The government has just submitted a new bill to Parliament the Universal Credit and Personal Independence Payment Bill which is expected to be voted on for the first time in the Commons at the beginning of July. Due to the rising tide of opposition to the proposed cuts to disability benefits the government has made some concessions. One of these is that people who are meet the severe conditions criteria won’t face any potential cuts to their benefits. However, to meet the severe conditions criteria a person must have a ‘level of function [which] constantly applies to the claimant.’ So, conditions that fluctuate in severity such as ME may not meet this requirement.
Having said this, there is plenty of scientific evidence with which to argue the case that pwME have an illness which meets this criteria. A new paper from a group of British scientists/doctors explores the chronic cognitive problems faced by pwME which are not alleviated by rest and have no current treatment. I recently interviewed Dr Amolok Bansal who co-wrote this paper about cognitive dysfunction in pwME.
Dr Amolak Bansal qualified in medicine in Southampton in 1982. Then trained at the Hammersmith Hospital, University Hospital of the West Indies in Jamaica, Aberdeen Royal Infirmary and finally Manchester Royal Infirmary. Subsequently worked as senior lecturer/consultant in clinical immunology with University of Queensland at the Princess Alexandra Hospital, Brisbane, Australia from 1993 to 1997. From 1997 to 2018 worked as Consultant in clinical immunology/immunopathology at the St Helier and Kingston Hospitals in Surrey and Honorary Senior Lecturer at St George's Hospital Medical School. Extensive research and publications in autoimmune disease, primary infertility and chronic fatigue syndrome. Involved in medical teaching and headed the Sutton CFS Service from 2005 to 2018. Retired from NHS in 2018 and from private practice in January 2025
Bronc How did you get involved in the field of ME research?
AB: In my early medical training I was fascinated by a patient with severe unrelenting fatigue who became worse with every viral infection and who had range of inexplicable symptoms. My investigations back in 1989 could not uncover a cause for this man's profound ill health. When I saw other patients with similar symptoms I undertook further detailed examination of the medical literature and it was then that I heard of myalgic encephalomyelitis which then became chronic fatigue syndrome (ME/CFS)(I will use both terms together). Since then I have been fascinated by this illness and how previously well people can become so astonishingly debilitated and quite often by a mild initial viral illness. Over the years I have approached the illness from an immunological perspective as I myself trained and then have worked as a clinical immunologist and allergist.
Bronc: Your recent paper Cognitive Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome—Aetiology and Potential Treatments highlights neuroinflammation and impaired neural connectivity as potential drivers of cognitive dysfunction in ME/CFS. Could you elaborate on which specific mechanisms (e.g., glial activation, cytokine profiles, or metabolic disruptions) show the strongest evidence for directly contributing to symptoms like ‘brain fog’?* (see glossary of terms)
AB: Almost certainly all three mechanisms are involved and linked. Certainly microglial activation leads to the local production of several inflammatory cytokines which then contribute brain neuronal disruption and partly by disturbing mitochondrial energy production. I also suspect that excessive absorption of certain amino acids such as glutamine from a leaky bowel epithelium contributes to the altered milieu of stimulatory and inhibitory neurotransmitters. Furthermore, gastrointestinal dysbiosis may lead to impaired production various important keto acids which are essential for brain function.
Bronc: The study acknowledges diverseness in ME/CFS patients. Are there emerging biomarkers or subtypes that could predict which patients are more likely to experience severe cognitive dysfunction, and might this inform personalised treatment approaches?
AB: Unfortunately, there are no biomarkers which correlate with the severity of cognitive dysfunction in those with ME/CFS. At one point I did wonder whether micro clots could explain the cognitive dysfunction but I am less convinced of this at present and as far as I'm aware nobody has correlated this parameter with brain fog. Peripheral markers of inflammation are insufficiently sensitive to provide any meaningful information but when they are markedly elevated as with a significant bacterial infection there is an increase in brain fog.
Bronc: The paper discusses overlaps between ME/CFS cognitive symptoms and conditions like Long COVID or fibromyalgia. Do you believe shared mechanisms (e.g., microglial priming, autoantibodies) could allow for repurposing of therapies across these conditions?
AB: I entirely agree with this notion and I have written a separate paper on the cognitive dysfunction in those with long COVID. I suspect that the brain fog seen in all these conditions has a common mechanism based on neuro inflammation and altered stimulatory and inhibitory neurotransmitters and associated with regional abnormalities of brain perfusion and neural dysfunction.*
Bronc: The review mentions pacing and CBT as common approaches, but critiques their limited efficacy for cognitive symptoms. What emerging interventions (e.g., antivirals, immunomodulators, or neuromodulation) show the most promise in targeting the root causes of cognitive dysfunction?
