My mother was a mother of 6 born between 1948 and 1961. She was a great advocate for lots of cuddles and physical contact with all of her children (as was my dad). This included baby massage directly on the skin as she emphasised touch as being very important. She passed this knowledge onto me when I became an aunt and then a mother. I am very grateful to have had such a hands on, affectionate and intuitive mother as a role model.
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.)
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.
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]

Wonderful column. My expertise is the psychology of risk perception, and I have done some reading on oxytocin and trust (not the kind you want to boost in a bar with Liquid Trust – you can the stuff with pheromones – to boost THAT kind of trust). It turns out there is a high concentration of oxytocin receptors on the amygdala, the area of the brain where fear starts. As oxytocin levels go up, the ability of the amygdala to be warry and more mistrustful goes down. I describe this in Ch. 3 of How Risky Is It, Really? Why Our Fears Don’t Always Match the Facts. A few graphs of which are below. I wonder whether the influence of oxytocin on the amygdala might be connected with the finding of the study you write about.
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:
The activity of the PAM enzyme system is dependent upon vitamin C (ascorbate), which is a necessary vitamin cofactor. By chance, sodium ascorbate by itself was found to stimulate the production of oxytocin from ovarian tissue over a range of concentrations in a dose-dependent manner.[23] Many of the same tissues (e.g. ovaries, testes, eyes, adrenals, placenta, thymus, pancreas) where PAM (and oxytocin by default) is found are also known to store higher concentrations of vitamin C.[24]
"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.
Oxytocin secreted from the pituitary gland cannot re-enter the brain because of the blood-brain barrier. Instead, the behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland. Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala, ventromedial hypothalamus, septum and brainstem.
Serotonin appears to be associated with panic attacks. Although studies that have used tryptophan depletion techniques in humans do not necessarily induce a panic attack[34][35][36] it appears it may sensitize the body by an increase in neurovegetative panic symptoms and increased anxiety[37] which suggests that serotonin is protective against panic attacks, at least acutely.[38][39] A study in 24 unmedicated panic disorder patients and normal participants given 200mg 5-HTP prior to a 35% CO2 test (used to induce a panic attack-like response) noted that the test was able to induce panic attack in both panic disorder patients and normal persons and that 200mg 5-HTP was protective in both conditions but to a greater degree in persons suffering from panic disorders.[40] This has been replicated with cholecystokinin-4 induced panic attack with 200mg 5-HTP in otherwise healthy persons.[41]
Hey Adrian, thanks for reaching out. Firstly, I am not a doctor and nothing I say should be taken as medical advice. For something like this I suggest you book a consult at
Hi..i had 3 major muscle tears(complete)..2 in shoulder and 1in bicep..they all needed surgery for reattachment.. ive done a 20 day round with 157 and believed it at 7 weeks post op and have about 5 month’s of recovery still to go.. thinking another round of 157..wondering if the TB500 might be a better option or stay with 157? As an athlete and top Spartan racer,im looking to speed up process by any %. Any thoughts/opinions or recommendations are greatly appreciated! Thanks for your help and this info :)
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.
MAPKs and NF-κB played pivotal roles in the development of osteoclasts downstream of RANK signaling [54]. In this study, we demonstrated that Tβ4 activation by Tβ4 peptide inhibited RANKL-induced p38, ERK, JNK MAPK, and NF-κB signaling pathways. These results suggested that Tβ4 activation might inhibit osteoclast differentiation via inhibition of the signaling cascades MAPK/NF-κB/NFATc1.
The promise of repairing sun parched aging skin is alluring, especially if damage control may be attained by applying a substance that is abundant in our body. Thymosin beta 4 (Tb4), a molecule that accelerates wound healing in animals and cultured cells, "may be valuable in repairing skin damage caused by sun or even by the wear and tear of aging?" This hopeful message of Tb4's potential to restore damaged human skin was voiced at the 5th International Symposium on Aging Skin, in California (May 2001), by Dr. Allan Goldstein, Chairman of the Biochemistry Department at George Washington University and founder of RegeneRX Biopharmaceuticals. RegeneRX is carrying out preclinical research on Tb4 as a wound healer, in collaboration with scientists at the National Institutes of Health.
