Introduction

I’ll write a series of posts in which I'll introduce alternative cancer care. I’ll explain why it can be a rigorous form of biohacking rather than mere quackery. I’ll review books popular in the alternative cancer care world like: Surviving Terminal Cancer by Ben Williams and How to Starve Cancer by Jane McLelland, both written by cancer survivors who overcame terminal stage 4 cancer. I’ll review the historical development of combination chemotherapy. I’ll review some famous cases e.g. the ‘spontaneous remission’ of Joe Tippens and the virologist Beta Halassy curing herself via self-experimentation. And I’ll review select phase 1/2 clinical trials. Throughout, I’ll criticize the FDA and the medical establishment for being too risk-averse, for having the wrong framework for clinical trials and having a frustratingly closed-minded epistemology. 

This is also my first post on this website so I welcome any (additional) feedback. And last, I don’t have a formal background in biology, and this is the result of my independent research. My perspectives are “strongly held views, loosely held” and as such nothing here should be taken as medical advice.

What is Alternative Cancer Care?

Traditional cancer care is defined by two major themes: (1) Oncologists stick to the Standard Of Care (SoC) and (2) if that fails patients can be recruited into clinical trials that are carefully regulated. These clinical trials tend to test the efficacy and safety of the addition / replacement of one of the agents in the SoC. For example they try to answer questions like, for patients with Stage 4 small cell lung cancer with biomarker X, does drug A when taken in combination with already approved drug B extend progression free survival (PFS) in a statistically significant way? PFS refers to the length of time in which the cancer of the patient doesn’t progress i.e. gets worse.

I define alternative cancer care through a negative, as any treatment that deviates from this framework. 

Summary of My Perspective.

1. Cancer is not a single disease; there is instead both inter-tumoral and intra-tumoral heterogeneity. Thus, it's better to think of it as a collection of diseases, even within a single tumor. These collections of diseases have independent vulnerabilities as well as independent capabilities to develop resistance to treatment.
2. As a result, cancer will be cured not with monotherapies or “silver bullet” solutions, but by protocols combining multiple treatment modalities, drug cocktails, and lifestyle optimizations that target multiple vulnerabilities simultaneously.
3. The bottleneck for curing cancer is the speed at which protocols can be tested. But protocols are not carefully designed to be tested as protocols. Instead, there is local search based on addition / replacement of a single agent one at a time. And since typically pharmaceutical companies sponsor clinical trials, promising treatments that can’t be patented are typically excluded from this local search. Worse, clinical trials take a lot of time and money, particularly in the US.
4. The causes for the malaise are over-determined but include among other reasons:  institutional inertia & red tape, lack of funding for repurposing generic drugs, regulations that often force companies to test only one new drug at a time against the standard of care (SoC), oncologists who refuse to deviate from SoC due to some combination of fear of medical liability and close-mindedness and coordination problems amongst pharmaceutical companies.
5. There are people who have cured their cancer through rigorously constructed protocols and self-experimentation, as well as dumb luck. But these cases tend to be completely ignored, rather than evoking curiosity, and rather than triggering follow-up experiments. Sometimes, however, these cases make their way into facebook groups of desperate patients who are willing to try anything.
6. There is a combination therapy ‘overhang’ and we can cure many more cases with the right sequencing and combination of treatments that we already have, including through repurposing generics and nutraceuticals.
7. There are many potential treatments that have limited toxic side effects and that have some theoretical justification and some Phase 1/2 trial evidence for efficacy. The median advice by the medical establishment that such potential treatments should be ignored because they are “unproven” fails a basic cost benefit analysis, particularly if such treatments rely on independent pathways vs the SoC limiting antagonistic interaction risk. On the contrary, such potential treatments have positive risk reward profiles for patients with poor prognosis.
8. Repurposing such potential treatments into a drug cocktail / protocol to be used in combination with the SoC also has a positive cost benefit profile. In this sense, alternative cancer care can be a rigorous form of biohacking.

