In some studies that record appetite suppression with 5-HTP supplementation, nausea appears to also be reported at higher freqencies than placebo,[9] although some interventions note this as the only relevant side effect.[10] Short term studies tend to note that nausea persists throughout the study period[10] while those expanding beyond three weeks note that reports of nausea tend to decline at this time point.[9]
To further determine the potential anti-inflammatory effects of Tβ4 activation, expressions of proinflammatory or osteoclastogenic cytokines were measured by RT-PCR (Fig 4A). The TNF-α, IL-1β, IL-6, IL-8, and IL-17 mRNA levels increased in the H2O2- stimulated PDLCs, and these increases were significantly decreased in a concentration-dependent manner by treatment with the Tβ4 peptide. Since receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) are two important osteoclastogenic factors, we next explored the effects of Tβ4 peptide on RANKL and OPG expressions in PDLCs. Tβ4 peptide reduced H2O2-stimulated up-regulation of RANKL, with a reciprocal increase in OPG mRNA in a dose-dependent manner (Fig 4B).
In 20 persons undergoing alcohol withdrawal taking 5-HTP (5mg) alongside Glutamine (150mg) and D-Phenylalanine (300mg) and some minerals such as Calcium and Magnesium, it was noted that after 40 days of nutritional therapy (in a hospital setting) that all withdrawal symptoms assessed via SCL-90-R except for anxiety noted a greater reduction with nutritional support relative to placebo.[1]
This sounds very promising and I have a question I’m sure you haven’t heard before. It’s regarding healing. I’m about 230 and avid lifter as well as running occasionally. But I’ve had severe injuries to my l3-s1 for years a d yes I’ve tried some stuff before as far as lifting. But when I was 2 I had encephalitis. I survived it back in 74 which most didn’t however the treatment had left me with migraines and seizures as a child and was told my adult teeth would be very weak when they grew in. So I’m 44 and most of my teeth have broken and I’ve been looking for alternatives to implants. You said both the products mentioned in this article would improve healing and I’ve heard stem cells are capable of regrowing teeth. Would this work for me and how or where would I inject it or maybe do a oral form and let it sit in my mouth for a bit? Never really thought about this but I’ve tried so many clinical trials and been turned down each time. Any info would be greatly appreciated thank you in advance.
I’m curious to know where you got your reconstitution calculation from; you recommend putting approx 3 cc’s in a 5 mg TB-500 which ‘almost fills’ the vial. I have been doing a ton of research on TB-500 and finding contradictory recommendations on how to reconstitute. Because the dosing for TB-500 is higher than what I’m used to with GHRH & GHRP – I felt a lower reconstitution mixture would reduce the amount I needed to take (but now I’m wondering if I’ve been over dosing based on your formula). Would really appreciate knowing how you arrived at filling an insulin syringe ‘three times’ equal to 3 cc’s – just want to make sure i’m dosing correctly
In persons with Panic Disorders (versus persons without as control) ingesting 200mg of 5-HTP, both groups experienced an increase in salivary cortisol within 3 hours but the persons with Panic Attacks continued to have greater increases after the 3 hour mark; this increased cortisol was independent of any percieved side-effects such as headache, fatigue, perspiration, nausea, etc.[43]
Angiogenesis is an essential step in the repair process that occurs after injury. In this study, we investigated whether the angiogenic thymic peptide thymosin beta4 (Tbeta4) enhanced wound healing in a rat full thickness wound model. Addition of Tbeta4 topically or intraperitoneally increased reepithelialization by 42% over saline controls at 4 d and by as much as 61% at 7 d post-wounding. Treated wounds also contracted at least 11% more than controls by day 7. Increased collagen deposition and angiogenesis were observed in the treated wounds. We also found that Tbeta4 stimulated keratinocyte migration in the Boyden chamber assay. After 4-5 h, migration was stimulated 2-3-fold over migration with medium alone when as little as 10 pg of Tbeta4 was added to the assay. These results suggest that Tbeta4 is a potent wound healing factor with multiple activities that may be useful in the clinic.
