OXYTOCIN
(WikiLinks : Oxytocin) - (Last Revision: 6/18/2022)
In a study published in the journal Nature Communications, researchers observed oxytocin levels in mice and found it declines with age. Older mice were observed to have fewer oxytocin receptors in muscle stem cells. Upon being injected with the hormone, the injured muscles of the older mice began to repair themselves after just nine days. "The action of oxytocin was fast," said Christian Elabd, a senior scientist in Conboy's lab and study co-author. "The repair of muscle in the old mice was at about 80 percent of what we saw in the young mice." Source: Yahoo News
A new paradigm is that individual detriments of aging might have a common cause: the concordant alteration of a few signal transduction networks, and points to a rational strategy of recalibrating a few key pathways for combatting many age-related diseases simultaneously, as a class. [6]
Oxytocin—a hormone best known for its role in lactation, parturition and social behaviours—is required for proper muscle tissue regeneration and homeostasis, and that plasma levels of oxytocin decline with age. Systemic administration of oxytocin rapidly improves muscle regeneration by enhancing aged muscle stem cell activation/proliferation through activation of the MAPK/ERK signalling pathway. Considering that oxytocin is an FDA-approved drug, this work reveals a potential novel and safe way to combat or prevent (Skeletal Muscle Aging [13]) (Muscle Atrophy, Sarcopenia [1]) (Cardiovascular Sisease [16]) (Osteoporosis [12]) (Telomer Shortening [11] (Cognitive Impairment [6]) (Erectile and Sexual Disfunction [18,20,21]) (Liver Degeneration [17]) (Immune Dis-Regulation [14,19]) and Age-Progression [6]).
⫸ A large number of studies have shown that autophagy (see Note Section) plays an important role in reversing cell aging and increase of autophagy can delay aging and extend longevity (Rubinsztein et al., 2011). Studies now reveal that OT promotes autophagy in either AML12 mouse hepatocytes or aged mice after partial hepatectomy or with CCl4-induced acute liver injury. In conclusion, OT promotes liver regeneration, especially in aged mice, which may be achieved by promoting autophagy. All these results support the possibility of OT and its analog being a potent anti-aging drug and promote liver rejuvenation. Taken together, the above results indicate that OT may promote liver cell regeneration by enhancing cell autophagy. ⫷[17]
⫸ The levels of oxytocin (OT) and the oxytocin receptor (OTR) decrease with age
OT and various Alk5 inhibitors [43] are already FDA approved for applications that are different from agerelated degenerative pathologies, and hence repositioning this combination is facilitated. OT is not associated with cancers or any other pathologies, and in fact a lack of OT is known to cause depression, obesity, osteoporosis and muscle wasting [12, 44–46]. Alk5 inhibitors are in clinical trials for combating cancer progression, because at high levels TGF-beta switches from inhibiting to promoting cancer metastasis, and from attenuating to promoting inflammation [14, 47, 48]. Of note, both Alk5i and OT have been shown to cross the blood brain barrier, enabling delivery to all organs and tissues [14, 49]. ⫷
◉ 2 W A R N I N G S ◉
In aging males, oxytocin augmentation may be counter indicated. Specifically men with enlarged prostrates or benign prostrate hyperplasia (BPH) are at risk of being in a precancerous state.
◉ Any male with an enlarged prostate commonly referred to as benign prostrate hyperplasa (BPH) and/or a PSA level that is above the normal range for your age, should not take Oxytocin. There is a strong risk of cancer because it raises your testosterone levels. I have wondered if this risk is why the Conboy's did not persue an obviously very beneficial treatment tract.
◉ In the testis, oxytocin has been shown not only to modulate testosterone production but also to increase the activity of the enzyme 5 alpha-reductase which converts testosterone to dihydrotestosterone (DHT). The prostate is an androgen-dependent organ with DHT being the active steroid. [2]
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◉ Within the prostate testosterone is converted by the enzyme, 5α-reductase, to dihydrotestosterone, which then stimulates growth of the gland. Oxytocin increases the activity of 5α-reductase (green arrow) resulting in increased concentrations of dihydrotestosterone and growth of the prostate. Conversely, androgens feedback (red arrows) reducing oxytocin concentrations in the prostate. [5]
◉ Age is, in and of itself, a risk factor for prostrate cancer. Your chronological age functions as a good indicator of your current risk level. If you are 75 years old, there is a 75% chance that you currently have some level of prostrate cancer.
