March 10, 2026: What's Going On With Shipping

Today’s focus is the Strait of Hormuz: what vessel traffic actually looks like, what the US military is saying about possible escort operations, and what the trade consequences are if this disruption continues.

What’s happening in the Strait of Hormuz

Some ships are still moving through the strait. Transit has not gone to zero. One example highlighted is a bulk carrier identified as having Chinese ownership and crew, because that may matter. The working assumption is similar to what happened in the Red Sea: some Chinese-linked shipping may keep operating where others pull back.

At the same time, the traffic picture is not fully trustworthy. AIS and public marine tracking data are being distorted by electronic interference and spoofing, attributed here to Iran. So when people look at public vessel maps and see ships apparently stacking up, stopping, or behaving strangely, part of that picture may be false or misleading.

What to make of the US escort discussion

The next issue is General Kaine’s remarks about possible US Navy escort missions in the Persian Gulf and Strait of Hormuz. As presented here, the military is assessing options, force requirements, command structure, and ways to reduce the risks if such a mission is ordered.

The basic interpretation is that no clear, executable public plan is being communicated yet. That matters, because commercial shipping is not going to regain confidence just because officials say options are under review. Confidence returns when there is a visible, credible demonstration that the strait is open and ships can be protected while transiting it.

There are also practical constraints:

• only so many escort ships are available
• carrier strike groups have to protect themselves
• ships need refueling and rearming
• logistics can become a bottleneck very quickly

UNCTAD trade numbers highlighted in the episode

A March 10 UNCTAD report on the Strait of Hormuz disruption is cited, with the trade moving through the strait broken down roughly as follows:

• 38% crude oil
• 29% liquefied petroleum gas
• 19% liquefied natural gas and refined oil products
• 13% chemicals, including fertilizer
• 3% containers
• 2% dry bulk

The report also provides the traffic collapse numbers highlighted in the video:

• 141 ships on February 27
• 81 ships on February 28
• 4 ships on March 8

That is framed as roughly a 97% drop relative to the February average of 129 ships.

Why Asia is especially exposed

Asia is presented as the main exposure point. Using the cited figures, about 14.3 million barrels per day moved through the area in 2024, and about 84% of that oil went to Asia. Around 83% of LNG flows through this route are also described as essential to Asia.

The argument here is that LNG may be the more immediate vulnerability than oil, because replacement capacity is more limited. Oil markets are extremely important, but LNG substitution can become constrained faster.

Fertilizer is a major issue too

This is not just an oil story. Fertilizer is another major vulnerability. About one-third of global seaborne fertilizer trade is said to pass through the strait. The cited product shares are approximately:

• 67% of urea
• 20% of DAP
• 9% of MAP

Countries described as especially exposed include Sudan, Sri Lanka, Australia, Tanzania, Somalia, Pakistan, Thailand, Kenya, New Zealand, and Mozambique.

Expected knock-on effects

If this disruption continues, the expected chain of effects looks like this:

• higher oil prices
• higher gas prices
• higher fertilizer prices
• higher food prices
• higher tanker and fuel costs
• broader supply-chain stress

The pressure is expected to fall hardest on developing economies with weak fiscal capacity and heavy import dependence.

Overall takeaway

The central point is straightforward:

1. the Strait of Hormuz disruption is already materially reducing vessel movement;
2. public ship-tracking data is only partially reliable because of spoofing and interference;
3. the biggest near-term risks are energy, LNG, fertilizer, and freight costs;
4. trade normalization likely requires a credible, operationally ready naval protection plan.

Final point

This is not a localized shipping inconvenience. It is a chokepoint crisis with global implications. If secure passage through the strait is not restored, the result is likely to be deeper shocks in energy, transport, fertilizer, and food markets, with developing countries taking the hardest hit.

Plaques and paradigm

• Alzheimer’s entered the field as plaques and tangles, but plaque burden never aligned cleanly with who did and did not become demented.
• The amyloid cascade model became the field’s organizing idea, drove funding and drug development, and turned plaque removal into the main therapeutic goal.
• A landmark 2006 Aβ*56 paper became a central support for this view, and its later retraction exposed how much confidence had rested on fragile data.
• The drug record followed the same pattern: anti-amyloid programs removed plaques more readily than they restored cognition or halted decline.

