5-HTP increases a chemical in the brain. This chemical is called serotonin. Some medications used for depression also increase serotonin. Taking 5-HTP with these medications used for depression might cause there to be too much serotonin. This could cause serious side effects including heart problems, shivering, and anxiety.

Some of these medications used for depression include phenelzine (Nardil), tranylcypromine (Parnate), and others.

The first dosage should be fairly small, as little as 0.3mg in order to gauge the reaction of the user's body. With increased dose first time user will deel warming ensation, flush in face and mild nausea, if these side effects occure dosage can be taken before going to bed, so any unpleasant effects take place while user is asleep. With regular use these side effects disapper and product can be taken at any tome of the day.
Indeed, the findings that progenitor cells of some form exist both in the regenerative zebrafish heart, and in the hearts of less-regenerative mammals supports this idea. Zebrafish have ostensibly found some method to optimize the activity of progenitor cells, perhaps either by maintaining more cells, or by harboring a more cultivating environment for regeneration. Also, both mammalian and nonmammalian hearts contain an epicardial cell layer, yet zebrafish have found some way to activate the epicardium after injury, a process linked with essential neovascularization of regenerating muscle (Lepilina et al., 2006. This result points to the adult mammalian epicardium as a potential cellular source to assist myocardial regeneration or survival. Indeed, mammalian myocardial infarcts typically show poor or insufficient neovascularization, a response that many are trying to improve experimentally. Recent findings have indicated that the G-actin sequestering protein, Thymosin-ß4, may influence the mammalian epicardium. Treatment of adult cardiac explants with Thymosin-ß4 induced the migration of fibroblasts, endothelial and smooth muscle cells as assessed by gene expression and cellular morphology (Smart et al., 2007). In addition, in vivo Thymosin-ß4 treatment could partially restore cardiac survival and function following coronary ligation (Bock-Marquette et al., 2004). Notably, Thymosin-ß4 expression is induced in the injured zebrafish heart, suggesting that fish naturally release this epicardial stimulant on injury (Lien et al., 2006).
5-HTP has been investigated for its role in hot flashes as Selective Serotonin Reuptake Inhibitors (SSRIs) have been noted to reduce the occurrence of hot flashes and menopausal symptoms.[30][31] In a study in menopausal females given 150mg 5-HTP daily (50mg taken thrice a day) for a period of one week failed to quantitivatively reduce the occurrance of hot flashes[32] as assessed by a Flashmark Pro recording device.[33]
The main functionality of TB500 hinges on the ability to upregulate cell building proteins such as actin, which is a protein that forms (together with myosin) the contractile filaments of muscle cells, and is also involved in motion and metabolism in many other types of cells.. Upregulation of actin allows TB500 to promote healing, cell growth, cell migration and cell proliferation. This not only helps build new blood vessel pathways but also upregulates the type of “good” inflammation that is directly correlated with faster wound healing.
Treated cells were washed with PBS and cytosolic protein extracts were prepared using 1X cell lysis buffer (Santa Cruz Biotechnology, CA) supplemented with protease inhibitor cocktail. Protein concentrations were determined using the Bradford assay (Bio-Rad, CA, USA) as per the manufacturer's protocol. Aliquots of protein lysates were separated on sodium dodecyl sulfate–10% polyacrylamide gels and Western blotting was performed. The proteins were transferred onto a polyvinylidene difluoride membrane (Bio-Rad, CA, USA) in transfer buffer (20 mm Tris, 150 mm glycine, 20% methanol, pH 8.0; TBS-T) at 4°C and 100 V for 1 hour. The membrane was blocked with 5% dry milk in TBS-T for 1 hour at room temperature and incubated with primary antibodies (1:1000) and horseradish peroxidase (HRP)-conjugated secondary antibodies. Protein bands were detected using an enhanced chemiluminescence (ECL) system (Amersham Biosciences, Backinghamshire, UK).
A study published last year in Biological Psychiatry was the first to assess whether people with variations in their oxytocin-receptor gene have a harder time maintaining romantic relationships than those who don’t. Hasse Walum, a graduate student at Karolinska Institute in Stockholm, and his colleagues took advantage of Swedish twin studies that included thousands of participants, their genetic information and their answers to questions about how affectionate they were with their romantic partners. They found that women with a specific variation weren’t as close to their partners as women without it: they kissed their partners less and didn’t desire physical proximity as often. These women were also more likely to report having had a marital crisis. Although researchers don’t know exactly how this variation affects the oxytocin system, it may result in a lower number of oxytocin receptors in the brain. People with fewer receptors would be less sensitive to the hormone’s effects.