◉ The addition of a androgen receptor blocking drug may provide a prophylactic solution to the increased risk of using oxytocin in older males. This process is described in the safety section of this page.
⫸ Indeed, while in the absence of androgens, oxytocin had no effect on prostate cancer cell lines (LNCaP and PC-3), in the presence of testosterone low oxytocin doses stimulated proliferation of PC-3 cells[81], supporting the notion that changes in levels of oxytocin in the prostate in aging and cancer may promote prostate epithelial cell proliferation. It is possible that increased levels of oxytocin might be involved in the mechanisms by which high ejaculation frequency is related to decreased risk of prostate cancer[82]. ⫷ [26]
◉ The Second Precaution: We have been informed by one subscriber of this site that they got very disorientated, lethargic and felt very “Stoned,” from taking what they ordered. When we investigated the individual obtained Oxycontin, an opioid/narcotic, not Oxytocin a hormone. Be cautious and make sure what your are ordering.
⫸ It is now well established that oxytocin is present in the mammalian testis and there is growing evidence that the peptide plays a role in the male reproductive tract by both assisting sperm transport and modulating steroidogenesis. In the testis, oxytocin has been shown not only to modulate testosterone production but also to increase the activity of the enzyme 5 alpha-reductase which converts testosterone to dihydrotestosterone (DHT). The prostate is an androgen-dependent organ with DHT being the active steroid. Oxytocin is present in the mammalian prostate. We have shown in the rat that levels of the peptide can be regulated by androgens, prostatic oxytocin concentrations being decreased by testosterone and increased following castration or treatment with an antiandrogen. Oxytocin treatment increases 5 alpha-reductase activity in the prostate of healthy young rats but, unlike the testis, this rise in enzyme activity is only transient. We thus propose that a local feedback mechanism may act to control prostatic levels of DHT and hence prostatic growth. Benign prostatic hyperplasia (BPH) is a common disease which affects both men and dogs. The aetiology of the disease is complex but both DHT and aging are important factors. Oxytocin levels are raised in prostatic tissue from dogs with BPH and the increase in peptide is accompanied by increased 5 alpha-reductase activity. Preliminary findings also suggest that prostatic oxytocin levels are raised in tissue from men with BPH. These data lead us to suggest that oxytocin may be involved in the pathophysiology of the prostate gland. ⫷ [2]
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⫸Oxytocin is a hormone produced mainly in the hypothalamus and secreted by the pituitary gland. Oxytocin plays well-known roles in female reproduction, including uterine contraction and milk ejection. The oxytocin receptor, a typical member of the class I G protein±coupled receptor superfamily, is expressed in a variety of tissues, such as the ovary, testis, adrenals, uterus, mammary glands, bone, brain, liver, and adipose [105]. Because the oxytocin receptor is present on diverse cell types, oxytocin has multiple positive physiological and psychological effects [106]. In particular, it influences a wide array of social behaviors through direct projections to other brain regions such as the nucleus accumbens, olfactory bulb, amygdala, and brain stem [107±110]. Although several studies of postmortem neural tissues have investigated whether aging affects the oxytocin system, some controversy persists regarding the number of oxytonergic cells in the brain of elderly subjects [111, 112]. In addition, reduced levels of oxytocin have been detected in postmenopausal women with osteoporosis [113]. Consistent with these observations, ovariectomized mice and rats have significantly lower plasma oxytocin levels than sham-operated mice. Oxytocin enhances osteoblast differentiation, and supplementation of oxytocin reverses bone loss induced by ovariectomy in rodents [114]. Interestingly, circulating oxytocin levels decline with age in rhesus macaques and mice [115, 116]. Elabd et al. [116]suggested that this age-related decline in oxytocin contributes to defects in muscle regeneration. They found that oxytocin rejuvenates muscle stem cells by promoting their proliferation after muscle injury. Furthermore, aged Oxt-/- mice exhibit premature sarcopenia. Because several lines of evidence have revealed that oxytocin improves social deficits associated with various psychiatric disorders, numerous clinical trials have investigated the effect of this protein on social dysfunction [117]. In addition to improvement of social behavioral dysfunction, oxytocin and the oxytocin-mediated signaling pathway represent new clinical targets for rejuvenation of aged skeletal muscle. ⫷ [1]
Oxytocin Production and Secretion within the Brain and in the Periphery
