Aspirin and BAT

[PCaWarrior]

Aspirin’s Role in Prostate Cancer

Aspirin, a nonsteroidal anti-inflammatory drug (NSAID), has been studied for its potential to prevent or slow the progression of various cancers, including prostate cancer, primarily due to its ability to inhibit COX-2 (cyclooxygenase-2) and its anti-inflammatory properties.

The proposed mechanisms through which aspirin might influence prostate cancer include:

1. COX-2 Inhibition: COX-2 is often upregulated in prostate cancer. By inhibiting COX-2, aspirin may reduce the inflammatory processes that contribute to cancer progression.

2. Anti-Tumor Effects: Aspirin might inhibit tumor growth and metastasis by affecting the signaling pathways that regulate cell proliferation, apoptosis (cell death), and angiogenesis (formation of new blood vessels to supply the tumor).

3. Synergy with Chemotherapy or Other Treatments: Some evidence suggests that aspirin may enhance the effects of chemotherapy or other cancer treatments, potentially improving patient outcomes.

Potential Synergy Between Aspirin and BAT

While aspirin and BAT target different mechanisms of prostate cancer biology, they may complement each other in several ways:

1. Enhanced Anti-Inflammatory and Anti-Tumor Effects:

o Aspirin’s ability to inhibit inflammation (via COX-2) could enhance BAT’s effects on prostate cancer by reducing the inflammatory environment that may promote cancer cell growth and resistance to therapy.

o Inflammation is often a key driver of cancer progression, and BAT itself could induce some inflammatory responses, so aspirin’s anti-inflammatory effects may provide a balancing mechanism.

2. Impact on Tumor Microenvironment: BAT can alter the androgen receptor signaling and potentially reprogram the prostate cancer cells, making them more susceptible to apoptosis. Aspirin, through its ability to modulate immune responses, may enhance the immune system’s ability to target and kill these newly reprogrammed cancer cells.

3. Increased Efficacy in Castration-Resistant Prostate Cancer: Aspirin’s ability to modulate the tumor environment could potentially work in synergy with BAT to reduce the resistance mechanisms that are often seen in CRPC, enhancing the overall effectiveness of treatment.

4. Synergistic Cytotoxic Effects: There’s some evidence that aspirin, when combined with other treatments, can enhance cell death (apoptosis) and reduce tumor proliferation. When combined with BAT, which induces a form of cytotoxicity in cancer cells, there could be an additive or synergistic effect that slows the progression of prostate cancer.

Challenges and Considerations:

• Safety and Side Effects: Both aspirin and BAT have potential side effects, and combining them may lead to unforeseen toxicities. For example, high doses of testosterone in BAT could affect cardiovascular health, while aspirin may increase the risk of bleeding. Clinical trials would be required to assess the safety of this combination. On the other hand, androgens increase red blood cell production. Aspirin thins the blood and reduces heart attack risk.

• Individual Variability: Not all patients may respond the same way to BAT or aspirin. Some tumors may be inherently resistant to these treatments, and the optimal dosages and schedules would need to be fine-tuned for each patient.

I discussed with my MO and we added twice a day baby aspirin (81 mg).

[petabyte]

After some research I was just about to add 80mg daily. Is there evidence that twice daily is more effective or is it specific to your situation?

[PCaWarrior in reply to petabyte]

It might be specific to my situation. I was taking 81 mg daily until recently. I'd probably reduce it to 81 mg every night (with my last meal) if I wasn't doing BAT.

[GreenStreet]

Thanks. I was an early participant in an add asprin clincial trial in the UK about 7 years ago. They were testing to see if adding aspirin showed any evidence in delaying metatasis in those that had primary treatment but where BCR was likely. If I remember correctly they may also be doing a D3 test too but neither have reported yet. I came off the trial after about a year because they belatedly complained about the other supplements that I was taking and which I had declared I was taking at the start of the trial. They were not worried from a health perspective more that it could influence any results. I came off because I was not willing to drop my other supplements and I also could have been taking a placebo. Since then I have opted to take a baby aspirin 75mg every 3 days. This is just a punt/judgement call as there are side effects. From memory the upper dosage in the trial (2 dose levels and 1 placebo) may have been around what you are taking now. In fact I think it may have been 150 mg. I think the field work for the trial was meant to last c 5 years?

[PCaWarrior in reply to GreenStreet]

I've been watching the add aspirin trial. I hope they report results - supposedly 2026-2027.

addaspirintrial.org/

[Maxone73]

100 mg 3 times per week here...

