HGH and Brain Trauma

Dr. Weeks’ Comment:  Brain trauma is terrifying and disrupts all aspects of a family’s life.  There is much offer to stack the cards in favor or regeneration.  HGH is one of the best options!   See below for other options also. 


J Neurotrauma. 2013 Jun 1;30(11):998-1006. doi: 10.1089/neu.2012.2705. Epub 2013 Jun 5.

Growth hormone replacement therapy in patients with traumatic brain injury.


In patients with severe traumatic brain injury (TBI), a growth hormone deficiency (GHD) is frequent and may contribute to the cognitive sequelae and reduction in quality of life (QoL). Recent studies have suggested thatGH replacement therapy (GHRT) can improve processing speed and memory. The aim of the study was to analyze the efficacy of GHRT on cognition, activities of daily living (ADL), and QoL and the factors that predicted and contributed to these effects. We included patients at least 1 year after their TBI and assessed pituitary functions (with stimulation tests), cognition (attention, memory, and executive function), participation in ADL and QoL. GHD was treated for at least 1 year in 23 patients, who were compared with 27 non-treated patients. Other deficiencies were also treated. Measurements were performed at baseline and 1 year later. An analysis of variance of the factors group and session (p ≤ 0.05) showed that most cognitive parameters had improved at 1 year (evidencing a session effect). A stronger effect of GHRT (i.e. a group x session interaction) was found for Rey Osterrieth complex figure recall and 2/6 domains in the QoL questionnaire (“personal” and “functional”). Trends (p ≤ 0.07) were also found for spatial orientation and immediate recall in the verbal memory test. Greatest improvements were associated with lower performance before treatment. The magnitude of the improvements in ADL and QoL was moderately correlated with the improvement in cognition. In conclusion, replacement therapy can improve cognition and QoL in patients with TBI who have GHD, especially in those with severe disabilities.

J Clin Endocrinol Metab. 2014 Jan;99(1):101-10. doi: 10.1210/jc.2013-2397. Epub 2013 Dec 20.

Prevalence of posttraumatic growth hormone deficiency is highly dependent on the diagnostic set-up: results from The Danish National Study on Posttraumatic Hypopituitarism.



Recent international guidelines suggest pituitary screening in patients with moderate and severe traumatic brain injury (TBI). Predominantly isolated GH deficiency (GHD) was reported in the literature, raising the question of potential methodological bias.


Our objective was to assess the prevalence of GHD in patients admitted in 2008 with TBI, with concurrent assessment of methodological bias.


We conducted a nationwide population-based cohort study at tertiary referral university hospitals.


Participants were Danish patients with a head trauma diagnosis from the Danish Board of Health diagnostic code registry; 439 patients and 124 healthy controls underwent dynamic assessment of GHsecretion 2.5 years (median) after TBI.


We evaluated the prevalence of GHD given use of 1) local versus guideline cutoffs, 2) insulin tolerance test (ITT), pyridostigmine (PD)-GHRH or GHRH-arginine (arg) test, 3) single versus repeated testing, and 4) GH assessment by assays with different isoform specificities.


The prevalence of GHD was lower by local than by guideline cutoffs (12% vs 19% [PD-GHRH/GHRH-arg, P<.001]; 4.5% vs 5% [ITT, P=.9]), and by ITT than by PD-GHRH/GHRH-arg (P=.006 [local cutoffs]; P<.001 [guideline cutoffs]). Only 1% of patients had GHD according to 2 tests. GH assessment by the Immulite or iSYS assay caused no significant diagnostic differences.


The study confirmed a high risk of bias in the management of pituitary testing of patients with TBI and stresses the importance of a proper control group and stringent GH testing including confirmatory testing in cohorts with low a priori likelihood of GHD such as in TBI. Our results question the evidence for newly introduced recommendations for routine pituitary assessment in TBI.

Curr Opin Endocrinol Diabetes Obes. 2013 Aug;20(4):354-8. doi: 10.1097/MED.0b013e32836318ba.

