1. And it is deuterium depleted because its already run thru TCA and neurons love lactate as a fuel source.
pubmed.ncbi.nlm.nih.gov/21593331/ x.com/DrEdCaddye/sta…
pubmed.ncbi.nlm.nih.gov/21593331/ x.com/DrEdCaddye/sta…
2. Lactate helps generate fuel as chemical energy (ATP) which powers every cell in the body. Lactate also operates like a light hormone due to its involvement in complex memory formation and neuroprotection. Not containing deuterium is a big part of this.
Astrocytes release lactate in response to neuronal activation. Lactate synthesizes substrates, including acetyl-CoA for the Krebs cycle.
During exercise, ATP is generated mostly from free-flowing blood glucose and the retrieval and breakdown of muscle glycogen stores. To keep moving when the glucose supply is short, the body looks for other ways to regenerate glucose and ATP. With plenty of oxygen, consumption and regeneration flow in a relatively steady state.
Astrocytes release lactate in response to neuronal activation. Lactate synthesizes substrates, including acetyl-CoA for the Krebs cycle.
During exercise, ATP is generated mostly from free-flowing blood glucose and the retrieval and breakdown of muscle glycogen stores. To keep moving when the glucose supply is short, the body looks for other ways to regenerate glucose and ATP. With plenty of oxygen, consumption and regeneration flow in a relatively steady state.
3. A shortage of oxygen, however, causes more lactate production. Pyruvate, a byproduct of glycolysis (glycogen breakdown), can convert to lactate to regenerate the chemical compound NAD+, which is necessary to make ATP.
When produced this way, lactate is typically shuttled to the liver where it’s used to synthesize glucose through gluconeogenesis. Then the glucose is shuttled back to the muscles as a primary energy source in glycolysis.
Fat cells (adipocytes) produce lactate under anaerobic conditions as well. The amount produced depends on a person’s total fat mass.
When produced this way, lactate is typically shuttled to the liver where it’s used to synthesize glucose through gluconeogenesis. Then the glucose is shuttled back to the muscles as a primary energy source in glycolysis.
Fat cells (adipocytes) produce lactate under anaerobic conditions as well. The amount produced depends on a person’s total fat mass.
4. Researchers are now investigating lactate’s ability to cross the blood-brain barrier and play a role in neuron metabolism.
Neuron cell death occurs with oxygen- and glucose-deprivation unless the cell receives lactate before the deprivation occurs. In fact, lactate, not glucose, is the necessary factor in neuron cell recovery from hypoxic conditions.
This process, called the astrocyte-neuron lactate shuttle (ANLS), is particularly active during excitatory neurotransmission and the conversion of neurotransmitters (such as glutamine from glutamate). ANLS both produces and consumes lactate.
Neuron cell death occurs with oxygen- and glucose-deprivation unless the cell receives lactate before the deprivation occurs. In fact, lactate, not glucose, is the necessary factor in neuron cell recovery from hypoxic conditions.
This process, called the astrocyte-neuron lactate shuttle (ANLS), is particularly active during excitatory neurotransmission and the conversion of neurotransmitters (such as glutamine from glutamate). ANLS both produces and consumes lactate.
5. Astrocytes are a type of glial cell in the brain which helps keep neurons healthy and function smoothly. Under resting conditions, apparently half of available glucose is used by the neurons and half by the astrocytes. Since astrocytes use only 10-15% of the brain’s total energy, researchers suggest lactate is the primary fuel source for neurons.
Is Lactate the Link to Improving Cognitive Function?
Is Lactate the Link to Improving Cognitive Function?
6. The ANLS pathway also may play a role in memory formation, causing researchers to question whether lactate could be the link between exercise and improved cognitive function.
In the hippocampus, the center of the brain where memories form, exercise induces an overflow of extracellular lactate. The lactate levels stay elevated for at least fifty minutes following exercise.
We need much more research to determine how lactate may correlate to memory formation and neuron plasticity, but these findings are progressive and promising.
In the hippocampus, the center of the brain where memories form, exercise induces an overflow of extracellular lactate. The lactate levels stay elevated for at least fifty minutes following exercise.
We need much more research to determine how lactate may correlate to memory formation and neuron plasticity, but these findings are progressive and promising.
7. Under strenuous exercise conditions, the highest level of effort the body can physically sustain without accumulating lactate and hydrogen ions (H+) in the blood and muscles is called the lactate threshold. Note not DEUTERIUM
The higher the lactate threshold, the greater the person’s physical fitness.
The point where lactate begins to accumulate in the blood stream creates the anaerobic threshold. Crossing the anaerobic threshold occurs when the body converts from primarily aerobic to anaerobic metabolism, shifting almost entirely from fat to carbohydrates as the primary fuel source.
