Jump up ^ Venkatesh B, Si-Hoe SL, Murphy D, Brenner S (November 1997). "Transgenic rats reveal functional conservation of regulatory controls between the Fugu isotocin and rat oxytocin genes". Proceedings of the National Academy of Sciences of the United States of America. 94 (23): 12462–6. Bibcode:1997PNAS...9412462V. doi:10.1073/pnas.94.23.12462. PMC 25001. PMID 9356472.

Bromodeoxyuridine (BrdU), a thymidine analogue, can be incorporated into the DNA of dividing cells and is widely used to label new cells.61-63 To label proliferating cells, BrdU (100 mg/kg) was injected i.p. daily starting at day 1 post TBI for 10 days. The number of BrdU-positive cells found in the ipsilateral cortex, DG, and CA3 areas was significantly increased 35 days after TBI compared with sham controls.18,34,64,65 Tβ4 treatment further increased the number of BrdU-positive cells compared to saline controls.34 The increased number of BrdU-positive cells may result from effects of Tβ4 on either increasing cell proliferation or reducing cell death of newborn cells. Our recent data show Tβ4 increases oligodendrocyte precursor cell proliferation and differentiation in animal models of stroke25 and experimental autoimmune encephalomyelitis.27 Tβ4 may not directly affect cell proliferation but inhibit cell death, for example, in corneal and conjunctival epithelial cells treated with benzalkonium chloride in vitro66 and endothelial precursor cells under serum deprivation.67 Our data further show that neurogenesis increases in TBI rats treated with Tβ4, suggesting that Tβ4 promotes newborn cells to differentiate into neurons. This is consistent with the effect of Tβ4 on promoting epicardium-derived progenitor cell differentiation into endothelial and smooth muscle cells to form the coronary vasculature.22 Whether the increased number of BrdU-positive cells in the brain of TBI rats treated with Tβ4 is tissue specific remains unknown. Tβ4 may not directly affect cell proliferation. Increased cell proliferation and neurogenesis are also possibly secondary to that Tβ4-mediated angiogenesis, as described later.
However, as I’ve said elsewhere, depression is kind of like a check engine light on car, it’s a quiet ambiguous sign that something is not working somewhere in your neurobiology. There is literally dozens (perhaps hundreds) of different ways to attempt to treat depression. Amongst the vast number of options for treating depression, there is a couple of low hanging fruits; things you would want to start with before moving onto more radical options, like…
When looking at studies that investigate carbohydrates per se, one study in overweight women given 8mg/kg 5-HTP for 5 weeks noted that while placebo did not reduce carbohydrate ingested (calories were reduced in placebo, but carbohdyrate remained at 38% of voluntary calorie intake) that 5-HTP also retained 38% of intake as carbohydrates despite consuming less calories and carbohydrates in total.[9] A decrease in both carbohydrate and dietary fat has been noted with 750mg 5-HTP daily for 2 weeks in diabetics (with no dietary guidelines given), but appeared to be reduced to a similar degree as calories overall.[10] Only one study supports these anecdotes, where the reduction in calories seemed to be acounted mostly for by carbohydrates (75% of observed reduction) and then fats (25%).[10]

