HIGHLIGHTS
- During a hypo, the brain depletes NAD+, a key molecule needed to convert glucose into usable energy.
- This results in an energy bottleneck that causes "post-hypo brain fog," even after blood glucose levels have returned to normal.
- Adaptive energy sources (like BHB and lactate) can bypass this bottleneck because they provide energy that is not dependent on NAD+.
- New solutions combine glucose with these adaptive fuels to support a faster, more complete recovery for both the body and the brain.
WHAT CAUSES POST-HYPO BRAIN FOG?
If you’ve ever treated a hypo (low blood glucose) and still felt drained, foggy, or wiped-out afterward, you’re not alone. Many people recover their numbers long before they feel like themselves again.
So what’s happening in the brain?
During a hypo, your brain uses up a molecule called NAD+, which it needs to turn glucose into usable energy. When NAD+ is depleted, the brain’s ability to turn glucose into fuel temporarily slows down. This creates an energy bottleneck.
Your glucose numbers recover quickly but your brain needs more time – this creates a lingering “post-hypo brain fog.”
This is where adaptive energy comes in.
WHAT IS ADAPTIVE ENERGY?
Most people think of glucose as the body’s main energy source – and most of the time, it is. But the body has other sources of energy for moments when glucose is low, like during fasting, intense exercise, or a hypo.
This system uses adaptive energy, which are fuels that can step in to support the brain and body when glucose isn’t enough.
Historically, these adaptive fuels were critical for survival, keeping people alert and functioning during fasting or food scarcity. Modern diets rely heavily on glucose, leaving these adaptive energy sources underused, but their ability to support your brain during low-glucose events remains.
The two most important adaptive energy sources are BHB (beta-hydroxybutyrate) and lactate.
BHB: Energy from Fat
When glucose is low, the liver converts stored fat into BHB which can be used directly by the brain. BHB is:
- Stable and long-lasting
- Highly efficient for the brain
- Able to cross the blood-brain barrier quickly
This makes BHB an important fuel source when glucose alone isn’t meeting the brain’s needs.
Lactate: Recycled Energy
Lactate is often misunderstood as a waste product of exercise – but in reality, it’s a valuable, recyclable fuel that can also be used by the brain during low-glucose events.
WHY DOES ADAPTIVE ENERGY MATTER DURING HYPO RECOVERY?
As a recap, during and after a hypo:
- The brain burns through NAD+
- NAD+ depletion slows glucose metabolism
- Blood glucose levels restore, but the brain can’t fully convert this to energy yet
- Fatigue, fogginess, and poor concentration continue
Adaptive fuels can bypass this bottleneck, providing the brain with energy that doesn’t require the same NAD+-dependent pathway.
This allows the brain to refuel faster – while glucose metabolism catches up.
Figure 1: During a hypo, the brain can’t efficiently turn glucose into energy because NAD+ is depleted, creating an energy bottleneck. Adaptive energy sources bypass this bottleneck, providing energy to the brain when glucose is low.
KLARIO: SUPPORTING THE BODY’S NATURAL ADAPTIVE ENERGY SOURCES
By supplying ready-to-use adaptive energy sources alongside glucose, Klario aims to support a more complete recovery after a hypo – fuelling both the body and the brain.
This approach is intended to help:
- Support faster cognitive recovery
- Reduce the risk of recurrent hypo events
- Improve confidence and control
Klario is backed by 2 independent clinical studies and proven in more than 1000 hypos. Want to dive deeper? Read more about the science of Klario and the clinical data supporting it here.
Disclaimer: Klario is a functional food for the dietary management of hypoglycaemia. It is not intended to replace medical advice. Always consult your healthcare provider for guidance on your diabetes management.
REFERENCES
De Angelis, L.C. et al. (2021) “Neonatal Hypoglycemia and Brain Vulnerability,” Frontiers in Endocrinology, 12. Available at: https://doi.org/10.3389/fendo.2021.634305.
Suh, S. et al. (2004) “Zinc release contributes to hypoglycemia-induced neuronal death,” Neurobiology of Disease, 16(3), pp. 538–545. Available at: https://doi.org/10.1016/j.nbd.2004.04.017.
Suh, S. et al. (2005) “Pyruvate Administered After Severe Hypoglycemia Reduces Neuronal Death and Cognitive Impairment,” Diabetes, 54(5), pp. 1452–1458. Available at: https://doi.org/10.2337/diabetes.54.5.1452.
Won, S.J. et al. (2012) “Prevention of Acute/Severe Hypoglycemia-Induced Neuron Death by Lactate Administration,” Journal of Cerebral Blood Flow & Metabolism, 32(6), pp. 1086–1096. Available at: https://doi.org/10.1038/jcbfm.2012.30.