AB: The marked disability caused by cognitive dysfunction has only recently been fully appreciated and this explains why research scales focusing on this important problem are very uncommon. There are few, if any, double-blind randomised controlled trials of anti-virals, immune modulators or anti-inflammatory agents used specifically for cognitive dysfunction. However, in my experience, anti-virals and vitamin B12 injections appear to provide the most consistent benefit and quite often this is maintained through several years of regular usage. Also important to reduce cognitive dysfunction is deep relaxation to reduce adrenaline levels and good quality restorative sleep. I hope that some of the new therapies for sleep such as the dual orexin receptor antagonists can be explored in the latter regard. I have not come across any supplements that consistently improve brain fog although in individual cases, optimising mitochondrial energy production can be helpful.*
Bronc: Many patients report post-exertional cognitive worsening (‘crash’). Does the evidence suggest this is due to metabolic dysfunction (e.g., lactate accumulation), neuroimmune exhaustion, or other factors? How should this guide clinical advice?
AB: Worsening cognitive function as part of the post exertional malaise has been the most difficult feature of ME/CFS to explain. I have been perplexed by this problem since I first became interested in ME/CFS. I suspect a combination of factors may be involved. These would include but not limited to:
a). increased neuro-endocrine hormones secreted during physical activity causing neural cell dysfunction – a sort of neural post-excitotoxic hypoactivity.
b). mild gastrointestinal ischaemia from diversion of blood flow to muscles leading to enhanced absorption of microbial factors that disrupt neural cell function and communication.
c). reduced cerebral perfusion from cardiac and autonomic dysfunction during exertion disrupting brain oxygen and nutrient delivery to neural cells that are already low on energy substrate.*
Bronc: What steps are needed to move mechanistic findings (e.g., neuroinflammation) into validated clinical treatments? Are there collaborations or funding priorities you see as critical for accelerating this process? How can patients support this research?
AB: As a first step it is critically important that we have better means of assessing cognitive dysfunction and ones that go beyond subjective questions on attention and memory. There are some computer programmes available and these and new methods need to be developed and assessed further. In my opinion monitoring and tracking eye movements, blink rate and changes in pupil diameter may offer new means of assessing cognitive dysfunction. These should be utilised alongside conventional measures in the first instance. I strongly believe they will provide an assessment of the balance of sympathetic and parasympathetic function. As such they will reflect the overall balance of factors that subserve cerebral perfusion and neural activity and which in turn regulate attention that is critical for cognitive and memory function. I am presently unaware of any collaborations in these areas but some researchers are trying to develop wearable technology for assessing all the above variables. The basic physical technology and software is already available but it requires effort to bring everything together. Perhaps crowdfunding may be helpful and especially if the income generated from the development of such a device could then be channelled back into ME/CFS research
Glossary of Terms used in interview
Glial Activation: Think of glial cells as the "support staff" and "security guards" of the brain and nerves. When they get "activated," it's like they've noticed a problem (like an injury or infection) and have switched from their normal maintenance duties into an alert, active state – cleaning up debris, trying to protect nerve cells, and sometimes sending out signals that can cause inflammation.
Cytokine Profiles: Cytokines are tiny chemical messengers used by your immune system to communicate (like text messages between immune cells). A "cytokine profile" is like a snapshot or list showing which specific cytokines are present and at what levels in a person's blood or tissues at a given time. It tells you what kind of "immune conversation" is happening (e.g., "fighting infection" vs. "calming down").
Metabolic Disruptions: Metabolism is how your body turns food into energy and building blocks. A "disruption" means this process isn't working smoothly anymore. It's like the factory (your cells) has broken machinery, clogged supply lines, or inefficient workers, leading to not enough energy being produced, waste piling up, or the wrong products being made.
Gastrointestinal Dysbiosis: This means the community of bacteria and other microbes living in your gut (your "gut microbiome") is out of balance. Imagine a garden where the weeds have taken over and the good plants are struggling. The "bad" or unhelpful microbes have become too numerous compared to the "good" ones, which can cause digestive problems and affect overall health.
Microglial Priming: Microglia are the brain's main "security guard" glial cells. "Priming" means they've been put on high alert by an initial problem (like an infection or injury). Once primed, they react much more strongly and quickly to even small subsequent triggers – like a guard who's been attacked once and is now jumpy and overreacts to minor noises.
