IngredientesTetrahydro iso-alpha acids, commonly called THIAA or Tetra, are modified hop acids extracted from hop (Humulus lupulus L.), which are frequently used in the brewing industry mainly to provide beer bitterness and foam stability. The compounds are also found in the research literature under the proprietary name META060, particularly in metabolic and inflammatory studies. Alpha acids can be converted to cis or trans iso-alpha acids/isohumulones by heat-induced isomerization, and these iso-alpha acids can in turn be converted to cis or trans reduced iso-alpha acids by hydrogenation. The three primary types of reduced iso-alpha acids are dihydro- (also known as rho-), tetrahydro-, and hexahydro-iso-alpha acids (RIAA, THIAA, and HIAA, respectively).
Humulus lupulus belongs to the Cannabaceae family, native to temperate zones across Europe, Western Asia, and North America. This climbing perennial vine can reach up to 7 meters, winding itself around supports with stout, hairy stems. Hops produce distinctive strobiles (cones), often mistaken for pine cones but softer, green, and papery. Alpha-acids are a family of structurally similar compounds extracted from the resin of mature hop strobili. This family is mainly composed of three molecules — humulone, cohumulone, and adhumulone. A thermal isomerization (acyloin-type ring contraction) of α-acids is required to reach the desired bitterness. This chemical process occurs during wort boiling, before cooling and fermentation. It generates six compounds: cis- and trans-isohumulone, isocohumulone, and isoadhumulone.
Hydrogenation of the C–C double bonds of the isoprenyl and isohexenoyl side chains of the iso-alpha-acids yields the tetrahydro-iso-alpha-acids. THIAA can be produced via two primary routes. Tetrahydroiso-α-acids can be derived from iso-alpha-acids by catalytic hydrogenation of the double bonds in the side chains at C4 and C5 of iso-α-acids. Alternatively, tetrahydroiso-α-acids are obtained from β-acids. In this multistep production process, β-acids are initially transformed to 6-deoxytetrahydro-α-acids. Following oxidation gives rise to tetrahydro-α-acids, which are then isomerized to tetrahydroiso-α-acids.
The THIAA compounds share a substituted 1,3-cyclopentadione motif, which is considered structurally important for their biological activity. Because these compounds are light-sensitive and generate a "stale off-flavor," stable reduced isomerized α-acids are regularly used to avoid this drawback in brewing. Specifically, these compounds are produced through hydrogenation of hop-derived iso-alpha acids, a process that stabilizes their molecular structure and eliminates their light sensitivity — making them highly valued in the brewing industry, particularly for beers stored in clear bottles.
Tetrahydro-iso-α-acids (THIAA) are obtained by the hydrogenation of both iso-α-acids double bonds in the side chain. These reduced compounds are light stable and preserve the beer's bitter flavor for a longer time. Additionally, tetrahydro- and hexahydro-iso-α-acids can stabilize beer foam, thanks to an increase in their hydrophobicity. In the context of dietary supplements, THIAA is commercially supplied as liquid extracts, potassium or magnesium salt solutions, and encapsulated powder preparations. The proprietary preparation META060 has been used in published preclinical and some clinical research. A variant called n-enriched THIAA (nTHIAA) has also been described in more recent investigations into joint health.
THIAA itself is a modern semi-synthetic derivative and has no independent history of traditional use. However, its parent plant, Humulus lupulus, has a documented history spanning centuries across multiple cultures.
The medicinal potential of hop (Humulus lupulus L.) is widely cited in ancient literature and is also allowed in several official pharmacopoeias for the treatment of a variety of ailments, mainly related to anxiety states. This is due to the plethora of phytoconstituents — including bitter acids, polyphenols, prenyl flavonoids — present in the female inflorescences, commonly known as cones or strobili, endowed with anti-inflammatory, antioxidant, antimicrobial, and phytoestrogen activities.
