I am not sure if my original question posted…I was wondering if I could use TB-500 to regenerate thyroid tissue? My endocrinologist said that my Hashimoto’s Thyroiditis has almost completely destroyed my thyroid. If yes, then where do I inject?? Additionally, I was wonder if the BPC-157 would have any benefits on thyroid as I plan to take orally for leaky gut/digestive issues.
This is a great product, I have been having digestive problems after 13 major surgeries and suffering from Crohn's Disease my whole life. Currently I can only tolerate a liquid diet. Was very depressed, found this and started taking it and it has made a HUGE difference to my life. Only have very mild depression symptoms now, and sleep better at night. Bought the powder to get the dose right, looks like 100mg suits my 50 kg frame. Only bad thing is the packaging. The 10 grams of powder is lost in the large packet, very hard to get it out and measure the same dose every night. I purchased miniature measuring spoons from ebay and they make life much easier. Sort out the correct spoon for your dosage with the scales then off you go. Can be tricky getting it in and out of the bag, often get powder everywhere, but usually just lick it off. A pill container would work much better for this power.

Good quality Griffonia Simplicifonia, however the pouch is a very inconvenient packaging choice! Why not use the small 25-50gm pill bottle type? I used to be a quality controller in food additives and it would be so perfect to take doses from and fairly cheap and easy to source. I can understand if this is a new product for your line however but you should invest in this for 5htp alone perhaps. Thank you though will be ordering more down the track!


In a study measuring oxytocin serum levels in women before and after sexual stimulation, the author suggests it serves an important role in sexual arousal. This study found genital tract stimulation resulted in increased oxytocin immediately after orgasm.[105] Another study reported increases of oxytocin during sexual arousal could be in response to nipple/areola, genital, and/or genital tract stimulation as confirmed in other mammals.[106] Murphy et al. (1987), studying men, found oxytocin levels were raised throughout sexual arousal with no acute increase at orgasm.[107] A more recent study of men found an increase in plasma oxytocin immediately after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted these changes "may simply reflect contractile properties on reproductive tissue".[108]

I’ve used powdered 5-HTP a couple times now, it doesn’t taste great and it’s resulted in an unpleasant stomach upset that lasted 45–60 minutes. For that reason I’ll likely not continue to use it. I did not find it’s effect on mood remarkable enough that I would want to put up with the stomach upset. My go to Nootropics for mood are Rhodiola and Phenibut and my go to Biohacks for mood are meditation and no fap, I don’t feel the need to use a whole lot more mood promoting strategies.
To pursue the sexual dysfunction agent, melanotan-II was licensed by Competitive Technologies to Palatin Technologies.[9] Palatin ceased development of melanotan-II in 2000 and synthesized, patented, and began to develop bremelanotide, a likely metabolite of melanotan-II that differs from melanotan-II in that it has a hydroxyl group where melanotan-II has an amide.[6][13] Competitive Technologies sued Palatin for breach of contract and to try to claim ownership of bremelanotide;[13] the parties settled in 2008 with Palatin retaining rights to bremelanotide, returning rights to melanotan-II to Competitive Technologies, and paying $800,000.[14]
The combination of supplemental 5-HTP and a dopamine decarboxylase inhibitor is also thought to reduce the risk for cardiovascular complications, as excess serum (but not neural) serotonin is associated with heart valve disease in rats.[56] Due to the accumulation of 5-HTP in neural tissue following the combination[54] it is plausible to assume a reduction in systemic serotonin; this has not been demonstrated yet, however.
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.
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.
Oxytocin (Oxt; /ˌɒksɪˈtoʊsɪn/) is a peptide hormone and neuropeptide. Oxytocin is normally produced by the paraventricular nucleus of the hypothalamus and released by the posterior pituitary.[3] It plays a role in social bonding, sexual reproduction, and during and after childbirth.[4] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding.[5] This helps with birth, bonding with the baby, and milk production.[5][6] Oxytocin was discovered by Henry Dale in 1906.[7] Its molecular structure was determined in 1952.[8] Oxytocin is also used as a medication to facilitate childbirth.[9][10][11]
Hypoxic heart disease is a predominant cause of disability and death worldwide. As adult mammals are incapable of cardiac repair after infarction, the discovery of effective methods to achieve myocardial and vascular regeneration is crucial. Efforts to use stem cells to repopulate damaged tissue are currently limited by technical considerations and restricted cell potential. We discovered that the small, secreted peptide thymosin beta4 (Tbeta4) could be sufficiently used to inhibit myocardial cell death, stimulate vessel growth, and activate endogenous cardiac progenitors by reminding the adult heart on its embryonic program in vivo. The initiation of epicardial thickening accompanied by increase of myocardial and epicardial progenitors with or without infarction indicate that the reactivation process is independent of injury. Our results demonstrate Tbeta4 to be the first known molecule able to initiate simultaneous myocardial and vascular regeneration after systemic administration in vivo. Given our findings, the utility of Tbeta4 to heal cardiac injury may hold promise and warrant further investigation.
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.
At least one study has actively differentiated between 'an increase in satiety' (sensation of fullness from food) and a 'decrease in appetite' (less desire to eat) and noted that 5-HTP causes an increase in satiety without a concomitant decrease in appetite.[9] Additionally, most studies are in exclusively females which may have more significance with interventions pertaining to serotonin metabolism; only one study mentioned above was conducted in men as well[10] but appears to suggest that it benefits both genders.
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.
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.