Brain insulin resistance

• A stronger fit is that Alzheimer’s is a brain insulin-resistance disorder in which neurons lose efficient access to glucose even when glucose is abundant.
• In this model, impaired insulin and IGF signaling drives energy shortage, tau dysregulation, weaker amyloid clearance, synaptic failure, and cognitive loss.
• de la Monte’s work anchors the “type 3 diabetes” term by tying worsening Alzheimer pathology to worsening defects in brain insulin signaling.
• Population data move in the same direction: diabetes tracks with higher dementia risk, and worse glycaemic history tracks with worse risk.

APOE4 and mechanism

• APOE4 fits this metabolic model because it can trap the insulin receptor inside neurons, weakening insulin signaling before late-stage pathology arrives.
• That gives APOE4 a direct route to brain fuel failure, tau disruption, and weaker amyloid clearance.

Ketones and practice

• The crucial asymmetry is that glucose handling falls early, while ketone uptake remains intact in mild cognitive impairment and early Alzheimer’s disease.
• PET work and post-mortem gene-expression work move in the same direction: glycolytic machinery falls broadly, while much of the ketolytic machinery stays usable outside oligodendrocytes.
• That makes ketones a rescue fuel, which is why ketogenic diets, MCT-based interventions, and exogenous ketones sit at the center of this account.
• The practical conclusion is to protect metabolic health early, lower chronic hyperinsulinaemia, and give special attention to carbohydrate restriction or ketone-raising strategies when brain glucose use is failing.

References

• [00:46] Alzheimer's Disease Is Type 3 Diabetes—Evidence Reviewed — https://doi.org/10.1177/193229680800200619
• [03:02] Alzheimer's Disease: The Amyloid Cascade Hypothesis — https://doi.org/10.1126/science.1566067
• [04:00] Frequent Amyloid Deposition Without Significant Cognitive Impairment Among the Elderly — https://doi.org/10.1001/archneur.65.11.1509
• [05:15] A specific amyloid-β protein assembly in the brain impairs memory — https://doi.org/10.1038/nature04533
• [06:30] Retraction Note: A specific amyloid-β protein assembly in the brain impairs memory — https://doi.org/10.1038/s41586-024-07691-8
• [10:41] Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease—is this type 3 diabetes? — https://doi.org/10.3233/JAD-2005-7107
• [11:23] Insulin and insulin-like growth factor expression and function deteriorate with progression of Alzheimer's disease: link to brain reductions in acetylcholine — https://doi.org/10.3233/JAD-2005-8304
• [14:04] Diabetes mellitus and risk of dementia: A meta-analysis of prospective observational studies — https://doi.org/10.1111/jdi.12087
• [14:17] The relationship between diabetes and the dementia risk: a meta-analysis — https://doi.org/10.1186/s13098-024-01346-4
• [14:33] Diabetes mellitus and the risk of dementia — https://doi.org/10.1212/WNL.53.9.1937
• [14:46] Associations of glycaemia-related risk factors with dementia and cognitive decline in individuals with type 2 diabetes: A systematic review and meta-analysis — https://doi.org/10.1111/dme.70123
• [15:09] Association between Age at Diagnosis of Type 2 Diabetes and Subsequent Risk of Dementia and Its Major Subtypes — https://doi.org/10.3390/jcm13154386
• [17:07] Apolipoprotein E4 Impairs Neuronal Insulin Signaling by Trapping Insulin Receptor in the Endosomes — https://doi.org/10.1016/j.neuron.2017.09.003
• [23:36] Can Ketones Help Rescue Brain Fuel Supply in Later Life? Implications for Cognitive Health during Aging and the Treatment of Alzheimer's Disease — https://doi.org/10.3389/fnmol.2016.00053
• [24:09] A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer's disease — https://doi.org/10.1016/j.exger.2017.07.004
• [25:04] Alzheimer's disease alters oligodendrocytic glycolytic and ketolytic gene expression — https://doi.org/10.1002/alz.12310
• [27:38] Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial — https://doi.org/10.1186/1743-7075-6-31
• [28:34] Regional Brain Glucose Hypometabolism in Young Women with Polycystic Ovary Syndrome: Possible Link to Mild Insulin Resistance — https://doi.org/10.1371/journal.pone.0144116