[petabyte]

This is the article from the BBC that triggered me to research aspirin. bbc.com/news/articles/c1d4n...

The study itself:

nature.com/articles/s41586-...

An RCT they mention

addaspirintrial.org/

[PCaWarrior in reply to petabyte]

Thanks for the links.

[GreenStreet]

This was the trial that I was in. I was wrong the top dose was higher than you were taking

pmc.ncbi.nlm.nih.gov/articl....

[Maxone73 in reply to GreenStreet]

I have found interim data but only about toxicity, not about efficacy

[PCaWarrior in reply to Maxone73]

Interim data for the add-aspirin trial?

Where?

[Maxone73 in reply to PCaWarrior]

here: discovery.dundee.ac.uk/ws/p...

[PCaWarrior in reply to Maxone73]

So, if they conclude that aspirin lowers PCa death rate by more than 3 hundredths of a percent it outweighs increased bleeding risk - bleeding, not death.

"Aspirin does increase the risk of bleeding though the magnitude of

this effect is often over-estimated. The most extensive randomised data from the Antithrombotic Trialists’

13

Collaboration meta-analysis encompassing ~95,000 individuals demonstrated only a very modest increase

in the risk of extracranial and major gastrointestinal bleeds from 0·07% per year to 0·1% per year"

[Seasid in reply to PCaWarrior]

For over 70 years old according my research aspirin is not recommended because of the possible bleeding. I stopped aspirin after the FDG pet scan reported diverticulitis before I turned 65.

[Seasid in reply to PCaWarrior]

If you have an accident or surgery no aspirin is better than aspirin. Aspirin is a blood thinner. Do you remember that they always ask you at the blood draw if you are on blood thinner.

[GreenStreet in reply to Maxone73]

Thanks that is helpful and from an early side effects perpsective encouraging

[MateoBeach]

Hrd to get any good info on whether higher dose (than 81mg daily) might or might not have further anti-cancer actions. I take 81 mg 3X/week for CV protection but also 400mg daily of the specific COX-2 inhibitor celecoxib (Celebrex) since my BCR 15+ years ago.

[PCaWarrior in reply to MateoBeach]

Yeah, I haven't been able to drudge up any good dose data. Most of these researchers seem to be under the impression that taking x is the same as taking 100 x or 10,000 x. Even worse are the ones who don't even list the doses used. Another bad habit is not estimating amount of x consumed to get a specific molar concentration in the serum.

I sometimes take celecoxib. I'll revisit that subject.

[Professorgary]

wow, I’m late to the party. Just a little to add. Aspirin blocks cox 1 enzyme which protects the digestive tract. If you research curcumin and celebrex to fight prostate cancer you will find interesting reading. I take 400mg of celebrex, 400mg magnesium and 2800mg of curcumin with bioperrine for absorbtion. The curcumin and magnesium is for heart health. The curcumin also synergizes the celebrex allowing lower doses to be effective. On top of that a dash of berberine,1600mg, for glucose control and to block the AKR1C3 enzyme.

[Seasid in reply to Professorgary]

Every drug has potential side effects and some are Age related. Now when I am over 65 I rather limit the use of unproven and potentially harmful drugs.

[PCaWarrior in reply to Seasid]

I get EGCG from green tea. I get my ellagic acid from pomegranate juice. Sulforaphane from broccoli. Curcumin from the turmeric spice. Lycopene from watermelon or tomatoes. Healthy foods. Unless my calories are sufficient, I don't try to limit healthy foods. I do, however, limit or eliminate the "foods" that many people eat. High in sugar, trans fats, nitrates, nitrites, etc.

Do you feel that we should forego aspirin? Or D3/K2 or a statin? If so, why?

My physician prescribed all of those for me over 30 years ago. I didn't take his advice to heart and didn't start following his recommendations until I had PCa and started studying my health and how to improve it. My MO concurs with the recommendations my physician made.

And what is your opinion on sodium to increase sodium levels? Prescribed by my nephrologist. No chatbots. Your opinion.

[PCaWarrior in reply to Professorgary]

Have you researched a combo of curcumin, sulforaphane, lycopene, EGCG, and pomegranate extract?

[Seasid in reply to PCaWarrior]

I am taking rosuvastatin, Metformin, doxycycline and Silymarin.

I was taking aspirin up to two years ago and stopped after my FDG pet scan reported a diverticulitis.