Thymosin beta(4), a small ubiquitous protein containing 43 aa, has structure/function activity via its actin-binding domain and numerous biological affects on cells. Since it is the major actin-sequestering molecule in eukaryotic cells and is found essentially in all cells and body fluids, thymosin beta(4) has the potential for significant roles in tissue development, maintenance, repair, and pathology. Several active sites with unique functions have been identified, including the amino-terminal site containing 4 aa (Ac-SDKP) that generally blocks inflammation and reduces fibrosis. Another active site at the amino terminus contains 15 aa, including Ac-SDKP, and promotes cell survival and blocks apoptosis, while a short sequence containing LKKTETQ, the central actin-binding domain (aa 17-23) plus 1 additional amino acid (Q), promotes angiogenesis, wound healing, and cell migration. Several additional biological activities have been identified but not yet localized in the molecule, including its antimicrobial activity, the induction of various genes (including laminin-5, MMPs, TGF beta, zyxin, terminal deoxynucleotidyl transferase, and angiogenesis-related proteins), and the ability to activate ILK/PINCH/Akt, and other signaling molecules important in both apoptosis and inflammatory pathways. This review details these important physiologically and pathologically active sites and their potential therapeutic uses.
A and B; Mouse BMMs were cultured with 200 μM H2O2 and indicated concentrations of Tβ4 peptide in the presence of M-CSF (30 ng/mL) and RANKL (100 ng/mL). C and D; PDLCs were co-cultured with mouse BMMs in the presence of M-CSF, RANKL, 200 μM H2O2, and indicated concentrations of Tβ4 peptide. To monitor osteoclast differentiation, both TRAP activity and the number of TRAP multinucleated cells were examined. * Statistically significant difference compared with control, p<0.05. The data presented were representative of three independent experiments.

“I didn’t think it would be that bad honestly, but since I weight lift multiple times a weak, this supplement is doing me more harm than good. On a typical weight lifting day my workout is split into 5 sections. After taking 5-htp the night before I barely have enough energy to get through 1 section, and that is a serious problem, because of this I am quitting 5-htp all together.”
5-HTP has been investigated for its role in hot flashes as Selective Serotonin Reuptake Inhibitors (SSRIs) have been noted to reduce the occurrence of hot flashes and menopausal symptoms.[30][31] In a study in menopausal females given 150mg 5-HTP daily (50mg taken thrice a day) for a period of one week failed to quantitivatively reduce the occurrance of hot flashes[32] as assessed by a Flashmark Pro recording device.[33]