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Oxytocin is mainly synthesized in by magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei within the hypothalamus. These nuclei have axons that project to the posterior pituitary, where oxytocin is stored for peripheral release. Magnocellular axonal neurons also project to the prefrontal cortex, hippocampus, arcuate nucleus, and amygdala for direct axonal release (solid arrows). Dendritically released oxytocin (dashed arrows) targets the amygdala and sensory cortices. Oxytocin is also synthesized in the parvocellular neurons of PVN that have axonal projections to the spinal cord and dorsal vagal complex (DVC). Image created with BioRender. [136]
Oxytocin Can Protect Telomeres from Social Stress
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Correlation studies have linked both oxytocin and the oxytocin receptor to telomere length (Yim et al., 2016),
Previous studies have demonstrated that oxytocin can protect against some endocrine and behavioral effects of social isolation, Stevenson et al. (2019) provided the first evidence that oxytocin can protect telomeres against the effects of social isolation. Thus, this suggests that social support and OXT can alleviate some of the negative consequences of social isolation, reducing glucocorticoid levels. Daily OXT injections in isolated voles was able to prevent the observed negative consequences of social isolation, including the telomeres shortening due to oxidative stress and the accelerated cellular aging process (Stevenson et al., 2019). Based on this evidence, OXT may completely prevent the effects of (chronic isolation) / (stress) on cellular aging. [11]
The National Geographic published an article describing a 2014 paper by the Conboy lab identifying: The Secret Ingredient in Young Blood:as Oxytocin?
“Oxytocin is an age-specific circulating hormone that is necessary for muscle maintenance and regeneration,”and provides a potent rational for including Oxytocin in an anti-aging strategy.
⫸ Here we report that oxytocin—a hormone best known for its role in lactation, parturition and social behaviors—is required for proper muscle tissue regeneration and homeostasis, and that plasma levels of oxytocin decline with age. Inhibition of oxytocin signalling in young animals reduces muscle regeneration, whereas systemic administration of oxytocin rapidly improves muscle regeneration by enhancing aged muscle stem cell activation/proliferation through activation of the MAPK/ERK signalling pathway.
The reduction in muscle mass in humans starts in the third decade of life and accelerates after the fifth decade, resulting in a decrease in strength and agility1. Muscle ageing is characterized by a deficiency in muscle regeneration after injury and by muscle atrophy associated with altered muscle function, defined as sarcopenia2.
These results demonstrate that myogenic proliferation and subsequent differentiation depend on ‘youthful’ levels of OT.
The role of OT in tissue homeostasis and regeneration is poorly documented and age-specific OT studies are lacking. The present work is the first to demonstrate that OT supports productive repair and maintenance of the skeletal muscle, and that age- imposed decline in OT contributes to sarcopenia. Moreover, we show that OT acts directly on muscle stem cells (in vitro and in vivo) and that pro-myogenic effects of OT are mediated by MAPK/ERK signalling.
The age-specific decrease in OT receptor levels in muscle stem cells compounds the decline of OT itself but, importantly, significant OT receptor levels still remain in the old cells, allowing for an enhancement of myogenesis by ectopic OT. Interestingly, these findings are a mirror image of the age-imposed deregulation of TGF-b/pSmad3 signalling in muscle stem cells, where with age there is an upregulation of TGF-b1 and simultaneous elevation of the TGF-b receptor24,40.
In contrast, OT is a naturally produced endocrine peptide that has little to no known detrimental side effects. Diminished circulating levels of OT are associated with pathological states such as autism in children44,45, osteoporosis46 and depression47.
The potent positive effects of OT on muscle tissue homeostasis and repair that were uncovered in this study are thus promising for developing an effective and safe new clinical strategy where OT and OTR agonists might be potentially used as systemically applicable and sustainable molecules for combating the deterioration of muscle mass, strength and agility in the elderly. ⫷ [2]
[2018] “Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age”
⫸ TGF-beta which activates ALK5/pSmad 2,3 and goes up with age, and oxytocin (OT) which activates MAPK and diminishes with age. The dose of Alk5 inhibitor (Alk5i) was reduced by 10-fold and the duration of treatment was shortened (to minimize overt skewing of cell-signaling pathways), yet the positive outcomes were broadened, as compared with our previous studies. Alk5i plus OT quickly and robustly enhanced neurogenesis, reduced neuro-inflammation, improved cognitive performance, and rejuvenated livers and muscle in old mice. Interestingly, the combination also diminished the numbers of cells that express the CDK inhibitor and marker of senescence p16 in vivo. Summarily, simultaneously re-normalizing two pathways that change with age in opposite ways (up vs. down) synergistically reverses multiple symptoms of aging.