Autoantibodies: Antibodies are proteins your immune system makes to fight foreign invaders (like viruses). Autoantibodies are "friendly fire" antibodies – they mistakenly target and attack your *own* body's healthy tissues or molecules, causing damage and disease.
Neuroinflammation: This is inflammation happening specifically within the brain or nervous system. Inflammation is the body's normal response to injury or threat (redness, swelling, heat), but when it happens in the brain, it's like a constant, low-grade alarm bell ringing where it shouldn't be, potentially harming delicate nerve cells and disrupting function.
Brain Perfusion: This simply means blood flow to the brain. Good perfusion is like a steady, strong flow of water (blood) bringing oxygen and nutrients to all parts of a garden (the brain). Poor perfusion means parts of the brain aren't getting enough blood supply.
Neural Dysfunction: This is a broad term meaning the nerve cells (neurons) in your brain or nervous system aren't working properly. It's like the wiring or electrical circuits in a house are faulty – lights might flicker, appliances might not turn on, or signals get crossed, leading to problems with thinking, moving, feeling, or regulating body functions.
Inhibitory Neurotransmitters: Neurotransmitters are chemical messengers nerve cells use to talk to each other. Inhibitory neurotransmitters are like "calm down" or "stop" signals. They tell the next nerve cell not to fire an electrical signal, helping to slow down brain activity and prevent over-excitement (e.g., GABA).
Immunomodulators: These are substances or treatments that help adjust or regulate the immune system. They don't just boost or suppress it entirely; they try to nudge it back towards balance – like a thermostat fine-tuning the temperature, or a conductor helping an orchestra play in harmony again.
Neuromodulation: This is the process of altering nerve activity, often using targeted electrical pulses, magnetic fields, or medication. Think of it like using a remote control to adjust the volume (activity level) or channel (signal pattern) of specific groups of nerves to treat problems like pain, tremors, or mood disorders.
Neuroendocrine Hormones: These are hormones produced by nerve cells (especially in the brain) that get released into the bloodstream. They act as a crucial link between your nervous system and your endocrine (hormone) system, helping control things like stress response (cortisol), sleep/wake cycles (melatonin), water balance, and metabolism. They're like chemical messengers that translate brain signals into body-wide hormonal commands.
Neural Post-Excitotoxic Hypoactivity: Excitotoxicity: Nerve cells get overstimulated (like a motor revved too high) to the point of damage or exhaustion.
Post-Excitotoxic: After this overstimulation damage happens.
Hypoactivity: The nerve cells become less active than normal.
Overall: After being severely overworked and damaged by too much stimulation, nerve cells become sluggish and underactive, like an engine that's been red-lined and now barely runs.
Mild Gastrointestinal Ischaemia: "Ischaemia" means reduced blood flow. This is a slight decrease in blood supply to parts of the stomach or intestines. It's like a gentle pinch in the hose supplying water to a section of the garden – not enough to cause immediate severe damage, but enough to stress the plants and make them function poorly over time.
Autonomic Dysfunction: Your autonomic nervous system automatically controls things you don't think about: heart rate, blood pressure, digestion, temperature, sweating, bladder. "Dysfunction" means this automatic control system is malfunctioning. It's like the autopilot system in your body is glitchy, leading to problems like dizziness, digestive issues, temperature sensitivity, or abnormal heart rate.
Metabolic Dysfunction = A Broken Engine - Your body’s cells are like tiny engines. They take fuel (sugar/fat from food) and oxygen, then burn them to make energy (like a car engine burning gas).
Metabolic dysfunction means these engines aren’t working properly: - They struggle to turn fuel into energy. - They might waste fuel or store it as fat instead of using it. - Waste products build up (like exhaust fumes in a car). - Result: You feel constantly tired, gain weight easily, and your body’s "systems" (like blood sugar) get messy.
Lactate Accumulation = Toxic Exhaust Build-up - When your cells work hard (like during exercise), they produce lactate (a.k.a. lactic acid) as a temporary byproduct – like exhaust from a revving engine. - Normally, your body quickly clears lactate by recycling it into energy or sending it to the liver. But in metabolic dysfunction your "engines" are so inefficient that they produce too much lactate even during normal activity. - Your body *can’t clear it fast enough (like a broken exhaust system). - Lactate builds up in your blood and muscles → lactate accumulation.