The historic use of hops is interesting, as its technical properties — use as flavor and for the preservation of beer — were discovered in the Middle Ages. Hildegard von Bingen, the noted German abbess, herbalist, and author (1098–1179), wrote in Physica that hops has little use for humans, noting that it "increases melancholy in men." However, she notes that "its bitterness fends off decomposition of beverages and increases shelf life." Between 1300 and 1600, there was a widespread use of hops as a remedy for fevers, spleen disorders, as a diuretic, and for liver purging.
Beyond its role in brewing, hop has long been employed in traditional medicine to relieve a variety of ailments, especially insomnia, excitability, and restlessness associated with nervous tension. Additionally, hop has been used to manage headaches and digestive complaints, making it a multifaceted remedy in folk medicine.
In traditional medicine, the dried flowers were recommended for the treatment of sleep disturbances, restlessness, mania, toothache, and earache. The use of hops as a mild sedative came from the observation of fatigue, tiredness, and sleepiness symptoms in the hop pickers, apparently due to resin absorption during harvesting or processing hops. Hops have been used in European herbal traditions since at least the 9th century, primarily for their sedative, bitter tonic, and digestive properties.
Traditional herbalists often combined hop extracts with other botanicals such as valerian, passionflower, and lemon balm, creating synergistic blends for relaxation, mood support, and digestive health. In these combinations, THIAA-rich hops contributed both bitterness to stimulate digestion and gentle calming effects to ease tension.
While tetrahydro iso-alpha acids themselves are modern laboratory derivatives, their origin — hop compounds — has a much older history in medicinal use. THIAA is the product of controlled industrial hydrogenation and does not occur in meaningful amounts in raw hops or traditional hop preparations such as teas or tinctures. As such, the traditional ethnobotanical record for hops applies to the parent plant and its crude preparations, not to THIAA specifically.
THIAA is a family of closely related molecules. The α-acid family is mainly composed of three molecules — humulone, cohumulone, and adhumulone. A thermal isomerization of α-acids is required to reach the desired bitterness. Following this isomerization, catalytic hydrogenation of the two double bonds in the side chains of the resulting iso-alpha acids produces the corresponding tetrahydro derivatives — primarily tetrahydroisohumulone, tetrahydroisocohumulone, and tetrahydroisoadhumulone — which together constitute the THIAA mixture used in brewing and supplement applications.
Hop cones contain a wealth of bioactive compounds, including phenolics, procyanidins, flavonoids, and chalcones such as xanthohumol. These compounds are renowned for their potent antioxidant, antimicrobial, antiviral, anti-inflammatory, sedative, and chemopreventive properties. THIAA represents one specialized class within this larger phytochemical profile.
Both RIAA and THIAA inhibited prostaglandin E2 (PGE2) production in lipopolysaccharide-stimulated RAW 264.7 macrophages by inhibiting inducible cyclooxygenase-2 (COX-2) protein expression. In the same cell model, RIAA and THIAA dose-dependently reduced NF-κB nuclear translocation and abundance. Similar to iso-α-acids, reduced iso-α-acids such as RIAA and THIAA have also been found to inhibit inflammatory signal transduction of NF-κB. In vitro investigations proved that both RIAA and THIAA (1–20 µg/mL) dose-dependently reduced NF-κB nuclear translocation and abundancy in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. This activity was shown to be similar to that of parthenolide, a natural NF-κB inhibitor that works through the inhibition of NF-κB activation and release from the cytoplasmic IκB complex.
THIAA's inhibition of prostaglandin production is mechanistically distinct from that of non-steroidal anti-inflammatory drugs (NSAIDs). A key component of inflammation is the increase in prostaglandin biosynthesis resulting from induction of the cyclooxygenase 2 (COX-2) gene. The COX-2 enzyme is the prime target of NSAID therapy. COX-2 is constitutively expressed in some tissues such as the gastrointestinal tract and its inhibition may result in GI toxicity. The research goal was to identify inhibitors of prostaglandin production that were not direct COX enzyme inhibitors. When RIAA or THIAA were added 1 hour prior to LPS stimulation, they both inhibited PGE2 formation, presumably by inhibiting the induction of COX-2 and/or other inducible components of the PGE2 biosynthetic machinery. THIAA is about 2–3 fold more inhibitory at any given dose tested.
