If one has already sequenced their genome, can they calculate this score by themselves? Or is it proprietary / unpublished?
The glucans in that study are 500 mg per capsule. You can get more than that in three grams of dried Oyster mushrooms.
Ī²-Glucan content and in vitro bile-acid binding capacity of Agaricus bisporus and Pleurotus spp. - Food & Function (RSC Publishing) DOI:10.1039/D4FO02416H(oyster%20mushroom,decreased%20by%2020.4%25%20when%20fried.
| Samples | Ī²-Glucan content, g per 100 g | G | Number of cups | Freeze dried powder amount (g) to provide 1 g of Ī²-glucan | ||
|---|---|---|---|---|---|---|
| Oats | Raw | 8.9 | 6.9 | 14 | 0.2 | 13.2 |
| Cooked | 80.2 | 1 | 100 | 0.4 | 20.4 | |
| Pleurotus, shimeji | Raw | 88.4 | 3.7 | 30 | 0.4 | 3.1 |
| Boiling | 91.8 | 2.6 | 40 | 0.2 | 3.2 | |
| Frying | 66.3 | 5.1 | 20 | 0.1 | 3.3 | |
| **Pleurotus, oyster | Raw | 91.4 | 3.2 | 30 | 0.4 | 2.7 |
| ** | Boiling | 92.2 | 3.7 | 30 | 0.2 | |
| Frying | 79.6 | 5.5 | 20 | 0.1 | 2.5 | |
| A. bisporus, button | Raw | 91.5 | 0.7 | 150 | 1.8 | 12.4 |
| Boiling | 92.2 | 1 | 100 | 0.6 | 7.5 | |
| Frying | 65 | 1.2 | 80 | 0.5 | 13 | |
| A. bisporus, cup | Raw | 92 | 0.5 | 200 | 2.4 | 15.7 |
| Boiling | 91.8 | 0.7 | 150 | 0.9 | 12.4 | |
| Frying | 72.7 | 0.8 | 120 | 0.7 | 14.4 | |
| A. bisporus, flat | Raw | 92.6 | 0.3 | 300 | 3.5 | 22.1 |
| Boiling | 93 | 0.5 | 200 | 1.2 | 13.9 | |
| Frying | 69.4 | 0.6 | 170 | 1 | 21.9 | |
| A. bisporus, brown | Raw | 91.3 | 0.7 | 150 | 1.8 | 13.2 |
| Boiling | 90.4 | 1.1 | 90 | 0.5 | 8.8 | |
| Frying | 64.3 | 1.2 | 90 | 0.5 | 13.8 |
Three grams of freeze dried oyster mushrooms provide one gram.
Raw freeze-dried Pleurotus spp. mushrooms had ā¼5 times more Ī²-glucan than A. bisporus per 100 g dry weight. The Ī²-glucan content was the highest in oyster (37.4 Ā± 1.3 g per 100 g dry weight) and shimeji mushrooms (32.5 Ā± 0.6 g per 100 g dry weight), followed by button (8.1 Ā± 0.0 g per 100 g dry weight), brown (7.6 Ā± 0.7 g per 100 g dry weight), and cup mushrooms (6.4 Ā± 0.4 g per 100 g dry weight), with flat mushrooms containing the lowest amounts (4.5 Ā± 0.1 g per 100 g dry weight). Freeze dried raw oats contained 7.6 Ā± 0.1 g per 100 g dry weight, similar to A. bisporus on a weight-for-weight basis for freeze dried samples (ESI Table 1ā ).
Peter Attia does lung cancer screening every year even as a non-smoker and never-smoker.
Is he talking about a CT scan annually? In combination with other routine screening scans itās a lot of radiation to take.
Talking of modifiable risk factors, thereās a big new study that showed exercise is actually more effective than drugs at preventing cancer reoccurrence:
structured exercise regime reduces risk of dying by a third, can stop tumours coming back or a new cancer developing
researchers enrolled 889 colon cancer patients between 2009 and 2023. Most (90%) had stage three disease. Patients were randomly assigned to take part in a structured exercise programme (445) or to just receive a healthy lifestyle booklet (444).
