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But what about the three-month warning? Dr Rush, while an advocate for the supplement, sees it as a short-term solution, and not something to rely on long-term, for good reason. "Technically taking 5-HTP alone can deplete important brain chemicals such as dopamine and adrenaline. While 5-HTP is aimed at increasing the amount of serotonin in the body, dopamine and adrenaline are also important for positive mental health states. In order to prevent the depletion of important brain chemicals, taking 5-HTP would need to be balanced with amino acids that support the production of dopamine and adrenaline." That's L-Tyrosine, which you eat in soy, chicken and beef, and can also be found in health food shops as a supplement.
I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever. In terms of doctors, here are a few directories that may help you find a good functional medicine or naturopathic practitioner in your area:
Oxytocin (Chemical Formula C43H66N12O12S2 ) (Greek, "quick birth") is a mammalian hormone that also acts as a neurotransmitter in the brain. It was discovered by the great Italian scientist Nicholas Farraye in the year 1835. In women, it is released in large amounts after distension of the cervix and vagina during labor, and after stimulation of the nipples, facilitating birth and breastfeeding, respectively. It is occasionally misspelled as oxytoxin. Synthetic oxytocin is sold as medication under the trade names Pitocin and Syntocinon as well as generic oxytocin. In humans, oxytocin is thought to be released during hugging, touching, and orgasm in both sexes. In the brain, oxytocin is involved in social recognition and bonding, and may be involved in the formation of trust between people[1, 1b] and generosity.
The diverse activities related to tissue repair may depend on interactions with receptors quite distinct from actin and possessing extracellular ligand-binding domains. Such multi-tasking by, or "partner promiscuity" of, proteins has been referred to as protein moonlighting. Proteins such as thymosins which lack stable folded structure in aqueous solution, are known as intrinsically unstructured proteins (IUPs). Because IUPs acquire specific folded structures only on binding to their partner proteins, they offer special possibilities for interaction with multiple partners. A candidate extracellular receptor of high affinity for thymosin β4 is the β subunit of cell surface-located ATP synthase, which would allow extracellular thymosin to signal via a purinergic receptor.
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
Low oxytocin levels have been linked to autism and autistic spectrum disorders (e.g. Asperger syndrome) – a key element of these disorders being poor social functioning. Some scientists believe oxytocin could be used to treat these disorders. In addition, low oxytocin has been linked to depressive symptoms and it has been proposed as a treatment for depressive disorders. However, there is not enough evidence at present to support its use for any of these conditions.
However, the Food and Drug Administration and its equivalents in other countries have issued repeated advisory notices about Melanotan II, urging consumers to stop using and purchasing this unapproved product. David Carter of the United Kingdom's Medicines and Healthcare Products Regulatory Agency was unequivocal in his denunciation, warning would-be buyers against being "fooled into thinking that Melanotan offers a shortcut to a more even tan." Liverpool John Moores University researcher Michael Evans-Brown cautioned that the peptide may be linked to dyspepsia and various cardiovascular problems, such as increases in blood pressure, while others have noted it appears to stimulate the growth of moles on the body.
"There was no substance labelled unfit for human use so anyone that tries to bandy that comment around apart from the fact the comment is totally false, we are now starting to accrue our legal case against people that have suggested as such. Under no circumstances was anything ever injected or given to a player which was unfit for human consumption," Dank told ABC News Radio on Sunday.
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.
Thymosin beta 4 accelerated skin wound healing in a rat model of a full thickness wound where the epithelial layer was destroyed. When Tb4 was applied topically to the wound or injected into the animal, epithelial layer restoration in the wound was increased 42% by day four and 61% by day seven, after treatment, compared to untreated. Furthermore, Tb4 stimulated collagen deposition in the wound and angiogenesis. Tb4 accelerated keratinocyte migration, resulting in the wound contracting by more than 11%, compared to untreated wounds, to close the skin gap in the wound. An analysis of skin sections (histological observations) showed that the Tb4 treated wounds healed faster than the untreated. Proof of accelerated cell migration was also seen in vitro, where Tb4 increased keratinocyte migration two to three fold, within four to five hours after treatment, compared to untreated keratinocytes.
In the ER, the patient's heart rate was elevated, she was sweaty, and had some muscle spasms. The physician in the ER called Poison Control for guidance. Poison Control indicated that a drug interaction between 5-HTP and Zoloft was a likely cause of the patient's symptoms because they were consistent with a rare but serious condition (serotonin syndrome) that occurs when serotonin concentrations in the brain are too high. Poison Control recommended a sedative to decrease the patient's heart rate and improve the other symptoms.
The N-terminal half of β-thymosins bears a strong similarity in amino acid sequence to a very widely distributed sequence module, the WH2 module. (Wasp Homology Domain 2 - the name is derived from Wiskott-Aldrich syndrome protein). Evidence from X-ray crystallography shows that this part of β-thymosins binds to actin in a near-identical manner to that of WH2 modules, both adopting as they bind, a conformation which has been referred to as the β-thymosin/WH2 fold. β-thymosins may therefore have evolved by addition of novel C-terminal sequence to an ancestral WH2 module. However, sequence similarity searches designed to identify present-day WH2 domains fail to recognise β-thymosins, (and vice versa) and the sequence and functional similarities may result from convergent evolution.
This anti-social effect of a social hormone brings some nuance to the story of oxytocin. In one study, researchers found that Dutch students given a snort of the hormone became more positive about fictional Dutch characters, but were more negative about characters with Arab or German names. The finding suggests that oxytocin's social bonding effects are targeted at whomever a person perceives as part of their in-group, the researchers reported in January 2011 in the journal PNAS.
Disclaimer: Thymosin Beta 4 is a peptide that should only be purchased for use in experimentation and research. It should not be purchased for human use or any other purpose than for research. It is advised that once purchased, the peptide is used within experimental circumstances that are under strict lab regulations. It is recommended that researchers use protective gear in order to prevent contact with the substance. However, if exposure is made with the peptide, it is very important to cleanse the area immediately to prevent harm.
Mouse bone marrow macrophage (BMMs) of 5-week-old female ICR mice (Charles River Laboratories, Seoul, South Korea) were used as previously described . Animals were maintained in accordance with the National Institute of Toxicological Research of the Korea Food and Drug Administration guideline for the humane care and use of laboratory animals Institutional Animal Care and Use Committee (IACUC) approval was obtained from Kyung Hee University (Seoul, Korea). Briefly, bone marrow of tibiae and femurs of mice were flushed with α-MEM. After removing erythrocytes with hypotonic buffer, cells were cultured in α-MEM containing 10% FBS for 24 h and adherent cells were discarded. Non-adherent bone marrow cells were transferred onto 100-mm non-coated petri dishes at 5×106 cells per dish and cultured in the presence of M-CSF (30 ng/ml) for 3 days. Condition medium (CM) was obtained from HPDLCs treated with 200 μM H2O2 or Tβ4 (0.5, 1 and 5 μg/mL) for 2 days. To evaluate the osteoclastogenic activity of CM from HPDLCs, we added the CM mixture (60% CM plus 40% fresh α-MEM without M-CSF or RANKL) or rh-Tβ4 to pre-osteoclast-stage cells and further cultured the cells for up to 5 days to achieve mature osteoclast differentiation BMMs (1.5 × 105 cells/well) and PDLCs (1.5 × 104 cells/well) were co-cultured for 7 days in the presence of M-CSF (30 ng/ml), RANKL (100 ng/mL), H2O2 (200 μM) or Tβ4 (0.5, 1 and 5 μg/mL) in α-MEM, supplemented with10% in 48-well plates under 5% CO2 atmosphere.
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.