Why This Matters: - Lactate feels like: Muscle burning, fatigue, or heavy breathing during minimal effort (like walking up stairs). It worsens metabolic dysfunction: High lactate signals your cells to slow down energy production → making fatigue and weakness worse. It’s a warning sign: Your engines are so broken, they’re poisoning themselves with their own exhaust.
Having said this, there is plenty of scientific evidence with which to argue the case that pwME have an illness which meets this criteria. A new paper from a group of British scientists/doctors explores the chronic cognitive problems faced by pwME which are not alleviated by rest and have no current treatment. I recently interviewed Dr Amolok Bansal who co-wrote this paper about cognitive dysfunction in pwME.
Dr Amolak Bansal qualified in medicine in Southampton in 1982. Then trained at the Hammersmith Hospital, University Hospital of the West Indies in Jamaica, Aberdeen Royal Infirmary and finally Manchester Royal Infirmary. Subsequently worked as senior lecturer/consultant in clinical immunology with University of Queensland at the Princess Alexandra Hospital, Brisbane, Australia from 1993 to 1997. From 1997 to 2018 worked as Consultant in clinical immunology/immunopathology at the St Helier and Kingston Hospitals in Surrey and Honorary Senior Lecturer at St George's Hospital Medical School. Extensive research and publications in autoimmune disease, primary infertility and chronic fatigue syndrome. Involved in medical teaching and headed the Sutton CFS Service from 2005 to 2018. Retired from NHS in 2018 and from private practice in January 2025
Bronc How did you get involved in the field of ME research?
AB: In my early medical training I was fascinated by a patient with severe unrelenting fatigue who became worse with every viral infection and who had range of inexplicable symptoms. My investigations back in 1989 could not uncover a cause for this man's profound ill health. When I saw other patients with similar symptoms I undertook further detailed examination of the medical literature and it was then that I heard of myalgic encephalomyelitis which then became chronic fatigue syndrome (ME/CFS)(I will use both terms together). Since then I have been fascinated by this illness and how previously well people can become so astonishingly debilitated and quite often by a mild initial viral illness. Over the years I have approached the illness from an immunological perspective as I myself trained and then have worked as a clinical immunologist and allergist.
Bronc: Your recent paper Cognitive Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome—Aetiology and Potential Treatments highlights neuroinflammation and impaired neural connectivity as potential drivers of cognitive dysfunction in ME/CFS. Could you elaborate on which specific mechanisms (e.g., glial activation, cytokine profiles, or metabolic disruptions) show the strongest evidence for directly contributing to symptoms like ‘brain fog’?* (see glossary of terms)
AB: Almost certainly all three mechanisms are involved and linked. Certainly microglial activation leads to the local production of several inflammatory cytokines which then contribute brain neuronal disruption and partly by disturbing mitochondrial energy production. I also suspect that excessive absorption of certain amino acids such as glutamine from a leaky bowel epithelium contributes to the altered milieu of stimulatory and inhibitory neurotransmitters. Furthermore, gastrointestinal dysbiosis may lead to impaired production various important keto acids which are essential for brain function.
Bronc: The study acknowledges diverseness in ME/CFS patients. Are there emerging biomarkers or subtypes that could predict which patients are more likely to experience severe cognitive dysfunction, and might this inform personalised treatment approaches?
AB: Unfortunately, there are no biomarkers which correlate with the severity of cognitive dysfunction in those with ME/CFS. At one point I did wonder whether micro clots could explain the cognitive dysfunction but I am less convinced of this at present and as far as I'm aware nobody has correlated this parameter with brain fog. Peripheral markers of inflammation are insufficiently sensitive to provide any meaningful information but when they are markedly elevated as with a significant bacterial infection there is an increase in brain fog.
Bronc: The paper discusses overlaps between ME/CFS cognitive symptoms and conditions like Long COVID or fibromyalgia. Do you believe shared mechanisms (e.g., microglial priming, autoantibodies) could allow for repurposing of therapies across these conditions?
AB: I entirely agree with this notion and I have written a separate paper on the cognitive dysfunction in those with long COVID. I suspect that the brain fog seen in all these conditions has a common mechanism based on neuro inflammation and altered stimulatory and inhibitory neurotransmitters and associated with regional abnormalities of brain perfusion and neural dysfunction.*
Bronc: The review mentions pacing and CBT as common approaches, but critiques their limited efficacy for cognitive symptoms. What emerging interventions (e.g., antivirals, immunomodulators, or neuromodulation) show the most promise in targeting the root causes of cognitive dysfunction?