Using a two-prong approach of simultaneously diminishing TGF-beta signaling and adding OT (which activates pERK via the oxytocin receptor (OTR) [12]), we were able to reduce the required dose of Alk5i, shorten the duration of treatment and to achieve a more broad rejuvenation of the three germ-layer derivative tissues: brain, liver and muscle. And, we found that Alk5i+OT down-regulated the number of cells that show an age-associated increase of the cyclin dependent kinase (CDK) inhibitor and marker of senescence, p16, thereby representing a pharmacological combination of two FDA approved drugs to normalize this checkpoint protein, which when chronically elevated negatively impacts tissue health [16-22].
This result is consistent with the OT/OTR and Alk5/TGF-beta/pSmad pathways inter- acting through pERK [2, 11, 24]. To confirm this possible mechanism, we studied the effects of Alk5i, OT and Alk5i+OT on the levels of oxytocin receptor (OTR). Interestingly, the combination of Alk5i+OT increased the expression of OTR above either drug alone or control (Figure 1B). And of note, OT and OTR signaling is needed for healthy muscle, bone, brain and metabolism [2, 12].
OT and various Alk5 inhibitors [43] are already FDA approved for applications that are different from age- related degenerative pathologies, and hence repositioning this combination is facilitated. (OT is not associated with cancers or any other pathologies, and in fact a lack of OT is known to cause depression, obesity, osteoporosis and muscle wasting [12, 44–46].)* Alk5 inhibitors are in clinical trials for combating cancer progression, because at high levels TGF-beta switches from inhibiting to promoting cancer metastasis, and from attenuating to promoting inflammation [14, 47, 48]. Of note, both Alk5i and OT have been shown to cross the blood brain barrier, enabling delivery to all organs and tissues [14, 49].
The translational ramifications of this study are in the attenuation and reversal of multi-tissue attrition and decline of cognitive performance in old mammals, leading to novel defined pharmacology for a number of degenerative and metabolic age-associated diseases, as a class.⫷[6]
◉ As this paper describes, by changing two determinants of aging; the up regulation of Oxytocin and down regulating TGFbeta1, it becomes possible to realize a synergistic improvement in biological age. Oxytocin as described on this page and Transforming Growth Factor beta-1(TGFbeta1). Please refer to that page for a complete description and rational for including both strategies.
• As the warning at the top of this page indicates, OT does pose an increase risk of cancer for a specific population of older males.
Interventional Opportunity: The Conboy’s paper excerpted in the overview section and indeed the vast majority of references incorporated on this page support Oxytocin as a viable interventional strategy to reverse loss of bone density, loss of muscle strength, improved organ function and as indicated by the graphs on the right, a dramatic improvement of cognitive function. The Conboy paper also describes a viable rational supporting a dramatic reduction in systemic inflammation. Combined these results constitute an age regressive intervention. Epigenetic studies would be very insightful.
Oxytocin
Oxytocin is a hormone produced mainly in the hypothalamus and secreted by the pituitary gland [174]. In humans, the level of this hormone is reduced in circulation in both genders [175, 176], and a high serum oxytocin level is positively associated with logical memory in aged females [176]. In male mice, aging led to a reduction of this hormone in plasma, and administration of oxytocin improved muscle regeneration through the activation of muscle stem cell activation and proliferation [177]. Oxytocin and two analogs reversed insulin resistance and glucose intolerance in obese mice [178]. A 4-week oxytocin treatment contributed to reducing body weight in obese humans [178]. Oxytocin also promoted liver regeneration especially in aged mice possibly through the activation of autophagic response [179]. Intranasal administration of oxytocin for 10 days was reported as safe in the aged population [180], and whether this mediates beneficial effects in individuals with cardiovascular-metabolic diseases remains an open question to be explored. [29]
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There are two components of this study, the proverbial signaling determinants that move in opposite directions; Oxytocin and TGFbeta1.
There are multiple agents that will block TGFbeta1 at ALK5 and referred to as ALK5 inhibitors (ALK5i) at different points in the signaling cascade after the TFGbeta1 receptor is activated by ligand. They are detailed on the TGFbeta1 page.
