PDGF-BB (Mustoe et al., 1994), FGF-2 (Inadomi et al., 2004), IGF I and II (Zhao et al., 1995), TGF-β (Greenalgh, 1996), and L-arginine (Shi et al., 2003) enhance fibroblast proliferation and deposition of collagen in chronic wounds. Thymosin β4 accelerates wound repair in both young and old diabetic mice by significantly increasing wound contraction and collagen deposition. A synthetic peptide that duplicated the actin-binding domain of thymosin β4 promoted wound repair in aged mice to a degree comparable to that of the whole molecule (Philp et al., 2003). In rats with wound healing impaired by mitomycin C, the formation of granulation tissue (angiogenesis and fibroblast proliferation) was significantly advanced by hydrogel sheets composed of alginate, chitin/chitosan, and fucoidin (Murakami et al., 2010).
Melanotan II can be of unknown quality and subject to contamination and stability concerns with use of multi-dose vials. There is no experience with the product other than through unregulated channels. There are health risks from the substance itself and its route of administration – documented in medical literature, case reports as well as reports from NSW PIC.

What to know about hormonal imbalances While it is natural to experience hormonal imbalances at certain times in life, such as puberty, menopause, and pregnancy, some hormonal changes are related to underlying medical conditions. This article looks at the causes and symptoms of hormonal imbalances in men and women, as well as treatment and home remedies. Read now
When you get your TB-500, it will come in a powder form. Just like BPC-157, you will need to “reconstitute” it by adding bacteriostatic water. Go back and read my article on BPC-157 to get access to a peptide calculator that will help you with the mixing/dosage math. Once your TB-500 is properly mixed, you then draw the dose into an insulin syringe, and inject it intramuscularly, subcutaneously, or intravenously (according to your preference).
About three months after quitting, I did have a major relapse, which was falling back into old habits for about two weeks. And the whole time I knew what was happening, I knew how dangerous it was, but I couldn't stop myself. I felt like I couldn't connect to anyone without drinking. I couldn't talk to my friends, I couldn't be open and honest with anybody in my life without already having had a few drinks. It was a really disconnected, really unpleasant feeling. That's what I couldn't sit with and I couldn't cope with that feeling, so I went back to drinking.

Monomeric β-thymosins, i.e. those of molecular weight similar to the peptides originally isolated from thymus by Goldstein, are found almost exclusively in cells of multicellular animals.[4] Known exceptions are monomeric thymosins found in a few single-celled organisms, significantly those currently regarded as the closest relatives of multicellular animals:[5] choanoflagellates [6] and filastereans.[7] Although found in very early-diverged animals such as sponges, monomeric thymosins are absent from arthropods and nematodes, which do nevertheless possess "β-thymosin repeat proteins" which are constructed from several end-to-end repeats of β-thymosin sequences.[8] Genomics has shown that tetrapods (land vertebrates) each express three monomeric β-thymosins, which are the animal species' equivalents (orthologues) of human β4, β10 and β15 thymosins, respectively. The human thymosins are encoded by the genes TMSB4X, TMSB10 and TMSB15A and TMSB15B. (In humans, the proteins encoded by the two TMSB15 genes are identical.) Bony fish in general express orthologues of these same three, plus an additional copy of the β4 orthologue.[9]

To evaluate the indirect effect of Tβ4 peptide on RANKL-induced osteoclastogenesis, mouse BMMs were incubated with RANKL and CM, prepared from HPDLCs treated with H2O2 and different concentrations of Tβ4, and allowed to differentiate into osteoclasts. As shown in Fig 6, Tβ4 peptide dose-dependently decreased the number of osteoclasts and TRAP activity. To determine whether the reduction in osteoclast generation by Tβ4 could be due to effects of Tβ4 peptide on viability of the BMMs, a cytotoxicity assay was performed. The viability of BMMs was not significantly affected by Tβ4 peptide (data not shown).
To evaluate the indirect effect of Tβ4 peptide on RANKL-induced osteoclastogenesis, mouse BMMs were incubated with RANKL and CM, prepared from HPDLCs treated with H2O2 and different concentrations of Tβ4, and allowed to differentiate into osteoclasts. As shown in Fig 6, Tβ4 peptide dose-dependently decreased the number of osteoclasts and TRAP activity. To determine whether the reduction in osteoclast generation by Tβ4 could be due to effects of Tβ4 peptide on viability of the BMMs, a cytotoxicity assay was performed. The viability of BMMs was not significantly affected by Tβ4 peptide (data not shown).
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.
“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.”
