Redefining
Cancer
Treatment
Redefining
Cancer
Treatment
| Formulation | Typical Price Range (£) | Quantity |
|---|---|---|
| 100–200 IU capsules | £8–£9 | 90–200 capsules |
| 400 IU capsules | £2.50–£26 | 30–100 capsules |
| 1000 IU capsules | £12–£40 | 30–90 capsules |
| Vitamin E oil/liquid | £9–£17 | 20,000 IU/59 ml |
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Vitamin E, a fat-soluble vitamin comprising eight isoforms (α (Alpha), β (Beta, γ (Gamma), δ (Delta) tocopherols and tocotrienols), has been extensively studied for its potential role in cancer prevention and therapy. Its anti-cancer properties are multifaceted, involving both antioxidant and non-antioxidant mechanisms.
Antioxidant Activity: Vitamin E neutralises free radicals, protecting cellular membranes and DNA from oxidative damage that can lead to mutations and cancer initiation67.
Anti-Inflammatory Effects: Chronic inflammation is a known contributor to cancer development. Vitamin E isoforms, particularly γ- and δ-tocopherols, suppress inflammatory pathways by inhibiting cyclooxygenase (COX) and lipoxygenase (LOX) enzymes, and modulating key signalling pathways such as NF-κB and JAK-STAT146.
Induction of Apoptosis: Certain forms of vitamin E can trigger programmed cell death in cancer cells, helping to eliminate abnormal cells and prevent tumour growth1467.
Cell Cycle Arrest: Vitamin E has been shown to halt the cell cycle in cancer cells, thereby inhibiting their proliferation147.
Anti-Angiogenic Effects: Some isoforms may reduce tumour blood supply by interfering with angiogenesis, thus limiting tumour growth and metastasis6.
Immune Modulation: Vitamin E may enhance immune system function, supporting the body’s ability to recognise and destroy cancer cells6.
DNA Repair and Stability: It supports DNA repair mechanisms, reducing the likelihood of mutations that can drive cancer progression6.
Recent research has highlighted that the anti-cancer efficacy of vitamin E is highly dependent on its specific isoform:
| Isoform | Key Findings |
|---|---|
| α-Tocopherol | Most common in supplements; strong antioxidant. Large trials (e.g., SELECT) did not show benefit and, in some cases, suggested possible harm at high doses235. Some protective effect observed in populations with low baseline vitamin E status27. |
| γ- and δ-Tocopherol | More effective than α-tocopherol at inhibiting cancer cell growth, inducing apoptosis, and scavenging reactive nitrogen species123457. Stronger anti-inflammatory and anti-cancer effects in preclinical models. |
| Tocotrienols | Exhibit unique anti-cancer mechanisms, including inhibition of HMG CoA reductase, NF-κB pathway, and antiangiogenic effects. δ-Tocotrienol, in particular, induces apoptosis, paraptosis, and autophagy in resistant prostate cancer cells45. |
Preclinical Studies: Both in vitro and animal studies consistently show that γ- and δ-tocopherols and tocotrienols inhibit cancer cell proliferation, induce apoptosis, and reduce tumour growth, often with greater efficacy than α-tocopherol1457.
Epidemiological Studies: Populations consuming diets rich in various vitamin E isoforms (such as those in the Mediterranean) have lower cancer rates, particularly for colon cancer27.
Clinical Trials: Large trials using high-dose α-tocopherol alone have failed to demonstrate cancer prevention and, in some cases, have raised concerns about increased risk (e.g., prostate cancer in the SELECT trial)235. There is limited but suggestive evidence that vitamin E may be protective in specific populations, such as smokers27.
Vitamin E’s anti-cancer effects are not limited to its antioxidant properties; they also include modulation of cell signalling, inhibition of key enzymes in inflammation and carcinogenesis, and direct effects on tumour cell survival and proliferation14567.
Novel mechanisms include the regulation of sphingolipid metabolism and the induction of endoplasmic reticulum stress, particularly by γ-tocopherol and its metabolites1.