Skin is the largest organ of the body, which makes up 16% of total body weight. It is also the largest organ that provides immune protection and plays a role in inflammation. Composed of specialized epithelial and connective tissue cells, skin is our major interface with the environment, a shield from the outside world and a means of interacting with it. As such, the skin is subjected to insults and injuries: burns from the sun’s ultraviolet radiation that elicit inflammatory reactions, damage from environmental pollutants and wear and tear that comes with aging.
Side effects: Nausea, fatigue, facial flushing, reaction at injection site, appetite suppression. The potential for side effects to occur increases with an increased dose of Melonotan, and decreases both with a lesser dose and with regular administration. The exception to this is physical signs of sexual arousal, namely male erection when using MT2. So it is important that users of MT II are aware of this before administering.
5-HTP increases a brain chemical called serotonin. Some medications for depression also increase serotonin. Taking 5-HTP along with these medications for depression might increase serotonin too much and cause serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking medications for depression.

Some of these medications for depression include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), amitriptyline (Elavil), clomipramine (Anafranil), imipramine (Tofranil), and others.

Every effort has been made to ensure that the information provided by on this page is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. The information on this page has been compiled for use by healthcare practitioners and consumers in the United States and therefore neither Everyday Health or its licensor warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Neither Everyday Health nor its licensors endorse drugs, diagnose patients or recommend therapy. The drug information above is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or combination is safe, effective or appropriate for any given patient. Neither Everyday Health nor its licensor assume any responsibility for any aspect of healthcare administered with the aid of the information provided. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have any questions about the drugs you are taking, check with your doctor, nurse or pharmacist.
The two main actions of oxytocin in the body are contraction of the womb (uterus) during childbirth and lactation. Oxytocin stimulates the uterine muscles to contract and also increases production of prostaglandins, which increase the contractions further. Manufactured oxytocin is sometimes given to induce labour if it has not started naturally or it can be used to strengthen contractions to aid childbirth. In addition, manufactured oxytocin is often given to speed up delivery of the placenta and reduce the risk of heavy bleeding by contracting the uterus. During breastfeeding, oxytocin promotes the movement of milk into the breast, allowing it to be excreted by the nipple. Oxytocin is also present in men, playing a role in sperm movement and production of testosterone by the testes.
Members agreed that the relevant matters under Section 52E(1) of the Therapeutic Goods Act 1989 included: (a) risks and benefits of the use of a substance; (b) the purpose for which a substance is to be used and the and extent of use; (c) the toxicity of a substance; (d) the dosage, formulation, labelling, packaging and presentation of a substance; (e) the potential for abuse of a substance; and (f) any other matters that the Secretary considers necessary to protect public health.
Cells were pretreated with indicated concentrations of Tβ4 peptide for 2 hours and then incubated with 200 μM H2O2 for 48 hours (A-E). Cell viability was measured by MTT assay (A). Protein and mRNA expressions were assessed by RT-PCR (B) and Western blot analysis (C), respectively. The production of NO (D) and PGE2 (E) were measured by Griess reaction and ELISA, respectively. Data replicated the quantifications of cytotoxicity, NO, and PGE2 with the standard deviation of at least three experiments (n = 4). The bar graph shows the fold increase in protein or mRNA expression compared with control cells. * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2—treated group.
Showa Denko, the source of up to 60% of all the tryptophan sold in the United States, had used an untested manufacturing process that reduced the amount of activated charcoal used to filter fermented raw tryptophan. Some reports suggest that purity may be a potential problem for 5-HTP as well. No cases of EMS resulting from 5-HTP use have been reported, however.

