tbResList Print — aLinA alpha Linolenic acid

Description: <b>Alpha Linolenic acid</b> naturally-occurring fatty acid. Found in vegetable oils, plant oils, nuts and meat.<br>
• Alpha linolenic acid (ALA) is an essential omega-3 fatty acid commonly found in plant sources such as flaxseed, chia seeds, walnuts, and certain vegetable oils.<br>
• As an essential fatty acid, ALA must be obtained from the diet and serves as a precursor to longer-chain omega-3 fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).<br>
• While ALA itself is not a strong antioxidant, its downstream metabolites can indirectly support antioxidant defense systems.<br>
• By reducing oxidative stress, ALA may help protect cellular DNA from damage that can trigger carcinogenesis.<br>

<br>
<b>Alpha-Linolenic Acid (ALA) — Cancer-Oriented Time-Scale Flagged Pathway Table</b><br>
<!-- Alpha-Linolenic Acid (ALA) — Cancer-Oriented Time-Scale Flagged Pathway Table -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer / Tumor Context</th>
<th>Normal Tissue Context</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>

<tr>
<td>1</td>
<td>Membrane lipid remodeling / lipid raft modulation</td>
<td>Growth signaling platform modulation (context-dependent)</td>
<td>Membrane fluidity ↑</td>
<td>R, G</td>
<td>Signal microdomain alteration</td>
<td>Incorporation into phospholipids can alter receptor clustering and downstream signaling; magnitude depends on conversion to EPA/DHA.</td>
</tr>

<tr>
<td>2</td>
<td>Inflammatory signaling (NF-κB / cytokine tone)</td>
<td>NF-κB ↓; pro-inflammatory cytokines ↓ (reported)</td>
<td>Inflammation tone ↓</td>
<td>R, G</td>
<td>Anti-inflammatory modulation</td>
<td>Anti-inflammatory effects are often attributed partly to downstream EPA/DHA conversion and altered eicosanoid balance.</td>
</tr>

<tr>
<td>3</td>
<td>Eicosanoid pathway shift (ω-6 → ω-3 balance)</td>
<td>Pro-tumor inflammatory eicosanoids ↓ (context)</td>
<td>Resolution mediators ↑ (if converted)</td>
<td>G</td>
<td>Lipid mediator rebalancing</td>
<td>Conversion efficiency to EPA/DHA is limited in humans; systemic effects depend on dose and metabolic status.</td>
</tr>

<tr>
<td>4</td>
<td>PI3K / AKT / mTOR signaling (reported)</td>
<td>Survival signaling ↓ (model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Growth modulation</td>
<td>Observed in some preclinical systems; not a universal or primary mechanism.</td>
</tr>

<tr>
<td>5</td>
<td>Apoptosis modulation</td>
<td>Apoptosis ↑ (reported in some tumor models)</td>
<td>↔</td>
<td>G</td>
<td>Cell fate shift</td>
<td>Usually secondary to membrane, redox, or inflammatory changes; not a strong direct cytotoxic lipid.</td>
</tr>

<tr>
<td>6</td>
<td>ROS / oxidative stress</td>
<td>ROS direction variable; lipid peroxidation risk ↑ at high PUFA levels</td>
<td>Oxidative injury ↓ or ↔ (context)</td>
<td>P, R, G</td>
<td>Redox modulation</td>
<td>PUFAs are oxidation-sensitive; effects depend on antioxidant status and dose.</td>
</tr>

<tr>
<td>7</td>
<td>AMPK activation (reported)</td>
<td>Metabolic stress signaling ↑ (context)</td>
<td>Metabolic regulation support</td>
<td>R, G</td>
<td>Energy sensing modulation</td>
<td>Some metabolic studies report AMPK activation, though stronger evidence exists for EPA/DHA.</td>
</tr>

<tr>
<td>8</td>
<td>Angiogenesis modulation (VEGF)</td>
<td>VEGF ↓ (reported in some models)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic support</td>
<td>Often secondary to inflammatory signaling shifts.</td>
</tr>

<tr>
<td>9</td>
<td>Chemo-sensitization (context-dependent)</td>
<td>Therapy sensitivity ↑ (reported in some systems)</td>
<td>—</td>
<td>G</td>
<td>Adjunct modulation</td>
<td>Omega-3 fatty acids are sometimes reported to enhance chemotherapy response; effect size and reproducibility vary.</td>
</tr>

<tr>
<td>10</td>
<td>Translation constraint (conversion efficiency)</td>
<td>Limited conversion to EPA/DHA in humans</td>
<td>Systemic effects dose-dependent</td>
<td>—</td>
<td>PK constraint</td>
<td>Only ~5–10% converts to EPA and much less to DHA in many individuals; effects may differ from marine omega-3s.</td>
</tr>

</table>

<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (lipid incorporation begins; oxidative interactions)</li>
<li><b>R</b>: 30 min–3 hr (early signaling + inflammatory shifts)</li>
<li><b>G</b>: &gt;3 hr (membrane remodeling, phenotype-level effects)</li>
</ul>






<br>
<b>Alpha-Linolenic Acid (ALA) — Alzheimer’s Disease (AD) Time-Scale Flagged Pathway Table</b><br>
<!-- Alpha-Linolenic Acid (ALA) — Alzheimer’s Disease (AD) Time-Scale Flagged Pathway Table -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>AD / Brain Context</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>

<tr>
<td>1</td>
<td>Neuroinflammation modulation</td>
<td>Microglial cytokine tone ↓ (reported)</td>
<td>R, G</td>
<td>Anti-inflammatory support</td>
<td>Anti-inflammatory effects are largely indirect and may depend on EPA/DHA conversion.</td>
</tr>

<tr>
<td>2</td>
<td>Membrane fluidity / synaptic integrity</td>
<td>Synaptic membrane composition modulation</td>
<td>G</td>
<td>Structural support</td>
<td>Omega-3 incorporation can influence neuronal membrane properties; DHA plays a stronger direct role than ALA.</td>
</tr>

<tr>
<td>3</td>
<td>Oxidative stress modulation</td>
<td>ROS injury ↓ (context); lipid peroxidation risk if imbalance</td>
<td>R, G</td>
<td>Redox balance shift</td>
<td>Balance between antioxidant defense and PUFA susceptibility to oxidation is important.</td>
</tr>

<tr>
<td>4</td>
<td>Vascular function / endothelial tone</td>
<td>Cerebrovascular support ↑ (reported)</td>
<td>G</td>
<td>Perfusion support</td>
<td>Omega-3 intake is associated with improved endothelial function in cardiovascular contexts.</td>
</tr>

<tr>
<td>5</td>
<td>Aβ / Tau pathology (direct evidence)</td>
<td>Limited direct evidence for ALA; stronger for DHA</td>
<td>G</td>
<td>Indirect modulation</td>
<td>ALA itself has limited direct mechanistic evidence in amyloid/tau models compared to DHA.</td>
</tr>

<tr>
<td>6</td>
<td>Translation constraint</td>
<td>CNS benefit depends on conversion to EPA/DHA</td>
<td>—</td>
<td>Metabolic limitation</td>
<td>Low conversion efficiency may limit brain-specific effects.</td>
</tr>

</table>

<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (lipid interaction begins)</li>
<li><b>R</b>: 30 min–3 hr (inflammatory/redox signaling shifts)</li>
<li><b>G</b>: &gt;3 hr (membrane remodeling and phenotype-level outcomes)</li>
</ul>