Vitamin E, especially in the form of γ- and δ-tocopherols and tocotrienols, demonstrates promising anti-cancer properties through antioxidant, anti-inflammatory, and direct anti-tumour mechanisms. While preclinical data are robust, clinical evidence is mixed, particularly for α-tocopherol at high doses. Future research should focus on the differential effects of vitamin E isoforms and their potential as adjuncts in cancer prevention and therapy, with an emphasis on personalised approaches and dietary sources over high-dose single-isoform supplementation.
A safe dosage for vitamin E has been established by several health authorities.
Recommended Daily Intake (Adults):
Tolerable Upper Intake Level (UL):
The European Food Safety Authority (EFSA) has set the UL for adults at 300 mg per day of α-tocopherol from all sources, including supplements and food510.
In the US, the upper limit is set at 1,000 mg per day (equivalent to 1,500 IU of natural or 1,100 IU of synthetic vitamin E)278.
The NHS advises that taking 540 mg (800 IU) or less per day is unlikely to cause harm1.
Safety Considerations:
Doses above 400 IU (approximately 268 mg) per day may be associated with increased risk of adverse effects, such as bleeding, especially in those with certain health conditions or on anticoagulant medications359.
High doses may also increase the risk of prostate cancer and other health issues in specific populations348.
General Advice:
Summary Table: Safe Dosage Guidelines for Adults
| Authority | Recommended Daily Intake | Upper Limit (UL) |
|---|---|---|
| NHS (UK) | 3–4 mg | 540 mg (800 IU) |
| EFSA (Europe) | 11–13 mg | 300 mg |
| US (NIH/FNB) | 15 mg | 1,000 mg (1,500 IU) |
Exceeding these upper limits may increase the risk of adverse effects, particularly bleeding disorders and, in some cases, cancer recurrence or progression358. Always consult a healthcare provider before starting high-dose vitamin E supplementation.
Vitamin E is generally safe at low doses, such as those found in a typical diet or standard multivitamin preparations35.
The risk of side effects rises with higher, therapeutic, or supplemental doses, especially above 400 IU (approximately 268 mg) per day235.
Increased Bleeding Risk: Vitamin E can impair blood clotting, increasing the risk of bruising and bleeding, particularly at doses above 400 IU/day. This risk is higher in those on anticoagulant or antiplatelet medications and can be significant enough to warrant stopping vitamin E before surgery234.
Haemorrhagic Stroke: Higher doses (≥400–800 IU/day) have been linked to an increased risk of haemorrhagic stroke23.
Coagulopathy: Cases of blood clotting disorders have been reported with excessive supplementation2.
Thrombophlebitis: Inflammation of veins due to blood clots has been observed in some cases2.
Lipogranuloma: Rare inflammatory reaction, usually with injectable vitamin E for cosmetic use2.
Prostate Cancer: Large clinical trials (e.g., SELECT) found that high-dose α-tocopherol supplementation (400 IU/day) increased the risk of developing prostate cancer in healthy men13.
Head and Neck Cancer: Supplementation above 400 IU/day may increase the risk of recurrence in head and neck cancer patients, especially smokers235.
Colorectal Adenoma and Mortality: Some studies link vitamin E supplementation to increased risk of colorectal adenoma and overall mortality in the general population5.
Lung Cancer: High-dose vitamin E may increase lung cancer risk, particularly in smokers45.
Chemotherapy and Radiotherapy: There is concern that vitamin E, as an antioxidant, could interfere with the effectiveness of some chemotherapy and radiotherapy regimens. Some evidence suggests it may reduce side effects (e.g., neuropathy, mucositis), but it may also reduce treatment efficacy or increase recurrence risk in certain cancers45.
Tamoxifen: In some studies, vitamin E with tamoxifen improved lipid profiles and enhanced anticancer effects, but interactions with other drugs can vary4.