I’ll start with the case history of Ben Williams, a UCSD psychology professor who, after being diagnosed with “terminal” glioblastoma in 1995, self-medicated alongside his standard of care treatments to become a 30 year survivor (he is still alive). In 2002, he wrote a book called Surviving Terminal Cancer that inspired me to conduct the research I now share. And he is the embodiment of the rigorous biohacker ethos I’ve argued for. 

Book Review: Surviving “Terminal” Cancer; Clinical Trials, Drug Cocktails, And Other Treatments Your Oncologist Won’t Tell You About

Surviving "Terminal" Cancer is part memoir, part manifesto and part proposal for a paradigm shift in oncology by Ben Williams, a UCSD psychology professor who, after being diagnosed with "terminal" glioblastoma in 1995, cured himself through a combination of self-medication and standard of care treatments. Written seven years later in 2002, the book argues that oncology is epistemically close-minded while FDA regulations are overly burdensome. This prevents the implementation of what Williams sees as obvious: concurrent therapy using drug cocktails of repurposed generics and supplements with anti-carcinogenic properties. Central to his argument is that terminal cancer patients, having nothing to lose, should be permitted to more aggressively utilize drugs that don't interfere with standard treatments and have established safety profiles. Williams argues that such compounds not only rarely antagonize each other, but often exhibit significant synergistic potential which can lead to complete response more frequently, such as in his case. In my review, I’ll document Prof Williams’ case history and the development of his protocol, his overall treatment philosophy based on drug cocktails and his criticisms of the medical establishment. I’ll then discuss how the field has evolved since the book was written.

Prof. Williams’ Case History & Development of His Drug Cocktail

In spring 1995, an MRI revealed a large tumor in the right hemisphere of Prof. Williams' brain. Surgery was promptly scheduled and executed without complications, though a significant portion of the tumor remained inoperable. Initial testing suggested a grade 3 anaplastic astrocytoma with a 3-4 year prognosis, and the surgeon expressed optimism about treating the remaining mass with brachytherapy - a targeted radiation treatment where radioactive material is implanted directly into the tumor site. While brachytherapy for brain tumors has largely fallen out of favor since the mid-1990s due to mixed clinical outcomes and the emergence of more precise external beam radiation techniques, at the time it was much more commonly used. However, a week later, the pathology report revealed the tumor to be glioblastoma - a far more aggressive cancer. Most patients with this diagnosis didn't survive beyond a year. Dr Chamberlain, his neuro-oncologist, the only one in the San Diego area, immediately scheduled him for radiation therapy.

Midway through radiation therapy, Prof. Williams approached Dr. Chamberlain to discuss alternative treatments he had researched. His own investigation confirmed the bleak prognosis - glioblastoma was uniformly fatal. Nevertheless, Williams pursued several promising leads: Dr. Friedman at Duke University was conducting clinical trials with monoclonal antibodies for brain cancers and agreed to enroll Williams three months after radiation completion. Dr. Burzynski in Houston, though under FDA investigation for fraud, had developed an antineoplaston treatment with vocal patient supporters. At Walter Reed Hospital, Dr. Salazar was investigating Poly ICLC with apparently remarkable results - all but one of his grade 3 glioma patients remained alive. Williams also discovered Dr. William Couldwell's research at USC on using tamoxifen for brain cancers. Dr. Chamberlain dismissed most of these options: he doubted Poly ICLC's results would replicate, was skeptical of the monoclonal antibody treatment, agreed with accusations against Burzynski, and despite conducting his own tamoxifen research, refused to prescribe it as "unproven." Instead, he too advocated for brachytherapy.

The refusal to prescribe tamoxifen led to a conflict. Williams, using his position as a UCSD professor, circumvented Dr. Chamberlain by appealing to his superior, ultimately forcing Chamberlain to agree to prescribe tamoxifen after radiation completion. Williams then formulated a strategic plan: complete radiation, undergo chemotherapy with tamoxifen in the interim, then join Friedman's monoclonal antibody trial after the required three-month waiting period. Despite his doctors' recommendations, he declined brachytherapy, to avoid additional brain damage.

