Feeding: a 2012 paper suggested that oxytocin neurons in the para-ventricular hypothalamus in the brain may play a key role in suppressing appetite under normal conditions and that other hypothalamic neurons may trigger eating via inhibition of these oxytocin neurons. This population of oxytocin neurons are absent in Prader-Willi syndrome, a genetic disorder that leads to uncontrollable feeding and obesity, and may play a key role in its pathophysiology.[54]
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In the hypothalamus, oxytocin is made in magnocellular neurosecretory cells of the supraoptic and paraventricular nuclei, and is stored in Herring bodies at the axon terminals in the posterior pituitary. It is then released into the blood from the posterior lobe (neurohypophysis) of the pituitary gland. These axons (likely, but dendrites have not been ruled out) have collaterals that innervate neurons in the nucleus accumbens, a brain structure where oxytocin receptors are expressed.[31] The endocrine effects of hormonal oxytocin and the cognitive or behavioral effects of oxytocin neuropeptides are thought to be coordinated through its common release through these collaterals.[31] Oxytocin is also produced by some neurons in the paraventricular nucleus that project to other parts of the brain and to the spinal cord.[32] Depending on the species, oxytocin receptor-expressing cells are located in other areas, including the amygdala and bed nucleus of the stria terminalis.
All of this becomes heavily ironic when you consider that the chemical in question – a hormone called oxytocin – is often billed as the “hormone of love”, and even marketed as “Liquid Trust”. As a new study shows, the reality is much more complicated. Describing oxytocin as the “hormone of love” is like describing a computer as a “writing tool” – it does other things too, some of which aren’t pleasant.

The reason for the difference is the density of oxytocin receptors in the brain. Life pair bonders, like prairie voles or, indeed, ourselves, have a high density of receptors in the reward centre of the brain. Non-pair bonders, like meadow voles, certainly enjoy sex, but their lower density of receptors means it doesn't matter so much who the partner is. So it's not the oxytocin itself making sex enjoyable. What it's doing is influencing our mating behaviour.
My physiotherapist suggested BCP-157. We injected this into the palm for a few weeks 3x week. We then worked up a 50/50 mix of BCP and TB500. I’ve upped my injections ( 5-7 injections) into the surrounding areas of the protruding nodes in my palm. The results have been significant. Into week 6 of a 3x injection program, and the chords are opening up (reacting to the ‘rematrixing’ of the cells). The TB seems to disperse the liquid throughout my palm. My ‘clutched palm’ is reduced and flexibility is restored. We’re going to stick with this for another couple of months.
Even if you did look after yourself adequately and monitor the amount of 5-HTP you were taking, it doesn't appear to be a permanent or lasting solution. A couple of the doctors talked about something that comes up time and time again with long-term SSRI use: a dissipating effect, meaning they can feel less and less effective over time. It seems that people may have the same problem with 5-HTP. "If you push on your biochemistry hard enough, it may downregulate," Dr Paddock explained. "If you're taking SSRIs your body may downregulate the amount of serotonin it puts out so you get waning effects over time. It's similar with 5-HTP. There may be a certain level of serotonin your body is keeping you at and if you raise it or push it, your body then may say, 'Okay, we're above the set point, let's then raise that point again.'"
5-HTP (5-Hydroxytryptophan) is a chemical by-product of the protein building block L-tryptophan. It is also produced commercially from the seeds of an African plant known as Griffonia simplicifolia 5-HTP is used for sleep disorders such as insomnia, depression, anxiety, migraine and tension-type headaches, fibromyalgia, obesity, premenstrual syndrome (PMS), premenstrual dysphoric disorder (PMDD), attention deficit-hyperactivity disorder (ADHD), seizure disorder, and Parkinson's disease..
Jump up ^ Rondanelli M, Opizzi A, Faliva M, Bucci M, Perna S (March 2012). "Relationship between the absorption of 5-hydroxytryptophan from an integrated diet, by means of Griffonia simplicifolia extract, and the effect on satiety in overweight females after oral spray administration". Eating and Weight Disorders. 17 (1): e22–8. doi:10.3275/8165. PMID 22142813.
Froemke's and Tsien's work fits into a broader theory: that one way oxytocin helps social interaction and recognition is by enhancing the brain's response to socially relevant sights, sounds or other stimuli. Young has shown that the hormone helps mice to recognize and pay attention to the smells of other mice7; others found that it promotes people's ability to recognize faces8.