Astrocytes constitute the largest population of cells in the central nervous system, constituting approximately 90% of human parenchymal cells. Astrocytes are highly responsive to injury, undergoing rapid hyperplasia and hypertrophy. Astrocytes act as physical and biochemical barriers to axonal regeneration by forming glial scars along ischemic lesions and producing axonal growth-inhibitory proteoglycans. Administration of MSCs significantly attenuates the glial scar in the ischemic boundary and reduces expression of inhibitory proteins, such as Nogo. Analysis of single-cell astrocytes isolated from the ischemic boundary by laser capture microdissection reveals that administration of MSCs dramatically down regulates neurocan, an axonal growth-inhibitory proteoglycan. Coculture of MSCs with astrocytes also substantially reduces neurocan expression in astrocytes activated by oxygen glucose deprivation. These findings suggest that injected MSCs reduce physical and biochemical barriers of astrocytes, which also contribute to axonal and neurite outgrowth.
In addition to its intracellular role as the major actin-sequestering molecule in cells of many multicellular animals, thymosin β4 shows a remarkably diverse range of effects when present in the fluid surrounding animal tissue cells. Taken together, these effects suggest that thymosin has a general role in tissue regeneration. This has suggested a variety of possible therapeutic applications, and several have now been extended to animal models and human clinical trials.
“This is a very ancient molecule,” says Sue Carter, a neuroscientist at Indiana University in Bloomington, whose lab pioneered many of the early studies of oxytocin in voles. “It has been used and reused for many purposes across the evolution of modern animals, and almost everybody who's tried to look at an effect of oxytocin on anything like social behaviour has found something.”
Oxytocin is a peptide of nine amino acids (a nonapeptide). The sequence is cysteine - tyrosine - isoleucine - glutamine - asparagine - cysteine - proline - leucine - glycine (CYIQNCPLG). The cysteine residues form a sulfur bridge. Oxytocin has a molecular mass of 1007 daltons. One international unit (IU) of oxytocin is the equivalent of about 2 micrograms of pure peptide.

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.[14] 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.[15] 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.[16]
In 1989, a nationwide outbreak sickened over 1500 people and caused at least 30 deaths in the US. The outbreak was characterized by severe muscle pain and high white blood cell count. The culprit was later determined to be tryptophan supplements made by a specific manufacturer that were thought to be contaminated. Shortly thereafter, the FDA recalled and banned all forms of tryptophan supplements. In the meantime, an alternative supplement called 5-hydroxytryptophan (5-HTP), which is a chemical byproduct of tryptophan, was introduced as an alternative and has since become popular.
In this study, Tβ4 mRNA down-regulation was detected in in vitro in PDLCs stimulated with the ROS. This down-regulation of Tβ4 was also observed in GCF of periodontitis patient [19] and endotoxin-induced septic shock of rats [39]. ROS were generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and involved in tissue destruction associated with periodontal diseases [40]. Thus, we chose to use ROS-stimulated PDLCs in this study since ROS, such as superoxide and H2O2, have been proposed as key players in bone resorption [41] and implicated in the pathogenesis of rheumatoid arthritis and periodontitis [29].
5-HTP can affect a brain chemical called serotonin. Dextromethorphan (Robitussin DM, others) can also affect serotonin. Taking 5-HTP along with dextromethorphan (Robitussin DM, others) might cause too much serotonin in the brain and can result in serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking dextromethorphan (Robitussin DM, and others).
Bartz found that when she averaged out the volunteers’ results, the sniffs of oxytocin hadn’t seemed to colour their memories of their mothers. But things changed when she looked at them individually. Those who felt more anxious about their relationships took a dimmer view of their mother’s parenting styles when they sniffed oxytocin, compared to the placebo. Those who were more secure in their relationships reacted in the opposite way – they remembered mum as being closer and more caring when they took the oxytocin.

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Oxytocin in a nine amino acid peptide that is synthesized in hypothalamic neurons and transported down axons of the posterior pituitary for secretion into blood. Oxytocin is also secreted within the brain and from a few other tissues, including the ovaries and testes. Oxytocin differs from antidiuretic hormone in two of the nine amino acids. Both hormones are packaged into granules and secreted along with carrier proteins called neurophysins.