• Median survival is near 8–14 months since 1926; John McCain died about 13 months after diagnosis.
• GBM spreads distally through the brain via Scherer infiltration patterns; complete surgical removal is unlikely.
• Death commonly follows rising intracranial pressure; debulking surgery rarely cures because cells already migrated.
• Standard of care uses surgery plus radiotherapy plus temozolomide; survival curves remain poor across institutions and countries.
• Radiotherapy, temozolomide, and steroids can increase glucose/glutamine availability and inflammation in the tumor microenvironment.
• Temozolomide gives modest progression-free benefit while adding toxicity; side effects reduce appetite and calories.

Mitochondrial dysfunction as a root defect

• Electron microscopy shows damaged cristae and abnormal mitochondrial structure in GBM compared with nearby tissue.
• Enzyme and electron-transport abnormalities accompany the structural defects; respiration via oxidative phosphorylation is impaired.
• Genetic heterogeneity is extensive, but aerobic fermentation is shared across tumor cells when respiration is insufficient.

Two fermentable fuels: glucose and glutamine

• Otto Warburg linked cancer growth to aerobic fermentation of glucose to lactate despite oxygen availability.
• Tumor cells also ferment glutamine via glutaminolysis and mitochondrial substrate-level phosphorylation (the Q-effect).
• Glucose feeds glycolysis and the pentose phosphate pathway; glutamine supplies carbon/nitrogen for biosynthesis and energy.
• Tumor cells cannot rely on fatty acids or ketone bodies when respiration is defective; normal brain tissue can.

Therapeutic goal: lower glucose, raise ketones, reduce inflammation

• Lowering blood glucose slows tumor growth; high glucose accelerates growth, yet clinic diets often include sugar.
• Calorie restriction and restricted ketogenic diets lower glucose and elevate ketones, placing metabolic stress on tumor cells.
• These diets also reduce inflammatory signaling and edema, limiting invasion-supporting microglia/macrophage activity.

Monitoring metabolic targeting with the Glucose Ketone Index

• GKI is the molar ratio of blood glucose to ketones; values near 1.0 or below indicate therapeutic ketosis.
• A Glucose Ketone Index Calculator supports daily tracking; many patients struggle to reach and sustain low GKI values.

Evidence and models

• Two pediatric brain tumor cases on ketogenic diets showed improved quality of life and longer-than-expected survival.
• Mouse models show diet restriction reduces tumor burden and invasion compared with standard high-carbohydrate feeding.
• Combining a restricted ketogenic diet with the glutamine antagonist DON further reduces tumor signal and improves survival in mice.

Press–pulse strategy for metabolic management

• Press therapy keeps glucose low and ketones high over time to stabilize the microenvironment before adding other hits.
• Pulse therapy adds intermittent glutamine targeting and other stressors while the tumor is metabolically constrained.

Human management example and implications

• A 24-month GBM follow-up combined ketogenic metabolic therapy with modified standard care and hyperbaric oxygen; later decline aligned with radiation necrosis.
• The strategy prioritizes ketogenic metabolic therapy as the core platform, using surgery for debulking but avoiding radiotherapy and temozolomide when possible.
• A global society for metabolic therapy is proposed to break stagnation and shift focus toward disease resolution.