Patients who began a structured exercise regime with the help of a personal trainer or health coach after they completed treatment had a 37% lower risk of death and a 28% lower risk of recurrent or new cancers developing, compared with patients who received only health advice, the trial found.
Drugs get approved for less than that, and theyāre expensive and theyāre toxic.
I think this is pretty amazing. Thatās stage 3 colon cancer, which is an absolutely devastating diagnosis. And youāre talking about lowering death by 37%. If a drug did that, it would be a massive blockbuster cost a fortune.
I also find that the ādoseā of exercise is very low:
Their weekly target was the equivalent of three to four walks of between 45 and 60 minutes, but patients could choose how they got more active. Some went kayaking or skiing, for instance.
Four hours per week is a very easy target to hit IMO.
Would this reduce risk of cancer in everyone else?
I remembered now that Inigo San Millan has discussed exercise and cancer a lot, this might validate that. Exercise increases the density and function of mitochondria, which increases ability to use more lactate (which lowers serum lactate both at rest and exercise for any given intensity with more training).
The theory that cancer is a metabolic and mitochondrial disease is gaining strength. In my view, the somatic mutation and mitochondrial theories of cancer are not rivals but rather two sides of the same coin.
Nuclear mutations can disrupt mitochondrial function and drive metabolic reprogramming toward glycolysis and chronic lactate production (the Warburg effect). This metabolic shift contributes to the over- or underexpression of key genes involved in cancer, as we and others have shown. Mitochondrial dysfunction, in turn, generates excess ROS, promotes DNA damage, and triggers further epigenetic changes.
Lactate is a central player in both hypotheses and, more broadly, a promising therapeutic target. Despite strong resistance from the ācancer establishment,ā which for decades has focused almost exclusively on the somatic mutation theory, we and others have demonstrated that lactate is a key oncometabolite which regulates gene transcription, fuels tumor growth, and shapes the tumor microenvironment. Lactate is the metabolic link between mitochondrial dysfunction and malignant transformation.
Ultimately, I believe that we should contemplate cancer is likely both a genetic and a metabolic diseaseāperhaps this dual nature explains why, as the āmother of all maladies,ā it continues to evade full understanding. Grasping the mutationāmitochondriaālactate axis is, in my opinion, essential if we are to truly understand and effectively treat cancer.
In our 2017 paper, Brooks and I bridged the somatic and mitochondrial theories of cancer by highlighting lactate as the key metabolic connector.
This was a good PSA.
I had an executive physical when I was almost 50 and they found a nodule on my lung. Iāve never smoked either, but exposed to a lot of secondhand smoke when I was youngā¦ grrr. After his heart attack, my father quit smoking when he was 40 but died of lung cancer at 63ā¦ yes, he went to the doc a year prior and complained about a coughā¦ and they blew him off, as commonly happens.
On that note, aprox 15 years ago, that same doc found lung cancer on our friend who is 88 and who can run circles around me. If not for that executive physical, he might not be here.
We followed it for years, but now that it has been stable for so long, my doc said we are done (I imagine Iāll take another look in a few years).
Same goes for a nodule on my thyroid. It was biopsied years ago after some quick growth, but has now been stable for ages, so we are done with that, too.
This year, through a whole body mri, they found a spot on my pancreasā¦ so, as advised, I will be taking another look next year.
Itās endless and all might turn out to be a waste in the end, but I have a friend who was just diagnosed with late stage pancreatic cancer, so Iād rather spend my money on this than on handbags 
Peter is suggesting to check for lung cancer every year regardless. I donāt know much about it, I just thought it was interesting.
Excellent point. I know a ct scan will show more, but I wonder about balancing that vs doing a whole body MRI each year, in order to catch things in more places, albeit, not as well. Iāll have to look into this topic. Thoughts?