Meta-analyses indicate that doses above 400 IU/day are associated with increased all-cause mortality, especially in those with chronic diseases. This risk appears lower in healthy individuals at doses up to 800 IU/day, but caution is still advised5.
| Dose | Common Side Effects | Serious Risks/Notes |
|---|---|---|
| < 400 IU/day | Rare, generally safe | Minimal for most people |
| 400–800 IU/day | Fatigue, headache, rash | Increased bleeding risk, haemorrhagic stroke, possible increased all-cause mortality |
| > 800 IU/day | As above, more likely | Higher risk of serious bleeding, stroke, possible increased cancer risk, mortality |
Avoid high-dose vitamin E supplementation (>400 IU/day), especially for cancer prevention or therapy, unless specifically advised by a healthcare provider345.
Cancer patients, particularly those with head and neck cancer or prostate cancer, or those undergoing chemotherapy/radiotherapy, should consult their medical team before using vitamin E supplements2345.
While dietary and low-dose vitamin E is generally safe, high-dose supplementation—often used in therapeutic or experimental cancer protocols—carries significant risks, including increased bleeding, stroke, and possible increased cancer recurrence or incidence. The therapeutic window for vitamin E in cancer remains narrow, and supplementation should only be considered with professional guidance.
Vitamin E has been studied alongside chemotherapeutic agents such as doxorubicin and camptothecin. In laboratory studies, combining vitamin E with doxorubicin increased the cytotoxicity against breast cancer cells while minimising toxicity to normal cells2. However, the combination did not show a significant synergistic effect in all cell lines, and some studies suggest that α-tocopherol may reduce the efficacy of certain chemotherapy drugs, such as tamoxifen and crizotinib25.
Clinical and preclinical evidence suggests vitamin E can help reduce chemotherapy-induced side effects, such as neurotoxicity and mucositis, without compromising the effectiveness of some drugs15.
Vitamin E, particularly tocotrienols, has demonstrated protective effects for normal tissues during radiation therapy and may reduce treatment-related toxicity3. Some studies also report that vitamin E supplementation can decrease DNA damage in patients receiving chemotherapy4.
Recent research shows that vitamin E supplementation can enhance the efficacy of immune-checkpoint therapy (ICT) in cancer patients. Analysis of clinical data and animal models demonstrates that vitamin E improves survival and boosts antitumour immunity by reinvigorating dendritic cells and enhancing T-cell responses6. Combining vitamin E with immunogenic chemotherapies or DC-recruiting cancer vaccines further increased the effectiveness of ICT in preclinical models6.
Vitamin E has been tested in combination with selenium, showing a synergistic effect in reducing mammary tumour development in animal models. Vitamin E alone was ineffective, but it potentiated selenium’s anticarcinogenic action when present during the tumour’s proliferative phase7.
In a phase 2 trial, a regimen of isotretinoin, interferon α-2a, and vitamin E prevented secondary cancers and relapse in head and neck cancer patients4.
| Therapy Type | Effect of Vitamin E Combination | Evidence Type |
|---|---|---|
| Chemotherapy | May increase cytotoxicity, reduce side effects, but can interfere with some drugs | Preclinical, Clinical |
| Radiotherapy | Protects normal tissue, reduces toxicity | Preclinical, Clinical |
| Immunotherapy | Enhances response and survival, boosts immune activity | Clinical, Preclinical |
| Selenium | Synergistic antitumour effect in animal models | Animal studies |
| Isotretinoin/Interferon | Reduced relapse/secondary cancers in head and neck cancer | Clinical trial |
Vitamin E has been tested in combination with chemotherapy, radiotherapy, immunotherapy, and other nutrients. It shows potential benefits in reducing side effects and, in some cases, enhancing therapeutic efficacy, particularly with immunotherapy and selenium. However, effects may vary by cancer type, therapy, and vitamin E isoform, and there is potential for negative interactions with some treatments. Clinical guidance is essential when considering vitamin E supplementation alongside cancer therapies.
US National Library of Medicine research on Vitamin E
Europe PMC research on Vitamin E
Pubmed research on Vitamin E
Reduction in Treatment-Related Side Effects
Several studies report that vitamin E supplementation, particularly at therapeutic doses (e.g., 300–800 mg/day), may help reduce certain side effects of cancer treatment:
Peripheral Neuropathy: Some trials show a reduction in chemotherapy-induced peripheral neuropathy, especially when vitamin E is combined with omega-3 fatty acids or other agents1345. However, results are mixed, and not all studies confirm this benefit.
