Increase Your Mitochondria, Your Body Will Thank You | The Acid Drop

DavidPerlmutterMD
5 Sept 202211:06

Summary

TLDR在这段视频中,Dr. David Perlmutter 讨论了线粒体的重要性,它们是细胞的能量工厂,尤其在大脑中至关重要。线粒体功能障碍与多种疾病有关,如癌症和心血管疾病。研究显示,低果糖和低钠饮食可以增加白细胞中线粒体的数量,减少氧化应激,从而改善线粒体功能。这项研究为通过饮食改善线粒体健康提供了有力的证据。

Takeaways

  • 🧠 线粒体是细胞内的能量生产者,尤其在大脑中,每个神经元可能含有多达一千个线粒体。
  • 🔍 线粒体功能良好对于维持免疫系统功能和控制炎症平衡至关重要。
  • 🚫 线粒体功能障碍与癌症、冠状动脉疾病等严重健康问题有关。
  • 🧬 通过检测血液中的线粒体DNA,可以评估身体内线粒体的数量和功能。
  • 🍽️ 研究表明,低果糖和低钠饮食可以增加血液中的线粒体DNA,从而提高线粒体密度。
  • 🥗 低钠和低果糖饮食有助于减少氧化应激,保护线粒体免受损害。
  • 📉 低钠和低果糖饮食可以显著降低氧化应激标志物DNPH的水平。
  • 📈 低钠和低果糖饮食可以减少尿酸水平,这与减少线粒体损伤和提高线粒体功能有关。
  • 🌟 线粒体的增加与减少氧化应激有关,这有助于线粒体的生存和复制。
  • 🔋 通过低钠和低果糖饮食,可以促进线粒体的再生和功能,有助于改善整体健康。

Q & A

  • 线粒体在细胞中扮演什么角色?

    -线粒体是细胞内的能量生产者,被称为细胞的发电厂。它们在几乎所有的细胞中都有分布,包括大脑中的神经元,每个神经元可能含有多达一千个线粒体。

  • 线粒体功能不佳与哪些健康问题有关?

    -线粒体功能障碍与多种健康问题有关,包括癌症、冠状动脉疾病、心血管疾病以及大脑疾病如痴呆症。

  • 大脑对能量的需求有多大?

    -尽管大脑只占人体总重量的3%到5%,但在休息状态下,它可能消耗掉整个身体25%的热量,显示出大脑对能量的高需求。

  • 如何通过简单的血液测试评估线粒体的数量?

    -可以通过检测血液中的线粒体DNA来评估线粒体的数量,这是一种简单的血液抽取测试,可以作为评估全身线粒体功能的一个替代指标。

  • 低果糖和低钠饮食对线粒体密度有什么影响?

    -研究表明,低果糖和低钠饮食可以显著增加线粒体密度,具体表现在白细胞中的线粒体DNA含量显著增加。

  • 线粒体功能障碍与肥胖、糖尿病和高血压有何关联?

    -线粒体功能障碍被认为是肥胖、糖尿病和高血压等健康问题的主要风险因素,这些问题又与冠状动脉疾病、阿尔茨海默病甚至癌症等更严重的健康问题有关。

  • 为什么高果糖和高钠饮食可能会降低线粒体的功能?

    -高果糖和高钠饮食可能会通过减少能量利用来降低线粒体的功能,这在食物稀缺的环境中可能是一种生存优势,因为这样可以减少能量消耗。

  • 研究中提到的低钠低果糖饮食对线粒体DNA的影响是什么?

    -在研究中,低钠低果糖饮食在八周后与线粒体DNA含量的显著增加有关,具体表现为白细胞中线粒体DNA的70倍增加。

  • 氧化应激与线粒体密度有何关系?

    -氧化应激水平的增加会威胁线粒体的生存,而低钠低果糖饮食通过降低氧化应激水平,有助于增加线粒体的数量和生存。

  • 研究中提到的dnph是什么,它与线粒体功能有何关联?

    -dnph是氧化应激的一个标志,它表示自由基的损伤作用。在低钠低果糖饮食的研究中,dnph的水平下降了52%,表明这种饮食有助于减少氧化应激,从而保护线粒体。

  • 低钠低果糖饮食如何影响尿酸水平?

    -低钠低果糖饮食可以降低尿酸水平,因为果糖直接提高尿酸水平,而钠间接通过增加葡萄糖转化为果糖的过程来提高尿酸水平。

Outlines

00:00

🧠 探讨线粒体的重要性与功能

Dr. David Perlmutter在视频中讨论了线粒体的重要性,线粒体是细胞内的能量生产者,尤其在脑细胞中数量众多。他指出,良好的线粒体功能对于免疫反应和炎症平衡至关重要。线粒体功能障碍与多种疾病如癌症、心血管疾病以及大脑疾病如痴呆症有关。大脑作为高能耗器官,对线粒体功能依赖性高。他提出增强线粒体生物合成的方法,即增加可用于能量生产的线粒体数量,并介绍了通过检测血液中红细胞的线粒体DNA来评估线粒体数量的方法。此外,他还提到了低果糖和低钠饮食对增加线粒体密度的影响,以及这种饮食方式如何与肥胖、糖尿病、高血压等健康问题相关联。