References

• [00:00] Cancer as a Metabolic Disease: On the Origin, Management and Prevention of Cancer — https://doi.org/10.1002/9781118310311
• [00:02] A classification of the tumors of the glioma group on a histogenetic basis with a correlated study of prognosis — https://catalog.hathitrust.org/Record/012447742
• [00:03] THE FORMS OF GROWTH IN GLIOMAS AND THEIR PRACTICAL SIGNIFICANCE — https://doi.org/10.1093/brain/63.1.1
• [00:08] On the Origin of Cancer Cells — https://doi.org/10.1126/science.123.3191.309
• [00:09] On the Origin of ATP Synthesis in Cancer — https://doi.org/10.1016/j.isci.2020.101761
• [00:11] Mitochondrial Substrate-Level Phosphorylation as Energy Source for Glioblastoma: Review and Hypothesis — https://doi.org/10.1177/1759091418818261
• [00:17] The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer — https://doi.org/10.1186/s12986-015-0009-2
• [00:18] Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports — https://doi.org/10.1080/07315724.1995.10718495
• [00:21] Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma — https://doi.org/10.1056/NEJMoa043330
• [00:23] Does the existing standard of care increase glioblastoma energy metabolism? — https://doi.org/10.1016/S1470-2045(10)70166-2
• [00:29] Therapeutic benefit of combining calorie-restricted ketogenic diet and glutamine targeting in late-stage experimental glioblastoma — https://doi.org/10.1038/s42003-019-0455-x
• [00:38] Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic Metabolic Therapy and Modified Standard of Care: A 24-Month Follow-Up — https://doi.org/10.3389/fnut.2018.00020
• [00:39] Provocative Question: Should Ketogenic Metabolic Therapy Become the Standard of Care for Glioblastoma? — https://doi.org/10.1007/s11064-019-02795-4

• Over ~12 months, a few intervention thoughts; focus on evidence and questions at the end.
• Relative had a minor heart attack; cath/angiogram team attempted a stent without prior consent; another patient learned a stent was placed without warning.
• Informed consent is an ethical and professional obligation.
• Consent is not only risks; it also includes realistic benefits and when benefits may be absent.
• Transparent benefit discussion would lead some people to decline some interventions.

Aspirin example: primary prevention drifted ahead of evidence

• Aspirin was recommended for decades for primary prevention until a large "Aspirri" trial found no longer life and substantial harms; routine primary-prevention advice shifted.
• Proving "better than nothing" requires placebo-controlled trials, not comparisons against another active agent.
• A secondary-prevention meta-analysis reviewed >250 papers and recommended lifelong aspirin after heart attack.
• Only a small subset of those trials compared aspirin to placebo.
• Surrogate outcomes are not enough; all-cause mortality is the cleanest outcome when available.
• In the placebo-controlled all-cause-mortality trials, most showed no benefit; the one with benefit used aspirin for about 4 weeks.
• Short-term post-MI clotting risk makes a short-course antiplatelet effect plausible, but that does not justify automatic lifelong use.

Surrogates vs outcomes that matter

• Blood pressure and cholesterol changes are surrogate markers; lower numbers are not automatically safer in every context.
• Evaluate interventions by outcomes that cannot be massaged: all-cause mortality.

Stents and PCSK9 inhibitors under the same standard

• Two large randomized trials with thousands comparing stenting vs no stenting show no mortality benefit and more early adverse events with stenting.
• PCSK9 inhibitors reliably lower cholesterol, but cholesterol is a surrogate; no demonstrated all-cause-mortality benefit on average.

Doctor as teacher; patient as decision-maker

• "Doctor" means teacher; the job is education plus support for the patient's choice.
• Communicate benefits and harms using absolute risk, not relative-risk spin.
• Example: 1% to 2% can be sold as "100% higher", but the absolute change is 1 percentage point.
• Focus on outcomes that matter to patients, especially mortality when data exist.

Uncertainty and population gaps

• Some clinicians reject "difficult" patients; time limits are real, but informed consent still includes evidence on risks and benefits.
• Patient-provided papers can change clinical practice.
• Many drug trials have few or no South Asians, especially women; risk calculators like "MISA" omit South Asians.
• When evidence is missing or unclear, be direct about uncertainty and let the patient decide with the best available data.

References

• [00:03] Effect of Aspirin on Cardiovascular Events and Bleeding in the Healthy Elderly — https://doi.org/10.1056/NEJMoa1805819

• Simon Thornley is an epidemiologist who uses numbers to decide what works and what does not in medicine.
• The talk collects nutrition topics from recent months: diet evidence, fasting, and major new weight-loss drugs.

