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Parkinson's disease, a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, is strongly associated with the death of dopaminergic neurons in the brain's substantia nigra. Although dopamine replacement therapy temporarily helps patients manage their motor symptoms, this current standard of care fails to address the underlying network of pathologies that contribute to the persistent death of dopaminergic neurons. Thus, new treatment approaches are needed that address the underlying pathologies and, thereby, slow or halt the progression of the actual disease. D-β-hydroxybutyrate – a ketone body produced by the liver to support brain function during periods of starvation – may provide an option. Lifestyle interventions that induce endogenous D-β-hydroxybutyrate production, such as caloric restriction and ketogenic diets, are known to increase healthspan and lifespan in animal models and are used to treat neurological disorders. The efficacy of these ketosis-inducing interventions, along with the recent development of commercially available D-β-hydroxybutyrate-based nutritional supplements, should inspire interest in the possibility that D-β-hydroxybutyrate itself exerts neuroprotective effects. This review provides a molecular model to justify the further exploration of such a possibility. Herein, we explore the cellular mechanisms by which the ketone body, D-β-hydroxybutyrate, acting both as a metabolite and as a signaling molecule, could help to prevent the development, or slow the progression of, Parkinson's disease. Specifically, the metabolism of D-β-hydroxybutyrate may help neurons replenish their depleted ATP stores and protect neurons against oxidative damage. As a G-protein-coupled receptor ligand and histone deacetylase inhibitor, D-β-hydroxybutyrate may further protect neurons against energy deficit and oxidative stress, while also decreasing damaging neuroinflammation and death by apoptosis. Restricted to the available evidence, our model relies largely upon the interpretation of data from the separate literatures on the cellular effects of D-β-hydroxybutyrate and on the pathogenesis of Parkinson's disease. Future studies are needed to reveal whether D-β-hydroxybutyrate actually has the potential to serve as an adjunctive nutritional therapy for Parkinson's disease.
고수의 한마디
'케톤상태는 혈당이 낮을때 한해서 전신염증을 줄인다. 혈당과 케톤수치가 높으면 건강에 해로울 수 있다. 케토제닉 다이어트로 인한 대부분의 부작용은 혈당수치가 높을때 발생한다. 토마스 세이프리드
뉴욕의 가정의학과 전문의 프레드 페스카토레는 햄튼 다이어트와 영원히 날씬하기(thin for good) 베스트셀러 저자.
프레드 페스카토레는 저탄수화물, 고지방 케톤식에 대하여 다음과 같이 말함.
'세상의 모든 의사들이 이 방법을 왜 사용하지 않는지 모르겠어요. 저는 20년전에 앳킨스 박사와 함께 일하면서 이 식단을 알게되었지요' '알레르기부터 체중감량에 이르는 모든 질환을 케톤식으로 치유했어요. 이 방식은 언제나 효과를 발휘하지요'
캐나다 의사 '제이 워트먼'은 2002년 2형 당뇨병이 발병하고 케토제닉 식이요법을 시행하고 완치함.
'의학교육을 받을때나 의사가 되어 진료를 하면서 탄수화물 제한이라는 치료법을 접한 적이 없어요. 하지만 탄수화물을 제거하자 곧바로 제 2형 당뇨병의 모든 징후와 증상이 극적으로 회복되더군요'
며칠안에 혈당이 정상화되고 몸상태가 아주 좋아졌으며 하루에 500g씩 체중이 빠지기 시작함. 식단을 바꿔서 치료효과를 얻을 수 있다는 이야기를 들은적이 없기 때문에 예상치 못한 기적적인 결과에 위트먼은 어리둥절함.
Keep carbs low
Eat more fat
Test ketons often
Overdoing protein is bad
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