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.

Maintenance doses are taken once the desired pigmentation has been reached and requires much less frequent dosing. Unfortunately, this is where too many variables come into play to give exact instructions. Skin type, bodyweight, metabolism regulating speed of skin fading, uv ray exposure, preferred tan level – all that makes impossible to give correct advice on maintenance dose. Everyone will find their own perfect dose and dosing frequency through some trial and error. To not leave you completely disinformed on this subject here is example of loading and maintenance which can be used as starting point where to adjust from:
Neurovascular units within the central nervous system consist of endothelial cells, pericytes, neurons and glial cells, as well as growth factors and extracellular matrix proteins that are close to the endothelium.72,73 Neurovascular units provide niches for neural stem/progenitor cells in the adult brain and, within these units, newly-generated immature neurons are closely associated with the remodeling vasculature. The generation of new vasculature facilitates several coupled neurorestorative processes including neurogenesis and synaptogenesis, which improve functional recovery.74-76 The vascular production of stromal-derived factor 1 and angiopoietin 1 is involved in neurogenesis and promotes behavioral recovery after stroke.77 The disruption of this neurovascular coordination has been observed in a variety of brain conditions including infection, stroke and trauma.78 The injured brain promotes angiogenesis and neurogenesis,13,32,69,79-84 that may contribute to spontaneous functional recovery from injuries such as stroke and TBI. Neurorestorative agents that increase angiogenesis and neurogenesis have been shown to improve functional outcome following brain injury.19,33 Vascular endothelial cells within the neurovascular niche affect neurogenesis directly via contact with neural progenitor cells, while soluble factors from the vascular system that are released into the CNS enhance neurogenesis via paracrine signaling.85 Here, we demonstrate that Tβ4 treatment promotes both angiogenesis and neurogenesis in rats after TBI, suggesting that the neurovascular remodeling at least partially contributes to Tβ4-mediated improvement in functional recovery. A better understanding of molecular mechanisms in the neurovascular niches will be important for developing novel angiogenic and neurogenic therapies for brain injuries.
Reconstituting tanning peptide is a part of the process required for use of the product and will require full attention to get proper results. 1 or 2ml sterile water is usually used, diluting with more water will improve dosing accuracy. Lovemelanotan peptide calculator is ideal tool for anyone just starting out and not sure how to reconstitute or dose the product properly.
Growth factors play an important role is enhancing structural repair of chronic wounds (Robson, 1997). KGF-2 (Robson et al., 2001), TGF-β (Robson et al., 1995), PDGF-BB (Mustoe et al., 1994; Kiritsy et al., 1995; Smiell et al., 1999), β-NGF (Muangman et al., 2004) have been shown to enhance re-epithelialization (Greenalgh, 1996 for review). The KGF-1 gene has been shown to improve cutaneous wound healing in a septic rat model when delivered in a plasmid (Lin et al., 2006). The PDGF-B gene carried in a plasmid mixed with a bovine collagen gel was reported to accelerate closure of patient diabetic ulcers (Mulder et al., 2009; Blume et al., 2011). KGF-2, PDGF-BB and FGF-L are commercially available as RepiferminTM, RegranexTM, and Trafermin to treat human chronic wounds. Data for the effects of PDGF-BB on back wounds of diabetic mice and for the effects of KGF-2 on chronic venous ulcers in patients is tabulated in Tables 10.3 and 10.4. Thymosin β4 accelerated keratinocyte migration in the wounds of old diabetic mice (Philp et al., 2003).
Side effects: Nausea, fatigue, facial flushing, reaction at injection site, appetite suppression. The potential for side effects to occur increases with an increased dose of Melonotan, and decreases both with a lesser dose and with regular administration. The exception to this is physical signs of sexual arousal, namely male erection when using MT2. So it is important that users of MT II are aware of this before administering.
Bonding. In the Prairie Vole, oxytocin released into the brain of the female during sexual activity is important for forming a monogamous pair bond with her sexual partner. Vasopressin appears to have a similar effect in males.[13] In people, plasma concentrations of oxytocin have been reported to be higher amongst people who claim to be falling in love. Oxytocin has a role in social behaviors in many species, and so it seems likely that it has similar roles in humans.
If you are not 100% satisfied with any purchase made directly from Life Extension®, just return your purchase within 12 months of original purchase date and we will either replace the product for you, credit your original payment method or credit your Life Extension account for the full amount of the original purchase price (less shipping and handling).
Oxytocin produces antidepressant-like effects in animal models of depression,[81] and a deficit of it may be involved in the pathophysiology of depression in humans.[82] The antidepressant-like effects of oxytocin are not blocked by a selective antagonist of the oxytocin receptor, suggesting that these effects are not mediated by the oxytocin receptor.[17] In accordance, unlike oxytocin, the selective non-peptide oxytocin receptor agonist WAY-267,464 does not produce antidepressant-like effects, at least in the tail suspension test.[83] In contrast to WAY-267,464, carbetocin, a close analogue of oxytocin and peptide oxytocin receptor agonist, notably does produce antidepressant-like effects in animals.[83] As such, the antidepressant-like effects of oxytocin may be mediated by modulation of a different target, perhaps the vasopressin V1A receptor where oxytocin is known to weakly bind as an agonist.[84][85]