The Scourcing / Resources section below identifies multiple agents capable of increasing systemic Oxytocin levels.
◉ The plasma half-life of Casodex is 4 and 8 days
◉ The plasma half-life of oxytocin ranges between 2 and 20 minutes.
◉ The plasma half-life of EGCG ranges between 3.9 and 5.5 hours*
◉ *This is typical for all of the ALK5i’s
◉ Supplemental magnesium is important to optimize the effectiveness of any Oxytocin administration.
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Potential Risk Reduction of Oxytocin Administration in Older Men
It may be possible to pharmacology block the negative effects produced by the increase in DHT production initiated by Oxytocin. The drug Bicalutamide, brand name; Casodex. does not inhibit the production of testosterone nor its conversion into dihydrotestosterone. It blocks the androgen receptor both utilize for signaling. Casodex has several off targets effect and they should be carefully reviewed with your physician prior to utilizing it as an adjunct testosterone receptor blocking agent. One of the effects is breast enlargement in men. This effect appears over time at relative high study state levels of drug. Blocking the adverse effect of testosterone in BPH or prostrate cancer in order to administer Oxytocin may be counter indicated in your specific situation and should not be implemented without consulting with your primary care physician.
Another effect of Casodex is the up regulation of Estrogen. Estrogen has been found to increase the synthesis and secretion of oxytocin. It also increases the expression of oxytocin receptors in the brain (25).
Casodex, acts as a highly selective competitive silent antagonist of the androgen receptor (AR) (IC50 = 159–243 nM), the major biological target of the androgen sex hormones testosterone and dihydrotestosterone (DHT).[16][17][18][19] It has no capacity to activate the AR under normal physiological circumstances.[20] In addition to competitive antagonism of the AR, bicalutamide has been found to accelerate the degradation of the AR, and this action may also be involved in its activity as an antiandrogen.[21] The activity of bicalutamide lies in the (R)-isomer, which binds to the AR with an affinity that is about 30-fold higher than that of the (S)-isomer.[22] Levels of the (R)-isomer also notably are 100-fold higher than those of the (S)-isomer at steady-state.[23][24] Source: The Wikipedia [] page for Bicalutamide/Casodex is a comprehensive. informative and well referenced compendium of information.
Bicalutamide levels after a single 10, 30, or 50 mg dose of bicalutamide in men.[194] The mean elimination half-life of bicalutamide in this study was 5.5 to 6.3 days. Source: The pharmacokinetics of Casodex in prostate cancer patients after single and during multiple dosing
Pulsed administration of Casodex one day before the first administration of Oxytocin may counteract the increased risk of taking Oxytocin in an older male population. Theoretically this makes sense, but no studies have been conducted to determine if Casodex is prophylactically effective at mitigating the risk that taking supplemental oxytocin may be causing. Oxytocin treatment increases 5 alpha-reductase activity in the prostate of healthy young rats but, unlike the testis, this rise in enzyme activity is only transient. As the graphs above indicate, Casodex has a fairly long half life of approximately 5 to 7 days depending on the dose(s) and you own metabolism. That translates to some level of coverage for 10 to 20 days. Again, what is effective coverage in this treatment scenario is not known. Taking additional doses on subsequent days/weeks extends the therapeutic window as indicated by the graph on the above-right, showing steady state levels achieved for each additional dose. For instance if you took 25mg for two days, the area under the curve would provide moderate to complete blockage of the testosterone receptors for 7 days. If you then took Oxytocin/ALK5i daily over a five day period within this window, you would be within the theoretical, androgen receptor blocking protective period. Oxytocin is a multi-faceted hormone that utilizes oxytocin receptors found on multiple cell types throughout the body. This should, again in theory, provide the benefit of administering oxytocin while at least minimally reducing the risk.
Oxytocin-producing cells and OXTR are sensitive to the oxytocin peptide. A form of autocrine feedback can regulate the synthesis of endogenous oxytocin levels in the central nervous system, moreover, availability of OXTRs can be dynamically modulated by increasing exogenous oxytocin administration.
◉ The plasma half-life of Casodex is 5 and 7 days.
◉ The plasma half-life of oxytocin ranges between 2 and 20 minutes.
◉ The plasma half-life of Demoxytocin (synthetic analogue of oxytocin) ranges between 30 and 60 minutes.
◉ The plasma half-life of EGCG ranges between 3.9 and 5.5 hours.*
◉ *This is typical for all of the ALK5i’s.