Radiation Toxicity: Vitamin E has been found to reduce the severity of radiation-induced side effects, such as mucositis, dry mouth (xerostomia), salivary gland dysfunction, and skin reactions34. Topical vitamin E may also help with radiation-induced vaginal toxicity and pain3.
Hot Flashes: Some evidence suggests vitamin E can reduce hot flashes in breast cancer survivors45.
Protection Against Cisplatin Toxicity: Vitamin E may help protect against cisplatin-induced kidney and ear toxicity45.
General Well-being
Vitamin E’s antioxidant properties may support immune function and help protect tissues from further damage during cancer therapy, potentially contributing to a better sense of overall well-being24.
Some studies report a reduced risk of death and recurrence in certain cancer populations, though these findings are not consistent across all studies2.
Increased Risk of Recurrence in Some Cancers
Notably, in head and neck cancer (especially among smokers), vitamin E supplementation at therapeutic doses has been associated with an increased risk of recurrence and second primary cancers during the intervention period2345. This risk appears to diminish or reverse after supplementation is discontinued3.
Some studies have also reported a higher recurrence rate for other cancers when vitamin E is used during active treatment35.
No Consistent Improvement in Overall Quality of Life
While vitamin E may reduce some specific side effects, overall quality of life scores (as measured in clinical trials) have not consistently shown significant improvement with supplementation3.
Diarrhoea and other gastrointestinal side effects may occur more frequently with vitamin E use at higher doses1.
Potential for Harm at High Doses
| Potential Benefit | Evidence Quality | Notable Risks/Limitations |
|---|---|---|
| Reduced neuropathy and mucositis | Mixed | Not consistent across all studies; diarrhoea |
| Reduced radiation-induced side effects | Moderate | Increased recurrence in head/neck cancer |
| Reduced hot flashes (breast cancer) | Limited | No improvement in overall quality of life |
| General well-being/antioxidant support | Theoretical | High-dose risks: bleeding, recurrence |
At therapeutic levels, vitamin E may modestly improve certain aspects of quality of life for some cancer patients, particularly by reducing specific treatment-related side effects like neuropathy and mucositis. However, the evidence is inconsistent, and there are significant risks—most notably, an increased risk of cancer recurrence in certain groups, especially head and neck cancer patients who smoke. There is no consistent evidence that vitamin E supplementation improves overall quality of life, and high doses may cause harm. Any consideration of vitamin E at therapeutic levels should be carefully discussed with an oncology team to weigh potential benefits against risks.
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Vitamin E supplements are widely available over the counter in pharmacies, health food stores, and online retailers. Natural food sources rich in Vitamin E, such as nuts, seeds, and vegetable oils, are also readily accessible in most grocery stores.
The patient demographic that might benefit most from vitamin E supplementation has been identified primarily in the context of prostate cancer prevention. The evidence from meta-analyses and large randomised controlled trials indicates the following:
Prostate Cancer Prevention:
Vitamin E supplementation is associated with a statistically significant reduction in the incidence of prostate cancer, particularly when used in combination with other supplements and at lower doses (<300 mg/day)2. The benefit is most notable among high-risk groups, including:
Other Cancers:
For other cancer types, such as breast, lung, colorectal, and others, vitamin E supplementation has not shown a clear benefit in reducing incidence or mortality, even among high-risk groups259. Some laboratory and animal studies suggest potential for certain forms of vitamin E (such as γ-tocopherol) in breast cancer models, but these findings have not yet translated into clinical recommendations for specific patient groups43.
Genetic and Ethnic Factors:
There is some evidence that the protective effect of dietary vitamin E may vary by genetic background. For example, higher dietary vitamin E intake was associated with less aggressive prostate cancer in men of European-American descent, but not in African-American men6.
| Cancer Type | Demographic Group | Evidence of Benefit |
|---|---|---|
| Prostate cancer | Men >55, high PSA, African Americans, family history | Statistically significant reduction in incidence28 |
| Other cancers | No specific group identified | No clear benefit established259 |
The clearest evidence for benefit from vitamin E supplementation is in the prevention of prostate cancer among older men, those with elevated PSA, African Americans, and men with a family history of prostate cancer. No specific demographic has been identified as benefiting from vitamin E for other cancer types, and in some cases, supplementation may be neutral or even detrimental. Further research is needed to clarify benefits in other populations and cancer types126.
