Do Energy Drinks Cause Cancer? Exploring the Latest Research

Reading time: 7 minutes

Preeti Prangya Panda

Energy drinks are treated like a fast, accessible, and powerful tool to regain energy. Their popularity is undeniable. More than 38% of young adults use energy drinks, and the use is generally high among athletes, shift workers, motivated workers, and students. 

Taurine is one of the most important ingredients in these drinks, which are normally present in a concentration between 750 and 1,000 mg per serving.

Since these beverages are flooding the international market, an important question continues to emerge: Can energy drinks cause cancer?

Although the cardiovascular or metabolic dangers of these drinks have been widely investigated, a novel study, “Taurine from tumour niche drives glycolysis to promote leukaemogenesis”, published in Nature, has opened the scientific community to the unknown role of taurine in cancer. Taurine is not just an additive but rather a key player in the metabolic potential of cancer stem cells¹.

The study suggests a strong link between endogenous taurine and cancer, but doesn’t seem to directly interrogate the contribution of taurine from energy drinks.

What Is Taurine—and Why It’s in Energy Drinks

Taurine is a non-essential amino acid typically consumed at 40–400 mg per day, with a recommended upper limit of 3,000 mg². It plays a role in calcium signaling, potentially affecting the brain, heart, and muscles. 

It plays a key role in maintaining homeostasis and protecting the body against oxidative stress. It is involved in preventing or mitigating conditions such as hypertension, neurological disorders, liver cirrhosis, and heart dysfunction, all of which are linked to oxidative damage³. 

However, when combined with caffeine—common in energy drinks—it may amplify cardiac effects like increased blood pressure and heart rate. 

Deep Dive: The Nature Study (Taurine–TAUT Axis in Leukemia)

Study Design

Researchers utilized temporal single-cell RNA sequencing (scRNA-seq) to compare populations of bone marrow stromal cells in mouse models of aggressive myeloid leukemia (blast-crisis CML and AML) at four distinct timepoints, during induction, employing established protocols.: 

• Naive: Healthy cells with no leukemia.
• Initiation: Tumor cells start growing and interacting with the tumor microenvironment.
• Expansion: Rapid proliferation of leukemic cells.
• Terminal disease: the last stage when cancer cells have increased to a great extent and the disease burden is maximum.

To investigate how non-immune bone marrow microenvironments change during myeloid leukaemia progression, researchers used blast-crisis chronic myeloid leukemia (bcCML)- leukemia stem cells (LSCs) in unirradiated mice and performed scRNA-seq on stromal populations at various disease stages. 

They identified 21 distinct cell clusters. After validating through flow cytometry, researchers found significant microenvironmental remodeling, including: 

• Increased MSCs: Leukemia cells form a supportive microenvironment for tumor growth, which prevents them from being treated.
• Increased osteolineage: The cancer cells remodel the bone marrow to support cancer cell formation instead of normal blood cells.
• Increased arteriolar endothelial cells: Arteriolar cells are small arteries present in the bone marrow that help in carrying oxygen-rich blood. Elevated arteriolar cells help cancer cells to survive. 
• Reduced sinusoidal endothelial populations: These are small vessels that help the blood to enter and exit the bone marrow. Losing these vessels can reduce the healthy blood formation and exchange.

Key Finding 1: Expanded Stromal Osteolineage Niche with Elevated CDO1

The stromal niche showed remodelling dynamics whereby mesenchymal stromal cells (MSCs) and osteolineage cells rose remarkably over the course of the disease. In the same niche, the expression of cysteine dioxygenase 1 (CDO1), an enzyme that produces taurine, was greatly increased with the development of the disease.

Key Finding 2: TAUT Expression in Leukemia Cells

By integrating scRNA-seq, human AML RNA-seq, and CRISPR screening, researchers identified TAUT (encoded by SLC6A6), which is a critical transporter expressed in leukemia stem cells (LSCs). 

It was found to be linked to poor prognosis and emerged as a critical regulator of leukaemia growth. Blocking taurine production impaired leukaemia stem cell function, and multi-omics analyses revealed how taurine supports disease progression.

Key Finding 3: Taurine from Niche Supports LSC Growth

Co-culture assays showed that murine and human AML stromal MSCs CDO1 decreased LSC viability by a factor of ~ 2 and their colony-forming potential by ~ 3-fold. Supplementation of taurine reversed these deficiencies.

Also, the taurine in the bone marrow interstitial fluid of leukemic mice was ~1.7-fold greater than in controls. This was consistent with the finding that MSC-specific CDO1 deletion increased the average lifespan of mice by ~13.5%. 

Thus, we can interpret that Taurine protects the LSCs while CDO1(an enzyme in MSCs that converts cysteine to cysteine sulfinate in the synthesis of taurine) reduces the taurine concentration by synthesizing cysteine internally. This helps taurine not to leak out of the space, and thus LSCs do not get much taurine to survive.

Key Finding 4: Exogenous Taurine Accelerates Disease

Supplementing taurine in mice increased the colony-forming potential of LSCs and accelerated AML progression, leading to ~3-fold higher mortality relative to controls.