Network meta-analysis for diet evidence

• Pair-wise meta-analysis compares one option against another; network meta-analysis links many options through shared comparators.
• Direct and indirect comparisons combine into a single network that ranks many diets at once.
• P-score ranks the chance that one diet beats the rest; a diet network meta-analysis puts low carbohydrate at about 0.9.
• Meta-analyses depend on inputs, yet many syntheses place keto/low carbohydrate ahead of low fat and Mediterranean patterns. Fasting and time-restricted eating
• Fasting is used as a way to rest the pancreas; solid academic evidence is scarce.
• A time-restricted eating trial with an 8-hour window (12 to 8) beats calorie restriction by about two-fold.

Carnivore diet survey paper

• Evidence in journals is sparse; a recent US paper by David S Ludwig and colleagues surveys adults on a carnivore diet.
• Recruitment runs through social media; eligibility is age ≥18 and carnivore diet duration ≥6 months.
• Mean BMI drops about 2.9 units, about 9.2 kg for a 1.78 m person.
• The survey answers include LDL rising, which supports honesty on other outcomes such as weight loss.

LDL thresholds and cardiovascular risk

• LDL cut-points sit far left on the distribution, so many people fall into the "abnormal" zone.
• Low LDL cut-points support a large market for lipid-lowering drugs.
• LDL links weakly with cardiovascular events in risk prediction; triglycerides track cardiovascular risk more strongly and move in the right direction on carnivore.

Drug effect size metrics and survival time

• Wegovy and similar drugs are promoted heavily at conferences; benefit numbers often use relative effects like 19% for all-cause mortality.
• Absolute effects matter: 0.44% absolute risk reduction maps to NNT ≈225 over 4 years to avert one death.
• Restricted mean survival time uses the area between Kaplan–Meier curves to express average survival gain as time.
• For one GLP-1 drug, 4 years of use yields about one week of average survival gain.
• For statins, 6 months to 6 years of use yields about one to three weeks of average survival gain in industry-funded trials.
• For dulaglutide, 6 years of use yields about 17 days of average survival gain; cost is about $500/month for one GLP-1 example.

Wrap-up

• Network meta-analysis helps sort nutrition evidence across many diet options.
• Early data on carnivore looks strong; LDL alarm is amplified by low thresholds.
• Restricted mean survival time makes drug benefits easier to understand as days or weeks of survival.

References

• [00:07] Behavioral Characteristics and Self-Reported Health Status among 2029 Adults Consuming a "Carnivore Diet" — https://doi.org/10.1093/cdn/nzab133

At our grocery stores and dinner tables, even the most thoughtful consumers are overwhelmed
 by the number of considerations to weigh when choosing what to eat—especially when it comes to meat. Guided by the noble principle of least harm, many responsible citizens resolve the ethical, environmental and nutritional conundrum by quitting meat entirely. But can a healthy, resilient and conscientious food system exist without animals?

Sacred Cow probes the fundamental moral, environmental and nutritional quandaries we face in raising and eating animals. In this project, we focus our lens on the largest and perhaps most maligned of farmed animals, the cow.

COMMON ASSUMPTIONS ABOUT MEAT...

• Red meat causes cancer, obesity and heart disease. 

• We’re eating too much meat.
• Humans don’t need to consume animal products to be healthy. 

• Raising livestock is bad for the environment.

• It’s unethical to eat animals. 

• If we can produce meat in labs, then why should we eat animals? 


The connection between nutrition and ecosystem health is starting to make some headway into mainstream media. Everyone is trying to figure out how to feed the world in the most sustainable and healthy way. However, we've allowed corporate interest, big food, flawed science, click-bait media and naïve celebrities to steer us away from what a truly nutrient-dense, ethical and sustainable, and regenerative food system really is. The mantra that “all meat is bad” influences how we're training dietitians, shaping our dietary guidelines, designing school lunch policies, and funding for nutrition-related research.

As we’ve become more globalized, the entire world is now pushing towards the "heart healthy" (and highly processed) Western diet. In the process, we're destroying entire ecosystems and human health through industrial, ultra-processed food.

Sacred Cow comes at a critical point in the nutrition and sustainability story. A meat tax is a very real possibility. Well intended yet highly misguided, The EAT Lancet Global Dietary Guidelines are calling for less than 1/2 an ounce of red meat per day, for human and planetary health.

