The CCI model we used causes cortical tissue loss. Traditionally, the target for neuroprotective treatment of TBI is to reduce the lesion volume.39,40 A major limitation of neuroprotection strategies is the short time window between injury and treatment. In the vast majority of preclinical TBI studies, the treatment compounds provide neuroprotection only when administered early (usually several hours after brain injury).11 The administration of a compound early in the clinical setting is not practical.41 The neuroprotective effects demonstrated in rodents may diminish if the treatment compounds are given in the clinical setting beyond the short neuroprotective window. We are able to stimulate recovery of neurological function without altering the lesion volume, which has also been demonstrated in our experimental studies of stroke,19,42,43 and is in essence, enhancement of neurorecovery.19 The extended 24-hour window for treatment which improves neurological recovery, without altering CCI cortical volume, is a major benefit of the neurorestorative therapy. Recently, we evaluated the efficacy of delayed Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by CCI.34 Briefly, TBI rats received Tβ4 at a dose of 6 mg/kg or a vehicle (saline) administered i.p. starting at 24 hours after injury and then every third day for 2 weeks. The dose of Tβ4 was selected based on our previous studies in animal models of stroke and EAE.25,27 Tβ4 did not alter lesion volume (14.2 ± 3.9% for saline treatment vs. 15.7 ± 3.6% for Tβ4 treatment). TBI caused neuronal cell loss in the ipsilateral CA3 and DG examined 35 days after injury compared to sham controls. Tβ4 treatment initiated 24 hours post injury significantly reduced cell loss in these two regions compared to saline controls. Tβ4-treated TBI rats showed significant improvement in spatial learning (MWM test) and sensorimotor (mNSS test) functional recovery compared to the saline-treated TBI rats.34


Naturalistic studies like ours can help unravel the evolutionary history and function of these hormones. Basically, the fact that hormone mechanisms have been tweaked during evolution suggests that the behaviors they promote have provided fitness benefits in the past. In this case, hunting and sharing meat must have increased men’s reproductive success.
It should be noted that, anecdotally, 5-HTP is said to reduce cravings for carbohydrates in particular. The serotonergic (related to serotonin) system plays a role in macronutrient selection particular in obese persons with a craving for carbohydrates[13] and enhancing serotonergic transmission is known to reduce these cravings.[14] Beyond this, depressed serotonergic tranmission (hypothalamus) is also implicated in increased eating and reduced satiety in general.[15]

Actual injection can be done Subq or IM that is - subcutaneous or intramuscular. Injection site does not matter, there is no one site better than others so use one which is more comfortabe to reach, after injection product is absorbed into bloodstream and spread through the body evenly. Subq injection takes place by pinching the skin loose from the muscle and raising it so the needle can be inserted in the fat layer of skin.
The need to balance hunting pride and social obligations, and the necessity to reconnect with a family that depends on their provisioning were likely experienced by men throughout much of human evolutionary history. Oxytocin is found in all mammals and originated in the mother-infant bond, where it helps with childbirth, nursing and bonding. In some species, this existing hormonal mechanism could then be harnessed for novel contexts – for instance, men investing in pair-bonding and family provisioning, which is rare among mammals.

When combined with antidepressants of the MAOI or SSRI class, very high parenteral doses of 5-HTP can cause acute serotonin syndrome in rats.[23][24] It is unclear if such findings have clinical relevance, as most drugs will cause serious adverse events or death in rodents at very high doses. In humans 5-HTP has never been clinically associated with serotonin syndrome, although 5-HTP can precipitate mania when added to an MAOI.[25]
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