thiamine and cancer

Thiamine and Cancer: Potential Mechanisms

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Before the COVID crisis, Dr. Lonsdale and I published a paper exploring the links between thiamine and cancer. We were particularly interested in discussing the current thiamine conundrum that suggests low dose thiamine promotes tumor growth while high dose prevents it. I think you’ll find the mechanisms involved the development of cancer, explored here, useful for understanding why thiamine is such an important dietary element.

Here is the abstract.

The resurgence of interest in cancer metabolism has linked alterations in the regulation and exploitation of metabolic pathways with an anabolic phenotype that increases biomass production for the replication of new daughter cells. To support the increase in the metabolic rate of cancer cells, a coordinated increase in the supply of nutrients, such as glucose, as well as micronutrients functioning as enzyme cofactors is required. The majority of co-enzymes are derivatives of water-soluble vitamins such as niacin, folate, pantothenic acid, pyridoxine, biotin, riboflavin and thiamine (Vitamin B1). Continuous dietary intake of these micronutrients is essential for maintaining normal health. How cancer cells adaptively regulate cellular homeostasis of cofactors and how they can regulate expression and function of metabolic enzymes in cancer is under-appreciated. Exploitation of cofactor-dependent metabolic pathways with the advent of anti-folates highlights the potential vulnerabilities and importance of vitamins in cancer biology. Vitamin supplementation products are easily accessible and patients often perceive them as safe and beneficial without full knowledge of their effects. Thus, understanding the significance of enzyme cofactors in cancer cell metabolism will provide for important dietary strategies and new molecular targets to reduce disease progression. Recent studies have demonstrated the significance of thiamine-dependent enzymes in cancer cell metabolism. Therefore, this hypothesis discusses the current knowledge in the alterations in thiamine availability, homeostasis, and exploitation of thiamine-dependent pathways by cancer cells.

The article is open source and can be accessed here.

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Chandler Marrs, PhD

Chandler Marrs MS, MA, PhD spent the last dozen years in women’s health research with a focus on steroid neuroendocrinology and mental health. She has published and presented several articles on her findings. As a graduate student, she founded and directed the UNLV Maternal Health Lab, mentoring dozens of students while directing clinical and Internet-based research. Post graduate, she continued at UNLV as an adjunct faculty member, teaching advanced undergraduate psychopharmacology and health psychology (stress endocrinology). Dr. Marrs received her BA in philosophy from the University of Redlands; MS in Clinical Psychology from California Lutheran University; and, MA and PhD in Experimental Psychology/ Neuroendocrinology from the University of Nevada, Las Vegas.

4 Comments

    • “That is, moderately high doses of thiamine (up to ∼ 75 times the RDI) seem to stimulate cell proliferation while supra-physiological doses (from ∼ 250-2500 times RDI) stifle it.” — from our article.
      Which was taken from this: Moderate doses of 12.5 to 37.5 times the RDI had the greatest stimulatory effect, peaking at approximately 250% greater tumor cell proliferation with 25 times the RDI. Interestingly, at values above 75 times the RDI, no change was found in tumor cell proliferation, and a slight decrease was found at 2,500 times the RDI. — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178204/
      Look at table 1 for values.
      The point we made that simply looking at these values was not enough; one had to look at the totality of the diet and where/why one had these values. Also, one should be looking at the totality of the environment. To that end, there was one more study addressed by Zastre et al. “In this study a normal-fat (NF) diet contained 10% of the calories from fat while the high-fat diet contained 60%. Low thiamine (LT) levels were defined as 2 mg of thiamine per 4,057 kcal and normal thiamine (NT) levels as 6 mg per 4,057 kcal. Tumor latency was significantly longer (295 days) in animals given a NF/LT diet compared with animals on NF/NT (225 days). Interestingly,the delay in tumor latency from LT was abolished when given a high-fat diet. This demonstrates an important interplay of dietary constituents on tumor progression that needs further characterization.” So it’s not a simply low/high question. It’s a question of the totality of diet and exposures, genetics, epigenetics relative to one’s need for thiamine. There would be no need for additional or higher dose thiamine absent those other factors. Those factors are the drivers of cancer. The exposure initiates it and the poor metabolic health supports it. Correct the metabolic health, e.g. heal the mitochondria, and as Seyfried’s research showed, cancer will not proliferate.

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