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Nathan Goodyear

Glucagon-like peptide 1 improves the ability of th... [Diabetes. 1998] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...9703326

glucagon-like peptid-1 insulin glucose control diabetes resistance

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • We concluded that low dosage GLP-1 improves the ability of the beta-cell to secrete insulin in both IGT and NIDDM subjects, but that the ability to sense and respond to subtle changes in plasma glucose is improved in IGT subjects, with only a variable response in NIDDM subjects. Beta-cell dysfunction was improved by GLP-1 infusion, suggesting that early GLP-1 therapy may preserve beta-cell function in subjects with IGT or mild NIDDM.
  • Nathan Goodyear on 06 Apr 11
     
    glucagon-like peptide-1 improves insulin/glucose regulation
Nathan Goodyear

Modulation of the glucagon-like peptide-1 receptor... [J Pharmacol Exp Ther. 2011] - Pu... - 0 views

www.ncbi.nlm.nih.gov/...21075839

flavonoids glucagon-like peptide-1

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Nathan Goodyear on 06 Apr 11
     
    natural flavonoids act as modulator of glucagon-like peptide-1
Nathan Goodyear

Incretin-based therapies: can we achieve glycemic control and cardioprotection? - 0 views

joe.endocrinology-journals.org/...T17.full

incretin incretins GLP-1 glucagon-like peptide 1) glucose homeostasis

shared by Nathan Goodyear on 24 Mar 14 - No Cached
  • Nathan Goodyear on 24 Mar 14
     
    Good discussion on the incretin: (Glucagon-like peptide 1 (GLP-1).
Nathan Goodyear

Exenatide can reduce glucose independent of islet hormones or gastric emptying - 0 views

ajpendo.physiology.org/...E269.full

glucagon-like peptide-1 exenatide insulin glucose regulation diabetes

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Nathan Goodyear on 06 Apr 11
     
    glucagon-like peptide-1 useful in glucose/insulin regulation
Nathan Goodyear

http://www.diabetologia-journal.org/files/Narendran.pdf - 0 views

www.diabetologia-journal.org/...Narendran.pdf

exercise inflammation growth hormone GH IGF-1 TNF-alpha IL-6 IL-1beta IL-1Ra interferon-gamma diabetes islet cells

shared by Nathan Goodyear on 28 Oct 14 - No Cached
  • Nathan Goodyear on 28 Oct 14
     
    Exercise is not just for calories out.  Exercise increases growth hormone, IGF-1, glucagon-like peptide 1, IL-6, and IL-1ra.  The effect is to GH increases beta islet cell mass and protects beta cell lines against IL-1beta, Interferon-gamma and TNF-alhpa induced apoptosis.  IL-6 increased production increases GLP-1 and IL-1ra which counters IL-1beta.  Interleukin-1beta induces islet cell apoptosis and thus IL-1ra counters this pro-inflammatory signal.
Nathan Goodyear

Extranuclear Actions of the Androgen Receptor Enhance Glucose-Stimulated Insulin Secret... - 0 views

www.cell.com/...S1550-4131(16)30118-8

Testosterone low Testosterone low T hormones male hormones DHT dihydrotestosterone insulin AR androgen receptor Diabetes

shared by Nathan Goodyear on 18 May 16 - No Cached
  • Nathan Goodyear on 18 May 16
     
    only abstract available here. Mouse model finds possible explanation for low Testosterone and diabetes link.  Actually, the link is between the metabolite DHT and the AR. The activity of AR from DHT binding induces beta cell insulin secretion in the presence of glucose.  This is dependent on glucagon-like peptide 1 receptor activation also, which AR activation by DHT does in fact do.
Nathan Goodyear