Neuroendocrine consequences of traumatic brain injury.



This article attempts to summarize findings of recent publications addressing the prevalence, effects, and treatment of pituitary hormone deficiency following traumatic brain injury (TBI).


A number of recent studies of TBI victims offer larger samples and much longer follow-up times. However, the prevalence of pituitary hormone deficiency continues to vary widely, underscoring the influence of patient selection, differences in endocrine testing, and patient’s comorbidities and age. Growth hormone deficiency (GHD) continues to be the most frequently detected type of pituitary dysfunction. Several reports show the influence of GHD on functional outcomes of TBI victims beyond what is predicted by traumaseverity. Emerging data support the notion growth hormone (GH) replacement as a useful intervention to improve symptomatology and functional outcomes among adequately selected GH-deficient patients recovering from TBI.


Pituitary dysfunction is prevalent following TBI. Pituitary dysfunction seems to influence functional outcomes in some patients recovering from brain injury. Adequately selected patients could benefit from hormonal replacement.

Neurosci Res. 2013 Aug;76(4):179-86. doi: 10.1016/j.neures.2013.03.014. Epub 2013 Apr 16.

Role of growth hormone (GH) in the treatment on neural diseases: from neuroprotection to neural repair.


Growth hormone (GH) is a pleiotropic hormone that exerts important functions in the control of braindevelopment as well as in the regulation neuronal differentiation and function, together with several behavioral and psychological effects that have been linked to its modulatory actions on brain neurotransmitters. In addition, the possibility that GH may play a role on brain repair after injury has been also envisaged, and a number of reports have shown that GH administration following injury confers neuroprotection and accelerates the recovery of some neural functions. In this review we have analyzed the state of the art of GHadministration in several neural diseases. Though more studies are still necessary in order to completely understand the importance of GH in these processes, the promising results obtained so far, together with the absence of untoward effects during GH therapy, encourages the development of clinical assays in order to further support the use GH treatment in neural diseases in which neuroprotection and/or neuroregeneration are involved.

Copyright © 2013. Published by Elsevier Ireland Ltd.

Scand J Trauma Resusc Emerg Med. 2013 Apr 20;21:33. doi: 10.1186/1757-7241-21-33.

Acute neuro-endocrine profile and prediction of outcome after severe brain injury.



The aim of the study was to evaluate the early changes in pituitary hormone levels after severe traumatic brain injury (sTBI) and compare hormone levels to basic neuro-intensive care data, a systematic scoring of the CT-findings and to evaluate whether hormone changes are related to outcome.


Prospective study, including consecutive patients, 15-70 years, with sTBI, Glasgow Coma Scale (GCS) score ≤ 8, initial cerebral perfusion pressure > 10 mm Hg, and arrival to our level one trauma university hospital within 24 hours after head trauma (n = 48). Serum samples were collected in the morning (08-10 am) day 1 and day 4 after sTBI for analysis of cortisol, growth hormone (GH), prolactin, insulin-like growth factor 1 (IGF-1), thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fT4), follicular stimulating hormone (FSH), luteinizing hormone (LH), testosterone and sex hormone-binding globulin (SHBG) (men). Serum for cortisol and GH was also obtained in the evening (17-19 pm) at day 1 and day 4. The first CT of the brain was classified according to Marshall. Independent staff evaluated outcome at 3 months using GOS-E.


Profound changes were found for most pituitary-dependent hormones in the acute phase after sTBI, i.e. low levels of thyroid hormones, strong suppression of the pituitary-gonadal axis and increased levels of prolactin. The main findings of this study were: 1) A large proportion (54% day 1 and 70% day 4) of the patients showed morning s-cortisol levels below the proposed cut-off levels for critical illness related corticosteroid insufficiency (CIRCI), i.e. <276 nmol/L (=10 ug/dL), 2) Low s-cortisol was not associated with higher mortality or worse outcome at 3 months, 3) There was a significant association between early (day 1) and strong suppression of the pituitary-gonadal axis and improved survival and favorable functional outcome 3 months after sTBI, 4) Significantly lower levels of fT3 and TSH at day 4 in patients with a poor outcome at 3 months. 5) A higher Marshall CT score was associated with higher day 1 LH/FSH- and lower day 4 TSH levels 6) In general no significant correlation between GCS, ICP or CPP and hormone levels were detected. Only ICPmax and LH day 1 in men was significantly correlated.