In regards to interventions, one study in treatment resistant depressed persons that combination therapy of 5-HTP with Carbidopa noted that 43 out of 99 (43.4%) patients improved with an average 200mg (variable 50-600mg) dosage of 5-HTP.[24] It has been noted[25] that since Cardidopa is a peripheral decarboxylase inhibitor that can prevent metabolism of monoamines including serotonin[26] that these results are unlikely to reflect monotherapy with 5-HTP, despite being within the 30-45% range sometimes seen with the placebo effect.[25][27]
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]
In addition to angiogenesis and neurogenesis, cell- and pharmacologically based therapies substantially remodel white matter in the ischemic brain. Treatment of experimental stroke with MCSs, rhEPO, or sildenafil significantly increases axonal density encapsulating the ischemic lesion. Dynamic changes of white matter structure along the ischemic boundary have been imaged in living animals by diffusion tensor imaging (DTI) and fractional anisotropy (FA) measurements. Data from these MRI indices demonstrate that administration of rhEPO or sildenafil augments axonal remodeling and angiogenesis and that both of them are spatially and temporally correlated. Administration of MSCs, rhEPO, and thymosin beta 4 (Tβ4) dramatically increases the number of oligodendrocyte progenitor cells in the corpus callosum, the striatum, and the V/SVZ of the ischemic hemisphere and mature oligodendrocytes in the ischemic boundary adjacent to myelinated axons. These findings suggest that cell- and pharmacologically based therapies promote generation of oligodendrocyte progenitor cells in the ischemic brain that migrate to target axons, where they extend their processes myelinating the axons.

About three months after quitting, I did have a major relapse, which was falling back into old habits for about two weeks. And the whole time I knew what was happening, I knew how dangerous it was, but I couldn't stop myself. I felt like I couldn't connect to anyone without drinking. I couldn't talk to my friends, I couldn't be open and honest with anybody in my life without already having had a few drinks. It was a really disconnected, really unpleasant feeling. That's what I couldn't sit with and I couldn't cope with that feeling, so I went back to drinking.
A number of factors can inhibit oxytocin release, among them acute stress. For example, oxytocin neurons are repressed by catecholamines, which are released from the adrenal gland in response to many types of stress, including fright. As a practical endocrine tip - don't wear a gorilla costume into a milking parlor full of cows or set off firecrackers around a mother nursing her baby.
Studies demonstrate that TB-500 is a potent, naturally occurring wound repair factor with anti-inflammatory properties. Tß4 is different from other repair factors, such as growth factors, in that it promotes endothelial and keratinocyte migration. It also does not bind to the extracellular matrix and has a very low molecular weight meaning it can travel relatively long distances through tissues. One of TB-500 key mechanisms of action is its ability to regulate the cell-building protein, Actin, a vital component of cell structure and movement. Of the thousands of proteins present in cells, actin represents up to 10% of the total proteins which therefore plays a major role in the genetic makeup of the cell.

"By understanding the oxytocin system's dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions," said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.
During clinic trials for its use as a tanning agent, melanotan II was found to be a potent stimulator of male erections. A new drug based on melanotan II, bremelanotide, was developed to take advantage of this property. It has been noted across several studies to increase rigidity and duration of male erection, as well as male sexual desire. It has also been shown to increase female sexual desire in patients with sexual arousal disorder.
A Risk Quiz; Let’s say you are one of the volunteers to whom researchers gave $100, and this option: you can either keep the money, or give it to an anonymous trustee who will either invest it and double it to $200 and return half of the extra hundred bucks to you–$50–or keep all the money for herself. So you can either increase your money by 50%, or lose it all. What would you do? Would you trust that anonymous trustee? (Remember Loss Aversion from Chapter Two, where in a similar experiment most people decided to avoid the gamble and take the sure cash.)
Toxicity effects of melanotan II from therapeutic and overdose exposures include renal dysfunction, rhabdomyolysis, sympathomimetic overdrive, change in size and pigmentation of pre-existing moles, rapid increase in the number of new moles, associated with causing melanomas, posterior reversible encephalopathy syndrome, refractory priapism, stretching and yawning syndrome, shortness of breath, chest pain, abdominal cramping and pain, dizziness and lethargy.