Meat is being vilified as causing cancer, heart disease and diabetes, yet there are no solid studies to back this up. Meanwhile, Silicon Valley has invested millions in highly processed meat alternatives, with the assumption that engineering our proteins in factories will be a better alternative to something nature has already figured out: grazing animals, restoring land while converting cellulose into protein.

The solution is regenerative agriculture.

The truth is, well-managed cattle are the unlikely heroes of this story. We can increase biodiversity, improve soil health, increase the water holding capacity of the land and raise high quality, nutrient-dense protein, while preserving family farming communities. Removing these animals from our food system could cause more harm than good. It’s not the cow, it’s the how.

• Meat should be traceable: farm, breed, and slaughter conditions should be known.
• Butchery should use the whole animal (nose-to-tail) so nothing is wasted.
• Local processing quality matters; farmers can control the animal’s life but often not its final day.

How industrial food became dominant

• Post–World War II agriculture scaled up through chemicals, monocultures, and efficiency goals.
• Processed food engineering amplified sugar/salt/flavor to drive repeat consumption.
• Public messaging shifted toward low-fat eating while ultra-processed foods expanded.

Health narratives around fat, meat, and processing

• Low-fat guidance did not prevent rising obesity, diabetes, and metabolic disease.
• Processed meats were framed as cancer-causing; red meat was framed as risky too.
• Nutrition guidance strongly shapes institutions (schools, healthcare) and food programs.

Plant Based identity, nutrient gaps, and personal health fallout

• Plant Based can become identity, making counter evidence hard to absorb.
• Some people do well for a time; many later develop health problems and leave the diet.
• Animal foods provide or simplify access to B12, bioavailable iron/zinc, EPA/DHA, and other nutrients.
• Supplements are a weak substitute in settings without clinicians, pharmacies, or supply chains.

Limits of observational nutrition claims

• Correlations between red meat and disease can reflect confounding behaviors (smoking, inactivity, low produce intake).
• Meat eaten within a whole-food, plant-rich pattern is not inherently harmful.
• Processed food is treated as the main driver behind modern chronic disease patterns.

Ethics conflict and activism pressure

• Activists targeted a butcher shop with protests and demanded public messaging concessions.
• The clash is shared opposition to factory farming but divergent solutions.

Alternatives to livestock: lab meat and plant-based substitutes

• Lab-grown and highly processed substitutes still depend on industrial crop inputs and fossil-fuel supply chains.
• Marketing is disguising the material inputs, processing, and ecological costs.

Regenerative grazing, soil, water, and biodiversity

• Managed grazing is rebuilding soil structure, water infiltration, and ecological function.
• Ruminants are co-creators of grassland soils via trampling, manure, and plant regrowth cycles.
• Portable infrastructure and multi-species rotations are stacking functions per acre.

Methane framing: biogenic vs fossil carbon

• Enteric methane is part of a short carbon cycle with ~10-year atmospheric lifetime.
• Fossil methane is adding ancient carbon and driving net atmospheric imbalance.

Land-use constraints and “marginal land” framing

• A large share of agricultural land is unsuitable for cropping but usable for grazing.
• Removing ruminants is creating a nutrient-dense food gap and degrading ecosystem function.

Desertification and restoration

• Poor management is accelerating erosion and water damage over decades.
• Rancher collectives are restoring grasslands and springs at very large scale.

Nutrition equity and child outcomes

• Adding small amounts of meat to children’s diets is improving school performance (45% figure).
• A proposed global dietary pattern restricting animal foods is unfair to regions needing more animal-source nutrients.

• Cancer growth follows chronic mitochondrial injury and disordered energy metabolism, not an initiating nuclear gene mutation.
• Tumor cells shift ATP production away from oxidative phosphorylation and toward substrate-level phosphorylation and fermentation.
• The somatic mutation theory dominates cancer care, and that focus blocks metabolic targeting.