Vitamin E’s therapeutic efficacy can be influenced by genetic, metabolic, and disease-related factors that reduce bioavailability, alter metabolism, or counteract its effects.
Key resistance markers include:
COMT (rs4680):
val/val genotype increases cancer risk with supplementation, while met/met reduces it6. This gene affects vitamin E’s interaction with oxidative stress pathways.
APOE isoforms (ε2, ε4):
ε4 carriers exhibit reduced responsiveness to supplementation despite higher baseline levels, while ε2 variants correlate with lower plasma α-tocopherol6.
CYP4F2 (rs2108622):
Alters vitamin E metabolism, leading to variable plasma levels and efficacy in liver disease6.
Fat malabsorption syndromes (e.g., Crohn’s disease, cystic fibrosis, abetalipoproteinemia) impair vitamin E uptake, causing deficiency even with adequate intake68.
Hepatic transport deficiencies (e.g., TTPA mutations) reduce tissue retention of α-tocopherol, limiting bioavailability6.
Elevated CRP levels: Vitamin E’s anti-inflammatory effects are weaker in individuals with high baseline CRP unless supplemented at ≥500 mg/day for ≥8 weeks4.
Insulin resistance and obesity: Central adiposity and metabolic dysfunction reduce serum α-tocopherol levels, blunting its antioxidant and anti-inflammatory benefits67.
Anticoagulants (e.g., warfarin): High-dose vitamin E exacerbates bleeding risk, limiting its safe use16.
Chemotherapy agents (e.g., tamoxifen, crizotinib): Vitamin E may interfere with drug efficacy or increase toxicity in certain regimens13.
High-dose α-tocopherol (>400 IU/day): Linked to increased prostate cancer risk and mortality, suggesting isoform-specific resistance616.
Synthetic vs. natural forms: Synthetic α-tocopherol has lower bioavailability, potentially reducing therapeutic effects6.
Summary Table: Key Resistance Markers
| Category | Marker/Context | Impact on Efficacy |
|---|---|---|
| Genetic | COMT val/val, APOE ε4, CYP4F2 T/T | Alters metabolism, increases cancer risk |
| Metabolic | Fat malabsorption, hepatic deficiencies | Reduces bioavailability, causes deficiency |
| Inflammatory | High CRP, insulin resistance | Diminishes anti-inflammatory effects |
| Pharmacological | Anticoagulants, chemotherapy | Increases toxicity or reduces drug efficacy |
| Dosage/Isoform | High-dose α-tocopherol | Raises cancer risk, mortality |
Genetic testing for COMT, APOE, and CYP4F2 variants may identify patients prone to resistance.
In malabsorption disorders, water-soluble vitamin E formulations (e.g., tocopheryl polyethylene glycol succinate) are preferred8.
Combination therapies (e.g., with selenium) or isoform-specific regimens (γ-tocopherol, tocotrienols) may overcome resistance in certain contexts6.
These markers highlight the need for personalised approaches to vitamin E supplementation in cancer and metabolic therapy.
Vitamin E has been extensively studied in preclinical (cellular and animal) models across various diseases, particularly cancer, neurodegenerative disorders, and metabolic conditions.
Key findings from these trials include:
Breast Cancer:
Mechanisms: Vitamin E isoforms (tocopherols, tocotrienols) delayed tumour development, reduced tumour size, and suppressed proliferation in animal models. They downregulated anti-apoptotic genes (BCL2) and upregulated pro-apoptotic genes (BAX), while enhancing immune responses23.
Combination Therapies: Synergistic effects were observed with estradiol, pterostilbene, and dendritic cell-based therapies, improving anti-tumour efficacy2.
