and demonstrate clinically that a KD may permanently restore normal brain function
Most studies report that the KD improves cognition (13–19), improves sociability and repetitive behaviors (20–23), and reduces nociception (24–26): all behavioral endpoints with relevance to dopamine-related behaviors (see below), including perseverative behaviors and potentially chronic pain – thought to share multiple mechanisms and comorbidities with addiction (27). Importantly, KD-related behavioral improvement in children with epilepsy is not solely due to seizure reduction (13, 28–32), thus indicating therapeutic benefits that are uncorrelated with the primary anticonvulsant/antiepileptogenic effects.
Diverse lines of evidence point to the neuromodulator adenosine as a key mechanism underlying short and long-term therapeutic benefits of metabolic therapy with a KD....in vivo evidence that KD feeding elevates brain adenosine
Manipulating the adenosine system is common – caffeine, a non-selective antagonist for adenosine A1 receptors (A1R) and adenosine A2 receptors (A2R), is the most widely used psychoactive drug worldwide
Some evidence suggests the KD alters dopamine directly.
Energy homeostasis – particularly changes in ATP and adenosine – is known to be relevant but poorly understood in neuroprotection, psychiatric disorders and addiction (81, 82). KDs supply a substrate (ketone bodies) for the citric acid cycle that elevates ATP and promotes mitochondrial function, including in impaired states
Brain hypometabolism has been reported with alcohol and online gaming addiction (98), with stimulant abuse (99, 100), in Alzheimer’s disease and mild cognitive impairment (101, 102), and indeed even with normal aging (103). As a dynamic and energy-demanding organ, and as a survival mechanism, it makes sense that metabolism is reflected in neurological function and behavior and that mitigating metabolic dysfunction is a potent therapeutic strategy
i.e. Keto improving metabolism improves brain metabolism, improves addictive behavior cycles.
Hyperglycemia causes inflammation (111, 112) and is associated with psychiatric re-hospitalization. Inflammation is a biomarker for and perhaps a cause of depression (113), and much evidence shows that KDs reduce inflammation in patients (114–117) and in pre-clinical models
Getting the blood glucose down helps with multiple psychiatric conditions.
KD feeding reduces both the responses to acute cocaine (day one of the sensitizing regimen; challenge day for saline-treated animals) and repeated cocaine. Considered together, these data were the first to show that KD treatment can modify behavioral responses to a monoaminergic stimulant, and suggest that KDs are a potential novel therapy for the treatment of addiction to these drugs.
KD feeding did not appear to modulate the acquisition of the cocaine-related place preference. However, when cocaine was withheld (i.e. extinction), mice on the KD more quickly lost the place preference. In addition, a cocaine priming injection after extinction reinstated the place preference only for the standard diet mice; mice that were on KD did not experience reinstatement.
Better recovery.
Regarding the commonly abused drug ethanol, in rat models of dependence KD-fed animals made fewer lever presses to receive alcohol during acute withdrawal (129) and had reduced withdrawal symptoms (130, 131). In mice, both KD and a ketone monoester (which is metabolized to ketone bodies) reduced withdrawal symptoms even when treatment was started during withdrawal
Food cravings, binge eating being an extreme form, are often considered to be a naturalistic analog of drug abuse. Excessive glucose and insulin spikes are thought to modify the brain leading to addiction-like binge eating; KD feeding will temper such spikes
I really feel this one.
high dietary sugar intake is associated with depression and anxiety in non-diabetic individuals (179–181). These associations do not determine causation but, intriguingly, there are suggestions that depression in the elderly might predispose the development of type II diabetes (182, 183). KDs minimize dietary sugar intake, and provided a stable, mild hypoglycemia which should counteract these deleterious effects on mood.
There is strong evidence of a metabolic underpinning of ASD, in addition to the genetic and environmental components. For example, this disorder has been found to involve hypoperfusion of specific brain regions (198–200) and to be associated with hyperglycemia, mitochondrial dysfunction, and adenosine dysfunction (201–204).
Taken together, the relationship between metabolic health and a broad range of neurological conditions is emerging, including mental health. The relationship among adenosine, dopamine, and ketogenic metabolic therapy is primary because of the ability to link cell energy, neuronal signaling, and gene expression for both short and long-term effects in key brain areas.
It's free, so why not try it?