Although maternal bonding may not always be hardwired — after all, human females can adopt babies and take care of them — oxytocin released during pregnancy "does seem to have a role in motivation and feelings of connectedness to a baby," Young said. Studies also show that interacting with a baby causes the infant's own oxytocin levels to increase, he added. 
Treatment with thymosin beta 4 (Tβ4) reduces infarct volume and preserves cardiac function in preclinical models of cardiac ischemic injury. These effects stem in part from decreased infarct size, but additional benefits are likely due to specific antifibrotic and proangiogenic activities. Injected or transgenic Tβ4 increase blood vessel growth in large and small animal models, consistent with Tβ4 converting hibernating myocardium to an actively contractile state following ischemia. Tβ4 and its degradation products have antifibrotic effects in in vitro assays and in animal models of fibrosis not related to cardiac injury. This large number of pleiotropic effects results from Tβ4’s many interactions with cellular signaling pathways, particularly indirect regulation of cellular motility and movement via the SRF–MRTF–G-actin transcriptional pathway. Variation in effects and effect sizes in animal models may potentially be due to variable distribution of Tβ4. Preclinical studies of PK/PD relationships and a reliable pharmacodynamic biomarker would facilitate clinical development of Tβ4.
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
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).
Neurovascular units within the central nervous system consist of endothelial cells, pericytes, neurons and glial cells, as well as growth factors and extracellular matrix proteins that are close to the endothelium.72,73 Neurovascular units provide niches for neural stem/progenitor cells in the adult brain and, within these units, newly-generated immature neurons are closely associated with the remodeling vasculature. The generation of new vasculature facilitates several coupled neurorestorative processes including neurogenesis and synaptogenesis, which improve functional recovery.74-76 The vascular production of stromal-derived factor 1 and angiopoietin 1 is involved in neurogenesis and promotes behavioral recovery after stroke.77 The disruption of this neurovascular coordination has been observed in a variety of brain conditions including infection, stroke and trauma.78 The injured brain promotes angiogenesis and neurogenesis,13,32,69,79-84 that may contribute to spontaneous functional recovery from injuries such as stroke and TBI. Neurorestorative agents that increase angiogenesis and neurogenesis have been shown to improve functional outcome following brain injury.19,33 Vascular endothelial cells within the neurovascular niche affect neurogenesis directly via contact with neural progenitor cells, while soluble factors from the vascular system that are released into the CNS enhance neurogenesis via paracrine signaling.85 Here, we demonstrate that Tβ4 treatment promotes both angiogenesis and neurogenesis in rats after TBI, suggesting that the neurovascular remodeling at least partially contributes to Tβ4-mediated improvement in functional recovery. A better understanding of molecular mechanisms in the neurovascular niches will be important for developing novel angiogenic and neurogenic therapies for brain injuries.