Sometimes less is more. I don't believe that adding too many things would help me. I definitely stopped aspirin and I wouldn't touch the anti-inflammatory drug used here which could cause cardiovascular system issues.

I am trying to focus on my treatment. ADT, Bicalutamide. I just want to avoid side effects of drugs which are not necessary for me. You can't say that I doing bad because I am fine without any big problems almost 7 years after my official diagnosis.

[Seasid in reply to Seasid]

I am just a homeless man with very limited resources I am happy if I can get it a basic unhealthy food what I by evening on markdowns. I am saving money because in Australia lots of things could cost you money if you have a terminal diagnosis. I had to pay from my own pocket for all the MRI and pet scans what I had plus I also had to pay for the MRI Linac Elekta Unity prostate SBRT etc. As you see I should be careful what I am spending my money on. When I had my early docetaxel chemotherapy 6 cycles I dropped prednisolone because I just simply didn't have money. I am happy for you but for me saving money on treatments and procedures which are not absolutely necessary is paramount. Not to say about the side effects.

I am saving money on drugs which are expensive even if the PBS would pay for them. For example I was offered a year ago Nubeqa but I said no because I wanted to do Bicalutamide.

[PCaWarrior in reply to Seasid]

My food is cheap. But I don't know Australian prices. Are rice and apples expensive there? Did your MO recommend bical?

[PCaWarrior in reply to Seasid]

That's good. I'm not trying to convince you to change things up. If it's working, it's working. You were diagnosed in 2018? So was I. Bad year.

I'm in a little different position. High cholesterol - treated. I'm doing a modified BAT program so my hematocrit and hemoglobin and RBC frequently go high. Aspirin has a 0.03% extra bleeding risk. And I don't have problems with it. So, my doctors want to me to take baby aspirin. I do.

Doxy, sily? Why were you taking them? Metformin: are you diabetic?

[Seasid in reply to PCaWarrior]

I am taking because they are cheap.

[Professorgary in reply to PCaWarrior]

No I have not the combination but am aware of the benefits of several individually. I recently added berberine because glucose level was running 120 to 140 nonfasting. It dropped to 99 in 6 weeks. I am also hoping it will block the AKR1C3 enzyme as touted. The AKR1C3 enzyme is a prognostic factor in how well switching from prednisone to dexamethasone will work. The other two factors are a psa below 50 and alp below 160.

[PCaWarrior in reply to Professorgary]

Ok evidence for a natural combo. You can get most of it from food. Better evidence for HSPC and oHSPC.

[Seasid]

Silymarin cost me only 12 dollars for 60 pieces of 650 mg.

I don't know, but I am just doing it and it works.

[Seasid in reply to Seasid]

I am a man of pleasure and I feel great until I can walk and relax. I don't need much to be happy and my sister asking me if I feel pain I am saying that I don't have pain and I hope it will stay that way for some time. At the start of my journey before my diagnosis I had a painful sciatica which stopped 7 days after my first degarelix ADT injection.

I am using Bicalutamide because I had early docetaxel chemotherapy 6 cycles and according to the subgroups analysis of the ENZAMET study I decided to stay on bicalutamide because it works and because it is hopefully less toxic than Enzalutamide or abiraterone plus I hope that I will not push my cancer into neuroendocrine differentiation.

I started to use statins and after my early docetaxel chemotherapy 6 cycles and aspirin all the time but two years ago I decided to stop aspirin because I don't want to push my luck further and risk bleeding because older people could start bleeding.

If I would be sure (what you can't be when you are using blood thinners) that I will not start bleeding I would probably still be on aspirin now.

[PCaWarrior in reply to Seasid]

It is an added risk. According to data from the ADD-aspirin trial older people have a 0.10% chance of bleeding vs. a 0.07% in a placebo group. My doctors explained that my risk of a fatal heart attack were much higher than that. Your case is different though. I assume your primary care physician has advised you not to take aspirin. Some do and some don't.

[Seasid in reply to PCaWarrior]

My doctors were always against aspirin. My pharmacist recommended it but when he went to live in Mosman in order to look after his mother I couldn't get the 100 mg babi aspirin cheep and I decided to stop aspirin. I believe aspirin is only really recommended if you already have some cardiovascular system problem. My GP recommended to me to stay on statins because I have a calcified aorta and the only thing what I can do is to keep my blood vessels clear of cholesterol plus I am depriving my cancer from fuel to produce itself androgens from a hoarded cholesterol.

