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.
Melanotan II first captured the public's imagination when the mainstream media briefly touted it as a Viagra-like panacea for middle-aged men. Norman Levine, a dermatologist who led the team that developed the drug, had first conducted experiments in which he darkened the pigments of frogs by injecting them with a hormone called Alpha MSH. After Melanotan II was modified for human use and put through clinical trials, Levine reported that "one very astute observer who took this drug told us that he was developing spontaneous erections."
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]
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For depression: Most commonly, 150-800 mg daily is taken for 2-6 weeks. These doses are sometimes divided up and administered as 50 mg to 100 mg three times a day. Sometimes the dose starts out low and steadily increases every 1-2 weeks until a target dose is reached. Less commonly, higher doses are used. In one study, the dose is steadily increased up to 3 grams per day.
Oxytocin is not only correlated with the preferences of individuals to associate with members of their own group, but it is also evident during conflicts between members of different groups. During conflict, individuals receiving nasally administered oxytocin demonstrate more frequent defense-motivated responses toward in-group members than out-group members. Further, oxytocin was correlated with participant desire to protect vulnerable in-group members, despite that individual's attachment to the conflict.[64] Similarly, it has been demonstrated that when oxytocin is administered, individuals alter their subjective preferences in order to align with in-group ideals over out-group ideals.[65] These studies demonstrate that oxytocin is associated with intergroup dynamics. Further, oxytocin influences the responses of individuals in a particular group to those of another group. The in-group bias is evident in smaller groups; however, it can also be extended to groups as large as one's entire country leading toward a tendency of strong national zeal. A study done in the Netherlands showed that oxytocin increased the in-group favoritism of their nation while decreasing acceptance of members of other ethnicities and foreigners.[66] People also show more affection for their country's flag while remaining indifferent to other cultural objects when exposed to oxytocin.[67] It has thus been hypothesized that this hormone may be a factor in xenophobic tendencies secondary to this effect. Thus, oxytocin appears to affect individuals at an international level where the in-group becomes a specific "home" country and the out-group grows to include all other countries.
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).
Jump up ^ Wermter AK, Kamp-Becker I, Hesse P, Schulte-Körne G, Strauch K, Remschmidt H (March 2010). "Evidence for the involvement of genetic variation in the oxytocin receptor gene (OXTR) in the etiology of autistic disorders on high-functioning level". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 153B (2): 629–39. doi:10.1002/ajmg.b.31032. PMID 19777562.
Differences among groups were analyzed using a one-way analysis of variance combined with the Bonferroni test. The relative intensities of mRNA and protein bands were assayed using Quantity-One software (Bio-Rad Co., Hercules, CA, USA); results were normalized to the mRNA and protein levels of beta-actin. All values were expressed as mean ± standard deviation. Differences were considered significant at p < 0.05.
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]
5-HTP has been shown in scientific studies to promote relaxation and alleviate stress and anxiety. The relaxation and anti-anxiety properties of 5-HTP appear to come from its ability to elevate levels of serotonin. Research has demonstrated that 5-HTP may reduce the risks of panic attacks and symptoms of panic, as well as anxiety and emotional stress. Research also indicates 5-HTP may be effective in helping to alleviate depression.

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]

One way to clarify that question is to give individuals oxytocin rather than just measure naturally occurring levels. In experiments by couple therapist and researcher Beate Ditzen at the University of Zurich, couples each sprayed a liquid containing oxytocin up their noses (which ensures that the hormone reaches the brain). Ditzen then got them to talk with each other about an issue that both partners said often lead to disagreement or fighting, such as who did the housework or how they spent their free time. She observed how they communicated with each other during the discussion compared with couples who didn’t get the hormone.
Mouse bone marrow macrophage (BMMs) of 5-week-old female ICR mice (Charles River Laboratories, Seoul, South Korea) were used as previously described [23]. Animals were maintained in accordance with the National Institute of Toxicological Research of the Korea Food and Drug Administration guideline for the humane care and use of laboratory animals Institutional Animal Care and Use Committee (IACUC) approval was obtained from Kyung Hee University (Seoul, Korea). Briefly, bone marrow of tibiae and femurs of mice were flushed with α-MEM. After removing erythrocytes with hypotonic buffer, cells were cultured in α-MEM containing 10% FBS for 24 h and adherent cells were discarded. Non-adherent bone marrow cells were transferred onto 100-mm non-coated petri dishes at 5×106 cells per dish and cultured in the presence of M-CSF (30 ng/ml) for 3 days. Condition medium (CM) was obtained from HPDLCs treated with 200 μM H2O2 or Tβ4 (0.5, 1 and 5 μg/mL) for 2 days. To evaluate the osteoclastogenic activity of CM from HPDLCs, we added the CM mixture (60% CM plus 40% fresh α-MEM without M-CSF or RANKL) or rh-Tβ4 to pre-osteoclast-stage cells and further cultured the cells for up to 5 days to achieve mature osteoclast differentiation BMMs (1.5 × 105 cells/well) and PDLCs (1.5 × 104 cells/well) were co-cultured for 7 days in the presence of M-CSF (30 ng/ml), RANKL (100 ng/mL), H2O2 (200 μM) or Tβ4 (0.5, 1 and 5 μg/mL) in α-MEM, supplemented with10% in 48-well plates under 5% CO2 atmosphere.
Serotonin influences sleep and sleep-wake cycles in many ways, and scientists continue to make discoveries about how this important neurochemical affects our sleeping and waking lives. One important way serotonin affects sleep and bio time is through its relationship with the “sleep hormone” melatonin. Melatonin is made from serotonin in the presence of darkness. (Remember, melatonin production in the body is triggered by darkness and suppressed by exposure to natural and artificial light.) Healthy serotonin levels are essential for maintaining healthy melatonin levels—and both serotonin and melatonin are critical to sleep and a well-functioning bio clock. With its ability to increase serotonin, 5-HTP supports a neurochemical process that can enable high-quality sleep and keep the body’s bio clock in sync.
A 2002 review concluded that although the data evaluated suggests that 5-HTP is more effective than placebo in the treatment of depression, the evidence was insufficient to be conclusive due to a lack of clinical data meeting the rigorous standards of today.[2] More and larger studies using current methodologies are needed to determine if 5-HTP is truly effective in treating depression.[3][4] In small controlled trials 5-HTP has also been reported to augment the antidepressant efficacy of the antidepressant clomipramine.[5][6][7]
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