I recently found a Wikipedia article (HERE) on a topic which made me really think about a critical element to what determines our overall height, which is our mental and emotional state.
We all know that genetics, sleep, nutrition, and exercise plays a role in determining our height, but what about our mental health? There are many claims going around the height increase and grow taller niche and one of them is that of using hypnosis. A lot of people state that for you to be taller, you have to really be positive and believe you WILL grow taller and increase your height. So the obvious question is. How much does our mental state affect our height?
From the article on Psychosocial Short Stature, it seems that the effects are really dramatic, at least when it some to how it can limit our grow if we are not in the healthiest of mental states.
From the wiki article…
Psychosocial short stature (PSS) or psychosocial dwarfism, sometimes called psychogenic or stress dwarfism, or Kaspar Hauser Syndrome, is a growth disorder that is observed between the ages of 2 and 15, caused by extreme emotional deprivation or stress.
The symptoms include decreased growth hormone (GH) secretion, very short stature, weight that is inappropriate for the height, and immature skeletal age. This disease is a progressive one, and as long as the child is left in the stressing environment, his or her cognitive abilities continue to degenerate. Though rare in the population at large, it is common in feral children and in children kept in abusive, confined conditions for extended lengths of time. It can cause the body to completely stop growing but is generally considered to be temporary; regular growth will resume when the source of stress is removed.
Children with PSS have extremely low levels of growth hormone. These children possibly have a problem with growth hormone inhibiting hormone (GHIH) or growth hormone releasing hormone (GHRH). The children could either be unresponsive to these hormones or too sensitive.
Children who have PSS exhibit signs of failure to thrive. Even though they appear to be receiving adequate nutrition, they do not grow and develop normally compared to other children of their age.
An environment of constant and extreme stress causes PSS. Stress releases hormones in the body such as epinephrine and norepinephrine, engaging what is known as the ‘fight or flight’ response. The heart speeds up and the body diverts resources away from processes that are not immediately important; in PSS, the production of growth hormone (GH) is thus affected. As well as lacking growth hormone, children with PSS exhibit gastrointestinal problems due to the large amounts of epinephrine and norepinephrine, resulting in their bodies lacking proper digestion of nutrients and further affecting development.
While the cure for PSS is questionable, some studies show that placing the child affected with the disease in a foster or group home increases growth rate and socialization skills.
Me: I asked a person I am working with on what she can find on the link between mental health and human growth and she pointed out two articles which I looked over. They are located HERE (resource 1) and HERE (resource 2).
From resource 1, HERE
Other endocrine interactions
Growth, reproductive function, and the thyroid axis are also influenced by stress system activation. In the acute setting of stress, glucocorticoids stimulate the growth hormone gene, leading to enhanced growth hormone secretion.53 However, with more prolonged stress, growth hormone release is suppressed by CRH‐induced elevations in somatostatin levels.54 This results in an inverse relationship between the diurnal concentrations of cortisol and growth hormone. Also, glucocorticoids directly inhibit growth hormone effects at target tissues by inhibiting insulin‐like growth factor‐1 (IGF‐1) and other growth factors.55 The effects of stress on the growth axis may account for the delay in growth often seen in chronic disease and emotional deprivation in childhood.
CRH, β‐endorphin, and glucocorticoids inhibit GnRH secretion from the hypothalamus. Glucocorticoids also suppress pituitary gonadotrophin release and inhibit gonadal tissue.56 Patients with illnesses associated with increased HPA‐axis activity, such as anorexia nervosa, hyperthyroidism, and malnutrition, may experience abnormalities of menstrual and reproductive function.57–,59
From resource 2, HERE
Me: I really coudn’t figure out the link to the study and how human height is effected. The conclusion is that behavior created from stress is from the Corticotropin-releasing hormone receptor, but don’t need the actual hormone. The Abstract below…
Stress-induced behaviors require the corticotropin-releasing hormone (CRH) receptor, but not CRH
- Stacie C. Weninger*†, Adrian J. Dunn‡, Louis J. Muglia†§, Pieter Dikkes¶, Klaus A. Miczek‖, Artur H. Swiergiel‡, Craig W. Berridge**, and Joseph A. Majzoub†‡‡
- *Program in Neuroscience, Howard Hughes Medical Institute, and †Division of Endocrinology and ¶Department of Neurology, Children’s Hospital, and Harvard Medical School, Boston, MA 02115; ‡Department of Pharmacology, Louisiana State University Medical Center, Shreveport, LA 71130; ‖Department of Psychology, Tufts University, Medford, MA 02155; and **Department of Psychology, University of Wisconsin, Madison, WI 53706
- Edited by Bruce S. McEwen, The Rockefeller University, New York, NY, and approved April 30, 1999 (received for review October 6, 1998)
Corticotropin-releasing hormone (CRH) is a central regulator of the hormonal stress response, causing stimulation of corticotropin and glucocorticoid secretion. CRH is also widely believed to mediate stress-induced behaviors, implying a broader, integrative role for the hormone in the psychological stress response. Mice lacking the CRH gene exhibit normal stress-induced behavior that is specifically blocked by a CRH type 1 receptor antagonist. The other known mammalian ligand for CRH receptors is urocortin. Normal and CRH-deficient mice have an identical distribution of urocortin mRNA, which is confined to the region of the Edinger–Westphal nucleus, and is absent from regions known to mediate stress-related behaviors. Since the Edinger–Westphal nucleus is not known to project to any brain regions believed to play a role in anxiety-like behavior, an entirely different pathway must be postulated for urocortin in the Edinger–Westphal nucleus to mediate these behaviors in CRH-deficient mice. Alternatively, an unidentified CRH-like molecule other than CRH or urocortin, acting through the CRH receptors in brain regions believed to mediate stress-induced behaviors, may mediate the behavioral response to stress, either alone or in concert with CRH.