Ibuprofen alters human testicular physiology to produce a state of compensated hypogona... - 0 views

www.pnas.org/...1715035115.full

ibuprofen Testosterone epigenetics hormones low Testosterone low T

shared by Nathan Goodyear on 09 Jan 18 - No Cached
  • The levels of LH in the ibuprofen group had increased by 23% after 14 d of administration
  • This increase was even more pronounced at 44 d, at 33%
  • We found an 18% decrease (P = 0.056) in the ibuprofen group compared with the placebo group after 14 d (Fig. 1A) and a 23% decrease (P = 0.02) after 44 d (Fig. 1C). Taken together, these in vivo data suggest that ibuprofen induced a state of compensated hypogonadism during the trial, which occurred as early as 14 d and was maintained until the end of the trial at 44 d
  • ...27 more annotations...
  • We first investigated testosterone production after 24 and 48 h of ibuprofen exposure to assess its effects on Leydig cell steroidogenesis. Inhibition of testosterone levels was significant and dose-dependent (β = −0.405, P = 0.01 at 24 h and β = −0.664, P < 0.0001 at 48 h) (Fig. 2A) and was augmented over time
  • The AMH data show that the hypogonadism affected not only Leydig cells but also Sertoli cells and also occurred as early as 14 d of administration
  • Sertoli cell activity showed that AMH levels decreased significantly with ibuprofen administration, by 9% (P = 0.02) after 14 d (Fig. 1B) and by 7% (P = 0.05) after 44 d compared with the placebo group
  • Examination of the effect of ibuprofen exposure on both the ∆4 and ∆5 steroid pathways (Fig. 2B) showed that it generally inhibited all steroids from pregnenolone down to testosterone and 17β-estradiol; the production of each steroid measured decreased at doses of 10−5–10−4 M. Under control conditions, production of androstenediol and dehydroepiandrosterone (DHEA) was below the limit of detection except in one experiment with DHEA
  • Measuring the mRNA expression of genes involved in steroidogenesis in vitro showed that ibuprofen had a profound inhibitory effect on the expression of these genes (Fig. 3 B–D), consistent with that seen above in our ex vivo organ model. Taken together, these data examining effects on the endocrine cells confirm that ibuprofen-induced changes in the transcriptional machinery were the likely reason for the inhibition of steroidogenesis.
  • Suppression of gene expression concerned the initial conversion of cholesterol to the final testosterone synthesis. Hence, expression of genes involved in cholesterol transport to the Leydig cell mitochondria was impaired
  • A previous study reported androsterone levels decreased by 63% among men receiving 400 mg of ibuprofen every 6 h for 4 wk
  • We next examined the gene expression involved in testicular steroidogenesis ex vivo and found that levels of expression of every gene that we studied except CYP19A1 decreased after exposure for 48 h compared with controls
  • the changes in gene expression indicate that the transcriptional machinery behind the endocrine action of Leydig cells was most likely impaired by ibuprofen exposure.
  • Together, these data show that ibuprofen also directly impairs Sertoli cell function ex vivo by inhibiting transcription
  • ibuprofen use in men led to (i) elevation of LH; (ii) a decreased testosterone/LH ratio and, to a lesser degree, a decreased inhibin B/FSH ratio; and (iii) a reduction in the levels of the Sertoli cell hormone AMH
  • The decrease in the free testosterone/LH ratio resulted primarily from the increased LH levels, revealing that testicular responsiveness to gonadotropins likely declined during the ibuprofen exposure. Our data from the ex vivo experiments support this notion, indicating that the observed elevation in LH resulted from ibuprofen’s direct antiandrogenic action
  • AMH levels were consistently suppressed by ibuprofen both in vivo and ex vivo, indicating that this hormone is uncoupled from gonadotropins in adult men. The ibuprofen suppression of AMH further demonstrated that the analgesic targeted not only the Leydig cells but also the Sertoli cells, a feature encountered not only in the human adult testis but also in the fetal testis
  • ibuprofen displayed broad transcription-repression abilities involving steroidogenesis, peptide hormones, and prostaglandin synthesis
  • a chemical compound, through its effects on the signaling compounds, can result in changes in the testis at gene level, resulting in perturbations at higher physiological levels in the adult human
  • The analgesics acetaminophen/paracetamol and ibuprofen have previously been shown to inhibit the postexercise response in muscles by repressing transcription
  • Previous ex vivo studies on adult testis have indeed pointed to an antiandrogenicity, only on Leydig cells, of phthalates (41), aspirin, indomethacin (42), and bisphenol A (BPA) and its analogs
  • ibuprofen’s effects were not restricted to Leydig and Sertoli cells, as data showed that the expression of genes in peritubular cells was also affected
  • short-term exposure
  • In the clinical setting, compromised Leydig cell function resulting in increased insensitivity to LH is defined as compensated hypogonadism (4), an entity associated with all-cause mortality
  • compensated hypogonadic men present with an increased likelihood of reproductive, cognitive, and physical symptoms
  • an inverse relationship was recently reported between endurance exercise training and male sexual libido
  • AMH concentrations are lower in seminal plasma from patients with azoospermia than from men with normal sperm levels
  • inhibin B is a key clinical marker of reproductive health (32). The function of AMH, also secreted by Sertoli cells, and its regulation through FSH remain unclear in men
  • the striking dual effect of ibuprofen observed here on both Leydig and Sertoli cells makes this NSAID the chemical compound, of all the chemical classes considered, with the broadest endocrine-disturbing properties identified so far in men.
  • after administration of 600 mg of ibuprofen to healthy volunteers
  • 14 d or at the last day of administration at 44 d
  • Nathan Goodyear on 09 Jan 18
     