To assess their effects on inflammatory signal transduction pathways, RIAA and THIAA were analyzed against several human protein kinases in cell-free enzyme assays. Both selectively inhibited kinases involved in inflammatory signal transduction, including SyK, PI3Kβ, γ, and δ. These kinases are involved in Fc receptor and B cell receptor signaling, and are therapeutic targets in asthma and related inflammatory conditions.
It has been proposed that hops iso-alpha acids, structurally similar to META060 (THIAA), increase liver fatty acid oxidation and normalize adipocyte hypertrophy via the co-activation of PPARα and PPARγ. Since the effect of META060 on insulin sensitivity is very similar to that of rosiglitazone, it is possible to think that these hop derivatives could act by activating PPARγ. However, unlike thiazolidinediones (TDZs), IAA and reduced IAA effectively prevent other effects related to PPARγ activation, such as weight gain. Thus, an alternative mechanism can be suggested — in particular, it is possible to speculate that IAAs' ability to improve glucose homeostasis and insulin sensitivities could be traced back to their partial agonism on PPARγ and their agonism on PPARα receptors.
Administration of tetrahydro iso-alpha acids (META060) to high-fat diet (HFD)-fed obese and diabetic mice for 8 weeks reduced body weight gain, the development of fat mass, glucose intolerance, and fasted hyperinsulinemia, and normalized insulin sensitivity markers. This was associated with reduced portal plasma LPS levels, gut permeability, and higher intestinal tight junction proteins Zonula occludens-1 and occludin. Moreover, META060 treatment increased the plasma level of the anti-inflammatory cytokine interleukin-10 and decreased the plasma level of the pro-inflammatory cytokine granulocyte colony-stimulating factor.
The molecular structure of tetrahydro-iso-alpha acids is close to a new type of estrogen receptor alpha (ERα) antagonist aimed at disrupting the binding of coactivators containing an LxxLL motif (NR-box). This extract fails to compete with estradiol for ERα binding and does not significantly impact the receptor turnover rate in MCF-7 cells, suggesting that it does not act like classical antiestrogens. THIAA is able to antagonize ERα estradiol-induced recruitment of the LxxLL binding motif.
Over the last decade, there has been growing scientific interest in the anti-inflammatory properties of both hops extracts and their purified components, including THIAA. Several preclinical studies, particularly in vitro and animal models, have shown that THIAA can suppress inflammatory pathways by inhibiting NF-κB activation and reducing the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6. Research has indicated that THIAA can reduce inflammation in models of arthritis and colitis, and may reduce oxidative stress in inflammatory environments. However, while these results are promising, the evidence is mostly limited to laboratory and animal studies. Human clinical trials evaluating the anti-inflammatory effects of THIAA specifically are limited in number and scope.
Evidence strength: Predominantly preclinical (in vitro and rodent models). Human clinical evidence is limited and often involves THIAA in combination with other agents.
Several in vivo/vitro studies and human interventional trials have demonstrated the beneficial effects of these molecules on weight gain, lipid metabolism, glucose homeostasis, insulin sensitivities, and inflammation by acting on different targets.
The most extensively characterized preclinical evidence involves the META060 preparation. Administration of tetrahydro iso-alpha acids (META060) to high-fat diet (HFD)-fed obese and diabetic mice for 8 weeks reduced body weight gain, the development of fat mass, glucose intolerance, and fasted hyperinsulinemia, and normalized insulin sensitivity markers. This was associated with reduced portal plasma LPS levels, gut permeability, and higher intestinal tight junction proteins Zonula occludens-1 and occludin. Moreover, META060 treatment increased the plasma level of the anti-inflammatory cytokine interleukin-10 and decreased the plasma level of the pro-inflammatory cytokine granulocyte colony-stimulating factor.