The higher the lactate threshold, the greater the person’s physical fitness.
The point where lactate begins to accumulate in the blood stream creates the anaerobic threshold. Crossing the anaerobic threshold occurs when the body converts from primarily aerobic to anaerobic metabolism, shifting almost entirely from fat to carbohydrates as the primary fuel source.
8. In this zone, hydrogen ion production accompanies lactate production. When glucose breaks down from the blood, the process releases two hydrogen ions. If glucose breaks down from muscle glycogen, it produces one ion.
The ions create an acidic environment, known as acidosis, which causes acute muscle fatigue, soreness, and delayed-onset muscle soreness (DOMS) twenty-four to forty-eight hours after exercise. Although lactate is not the direct source of H+ generation, it’s often blamed for muscle fatigue and soreness. This is how the binary code works in muscles. It isn't what you were taught in medical school biochemistry.
Lactic acid production, however, plays an essential role in chemical buffering to regenerate NAD+ and remove pyruvate from the cell to supply the next cycle of energy production when 380 nm light is present. The blood can take lactic acid from resting or slowly working muscles. This is why muscles appear to recover during the rest periods of interval training occurring at, or above, the lactate threshold.
Proia, P., Di Liegro, C. M., Schiera, G., Fricano, A., and Di Liegro, I. (2016). Lactate as a Metabolite and a Regulator in the Central Nervous System. International Journal of Molecular Sciences, 17(9), 1450. doi:10.3390/ijms17091450.
The ions create an acidic environment, known as acidosis, which causes acute muscle fatigue, soreness, and delayed-onset muscle soreness (DOMS) twenty-four to forty-eight hours after exercise. Although lactate is not the direct source of H+ generation, it’s often blamed for muscle fatigue and soreness. This is how the binary code works in muscles. It isn't what you were taught in medical school biochemistry.
Lactic acid production, however, plays an essential role in chemical buffering to regenerate NAD+ and remove pyruvate from the cell to supply the next cycle of energy production when 380 nm light is present. The blood can take lactic acid from resting or slowly working muscles. This is why muscles appear to recover during the rest periods of interval training occurring at, or above, the lactate threshold.
Proia, P., Di Liegro, C. M., Schiera, G., Fricano, A., and Di Liegro, I. (2016). Lactate as a Metabolite and a Regulator in the Central Nervous System. International Journal of Molecular Sciences, 17(9), 1450. doi:10.3390/ijms17091450.
10. Where is the binary code lurking in your biochemistry? It is in the biophysics.
An elevated lactate is a sign of an imbalance between production and consumption of hydrogen isotopes. It is the Morse Code of biology that centralized science missed.
It is redox coupled to NAD+ and pyruvate, and to mitochondrial oxidative phosphorylation.
My decentralized integration of lactate biology into the deuterium-timing-light framework is Nature's masterful pivot because it reframes elevated lactate not as mere "waste" or acidosis culprit, but as a deuterium-depleted signaling molecule that encodes metabolic "binary code" through its production, shuttling, and light-dependent context.
An elevated lactate is a sign of an imbalance between production and consumption of hydrogen isotopes. It is the Morse Code of biology that centralized science missed.
It is redox coupled to NAD+ and pyruvate, and to mitochondrial oxidative phosphorylation.
My decentralized integration of lactate biology into the deuterium-timing-light framework is Nature's masterful pivot because it reframes elevated lactate not as mere "waste" or acidosis culprit, but as a deuterium-depleted signaling molecule that encodes metabolic "binary code" through its production, shuttling, and light-dependent context.
11. The evidence aligns strikingly:
Lactate as deuterium-depleted fuel/signaler: Emerging work (e.g., from Boros, Seneff, and others) positions lactate produced via glycolysis (especially in Warburg-like states) as relatively deupleted compared to mitochondrial matrix water under high-deuterium stress.
Cancer cells, for instance, hoard deuterium while exporting deupleted lactate, potentially as a "rescue" nutrient for surrounding cells' mitochondria.
In the brain, the astrocyte-neuron lactate shuttle (ANLS) delivers this lactate preferentially to neurons, where it's oxidized to pyruvate, fueling TCA/oxidative phosphorylation with lower deuterium load.
Neurons thrive on lactate (often over glucose) during activation, hypoxia recovery, or high demand, exactly at the time where deuterium depletion would protect ATPase rotors and sustain efficiency. People who tell you glucose drives stress brain metabolism or tumors need to be avoided at all costs. They believe old data that is now refuted.
Lactate as deuterium-depleted fuel/signaler: Emerging work (e.g., from Boros, Seneff, and others) positions lactate produced via glycolysis (especially in Warburg-like states) as relatively deupleted compared to mitochondrial matrix water under high-deuterium stress.
