Dataset Information

Effect of a Ketogenic Diet on the Nutritional Parameters of Obese Patients: A Systematic Review and Meta-Analysis.

ABSTRACT: The effect of a ketogenic diet (KD) on biochemical parameters and nutritional status has been the subject of debate over the years, as several randomized clinical trials (RCTs) obtained different results.

Method

A systematic review and random-effects meta-analysis of RCTs comparing KD with a balanced diet was performed by means of a search of PubMed, Cochrane Library, Scopus, and Web of Science. Trials where the method for measuring the response variables was unclear, those that considered pathologies other than chronic non-communicable diseases and those with participants receiving pharmacological treatment for obesity were excluded from the comparison.

Results

Of the studies included in the meta-analysis, no statistically significant standardized mean differences were observed for body mass index (BMI) (d = -0.457, p = 0.359), total cholesterol, COL-T (d = 0.230, p = 0.591), high-density lipoprotein, HDL (d = -0.028, p = 0.934), low-density lipoprotein, LDL (d = 0.528, p = 0.173), or triglycerides, TG (d = -0.283, p = 0.222), with high values of heterogeneity. The percentage of women included in the studies is a significant moderating variable in terms of BMI ratio (z = -6.68, p < 0.001) and TG (z = -2.27, p = 0.023).

Conclusion

A KD shows no more benefits on nutritional parameters than a balanced diet, and adverse effects of being on the diet are sometimes reported.

SUBMITTER: Lopez-Espinoza MA

PROVIDER: S-EPMC8467306 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundNo curative therapy for mitochondrial disease (MD) exists, prioritizing supportive treatment for symptom relief. In animal and cell models ketones decrease oxidative stress, increase antioxidants and scavenge free radicals, putting ketogenic diets (KDs) on the list of management options for MD. Furthermore, KDs are well-known, safe and effective treatments for epilepsy, a frequent symptom of MD. This systematic review evaluates efficacy and safety of KD for MD.MethodsWe searched Pubmed, Cochrane, Embase and Cinahl (November 2020) with search terms linked to MD and KD. From the identified records, we excluded studies on Pyruvate Dehydrogenase Complex deficiency. From these eligible reports, cases without a genetically confirmed diagnosis and cases without sufficient data on KD and clinical course were excluded. The remaining studies were included in the qualitative analysis.ResultsOnly 20 cases (14 pediatric) from the 694 papers identified met the inclusion criteria (one controlled trial (n = 5), 15 case reports). KD led to seizure control in 7 out of 8 cases and improved muscular symptoms in 3 of 10 individuals. In 4 of 20 cases KD reversed the clinical phenotype (e.g. cardiomyopathy, movement disorder). In 5 adults with mitochondrial DNA deletion(s) related myopathy rhabdomyolysis led to cessation of KD. Three individuals with POLG mutations died while being on KD, however, their survival was not different compared to individuals with POLG mutations without KD.ConclusionData on efficacy and safety of KD for MD is too scarce for general recommendations. KD should be considered in individuals with MD and therapy refractory epilepsy, while KD is contraindicated in mitochondrial DNA deletion(s) related myopathy. When considering KD for MD the high rate of adverse effects should be taken into account, but also spectacular improvements in individual cases. KD is a highly individual management option in this fragile patient group and requires an experienced team. To increase knowledge on this-individually-promising management option more (prospective) studies using adequate outcome measures are crucial.