Good news for all those going for self-improvement by low-carb dieting: Such a diet is not only good for the body but can also have a preventive effect on the development of certain subtypes of primary open-angle glaucoma (POAG). The prerequisite for this is, of course, that there are no metabolic diseases that could deem a low-carb diet risky. The neuroprotective effect of a low-carb diet is already known from preventive measures against Alzheimer's disease, epilepsy, and Parkinson's disease. However, carbohydrates should not be completely avoided, as this can lead to the so-called "keto flu".1-5
The influence of low-carb nutrition on the development of primary open-angle glaucoma (POAG) was investigated for the first time at the New York Eye and Ear Infirmary of Mount Sinai, USA. According to the low-carb diet guidelines from the recently published study, the key source of protein and fat were mainly from vegetables. Ketone bodies are formed in this catabolic state, and play a central role in the neuroprotection of the optic nerve. They are particularly beneficial in supplying the mitochondria-rich optic nerve head (a.k.a. optic disk). The low-carbohydrate diet results in ketone bodies being metabolized as energy suppliers instead of glucose. The metabolism of the ketone bodies leads to a much higher energy yield compared to glucose. This can be accompanied by an improvement in mitochondrial function, a reduction in free radicals, and a stabilization of the synapses.1
The research group filtered out the data for the present study from three larger prospective American cohort studies with 185,638 study participants. The research group obtained the necessary data for their analysis by means of a special questionnaire obtained from the study participants about their dieting practices. A total of 78,210 persons were included in the analysis who had an age of at least ≥ 40 years, whose eating habits had been recorded by means of a questionnaire and who were under ophthalmological control. In 2,122 of these persons, the development of POAG occurred within the course of the studies.1
For statistical analysis, glaucoma cases were divided into further subtypes depending on the intraocular pressure and the occurrence of paracentral or peripheral visual field failure. The "high-tension" POAG group showed intraocular pressure values of ≥ 22 mmHg. In the normal-tension POAG group, the intraocular pressure was 22 mmHg at ≤. A further division was made on the basis of perimetric data: Patients with peripheral visual field defects without paracentral visual field loss belonged to one subtype and patients with early paracentral visual field defects to another subtype. In the former group, in addition to peripheral visual field defects, a Bjerrum scotoma or nasal step was allowed to occur.1
The evaluation included perimetric data, intraocular pressure values, gonioscopic data, structural information about the respective optic nerve, and the necessity of a pressure-lowering surgery. It was shown that a plant-based low-carbohydrate diet was associated with a 20% risk reduction for the POAG subtype associated with early paracentral defects. This subtype is associated with a loss of retinal ganglion cells (RGCs) in the maculopapular bundle. The subtype is particularly vulnerable to mitochondrial and dysfunctional vascular autoregulatory mechanisms because the optic nerve has a high cellular mitochondrial density. This reflects its high-energy demand and its vulnerability to a lack of energy supply. Scientists believe that mitochondrial dysfunction may be relevant to the pathomechanism of glaucoma. The results of this comprehensive study support this hypothesis.1
References:
1. Hanyuda A. et al. (2020). Low-carbohydrate-diet scores and the risk of primary open-angle glaucoma: data from three US cohorts. Eye (Lond). 2020;34(8):1465-1475.
2. Roehl K. et al. (2019). Modified ketogenic diets in adults with refractory epilepsy: efficacious improvements in seizure frequency, seizure severity, and quality of life. Epilepsy Behav. 2019;93:113–18.
3. Freeman J. et al. (2006). The ketogenic diet: from molecular mechanisms to clinical effects. Epilepsy Res. 2006;68:145–80.
4. Vanitallie T. B. et al. (2005). Treatment of Parkinson's disease with diet-induced hyperketonemia: a feasibility study. Neurology. 2005;64:728–30.
5. Ota M. et al. (2019). Effects of a medium-chain triglyceride-based ketogenic formula on cognitive function in patients with mild-to-moderate Alzheimer’s disease. Neurosci Lett. 2019;690:232–6.