    ibuprofen alters genetic expression that results in decreased Testosterone production.
Nathan Goodyear

Thymosin alpha 1: A comprehensive review of the literature - 0 views

www.ncbi.nlm.nih.gov/...PMC7747025

peptides cancer thymosin alpha-1 TA-1

shared by Nathan Goodyear on 15 Aug 21 - No Cached
  • Nathan Goodyear on 15 Aug 21
     
    Awesome review article on TA-1 and its broad immunomodulatory effects, i.e. increase IL-1, IFN-gamma, increase dendritic cell activity, inhibition of tumor growth…
Nathan Goodyear

Thymosin alpha 1 suppresses proliferation and induces apoptosis in breast cancer cells ... - 0 views

pubmed.ncbi.nlm.nih.gov/26002438

TA-1 peptides PI3K_Akt_mTOR breast cancer thymosin alpha-1 PTEN

shared by Nathan Goodyear on 15 Aug 21 - No Cached
  • Nathan Goodyear on 15 Aug 21
     
    TA-1 induces apoptosis through PTEN mediated PI3k/Akt/mTOR pathway inhibition. Sorry, only abstract available here. Significant in that TA-1 works beyond just immune stimulation.
Nathan Goodyear

Ghrelin-Induced Food Intake Is Mediated via the Orexin Pathway - 0 views

endo.endojournals.org/...1506.long

ghrelin orexin orexins appetite

shared by Nathan Goodyear on 28 May 13 - No Cached
  • Ghrelin, a peptide produced in the stomach and hypothalamus, stimulates feeding and GH secretion
  • Centrally administered ghrelin exerts an orexigenic activity through the neuropeptide Y (NPY)
  • though ghrelin is predominantly produced in endocrine cells of the stomach (17, 18), it is also synthesized in the hypothalamic arcuate nucleus (1, 19), a critical region for feeding
  • Nathan Goodyear on 28 May 13
     
    ghrelin stimulates feeding through orexin signaling.
Nathan Goodyear

Zadaxin (Thymalfasin): Uses, Dosage, Side Effects, Interactions, Warning - 0 views

www.rxlist.com/zadaxin-drug.htm

peptide cancer TA-1 thymosin alpha-1

shared by Nathan Goodyear on 15 Aug 21 - No Cached
  • Nathan Goodyear on 15 Aug 21
     
    Not an article, but a drug review of the medication Zadaxin, which is a commercial synthetic form of TA-1; Thymosin alpha 1 improved immunological parameters increased tumor response rates, and improved survival and quality of life
Nathan Goodyear