“People got quite excited,” recalls clinical neuroscientist Evdokia Anagnostou, who co-directs the Autism Research Centre at Holland Bloorview Kids Rehabilitation Hospital in Toronto, Canada. But Anagnostou says that some preliminary steps were skipped over as researchers rushed to test oxytocin as a psychiatric drug. “To be honest, if we had done it properly, we wouldn't have done it the way we did. It went a little bit too fast,” she says. Because oxytocin had cleared the early, standard steps of drug development decades earlier, some researchers did not systematically test a range of doses to see whether they had differing psychological effects.

Oxytocin is a peptide of nine amino acids (a nonapeptide) in the sequence cysteine-tyrosine-isoleucine-glutamine-asparagine-cysteine-proline-leucine-glycine-amide (Cys – Tyr – Ile – Gln – Asn – Cys – Pro – Leu – Gly – NH2, or CYIQNCPLG-NH2); its C-terminus has been converted to a primary amide and a disulfide bridge joins the cysteine moieties.[116] Oxytocin has a molecular mass of 1007 Da, and one international unit (IU) of oxytocin is the equivalent of about 2 μg of pure peptide.
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.
The soluble form of Ac-SDKP peptide, derived from thymosin beta-4, has been described as a natural inhibitor of pluripotent hematopoietic stem cell proliferation and as a stimulator of angiogenesis, both in vitro and in vivo (Koutrafouri et al., 2001; Wang et al., 2004). This peptide has been selectively bound to acrylated hyaluronic acid hydrogels via thiol groups from cysteine residues (Song et al., 2014). Unfortunately, the immobilization process was poorly characterized and the effect of hydrogels on EC function was not tested in vitro. In a mouse model of chronic myocardial infarction, hydrogels with immobilized Ac-SDKP did not show improved regeneration potential. Yet, Ac-SDKP-HA hydrogels with entrapped stem cell homing factor SDF-1 showed a significant increase of myocardial regeneration and recovery of heart function, as compared to groups with only one or none of these factors, suggesting a potentially interesting synergistic effect.
Treatment of patients with hyperbaric oxygen has been shown to improve the healing of chronic lower extremity wounds of diabetic patients (Londahl et al., 2010). In a pilot study, this treatment has been shown to more than double the number of circulating vascular stem/progenitor cells in these patients by a mechanism that elevates platelet NOS activity and to stimulate recruitment of vascular progenitor cells to wounds made in their abdominal skin (Thom et al., 2011). This treatment might be combined with topical agents for even greater efficacy in healing chronic wounds.

On a personal note, 5-HTP is actually one of the 1st nootropics I ever used. When I was a teenager and would go to raves me and my friends would use 5-HTP the next day because ecstasy (MDMA) diminishes the serotonin levels. Anyone with much experience with ecstasy knows that the day(s) after can be pretty hellish because the drug so depletes your feel good neurotransmitters, 5-HTP is sort of a Biohack for this.
But long before that, say researchers, oxytocin could use a rebranding. “It doesn't induce love; it doesn't induce massive amounts of trust,” Guastella says. “The problem we've got ourselves into is that we're trying to look for a simple answer: either oxytocin does or does not work in a patient population, or it does or does not enhance a certain social process.”
Jump up ^ Gauquelin G, Geelen G, Louis F, Allevard AM, Meunier C, Cuisinaud G, Benjanet S, Seidah NG, Chretien M, Legros JJ (1983). "Presence of vasopressin, oxytocin and neurophysin in the retina of mammals, effect of light and darkness, comparison with the neuropeptide content of the neurohypophysis and the pineal gland". Peptides. 4 (4): 509–15. doi:10.1016/0196-9781(83)90056-6. PMID 6647119.
Trust is increased by oxytocin.[95][96][97] Disclosure of emotional events is a sign of trust in humans. When recounting a negative event, humans who receive intranasal oxytocin share more emotional details and stories with more emotional significance.[96] Humans also find faces more trustworthy after receiving intranasal oxytocin. In a study, participants who received intranasal oxytocin viewed photographs of human faces with neutral expressions and found them to be more trustworthy than those who did not receive oxytocin.[95] This may be because oxytocin reduces the fear of social betrayal in humans.[98] Even after experiencing social alienation by being excluded from a conversation, humans who received oxytocin scored higher in trust on the Revised NEO Personality Inventory.[97] Moreover, 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 they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk aversion.[99] When there is a reason to be distrustful, such as experiencing betrayal, differing reactions are associated with oxytocin receptor gene (OXTR) differences. Those with the CT haplotype experience a stronger reaction, in the form of anger, to betrayal.[100]