◉ Supplemental magnesium is important to optimize the effectiveness of any Oxytocin administration.
Multitude of Drugs, Supplements and Probiotics that increase Oxytocin
Drugs:
A Large variety of sublingual tablets, nasal sprays, injectable formulation of Oxytocin are available through pharmacist and online. Prescriptions are required for many of them but not all. Search online and the physicians desk reference. The list we provide below contains just a few examples of commonly utilized preparations.
OxyPro Oxytocin 5 IU Lozenges, Profound Products www.profound-products.com (Discounted Links provided below.)
Desaminooxytocin® [Demoxytocin] is a synthetic analogue of oxytocin. The mechanism of action and pharmacological properties of demoxytocin and oxytocin are similar. the hormone of the posterior pituitary gland.
With buccal administration, demoxytocin, unlike oxytocin, is not cleaved by saliva enzymes, and easily penetrates the oral mucosa into the systemic circulation. The effect is dose dependent and lasts up to 180 minutes.
Pharmacokinetics Demoxytocin is rapidly and completely absorbed through the mucous membrane of the oral cavity and enters the bloodstream. With buccal administration of 1 tablet of 50 IU, demoxytocin is absorbed within 15-30 minutes. Saliva enzymes do not destroy the drug because it is resistant to oxytocinase; elimination of demoxytocin is carried out within 30-60 minutes.
Nutritional Supplements that increase Oxytocin Systemically:
◉ Vitamin C (sodium ascorbate) stimulates the production oxytocin, in a dose dependent manor and the synthesis of oxytocin is dependent upon Vitamin C. Additionally the activity of PAM enzyme system is dependent upon vitamin C.[8] This crucial PAM enzyme is a copper and Vitamin C dependent enzyme that is responsible for activating these neuropeptides. And another study found that supplementing with a high dose of Vitamin C increases the release of oxytocin, which then increases intercourse frequency, improves mood and decreases stress (24).
◉ Vitamin D hormone would regulate both the production of the oxytocin hormone and the response to it we confirmed that OXT contains a proximal and 3 distal VDREs and OXTR has 1 distal VDRE as observed in serotonin producing VDREs. [9]
◉ Tryptophan and Vitamin D supplementation may be a simple method of increasing brain serotonin/ oxytocin levels without negative side effects. [126]
◉ PGC-1 directly regulates the expression of the hypothalamic neuropeptide oxytocin, PGC-1_ is both necessary and sufficient for the production of oxytocin, implicating hypothalamic PGC-1_ in the direct activation of a hypothalamic hormone known to control energy intake. [23]
◉ Metformin induced AMPK phosphorylation in skeletal muscle increases PGC-1., mitochondrial oxidative enzymes, and cytochrome C expression, ultimately amplifying mitochondrial function. [71]
◉ Melatonin produced a significant increase in plasma oxytocin in the nonpregnant though not the pregnant ewe. These data suggest a possible interaction between melatonin and oxytocin in the integration of mammalian reproduction cycles.[22]
◉ Caffeine increase AMPK phosphorylation, as well as cAMP accumulation which activates CREB, ultimately leading to PGC-1 expression. [71]
◉ EGCG increased mRNA levels of several mitochondrial biosynthetic genes including NRF-1 and UCP3 (downstream targets of PGC-1), as well as PPARα. EGCG was also shown to increase AMPK and p38 MAPK phosphorylation which promotes PGC-1 phosphorylation and activation. [71]
◉ Resveratrol treatment appears to increase expression and deacetylation of PGC-1 leading to significantly elevated mitochondrial DNA and content which appears to function in part through AMPK activation and through increased SIRT expression. Supplementation with resveratrol has been shown to improve many clinically meaningful characteristics including circulating lipids, glucose, and inflammatory markers. Despite some controversy regarding the exact mechanism(s) of action, resveratrol appears to be a potent stimulator of PGC-1and mitochondrial biogenesis in skeletal muscle. [71]
◉ Leucine treatment increases PGC-1 expression with simultaneous increase in mitochondrial content using human and mouse cell models. [71]
◉ Magnesium The presence of magnesium is essential for effective oxytocin receptor / ligand functionality. In the absence of magnesium the afinity of the receptor for OT decreased by about 1500-fold.