It didnāt sound like he did a MRI as he mentioned radiation.
Attia does low dose CT scan, to my knowledge. I think the radiation isnāt something to worry about, in the context of life in general
I would have to assume so, but I think it would be super difficult to prove with a trial. But in general, people who are sedentary get more cancer, people who are active get less, and now we have like the joining part, where people with cancer have better outcomes with exercise. So IMO itās likely that exercise ticks box boxes.
What Iād be really interested in is knowing the dose and type of exercise. For example, I wonder if resistance training would qualify under the 4 hours per week.
And FWIW, I find it really hard to believe thereās any sort of āone size fits allā general statement for cancer. Iām sure lactate and mitochondria are important, but you get foetuses with cancerous growths in the womb, or really young kids tragically getting fatal cancers. Itās hard to imagine they have metabolic health or mitochondrial problems, and if they did, how that wouldnāt have been determined already.
Thatās like the trial that could be powered to detect any effect in cancer prevention. But if prospective cohort studies show a reduction in cancer as well, Iād act as if it is causal until further evidence. Itās like cholesterol lowering meds only being powered to detect effects in people with high risk of CVD. We still believe it will be the case in those with low risk over time. But we have genetic studies as well, I donāt know if that could be established for exercise ā cancer. Maybe future studies can find a biomarker that exercise improves and which explains the reduction in cancer, which thereās genetic variation in that exposure. Then itād be easy to see if itās causal and even have an important biomarker to track. Pharma would probably find a way to drug it as well.
Yes, but youād need an enormous population. These people already had cancer, and thereās a very high percentage of reoccurrence. If you grabbed random people from the general population, the general chance of cancer within the trial period is pretty low.
As for exercise biomarkers, you might be interested in this: https://www.motrpac.org Theyāve published a ton of papers now, omics (transcriptomic, proteomic, kinome, metabolome etc) datasets etc showing acute responses to exercise.
Awesome paper from a team at UCLA: Serotonin transporter inhibits antitumor immunity through regulating the intratumoral serotonin axis (Cell, 2025)
Identifying additional immune checkpoints hindering antitumor T cell responses is key to the development of next-generation cancer immunotherapies. Here, we report the induction of serotonin transporter (SERT), a regulator of serotonin levels and physiological functions in the brain and peripheral tissues, in tumor-infiltrating CD8 T cells. Inhibition of SERT using selective serotonin reuptake inhibitors (SSRIs), the most widely prescribed antidepressants, significantly suppressed tumor growth and enhanced T cell antitumor immunity in various mouse syngeneic and human xenograft tumor models. Importantly, SSRI treatment exhibited significant therapeutic synergy with programmed cell death protein 1 (PD-1) blockade, and clinical data correlation studies negatively associated intratumoral SERT expression with patient survival in a range of cancers. Mechanistically, SERT functions as a negative-feedback regulator inhibiting CD8 T cell reactivities by depleting intratumoral T cell-autocrine serotonin. These findings highlight the significance of the intratumoral serotonin axis and identify SERT as an immune checkpoint, positioning SSRIs as promising candidates for cancer immunotherapy.
Any thoughts on Dr Aubrey de Greyās theory of telomerase being more active in cancers and the solution to cancer is to actually turn telomerase off and do stem cell replacement of cells to over one a lack of telomerase?
Hopefully I didnāt butcher that. I read it in one of his books.
