Description: <b>Hops (Humulus lupulus)</b> – Hops (known for beer brewing) contain compounds like xanthohumol that have demonstrated anticancer activity, particularly in breast and prostate cancer.<br>
-Phytochemicals, including flavonoids and polyphenols, which have antioxidant properties.<br>
-8-prenylnaringenin, may have estrogenic effects. (Hormone related cancers)<br>
-Anti-inflammatory properties <br>
Dose: Tea 1-3g/d, 1-3x/d. Extract 300-500mg/d<br>
<p><b>Hops (Humulus lupulus)</b> — the dried female inflorescences or hop cones of <i>Humulus lupulus</i> L., a perennial plant in the Cannabaceae family, are a complex botanical mixture containing prenylated flavonoids, polyphenols, α- and β-bitter acids, proanthocyanidins and volatile terpenes. Hops are classified as a botanical/natural-product mixture; the recommended abbreviation is <b>Hops</b> or <b>HL</b>. This entry represents whole hops and hop extracts rather than purified
<a href="https://nestronics.ca/dbx/tbProdEdit.php?pid=390">xanthohumol</a>, which has substantially stronger and more specific anticancer evidence and is appropriately maintained as a separate product. Extract composition varies markedly with cultivar, processing and extraction method, so biological effects cannot be assumed to be uniform across commercial hop preparations.</p>
<p><b>Primary mechanisms (ranked):</b></p>
<ol>
<li>Suppression of tumor invasion and migration by polyphenol-rich spent-hop extract, associated with reduced MMP-2 and MMP-9 expression and activity.</li>
<li>Antiangiogenic activity through reduced HIF-1α and VEGF expression in colorectal cancer cells.</li>
<li>Modulation of carcinogenic estrogen metabolism, including suppression of CYP1A1/CYP1B1 induction, reduced estradiol 4-hydroxylation and inhibition of estrogen-induced malignant transformation in mammary epithelial cells.</li>
<li>Anti-inflammatory signaling, including reduced NF-κB activity, COX-2, iNOS and inflammatory cytokines such as IL-6 in experimental hop-extract models.</li>
<li>Direct antiproliferative effects have been reported for some whole or spent-hop extracts in colorectal and other cancer-cell models, but these effects are less extensively characterized than those of isolated hop constituents.</li>
<li>Estrogen-receptor modulation is constituent- and preparation-dependent because hop extracts can contain the potent phytoestrogen 8-prenylnaringenin; whole-hop preparations therefore cannot be categorized simply as estrogen suppressive.</li>
</ol>
<p><b>Bioavailability / PK relevance:</b> Whole-hop extracts do not have a single definable pharmacokinetic profile because their constituent concentrations and extraction ratios vary substantially. Human studies with standardized hop preparations demonstrate systemic absorption of prenylated hop phenols, including 8-prenylnaringenin and isoxanthohumol-derived metabolites, with considerable inter-individual variability. Gut microbial conversion of isoxanthohumol to 8-prenylnaringenin can materially influence estrogenic exposure. Pharmacokinetic results from one standardized extract should therefore not be generalized to teas, beer, spent-hop extracts or unrelated commercial hop supplements.</p>
<p><b>In-vitro vs systemic exposure relevance:</b> The strongest whole-extract cancer studies are concentration-driven in-vitro experiments. For example, spent-hop extract produced pronounced inhibition of colorectal-cancer invasion and migration at approximately 200 µg/mL, whereas estrogen-metabolism effects have been reported at lower extract concentrations such as 5 µg/mL. Whether these concentrations and phytochemical ratios are achieved in human tumors after conventional oral hop supplementation is unknown. Direct systemic anticancer exposure from ordinary dietary hops or beer should not be assumed equivalent to experimental extracts.</p>