Solvent-free Bulletproof Medium-Chain-Triglyceride (MCT) oil. Pure Caprylic and Capric acids. No Lauric Acid. A rapidly metabolised source of energy. Very little MCT oil is stored as fat because it is used for energy so quickly! Formulated supplementary sports food to be consumed as part of a nutritious diet and as part of a program of physical activity. Also available: Bulletproof...
This is exactly the type of question myself, my team of coaches and the community in my Inner Circle can help to answer for you. The Inner Circle is a collective of people who are pursuing the same goals you are – trying to live a healthy, happy, adventurous, fulfilling and limitless life in a modern world. In the Inner Circle, we all help each other with questions, ideas, motivation, suggestions and much more!
Oxytocin's story starts back in the early 1900s, when biochemists discovered that a substance from the posterior pituitary gland could promote labour contractions and lactation. When scientists later discovered the hormone responsible, they named it oxytocin after the Greek phrase meaning 'rapid birth'. Oxytocin is produced mainly by the brain's hypothalamus; in the 1970s, studies revealed that oxytocin-producing neurons send signals throughout the brain, suggesting that the hormone had a role in regulating behaviour.
Down syndrome. Some research shows that giving 5-HTP to infants with Down syndrome might improve muscle and activity. Other research shows that it does not improve muscle or development when taken from infancy until 3-4 years of age. Research also shows that taking 5-HTP along with conventional prescription drugs does improve development, social skills, or language skills.
Recently, therapeutic biomolecules such as growth factors provide great potential as an alternative therapeutic approach to traditional periodontal wound healing [61]. However, because of the short half-lives of growth factors and polynucleotides in the body and the necessity to deliver to specific target sites, those medicinal substances do not always exhibit the anticipated therapeutic potency and outcomes [62]. Thus, optimized delivery regimes and well-defined release kinetics appear to be logical prerequisites for safe and efficacious clinical application of biomolecules. For considering the application of Tβ4 in clinical trials, target cells of exogenous Tβ4 should be restricted to cells in the periodontal tissue.
Nolen, W. A., van de Putte, J. J., Dijken, W. A., Kamp, J. S., Blansjaar, B. A., Kramer, H. J., and Haffmans, J. Treatment strategy in depression. II. MAO inhibitors in depression resistant to cyclic antidepressants: two controlled crossover studies with tranylcypromine versus L-5-hydroxytryptophan and nomifensine. Acta Psychiatr.Scand 1988;78:676-683. View abstract.
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.
This mother-child bonding is the most glorified myth that is not re-thought as often as it should. Its apparant purpose is just to make a dangerously selfish mother (such frustrated mothers do exist a lot more than we read in the news) to think twice before harming her defenseless child which is oftentimes in her sole custody in our society. Acts of such mothers are branded as mental illness rather than plain cruelty. While most people (men and women alike) tend to protect, and not harm a child, the real bonding can happen beetween two independent, mature adults.
Exogenous Tβ4 can function like a hormone on cells in terms of its ability to modulate their biological behavior. Since one of the primary roles of Tβ4 in cells is the sequestration of actin monomers, and the protein is not secreted, previously indicated that it was unlikely that Tβ4 could have a hormonal function [42]. However, other studies have shown that the intracellular level of Tβ4 or its mRNA can be significantly and rapidly altered by external stimuli and that change in the level of Tβ4 often are correlated with cell differentiation [18, 43]. In the present study, exogenous Tβ4 peptide activate intracellular Tβ4, which results suggested that exogenous Tβ4 spontaneously enter the cytoplasm through rapid internalization, and acts their functions same as endogenous one [8, 18].
TBI patients frequently suffer from long-term deficits in cognitive and motor performance. No single animal model can adequately mimic all aspects of human TBI owing to the heterogeneity of clinical TBI.11 Some features of cognitive and motor function in humans have been successfully demonstrated in experimental brain trauma models.28-30 The controlled cortical impact (CCI) model is one of the most widely used TBI models. The CCI-TBI model has many clinically relevant features in that CCI causes not only cortical damage but also selective neuronal death in the hippocampus in rodents, leading to sensorimotor dysfunction and spatial learning and memory deficits, respectively.18,31-33
Chae, H. S., Kang, O. H., Choi, J. G., Oh, Y. C., Lee, Y. S., Jang, H. J., Kim, J. H., Park, H., Jung, K. Y., Sohn, D. H., and Kwon, D. Y. 5-hydroxytryptophan acts on the mitogen-activated protein kinase extracellular-signal regulated protein kinase pathway to modulate cyclooxygenase-2 and inducible nitric oxide synthase expression in RAW 264.7 cells. Biol Pharm Bull 2009;32:553-557. View abstract.
Our nutrition team created these easy mix-and-match menus using the same guidelines that helped 5-HTP dieters lose weight at top speed during the University of Rome study. The idea here is simple: You’ll eat balanced meals that keep you feeling energized and awesome, but you’ll also watch portions so you’re not overeating out of habit. While using these menus, be sure to drink plenty of water and add any other zero-cal beverages you like. You’re also encouraged to season meals to your liking with unlimited herbs, spices, vinegar, mustard, and citrus juice. As always, get a doctor’s OK before trying any new plan.