Interestingly, there are numerous differences in the biology of teleosts and mammals, as well as specific differences in cardiomyocyte cellular structure and anatomy, all of which might contribute to regenerative variability. Unlike mammals, zebrafish can grow throughout most of adulthood, a phenomenon called “indeterminate growth” (Jordan, 1905). In fact, their growth can be affected markedly by changes in nutrition and population density (Goldsmith et al., 2006). It is thus possible that the capacity to replace cardiac tissue rapidly in teleosts has been retained in evolution as a function of the need for robust animal and cardiac growth. Indeed, a recent study has found that experimentally-induced adult cardiac growth in zebrafish is hyperplastic, and appears to rely on the same signals present or required during cardiac regeneration (Wills et al., 2008).
TB-500 was identified as a gene that was up-regulated four-to-six fold during early blood vessel formation and found to promote the growth of new blood cells from the existing vessels. This peptide is present in wound fluid and when administered subcutaneously, it promotes wound healing, muscle building and speeds up recovery time of muscles fibres and their cells. An additional key factor of TB-500 is that it promotes cell migration through a specific interaction with actin in the cell cytoskeleton. It has been demonstrated that a central small amino acid long-actin binding domain has both blood cell reproduction and wound healing characteristics. These characteristics are uncovered by accelerating the migration of endothelial cells and keratinocytes. It also increases the production of extracellular matrix-degrading enzymes.
"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.
That view has led some clinicians to try oxytocin as a treatment for psychiatric conditions such as autism spectrum disorder. But the early trials have had mixed results, and scientists are now seeking a deeper understanding of oxytocin and how it works in the brain. Researchers such as Froemke are showing that the hormone boosts neuronal signals in a way that could accentuate socially relevant input such as distress calls or possibly facial expressions. And clinical researchers are starting a wave of more ambitious trials to test whether oxytocin can help some types of autism.
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.

It turns out oxytocin is responsible for a lot more than just love. New science has found that this amazing molecule also influences how sociable each of us is, allowing us to 'tune in' to the social information around us, perceiving it in much higher resolution. Scientists are now applying this new knowledge in the lab, and as reporter Dr Graham Phillips finds out, they're discovering oxytocin's great potential to treat social disorders, like drug addiction and alcoholism.
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.
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.
I’ve tried researching this on my own but haven’t been able to find much. I have Hashimoto’s Thyroiditis & my endocrinologist says I barely have any thyroid left. Would TB-500 help regenerate new thyroid growth & if so where would I inject it?? I plan on taking this along with the BPC-157 (orally) for gut inflammation to see if it can repair leaky gut & digestive issues. Thoughts?
Thymosin beta-4 is a naturally occurring peptide, and is found ubiquitously in our cells. A range of studies on animal models have indicated several key biological activities for Tβ4, such as “promot[ing] wound repair, tissue protection, and regeneration in the skin, eye, heart and central nervous system”. Only a handful of clinical trials in humans have attempted to explore these roles practically.
We had previously reported that successful hunters experienced a surge in testosterone that lasted from the moment they made a kill until their return home – a “winner effect,” rewarding them for their work. Testosterone reinforces the hunting activity and simultaneously helps with muscle regeneration afterwards - similar to the elated feeling we might have after doing sports or other exercise.
I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. I would say yes though. Just because you dont “know” or “feel” any injury, you might be one functional movement away from a weakened tendon or muscle – snap, crackle and POP! These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever.
Melanotan II non-selectively mimics the action of melanocortin peptides. These are natural hormones involved with pigmentation, energy homeostasis, sexual functioning, the immune system, inflammation, and the cardiovascular system. Much like melanotan I (afamelanotide), melanotan II stimulates the production of eumelanin, causing the skin to go darker (tanning).
Tβ4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners. Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs. Tβ4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-κB in PDLCs. Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs. In addition, H2O2 up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2 in PDLCs. Wnt5a inhibition by Wnt5a siRNA enhanced the effects of Tβ4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.
"Just that it is completely false that these particular substances and the program wasn't discussed through the highest levels of the club. We have been very firm in terms of our belief in what ASADA, the AFL and Essendon know and for them to remotely suggest that no one knew, to be really blunt, is completely wrong and in some ways offending the process we set up at Essendon Football Club. We were very strict in the protocols we set up."
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.
Nasally administered oxytocin has been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).[76] Indeed, studies in rodents have shown oxytocin can efficiently inhibit fear responses by activating an inhibitory circuit within the amygdala.[77][78] Some researchers have argued oxytocin has a general enhancing effect on all social emotions, since intranasal administration of oxytocin also increases envy and Schadenfreude.[79] Individuals who receive an intranasal dose of oxytocin identify facial expressions of disgust more quickly than individuals who do not receive oxytocin.[75][qualify evidence] Facial expressions of disgust are evolutionarily linked to the idea of contagion. Thus, oxytocin increases the salience of cues that imply contamination, which leads to a faster response because these cues are especially relevant for survival. In another study, after administration of oxytocin, individuals displayed an enhanced ability to recognize expressions of fear compared to the individuals who received the placebo.[80] Oxytocin modulates fear responses by enhancing the maintenance of social memories. Rats that are genetically modified to have a surplus of oxytocin receptors display a greater fear response to a previously conditioned stressor. Oxytocin enhances the aversive social memory, leading the rat to display a greater fear response when the aversive stimulus is encountered again.[74]
As reactive oxygen species (ROS) have been implicated in the pathogenesis of periodontitis [24], we examined whether H2O2 could down-regulate or up-regulate Tβ4 expression in PDLCs. As shown in Fig 1A and 1B, Tβ4 mRNA and protein expressions were down-regulated by H2O2 in a time- and concentration-dependent manner. Because maximal Tβ4 mRNA and protein expressions were achieved with 200 μM H2O2 within 48 hours in PDLCs, this concentration was used in subsequent experiments.