<p><b>Clinical evidence status:</b> <b>Preclinical for cancer.</b> Whole-hop and spent-hop extracts have demonstrated chemopreventive, anti-invasive, antiangiogenic and estrogen-metabolism effects in cell and animal models, but there is no established randomized clinical evidence that whole hops treat human cancer. Human hop-extract trials have primarily evaluated menopausal symptoms, sleep, metabolic effects, joint health, safety and pharmacokinetics rather than oncology efficacy. Hops are used as traditional herbal products for mild stress and sleep-related indications in European regulatory monographs, not for cancer treatment.</p>
<h3>Hops Cancer-Relevant Mechanisms</h3>
<table>
<thead>
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
</thead>
<tbody>
<tr>
<td>1</td>
<td>MMP-2 and MMP-9 Invasion Axis</td>
<td>↓ MMP-2<br>↓ MMP-9<br>↓ invasion<br>↓ migration</td>
<td>↔ / unclear</td>
<td>G</td>
<td>Reduced metastatic phenotype</td>
<td>Demonstrated with polyphenol-rich spent-hop extract in SW-480 and HT-29 colorectal cancer cells. Strong inhibition required relatively high extract concentrations.</td>
</tr>
<tr>
<td>2</td>
<td>HIF-1α VEGF Angiogenesis</td>
<td>↓ HIF-1α<br>↓ VEGF<br>↓ angiogenic signaling</td>
<td>↓ pathological endothelial response (context-dependent)</td>
<td>G</td>
<td>Antiangiogenic activity</td>
<td>Spent-hop extract reduced HIF-1α and VEGF expression in colorectal cancer models and inhibited angiogenesis-related behavior.</td>
</tr>
<tr>
<td>3</td>
<td>Estrogen Oxidative Metabolism</td>
<td>↓ CYP1B1<br>↓ CYP1A1 induction<br>↓ estradiol 4-hydroxylation</td>
<td>↓ estrogen-induced malignant transformation</td>
<td>G</td>
<td>Reduced formation of potentially genotoxic estrogen metabolites</td>
<td>A standardized hop extract inhibited oxidative estrogen metabolism and estrogen-induced transformation in MCF-10A mammary epithelial cells. This is primarily chemopreventive rather than evidence of tumor treatment.</td>
</tr>
<tr>
<td>4</td>
<td>NF-κB Inflammatory Signaling</td>
<td>↓ inflammatory signaling (context-dependent)</td>
<td>↓ NF-κB<br>↓ inflammatory response</td>
<td>R-G</td>
<td>Anti-inflammatory activity</td>
<td>Best characterized with polyphenol-rich spent-hop extract in activated macrophage and inflammatory models rather than directly in cancer cells.</td>
</tr>
<tr>
<td>5</td>
<td>COX-2 iNOS and Cytokines</td>
<td>↓ inflammatory tumor-supportive signaling (context-dependent)</td>
<td>↓ COX-2<br>↓ iNOS<br>↓ IL-6</td>
<td>R-G</td>
<td>Reduced inflammatory mediator production</td>
<td>Spent-hop extract markedly reduced COX-2 and IL-6 expression in LPS-activated macrophages. Cancer relevance is primarily through modulation of inflammatory microenvironment mechanisms.</td>
</tr>
<tr>
<td>6</td>
<td>Cell Proliferation</td>
<td>↓ proliferation (extract-dependent)</td>
<td>Less affected in limited comparative studies</td>
<td>G</td>
<td>Growth inhibition</td>
<td>Reported for spent-hop and other hop extracts, particularly in colorectal cancer models, but potency and composition vary substantially among extracts.</td>
</tr>
<tr>
<td>7</td>
<td>Estrogen Receptor Activity</td>
<td>↑ / ↓ ER signaling (constituent-dependent)</td>
<td>↑ estrogenic signaling possible</td>
<td>R-G</td>
<td>Mixed estrogenic modulation</td>
<td>Whole hops contain 8-prenylnaringenin, a potent phytoestrogen. Estrogenic activity depends strongly on extract composition, dose and conversion of isoxanthohumol to 8-prenylnaringenin. Do not classify whole hops simply as ER inhibition.</td>
</tr>
<tr>
<td>8</td>
<td>Clinical Translation Constraint</td>
<td>Extract-dependent effects<br>high experimental concentrations frequently required</td>
<td>Estrogenic exposure is formulation-dependent</td>
<td>G</td>
<td>Limits oncology translation</td>
<td>Whole-hop preparations vary in polyphenols, bitter acids and prenylated flavonoids. Human anticancer efficacy has not been established, and pharmacokinetic equivalence among experimental extracts and commercial products is unknown.</td>
</tr>
</tbody>
</table>
<p>P: 0–30 min R: 30 min–3 hr G: >3 hr</p>