Oxytocin affects social distance between adult males and females, and may be responsible at least in part for romantic attraction and subsequent monogamous pair bonding. An oxytocin nasal spray caused men in a monogamous relationship, but not single men, to increase the distance between themselves and an attractive woman during a first encounter by 10 to 15 centimeters. The researchers suggested that oxytocin may help promote fidelity within monogamous relationships.[109] For this reason, it is sometimes referred to as the "bonding hormone". There is some evidence that oxytocin promotes ethnocentric behavior, incorporating the trust and empathy of in-groups with their suspicion and rejection of outsiders.[66] Furthermore, genetic differences in the oxytocin receptor gene (OXTR) have been associated with maladaptive social traits such as aggressive behavior.[110]
Studies on diabetic rats indicated significant increases in the amount of collagen and in tensile strength of light-treated wounds over controls (Stadler et al., 2001; Reddy et al., 2001). In combination with hyperbaric oxygen, light-treated skin wounds in rats closed faster (Yu et al., 1997), an effect that was associated with a more uniform rise and fall in VEGF and FGF-2 instead of the sharp peaks at day four and subsequent rapid drop-off observed in control wounds (Whelan et al., 2001). In vitro, proliferation of mouse fibroblasts was increased by over 150% and that of human epithelial cells by 155–171% (Whelan et al., 2001). Whelan et al. (2001) also reported that wound-healing time was decreased by 50% aboard a submarine, where the atmosphere is lower in oxygen and higher in carbon dioxide, and that children suffering from oral mucositis as a result of chemotherapy experienced a 47% reduction in pain. Recently, however, a randomized trial using a 980 nm diode laser to treat venous leg ulcers of 18 patients indicated no difference in reduction of ulcer size compared to the 16 control patients (Leclere et al., 2010).
Oxidative stress is characterized by an accumulation of ROS and plays a key role in the progression of periodontal diseases [24]. Damage of tissues in inflammatory periodontal disease can be mediated by ROS resulting from the physiological activity of PMN during the phagocytosis of periodontopathic bacteria [27]. In addition, LPS from Porphyromonas gingivalis as well as hypoxia induces a NOX4-dependent increase in H2O2 release in PDLCs [28]. Furthermore, ROS such as H2O2 are small, diffusible, and ubiquitous molecules, can affect human PDLCs and gingival fibroblasts cell injury indirectly by enhancing pro-inflammatory factors such as cytokines, NO, PGE2, and ROS [29–31]. This ROS is known to stimulate osteoclast differentiation and participate in early signaling events associated with osteoclast activation for bone resorption [32]. Since LPS from P. gingivalis increases oxidative stress in PDLCs and contributes to periodontitis [28], human PDLCs treated with H2O2 may serve as an in vitro model relevant to periodontitis.
The uterine-contracting properties of the principle that would later be named oxytocin were discovered by British pharmacologist Sir Henry Hallett Dale in 1906,[125][46] and its milk ejection property was described by Ott and Scott in 1910[126] and by Schafer and Mackenzie in 1911.[127] In the 1920s, oxytocin and vasopressin were isolated from pituitary tissue and given their current names. The word oxytocin was coined from the term oxytocic, Greek ὀξύς, oxys, and τοκετός , toketos, meaning "quick birth".
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.
The short half-life (<2h)[16] of 5-HTP may inherently limit the therapeutic potential of 5-HTP,[17] as the systemic 5-HTP exposure levels will fluctuate substantially, even with relatively frequent dosing. Such exposure fluctuations are usually associated with increased adverse event burden, resulting from Cmax drug spikes, and decreased clinical efficacy resulting from sub-therapeutic exposure for large parts of the day. It has been proposed that 5-HTP dosage forms achieving prolonged delivery would be more effective,[17] as is generally the situation with short-acting active pharmaceutical ingredients.[18]