AB: The marked disability caused by cognitive dysfunction has only recently been fully appreciated and this explains why research scales focusing on this important problem are very uncommon. There are few, if any, double-blind randomised controlled trials of anti-virals, immune modulators or anti-inflammatory agents used specifically for cognitive dysfunction. However, in my experience, anti-virals and vitamin B12 injections appear to provide the most consistent benefit and quite often this is maintained through several years of regular usage. Also important to reduce cognitive dysfunction is deep relaxation to reduce adrenaline levels and good quality restorative sleep. I hope that some of the new therapies for sleep such as the dual orexin receptor antagonists can be explored in the latter regard. I have not come across any supplements that consistently improve brain fog although in individual cases, optimising mitochondrial energy production can be helpful.*
Bronc: Many patients report post-exertional cognitive worsening (‘crash’). Does the evidence suggest this is due to metabolic dysfunction (e.g., lactate accumulation), neuroimmune exhaustion, or other factors? How should this guide clinical advice?
AB: Worsening cognitive function as part of the post exertional malaise has been the most difficult feature of ME/CFS to explain. I have been perplexed by this problem since I first became interested in ME/CFS. I suspect a combination of factors may be involved. These would include but not limited to:
a). increased neuro-endocrine hormones secreted during physical activity causing neural cell dysfunction – a sort of neural post-excitotoxic hypoactivity.
b). mild gastrointestinal ischaemia from diversion of blood flow to muscles leading to enhanced absorption of microbial factors that disrupt neural cell function and communication.
c). reduced cerebral perfusion from cardiac and autonomic dysfunction during exertion disrupting brain oxygen and nutrient delivery to neural cells that are already low on energy substrate.*
Bronc: What steps are needed to move mechanistic findings (e.g., neuroinflammation) into validated clinical treatments? Are there collaborations or funding priorities you see as critical for accelerating this process? How can patients support this research?
AB: As a first step it is critically important that we have better means of assessing cognitive dysfunction and ones that go beyond subjective questions on attention and memory. There are some computer programmes available and these and new methods need to be developed and assessed further. In my opinion monitoring and tracking eye movements, blink rate and changes in pupil diameter may offer new means of assessing cognitive dysfunction. These should be utilised alongside conventional measures in the first instance. I strongly believe they will provide an assessment of the balance of sympathetic and parasympathetic function. As such they will reflect the overall balance of factors that subserve cerebral perfusion and neural activity and which in turn regulate attention that is critical for cognitive and memory function. I am presently unaware of any collaborations in these areas but some researchers are trying to develop wearable technology for assessing all the above variables. The basic physical technology and software is already available but it requires effort to bring everything together. Perhaps crowdfunding may be helpful and especially if the income generated from the development of such a device could then be channelled back into ME/CFS research
Glossary of Terms used in interview
Glial Activation: Think of glial cells as the "support staff" and "security guards" of the brain and nerves. When they get "activated," it's like they've noticed a problem (like an injury or infection) and have switched from their normal maintenance duties into an alert, active state – cleaning up debris, trying to protect nerve cells, and sometimes sending out signals that can cause inflammation.
Cytokine Profiles: Cytokines are tiny chemical messengers used by your immune system to communicate (like text messages between immune cells). A "cytokine profile" is like a snapshot or list showing which specific cytokines are present and at what levels in a person's blood or tissues at a given time. It tells you what kind of "immune conversation" is happening (e.g., "fighting infection" vs. "calming down").
Metabolic Disruptions: Metabolism is how your body turns food into energy and building blocks. A "disruption" means this process isn't working smoothly anymore. It's like the factory (your cells) has broken machinery, clogged supply lines, or inefficient workers, leading to not enough energy being produced, waste piling up, or the wrong products being made.
Gastrointestinal Dysbiosis: This means the community of bacteria and other microbes living in your gut (your "gut microbiome") is out of balance. Imagine a garden where the weeds have taken over and the good plants are struggling. The "bad" or unhelpful microbes have become too numerous compared to the "good" ones, which can cause digestive problems and affect overall health.
Microglial Priming: Microglia are the brain's main "security guard" glial cells. "Priming" means they've been put on high alert by an initial problem (like an infection or injury). Once primed, they react much more strongly and quickly to even small subsequent triggers – like a guard who's been attacked once and is now jumpy and overreacts to minor noises.
Autoantibodies: Antibodies are proteins your immune system makes to fight foreign invaders (like viruses). Autoantibodies are "friendly fire" antibodies – they mistakenly target and attack your *own* body's healthy tissues or molecules, causing damage and disease.