After six weeks of radiation therapy, Prof. Williams' tumor remained stable i.e. neither growing nor shrinking. As he prepared to start BCNU chemotherapy, Williams began taking tamoxifen. Dissatisfied with Dr. Chamberlain's conservative dosing, he traveled to Tijuana to purchase additional tamoxifen, secretly increasing his dosage to match the levels used in Dr. Couldwell's clinical trials. His research into glioblastoma chemotherapy revealed two critical insights: while combined chemotherapy and radiation didn't significantly extend median survival time, the two-year survival rate increased from 2-10% to 15-30%. Furthermore, he discovered that tumor cells could defend themselves using a pump-like mechanism to expel chemotherapy agents. Williams hypothesized that blocking this mechanism could enhance his chemotherapy's efficacy, potentially placing him among the responsive minority. He identified verapamil, a calcium channel blocker, as a potential solution and obtained a prescription from his internist for the maximum tolerable dose, despite Dr. Chamberlain's dismissal of it as unproven.

Williams' rigor extended to the administration of his treatment. After studying the Physician's Desk Reference (PDR), he learned that BCNU requires storage in glass containers and protection from light to maintain its cytotoxicity. When he observed nurses preparing to administer BCNU from light-exposed plastic bags, he demanded and obtained properly stored replacement medication. Finally, Williams began his protocol: chemotherapy combined with high-dose tamoxifen and verapamil.

Between his first round of chemotherapy and next scheduled MRI, Prof. Williams discovered accutane through a BrainTmr forum post referencing Dr. Levin, then head of MD Anderson's brain tumor center. Accutane, an FDA-approved acne medication, is an acid form of vitamin A with lower toxicity at high doses compared to standard vitamin A supplements. Understanding accutane's anti-oxidant properties, Williams theorized it might interfere with chemotherapy and developed a carefully timed protocol: taking accutane during his chemotherapy off-weeks while suspending its use during active treatment. Rather than consulting Dr. Chamberlain, he again traveled to Tijuana to secure a large supply. Managing his only significant side effect - tamoxifen's risk of blood clots - Williams implemented a simple preventive strategy: daily beach walks combined with two aspirin tablets. Aspirin itself is speculated to have anti-carcinogenic properties since it can be a COX-1/2 inhibitor, but Prof Williams was only focused on aspirin's blood thinner property.

The strategy proved effective: the next MRI revealed significant tumor shrinkage, prompting a revision of the treatment plan. Dr. Chamberlain abandoned his push for brachytherapy, and Williams opted to continue chemotherapy rather than pursue Dr. Friedman's monoclonal antibody treatment. For the next phase, they agreed to switch to the PCV regimen. Despite this success, Williams remained cautious: research showed that patients achieving partial response to chemotherapy averaged only 72 weeks of survival compared to the 50-week baseline, as residual tumors typically developed resistance and returned more aggressively.

Determined to maintain momentum, Prof. Williams expanded his protocol with two additional agents: melatonin and polysaccharide krestin (PSK). An Italian clinical trial had demonstrated melatonin's ability to double survival time for various cancers, including glioblastoma. Despite its low toxicity profile and mechanism of action as a broad immune system booster, this finding had been largely ignored by American oncologists. Similarly, PSK, a mushroom extract with documented success in Japanese cancer treatment for over a decade, had demonstrated doubled survival times in international clinical trials, yet also failed to gain traction in American oncology. Williams could only obtain PSK through a single source: an Oregon-based physician who distributed it by mail order. After incorporating these two agents into his protocol and commencing his next round of PCV chemotherapy, the subsequent MRI revealed another dramatic reduction in tumor size - so significant that, for the first time, Williams had genuine cause for optimism.

Continuing his aggressive approach, Prof. Williams identified yet another compound to add to his protocol: Gamma-linoleic acid (GLA). An Indian study had demonstrated dramatic tumor reduction in glioma patients when GLA was injected directly into the tumor cavity - another promising finding that had failed to gain traction in American oncology. Williams calculated that 10 capsules of borage seed oil daily would provide 2-2.5g of GLA. Though uncertain about both the optimal dosage and GLA's ability to cross the blood-brain barrier when taken orally, he reasoned that given its safety profile, the potential benefit outweighed any risk. His third MRI brought remarkable news: one tumor site had completely disappeared, while the other showed further shrinkage. Buoyed by these results and struggling with PCV's side effects, Williams made the strategic decision to switch back to BCNU chemotherapy.

