Evidence map›Paper›PMID 24847102›Full record

ReviewJournal of lipid research2014

Ketogenic diets, mitochondria, and neurological diseases.

Lindsey B Gano, Manisha Patel, Jong M Rho

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 2 pooled it
9.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

149 citing papers in PubMed, 2 syntheses or guidelines pooled it, 265 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Aspartate-Glutamate Carrier 1 (International journal of molecular sciences · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. The Ketogenic Diet in Obesity Management: Friend or Foe?Cell biochemistry and biophysics · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Ketogenic diet and Parkinson's disease.Frontiers in molecular neuroscience · 2026
    Review
  17. Review
  18. Review
  19. Review
  20. Review

89 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Lindsey B GanoDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Colorado, Denver, CO.
Manisha PatelDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Colorado, Denver, CO.
Jong M RhoDepartments of Pediatrics and Clinical Neurosciences, Alberta Children's Hospital Research Institute for Child and Maternal Health, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada.
University of Colorado Denver · USAlberta Children's Hospital · CA

Funding

SUPEROXIDE RADICALS IN SEIZURE-INDUCED NEURONAL DEATHR01NS039587 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2000 to 2019
$5.9M
Redox Control of Seizure-Induced Neuroinflammation.R01NS086423 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2013 to 2022
$3.0M
CIHRNINDS NIH HHS NS086423NINDS NIH HHS R01 NS039587NINDS NIH HHS R01 NS086423
6 · The paper itself

Abstract

The ketogenic diet (KD) is a broad-spectrum therapy for medically intractable epilepsy and is receiving growing attention as a potential treatment for neurological disorders arising in part from bioenergetic dysregulation. The high-fat/low-carbohydrate "classic KD", as well as dietary variations such as the medium-chain triglyceride diet, the modified Atkins diet, the low-glycemic index treatment, and caloric restriction, enhance cellular metabolic and mitochondrial function. Hence, the broad neuroprotective properties of such therapies may stem from improved cellular metabolism. Data from clinical and preclinical studies indicate that these diets restrict glycolysis and increase fatty acid oxidation, actions which result in ketosis, replenishment of the TCA cycle (i.e., anaplerosis), restoration of neurotransmitter and ion channel function, and enhanced mitochondrial respiration. Further, there is mounting evidence that the KD and its variants can impact key signaling pathways that evolved to sense the energetic state of the cell, and that help maintain cellular homeostasis. These pathways, which include PPARs, AMP-activated kinase, mammalian target of rapamycin, and the sirtuins, have all been recently implicated in the neuroprotective effects of the KD. Further research in this area may lead to future therapeutic strategies aimed at mimicking the pleiotropic neuroprotective effects of the KD.

Indexed as

Diet, KetogenicMitochondriaAnimalsHumansKetone BodiesNervous System DiseasesKetone Bodiescellular signalingfatty acidsketoneoxidative stress

Identifiers

PMID24847102
PMCPMC4617125
OpenAlexW2153413087

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.