Loading is not absolutely necessary, it is only done to achieve results faster. Loading means taking doses more frequently to build up initial tan faster thus getting in tan maintenance mode sooner. Typical loading is done by taking 0.5mg once a day until desired skin tone is achieved. Loading dose can slightly vary from person to person, depending on skin type, bodyweight and other factors, but 0.5mg is pretty standard for most
^ Jump up to: a b Low TL, Hu SK, Goldstein AL (February 1981). "Complete amino acid sequence of bovine thymosin beta 4: a thymic hormone that induces terminal deoxynucleotidyl transferase activity in thymocyte populations". Proceedings of the National Academy of Sciences of the United States of America. 78 (2): 1162–6. Bibcode:1981PNAS...78.1162L. doi:10.1073/pnas.78.2.1162. PMC 319967. PMID 6940133.

The oxytocin peptide is synthesized as an inactive precursor protein from the OXT gene.[18][19][20] This precursor protein also includes the oxytocin carrier protein neurophysin I.[21] The inactive precursor protein is progressively hydrolyzed into smaller fragments (one of which is neurophysin I) via a series of enzymes. The last hydrolysis that releases the active oxytocin nonapeptide is catalyzed by peptidylglycine alpha-amidating monooxygenase (PAM).[22]
Animal studies have found high levels of both stress and oxytocin in voles that were separated from other voles. However, when the voles were given doses of oxytocin, their levels of anxiety, cardiac stress, and depression fell, suggesting that stress increases internal production of the hormone, while externally supplied doses can help reduce stress.
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]
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5-HTP, along with other L-Tryptophan supplements, have been implicated in the flu-like, potentially fatal Eosinophilic Myalgia Syndrome. This syndrome was initially tied to  impurities - Amino Acids called "Peak E" and "Peak X" - which were present in these products because of poor manufacturing processes by a single major supplier. Some people reject this idea and believe that the syndrome is caused by an excess of tryptophan itself (10, 11).
The group had first identified the thymosin sulfoxide as an active factor in culture fluid of cells responding to treatment with a steroid hormone, suggesting that its formation might form part of the mechanism by which steroids exert anti-inflammatory effects. Extracellular thymosin β4 would be readily oxidised to the sulfoxide in vivo at sites of inflammation, by the respiratory burst.[21]
For this study, one of us, Ben Trumble, followed Tsimane men as they went hunting for food. Typically, Tsimane men set out alone or with a partner in the early morning and search in the forest for prey such as wild pigs, deer, monkeys, or the rare tapir. Following long looping trails they might be gone for eight or nine hours, traveling about six miles (ten kilometers). Ben collected saliva samples throughout the hunt in order to measure changes in men’s hormone levels.

The relationship between oxytocin and human sexual response is unclear. At least two non-controlled studies have found increases in plasma oxytocin at orgasm in both men and women.[5][6] The authors of one of these studies speculated that oxytocin's effects on muscle contractibility may facilitate sperm and egg transport.[5] Murphy et al. (1987), studying men, found that oxytocin levels were raised throughout sexual arousal and there was no acute increase at orgasm. [7] A more recent study of men found an increase in plasma oxytocin immediantly after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted that these changes "may simply reflect contractile properties on reproductive tissue."[8]
In addition, in the Phase 1 clinical trial in healthy volunteers using a randomised, double-blind, placebo-controlled single- and multiple-dose Phase 1 clinical trial, the safety and pharmacokinetics of the intravenous administration of TB-4 was evaluated. From this, intravenous administration of TB-4 appears to be safe and well-tolerated by all subjects with no dose limiting toxicity or serious adverse events reported.
It is highly important to understand that MT2 itself does not protect skin from burning, tan protects your skin. Until some base tan is developed users should still take care not to over-expose skin to uv rays. Starting only with the amount of exposure that the user's skin can handle without burning. It should not take long before the user can handle longer exposures to strong sunlight without adverse effects.
Combined treatments of 5-HTP and SSRI seem to have strong synergistic effects on serotonin levels in rats and humans so that some clinicians recommend the use of slow-released 5-HTP in combination with SSRIs (R, R2, R3). However, additional clinical trials are required to demonstrate the safety and effectiveness of this approach, and combinations of 5-HTP and medications should only be used under medical supervision.
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