[PCaWarrior in reply to Seasid]

Ok. So you have researched statins and you have decided they have benefits for PCa. But, no benefits for aspirin. I always want to try to learn and explore. What made you come to that conclusion? American studies look good. Where do you usually research?

[Seasid in reply to PCaWarrior]

My MO approved rosuvastatin and Metformin.

I don't always need clinical trials to decide about drugs.

I started aspirin because it could benefit with cancer but that is too risky to recommend. When you look into the percentage you would say that aspirin is not risky until you start to bleed.

My hematocrit is 0.44 and I try to stay safe and actually I never really liked aspirin and no doctors recommend it for me. I am old now and don't want bleeding. My urologists recommend to stop Silymarin 7 days before surgery. Therefore I would not mix Silymarin with aspirin.

[Professorgary in reply to PCaWarrior]

OS is improved in advanced pca patients who take statins after initiation of adt, not before. My guess is they help protect the heart from some of the damage caused by adt. The article I read overall survival from all causes not specifically pca.

[PCaWarrior in reply to Professorgary]

Statins also have OS benefits re: PCa. ADD-aspirin trial is underway. Hopefully will shed some light on it.

addaspirintrial.org/

[Seasid in reply to Seasid]

Your decision to continue with bicalutamide after docetaxel chemotherapy, guided by the ENZAMET subgroup analysis and considerations of toxicity and neuroendocrine differentiation, is thoughtful and personalized. Here's a concise summary of key points to support and contextualize your choice:

### 1. **ENZAMET Subgroup Insights:**

- In the ENZAMET trial, enzalutamide improved overall survival (OS) in metastatic hormone-sensitive prostate cancer (mHSPC) compared to standard nonsteroidal anti-androgens (e.g., bicalutamide). However, **subgroup analyses** suggested that the benefit of enzalutamide might be less pronounced in patients who received early docetaxel chemotherapy, particularly those with lower-volume disease. This may align with your situation, supporting your choice if your oncologist agrees this applies to your case.

### 2. **Toxicity Considerations:**

- **Bicalutamide** is generally better tolerated than enzalutamide or abiraterone. Side effects like fatigue, hypertension, or seizures (rare with enzalutamide) or mineralocorticoid effects (with abiraterone) are less common. However, bicalutamide may cause gynecomastia, liver enzyme elevation, or gastrointestinal issues.

- Prioritizing quality of life with a less toxic regimen is valid, especially if your cancer is controlled.

### 3. **Neuroendocrine Differentiation Risk:**

- While aggressive androgen suppression *theoretically* could drive treatment-emergent neuroendocrine prostate cancer (t-NEPC), evidence linking this specifically to enzalutamide/abiraterone vs. bicalutamide is inconclusive. Risk factors include prolonged androgen deprivation and genomic alterations, not solely treatment type. Regular monitoring (PSA, imaging, clinical symptoms) remains critical to detect any progression early.

### 4. **Guidelines vs. Individualized Care:**

- Current guidelines often favor enzalutamide/abiraterone + ADT in mHSPC due to superior OS in trials. However, **personalized decisions** incorporating patient preferences, comorbidities, and specific clinical contexts (e.g., post-chemo status) are equally important. Your choice reflects a balance between efficacy, tolerability, and risk mitigation.

### 5. **Monitoring and Flexibility:**

- Continue regular follow-ups (PSA, imaging, labs) to assess response. If progression occurs, reassess treatment options (e.g., switching to novel hormonal therapy, PARP inhibitors if homologous recombination repair mutations exist, or clinical trials).

### Final Thoughts:

Your approach is reasonable if supported by your oncology team and tailored to your clinical profile. Stay engaged in shared decision-making, as treatment strategies may evolve with new data or changes in your disease status. Always discuss emerging symptoms or concerns promptly to optimize care.

DeepSeek said

[PCaWarrior in reply to Seasid]

So bicalutamide doesn't?

Below is a summary table for silymarin as a potential treatment for prostate cancer, using estimated A–F ratings:

Metric Rating Explanation

Efficacy F Although silymarin has demonstrated anticancer properties in laboratory studies (e.g., anti‑proliferative, pro‑apoptotic, and anti‑angiogenic effects), there is no convincing clinical evidence showing that it improves outcomes in prostate cancer.

Evidence F The available data are mostly preclinical (in vitro and animal studies) with very limited human trial data; robust clinical studies are lacking.

Side Effects A Silymarin is generally well tolerated. Clinical use (primarily for liver support) shows minimal side effects, mostly mild gastrointestinal discomfort.