“Further analysis by gender revealed that females in the 5-HTP group had a significantly lower panic rate and intensity of cognitive symptoms whereas, in males, the effect of 5-HTP was limited to lowering the intensity of somatic panic symptoms. Thus, an increased availability of 5-HT may have a gender-dependent protective effect in CCK-4-induced panic.”
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 identify newborn neurons, double immunofluorescent staining for BrdU/NeuN (mature neuronal marker) was performed (Fig.1). TBI alone significantly increased the number of newborn neurons (NeuN/BrdU-colabeled cells) in the DG of injured hemisphere. Tβ4 treatment significantly further increased the number of newborn neurons compared to saline controls. These data suggest that Tβ4 administration initiated 24 hours after TBI promotes neurogenesis in rats.
People are using 5-HTP for absolutely everything from sleep disorders to OCD symptoms. After asking people in mental health Facebook groups whether they used it and why, I was inundated with responses. Sach Tennant, from London, takes it for her PMDD (premenstrual dysphoric disorder). "I only take it when I feel low and it only takes one hour to feel calm," she told me. "This month I only needed one to feel better. I don't get the zombie antidepressant feeling – you still have your emotions. Sleep is good on it. I used to have an inner voice that was male and used to bully me during PMT time. Noises seemed too loud, even like somebody eating a bag of crisps. Topping up with 5-HTP has stopped all this."
The sequence LKKTET, which starts at residue 17 of the 43-aminoacid sequence of thymosin beta-4, and is strongly conserved between all β-thymosins, together with a similar sequence in WH2 domains, is frequently referred to as "the actin-binding motif" of these proteins, although modelling based on X-ray crystallography has shown that essentially the entire length of the β-thymosin sequence interacts with actin in the actin-thymosin complex.[13]
Many early studies of oxytocin for autism were limited because they assessed only a single dose and had relatively few participants, and later experiments with more doses failed to show the same promise. In 2010, clinical psychologist Adam Guastella at the University of Sydney in Australia studied 16 male adolescents with autism spectrum disorder, and found that one dose of oxytocin could improve their ability to gauge the emotions of others by looking at their eyes13. But when he tried giving twice-daily doses of the hormone for two months, he found no significant improvements in social interaction or social cognition14. “Studies to this point have really shown limited benefit of oxytocin in improving psychiatric illnesses over time,” he says. Guastella says that getting to the bottom of oxytocin's complex neurological effects will take time. “If we want a simple answer, we're not going to get it.”
Melanotan II was originally developed as a treatment for sexual dysfunction. However, this was abandoned when the metabolite bremelanotide was developed instead for treatment of haemorrhagic shock. Melanotan II is usually injected subcutaneously for the purposes of sunless tanning, appetite suppression, inducing sexual desire and penile erection and other conditions such as rosacea and fibromyalgia. There are also dose forms available for nasal administration. The therapeutic dose is considered to be 0.01 mg/kg.
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.
20 patients (nine from the 5-HTP group and 11 from the Placebo group) completed the study. Brain tryptophan availability in diabetic patients was significantly reduced when compared to a group of healthy controls. Patients receiving 5-HTP significantly decreased their daily energy intake, by reducing carbohydrate and fat intake, and reduced their body weight.”
Oxytocin is known to be metabolized by the oxytocinase, leucyl/cystinyl aminopeptidase.[25][26] Other oxytocinases are also known to exist.[25][27] Amastatin, bestatin (ubenimex), leupeptin, and puromycin have been found to inhibit the enzymatic degradation of oxytocin, though they also inhibit the degradation of various other peptides, such as vasopressin, met-enkephalin, and dynorphin A.[27][28][29][30]
Maternal behavior: Female rats given oxytocin antagonists after giving birth do not exhibit typical maternal behavior.[59] By contrast, virgin female sheep show maternal behavior toward foreign lambs upon cerebrospinal fluid infusion of oxytocin, which they would not do otherwise.[60] Oxytocin is involved in the initiation of maternal behavior, not its maintenance; for example, it is higher in mothers after they interact with unfamiliar children rather than their own.[61]
Some work has pointed to a potential dark side to oxytocin. Carter's group found that a single low dose of the hormone given to baby prairie voles improved their pair bonding as adults, but that higher doses interfered with that behaviour — possibly because oxytocin started to activate other receptors16. And human studies have suggested that in certain contexts, a puff of oxytocin can cause people to be more aggressive in defending themselves against outsiders or competitors17. In patients with a psychiatric condition known as borderline personality disorder, a single dose of oxytocin has been found to hinder trust and cooperation18.