Key Finding 5: TAUT Deletion Impairs Leukemia Initiation & Progression

In mice, a global TAUT knock-out, meaning that the mice lack the TAUT protein entirely, showed:

• Decreased leukemia stem cell growth and colony generation.
• Late onset of disease; 3.8-fold and 6.1-fold increased survival in CML and MLL-driven AML, respectively.
• In the absence of TAUT, the percentage of LSCs was almost completely depleted in secondary transplantation (extracting leukemic cells from the first mouse and transplanting to another mouse).

Key Finding 6: TAUT Dependency in Human AML

• SLC6A6 expression was enriched in LSCs across AML subtypes, especially venetoclax-resistant and RAS-mutated cases.
• TAUT knockdown via shRNA decreased taurine uptake 2–3.4-fold and reduced colony formation in AML cell lines (2–12× reduction) and patient-derived AML cells (2.3–9.1× reduction), without impacting normal CD34+ hematopoietic stem/progenitor cells.
• In xenograft models, where human cancer lines are used in murine models, TAUT knockdown greatly reduced AML engraftment but had minimal effect on healthy HSPC engraftment.
  

Key Finding 7: Taurine Drives Glycolysis via mTOR Activation

Absence of TAUT had the following findings:

• LSCs showed significant downregulation of glycolysis and TCA cycle metabolites (e.g., pyruvate, glyceraldehyde‑3‑phosphate, 3‑phosphoglycerate).
• Reduced baseline basal glycolysis, capacity, oxygen consumption, and spare respiratory capacity.
• Colony-forming defects could be rescued with pyruvate, acetate, lactate—but not glucagon—suggesting a specific glycolytic dependency.
• Taurine activates mTOR activity to control colony growth through Rag GTPases: Losing TAUT decreased phospho-mTOR and other downstream targets. mTOR activation mutants or taurine could also rescue colony formation.
• Taurine uptake activated mTOR signaling via Rag GTPases: TAUT loss reduced phospho-mTOR and downstream targets. mTOR activation mutants or taurine restored colony formation.

In summary, taurine uptake through TAUT activates mTOR signaling, which promotes metabolic activity and growth of leukemia stem cells.

What This Study Shows?

• Bone marrow stromal cells increase taurine production via CDO1 during leukemia progression.
• Taurine uptake (via TAUT) is physiologically exploited by the leukemia stem cells to drive glycolysis and growth by the mTOR pathway.
• Inhibition of leukemia in the mouse and human AML models blocks taurine synthesis or utilization.

In this study, the researchers emphasize the necessity of evaluating the addition of taurine to energy drinks.

Takeaway

Taurine, an energy drink and a substance sometimes utilized to curb the side effects of chemotherapy, could be beneficial to leukemia patients. However, this study raises questions about the overall impact presence of taurine in energy drinks for leukemia patients. 

It reveals a taurine-TAUT-mTOR glycolysis node as a prerequisite to aggressive myeloid leukemia in preclinical models. It brings to the fore the metabolic fuelling of cancer stem cells by the tumor microenvironment. 

This study has uncovered the previously unrecognized dependency of leukemia cells on the taurine-TAUT-mTOR-glycolysis pathway. Though this study does not directly imply that taurine causes cancer but researchers think a careful consideration of supplemental taurine in patients with leukemia is needed. Thus, further research is needed for this. In the future, the targeted strategies or inhibitors against taurine would be assessed in clinical trials. 

Header Image Source: Wikimedia Commons

Figure 1 Image Source: https://commons.wikimedia.org/w/index.php?search=taurine&title=Special%3AMediaSearch&type=image

Edited by Karli Norville

References

1. Sharma S, Rodems BJ, Baker CD, Kaszuba CM, Franco EI, Smith BR, Ito T, Swovick K, Welle K, Zhang Y, Rock P, Chaves FA, Ghaemmaghami S, Calvi LM, Ganguly A, Burack WR, Becker MW, Liesveld JL, Brookes PS, Munger JC, Jordan CT, Ashton JM, Bajaj J. Taurine from tumour niche drives glycolysis to promote leukaemogenesis. Nature. 2025 May 14. doi: 10.1038/s41586-025-09018-7. Epub ahead of print. PMID: 40369079.
2. Curran CP, Marczinski CA. Taurine, caffeine, and energy drinks: Reviewing the risks to the adolescent brain. Birth Defects Res. 2017 Dec 1;109(20):1640-1648. doi: 10.1002/bdr2.1177. PMID: 29251842; PMCID: PMC5737830.
3. Baliou S, Adamaki M, Ioannou P, Pappa A, Panayiotidis MI, Spandidos DA, Christodoulou I, Kyriakopoulos AM, Zoumpourlis V. Protective role of taurine against oxidative stress (Review). Mol Med Rep. 2021 Aug;24(2):605. doi: 10.3892/mmr.2021.12242. Epub 2021 Jun 29. PMID: 34184084; PMCID: PMC8240184.