What to know about hormonal imbalances While it is natural to experience hormonal imbalances at certain times in life, such as puberty, menopause, and pregnancy, some hormonal changes are related to underlying medical conditions. This article looks at the causes and symptoms of hormonal imbalances in men and women, as well as treatment and home remedies. Read now

Melanotan peptides are stable and durable when shipped, surviving about 37 degrees temperatures for around a month or more. Even during summer, this peptide can be shipped without hassles. Once they have been received, they ought to be put away in the refrigerator or better still, freezer to avert conceivable deterioration until ready to be mixed, which then the mixed Melanotan is stored in the refrigerator.
Thymosins were discovered in the mid 1960’s, when Allan Goldstein from the Laboratory of Abraham White at the Albert Einstein College of Medicine in New York studied the role of the thymus in development of the vertebrate immune system. Since then, Dr. Goldstein founded a company that creates thymosin alpha 1 for the purpose of increasing immune cell activity, and thymosin beta 4 (TB-500) to promote wound repair and healing.
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
In women, oxytocin is responsible for signaling contractions of the womb during labor. The hormone stimulates the uterine muscles to contract, so labor begins. It also increases the production of prostaglandins, which move labor along and increases the contractions even more. Because of this effect, synthetic oxytocin (pitocin) is sometimes used to induce a woman to start labor if she cannot start naturally, or it can be given to make contractions stronger if a woman's labor is slowing.

Work with cell cultures and experiments with animals have shown that administration of thymosin β4 can promote migration of cells, formation of blood vessels, maturation of stem cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. These multiple properties have provided the impetus for a worldwide series of on-going clinical trials of potential effectiveness of thymosin β4 in promoting repair of wounds in skin, cornea and heart.[17]

Sexual activity: The relationship between oxytocin and human sexual response is unclear. At least two uncontrolled studies have found increases in plasma oxytocin at orgasm – in both men and women.[103][104] Plasma oxytocin levels are notably increased around the time of self-stimulated orgasm and are still higher than baseline when measured five minutes after self arousal.[103] The authors of one of these studies speculated that oxytocin's effects on muscle contractibility may facilitate sperm and egg transport.[103]
A warning: unlike BPC-157, TB-500 is absolutely, 100% banned by WADA and most other global sporting organization both in-competition and out-of-competition. You should NOT use this if you are competing in any such sanctioned sport as it definitely falls under the banned category of “Peptide Hormones, Growth Factors, Related Substances and Mimetics (S2)”.
Increasing trust and reducing fear. In a risky investment game, experimental subjects given nasally administered oxytocin displayed “the highest level of trust” twice as often as the control group. Subjects who were told that they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk-aversion.11 Nasally administered oxytocin has also been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).12 There is no conclusive evidence for access of oxytocin to the brain through intranasal administration, however.

Research in the early 1960s showed that in rats, administration of α-MSH caused sexual arousal, and work on this continued in many labs up through the 1980s, when scientists at University of Arizona began attempting to develop α-MSH and analogs as potential sunless tanning agents, and synthesized and tested several analogs, including melanotan-I and melanotan II.[6][9]

A handful of large-scale clinical trials are now getting under way to test oxytocin and oxytocin-based therapies for autism spectrum disorder, and to work out who could benefit. Linmarie Sikich, a child psychiatrist at the University of North Carolina is heading the largest of these trials. Sikich plans to recruit 300 people with autism spectrum disorder, ranging in age from 3 to 17, and give them 6 months of either oxytocin or a placebo, followed by 6 months in which everyone will receive oxytocin.

