropsychology, edited by Jeffrey S. Kreutzer, John DeLuca, and Bruce Caplan, 2737–38. New York, NY: Springer, 2011. https://doi.org/10.1007/978-0-387-79948-3_1340.
[4]Longo, Valter D, and Mark P Mattson. “Fasting: molecular mechanisms and clinical applications.” Cell metabolism vol. 19,2 (2014): 181-92. doi:10.1016/j.cmet.2013.12.008
[5] de Cabo, Rafael, and Mark P Mattson. “Effects of Intermittent Fasting on Health, Aging, and Disease.” The New England journal of medicine vol. 381,26 (2019): 2541-2551.
[6] Porta, Camillo et al. “Targeting PI3K/Akt/mTOR Signaling in Cancer.” Frontiers in oncology vol. 4 64. 14 Apr. 2014, doi:10.3389/fonc.2014.00064
[7]https://pubmed.ncbi.nlm.nih.gov/15677391/
[8][8] Shilpa, Joshi, and Viswanathan Mohan. “Ketogenic diets: Boon or bane?.” The Indian journal of medical research vol. 148,3 (2018): 251-253. doi:10.4103/ijmr.IJMR_1666_18
[9] Santin, Ana Paula, and Tania Weber Furlanetto. “Role of estrogen in thyroid function and growth regulation.” Journal of thyroid research vol. 2011 (2011): 875125. doi:10.4061/2011/875125
[10] Sex Differences in the Response of C57BL/6 Mice to Ketogenic Diets
JESSE COCHRAN, PAUL V. TAUFALELE, KEVIN D. LIN, YUAN ZHANG, E. DALE ABEL
Diabetes Jul 2018, 67 (Supplement 1) 1884-P; DOI: 10.2337/db18-1884-P
[11] Stimson, Roland H et al. “Dietary macronutrient content alters cortisol metabolism independently of body weight changes in obese men.” The Journal of clinical endocrinology and metabolism vol. 92,11 (2007): 4480-4. doi:10.1210/jc.2007-0692
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