The effect of 100 mg/kg tetrahydro iso-α-acids (META060) was compared with that of 1 mg/kg rosiglitazone (a PPARγ agonist) in C57Bl/6J male mice fed with HFD. Both META060 and rosiglitazone were found to improve glucose homeostasis and prevent HFD-induced insulin resistance in the short and long term. The oral glucose tolerance test, performed during week 5 of the dietary intervention, showed that both META060 and rosiglitazone significantly decreased plasma glucose levels, as demonstrated by the mean AUC, which was 20% and 15% lower than HFD-fed mice (p < 0.05), respectively.
These results strongly suggest that tetrahydro iso-alpha acids exert beneficial effects on plasma glucose, inflammation, and insulin resistance independently of body weight loss or lower body fat accumulation. Altogether, these data support the need to test this compound in obese and type 2 diabetic patients.
C57BL/6J mice fed with an HFD supplemented with 0.1% META060 exhibited a significant decrease in total adiposity compared to HFD mice, as both subcutaneous and visceral adipose depots were significantly decreased. Moreover, META060 appears to work by inhibiting fat accumulation in HFD-fed mice, but at the end of the treatment, mice quickly began to gain weight.
Evidence strength: Robust preclinical (multiple rodent studies). Human clinical translation has been called for explicitly by authors, but large-scale human RCTs specifically testing THIAA for metabolic outcomes have not yet been published in the peer-reviewed literature as of the available systematic review data.
In a mouse model of rheumatoid arthritis (RA), THIAA decreased bone, joint, and cartilage degradation, reduced carrageenan-induced footpad swelling, and reduced plasma levels of interleukin (IL)-6 in a dose-dependent manner.
Both RIAA and THIAA dose-dependently reduced the arthritis index and joint degradation, and at a dose of 250 mg/kg, their efficacy was similar to that of 20 mg/kg of celecoxib, the positive control. These hop-derived molecules may be of great value as an efficacious and safer alternative to treat chronic inflammation. Significant reductions were observed for celecoxib (days 32–42), THIAA at 250 mg/kg (days 34–42), and THIAA at 50 mg/kg (days 34–40), also demonstrating the effectiveness of THIAA as an antiarthritic agent. The results from histological examination of joint tissue damage show the absence or minimal evidence of joint destruction in the THIAA-treated individuals. There are clearly signs of a dose response, and the reduction in the histology score at 250 mg/kg and 50 mg/kg was 40% and 28%, respectively. This compares favorably with the celecoxib-treated group where joint destruction was scored as mild.
A human open-label case series investigated a combination preparation. This 12-week study evaluated the efficacy and safety of a nutritional product containing n-enriched tetrahydro iso-alpha acids and undenatured type 2 collagen in participants with chronic joint pain (including pain from symptomatic osteoarthritis and from rheumatoid arthritis). Tetrahydro iso-α acids (THIAAs), derived from Humulus lupulus (hops), have demonstrated anti-inflammatory effects in vitro and in an animal model of rheumatoid arthritis (RA). Undenatured type 2 collagen has been found to be effective in clinical studies in RA and osteoarthritis (OA). The study intended to evaluate the efficacy and safety of a proprietary tablet containing 150 mg of n-enriched THIAA (nTHIAA) and 10 mg of undenatured type 2 collagen (UC-II) in patients with arthritis. This study was an open-label design without a control arm, which substantially limits the conclusions that can be drawn from it.
Evidence strength: Strong in animal models. Human evidence is limited to an uncontrolled open-label case series using a combination product; no blinded, placebo-controlled human RCTs for THIAA alone in arthritis have been identified in the literature.