◉ Leucine and Resveratrol treatment of cultures 3T3 adipocytes and C2C12 myocytes and found that concurrent treatment synergistic effect of simultaneous treatment significantly elevated SIRT1 and SIRT3 in both cell models [10]. Additionally, they found that combination leucine and resveratrol increased AMPK content and fatty acid oxidation under both high and low glucose in cultured adipocytes. [71]
◉ Lipoic acid and ubiquinol (◉ CoQ10) have been shown to increase nuclear PGC-1 levels with heightened PPARγ activation, NRF-2, TFAM, and mitochondrial content in C2C12 mouse myoblasts. [71]
◉ Fenugreek Stimulates Oxytocin Expression at the Pituitary Level and Upregulates the Expression of Insulin, GH and IGF-1 Receptors. [4]
Probiotics:
◉ Lactobacillus reuteri (Prototype probiotic bacterium) has been found to upregulate hormone oxytocin and systemic immune responses to achieve a wide array of health benefits involving wound healing, mental health, metabolism, and myoskeletal maintenance.
The YouTube video linked below provides a broad overview of the benefits of Oxytocin as well as how to culture your own yougert containing the Lactobacillus Reuteri bacteria.
ProfoundHealth is one component of a integrated group of sites that provides anti-aging information and high quality, reasonably priced products.
ARC readers/subscribers have been offered a 15% discount. Use the Coupon Code ⫸ ARC ⫷ at checkout. The logo on the left is a direct links to their sites.
This page contains a complete description of Demoxytocin including ordering information from My Salve.
A Large number of Nasal Sprays are also available over the internet
For a complete listing of all available discounts please go to the Discounts and Resources page under the News and Info Sources Heading at the top of each page.
ONE PHYSICIAN’S EXPERIENCE WITH OXYTOCIN
[1] [2022] Circulating plasma factors involved in rejuvenation
[3] [1995] Oxytocin and prostatic function
[5] [2020] Oxytocin: a paracrine regulator of prostatic function
[7] [] Catecholamines and ascorbic acid as stimulators of bovine ovarian oxytocin secretion
[8] Vitamin D hormone regulates serotonin synthesis
[9] Fenugreek Stimulates the Expression of Genes Involved in Milk Synthesis and Milk Flow through Modulation of Insulin/GH/IGF-1 Axis and Oxytocin Secretion
[10] [1989] Essential role of magnesium in oxytocin-receptor affinity and ligand specificity
[11] [2021] The Anti-Aging Role of Oxytocin
[14] [2020] Is Oxytocin “Nature’s Medicine?
[15] [2020] An Allostatic Theory of Oxytocin
[17] [2021] Oxytocin promotes hepatic regeneration in elderly mice
[18] ]2021] Oxytocin, Erectile Function and Sexual Behavior: Last Discoveries and Possible Advances
[19] [2017] Approaches Mediating Oxytocin Regulation of the immune System
[20] [2011] The orgasmic history of oxytocin- Love, lust, and labor
[21] [2007] Oxytocin- The Neuropeptide of Love Reveals Some of Its Secrets
[22] [1985] Oxytocin Release Induced by Melatonin in the Ewe
[23] [2021] Metabolic Effects of Oxytocin
[25] [2022] Wikipedia;Oxytocin
[26] [2018] Oxytocin and cancer: An emerging link
[27] [2011] Autophagy and Aging
[28] [2022] Oxytocin promotes hepatic regeneration in elderly mice
[29] [2022] Role of circulating molecules in age-related cardiovascular and metabolic disorders
Keep Reading ;√), If you find something important please use the “contribute content,” and share it with us.
Ethanol-oxytocin Interactions at Homomeric Glycine Receptors
Oxytocin, the sweet hormone? Trends in Endocrinology and Metabolism
The Oxytocin Receptor: From Intracellular Signaling to Behavior
Catecholamines and ascorbic acid as stimulators of bovine ovarian oxytocin secretion
Vitamin D hormone regulates serotonin synthesis.
Autophagy:
Autophagy is also a critical regulator of organellar homeostasis, particularly of mitochondria. Dysfunctional mitochondria that have lost their membrane potential and are more likely to release toxic apoptotic mediators and reactive oxygen species are apparently selectively removed by autophagy relative to “healthy” mitochondria via phosphorylation reactions mediated by the kinase PINK1 and subsequent ubiquitination of mitochondrial membrane proteins by the E3 ligase Parkin. Autophagy can also enhance degradation of various bacteria and viruses and may play protective roles in numerous infectious diseases