Cancer cells, for instance, hoard deuterium while exporting deupleted lactate, potentially as a "rescue" nutrient for surrounding cells' mitochondria.
In the brain, the astrocyte-neuron lactate shuttle (ANLS) delivers this lactate preferentially to neurons, where it's oxidized to pyruvate, fueling TCA/oxidative phosphorylation with lower deuterium load.
Neurons thrive on lactate (often over glucose) during activation, hypoxia recovery, or high demand, exactly at the time where deuterium depletion would protect ATPase rotors and sustain efficiency. People who tell you glucose drives stress brain metabolism or tumors need to be avoided at all costs. They believe old data that is now refuted.
12. Neuroprotection and memory as "hormone-like" roles: Lactate crosses the blood-brain barrier, acts as a lactormone (signaling via HCAR1 receptors), boosts BDNF, modulates NMDA activity for plasticity, and supports long-term memory consolidation (e.g., hippocampal overflow post-exercise lasting >50 min).
Pre-conditioning with lactate prevents neuron death in oxygen/glucose deprivation, mirroring the GOE parallels in my blogs, where harnessing "stress" metabolites (post-oxygen rise) enabled complex cognition.
Pre-conditioning with lactate prevents neuron death in oxygen/glucose deprivation, mirroring the GOE parallels in my blogs, where harnessing "stress" metabolites (post-oxygen rise) enabled complex cognition.
13. The binary code in acidosis/threshold: —it's H⁺ ions (protium, not deuterium) from glycogen/glucose breakdown that drive the burn and fatigue, while lactate buffers and shuttles away.
At the lactate threshold, the shift to anaerobic glycolysis amplifies this: more H⁺ signaling "limit reached," forcing adaptation (higher threshold = fitter).
But under 380 nm UVA (neuropsin activation), this could flip to repair/mTOR modulation, my photorepair slide nails it: violet/UVA drives clock periodicity, AMPK/LKB sensing, NAD⁺ recycling, and metabolic flux shifts that favor lactate utilization over accumulation.
At the lactate threshold, the shift to anaerobic glycolysis amplifies this: more H⁺ signaling "limit reached," forcing adaptation (higher threshold = fitter).
But under 380 nm UVA (neuropsin activation), this could flip to repair/mTOR modulation, my photorepair slide nails it: violet/UVA drives clock periodicity, AMPK/LKB sensing, NAD⁺ recycling, and metabolic flux shifts that favor lactate utilization over accumulation.
14. Tying my thesis to the photorepair diagram: 380 nm neuropsin (OPN5) directly entrains local clocks, photorepairs DNA/membranes, and interfaces with mTOR/AMPK via redox (NAD⁺/NADH).
Lactate feeds into this by regenerating NAD⁺ (as I've noted for years), providing deupleted substrate, and signaling via ROS/redox for Nrf2/antioxidant responses.
In low-UV/modern nnEMF environments, disrupted neuropsin timing scatters "this biophysical code because chronic lactate without resolution mimics unresolved GOE stress.
The "Morse" here is probabilistic/timed: lactate pulses (exercise, activation) encode environmental cues (oxygen availability, light cycles, deuterium load) into bioelectric/redox oscillations, scaling to memory, adaptation, or pathology if desynchronized.
This decentralizes my narrative beautifully because lactate isn't "bad" in elevation; it's informational, especially when deupleted and timed right.
Neurons "love" it because it bypasses deuterium-stutter risks while signaling growth/plasticity. The smoking gun? Track lactate shuttling + deuterium content in high vs. low UVA exposure models, or latitude gradients in ANLS efficiency/memory performance. This is how I unmasked the deuterium code in my patients. @ricciflowhealth you might like this thread on biophysics.
Lactate feeds into this by regenerating NAD⁺ (as I've noted for years), providing deupleted substrate, and signaling via ROS/redox for Nrf2/antioxidant responses.
In low-UV/modern nnEMF environments, disrupted neuropsin timing scatters "this biophysical code because chronic lactate without resolution mimics unresolved GOE stress.
The "Morse" here is probabilistic/timed: lactate pulses (exercise, activation) encode environmental cues (oxygen availability, light cycles, deuterium load) into bioelectric/redox oscillations, scaling to memory, adaptation, or pathology if desynchronized.
This decentralizes my narrative beautifully because lactate isn't "bad" in elevation; it's informational, especially when deupleted and timed right.
Neurons "love" it because it bypasses deuterium-stutter risks while signaling growth/plasticity. The smoking gun? Track lactate shuttling + deuterium content in high vs. low UVA exposure models, or latitude gradients in ANLS efficiency/memory performance. This is how I unmasked the deuterium code in my patients. @ricciflowhealth you might like this thread on biophysics.
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