Clostridium scindens: a human gut microbe with a high potential to convert glucocortico... - 0 views

www.jlr.org/...2437.full

gut microbiota gut microbiome gut bacteria androgens hormones clostridium scindens

shared by Nathan Goodyear on 29 Apr 15 - No Cached
  • During the enterohepatic circulation (EC), bile salts are synthesized in the liver, concentrated in the gallbladder, and function in the lumen of the small intestine to absorb dietary lipids and limit microbial growth at the site of nutrient uptake
  • Bile acid 7α/β-dehydroxylating bacteria are organisms capable of converting primary bile acids made by the host to harmful secondary bile acids, deoxycholic acid, and lithocholic acid
  • These bacteria normally comprise a small proportion of the gut microbiota (∼103–104/g wet weight) and consist of species within the genus Clostridium
  • ...3 more annotations...
  • C. scindens and a small number of species belonging to the genus Clostridium are responsible for significant alterations in the human bile acid pool composition through bile acid 7α/β dehydroxylation
  • bile acids play an important role in maintaining intestinal barrier function as antimicrobial agents in the small bowel (37, 38) and inducers of antimicrobial peptides
  • Perturbations in the biliary bile acid pool composition can be indicative of hepatogastrointestinal diseases such as fat malabsorption (40), gallstones (3), gastrointestinal cancers (41), and possibly type II diabetes
  • Nathan Goodyear on 29 Apr 15
     
    Gut microbiota appears to be source of androgen production that originates from the gut.  Who would have thought that the Gut as an androgen producing endocrine gland.
Nathan Goodyear

Redefining Metabolic Syndrome in Men (July 2012) Townsend Letter for Doctors & Patients - 0 views

www.townsendletter.com/...metsyndrome0712.html

testosterone male men hormone hormones saliva salivary low T low metabolic syndrome MetS

shared by Nathan Goodyear on 28 Aug 12 - No Cached
  • Approximately 95% to 98% of testosterone is bound to a carrier protein at any given time, leaving just the remaining 2% to 5% as completely unbound and available for tissues to use
  • most serum laboratories offer a free testosterone level, which is a calculated value based on SHBG levels or determined with equilibrium dialysis
  • the hormone enters the salivary gland by passive diffusion
  • ...11 more annotations...
  • Testosterone has a known age-related decline, and total levels typically drop by approximately 1.6% per year beginning for most men in their 30s
  • As estrogen levels rise, they prompt the body to produce more SHBG, which in turn has a higher binding affinity for testosterone, and drives the unbound fraction of the testosterone pool down even further
  • When the increase in SHBG is taken into account, the age-related decline in the level of hormone that can be used by the body is closer to 2% to 3% per year.
  • Stinging nettle (Urtica dioica), an herb commonly used for allergies, can also be employed to bind to SHBG, which leaves more testosterone available to tissues
  • Leptin, an adipose-derived peptide hormone that regulates appetite and metabolism, has been shown to directly inhibit testosterone production in animal models
  • tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) further inhibit Leydig cell testosterone production
  • Natural aromatase inhibitors include the bioflavonoids chrysin and luteolin
  • Zinc deficiency causes an upregulation of the aromatase enzyme
  • Testosterone reduces lipoprotein lipase (LPL) activity
  • there are several herbs that can work to boost testosterone levels, including longjack (Eurycoma longifolia), horny goat weed (Epimedium grandiflorum), and tribulus (Tribulus terrestris).
  • the majority of the hormone is bound to carrier proteins including sex hormone binding globulin (SHBG) and albumin
  • Nathan Goodyear on 28 Aug 12
     
    nice and short review on testosterone and men's  health.
Nathan Goodyear

Effects of glucagon-like peptide 1 on appetite and body weight: focus on the CNS - 0 views

joe.endocrinology-journals.org/...T1.full

incretins incretin appetite

shared by Nathan Goodyear on 24 Mar 14 - No Cached
  • Nathan Goodyear on 24 Mar 14
     