At SelfHacked, it’s our goal to offer our readers all the tools possible to get optimally healthy. When I was struggling with chronic health issues I felt stuck because I didn’t have any tools to help me get better. I had to spend literally thousands of hours trying to read through studies on pubmed to figure out how the body worked and how to fix it.
In the experiments, an epithelial wound was made in the corneas of sedated rats. A Tb4 solution was applied at several concentrations to the injured eyes in one group of rats while another group was treated with a solution without Tb4. Following 12, 24 and 36 hours, the eyes were tested by microscopic observation for epithelial growth over the injured site. Investigators found the Tb4 accelerated corneal wound repair at doses of Tb4 similar to those found to repair skin wounds. When tested 24 hours after treatment, the rate of accelerated repair was proportional to the concentration of Tb4, with the highest dose (25 microgram) showing a threefold acceleration of epithelial cell migration, compared to untreated. Treatment with Tb4 showed anti-inflammatory effects, helping resolve the injury. An application to human cells in a model of human corneal cells in culture showed that Tb4 enhanced epithelial cell migration in vitro.
An estimated 1.4 million people sustain traumatic brain injury (TBI) each year in the United States, and more than 5 million people are coping with disabilities from TBI at an annual cost of more than $56 billion.1 There are no commercially-available pharmacological treatment options available for TBI because all clinical trial strategies have failed.2,3 The disappointing clinical trial results may be due to variability in treatment approaches and heterogeneity of the population of TBI patients.4-9 Another important aspect is that most clinical trial strategies have used drugs that target a single pathophysiological mechanism, although many mechanisms are involved in secondary injury after TBI.4 Neuroprotection approaches have historically been dominated by targeting neuron-based injury mechanisms as the primary or even exclusive focus of the neuroprotective strategy.3 In the vast majority of preclinical studies, the treatment compounds are administered early and, frequently, even before TBI.10,11 Clinically, the administration of a compound early may be problematic because of the difficulty in obtaining informed consent.12
Thymosin is a hormone secreted from the thymus. Its primary function is to stimulate the production of T cells, which are an important part of the immune system. Thymosin also assists in the development of B cells to plasma cells to produce antibodies. The predominant form of thymosin, thymosin b4, is a member of a highly conserved family of actin monomer-sequestering proteins. b-thymosins are the primary regulators of unpolymerized actin, and are essential for maintaining the small cytoplasmic pool of free G-actin monomers required for rapid filament elongation and allowing for the flux of monomers between the thymosin-bound pool and F-actin.
In January 1955, adreno-corticotrophic hormone (ACTH) was included in the very first Poisons Schedules. It was included in Schedule 4, Part A, which is equivalent to the current Schedule 4 of the Poisons Standard. Provisions for a repeated script must be authorised by an authorised prescriber, including general practitioners, veterinarian or dentist (if required for the purposes of the dental profession or are permitted to be prescribed by a dentist).
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]
Thymosin beta-4 (Tβ4) is a water-soluble, 43-amino acid, and 4.9 kDa protein that was originally isolated from bovine thymus [6]. Since Tβ4 is the major actin-sequestering molecule in eukaryotic cells and is found in all cells [7], Tβ4 has multiple diverse cellular functions, including tissue development, migration, angiogenesis, and wound healing [7]. We previously reported that Tβ4-overexpressing transgenic mice, using a construct on the skin-specific keratin-5 promoter, have abnormal tooth development and enhanced stimulation of hair growth [8]. Moreover, exogenous Tβ4 has anti-inflammatory effects in the bleomycin-induced mouse model of lung fibrosis [9], tooth extraction sockets in rats [10], rat model of myocardial ischemia [11], corneal wound healing [12], wound healing of rat palatal mucosa [13], in vitro model of cultured human gingival fibroblasts [14], and cardiac fibroblasts [15]. However, the effects of Tβ4 over expression or inhibition on differentiation are controversial. Exogenous β4 peptide inhibited osteogenic differentiation but facilitated adipogenic differentiation in human bone marrow-derived-mesenchymal stem cells (MSCs) [16]. In contrast, Tβ4 inhibition by Tβ4 siRNA attenuated odontoblastic differentiation in the odontoblast-like cells, MDPC-23 [17]. Moreover, we recently demonstrated that odontoblastic differentiation was enhanced by activation of Tβ4 by Tβ4 peptide but was decreased by Tβ4 siRNA in human dental pulp cells (HDPCs) [18]. However, the effects of Tβ4 on osteoclastic differentiation have not been reported.

“The study was double-blinded and was for two consecutive 6-wk periods. No diet was prescribed during the first period, a 5040-kJ/d diet was recommended for the second. Significant weight loss was observed in 5-HTP-treated patients during both periods. A reduction in carbohydrate intake and a consistent presence of early satiety were also found. These findings together with the good tolerance observed suggest that 5-HTP may be safely used to treat obesity.”