In an in vitro model, a THIAA+niacin mixture inhibited several TNF-α-induced cytokines in human aortic endothelial cells and in human monocytic cells and was significantly more efficacious than niacin alone. Subsequently, the effect of 125 mg THIAA and 500 mg niacin on endothelial-regulated flow-mediated vasodilation (FMD) was explored in a pilot study of 11 dyslipidemic volunteers. The 12-week treatment (2 tablets/day) resulted in a clinically relevant FMD increase compared to a trend toward an FMD decrease with placebo; the between-arm difference was statistically significant.
In a mouse model of rheumatoid arthritis (RA), THIAA decreased bone, joint, and cartilage degradation, reduced carrageenan-induced footpad swelling, and reduced plasma levels of IL-6 in a dose-dependent manner. Since systemic chronic inflammation associated with RA in humans has been associated with atherosclerosis and increased cardiovascular events, THIAA's anti-inflammatory properties may be efficacious in ameliorating the inflammation-mediated monocyte-endothelial interaction. Supporting this notion is a recent publication that demonstrated that THIAA indeed attenuated monocyte adhesion to endothelial cells and suppressed multiple inflammatory biomarkers in both monocytic and endothelial cell lines.
Evidence strength: The cardiovascular endothelial function pilot study (n=11) is the only available human clinical data in this area. It was small and used a combination product (THIAA plus niacin); therefore, the specific contribution of THIAA alone cannot be isolated. Evidence should be characterized as preliminary.
Because tetra- and hexahydro isoalpha acids (THIAA and HHIAA) from hops elicit anti-inflammatory properties, they were evaluated for antitumor effects in vitro in human HCC cell lines (HepG2, Hep3B, Huh7) and in vivo in a diethylnitrosamine (DEN)-induced animal model of HCC. In human HCC cell lines, THIAA and HHIAA reduced cell proliferation and viability, which was associated with the inhibition of NF-κB-DNA binding and tumor necrosis factor α mRNA expression. Both compounds also inhibited phosphorylation of the mTOR effector p70S6 kinase without affecting ERK, AKT, JNK, and GSK3β phosphorylation or activator protein-1 activation.
In DEN-treated rats, administration of THIAA and HHIAA in food reduced the tumor numbers and the expression of the cellular transformation marker glutathione S-transferase pi.
Evidence strength: In vitro and animal model evidence only. No human clinical data are available for THIAA in the context of liver disease or hepatocellular carcinoma prevention.
THIAA decreases estradiol-stimulated proliferation of MCF-7 (ERα-positive breast cancer) cells. It also inhibits ERα transcriptional activity. This extract fails to compete with estradiol for ERα binding and does not significantly impact the receptor turnover rate in MCF-7 cells, suggesting that it does not act like classical antiestrogens. THIAA is able to antagonize ERα estradiol-induced recruitment of the LxxLL binding motif.
Evidence strength: In vitro cell line work only (MCF-7 breast cancer cells). No animal models or human clinical data have been published for this application. These findings are exploratory and mechanistic only.
THIAA does not have an established recommended daily intake or a pharmacopeial monograph defining its dosage. All dosage information below is drawn from published research and is reported as stated in those sources.
Hops is generally recognized as safe (GRAS) as a food by the U.S. Food and Drug Administration. Essential oils, oleoresins, and natural extracts of Humulus lupulus (hops) are GRAS for human consumption. Purified THIAA as a dietary supplement ingredient operates within this broader regulatory context, though it is a processed derivative rather than a crude botanical preparation.
Hops can cause sedation and should be avoided while taking other sedating drugs and in patients with depression. The sedative property is primarily attributed to the compound 2-methyl-3-butene-2-ol, a metabolic oxidation product of the hop bitter acids. 2-methyl-3-butene-2-ol has sedative properties. While THIAA is a chemically distinct fraction from the sesquiterpene-rich hops volatile fraction most associated with sedation, potential additive CNS depressant effects with relevant medications (benzodiazepines, barbiturates, other sedative hypnotics) cannot be excluded.