    To be read article on incretins
Nathan Goodyear

Hyperthermia as an immunotherapy strategy for cancer - 1 views

www.ncbi.nlm.nih.gov/...PMC2828267

cancer hyperthermia

shared by Nathan Goodyear on 29 Nov 18 - No Cached
  • the notion of treating human cancers with heat dates back to the writings of Hippocrates
  • enhance the efficiency of standard cancer therapies, such as chemotherapy and radiation treatment
  • After antigen uptake at tumor sites, APCs have the ability to create a robust response by entering lymphoid compartments and programming lymphocytes
  • ...36 more annotations...
  • Hyperthermia differs fundamentally from fever in that it elevates the core body temperature without changing the physiological set point
  • hyperthermia is induced by increasing the heat load and/or inactivating heat dissipation
  • mor cells [2]. Although significant cell killing could be achieved by heating cells or tissues to temperatures > 42°C for 1 or more hours, the application, measurement and consistency of this temperature range within the setting of cancer clinical trials
  • mild temperature hyperthermia (ie, within the fever-range, 39–41°C)
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      101.2 to 105.8
  • moderate hyperthermia (41°C)
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      105.8 F
  • Hsps are a family of stress-induced proteins
  • they are key regulators of cellular protein activity, turnover and trafficking
  • Hsps ensure appropriate post-translational protein folding, and are able to refold denatured proteins, or mark irreversibly damaged proteins for destruction
  • the ability of fever-range hyperthermia to induce reactive immunity against tumor antigens through DCs and NK-cells is likely mediated by Hsps
  • thermotolerance
  • Hsps support the malignant phenotype of cancer cells by not only affecting the cells’ survival, but also participating in angiogenesis, invasion, metastasis and immortalization mechanisms
  • Hsps released from stressed or dying cells activate dendritic cells (DCs), transforming them into mature APCs
  • In theory, fever-range hyperthermia may take advantage of tumor cell Hsps by inducing their release from tumor cells and augmenting DC priming against tumor antigens
  • In several models of hyperthermia, heat-treated tumors exhibited improved DC priming and generation of systemic immunity to tumor cell
  • hyperthermia alone can enhance antigen display by tumor cells, thus rendering them even more susceptible to programmed immune clearance
  • Fever-range hyperthermia may also induce Hsps
  • Hsps may exert an adjuvant effect by bolstering MHC class II and co-stimulatory molecule expression by DCs
  • thermal ablation of liver tumors in particular has demonstrated an ability to potentiate immune responses [57, 58] and elicit robust T-cell infiltrates at ablation sites
  • specific Hsp, Hsp70, directly inhibits apoptosis pathways in cancer cells, as demonstrated in human pancreatic, prostate and gastric cancer cells
  • Cross-priming is the ability of extracellular Hsps complexed to tumor peptides to be internalized and presented in the context of MHC class I molecules on APCs, thus allowing potent priming of CTLs against tumor antigens
  • It has been reported that Hsps are generated from necrotic tumor cell lysates, but not from tumor cells undergoing apoptosis
  • tumor cells exposed to hyperthermia in the heat shock range (42°C for 4h) prior to lysing, DC activation and cross-priming were significantly enhanced with the application of heat
  • Due to the ability of Hsps to activate DCs directly by chaperoning tumor antigens upon their release [28], it is possible that both local and regional immune stimulation can be achieved with hyperthermia.
  • support the use of hyperthermia as an inducer of Hsps to serve as ‘danger signals’, activating antitumor immune responses
  • whole-body hyperthermia not only augments immune responses, but also stimulates the migration of skin-derived DCs to draining lymph nodes
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      This allows for the activation of lymphocytes by the activated dendritic cells.
  • suggest a valuable role of hyperthermia in DC cancer vaccine strategies
  • In mice treated with fever-range whole-body hyperthermia, tumor growth was significantly inhibited and NK-cell infiltration increased
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      Hyperthermia increased NK cell activation, proliferation, and infiltration, which equals increased cytotoxicity.
  • exposure to fever-range hyperthermia resulted in improved endogenous NK-cell cytotoxicity to several cancer types
  • improved activation and function of DCs and NK cells following hyperthermia
  • Hyperthermia increases the expression ICAM-1 a key adhesion molecule,
  • The combined effects of hyperthermia on lymphoid tissue endothelium and lymphocytes can promote immune surveillance and increase the probability of naive lymphocytes leaving the circulation and encountering their cognate antigen displayed by DCs in lymphoid organs.
  • In independent clinical studies, whole-body hyperthermia resulted in a transient decrease in circulating lymphocytes in patients with advanced cancer [12, 94, 99, 100], a finding which mirrored observations in animal models in which lymphocyte entry into lymph noeds was increased following hyperthermia treatment [93]. Enhanced recruitment of lymphocytes to lymphoid tissues may be exploited in the treatment of malignancies.
  • The initial tumor antigen presentation and initiation of clonal expansion of CTLs transpires in the lymph nodes and cannot take place outside this specialized compartment
  • the ability of DCs present in the lymph nodes to stimulate an anti-tumor immune response is critical
  • hyperthermia has been shown to improve immune surveillance by T-cell
  • and to increase DC trafficking to lymph nodes
  • Nathan Goodyear on 29 Nov 18
     