With his prognosis improving, Prof. Williams traveled to Washington DC for Christmas with his wife's family - a decision that proved ill-advised when he fell ill and remained housebound at his in-laws' residence. However, upon returning to San Diego, his fourth MRI delivered extraordinary news: the tumor had completely disappeared. Yet Williams remained cautious, recognizing that a single clear MRI could be anomalous and true remission required confirmation. He proceeded with a fourth round of BCNU chemotherapy. The subsequent MRI confirmed remission. Williams' research indicated the rarity of his situation: only 5% of glioblastoma patients ever achieved a clean MRI, and of those, half suffered recurrence and death within a year, while the other half appeared to achieve lasting remission. Taking no chances, Williams underwent one final round of chemotherapy - a half-dose PCV regimen.

Two additional clean MRIs marked the beginning of Prof. Williams' transition back to normal life, as he resumed attending conferences and established an exercise routine centered on walking. Though he noted a persistent decline in his cognitive sharpness and memory, subsequent clean MRIs finally convinced him of his remarkable achievement: he had become Dr. Chamberlain's first glioblastoma patient to achieve a cure. Despite reaching this milestone, Williams maintained his protocol, including tamoxifen, choosing to endure its side effects rather than risk recurrence.

The Drug Cocktail Treatment Philosophy

Prof. Williams' approach followed a precise logic: he identified promising compounds that showed efficacy in 20-30% of patients, theorizing that combining multiple such agents could produce not just additive but synergistic effects. His most compelling insight drew from the HIV treatment paradigm, which I'll quote in full as its my favorite passage of the book:

The HIV virus and cancer cells are biological entities that mutate rapidly. Because mutations can develop resistance to treatment agents, treatments for these diseases often seem effective at first, but may become less effective over time. 

The major advance in AIDS treatment was the discovery that a combination of agents is more effective in overcoming this resistance than individual agents. When a mutated cell becomes resistant to a treatment agent, that resistance is transmitted to a subsequent generation of cells. The result is a virulent cell population that is much less likely to respond to the treatment in the future. But when that same treatment is part of a treatment cocktail, along with several other agents having different mechanisms of action, the other agents can prevent the cell from dividing, causing the mutation to die on the vine. It seemed that the same concept could apply to cancer cells. Perhaps my outcome had been successful because I used a drug cocktail that included agents with different mechanisms of action and this prevented my tumor from developing resistance to my treatments.

I was impressed by another detail with the AIDS treatment, the development of AZT as an early approach to treating HIV showed great promise, but optimism quickly changed to disappointment as most patients developed resistance to the drug, and those patients were switched to the drug cocktails their outcomes were significantly worse than patients who had not prior exposure to AZT.

If this analogy between AIDS and cancer is valid, then it implies that simultaneous drug combinations are best used as initial approach treatments, not after the individual treatment agents are shown to fail. Yet the typical approach to glioblastoma treatment is to prescribe a single best agent, then after it fails to prescribe another drug, and so until the patient's vital resources are depleted. Such an approach will never exploit the synergistic effects of combined treatments, thus depriving patients of their best chance for survival.

While combination therapy exists in cancer treatment - exemplified by the PCV regimen's three chemotherapy agents - it faces two major limitations. First, the combined toxicity of multiple chemotherapy drugs creates a ceiling on how many can be used together. Prof. Williams circumvented this by identifying at least half a dozen compounds with demonstrated anti-cancer effects but minimal toxicity. The second limitation stems from oncologists' concerns about potential negative interactions, which they frequently cite when discouraging patients from combining alternative treatments with standard protocols.

Williams dismissed this as intellectual complacency. His reasoning was twofold: for terminal patients, the standard of care's inadequacy justifies greater risk-taking, and the mechanisms of action described in literature allow for informed speculation about drug interactions. He noted the distinct pathways: GLA's free-radical release for cancer cell death, PSK and melatonin's immune system enhancement, accutane's blocking of epidermal growth factor receptors, and tamoxifen's protein kinase C suppression. With such diverse mechanisms, Williams concluded the risk of antagonistic interactions was limited.