Information regarding safety and efficacy in pregnancy and lactation is lacking for hops preparations, and by extension for purified THIAA. No data exist on the excretion of any components of hops into breastmilk or on the safety and efficacy of hops in nursing mothers or infants. Given that THIAA has demonstrated ERα modulating activity in cell line studies, and given that hops contain compounds with known phytoestrogenic properties, additional caution in hormonal contexts is warranted until human safety data are available.
Hops may uncommonly induce symptoms of food allergy in non-occupationally sensitised individuals. Occupational allergy may commonly be associated with exposure to hops. Hops are an uncommon cause of occupational asthma and anaphylaxis. Skin contact with the plant causes dermatitis in susceptible people. Systemic and contact urticaria have been documented. In a survey of Humulus lupulus (hops) farmers, exposure to hops was reported to cause the greatest number of skin problems; 14 of 73 (19.2%) of the farmers reported work-related skin symptoms.
In a study of occupational exposure of brewery workers to organic dusts, including Humulus lupulus, the potential to affect respiratory function and immunological status was examined. A large number of brewery workers complained of acute symptoms that developed during the work shift. Lung function tests were decreased compared to predicted levels. There was a greater instance of positive skin prick tests (SPTs) in brewery workers for hops than in controls (15% vs 3%). There were increased serum levels of total IgE in 34 of 97 (45.1%) brewery workers compared to controls, 1 of 76 (2.7%). These findings are specific to occupational inhalation exposure and are not directly applicable to oral supplemental use of purified THIAA.
No specific, formally characterized pharmacokinetic drug-drug interactions with purified THIAA as a supplement ingredient have been identified in the published peer-reviewed literature. Contraindications for hops have not yet been identified. However, given THIAA's demonstrated inhibitory activity on NF-κB, COX-2 induction, and multiple protein kinases — pathways shared by various pharmaceutical agents — caution is theoretically warranted when combining THIAA with:
The GI safety advantage of THIAA relative to classical NSAIDs has been suggested by preclinical models. RIAA, IAA, THIAA, HHIAA, BA, and AA have strong potential as anti-inflammatory agents, and predict, from in vitro models, that they may have a low GI toxicity. However, this comparative assessment has not been confirmed in human clinical trials.
The overall safety profile of THIAA as a purified dietary supplement ingredient has not been formally assessed in long-term human clinical trials. The available clinical evidence is restricted to short-duration pilot studies (12 weeks maximum in the identified literature), and the number of human participants studied is small. The ERα antagonist activity observed in breast cancer cell lines raises a theoretical consideration for individuals with hormone-sensitive conditions, though this has not been evaluated in a human context.
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THIAA suppresses TNF-α-mediated inflammatory cytokines in human aortic endothelial cells and inhibits monocyte adhesion — early steps in atherosclerotic plaque formation. Combined with niacin in a small human trial, THIAA improved flow-mediated vasodilation in dyslipidemic subjects. Research has proposed THIAA may ameliorate inflammation and plaque destabilization characteristic of atherosclerosis.
THIAA has been studied in both osteoarthritis and rheumatoid arthritis contexts. In preclinical models it inhibits NF-κB, MMP-9, and TNF-α and attenuates joint swelling. A 12-week open-label case series used 150 mg nTHIAA with undenatured type II collagen in patients with chronic joint pain from OA and RA. Taylor & Francis references THIAA for inhibition of NF-κB, TNF-α, and MMP-9 relevant to osteoarthritis.
THIAA inhibits BTK, Syk, and PI3K isoforms — kinases central to B-cell receptor signaling implicated in autoimmune pathogenesis. In a collagen-induced RA model (an established autoimmune disease model), THIAA reduced arthritis index and joint degradation dose-dependently. These kinase targets overlap with those of approved autoimmune therapeutics.
THIAA (META060) supplementation in HFD-fed obese/diabetic mice for 8 weeks reduced glucose intolerance and fasting hyperinsulinemia, and improved glucose homeostasis. Related iso-alpha acids have shown similar effects in human interventional data. THIAA may activate PPARα/γ pathways that influence glucose metabolism in adipocytes.
