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The 3 S's Part II - Stress

I have been wanting to release this for a while now, but unfortunately other projects have kept getting in the way. Now, it would be easy to simply get stressed out about the delay, but then I wouldn't be heeding my own advice. So let's just dive a little deeper here in Part II and focus in on stress. If you missed Part I, check it out here!

All life, from bacteria, through plants, to animals including humans have had to deal with and adapt stress on varying levels. It's an inescapable part of life. When it is acute or short term, it can actually be beneficial, but it is the general, chronic stresses of modern every day life that tends to be the problem.

When using the ancestral framework with respect to nutrition and lifestyle, it is easy to get caught up in trying to make it a reenactment. But this is a mistake, it should only be that, a framework. We shouldn't avoid grains and legumes, or processed foods simply because our ancestors did, but rather because represent novel foods that perhaps our bodies have not had adequate time to adapt to.

For example, lactose intolerance is the genetic norm; however, some populations in Europe adapted to environmental stressors and developed lactase persistence, or the ability to digest the lactose sugar found in milk, after weaning from their mother [1]. Similarly, selective pressures increased the expression of the amylase enzyme, essential to the digestion of starches [2].

But back to the stress we came here to talk about. As we discussed last time, in the event a lion came to eat you, you want to be able to fight or run away, i.e. “fight or flight.” In a more modern example, think about how your body reacts if you almost get into a car accident. You get a quick surge of adrenaline, your heart rate goes up, you may even yell at the person in the other car, but eventually your body returns back to baseline, to homeostasis.

Now, the body wants to be in that homeostasis at all times and while it has adapted to be able to handle those acute stressors, the things we deal with today are often entirely novel. As such, just as with diet, our bodies simply do not know how to deal with chronic and prolonged stress efficiently. This dysregulation sets off a cascade of deleterious effects on various body systems, including metabolism, circulation, immune/inflammatory response, reproduction and the microbiome [3, 4, 5].

In part one, we briefly touched upon some of the stress response, but let's really dive in now. When the stress response is initiated, it affects the hypothalamus-pituitary-adrenal (HPA) axis. The hypothalamus is activated and secretes corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH). This activates the adrenals to produce cortisol, dopamine, norepinephrine and epinephrine [6]. To see this a little better, take a look at the bottom section of the graphic.

All of this makes sense insomuch as it will raise the blood pressure and release sugar and fatty acids for energy, as well as increase alertness and muscle tension, so as to mount a prepared response [7]. Again, if this is an acute response, it is not a problem. Have I said that enough? But what happens in the chronic situation?

Well referring back to the figure again, the hypothalamus also releases thyrotropin-releasing hormone (TRH), which tells the pituitary to secrete thyroid-stimulating hormone (TSH). In turn, the thyroid produces thyroxine (T4), which converts into the more biologically active triiodothyronine (T3) [8]. This is known as the HPT axis and it is inexorably linked to the HPA axis. The chronic release of CRH and cortisol will down-regulate, or decrease, the production of TSH and T4, subsequently impairing thyroid function [9].

Moreover, dysregulation of the sympathetic nervous system, particularly the HPA and HPT axes, is associated with the development of obesity and metabolic syndrome [10, 11, 12], as well as psychological issues and sleep disturbance [13, 14, 15]. Unfortunately, in the latter case, given the relationship between the thyroid and neurotransmitters, such as serotonin and dopamine, the drugs given for psychological conditions may actually further impair thyroid function [16].

So, now we have a looked a little bit at how our body immediately reacts to stress and some of the many other systems negatively impacted by chronic, prolonged stress, but let's examine some other ways stress can impact us. As we have previously discussed, our gut and the bacteria that inhabit it have a reciprocal relationship with respect to reacting to stress. Stress is able to increase intestinal permeability, bacterial overgrowth and the subsequent bacterial release of the endotoxin, lipopolysaccharide (LPS) [17, 18]. This increased LPS circulation can then result in neurological and metabolic dysregulation within the body [19, 20], which brings everything back full circle.

If that weren't enough, among the micronutrients depleted by chronic stress are vitamins A, B1, B2, B3, B5, B6, B7, B9, B12, choline, C, D, E, calcium, chromium, copper, iodine, iron, magnesium, potassium, selenium, zinc, omega-3 and carnitine [21]. That laundry list represents many of the same nutrients required for maintenance of proper hormonal/neurotransmitter function, intestinal wall integrity and proper metabolism.

Again, are we starting to see the importance of managing our stress??

Now, to be clear, this article and the graphic I created are not intended to be a comprehensive picture of all the issues that may develop from stress. There are many other immensely important systems that I did not include or only peripherally addressed, such as the heart, liver, kidneys and reproductive organs. Moreover, the graphic was not meant to stress you out more. The point was to simply try to elucidate the magnitude of things affected by stress.