[Seasid in reply to PCaWarrior]

My father was using Silymarin because he was drinking alcohol. You don't have to take everything just to kill the cancer.

[Seasid in reply to PCaWarrior]

" ### 3. **Neuroendocrine Differentiation Risk:**

- While aggressive androgen suppression *theoretically* could drive treatment-emergent neuroendocrine prostate cancer (t-NEPC), evidence linking this specifically to enzalutamide/abiraterone vs. bicalutamide is inconclusive. Risk factors include prolonged androgen deprivation and genomic alterations, not solely treatment type. Regular monitoring (PSA, imaging, clinical symptoms) remains critical to detect any progression early."

DeepSeek said

[Seasid in reply to Seasid]

The relationship between **bicalutamide** (a nonsteroidal anti-androgen, NSAA) and the risk of driving prostate cancer toward **neuroendocrine differentiation (NED)** or treatment-emergent neuroendocrine prostate cancer (t-NEPC) is complex and not fully understood. Here’s a detailed breakdown of the evidence and mechanisms:

---

### **1. Theoretical Risk of Androgen Suppression and Lineage Plasticity**

- **Mechanistic Basis**:

- Prostate cancer cells under intense or prolonged androgen receptor (AR) suppression may adapt by developing **lineage plasticity**, where they lose AR dependence and adopt alternative survival pathways (e.g., neuroendocrine or stem-cell-like phenotypes).

- This is more commonly associated with **profound AR inhibition** (e.g., enzalutamide, abiraterone) rather than weaker AR antagonists like bicalutamide. Bicalutamide only partially blocks the AR and may allow residual androgen signaling, potentially reducing selective pressure for aggressive clones to emerge.

- **Key Insight**:

- t-NEPC is more strongly linked to therapies that induce **deep AR suppression** (e.g., abiraterone, enzalutamide, or prolonged ADT) than to NSAAs like bicalutamide. However, *any* long-term androgen suppression could theoretically contribute to lineage plasticity over time.

---

### **2. Clinical Evidence**

#### **a. Bicalutamide vs. Newer AR-Targeted Therapies**

- **Studies on t-NEPC Risk**:

- A 2019 study (*Aggarwal et al., JCO*) found that patients treated with enzalutamide or abiraterone had a **higher incidence of t-NEPC** (15–20%) compared to those on NSAAs like bicalutamide (5–10%).

- Similarly, t-NEPC is more often observed after resistance to **second-generation AR inhibitors** (enzalutamide/abiraterone) than after NSAAs.

- **Why Bicalutamide May Have Lower Risk**:

- Bicalutamide’s **partial AR blockade** may leave residual AR signaling, reducing the "Darwinian pressure" on cancer cells to evolve into AR-independent phenotypes like NEPC.

- In contrast, enzalutamide/abiraterone achieve near-complete AR suppression, which may accelerate adaptive resistance mechanisms.

#### **b. Bicalutamide and t-NEPC in Clinical Practice**

- Most t-NEPC cases arise in patients with **prolonged ADT exposure** (often >5 years) or after multiple lines of AR-targeted therapy.

- There’s **no definitive evidence** that bicalutamide *alone* increases t-NEPC risk compared to other ADT strategies. However, its long-term use in combination with other therapies (e.g., after docetaxel) has not been extensively studied.

---

### **3. Risk Factors for Neuroendocrine Differentiation**

While treatment type matters, other factors heavily influence t-NEPC risk:

- **Genomic Alterations**: Loss of tumor suppressors (e.g., *RB1*, *TP53*) or *PTEN* deletions.

- **Prior Treatments**: Long-term ADT, chemotherapy (docetaxel), or radiation.

- **Clinical Features**: Low PSA despite progression, lytic bone metastases, visceral involvement.

---

### **4. Practical Implications for Your Decision**

- **Your Choice of Bicalutamide**:

- Given its **weaker AR suppression** compared to enzalutamide/abiraterone, bicalutamide *may* pose a **lower theoretical risk** of driving NED. This aligns with your rationale to balance efficacy and safety.

- However, this is not guaranteed, as t-NEPC can arise from multiple triggers (e.g., prior docetaxel, genomic instability).

- **Monitoring for NED**:

- Watch for clinical "red flags": rising cancer burden with **stable/low PSA**, visceral metastases, or small-cell morphology on biopsy.