To investigate whether the newborn neurons generated in the DG are capable of projecting their axons into the CA3 region of the hippocampus after TBI, we stereotactically injected a fluorescent tracer, 1,1″-dioleyl-3,3,3″,3″-tetramethylindocarbocyanine methanesulfonate (Dil, Delta 9-DiI; AnaSpec, San Jose, CA) into the ipsilateral CA3 region (stereotaxic coordinates AP, -3.6 mm bregma, ML, 3.6 mm, DV, 3.0 mm, Paxinos and Watson, 1994) at day 28 after TBI. BrdU (100mg/kg, ip) was injected i.p. daily starting at day 1 after TBI for 10 days to label newly generated cells. One week after DiI injection (i.e., 35 days after TBI), the animals were anesthetized and sacrificed. Their brains were fixed in 4% paraformaldehyde. The brain was cut into seven equally spaced 2-mm coronal blocks using a rat brain matrix. The brain blocks containing the hippocampus were processed for vibratome sections (100 μm) followed by BrdU staining. BrdU and DiI labeling in the hippocampus on brain sections was analyzed with a Bio-Rad MRC 1024 (argon and krypton) laser-scanning confocal imaging system mounted onto a Zeiss microscope (Bio-Rad, Cambridge, MA). Co-localization of BrdU-positive nuclei within retrogradely DiI-labeled granule cells was found, indicating that newborn granule neurons extend axons into the CA3 region that are capable of retrogradely transporting DiI from the CA3 to their cell bodies within the DG after TBI (Fig.2). This finding suggests that newborn granule neurons may be incorporated into functional hippocampal circuitry after TBI.
It has been reported that deficiencies in the amino acid tryptophan (precursor to 5-HTP) are correlated with depression, as evidence by serum tryptophan in depressed persons.[16][17] Decreased levels of tryptophan in the body can come from various means but are most likely caused by a diet lacking in the amino acid as substrate, or by upregulation of enzymes (most notably indoleamine 2,3-dioxygenase(IDO) and tryptophan 2,3-dioxygenase(TDO)) that degrade tryptophan or direct it to paths that are not serotonin synthesis causing a relative deficiency.[18][19] These enzymes can be upregulated in states of chronic inflammation[18][20] and injection of some pro-inflammatory cytokines has been implicated in depression[21] and increasing the kyurenine:tryptophan ratio, which is indicative of IDO activity being increased.[22] The activity of tryptophan hydroxylase can also be further downregulated in cases of Magnesium or vitamin B6 deficiency, stress, or excessive tryptophan levels.[7]
She recruited 31 men* and asked them to sniff either an oxytocin nasal spray or another spray with the same ingredients minus oxytocin – a placebo. A few weeks later, the sprays were swapped so that the men who took oxytocin now took the placebo, and vice versa. At the time, neither the scientists nor the volunteers knew which was which – that was only revealed after the experiment was over.
Tβ4 is not a thymus-specific peptide but also present in most tissue and all cells except red blood cells [35]. High amounts of Tβ4 were detected in human white blood cells, especially in neutrophils and in macrophages [34], expressed in developing mandible (embryonic day 12) [36] and hair follicles (HF) of mice [37]. In addition, the peptide is also detected outside cells, in blood plasma and in wound and blister fluids [34]. Although the mechanism(s) of action of exogenous Tβ4 on anti-inflammatory effects remains unclear, the high levels of Tβ4 present in human wound fluid (13 μg/mL) suggest its importance in wound healing or anti-inflammation [38]. However, the level of Tβ4 is variable (unchanged, decreased, and increased) in GCF or biopsied gingival tissue of periodontal patients [20, 21]. Based on the observations that Tβ4 has anti-inflammatory effects [11–14], the hypothesis is that Tβ4 regulates inflammatory mediators and osteoclastogenesis in osteolytic bone disease, such as periodontitis.
We have evaluated the efficacy of early Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by unilateral CCI.34 In brief, TBI rats received Tβ4 at a dose of either 6 or 30 mg/kg (RegeneRx Biopharmaceuticals Inc, Rockville, MD) or a vehicle control (saline) administered i.p. starting at 6 hours after injury and then at 24 and 48 hours. Spatial learning was performed during the last five days (31-35 days post injury) using the modified Morris water maze (MWM) test, which is extremely sensitive to the hippocampal injury.35-37 Tβ4-treated TBI rats showed significant improvement in spatial learning when compared to the saline-treated TBI rats. Tβ4 treatment also significantly reduced the swim latency to reach the hidden platform by rats post TBI compared to saline treatment. Using the modified Neurological Severity Score (mNSS) test, our data show that significantly improved scores were observed after TBI in the Tβ4-treated group compared to the saline-treated group. Our data also show that Tβ4 reduced the incidence of both right forelimb and hindlimb footfaults in TBI rats.34 Histological data show that early Tβ4 treatment reduced cortical lesion volume by 20% and 30% for 6 mg/kg and 30 mg/kg, respectively, and reduced hippocampal cell loss. These findings suggest that TB4 provides neuroprotection even when the treatment was initiated 6 hours post injury. In addition, 6-hour Tβ4 treatment promotes neurogenesis in the dentate gyrus (DG) of the hippocampus,38 which may contribute to improvement in spatial learning.
Last month, in the article “How To Use BPC-157: A Complete Dummies Guide To Healing The Body Like Wolverine“, I introduced the little-known concept of using BPC-157 peptide self-injections and oral BPC-157 peptide consumption (currently completely legal and not banned by sporting organizations) for everything from rapidly healing leaky gut to fixing tendon, ligament and muscle injuries.

