High Lactate Levels in MS Patients Tied to Disease Progression, Mitochondrial Dysfunction

High Lactate Levels in MS Patients Tied to Disease Progression, Mitochondrial Dysfunction

Scientists in recent years have wondered whether a link exists between high lactate levels resulting from mitochondrial dysfunction and multiple sclerosis (MS) progression. Now researchers in Italy showed that lactate, a metabolic byproduct, is indeed increased in the cerebrospinal fluid of MS patients and may be a disease driver.

Mitochondria are the body’s energy factories, converting nutrients into energy with the help of oxygen. When mitochondrial function in brain neurons is disrupted, these powerhouses produce excess levels of lactate, normally only used to meet neuronal energy demands. (Neurons are believed to use lactate, and not glucose, as their primary source of energy.)

Earlier studies investigating lactate in MS patients reported contradictory findings, with data revealing increased, decreased, or unchanged levels of lactate depending on the study at hand. Researchers from the University of Rome, Tor Vergata, Italy, argued that these studies were either too small or explored the issue in too widely diverse groups of patients to be definitive.

Their study, Cerebrospinal fluid lactate is associated with multiple sclerosis disease progression,” measured lactate, along with tau protein and neurofilament light, two other markers of damage to myelinated neurons in patients with relapsing-remitting MS (RRMS). The study included 118 patients, followed for an average of five years, and 157 controls.

Findings, published in the Journal of Neuroinflammation, showed that lactate was higher in the cerebrospinal fluid of patients than in controls. Moreover, the levels were higher in those with longer disease duration. High lactate levels in MS patients were also linked to disease severity, with progression assessed through the multiple sclerosis severity scale (MSSS), progression index (PI), and the Bayesian risk estimate for multiple sclerosis (BREMS). The research team also noted that the levels were linked to the levels of tau and neurofilament light proteins.

These findings point to the possibility of a link between energy metabolism and MS severity. The authors speculated that such an association could be, in part, dependent on the increased energy demands of neurons that have lost their protective myelin coating. This increased stress on the neuronal energy production system could, in itself, lead to mitochondrial damage.

Study findings imply that pursuing therapies targeting mitochondrial injury could prevent disease progression and the accumulation of disability in RRMS patients.


  1. spiro spyratos says:

    This has been the thinking all along: it’s called virtual hypoxia. Due to the injury of axons and lack of myelin protection, metabolically, mitochondria end up dying. That’s why antioxidants and especially some specialty ones, like MitoQ, a targeted mitochondrial Coenzyme Q have been shown in clinical trials to slow or even halt the progression of EAE in mice. Also, exercise is associated with an increase in mitochondria numbers especially aerobic.

  2. Shasha says:

    Yes…when mitochondria are hurt and low in oxygen burning they make lactic acid like a person who exercises too much and muscles ache. Antibiotics/heavy metals/inheriting hurt mitochondria from the mom/chemicals may hurt mitochondria. Coenzyme Q10 is the spark plug for the mitochondria. PQQ in certain foods or supplement helps make more mitochondria. Fixing the DNA of mitochondria is hard. Exercise may make more neurons and mitochondria. MS is due to low oxygen in the brain. Carnitine/acetylcarnitine help get fats into the mitochondria to burn as fuel. Mg may help protect mitochondria. Ribose may help make more ATP in mitochondria. Amour thyroid may help speed up mitochondria. Many MS people are not getting thyroid medicine due to low TSH when they need thyroid medicine. A thyroid test…Free T4 and Free T3 need to be in the upper middle of the range..not go by TSH since gluten may have hurt the thyroid/pituitary that makes TSH. Stress may make cortisol that blocks thyroid. Soy may block thyroid. Sugar may slow mitochondria. Gluten may hurt intestines so minerals/fat/nutrients don’t absorb. Zinc/Se/enough iron/probiotic are need to convert T4 to T3 for thyroid energy. Gluten may not allow these minerals to absorbed in food/supplement. Probiotics may help make B vitamins which may help the citric acid cycle to make ATP energy. Probiotics help thyroid medicine convert to T3 so the cell can use the medicine. Probiotics may help detox. Detoxing heavy metals may help mitochondria work better. Far Infrared sauna may help detox heavy metals and speed up mitochondria. Coconut oil may speed up mitochondria, but it clogs my blood vessels. I can’t have saturated fat which would help all glands. I can have raw walnuts (open shells to avoid hidden gluten) which are high in polyunsaturated fat and fish oil 2000mg/evening primrose oil 2000mg/krill oil/phosphatidylserine/DMAE/CLA/lecithin. Lecithin may help defat the liver and help memory. Parsley may help memory and has PQQ. Zinc, iron, carnosine, Mg, Mn, Vit C, Vit A, resveratol, alpha lipoic acid and more may help mitochondria.



  3. daan says:

    I keep reading “lactate” over and over again in this article and it got me wondering… Does milk/dairy products intake have something to do with the findings of high lactate levels resulting from mitochondrial dysfunction?

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