Starving Lyme: How to Exploit Borrelia’s Metabolic Weakness
A 2025 study published in mBio, a journal of the American Society for Microbiology, titled “Lactate dehydrogenase is the Achilles’ heel of Lyme disease bacterium Borreliella burgdorferi” revealed a key insight: the Lyme bacteria relies entirely on a single enzyme — lactate dehydrogenase (LDH) — for its metabolism and survival.
The researchers concluded that this enzyme could be a promising drug target. But the same observations also point toward natural, non-pharmaceutical solutions. By understanding how Borrelia depends on lactate for its energy and redox balance, we can apply this knowledge to how we live, eat, and manage our metabolism to create unfavorable conditions for the bacteria.
What the Study Found
The 2025 study highlighted that Borrelia burgdorferi has a highly restricted metabolism, relying solely on the anaerobic fermentation of glucose—glycolysis—for ATP production. To keep glycolysis running, the bacteria depend critically on the lactate dehydrogenase enzyme, which interconverts pyruvate and lactate, helping to recycle NAD⁺ and maintain the NAD⁺/NADH redox balance.
Redox refers to reduction-oxidation, or the transfer of electrons between molecules. NAD⁺ acts as an electron acceptor, becoming NADH once it receives an electron. NADH then donates that electron to power metabolic reactions, converting back into NAD⁺ so the cycle can continue.
Without lactate dehydrogenase, Borrelia loses the ability to regenerate NAD⁺, halting glycolysis — and therefore halting its only way of making energy. In essence, it can no longer recharge its redox batteries and quickly loses its charge.
Borrelia’s Adaptability
Borrelia’s ability to run lactate dehydrogenase in both directions — converting pyruvate to lactate or lactate to pyruvate — is a key adaptation that enables it to survive in two completely different environments: the tick gut and the mammalian host.
Inside the tick gut, glucose is scarce but lactate accumulates. Lyme bacteria import this lactate through a transporter called lactate permease (LctP), converting it into pyruvate for energy.
Inside mammals, where glucose is abundant, the bacteria reverse this process — fermenting glucose into lactate to regenerate NAD⁺ and sustain glycolysis.
This simple enzyme provides the metabolic adaptability that allows Borrelia to thrive in both environments.
Human Comparison
Humans can also produce energy through glycolysis. But unlike Borrelia, we have mitochondria that provide another, far more efficient energy pathway.
Inside the mitochondria, electrons from the breakdown of food are passed through the electron transport chain (ETC), generating an electrical current and proton gradient that drives the production of ATP and metabolic water — together creating the energy that powers life.
This process, called oxidative phosphorylation, can run on electrons derived from carbohydrates, fats, or proteins, unlike glycolysis, which relies solely on glucose.
When mitochondrial function breaks down — due to circadian disruption, diets high in processed and deuterium-loaded foods, chronic infections, or overexposure to mitochondrial stressors like artificial blue light and non-native electromagnetic fields (nnEMFs) — the cell reverts to glycolysis as a survival mechanism.
This shift represents metabolic hypoxia, where the cell loses redox potential and oxygen efficiency. Glycolysis produces far less ATP, generates no metabolic water, and produces large amounts of lactate as a byproduct — creating the very conditions that Borrelia exploits.
Targeting Lyme’s Vulnerability Through Diet
Knowing that Borrelia depends on glucose and lactate for its metabolism, and that it can parasitically import lactate through LctP, it stands to reason that environments low in both glucose and lactate are unfavorable for its survival.
Our mitochondrial flexibility gives us the unique ability to create such an environment. When we shift into a ketogenic metabolic state, relying primarily on fats and ketones for energy, we activate mitochondrial respiration and move away from glycolysis.
Two things happen simultaneously:
There’s less glucose available for the bacteria to ferment.
There’s less lactate produced for it to scavenge.
A targeted, intelligently implemented ketogenic diet can therefore cut off Borrelia’s two main fuel lines — glucose and lactate.
This doesn’t mean there’s zero glucose or lactate in the system, but their availability can be dramatically reduced, creating a metabolic terrain that stresses the bacteria and limits its growth.
When chronic infection, inflammation, and hypoxia drive our own cells toward glycolysis, we essentially recreate the low-oxygen, high-lactate conditions of the tick gut inside our own bodies.