Supplementation of 5-HTP has been shown to be more effective than tryptophan supplementation alone. This additional benefit of 5-HTP supplementation arises because 5-HTP bypasses the cell's L-tryptophan's own self-regulation on the IDO enzyme, in which it upregulates the activity of IDO (discussed in next section) to maintain body homeostasis of tryptophan[6] and it bypasses the tryptophan hydroxylase enzyme, which is the rate limiting step in serotonin biosynthesis.[7]

I am not a doctor and nothing I say should be taken as medical advice. If you have a read through the article, I would suggest following the recommendations there. If you want to go into detail book a consult at
There have been some side effects reported while using Melanotan 2, typically these effects appear during the first few days of dosing and will become increasingly less obvious as the body adjusts to the peptide. These effects include: nausea, appetite loss, drowsiness and increased sex drive. In order to combat nausea, an anti-histamine can be taken when injecting until the body gets used to it. But most common way to deal with this is to inject Melanotan before bed, this is also beneficial to combat any drowsiness.
Bone loss associated with inflammatory diseases, such as rheumatoid arthritis, periodontal disease, and osteoporosis, and elevated osteoclast activity leads to bone destruction [1]. The most common osteolytic disease, periodontitis, is a multi-factorial irreversible and cumulative condition, initiated and propagated by bacteria and host factors [2]. Destruction of peridontal tissue is mediated via the expression of various tissue-destructive enzymes or inflammatory mediators such as interleukins-1 (IL-1), IL-6 and IL-8, tumor necrosis factor- α (TNF- α), nitric oxide (NO), and prostaglandin E2 (PGE2) [2]. Receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) and osteoprotegerin (OPG) are critical for homeostatic control of osteoclast activity, suggesting that they have vital roles in the progression of bone loss in periodontitis [3, 4]. Therefore, resolution of inflammation and blocking osteoclast differentiation might be a potential therapeutic approach for the prevention and treatment of osteolytic inflammatory disease, such as periodontitis [5].

Froemke's study1, published in April, showed that oxytocin temporarily suppresses inhibitory neurons — those that dampen neural activity — which allows excitatory cells to respond more strongly and reliably. “Our hypothesis is that the virgin brain is a blanket of inhibition, and that pairing the pup calls with oxytocin allows the network to be reconfigured,” says Froemke. The hormone may serve to amplify incoming signals and allow them to be recognized as behaviourally important. (It is at least possible, he says, that this same mechanism could explain why some human mothers feel they are uniquely tuned to a baby's cries.)


On the most basic level, a peptide is essentially a small protein. Billions of unique peptides exist, all with different effects and functions in the body. Physiological examples include insulin, oxytocin, and casein, the main protein in milk. Thus, to taunt Essendon supporters for the use of “peptides” is rather non-specific. A much more intelligent insult would be to focus on the administration of thymosin beta-4.
A user knowing their skin type in relation to the Fitzpatrick scale is important because it will dictate dosing needs. It should be noted that those who will benefit the most from this product are those in the upper spectrum of the Fitzpatrick scale (Types 1, 2 and 3 especially). Skin type 1 and 2 users will typically take longer to see any results from this product, however once beautiful tan is obtained maintenance is easy.
A: 5-HTP (5-hydroxy-tryptophan) 5-htp-5-hydroxytryptophan is converted to serotonin in the body. Because 5-HTP is related to serotonin, it should not be taken with drugs, which may affect serotonin level. These drugs are SSRI (selective serotonin reuptake inhibitors) such as Paxil (paroxetine), Zoloft (sertraline), Prozac (fluoxetine), Celexa (citalopram) and others. The list of drugs: Plavix (clopidogrel), Lipitor (atorvastatin), Uroxatral (alfuzosin), bisoprolol, aspirin and lisinopril do not affect serotonin in the body. Tramadol, however, has a weak inhibition of serotonin reuptake and can increase serotonin levels. It is therefore recommended that tramadol and 5-HTP be used with caution. The patient needs to be monitored for serotonin syndrome, which may include changes in mental status, tremor, hyperthermia, rigidity, seizure, increase sweating and shaky movement. The interaction may also cause a cerebral vasoconstrictive disorder such as Call-Fleming syndrome. It is important to discuss the use of tramadol and 5-HTP with your healthcare provider before taking 5-HTP. Lori Mendoza, RPh