Profound dynamic changes in hormone levels are found in the acute phase of sTBI. This is consistent with previous findings in different groups of critically ill patients, most of which are likely to be attributed to physiological adaptation to acute illness. Low cortisol levels were a common finding, and not associated with unfavorable outcome. A retained ability to a dynamic hormonal response, i.e. fast and strong suppression of the pituitary-gonadal axis (day 1) and ability to restore activity in the pituitary-thyroid axis (day 4) was associated with less severe injury according to CT-findings and favorable outcome.


Behav Brain Res. 2013 Jun 15;247:48-58. doi: 10.1016/j.bbr.2013.03.012. Epub 2013 Mar 18.

Early growth hormone (GH) treatment promotes relevant motor functional improvement after severe frontal cortex lesion in adult rats.


A number of studies, in animals and humans, describe the positive effects of the growth hormone (GH) treatment combined with rehabilitation on brain reparation after brain injury. We examined the effect of GHtreatment and rehabilitation in adult rats with severe frontal motor cortex ablation. Thirty-five male rats were trained in the paw-reaching-for-food task and the preferred forelimb was recorded. Under anesthesia, the motor cortex contralateral to the preferred forelimb was aspirated or sham-operated. Animals were then treated with GH (0.15 mg/kg/day, s.c) or vehicle during 5 days, commencing immediately or 6 days post-lesion. Rehabilitation was applied at short- and long-term after GH treatment. Behavioral data were analized by ANOVA following Bonferroni post hoc test. After sacrifice, immunohistochemical detection of glial fibrillary acid protein (GFAP) and nestin were undertaken in the brain of all groups. Animal group treated with GHimmediately after the lesion, but not any other group, showed a significant improvement of the motor impairment induced by the motor lesion, and their performances in the motor test were no different from sham-operated controls. GFAP immunolabeling and nestin immunoreactivity were observed in the perilesional area in all injured animals; nestin immunoreactivity was higher in GH-treated injured rats (mainly in animals GH-treated 6 days post-lesion). GFAP immunoreactivity was similar among injured rats. Interestingly, nestin re-expression was detected in the contralateral undamaged motor cortex only in GH-treated injured rats, being higher in animals GH-treated immediately after the lesion than in animals GH-treated 6 days post-lesion. EarlyGH treatment induces significant recovery of the motor impairment produced by frontal cortical ablation. GHeffects include increased neurogenesis for reparation (perilesional area) and for increased brain plasticity (contralateral motor area).

Copyright © 2013 Elsevier B.V. All rights reserved.

Acta Neurochir (Wien). 2013 Nov;155(11):2053-62. doi: 10.1007/s00701-013-1670-8. Epub 2013 Mar 15.

Somatotropic and thyroid hormones in the acute phase of subarachnoid haemorrhage.



Somatotropic and thyroid hormones are probably important for the recovery after acute braininjury. Still, the dynamics of these hormones after spontaneous subarachnoid haemorrhage (SAH) is not well described. The purpose of this study was to investigate the relation between somatotropic and thyroid hormones and clinical factors after SAH.


Twenty patients with spontaneous SAH were included prospectively. Serum concentrations of TSH, fT4, T3, IGF-1 and GH were measured once a day for 7 days after SAH. Hormone patterns and serum concentrations were compared to the severity of SAH, neurological condition at admission, clinical course and outcome of the patients.