Evidence base

• Nuclear–mitochondrial transfer experiments: normal nucleus placed into tumor cytoplasm yields tumor; tumor nucleus placed into normal cytoplasm yields normal growth control.
• Driver mutations can exist without forming cancer, so mutations do not explain initiation by themselves.
• Environmental exposures and inherited risk interact, so separating “genes” from environment in real people is difficult.
• Hereditary cancer syndromes align with impaired oxidative phosphorylation in a recent Oncology paper with Bob Kaplan.
• Keeping cancer as a gene-only problem leaves about 1,700 people per day dying from cancer in the US.

Fuel logic and therapeutic targets

• The two fuels driving dysregulated tumor growth are glucose and the amino acid glutamine.
• Tumor cells cannot shift to ketone bodies or fatty acids the way healthy cells can.
• Cutting fermentable fuel availability and blocking glutamine use is the direct way to stress tumor metabolism.

Metabolic therapy: baseline approach

• Nutritional ketosis and water-only fasting lower glucose, raise ketones, and reduce inflammatory drive in tumors.
• The glucose–ketone index (GKI) tracks the glucose-to-ketone ratio as a single number to monitor metabolic pressure.
• Achieving ketosis is harder in modern food environments because sugar and ultra-processed foods are engineered for craving and convenience.

Combining metabolic therapy with standard care

• Metabolic therapy is non-toxic in practice; people generally get healthier during it.
• Chemo, radiation, and immunotherapy remain options, but metabolic control first aims to shrink and de-inflame the tumor.
• After the tumor burden and inflammation drop, smaller doses of standard agents can be used with less collateral damage.
• Some immunotherapies help some people, and they also can cause hyperprogressive disease and death; metabolic therapy avoids that risk profile.

Antiparasitic drugs and cancer

• Mebendazole and fenbendazole can hit cancer metabolism because parasites and tumor cells share a survival pathway.
• The shared pathway is mitochondrial substrate-level phosphorylation, fermentation inside mitochondria.
• In pediatric high-grade glioma work, antiparasitic drugs paired with nutritional ketosis are a practical, low-cost direction.
• “Cancer is a parasite” is rejected; parasites are different organisms, even when drug targets overlap.

Obesity, inflammation, and GLP-1 drugs

• Weight alone is less informative than inflammation; some people carry weight without chronic inflammatory drive.
• Ultra-processed carbs and sugar push inflammation; removing them and using fasting or ketosis pulls it down.
• GLP-1 drugs can reduce appetite and body weight, and they do not fix the food environment that drove the problem.
• When lifestyle change fails for years, GLP-1 drugs can be a last-resort tool to break the cycle.

Industry and incentives

• Cancer care is a revenue generator, with multi-billion-dollar drug markets anchored to the genetic model.
• Drug advertising spends heavy time on fatal risks, and metabolic therapy remains underused despite low toxicity.
• A “firewall of ignorance” exists across patients and caregivers who do not read or understand the scientific literature.

Virus, vaccines, and “turbo cancer” talk

• SARS-CoV-2 infection damages mitochondria and can contribute to downstream chronic disease.
• Sorting vaccine damage from virus damage is hard when many people experienced both.
• Regardless of trigger, metabolic behavior is the same: fermentation of glucose and glutamine.
• No clinical trial targets glucose and glutamine together while maintaining nutritional ketosis.

Risk reduction starting now

• Exercise is the top lever for mitochondrial health.
• Reduce ultra-processed foods, especially addictive sugar, and favor more natural foods even when cost is higher.
• Sleep, social connection, and reducing sedentary “doom scrolling” support healthier mitochondria.
• Chronic disease occurs at younger ages, with type 2 diabetes and obesity in children as warning signals.

References

• [00:01] Cancer as a Metabolic Disease: On the Origin, Management and Prevention of Cancer — https://doi.org/10.1002/9781118310311
• [00:03] Hereditary cancer syndromes linked to oxidative phosphorylation insufficiency — https://doi.org/10.1515/oncologie-2025-0301
• [00:12] The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer — https://doi.org/10.1186/s12986-015-0009-2
• [00:19] Ketogenic diet as a metabolic vehicle for enhancing the therapeutic efficacy of mebendazole and devimistat in preclinical pediatric glioma — https://doi.org/10.1101/2023.06.09.544252