Oxidative Stress: Results were conflicting—some studies reported reduced oxidative damage, while others found no significant changes210.
Pancreatic Cancer:
δ-Tocotrienol demonstrated anti-neoplastic activity in preclinical models, prompting progression to human Phase I trials11.
Alzheimer’s Disease (AD):
Non-Alcoholic Steatohepatitis (NASH):
Vitamin E improved liver histology, reduced fibrosis, and normalised transaminase levels in rodent models. Benefits were linked to antioxidant effects and insulin sensitivity enhancement10.
Atopic Dermatitis (AD):
Acute Toxicity: Vitamin E showed very low acute toxicity in laboratory animals, with LD₅₀ values >2,000 mg/kg body weight1419.
Subchronic Studies: No-observed-adverse-effect levels (NOAEL) were established at 150 mg/kg/day in rats1417.
Organ-Specific Effects: High doses (≥500 mg/kg/day) caused reversible liver and testicular weight changes in rats, but no genotoxicity1718.
Isoform-Specific Effects: Most studies focused on α-tocopherol, while γ-/δ-tocopherols and tocotrienols showed superior anti-cancer activity in limited trials215.
Oxidative Stress Biomarkers: Inconsistent results in oxidative stress markers (e.g., MDA, SOD) highlight the complexity of vitamin E’s antioxidant role210.
Translation to Humans: Benefits observed in animals (e.g., tumour regression) often fail to replicate in human trials due to differences in dosage, timing, and disease progression10.
| Disease/Context | Model | Key Outcomes |
|---|---|---|
| Breast Cancer | Rodents, cell lines | Reduced tumour size, enhanced apoptosis, immune activation23 |
| Pancreatic Cancer | Xenografts | δ-Tocotrienol inhibited tumour growth11 |
| Alzheimer’s Disease | Transgenic mice | Improved cognition, reduced oxidative stress8 |
| NASH | Rodents | Improved liver histology, reduced fibrosis10 |
| Atopic Dermatitis | NC/Nga mice | Reduced inflammation, restored skin barrier45 |
Preclinical trials highlight vitamin E’s potential in cancer, neurodegeneration, and metabolic diseases through antioxidant, anti-inflammatory, and pro-apoptotic mechanisms. However, outcomes vary by isoform, dosage, and disease stage, underscoring the need for further research to optimise therapeutic strategies.
Vitamin E is currently being investigated in clinical trials for cancer and related conditions, often in combination with other therapies.
The trials are primarily in Phase II and focus on both direct anti-cancer effects and supportive care.
1. Radiation Necrosis Prophylaxis (Phase II)
A Phase II trial is evaluating the use of vitamin E (400 IU twice daily) in combination with Trental (pentoxifylline) to reduce the risk of radiation necrosis after radiosurgery for metastatic brain tumours. The regimen begins the day after radiosurgery and continues for six months. The primary endpoint is the incidence of symptomatic radiation necrosis5.
2. Combination with Selenium in Bladder Cancer (Completed)
The SELENIB trial investigated whether selenium and vitamin E could prevent recurrence in early-stage bladder cancer. The trial is now closed and results published in 2023. It was a randomised, placebo-controlled study, but did not show a benefit for vitamin E; in fact, recurrence was higher in those taking vitamin E2.
3. Supportive Care During Chemotherapy
Several recent randomised controlled trials (RCTs) have tested vitamin E, often in combination with other supplements (e.g., vitamin C or omega-3), to reduce chemotherapy-induced peripheral neuropathy (CIPN) and mucositis. These studies are typically small and heterogeneous, but some have shown benefit in reducing side effects1.
4. Liver Disease (MASH) – Not Cancer, but Metabolic Context
A multicentre, randomised, double-blind, placebo-controlled trial (NCT02962297) recently completed, tested 300 mg of vitamin E daily in patients with metabolic dysfunction-associated steatohepatitis (MASH). While not a cancer trial, it is relevant to metabolic therapy. The study found improvements in liver histology, with no serious adverse events attributed to vitamin E3.