During the first week after SAH, all patients showed increased GH and IGF-1 concentrations. In the whole group, concentrations of TSH increased, whereas T3 and fT4 decreased. There were no relations of serum concentrations of IGF-1 or GH to clinical condition at admission, clinical course or outcome of the patients. Half of the patients showed low T3 serum concentrations. A complicated course was associated with a deeper fall in TSH and T3 concentrations. There were negative correlations for mean concentrations of TSH and T3 versus WFNS grade and a positive correlation for T3 versus GOS after 6 months, indicating that low concentrations of TSH and T3 were connected to worse SAH grade and poor outcome.


All patients showed increased GH and IGF-1 concentrations irrespective of the grade of SAH or clinical course. Patients with a complicated clinical course showed a more pronounced fall in TSH and T3 concentrations and low serum T3 concentrations were related to a more serious SAH and poor patient outcome. These results need to be studied further and they may contribute to the accumulated knowledge needed to understand the complex mechanisms influencing the unpredictable clinical course after SAH.

Brain Inj. 2013;27(2):200-8. doi: 10.3109/02699052.2012.672786.

Neuropsychological recovery and quality-of-life in children and adolescents with growth hormone deficiency following TBI: a preliminary study.



To compare neurocognition and quality-of-life (QoL) in a group of children and adolescents with or without growth hormone deficiency (GHD) following moderate-to-severe traumatic brain injury (TBI).


Thirty-two children and adolescents were recruited from the TBI clinic at a children’s hospital. Growth hormone (GH) was measured by both spontaneous overnight testing and following arginine/glucagon stimulation administration. Twenty-nine subjects participated in extensive neuropsychological assessment.


GHD as measured on overnight testing was significantly associated with a variety of neurocognitive and QoL measures. Specifically, subjects with GHD had significantly (p”‰<”‰0.05) lower scores on measures of visual memory and health-related quality-of-life. These scores were not explained by severity of injury or IQ (p”‰>”‰0.05). GHD noted in response to provocative testing was not associated with any neurocognitive or QoL measures.


GHD following TBI is common in children and adolescents. Deficits in neurocognition and QoL impact recovery after TBI. It is important to assess potential neurocognitive and QoL changes that may occur as a result of GHD. It is also important to consider the potential added benefit of overnight GH testing as compared to stimulation testing in predicting changes in neurocognition or QoL.

Growth Horm IGF Res. 2008 Dec;18(6):472-8. doi: 10.1016/j.ghir.2008.08.007. Epub 2008 Oct 1.

Growth hormone deficient patients after traumatic brain injury–baseline characteristics and benefits after growth hormone replacement–an analysis of the German KIMS database.



In recent years, traumatic brain injury (TBI) has been identified as a significant cause of growth hormone deficiency (GHD). The aim of the present study was to characterize adult TBI patients with GHD to elucidate the effect of human growth hormone (hGH) replacement in TBI patients as documented in the German Pfizer International Metabolic (KIMS) database.


As of October 2006, 84 TBI patients had been included in the German KIMS database (n=28 childhood-onset and 54 adult-onset GHD). All 84 TBI patients were matched with 84 patients with GHD due to non-functioning pituitary adenoma (NFPA) also included in this database. Analysis of clinical and outcome variables was performed, with comparisons of childhood vs. adult TBI, and TBI vs. NFPA patients, at baseline and one-year follow-up.


TBI patients with GHD were significantly younger at the onset of pituitary disease and exhibited a significantly longer time span between GHD diagnosis and KIMS entry than NFPA patients. Those KIMS patients who had sustained their TBI in childhood were of significantly shorter stature than adult-onset TBI patients. At 1-year follow-up, insulin-like growth factor I (IGF-I) standard deviation score levels had returned to the normal range and quality of life (QoL), as measured by QoL- Assessment of Growth Hormone Deficiency in Adults (AGHDA) questionnaire, improved significantly in TBI as in NFPA patients.


This analysis provides preliminary data that TBI patients with GHD benefit from hGHreplacement in terms of improved QoL in a similar fashion as do NFPA patients. Moreover, it suggests that belated diagnosis and treatment in childhood-onset GHD due to TBI might be related to a shorter final height in these children.