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]


TB-500 is a synthetic version of the naturally occurring peptide present in virtually all human and animal cells, Thymosin Beta-4. This potent peptide is a member of a ubiquitous family of 16 related molecules with a high conservation of sequence and localization in most tissues and circulating cells in the body. TB-500 not only binds to actin, but also blocks actin polymerization and is the actin-sequestering molecule in eukaryotic cells.
In 1999 researchers in Glasgow University found that an oxidised derivative of thymosin β4 (the sulfoxide, in which an oxygen atom is added to the methionine near the N-terminus) exerted several potentially anti-inflammatory effects on neutrophil leucocytes. It promoted their dispersion from a focus, inhibited their response to a small peptide (F-Met-Leu-Phe) which attracts them to sites of bacterial infection and lowered their adhesion to endothelial cells. (Adhesion to endothelial cells of blood vessel walls is pre-requisite for these cells to leave the bloodstream and invade infected tissue). A possible anti-inflammatory role for the β4 sulfoxide was supported by the group's finding that it counteracted artificially-induced inflammation in mice.
A and B; Mouse BMMs were cultured with 200 μM H2O2 and indicated concentrations of Tβ4 peptide in the presence of M-CSF (30 ng/mL) and RANKL (100 ng/mL). C and D; PDLCs were co-cultured with mouse BMMs in the presence of M-CSF, RANKL, 200 μM H2O2, and indicated concentrations of Tβ4 peptide. To monitor osteoclast differentiation, both TRAP activity and the number of TRAP multinucleated cells were examined. * Statistically significant difference compared with control, p<0.05. The data presented were representative of three independent experiments.

Moreover, Tβ4 concentration revealed wide variability, and it decreased in the gingival crevicular fluid (GCF) as periodontal disease progressed [19]. In contrast, Tβ4 mRNA expression was 3.76 fold higher in periodontitis-affected gingival tissue, compared with healthy individuals’ tissue obtained from public microarray data (GEO assession: GSE 23586) [20]. However, the Tβ4 mRNA level did not change in the periodontal-diseased gingival tissue (arbitrary units; 6.249) when compared with healthy tissue (arbitrary units; 6.242) (GEO assession: GSE 10334) [21]. Although Tβ4 exerts anti-inflammatory effects in vivo and in vitro, the precise role of Tβ4 in the inflammatory response remains unclear.


In mammals, many mysteries remain. Oxytocin is difficult to measure reliably in the brain, making it hard to know exactly where, when and how much is normally released; nor do scientists understand precisely how it works to alter behaviour. “What we need to start thinking about is the more fundamental role that oxytocin plays in the brain,” Young says. The determination to find out has been strengthened by a growing move in neuroscience to characterize circuits that are important in brain operations. “That's the level that's critical for understanding how the brain is regulating behaviour,” says Thomas Insel, director of the US National Institute of Mental Health in Bethesda, Maryland, who has studied oxytocin in voles.


Delayed Tβ4 treatment increases vascular density in the injured cortex, ipsilateral dentate gyrus, and CA3 region 35 days after TBI. Arrows show vWF-stained vascular structure. TBI alone (B) significantly increases the vascular density in the injured cortex compared to sham controls (A, P < 0.05). Tβ4 treatment (C) further enhances angiogenesis after TBI compared to the saline-treated groups (P < 0.05). The density of vWF-stained vasculature in different regions is shown in (D). Scale bar = 25 μm (C). Data represent mean + SD. *P < 0.05 vs Sham group. #P < 0.05 vs Saline group. N (rats/group) = 6 (Sham); 9 (Saline); and 10 (Tβ4).
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(6):676-683. View abstract.