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    1. Amore practical alternative could be ketone bodies, which enter thebrain via the same MCTs as acetate, raising their possible use astherapy for AUD [67–69]. A ketogenic diet raises ketone bodies inblood for subsequent use by the brain to replace glucose partially[70]. Previous studies [17, 65] tested this idea with the introductionof a ketogenic diet to AUD patients [65], and that work showedthat the diet reduced withdrawal symptoms in AUD patientsrelative to those on a standard diet.

      If the brain's doors for acetate are supposedly blocked or damaged right after quitting alcohol, how would feeding someone a keto diet or ketone drinks actually help them feel better during withdrawal?

    2. Chronically, plasma acetate (daily, not sporadic) could leadthe brain to protect against importing acetate, possibly byreduced MCT across the blood-brain barrier. Mews et al.reported histone acetylation with alcohol exposure in themouse brain [56], which may be harmful when it occurschronically [57, 58].

      Could the brain be intentionally shutting down its transporters just to protect its genes from getting messed up by too much acetate from constant binge drinking?

    3. In brain, acetateis selectively utilized by astrocytes [30], so isotopically labeledacetate can be used to trace glial metabolism and the glutamate-glutamine neurotransmitter cycle [31–33], which relates directly tothe rate of synaptic glutamate release.

      Why can only astrocytes use acetate instead of regular brain cells, and how does watching what astrocytes do tell us anything about how brain cells talk to each other?