The first bit of evidence that points to oxytocin as nature’s love glue comes from researchers who measured the hormone in couples. Psychology professor Ruth Feldman at Bar-Ilan University in Israel, spent years studying oxytocin’s role in the mother–child bond and recently decided to dive into the uncharted waters of romantic bonds by comparing oxytocin levels in new lovers and singles. “The increase in oxytocin during the period of falling in love was the highest that we ever found,” she says of a study she and her colleagues published in Psychoneuroendocrinology. New lovers had double the amount Feldman usually sees in pregnant women.


^ Jump up to: a b Marazziti D, Dell'Osso B, Baroni S, Mungai F, Catena M, Rucci P, Albanese F, Giannaccini G, Betti L, Fabbrini L, Italiani P, Del Debbio A, Lucacchini A, Dell'Osso L (October 2006). "A relationship between oxytocin and anxiety of romantic attachment". Clinical Practice and Epidemiology in Mental Health. 2 (1): 28. doi:10.1186/1745-0179-2-28. PMC 1621060. PMID 17034623.
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.
Three groups of mice were individually placed in cages with aggressive mice and experienced social defeat, a stressful experience for them. One group was missing its oxytocin receptors, essentially the plug by which the hormone accesses brain cells. The lack of receptors means oxytocin couldn't enter the mice's brain cells. The second group had an increased number of receptors so their brain cells were flooded with the hormone. The third control group had a normal number of receptors.
Ive been struggling with my left brachialis and so after listening to a podcast in which you mentioned BPC-157 I tried it out. I was hoping for a miracle cure, which I did not get. However, I believe it certainly helped a lot. I am considering a second round. But the peptide rabbit hole is certainly interesting and I am most keen to try some others. But I would like to see if you have some advise for me on another topic. After having listened to your podcast with Dr Gains I thought that either you or Dr Gains may be able to at least point me in the right direction. My wife suffers from a condition called Pelvic Vein Congestion which causes her a lot of pain. From what I understand, she has a seemingly unnatural mass of veins around her uterus which may also suffer from a “valve” type problem in which blood can potentially run in the opposite direction and pool in locations which causes pain. She has been to doctors which offer invasive solutions with unattractive success rates. I have been searching for other cures, but the only thing that I found (supplement with Diosmin and Hisperidan) had some psychological effects. Any thoughts?
Horvath, G. A., Stockler-Ipsiroglu, S. G., Salvarinova-Zivkovic, R., Lillquist, Y. P., Connolly, M., Hyland, K., Blau, N., Rupar, T., and Waters, P. J. Autosomal recessive GTP cyclohydrolase I deficiency without hyperphenylalaninemia: evidence of a phenotypic continuum between dominant and recessive forms. Mol.Genet.Metab 2008;94:127-131. View abstract.
5-HTP supplements are made using an extract from the seeds of Griffonia simplicifolia,a tree native to Africa (2). 5-HTP very rarely occurs naturally in what we eat, but tryptophan, from which 5-HTP is made in the body, is found in a variety of foods. The richest natural food sources include cheese, poultry, eggs, fish, nuts, soy, and various greens.
To determine the effects of Tβ4 peptide and H2O2 on cytotoxicity, its cell viability was evaluated. A 48-h exposure to 0.1–5 μg/mL Tβ4 peptide did not affect H2O2-mediated cell viabilities (Fig 2A). In order to examine whether Tβ4 peptide suppressed ROS-induced inflammatory mediators, the ability of Tβ4 peptide on production of NO and PGE2, and expressions of COX-2 and iNOS were measured by RT-PCR, Western blot, and ELISA. Pretreatment with Tβ4 peptide dose-dependently inhibited H2O2-induced mRNA and protein expressions of COX-2 and iNOS, and NO and PGE2 production (Fig 2B–2E).
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 serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking dextromethorphan (Robitussin DM, and others).
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