THIAA reduced cartilage degradation in collagen-induced arthritis mice. Related rho-iso-alpha acids inhibit MMP-13 (the primary type II collagen-degrading enzyme) in chondrosarcoma cells and reduce RANKL-mediated osteoclast activity. THIAA is highlighted in Taylor & Francis literature specifically for its inhibition of NF-κB, TNF-α, and MMP-9 relevant to OA cartilage protection.
THIAA inhibits NF-κB nuclear translocation, COX-2 expression, and PGE2 production in macrophages, suppressing key pro-inflammatory mediators including TNF-α, IL-1β, and IL-6. These mechanisms have been demonstrated in multiple in vitro and animal models. Ex vivo data in human peripheral blood mononuclear cells further support anti-inflammatory activity. Clinical evidence in humans remains limited in scope.
A 12-week open-label clinical case series evaluated 150 mg n-enriched THIAA combined with undenatured type II collagen in patients with chronic joint pain from OA and RA. THIAA's inhibition of COX-2, NF-κB, and PGE2 pathways underpins a plausible mechanism for pain modulation. Evidence is preliminary, limited to a single small open-label study.
THIAA's molecular structure is close to a class of ERα antagonists that disrupt coactivator binding via the LxxLL motif. In MCF-7 ERα-positive breast cancer cells, THIAA inhibited estradiol-stimulated proliferation and ERα transcriptional activity. Uniquely, it does not compete directly with estradiol for receptor binding, suggesting a novel coactivator-displacement mechanism.
In HFD-fed mice, THIAA (META060) reduced metabolic endotoxemia, decreased portal plasma LPS, and was associated with improved gut barrier markers, including restoration of tight junction proteins ZO-1 and occludin. These effects indicate indirect modulation of gut microbiome-driven systemic inflammation. This study provides mechanistic evidence linking THIAA to gut microbiome-related outcomes.
In an 8-week HFD mouse study, THIAA (META060) administration at 0.1% dietary dose significantly reduced body weight gain and fat mass development compared to HFD controls. The mechanism may involve PPARα/γ activation and improved adipocyte metabolism. Human weight data are not available for THIAA specifically.
In a 12-week pilot RCT (n=11 dyslipidemic subjects), THIAA+niacin treatment produced a statistically significant and clinically relevant improvement in flow-mediated vasodilation compared to placebo, with improvements in total cholesterol, LDL-C, and uric acid. THIAA inhibits monocyte-endothelial inflammatory interactions directly implicated in atherosclerosis development.
Administration of THIAA (META060) to HFD-fed obese and diabetic mice for 8 weeks normalized insulin sensitivity markers and reduced fasting hyperinsulinemia. A PMC review cites human evidence that THIAA-class compounds can restore insulin sensitivity in type II diabetes patients. THIAA may also act via PPARα/γ co-activation affecting adipocyte metabolism.
THIAA administration in HFD-fed mice reduced gut permeability and increased intestinal tight junction proteins ZO-1 and occludin, protecting against diet-induced gut barrier dysfunction and metabolic endotoxemia. These are direct molecular markers of gut barrier integrity. The evidence is from a single preclinical study; human data are not yet published.
A 2021 systematic review specifically examined iso-α-acids including THIAA against metabolic syndrome and its related disorders (diabetes, dyslipidemia, inflammation) using PubMed/Scopus. THIAA reduced body weight gain, fat mass, glucose intolerance, and metabolic endotoxemia in HFD mice. Iso-alpha acid class compounds have been studied in human interventional trials for metabolic syndrome components.
In a collagen-induced arthritis mouse model, THIAA dose-dependently reduced arthritis index and joint degradation, with efficacy at 250 mg/kg comparable to celecoxib at 20 mg/kg. A 12-week open-label human case series evaluated 150 mg nTHIAA plus undenatured type II collagen in arthritis patients including those with rheumatoid arthritis. THIAA inhibits kinases in the B-cell receptor pathway relevant to autoimmune-mediated joint destruction.
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