Touting their discovery as “a great step forward in weight loss history,” the panel were quick to offer up their hard earned cash to back the entrepreneurial pair. “We were shocked. The most we were hoping for was some advice…we weren’t even sure that we would manage to get any investors,” explained Samantha. After outstanding offers from each panel member, the sisters burst into tears.
I was kind of scared because I ran across some threads that said TB500 leads to cancer or promotion of benign tumors…most of these were at least 4-5 years old though and it seems there are countless logs online all with good experiences. Nonetheless I was still worried so I did some more research and came across a pharmaceutical company in the US doing clinical trials for thymosin beta 4 to help with dry eye syndrome. I have attached some links. This makes me feel much safer but if you have any more insight I’d really appreciate it.
Stimulation of milk ejection (milk letdown): Milk is initially secreted into small sacs within the mammary gland called alveoli, from which it must be ejected for consumption or harvesting. Mammary alveoli are surrounded by smooth muscle (myoepithelial) cells which are a prominant target cell for oxytocin. Oxytocin stimulates contraction of myoepithelial cells, causing milk to be ejected into the ducts and cisterns.
Oxytocin has been of keen interest to neuroscientists since the 1970s, when studies started to show that it could drive maternal behaviour and social attachment in various species. Its involvement in a range of social behaviours2, including monogamy in voles, mother–infant bonding in sheep, and even trust between humans, has earned it a reputation as the 'hug hormone'. “People just concluded it was a bonding molecule, a cuddling hormone, and that's the pervasive view in the popular press,” says Larry Young, a neuroscientist at Emory University in Atlanta, Georgia, who has been studying the molecule since the 1990s.
Exposure to ultraviolet (UV) light prompts an increased release of Alpha-MSH, which in turn stimulates the production of melanin in the skin. The more melanin produced the greater pigmentation level becomes, making the skin progressively darker and tan lasts significantly longer. This makes Melanotan peptide unique, people do not require as much exposure to UV light to produce more melanin, very attractive for people wishing to develop greater tanning of the skin in fastest way possible.
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.
Jump up ^ Hicks C, Ramos L, Reekie T, Misagh GH, Narlawar R, Kassiou M, McGregor IS (June 2014). "Body temperature and cardiac changes induced by peripherally administered oxytocin, vasopressin and the non-peptide oxytocin receptor agonist WAY 267,464: a biotelemetry study in rats". British Journal of Pharmacology. 171 (11): 2868–87. doi:10.1111/bph.12613. PMC 4243861. PMID 24641248.
Our research mainly focusses on this early social experiences that people have that can be positive or negative, and that can really shape our developing brain. There have been some very interesting studies, for example, with children that grew up in Romanian orphanages. And we know that that early start, where it's really deprived from social contact and physical contact, had a massive impact. So we see that oxytocin levels, for example, are much lower than we would expect in other kids.
This may be an odd question. But would this be good to inject or spray on those that have undergone hair transplants in the first month of surgery. Fue microscars. I see you mention it improves hair growth and blood flow. both which basically what rogaine claims to do. Surely this would benefit new transplanted hair follicles in taking and holding? Interested in your thoughts in the matter.
But this isn’t the only study to show the subtle side of oxytocin. Just three months ago, I wrote about research from Heejung Kim at the University of California, which showed how oxytocin’s effects vary across different cultures. To fulfil its many roles, oxytocin has to dock at a protein called the ‘oxytocin receptor’, encoded by a gene called OXTR.
But Carter and other scientists are concerned by reports from the physicians and parents of children with autism spectrum disorder who say that they are already using oxytocin off-label — before it has been thoroughly tested. “We do not understand how the hormone works yet, or have enough information about what happens when it's given repeatedly,” Carter says. “This is not a molecule that people should be self-administering or playing with.”
To determine whether MAPK and NF-κB signaling pathways were involved in the anti-osteoclastogenic function of Tβ4, the effect of Tβ4 peptide on the phosphorylation levels of ERK, JNK, and p38 MAPK(s) as well as the nuclear translocation of NF-κB p65 in RANKL-stimulated BMMs were examined. As shown in Fig 8B, Tβ4 peptide inhibited the RANKL-induced phosphorylation of p38, ERK, and JNK and nuclear translocation of NF-κB p65.
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…
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