People  with brain injury would mostly likely benefit from  these options all of which offer no deleterious side-effects

1)  pulsed electromagnetic  frequency treatment 
2) LENS treatment  www.ochslabs.com
Dr. Weeks’ Comment: Many patients come to be having suffered brain trauma from falls or accidents which were never worked up by their doctors. LENS brain  …
3) HGH is excellent for brain trauma recovery 
see above
4) Xyrem (GHB) is neuroprotective.
Yao Xue Xue Bao. 2007 Aug;42(8):838-42.
[Effect of gamma-hydroxybutyric acid receptor on focal cerebral ischemia-reperfusion injury in rats]

[Article in Chinese]

Jin RJiang XYMa XGu SLDai TJ.

Department of Pharmacology, Xuzhou Medical College, Xuzhou 221002, China.

This study is to investigate the effect of gamma-hydroxybutyric acid receptor (GHBR) on focal cerebral ischemia-reperfusion injury in rats and its mechanism. NCS-356 (the agonist of GHBR) and NCS-382 (the antagonist of GHBR) were adopted as the tool medicine. The ripe male Sprague-Dawley rats weighing 240 – 280 g were randomly divided into seven groups: sham operation group (sham), ischemia-reperfusion group (Isc/R), NCS-356 160 microg x kg(-1) group (N1), NCS-356 320 microg x kg(-1) group (N2), NCS-356 640 microg x kg(-1) group (N3), NCS-382 640 microg x kg(-1) + NCS-356 640 microg x kg(-1) group (NCS-382 + N3), and nimodipine (Nim) 600 microg x kg(-1) group. The middle cerebral artery occlusion (MCAO) model referring to Longa’s method with modifications was adopted. The effect of GHBR on behavioral consequence of MCAO rats was studied after 2 h of ischemia-reperfusion. After 24 h of ischemia-reperfusion, part of animals were used to measure the cerebral infarction volume by TTC staining; ischemic cortex of another part of animals were used to measure the content of intracellular free calcium by flow cytometry, the tNOS, iNOS activity and the content of NO by spectrophotometric method, the content of cGMP by radioimmunoassay. The neurological function score and infarction volume rate in Isc/R group rats increased significantly than that in sham group; The content of intracellular calcium ([Ca2+]) of cortex neuron and cGMP, the activities of tNOS and iNOS, and the content of NO in Isc/R group were higher than that in sham group obviously (P < 0.01); These consequence we mentioned of N1, N2, N3 and Nim group were lower than that of Isc/R. NCS-382 + N3 group could significantly antagonize the above effect of N3. Thus, NCS-356 has protective effects against ischemia-reperfusion brain injury by activating GHBR. The neuroprotective effect of GHBR is related with decreasing the content of [Ca2+]i, NO, cGMP and tNOS, iNOS activity in MCAO rats.

5)  DMSO is excellent for brain trauma recovery 
Apr 30, 2010  Traumatic brain injury is the most common injury of soldiers returning from the war in Iraq. In light of this, new clinical trials using DMSO to …
6) Testosterone and low dose Lithium
weeksmd.com/…/prescribing-testosterone-to-older-men-a-smart-move-after- all/
Jul 31, 2009  … lowest quartile of testosterone values demonstrated an increased risk of low- traumafractures.15 …. Low Dose Lithium – protects the brain.
7) Progesterone  is excellent for brain trauma recovery 
weeksmd.com/…/why-i-have-prescribed-progesterone-as-a-nerve-repair- agent-for-years/
Jul 3, 2009  Several potential treatments for brain injury and stroke have failed in … promise in warding off brain damage from head trauma and stroke.
8)  Metformin
Jul 6, 2012  Miller says they now hope to test whether metformin might help repair the brains of those who have suffered brain injury due to trauma or …
9) And of course SOUL 
Dec 9, 2013  Prevents Radiation Damage: Nigella sativa oil (NSO) and its active component, thymoquinone, protect brain tissue from radiation-induced …





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