Last month's blog discussed the disturbing rise in colorectal cancer in young adults and some steps that may reduce risk and improve treatment outcomes. This week we will take a deep dive into brain cancer – specifically Glioblastoma multiforme – the most aggressive type of brain cancer. Glioblastoma (GBM) accounts for over 60% of all brain cancer diagnoses in adults, and it has the worst prognosis, with an overall median survival of approximately 14 months.
GBM is one of the most clinically challenging types of cancer to treat, with few historical improvements to point to. Surgery and radiation – both of which have been around for hundreds of years – comprise the frontline, standard-of-care treatment. The only approved adjunctive treatment for GBM is Temozolomide, a chemotherapy approved almost 20 years ago. Temozolomide increases overall median survival from 12 to 14 months.
Although most studies report that total brain cancers diagnoses have remained stable over the past few decades, the incidence of GBM is on the rise. A U.K. study published in 2018 looked at 81,135 people diagnosed with brain tumors in England between 1995–2015. Within this group, the number of GBMs diagnosed doubled over the 20 years while the number of lower-grade brain cancers decreased. So, while the total incidence of brain cancer remained stable, there was a pronounced shift toward the more aggressive GBM.(1) A 2020 study on GBM in Malta reported similar results. The study looked at the total incidence of GBM in Malta over the ten years between 2008 and 2018. During this period, GBM diagnoses went from 3 patients diagnosed in 2008 to 21 in 2017 – a shocking increase.(2) The U.K. and Malta studies reflect other studies spanning the globe. SEER data in the U.S. for the 14 years between 1992–2006 reported a rising trend in frontal and temporal lobe tumors – the majority of which were GBM – with a decreased incidence of tumors across all other anatomical subsites.(3)
The increase in GBM incidence worldwide raises the question: What is causing this increase? The authors of these studies mostly point to 3 possible causes:
Radiation (primarily from an increase in CT scans)
Increased air pollution
Increased cell phone usage
While the first two, radiation and air pollution, demonstrate strong correlations, the effect of cell phone usage on brain cancer rates remains inconclusive; some studies report an association, whereas others do not. If history is a guide, the science on the health impact of new chemicals and technologies is rarely definitive from the start. Take aspartame; in 1983, the year the FDA approved it for use in soft drinks, a New York Times article reported on the scientific consensus regarding its safety: “As for the most frightening prospect - cancer - there is as yet no evidence in animals of any possible harm.” (4)
Yet, recently (40 years later), the WHO declared aspartame a possible cancer-causing agent.
Waffling like this hardly inspires confidence in our public health agencies and should make people generally question any definitive declaration of a new chemical or technology as “safe.”
A 2011 study raised concerns about cell phones held directly to the ear. The study administered PET scans to 47 subjects while they had "on" cell phones held up to their ear for 50 minutes and then repeated the procedure while the subjects held an “off” cell phone up to their ear for the same time. The results were surprising: “Whole-brain metabolism did not differ between on and off conditions. In contrast, metabolism in the region closest to the antenna (orbitofrontal cortex and temporal pole) was significantly higher for on than off conditions.”(5)
The significant metabolism increase in the brain region closest to the antenna was specifically glucose metabolism. Researchers have proposed ideas on why this shift in metabolism occurs. Based on findings from in vivo animal and in vitro experiments, the metabolic change could reflect the effects of RF-EMF exposure on neuronal activity mediated by changes in cell membrane permeability, calcium efflux, cell excitability, and neurotransmitter release. Of course, this study should raise some red flags – any forced alteration in metabolism is concerning.
Considerations for the prevention and treatment of GBM
Radiation exposure is a well-established risk factor for brain cancer. Acute doses of radiation lead to a sharp increase in free radicals that damaged DNA. The most common exposure to acute radiation comes from CT scans. One possible way to mitigate the damage from CT scans is an over-the-counter product called a ketone ester sold by KetoneAid and some other companies. Ketone esters get converted into a molecule called beta-hydroxybutyrate in the liver. Multiple studies have shown that beta-hydroxybutyrate can dramatically increase the cell's antioxidant capacity. A 2016 study demonstrated the potent ability of ketone ester to mitigate the DNA damage caused by radiation. The study exposed two groups of mice to γ-radiation. One group was administered ketone ester 24 hours after exposure, and the other was not. In the ketone ester group, the bone marrow chromosomal damage markers were attenuated by 50%.(6)
At Meakin Metabolic Care, we also developed a product to mitigate the risk of radiation exposure from scans called Scan Shield. The product contains an amalgam of antioxidants that were reported to have reduced cancer risk in the years following Nagasaki and Hiroshima.