Stress, defined as the response of the body to any threatening demand (1), can be broadly separated into physiological responses, including the stimulation of adrenal glucocorticoid secretion, and behavioral responses, including anxiety and fearful behavior. Alterations in the stress-response system are believed to underlie many anxiety-related disorders (2–5). Corticotropin-releasing hormone (CRH) has been implicated in both physiological and behavioral stress responses. CRH was identified by its ability to stimulate adrenocorticotropic hormone (ACTH) secretion from anterior pituitary corticotrophs, thus activating the hypothalamic–pituitary–adrenal (HPA) axis (6). In addition, infusion of CRH into the brain was found to cause stress-like behaviors (7), suggesting that CRH integrates physiological and behavioral activities into a generalized stress response. Subsequently, many other pharmacological studies have implicated CRH in the behavioral response to stressors. These studies confirmed that intracerebral infusion of CRH induces stress-like behaviors and additionally that intracerebral infusions of CRH antagonists blunt the behavioral response to a stressor (8–10). Furthermore, transgenic mice that overexpress CRH exhibit increased anxiety-like behavior (11).
The role of the CRH receptor in the behavioral stress response has been further evaluated. The two known CRH receptors, type 1 and type 2 (12), both consist of a 7-transmembrane helix functionally coupled to adenylate cyclase via Gs. For the most part, the anatomical distributions of the two CRH receptors are distinct, with the type 1 receptor expressed in the central nervous system in regions including neo-, olfactory, and hippocampal cortices, subcortical limbic structures in the septal region and amygdala, certain relay nuclei in the brainstem, and the cerebellum (13). One splice variant of the type 2 receptor is expressed in the periphery, whereas another splice variant is expressed in specific subcortical structures, the lateral septal nuclei, and the hypothalamus (14, 15). Two reports of mice lacking the CRH type 1 receptor have confirmed a role for this receptor in anxiety-related behavior (16, 17). CRH type 1 receptor-deficient mice display decreased anxiety-like behavior in the dark–light emergence task and the elevated-plus maze, both behavioral paradigms thought to measure anxiety in rodents. Both studies conclude that CRH mediates the behavioral responses to stressors by means of the CRH type 1 receptor (16, 17). More recently, a CRH type 1 receptor antagonist has been found to block both the acquisition and expression of stress-induced behaviors in rats (18).
Thus, the CRH type 1 receptor clearly mediates behavioral responses to stress, with the evidence to date implicating CRH as its most likely ligand (9, 10, 19). The other known mammalian ligand for CRH receptors is urocortin (20). Urocortin, acting either alone or in concert with CRH, is a potential mediator of in vivo stress responses, because in the studies cited above, infused or transgenically overexpressed CRH could act at receptor sites normally occupied by urocortin, and CRH antagonists could block urocortin actions as well as those of CRH (21). Therefore, we examined the role of CRH in this pathway by characterizing the behavioral responses to stressors of CRH-deficient (knockout, KO) mice (22) and the effects of CRH antagonists on these responses. We also examined the expression of urocortin mRNA in wild-type (WT) and CRH KO mouse brain to assess whether its distribution provides insight into its potential role in mediating stress-induced behaviors.
Me: What I can say is that stress does cause the human brain to release certain hormones that seems to inhibit the human longitudinal growth process. Here is my theory, from using evolutionary biology. The human body can be viewed as a system of work done that needs energy input. For the body/system to become bigger, it needs a lot more energy than before to even get it to grow to that size.
So, while you are still young, stay happy and dont get too stress out. There is really no good point and you won’t be inhibiting your growth process.
If we view stress, as a form of resistance or internal conflict, we can use the analogy froom physics that stress is like friction, which is lost energy. If we are losing the energy, we don’t have the energy to go through our growth spurts. So stress is taking away the energy our young bodys/minds need to make that quantum energy leap.
From the researcher, she states…
“cortisol is released during stress, and cortisol inhibits growth,….Yes, being in a happier less stressful situation, a person raising their chances of growing.”