Lyme disease thrives on the byproducts of our metabolic inefficiency. It exploits a terrain of low redox potential and poor mitochondrial function — the same terrain that underlies many chronic illnesses. By restoring mitochondrial health and returning to oxidative phosphorylation, we produce clean energy with no lactate output, starving Borrelia of the very resources it depends on.
Restoring Mitochondrial Function
To shift out of glycolysis and back into mitochondrial energy production, the health of the mitochondria themselves — which have their own genome separate from the human nuclear genome — is foundational.
Supporting mitochondrial health involves providing them with the environmental inputs they depend on while mitigating known mitochondrial stressors and toxins. This means aligning with natural circadian rhythms (morning sunlight exposure, blocking artificial blue light after sunset), reducing nnEMF exposure, grounding whenever possible, maintaining a low deuterium load, and ensuring regular exposure to infrared and full-spectrum sunlight — all of which help optimize the electron transport chain.
Deuterium, for example, is a heavy isotope of hydrogen that is heavily concentrated in industrial seed oils, processed foods, and carbohydrates. It is twice as large and heavy as regular hydrogen (protium) and can jam the ATP synthase nanomotor at the end of the ETC, which is only designed to pump protium. This disrupts electron and proton flow, forcing metabolism back toward glycolysis.
Infrared light powers Complex IV of the ETC, stimulating the production of deuterium-depleted metabolic water — which forms structured, charge-separated Exclusion Zone (EZ) water — and supporting local melatonin production, which is essential for managing oxidative stress and maintaining redox balance.
The production of EZ water through oxidative phosphorylation is also critical, as layers of structured water inside and around our cells support detoxification and provide shielding against intracellular pathogens or membrane damage — including Borrelia’s scavenging of host membrane lipids, which it uses to cloak itself from immune recognition.
In other words, fixing your circadian rhythm, getting plenty of natural full-spectrum and infrared-rich sunlight, avoiding excess artificial blue light and nnEMF (which can create hypoxic conditions), and strategically implementing ketosis all help deplete the body of excess deuterium and restore mitochondrial electron transport efficiency. This reactivates oxidative phosphorylation — enabling you to produce energy cleanly, rather than through glycolysis, which generates the lactate that Lyme uses as fuel.
The Seasonal Diet Connection
A best practice to support metabolic health is to consume a diet that is both local and seasonal to where you live.
At northern latitudes, as sunlight and UV exposure drop in winter, carbohydrate availability naturally declines. Ancestrally, this would have shifted our metabolism into a mild, fat-based ketogenic state — an AMPK-dominant phase focused on repair, autophagy, and regeneration.
In summer, with higher UV exposure and carbohydrate abundance, metabolism shifts toward mTOR activation, promoting growth, protein synthesis, and energy storage. Both phases are essential.
Today, artificial light environments and the constant availability of imported, out-of-season foods keep us stuck in perpetual summer — high glucose, high lactate, high deuterium, and chronic inflammation.
We cut ourselves off from the restorative processes of winter — autophagy, ketosis, and deuterium depletion.
Returning to seasonal patterns — higher fat intake in winter, higher carbohydrate intake in summer — helps restore the metabolic rhythms that support mitochondrial health and keep pathogens like Borrelia in check.
The Takeaway
The 2025 study by Sze et al. identified Borrelia’s dependence on lactate dehydrogenase as its metabolic weakness — its Achilles’ heel.
While the researchers proposed that lactate dehydrogenase could serve as a target for developing pharmaceutical drugs that impair Borrelia’s metabolism, the same observation reveals another, more immediate path: restore mitochondrial function and shift metabolism away from glycolysis.
We have mitochondria and can run on fats and ketones where Lyme cannot. This is where our advantage lies.
By focusing on mitochondrial health and producing energy through oxidative phosphorylation, we can create a coherent metabolic terrain in which Lyme cannot thrive.
CITE:
Sze CW, Lynch MJ, Zhang K, Neau DB, Ealick SE, Crane BR, Li C. Lactate dehydrogenase is the Achilles' heel of Lyme disease bacterium Borreliella burgdorferi. mBio. 2025 Apr 9;16(4):e0372824. doi: 10.1128/mbio.03728-24. Epub 2025 Mar 20. PMID: 40111021; PMCID: PMC11980376.
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