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 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.
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.
At first, the mice showed an irregular smattering of neural impulses when they heard the baby's cries. Then, as the oxytocin kicked in, the signal evolved into a more orderly pattern typical of a maternal brain. The study showed in unusual detail how the hormone changed the behaviour of neurons1. “Oxytocin is helping to transform the brain, to make it respond to those pup calls,” Froemke says.
Thymosin Beta 4 is a peptide that was first found within the thymus gland. Since its discovery, other types of thymosin have been found in different tissues throughout test subjects. Thymosin Beta 4 is typically found in both types of muscles – skeletal (the muscles that are required to move) and smooth muscles (such as the heart). When damage occurs in a tissue, Thymosin Beta 4 is upregulated. Then when traumas take place, Thymosin Beta 4 is released in order to help the subject heal from the trauma. This peptide also helps to prevent adhesions from forming, which means there will be less scar tissue and potentially more flexibility. It has potent anti-inflammatory characteristics.
How does MT-1 compare to MT-2? In terms of darkening the pigmentation of skin to enhance and individuals tan, both types have been proven to work in a number of clinical trials. However, the side effects using MT-2 are more common, but offsetting this is the fact that the darkening effect using MT-2 can be seen faster. It's important to note that the dosages for Melanotan-1and Melanotan-2 are different. For example, a sometimes recommended beginning dose of MT1 is 1mg, while a beginning dose of MT2 is often only 0.25mg.
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]
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.
Toxicity includes renal dysfunction, rhabdomyolysis, sympathomimetic overdrive, change in size and pigmentation of new moles, with one report of melanoma associated with use of melanotan II. Other case reports include posterior reversible encephalopathy syndrome (consisting of seizures, visual disturbance, confusion, headache, vomiting); refractory priapism, stretching and yawning syndrome; shortness of breath, chest pain, abdominal cramping & pain, dizziness and lethargy.
I’ve been on this stuff for lots of years. I really needed it when I was depressed like hell, and I had an emotional pain that simply didn’t go away for 2 decades prior to starting that stack. Did it help? yes. Was it the best intervention possible? probably not. I was able to get off all this stuff with the uridine stack, and I believe it partly fixed a part of my brain that was damaged from this decade long suffering. So this is, why I am now more into brain regeneration and psychotherapeutic interventions (even though I do them myself), and I would only go back to this stack if I was completely fucked up again. There are a lot of side effects, and its a fine line to balance the supplements, to get rid of the side effects…
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.

CONDITIONS OF USE AND IMPORTANT INFORMATION: This information is meant to supplement, not replace advice from your doctor or healthcare provider and is not meant to cover all possible uses, precautions, interactions or adverse effects. This information may not fit your specific health circumstances. Never delay or disregard seeking professional medical advice from your doctor or other qualified health care provider because of something you have read on WebMD. You should always speak with your doctor or health care professional before you start, stop, or change any prescribed part of your health care plan or treatment and to determine what course of therapy is right for you.
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