As for cell phones, the simple solution is don't hold your phone to your ear. When placing or taking a call, press the “speaker” button.
The same lifestyle variables that hold true for the prevention and treatment of most cancers apply to GBM. A 2011 study reported that exercise can significantly improve outcomes. The study followed 243 patients aged 20 to 77 who had advanced recurrent malignant gliomas. Those who exercised briskly and regularly (the equivalent of a brisk 30-minute walk five days a week) lived nearly 22 months compared to 13 months for those who were less active.(7)
The ketogenic diet has sparked researchers’ interest as an adjunctive therapy for cancer, particularly for GBM, where the evidence is the strongest. Dr. Jethro Hu conducted a phase 1 trial at Cedars Sinai on the effect of the ketogenic diet concurrent to standard of care on 17 GBM patients. The overall survival of the cohort was 28.6 months – over double the historical average of 14 months.(8) Even though the trial was small, the dramatic increase in overall survival inspired Dr. Hu to organize a more extensive phase 2 trial. If the results of the phase 2 trial even approach the phase 1 trial, it would be the most significant step-change in GBM treatment since temozolomide was approved over 20 years ago. Below is a short clip of Dr. Hu presenting data from the phase one trial at the 2021 Metabolic Heath Summit in Santa Barbara, CA. Next week we will look at an exciting new study on the role of repurposed drugs in GBM.
KEY POINTS
The incidence of GBM is rising globally
Most experts agree that air pollution, radiation, and possibly cell phone usage may be responsible for this rise.
Ingesting a ketone ester and Scan Shield may help mitigate the risk of CT scan radiation exposure.
When placing or taking a call on your cell phone, press "speaker" rather than holding the phone up to your ear
Exercise may help improve GBM outcomes
The ketogenic diet shows promise as an adjunctive treatment for GBM
Stay Strong and Curious,
Charles Meakin MD, MS, MHA
Travis Christofferson MS
Meakin Metabolic Care Website
Meakin Metabolic Care Service Plans
CoachItForwardChuck.com - Questions from the Clinic (rationally researched for you)
Chronic Disease Prevention Program- Metabolic Optimization Protocol (MOP)
Heal Navigator (care partner) - Oncology Nurse Navigators
Disclaimer: This information is not meant as direct medical advice. Readers should always review options with their local medical team. This is the sole opinion of Dr. Meakin based on a literature review at the time of the blog and may change as new evidence evolves.
Alasdair Philips, Denis L. Henshaw, Graham Lamburn, Michael J. O’Carroll, "Brain Tumours: Rise in Glioblastoma Multiforme Incidence in England 1995–2015 Suggests an Adverse Environmental or Lifestyle Factor", Journal of Environmental and Public Health, vol. 2018, Article ID 7910754, 10 pages, 2018.
Grech N, Dalli T, Mizzi S, et al. (May 19, 2020) Rising Incidence of Glioblastoma Multiforme in a Well-Defined Population. Cureus 12(5): e8195. doi:10.7759/cureus.8195
G. Zada, A. E. Bond, Y.-P. Wang, S. L. Giannotta, and D. Deapen, “Incidence trends in the anatomic location of primary malignant brain tumors in the United States: 1992–2006,” World Neurosurgery, vol. 77, no. 3-4, pp. 518–524, 2012.
Volkow ND, Tomasi D, Wang G, et al. Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. JAMA. 2011;305(8):808–813. doi:10.1001/jama.2011.186
Martin F Kemper, Alexandra Miller, Robert J Pawlosky, Richard Veech, Administration of a novel β-hydroxybutyrate ester after radiation exposure suppresses in vitro lethality and chromosome damage, attenuates bone marrow suppression in vivo, FASEB journal, 01 April 2016
Ruden E, Reardon DA, Coan AD, Herndon JE 2nd, Hornsby WE, West M, Fels DR, Desjardins A, Vredenburgh JJ, Waner E, Friedman AH, Friedman HS, Peters KB, Jones LW. Exercise behavior, functional capacity, and survival in adults with malignant recurrent glioma. J Clin Oncol. 2011 Jul 20;29(21):2918-23. doi: 10.1200/JCO.2011.34.9852. Epub 2011 Jun 20. PMID: 21690470; PMCID: PMC3138718.
DOI: 10.1200/JCO.2023.41.16_suppl.2076 Journal of Clinical Oncology 41, no. 16_suppl (June 01, 2023) 2076-2076.