I'll be discussing more in the following parts of this series, so stay tuned! But if you really want to dive right in, be sure to check out the Primal90 Program, it features continually updated information from some of the brightest minds in the world on nutrition, health and lifestyle!


1) Itan, Y., Powell, A., Beaumont. M.A., Burger, J. & Thomas, M.G. (2009). The origins of lactase persistence in Europe. PLoS Comput Biol. Vol. 5(8):e1000491.

2) Perry, G.H., Dominy, N.J., Claw, K.G., Lee, A.S., Fiegler, H., Redon, R., Werner, J., Villanea, F.A., Mountain, J.L., Misra, R., Carter, N.P., Lee, C. & Stone, A. C. (2007). Diet & the evolution of human amylase gene copy number variation. Nat Genet. Vol. 39(10):12561260.

3) Segerstrom, S.C. & Miller, G.E. (2004). Psychological stress & the human immune system: A meta-analytic study of 30 years of inquiry. Psychol Bull. Vol. 130(4):601-630.

4) Tamashiro, K.L., Sakai, R.R., Shively, C.A., Karatsoreos, I.N. & Reagan, L.P. (2011). Chronic stress, metabolism & metabolic syndrome. Stress. Vol. 14(5):468-474.

5) Dinan, T.G. & Cryan, J.F. (2012). Regulation of the stress response by the microbiota: Implications for psychoneuroendocrinology. Psychoneuroendocrinology. Vol. 37(9):1369-1378.

6) Xiong, F. & Zhang, L. (2013). Role of the hypothalamic-pituitary-adrenal axis in developmental programing of health & disease. Front Neuroendocrinol. Vol. 34(1):27-46.

7) Goldstein, D.S. (2010). Adrenal responses to stress. Cell Mol Neurobiol. Vol. Vol. 30(8):1433-1440.

8) Fekete, C. & Lechan, R.M. (2014). Central regulation of hypothalamic-pituitary-thyroid axis under physiological & pathological conditions. Endocrine Res. Vol. 35(2):159-194.

9) Ranabir, S. & Reetu, K. (2011). Stress & hormones. Indian J Endocrinol Metab. Vol. 15(1):18-22.

10) Bose, M., Oliván, B. & Laferrère, B. (2010). Stress & obesity: The role of the hypothalamic-pituitary-adrenal axis in metabolic disease. Curr Opin Endocrinol Diabetes Obes. Vol. 16(5):340–346.

11) Gyawali, P., Takanche, J.S., Shrestha, R.K., Bhattarai, P., Khanal, K., Risal, P. & Koju, R. (2015). Pattern of thyroid dysfunction in patients with metabolic syndrome & its relationship with components of metabolic syndrome. Diabetes Metab J. Vol. 39(1):66-73.

12) Moreira, M.C., Pinto, I.S., Mourão, A.A., Fajemiroye, J.O., Colombari, E., Reis, Â.A., Freiria-Oliveira, A.H., Ferreira-Neto, M.L. & Pedrino, G.R. (2015). Does the sympathetic nervous system contribute to the pathophysiology of metabolic syndrome? Front Physiol. Vol. 6:234:11pp.

13)Chakrabarti, S. (2011). Thyroid functions & bipolar affective disorder. J Thyroid Res. Vol. 2011:306367.

14) Holsen, L.M., Lancaster, K., Klibanski, A., Whitfield-Gabrieli, S., Cherkerzian, S., Buka, S. & Goldstein, J.M. (2013). HPA-axis hormone modulation of stress response circuitry activity in women with remitted major depression. Neuroscience. Vol. 250:733-742.

15) Xia, L., Chen, G.H., Li, Z.H., Jiang, S. & Shen, J. (2013). Alterations in hypothalamus-pituatary-adrenal/thyroid axes & gonadotropin-releasing hormone in the patients with primary insomnia: A clinical research. PLoS ONE. Vol. (8):e71065:6pp.

16) Bou Khalil, R. & Richa S. (2011). Thyroid adverse effects of psychotropic drugs: A review. Clin Neuropharmacol. Vol. 34(6):248-255.

17) Bures, J., Cyrany, J., Kohoutova, D., Förstl, M., Rejchrt, S., Kvetina, J., Vorisek, V. & Kopacova, M. (2010). Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. Vol. 16(24):2978-2990.

18) Campbell, A.W. (2014). Autoimmunity & the gut. Autoimmune Dis. Vol. 2014:152428.

19) Maes, M., Kubera, M. & Leunis, J.C. (2008). The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuro Endocrindol Lett. Vol. 29(1):117-124.

20) Festi, D., Schiumerini, R., Eusebi, L.H., Marasco, G., Taddia, M. & Colecchia, A. (2014). Gut microbiota & metabolic syndrome. World J Gastroenterol. Vol. 20(43):16079-16094.

21) Calton, J. & Calton, M. (2015). The micronutrient miracle: The 28-day plan to lose weight, increase your energy, and reduce disease. New York, NY: Rodale.

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