Long-term use of low-dose aspirin has been demonstrated to reduce cancer risk, but the duration of necessary medication use remains uncertain. This study aimed to investigate the long-term chemoprotective effect of aspirin among the Chinese population. This population-based study included all aspirin users between 2000 and 2019. Aspirin users were age-sex matched with non-users at a 1:2 ratio. Cancer incidence and mortality were the main outcomes measured. Survival analyses with the Fine-Gray modelling were performed. The chemoprotective effects were measured by the sub-distribution hazard ratios (SHR) with control for the competing risks. A total of 538,147 aspirin users and 968,378 non-users were included, with a mean age of 64.8 years, 9,543,399 person-years of follow-up and 90% of users with 80 mg aspirin. The long-term use of aspirin was associated with a reduced risk of cancer (SHR 0.92, 95% CI 0.91-0.94) and a reduced risk of cancer mortality (SHR 0.80, 95% CI 0.79-0.82). Stronger chemopreventive effects were observed among those who used aspirin for more than 10 years, including risk reductions for lung (SHR 0.56, 95% CI 0.51-0.60), breast (SHR 0.34, 95% CI 0.29-0.38) and colorectal (SHR 0.37, 95% CI 0.33-0.40) cancers, but not for bladder cancer and leukaemia. Low-dose use of aspirin was associated with lower risk of cancer among Chinese. The association was even stronger for those using aspirin for more than 10 years. Prescription of aspirin may be started as early as at age of 40, as the chemoprotective effect also applied for early cancers.
An abortion drug for breast cancer is being blocked by moral and political interests
A group of experts says that conservative politics have hampered research on mifepristone. āItās scary to investigate it and look pro-abortionā
On December 1, 2006, the journal Science flagged up a promising development. āIn the future, perhaps, drugs can be used to prevent breast cancer,ā the article predicted. Almost 20 years later, that hasnāt happened. The āmaybesā in scientific journals should be written in capital letters. Science advances slowly and there are many obstacles in its path: lack of funding, errors, dead endsā¦ But in this case, the research has also been impeded by moral prejudice and political bias.
The drug Science was talking about is called mifepristone and is used to induce abortions. And this is a problem. āItās scary to investigate it and look pro-abortion,ā Swedish researcher Kristina Gemzell Danielsson, from the Karolinska Institutet, explains. Danielsson is one of the signatories of a recent editorial published in The Lancet denouncing the situation. āWe have very promising data, but no efforts are being made to continue with the research,ā she explains. āMifepristone is also extremely expensive to use for research and the regulatory hurdles are absurd, probably because it is associated with induced abortion.ā
Squelching Progesteroneās Signal May Prevent Breast Cancer
Leeās team also showed that mifepristone, a drug that induces abortions by inhibiting the progesterone receptor, blocks the development of mammary tumors in mice that have had the rodent version of BRCA1 inactivated in their mammary glands. āThe paper has a mechanism [of BRCA1 activity] and has clinical implications. Itās potentially important,ā says Eliot Rosen of Georgetown University School of Medicine in Washington, D.C., who is also studying the interaction between BRCA1 and progesterone.
Read the full article:
https://www.science.org/doi/10.1126/science.314.5804.1370
The potential role of mifepristone in breast cancer prevention: beyond medical abortion
Breast cancer is the leading cause of cancer-related deaths among women globally. Yet, current management strategies emphasise detection and treatment over primary prevention. For groups at high risk of breast cancer, such as carriers of BRCA1 or BRCA2 pathogenic variants, salpingo-oophorectomy and mastectomy are risk-reducing surgical options, but these approaches affect quality of life and evidence for a mortality benefit is sparse. Non-surgical treatments, such as selective oestrogen receptor modulators, have low efficacy against breast cancers with poor prognosis (eg, triple-negative cancers), and toxicity can often lead to poor adherence. Emerging evidence indicates that progesterone plays a part in breast carcinogenesis, particularly in carriers of BRCA1 pathogenic variants. Mifepristone, a selective progesterone receptor modulator, has shown potential to reduce breast epithelial proliferation. However, the association of this drug with medical abortion, besides long-standing availability and patent restrictions, has hindered its development for breast cancer prevention. Regulatory, political, and legal barriers, along with minimal pharmaceutical investment, have further restricted research. Collaborative efforts are needed to accelerate research on mifepristone as a non-surgical risk-reducing option. Overcoming current barriers is essential to expand prevention strategies, particularly for women at high risk of breast cancer worldwide.
https://www.thelancet.com/journals/lanogw/article/PIIS3050-5038(25)00013-5/abstract
ChatGPT:
Identify the research papers that suggest that mifepristone may be helpful against breast cancer
Hereās a concise, citation-backed list of peer-reviewed papers (plus a few registered trials) that have reported signals suggesting mifepristone (RU-486) could be helpful against breast cancerāeither directly as an anti-tumor agent or by enhancing other therapies.