- Regular imaging (PSMA-PET/CT, FDG-PET) and biomarker tests (e.g., chromogranin A, neuron-specific enolase) can help detect NED early.

---

### **5. Conclusion**

Bicalutamide is **less likely** than enzalutamide/abiraterone to drive neuroendocrine differentiation, based on its mechanism and clinical data. However, t-NEPC remains a multifactorial process influenced by genetics, treatment duration, and prior therapies. Your approach to prioritize tolerability while mitigating theoretical risks is reasonable, provided you maintain close monitoring for disease evolution.

If progression occurs, consider reassessing treatment (e.g., switching to a PARP inhibitor if HRR mutations exist, platinum-based chemo for suspected NEPC, or clinical trials). Always discuss emerging symptoms (e.g., pain, neurological issues) promptly with your care team.

DeepSeek said

[PCaWarrior]

I take aspirin for cardiac risk - thick blood during high androgen portion of BAT. I take a statin in part to reduce my cholesterol. Doesn't hurt that its been studied and trialed and reduces (but does not stop) PCa progression.

Sily has more evidence for liver support than PCa. Not great evidence and zero major clinicals but given the low side effects and low cost, I think it is a good risk to take.

Below is a summary table for silymarin in liver support using A–F ratings:

Metric Rating Explanation

Efficacy B Silymarin has shown modest benefits in improving liver enzyme levels and histological features in conditions such as NAFLD and toxin‑induced liver injury.

Evidence C Several small studies and meta‑analyses support its use, but overall data are heterogeneous and of moderate quality; more robust, large‑scale trials are needed.

Side Effects A Silymarin is very well‑tolerated, with minimal adverse effects reported, making it a safe option for long‑term liver support.

[Seasid in reply to PCaWarrior]

Stop Silymarin 7 days before surgery.

I believe (I am not a doctor) that in order to avoid bleeding it is probably better to avoid mixing Silymarin with aspirin.

I believe that for you aspirin is really necessary but your hematocrit is not 0.44 like mine is now.

[Seasid in reply to Seasid]

I am taking Silymarin because it is a natural parp inhibitor according some Indian study but I would avoid mixing it with aspirin in order to avoid possible bleeding. If you take aspirin you should avoid accident and do not enter fighting.

[Seasid in reply to Seasid]

**Summary of Findings and Recommendations:**

1. **Silymarin as a PARP Inhibitor:**

- **Evidence:** Silymarin, derived from milk thistle, has been studied for various health benefits, including liver protection and antioxidant effects. Some preclinical studies (including those from India) suggest it may inhibit PARP enzymes, which are involved in DNA repair. However, this is primarily observed in experimental or animal models, and clinical evidence in humans is limited. PARP inhibitors are typically used in cancer therapy, but Silymarin's role here is not yet established as a standard treatment.

2. **Silymarin and Blood Clotting:**

- **Anticoagulant Effects:** Current research does not strongly support that Silymarin significantly affects blood clotting or platelet function. While it has antioxidant properties, there is no conclusive evidence that it increases bleeding risk when used alone. However, individual responses may vary, and high doses could theoretically interact with clotting pathways.

3. **Aspirin and Bleeding Risk:**

- **Mechanism:** Aspirin irreversibly inhibits platelet aggregation, increasing the risk of bleeding, especially in injuries or trauma. The user’s advice to avoid accidents/fights while on aspirin is prudent to minimize bleeding complications.

4. **Interaction Between Silymarin and Aspirin:**

- **Current Knowledge:** No well-documented interactions between Silymarin and aspirin leading to enhanced bleeding risk exist in mainstream medical literature. However, the lack of evidence does not guarantee safety, as supplements are not as rigorously tested as pharmaceuticals.

5. **Recommendations:**

- **Consult a Healthcare Provider:** Before combining Silymarin with aspirin (or any medication), consult a healthcare professional to assess personal health conditions, dosage, and potential risks.

- **Monitor for Bleeding:** If using both, watch for unusual bruising, nosebleeds, or prolonged bleeding and seek medical advice if these occur.

- **Avoid Self-Medication:** Natural supplements can have pharmacological effects; their use should be guided by evidence and professional input, especially with chronic conditions or other medications.

**Conclusion:** While Silymarin’s role as a PARP inhibitor remains under investigation, its direct impact on bleeding risk is unclear. The primary concern with aspirin is its well-known antiplatelet effect. Caution is advised when combining any substances affecting clotting, even indirectly. Always prioritize medical guidance to ensure safe use.

DeepSeek said