Osteoclast differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) staining and activity. After 5 days of culture, cells were stained for TRAP kit using a leukocyte acid phosphatase kit (Sigma Aldrich, St Louis, MO, USA). Cells with three or more nuclei were counted as multinucleated mature osteoclasts. To measure TRAP activity, cells were fixed with 10% formalin for 10 min and 95% ethanol for 1 min, and then 100 μl of citrate buffer (50 mM, pH 4.6) containing 10 mM sodium tartrate and 5 mM p-nitrophenylphosphate (Sigma-Aldrich) was added to the wells containing fixed cells in the 48-well plates. After incubation for 1 h, enzyme reaction mixtures in the wells were transferred to new plates containing an equal volume of 0.1 N NaOH. Absorbance was measured at 410 nm using a microplate reader.

Oxytocin has been of keen interest to neuroscientists since the 1970s, when studies started to show that it could drive maternal behaviour and social attachment in various species. Its involvement in a range of social behaviours2, including monogamy in voles, mother–infant bonding in sheep, and even trust between humans, has earned it a reputation as the 'hug hormone'. “People just concluded it was a bonding molecule, a cuddling hormone, and that's the pervasive view in the popular press,” says Larry Young, a neuroscientist at Emory University in Atlanta, Georgia, who has been studying the molecule since the 1990s.

Robert Love, a urologist in Dallas, understands why there is such back-channel demand for a product like Melanotan II. "People sometimes want to handle performance issues on their own, without a physician involved, either because they are embarrassed or because they may be uninsured or lack adequate insurance," he told Motherboard. "Handling things this way is not advisable. We have prescription drugs that address erectile dysfunction issues. And although this isn't my area, there are alternative ways of getting suntans—tanning beds, spray tans—though of course extended outdoor sun exposure should be avoided if possible."

Sexual activity: The relationship between oxytocin and human sexual response is unclear. At least two uncontrolled studies have found increases in plasma oxytocin at orgasm – in both men and women.[103][104] Plasma oxytocin levels are notably increased around the time of self-stimulated orgasm and are still higher than baseline when measured five minutes after self arousal.[103] The authors of one of these studies speculated that oxytocin's effects on muscle contractibility may facilitate sperm and egg transport.[103]

“Ultimately you’re body is going to down-regulate the enzymes needed to convert the tyrosine/l-phenylalanine into dopamine and norepinephrine; this also counts for 5 -htp being converted into serotonin. As far as I’m aware when simply supplementing amino acids to improve neurotransmitter prevalence in the brain, tolerance will build very rapidly within a one week to two week period (from personal experience). Not saying it’s not viable to help out with mood when used sparingly, just saying there’s most likely better ways for continued treatment.”

Interestingly, there are numerous differences in the biology of teleosts and mammals, as well as specific differences in cardiomyocyte cellular structure and anatomy, all of which might contribute to regenerative variability. Unlike mammals, zebrafish can grow throughout most of adulthood, a phenomenon called “indeterminate growth” (Jordan, 1905). In fact, their growth can be affected markedly by changes in nutrition and population density (Goldsmith et al., 2006). It is thus possible that the capacity to replace cardiac tissue rapidly in teleosts has been retained in evolution as a function of the need for robust animal and cardiac growth. Indeed, a recent study has found that experimentally-induced adult cardiac growth in zebrafish is hyperplastic, and appears to rely on the same signals present or required during cardiac regeneration (Wills et al., 2008).
Dietary supplements containing 5-HTP are claimed to help promote feelings of happiness and general well-being as well as a wide range of other positives such as appetite control, reduced anxiety, and improved mood, sleep and feelings of relaxation. However, there is no conclusive evidence showing that it is effective, and there is no clear "therapeutic" dose of 5-HTP.
Hey Adrian, thanks for reaching out. Firstly, I am not a doctor and nothing I say should be taken as medical advice. For something like this I suggest you book a consult at ×