Clinical and translational studies in humans
-
MIPRA trial (biomarker-selected neoadjuvant study).
Single-arm window-of-opportunity trial showing Ki-67 reductions and molecular responses to short-course mifepristone in patients whose tumors had a high PR-A:PR-B isoform ratio (PRA-H)āsupporting antiprogestins in a selected subset. (PMC) -
Randomized phase I (nab-paclitaxel Ā± mifepristone) in advanced breast cancer.
Demonstrated feasibility and signals of activity (including complete and partial responses) when pretreating with mifepristone; rationale was glucocorticoid receptor (GR) antagonism to overcome chemo-resistance. (PMC) -
Randomized phase II (nab-paclitaxel Ā± mifepristone) in advanced TNBC.
Under-accrued study; no PFS benefit overall, but responders were seen and authors note the need for biomarker-driven selection for GR/PR targeting. Useful as context for where mifepristone may (or may not) help. (PMC) -
Single-agent phase II in metastatic PR-positive disease (1990s).
Early trials of mifepristone (and related antiprogestins) in metastatic breast cancer reported modest activity in small cohortsāimportant historically for the antiprogestin concept. (PubMed) -
Short-term exposure study in healthy/premenopausal women.
50 mg/day mifepristone for 3 months reduced breast epithelial proliferation (Ki-67), a prevention-relevant endpoint. (Oxford Academic) -
Case reports suggesting benefit.
Isolated reports describe marked clinical responses with mifepristone, including a complete remission after short exposure; these are hypothesis-generating only. (IIAR Journals)
Preclinical/mechanistic work underpinning benefit
-
GR antagonism as a strategy in TNBC.
Foundational lab paper showing that mifepristone blocks GR-mediated pro-survival signaling and enhances taxane-induced apoptosis in GR-positive triple-negative modelsāproviding the mechanistic basis for clinical combinations. -
TNBC xenograft study (Theranostics).
Additional in-vivo work supporting mifepristoneās anti-proliferative and anti-metastatic effects in TNBC models. (PMC)
Ongoing/related clinical efforts (context)
-
Pembrolizumab + mifepristone (HER2-negative metastatic breast cancer).
Phase II trial exploring GR blockade with immunotherapy; abstracted results presented (safety/efficacy signals). (ASCO Publications, ClinicalTrials.gov, Cancer.gov) -
Enzalutamide Ā± mifepristone vs. physicianās choice in AR-expressing disease.
A current phase II design testing whether adding mifepristone can improve outcomes; included here to show how investigators are operationalizing the hypothesis. (ClinicalTrials.gov, Cancer.gov)
How to read this evidence
- The strongest positive human signal so far is biomarker-selected (PRA-H in the MIPRA study).
- Attempts to use mifepristone broadly (e.g., unselected TNBC with nab-paclitaxel) have not yet shown clear PFS benefit, reinforcing the need for selection by PR isoforms and/or GR activity. (PMC)
If you want, I can filter these into a mini-bibliography (APA/AMA) or pull out key data (dose, schedule, endpoints, effect sizes) for the papers most relevant to your use case.
Old post I missed, purple Owsley blotter was quite popular in my day
For a couple years my buddies and I would take a trip every couple months We went on one run doing it every weekend for about 3 months in 1972. As a bunch of farmer boys most of our trips were at a cabin we built in the woods.
Green Frog and Yellow Sunshine and a few other come to mind but that was 50+ years ago.
The stories I could tell.