    Great review of hyperthermia.
Nathan Goodyear

Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation o... - 0 views

www.jnutbio.com/...abstract

chylomicron inflammation atherosclerosis CAD arteriosclerosis plaque vascular disease

shared by Nathan Goodyear on 01 May 13 - No Cached
  • Nathan Goodyear on 01 May 13
     
    Inflammatory foods coupled with elevated glucose levels and hypertriglyceridemia induces endotoxemia, oxidative damage and immune,inflammatory dysfunction; thus activated chylomicrons
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

endo.endojournals.org/...4109.full

inflammation obesity overweight hypothalamus HPA

shared by Nathan Goodyear on 04 Oct 12 - No Cached
  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
  • Nathan Goodyear on 04 Oct 12
     
    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Effect of Tongkat Ali on stress hormones and psychological mood state in moderately str... - 0 views

www.ncbi.nlm.nih.gov/...PMC3669033

Tongkat Ali long jack cortisol stress testosterone hormone hormones

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • At the age of 60, testosterone levels are typically only 40-50% of youthful levels and may be lower
  • Eurycoma contains a group of small peptides referred to as “eurypeptides” that are known to have effects in improving energy status and sex drive in studies of rodents
  • The effects of tongkat ali in restoring normal testosterone levels appears to be less due to actually “stimulating” testosterone synthesis, but rather by increasing the release rate of “free” testosterone from its binding hormone, sex-hormone-binding-globulin (SHBG)
  • ...6 more annotations...
  • The current study found that daily supplementation with tongkat ali root extract (200 mg/day) improves stress hormone profile (lower cortisol; higher testosterone) and certain mood state parameters (lower tension, anger, and confusion)
  • tongkat ali supplementation (100 mg/day) improved lean body mass, 1-RM strength, and arm circumference to a significantly greater degree compared to a placebo group.
  • In a recent 12-week trial [46] of Eurycoma longifolia supplementation (300 mg/day), men (30–55 years of age) showed significant improved compared to placebo in the Physical Functioning domain of the SF-36 quality of life survey
  • sexual libido was increased by 11%
  • In men with low testosterone levels (average age 51 years), one month of daily supplementation with tongkat ali extract (200 mg/day) resulted in a significant improvement in serum testosterone levels and quality-of-life parameters
  • rise in cortisol and drop in testosterone is an early signal of “overtraining”
  • Nathan Goodyear on 09 Mar 15
     
    Tongkat Ali, commonly known as long jack, is found to reduce stress and increase Testosterone.  Stress is one of the common causes of low T in men.  It appears that long Jack functions as an adaptogen.
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