Criticisms of the Medical Establishment

After Williams' story spread through the BrainTmr forums, he began receiving requests for advice. However, a pattern emerged: while patients were initially receptive to his approach, their oncologists consistently discouraged them from pursuing it. Most of these patients ultimately followed their oncologists' advice and subsequently died. During the period covered in the book, Williams was aware of only one patient who adopted the cocktail protocol for glioblastoma treatment; though they ultimately succumbed to the disease, demonstrating that his approach didn't guarantee success.

The 2015 documentary "Surviving Terminal Cancer" interviewed two additional cases of terminal glioblastoma patients who survived by following Williams' approach. Dr. Richard Gerber, a computer science professor given months to live, developed a protocol incorporating over a dozen compounds, ultimately resorting to prescription forgery when his oncologist refused to cooperate. Dr. Anders Ferry, a Swedish chemist, also survived glioblastoma using a similar cocktail approach, aided by physician relatives willing to write off-label prescriptions. These cases, while still anecdotal, suggest Williams' success wasn't entirely unique. 

This resistance to the cocktail approach stems largely from oncologists' adherence to standardized treatment protocols. Their typical progression follows a rigid pattern: first proposing the standard of care, then upon its failure, steering patients toward clinical trials that usually test single additional agents. This conservative approach is partly driven by FDA regulations, which discourage physicians from recommending 'unproven' treatments.

Prof. Williams condemns the current medical system as fundamentally unethical, arguing that strict adherence to it would have cost him his life. He identifies a systemic catch-22: doctors won't recommend drugs without FDA approval, yet drugs can't establish efficacy records without this recommendation. While large-scale phase 3 clinical trials could break this cycle, pharmaceutical companies lack financial incentive to conduct expensive trials for generic drugs. Without National Cancer Institute funding, potentially effective treatments remain in perpetual limbo, lacking the formal efficacy records required for widespread adoption. The FDA's preference for evaluating drugs individually before combinations, while not absolute, creates additional regulatory burdens for developing multi-drug protocols.

This systemic failure particularly affects drugs that are inexpensive, safe, and show promise in phase 2 trials. Despite favorable cost-benefit analyses supporting their use, these treatments remain largely inaccessible to patients. Williams' own experience illustrates this barrier: despite identifying safe, potentially efficacious treatments through his research, he had to resort to traveling to Mexico and engaging in conflicts with Dr. Chamberlain simply to access them.

Williams proposes a pragmatic alternative: a National Cancer Institute maintained database tracking longitudinal patient outcomes, treatment protocols and patient profiles. Using standard-of-care median outcomes as a control group, this system would allow terminal cancer patients to access promising phase 2 trial drugs without phase 3 confirmation. This approach challenges current medical standards and FDA regulations, arguing that rigidly adhering to standard protocols becomes illogical when facing diseases with fatal outcomes.

Drawing another parallel to HIV treatment, Williams notes that the successful HIV cocktail wasn't developed through traditional phase 3 trials but gained FDA approval through patient activism. He envisions a similar "Bastille Day" for cancer treatment - where patients gain freedom to pursue promising, low-toxicity treatments without waiting for phase 3 trials that may never materialize due to funding constraints. However, writing this review 22 years after Williams' book, it's evident that his hoped-for revolution has not materialized. 

Williams concludes with a survey of potentially overlooked treatments and emerging trends in oncology. His speculations are from 22 years ago and so are now a little outdated. I will not review those for the purposes of this book review.

Conclusion

Williams' survival is difficult to dismiss as pure chance. That the singular patient who systematically researched every promising treatment, methodically reviewed phase 2 trials with the rigor of a smart professor, developed a novel treatment paradigm, and engineered his own drug cocktail managed to survive an otherwise uniformly fatal disease suggests he uncovered something significant, even if luck played a role in his complete response.

Twenty years later, the remarkable case of Prof. Williams remains largely ignored. The field of neuro-oncology's indifference to his success is telling - glioblastoma survival rates remain dismally low, yet his cocktail approach has neither been systematically studied nor replicated. A Google Scholar search reveals a stark absence of academic literature examining his case.

