There is a rapidly growing amount of research regarding Intermittent and Extended Fasting and its benefits on brain and body health. From an evolutionary standpoint, humans did not sustain themselves eating three meals a day. Those who operated well in a fasted state were more successful at finding food, enabling survival and reproduction. [3] Fasting has shown to produce healthy stress on the brain and help to combat injury and disease. The following studies display some of the benefits of fasting and its ability to enable neuroplasticity, our brain’s natural ability to grow.

DPDR is marked by decreased activity within emotional and attention based networks like the Salience Network. There are alterations within the sympathetic and parasympathetic nervous systems as well. While sympathetic-associated regions predominate in executive- and salience-processing networks, parasympathetic regions predominate in the default mode network. [5] These studies show that fasting may help to alleviate the symptoms of DPDR as they address critical aspects of this disorder by increasing activity within Salient regions.

Positive Effects Of Fasting On Health
  • Intermittent Fasting (IF) is a term used to describe a variety of eating patterns in which no or few calories are consumed for time periods that can range from 12 hours to several days, on a recurring basis. IF regimens can help induce a metabolic switch that can assist in facilitating our immune response and initiate neuroplasticity. [2]
  • Lifestyles characterized by little or no Intermittent Metabolic Switching (three meals per day, plus snacks and negligible exercise) result in suboptimal brain functionality and increase the risk of major neurodegenerative and psychiatric disorders. [3]
  • A 48 hour fast resulted in higher Parasympathetic Nervous System activity and decreased resting frontal brain activity.  It also resulted in improved prefrontal-cortex-related cognitive functions, such as mental flexibility. [1]
  • IF regimens also induce the coordinated activation of signaling pathways that optimize physiological function, enhance performance, and slow aging and disease processes. [2]
  • Findings show complex and coordinated adaptations of the brain and body that enable the individual to maintain and even enhance their cognitive and physical performance for extended time periods in the fasted state. [3]
  • With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced [This is where the name for the ketogenic diet comes from]. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. This metabolic switch promotes neuroplasticity and resistance of the brain to injury and disease. [3]
  • Cognition, sensory-motor function and physical performance can be enhanced by IMS protocols involving IF and/or vigorous exercise. Fasting and exercise upregulate neurotrophic factor signalling, antioxidant and DNA repair enzymes, protein deacetylases and autophagy, which protects neurons against stress and sets the stage for mitochondrial biogenesis and cell growth and plasticity during recovery periods. [3]
  • Based on stress influence on the body, [stress] is classified into eustress and distress. Chronic stressors are generally well-known for adverse effects on the body, particularly cognitive decline. IF could improve cognitive function and preserve the brain against distress by regulation of inflammatory response pathway. The current findings demonstrated that intermittent fasting would be a useful tool in distressful conditions to improve learning and memory. [4]
Fasting And Treating DPDR
  • We examined the Salience Network (SN) response to meal intake and potential genetic and acquired influences on SN function. Excluding genetic confounders (variables that influence both dependent and independent variables), the percentage change in SN connectivity by a meal correlated to body fat percentage. [6] This suggests that body fat percentage may play a role in SN activity.
  • SN connectivity was reduced by a meal, indicating potential participation of the SN in control of feeding. The findings support the involvement of the SN in feeding behavior as well as genetic influences on SN connectivity. The degree of change in SN connectivity evoked by a meal appears to be a malleable response reflecting flexibility within the regulatory system to adapt to shifts in environmental or homeostatic conditions. [6]
  • We found an extensive modulation elicited by food stimuli in the 2 visual and salience networks. Specifically, only in lean subjects, the salience network was modulated by caloric content, whereas overweight and obese subjects showed a generalized augmented response in the salience network. [7]
  • In conclusion, obesity is marked by alterations in functional connectivity networks involved in food reward and salience. Prolonged fasting differentially affected hypothalamic connection with the dACC and the insula between obese and lean subjects. [7]
  • We hypothesized that brain circuits involved in reward and salience respond differently to fasting in obese versus lean individuals. We compared functional connectivity networks related to food reward and saliency after an overnight fast (baseline) and after a prolonged fast of 48 h in lean versus obese subjects. [8]
  • At baseline, we found a stronger connectivity between hypothalamus and left insula in the obese subjects. This effect diminished upon the prolonged fast. After prolonged fasting, connectivity of the hypothalamus with the dorsal anterior cingulate cortex (dACC), which is a Primary Hub within the Salience Network, increased in lean subjects and decreased in obese subjects. Amygdala connectivity with the ventromedial prefrontal cortex was stronger in lean subjects at baseline, which did not change upon the prolonged fast. No differences in posterior cingulate cortex connectivity were observed. [8]
  • In conclusion, obesity is marked by alterations in functional connectivity networks involved in food reward and salience. Prolonged fasting differentially affected hypothalamic connections with the dACC and the insula between obese and lean subjects. Our data support the idea that food reward and nutrient deprivation are differently perceived and/or processed in obesity. [8]