Neuroinflammation: This is inflammation happening specifically within the brain or nervous system. Inflammation is the body's normal response to injury or threat (redness, swelling, heat), but when it happens in the brain, it's like a constant, low-grade alarm bell ringing where it shouldn't be, potentially harming delicate nerve cells and disrupting function.
Brain Perfusion: This simply means blood flow to the brain. Good perfusion is like a steady, strong flow of water (blood) bringing oxygen and nutrients to all parts of a garden (the brain). Poor perfusion means parts of the brain aren't getting enough blood supply.
Neural Dysfunction: This is a broad term meaning the nerve cells (neurons) in your brain or nervous system aren't working properly. It's like the wiring or electrical circuits in a house are faulty – lights might flicker, appliances might not turn on, or signals get crossed, leading to problems with thinking, moving, feeling, or regulating body functions.
Inhibitory Neurotransmitters: Neurotransmitters are chemical messengers nerve cells use to talk to each other. Inhibitory neurotransmitters are like "calm down" or "stop" signals. They tell the next nerve cell not to fire an electrical signal, helping to slow down brain activity and prevent over-excitement (e.g., GABA).
Immunomodulators: These are substances or treatments that help adjust or regulate the immune system. They don't just boost or suppress it entirely; they try to nudge it back towards balance – like a thermostat fine-tuning the temperature, or a conductor helping an orchestra play in harmony again.
Neuromodulation: This is the process of altering nerve activity, often using targeted electrical pulses, magnetic fields, or medication. Think of it like using a remote control to adjust the volume (activity level) or channel (signal pattern) of specific groups of nerves to treat problems like pain, tremors, or mood disorders.
Neuroendocrine Hormones: These are hormones produced by nerve cells (especially in the brain) that get released into the bloodstream. They act as a crucial link between your nervous system and your endocrine (hormone) system, helping control things like stress response (cortisol), sleep/wake cycles (melatonin), water balance, and metabolism. They're like chemical messengers that translate brain signals into body-wide hormonal commands.
Neural Post-Excitotoxic Hypoactivity: Excitotoxicity: Nerve cells get overstimulated (like a motor revved too high) to the point of damage or exhaustion.
Post-Excitotoxic: After this overstimulation damage happens.
Hypoactivity: The nerve cells become less active than normal.
Overall: After being severely overworked and damaged by too much stimulation, nerve cells become sluggish and underactive, like an engine that's been red-lined and now barely runs.
Mild Gastrointestinal Ischaemia: "Ischaemia" means reduced blood flow. This is a slight decrease in blood supply to parts of the stomach or intestines. It's like a gentle pinch in the hose supplying water to a section of the garden – not enough to cause immediate severe damage, but enough to stress the plants and make them function poorly over time.
Autonomic Dysfunction: Your autonomic nervous system automatically controls things you don't think about: heart rate, blood pressure, digestion, temperature, sweating, bladder. "Dysfunction" means this automatic control system is malfunctioning. It's like the autopilot system in your body is glitchy, leading to problems like dizziness, digestive issues, temperature sensitivity, or abnormal heart rate.
Metabolic Dysfunction = A Broken Engine - Your body’s cells are like tiny engines. They take fuel (sugar/fat from food) and oxygen, then burn them to make energy (like a car engine burning gas).
Metabolic dysfunction means these engines aren’t working properly: - They struggle to turn fuel into energy. - They might waste fuel or store it as fat instead of using it. - Waste products build up (like exhaust fumes in a car). - Result: You feel constantly tired, gain weight easily, and your body’s "systems" (like blood sugar) get messy.
Lactate Accumulation = Toxic Exhaust Build-up - When your cells work hard (like during exercise), they produce lactate (a.k.a. lactic acid) as a temporary byproduct – like exhaust from a revving engine. - Normally, your body quickly clears lactate by recycling it into energy or sending it to the liver. But in metabolic dysfunction your "engines" are so inefficient that they produce too much lactate even during normal activity. - Your body *can’t clear it fast enough (like a broken exhaust system). - Lactate builds up in your blood and muscles → lactate accumulation.
Why This Matters: - Lactate feels like: Muscle burning, fatigue, or heavy breathing during minimal effort (like walking up stairs). It worsens metabolic dysfunction: High lactate signals your cells to slow down energy production → making fatigue and weakness worse. It’s a warning sign: Your engines are so broken, they’re poisoning themselves with their own exhaust.