Nevertheless, in oncology, there has been a growing recognition that combination treatments represent the future, yet progress remains frustratingly slow. In the case of glioblastoma, the standard of care has evolved to the Stupp protocol (developed in 2005), which combines radiation and temozolomide chemotherapy concurrently rather than sequentially as in Prof. Williams' era, the fundamental approach remains conservative. Alternative treatments and repurposed drugs, despite growing evidence of their potential efficacy, have not been integrated into comprehensive treatment cocktails. A glioblastoma diagnosis remains, for almost all patients, a death sentence - with median survival times improving only marginally over the past two decades; but with 2 year survival rates increasing from about 10% to 20-25% and 5 year survival rates increasing from about 2% to 10% as a result of the Stupp protocol.

One exception has been Dr. Marc-Eric Halatsch’s experimental glioblastoma treatment protocol CUSP9v3 [NCT02770378]. Interestingly, Dr. Halastch also featured extensively in the documentary. He proposed re-purposing 9 generic drugs (aprepitant, auranofin, celecoxib, captopril, disulfiram, itraconazole, minocycline, ritonavir, and sertraline) into a glioblastoma treatment protocol. He first proposed CUSP in 2013. With a 325,000 Euro donation from the anti-cancer fund, a Phase 1/2 clinical trial commenced in April 2016. A paper describing the results was published in 2021. A phase 3 clinical trial is anticipated to start in 2026.

In the study, 10 patients with recurrent glioblastoma were recruited. In recurrent GBM, single-agent trials have a reported PFS at 6 months of up to 20–30%. The treatment was well-tolerated by all patients though side effects like diarrhea and fatigue were observed in some. 5 patients progressed quickly, dying within a range of 1.5–7 months. The other 5 patients all had PFS of 12 or more months. 3 patients had a complete response and became long-term survivors. It is standard practice for the administration of the protocol to stop when the clinical trial ends. So in December 2020 these 3 patients stopped receiving the CUSP9v3 protocol. One is still alive. However, two of the patients have since passed away, as their cancer recurred after the cessation of the protocol: on 2023-04 and 2022-11, 81 and 70 months since the beginning of the trial. In another trial with recurrent GBM in contrast, a single-agent trial reported complete response in only 1 out of 49 patients (vs 3 out of 10 for the cusp9v3 protocol). 

Of course, you know given the sample size and the lack of a randomized and blinded placebo arm, we possibly can’t infer anything regarding the efficacy of this protocol. Maybe it was all a chance. Therefore, we must protect glioblastoma patients from this potentially dangerous and unknown protocol. God forbid if people get on this protocol as a first line treatment, it might interfere with their SoC with a 95% failure rate. 

My broader critique as an outsider is, it doesn’t seem like the field of oncology is acting with any urgency, it’s not making correct decisions under uncertainty, its epistemology is failing to deliver the patients the best survival odds. Why hasn’t anyone run a clinical trial that attempts to replicate the success of the “Williams Protocol”? In Machine Learning we say look at the data. Shouldn’t researchers study the case studies of “radical” or “spontaneous” remission? Why are patients with terminal disease denied access to cheap and generally safe drugs? Why does it take 15 years for Dr Halatsch to go from idea to phase 3 clinical trial? The answer to all of these questions seem to me to be some combination of status quo bias and a lack of commercial incentives to repurpose generic drugs. If so, streamlining clinical trial regulations and a prize system for generic drug repurposing seem to be appropriate policy responses.

Williams' case exemplifies Kant's enlightenment motto 'Sapere aude' - dare to know, have the courage to use your own reason. The systematic failures of oncology stem from a lack of doctors, regulators and patients willing to think independently. What is obvious to many outsiders remains blasphemy to those whose epistemology centers on rejecting any evidence not derived from expensive phase 3 clinical trials; a close mindedness that becomes catastrophic for integrating unpatentable compounds into the standard of care. Perhaps this is a corny line, but maybe the reason the war on cancer failed is because we fought it like the invasion of Afghanistan.