Please do your research before engaging in any fasting. Based on health conditions or lifestyles, fasting may not be for you and improper fasts can lead to potential long term damages. There may also be damages, such as muscle cramps, during the fast if healthy vitamin levels, such potassium and magnesium are not maintained. Adding these to the regimen can be of assistance, but everyone reacts differently. It is suggested to begin with intermittent and smaller fasts to prepare yourself. Addressing other stressors, healthy eating, consistent bed times, pain management, etc. are all very important as well.

  • Despite the many longer-term studies with very few adverse events, safety remains a potential concern. If findings of the research outlined above provide additional support for the metabolic benefits of IF, it is foreseeable in the near future that healthcare professionals may recommend IF regimens to patients who are overweight, insulin resistant, and/or hypertensive. [2]
  • Many different IMS regimens are likely to improve brain health such that individuals may choose an approach that suits their particular daily and weekly schedules. [That being said] there are many gaps in our knowledge of the neurobiology of IMS and the application of such knowledge to the prevention and treatment of neurological disorders. Several randomized controlled trials of IF in subjects with or at high risk of a neurological disorder are in progress and results will be forthcoming. [3]
– A lot of this info may be subjective claims, so it is important to recognize and state that, but still support those claims with existing scientific literature.

– potential therapeutic benefits of fasting. differences in something like CBT and Fasting (i.e. physiological response vs cognitive response). CBT may be helpful for coping mechanisms, but has shown to be unsuccessful at addressing the neurological impacts and dysregulation of major brain networks.

– starting a healthy fast

– Fasting within the public eye (potentially) – this isn’t as much focused on the information, so maybe

– Treatment options – dementia, depression, dpdr, other neurological malfunctions, like seizures, etc.

– May prove fruitful in addressing rumination, certain types of depression, numbness, fatigue, apathy or otherwise.

-Alleviating general stressors, which is one of, if not the single greatest indicator of cognitive decline and general health problems.

– Lots of studies need to be done – salience network activity may be impacted basy on body fat percentage, medicines being taken, etc.


Neurological Impacts of Fasting

Disclaimer: Many of these claims are subjective, and while existing studies suggest that intermittent fasting may have a number of therapeutic benefits, more research must be done in order to better understand these potential benefits.

The Salience Network and Attentional Mechanisms
  • The Salience Network (SN) is responsible for the transition between the Default Mode Network (DMN) and the Task-Positive Network (TPN). Research shows that meals significantly reduce SN connectivity (source 6 from above), therefore impairing one’s ability to go between the DMN and TPN as needed.
  • Overactivity of the DMN (seen in disorders such as DPDR, depression, and dementia variants, among others) can result in rumination, numbness, apathy, and other forms of physical and cognitive dysregulation. Preventing the reduction of SN activity through fasting has the potential to alleviate the effects of DMN overactivity by facilitating the transition. 
  • All known clinically effective treatments for depression (SSRIs, CBT, meditation, Psilocybin, etc.) also result in the reduction of DMN activity.