5. Immunotherapy Enhancement (Preclinical and Translational)
Recent preclinical research has shown that vitamin E succinate (VES) can enhance tumour sensitivity to immunotherapy by promoting the degradation of FTO, a protein linked to tumour growth and resistance. These findings are promising, but as of early 2025, they are still in the preclinical or early translational phase and not yet in large-scale human clinical trials4.
| Indication/Use | Trial Phase | Status | Notes |
|---|---|---|---|
| Radiation necrosis prophylaxis (brain metastases) | II | Ongoing | Vitamin E + Trental, 6 months post-radiosurgery5 |
| Bladder cancer recurrence prevention | III | Completed | SELENIB trial, no benefit for vitamin E2 |
| Chemotherapy side effect reduction | II/III | Recent/Ongoing | RCTs in various cancers, mixed results1 |
| MASH (liver disease, metabolic context) | II/III | Completed | 300 mg daily, improved liver histology3 |
| Immunotherapy enhancement (VES) | Preclinical | Early phase | Positive results in animal models, not yet in human trials4 |
Vitamin E is part of several current and recent clinical trials, mainly in Phase II, focusing on supportive care (reducing side effects of cancer therapy), recurrence prevention, and as an adjunct in combination therapies. While some trials have completed (such as SELENIB for bladder cancer), ongoing studies continue to explore its potential, particularly in combination with other agents. Results so far are mixed, and large-scale, well-designed trials are still needed to establish clear therapeutic roles and safety profiles for vitamin E in cancer treatment.
Information on active clinical trials involving Vitamin E and cancer can be found on platforms like ClinicalTrials.gov.
Several genetic markers have been identified that influence vitamin E’s efficacy, particularly in cancer prevention and metabolic contexts. These markers affect absorption, metabolism, and biological activity, leading to variable outcomes in different populations.
Key findings include:
Effect: The COMT gene (catechol-O-methyltransferase) influences whether vitamin E supplementation reduces or increases cancer risk.
Mechanism: The val/val variant produces a more active COMT enzyme, altering vitamin E’s interaction with oxidative stress pathways68.
Effect: This cytochrome P450 enzyme variant affects vitamin E metabolism.
Implication: Genetic differences in vitamin E catabolism may explain variable efficacy in liver disease and cancer prevention210.
Effect: APOE isoforms influence vitamin E transport via lipoproteins.
Cancer relevance: APOE-ε4 is linked to increased prostate cancer risk, while higher vitamin E status in ε2 carriers may be protective14.
Effect: Variants in the SCARB1 gene (involved in vitamin E uptake) correlate with lower plasma α-tocopherol levels, potentially limiting bioavailability1015.
Effect: Mutations in the α-tocopherol transfer protein (TTPA) gene reduce hepatic vitamin E retention, leading to deficiency. The TT genotype is associated with 3% lower α-tocopherol levels and diminished response to supplementation10.
| Gene/SNP | Effect on Vitamin E Efficacy | Cancer Relevance |
|---|---|---|
| COMT | met/met: ↓ cancer risk; val/val: ↑ risk | Modulates overall cancer incidence |
| CYP4F2 | Alters metabolism; no direct treatment link | NAFLD, liver-related outcomes |
| APOE | ε2: lower levels; ε4: higher baseline but poor response | Prostate cancer risk modulation |
| SCARB1 | Reduces bioavailability | General antioxidant capacity |
| TTPA | Limits hepatic retention, reduces efficacy | Deficiency-linked disorders |
Personalised Supplementation: Genetic testing for COMT, APOE, and CYP4F2 variants could identify individuals likely to benefit (e.g., COMT met/met) or face risks (e.g., COMT val/val) from vitamin E6814.
Dose Adjustments: Carriers of TTPA or SCARB1 variants may require higher doses to achieve therapeutic effects1015.
These findings underscore the importance of genetic profiling to optimise vitamin E’s use in cancer prevention and therapy.
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Drugs and supplements that inhibit cell proliferation help prevent the rapid multiplication of cancerous cells, slowing down or stopping the progression of the disease.
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Targeting specific pathways is a key strategy in precision medicine, offering a tailored approach to combat cancer at its core.
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