05:02

🍽 低钠低果糖饮食对线粒体密度的影响

研究中,36名超重的前高血压成年人被分为两组,一组实行低钠饮食(每天不超过6克),另一组实行等热量的低钠低果糖饮食(每天果糖摄入量少于20克)。研究持续了八周,通过血液测试测量了白细胞中线粒体DNA的数量,以评估线粒体的密度。结果显示,仅仅实行低钠饮食就能在第八周时观察到线粒体DNA的增加,而低钠低果糖饮食组的线粒体DNA增加了70倍。研究提出,这种饮食方式通过减少氧化应激来保护线粒体,从而促进了线粒体的生成和存活。此外,研究还发现低钠低果糖饮食显著降低了氧化应激标志物dnph的水平,以及降低了尿酸水平,这与减少果糖摄入有关,因为果糖会直接提高尿酸水平。

10:06

🔬 低钠低果糖饮食与线粒体健康

Dr. David Perlmutter强调了尿酸作为氧化应激的引发因素,能够损害线粒体、影响细胞功能、增加炎症、影响一氧化氮的产生,进而影响血液供应和胰岛素敏感性。他指出,高钠和高果糖饮食会导致尿酸水平升高,这是线粒体受损的下游效应。通过八周的低钠低果糖饮食,观察到线粒体DNA在白细胞中显著增加,这表明了线粒体密度的增加。他提出,我们应采取行动帮助线粒体工作、促进线粒体再生、增强线粒体生物合成,并清除有缺陷的线粒体,这是自噬过程的一部分。最后,他总结了低钠低果糖饮食在减少氧化应激和增加线粒体密度方面的积极效果。

Mindmap

Keywords

💡线粒体

线粒体是细胞内的能量生产者,被称为细胞的‘动力工厂’。在视频中,线粒体被强调为细胞功能和健康的关键因素,尤其是在脑细胞中,每个神经元可能含有多达一千个线粒体。线粒体的功能与数量对于维持有效的免疫功能和平衡炎症至关重要。

💡能量消耗

能量消耗在视频中被用来描述线粒体在细胞内的作用,即产生能量。大脑是一个能量消耗大的器官,尽管只占身体总重量的3-5%,但在休息状态下可能消耗整个身体25%的热量。因此,大脑高度依赖于线粒体的功能。

💡线粒体功能障碍

线粒体功能障碍是指线粒体出现问题,这在视频中被提到是一些普遍问题的核心,如癌症和冠状动脉疾病。线粒体功能障碍与多种退行性疾病,包括阿尔茨海默病有关,这些疾病与线粒体的生物合成和功能密切相关。

💡线粒体生物合成

线粒体生物合成是指增加可用于能量生产的线粒体数量的过程。视频中提到,通过低果糖和低钠饮食可以增加线粒体密度,这是通过测量白细胞中的线粒体DNA来评估的。

💡氧化应激

氧化应激是指由自由基引起的细胞损伤。在视频中,氧化应激与线粒体的损伤和功能障碍有关,而低钠低果糖饮食可以降低氧化应激,从而保护线粒体。

💡果糖

果糖是一种简单的糖,视频中提到高果糖摄入与线粒体功能障碍有关。低果糖饮食有助于减少氧化应激,增加线粒体密度,从而改善线粒体功能。

💡

钠是饮食中的一种电解质,视频中提到高钠摄入与线粒体功能障碍有关。低钠饮食有助于减少氧化应激,增加线粒体密度,对维持线粒体健康有积极作用。

💡尿酸

尿酸是体内的一种代谢产物,视频中提到高尿酸水平与氧化应激和线粒体损伤有关。低钠低果糖饮食可以降低尿酸水平,减少对线粒体的损害。

💡自噬作用

自噬作用是细胞清除和回收受损或不需要的组分的过程。视频中提到,通过自噬作用可以清除有缺陷的线粒体,这是维持线粒体健康和功能的重要机制。

💡线粒体DNA

线粒体DNA是存在于线粒体内的遗传物质,与细胞核DNA不同。视频中提到,通过测量白细胞中的线粒体DNA可以作为评估全身线粒体数量和功能的代理标志。

Highlights

线粒体是细胞内的能量生产者,被称为细胞的发电厂。

大脑中的神经元可能每个含有多达一千个线粒体。

线粒体功能良好对于有效的免疫功能和平衡炎症至关重要。

线粒体功能障碍与癌症、冠状动脉疾病等严重健康问题有关。

大脑是能量消耗大户,尽管只占体重的3-5%,却可能消耗25%的能量。

线粒体功能对于大脑的能量供应至关重要。

增强线粒体生物生成是提升能量生产的关键。

通过检测红细胞中的线粒体DNA水平可以评估线粒体数量。

研究发现低果糖和低钠饮食可以增加线粒体密度。

线粒体功能障碍是肥胖、糖尿病和高血压等健康问题的主要风险因素。

线粒体功能受损可能导致脂肪生成,这在食物稀缺时是一种生存机制。

研究显示,低钠和低果糖饮食可以显著增加线粒体DNA的数量。

低钠和低果糖饮食可以减少氧化应激,保护线粒体。

氧化应激水平的降低与线粒体密度的增加有关。

低钠低果糖饮食可以减少氧化应激标志物dnph的水平。

低钠低果糖饮食可以降低尿酸水平,减少线粒体损伤。

低钠和低果糖饮食有助于促进线粒体的再生和清除缺陷线粒体。

降低饮食中的钠和果糖可以减少尿酸的产生,减少氧化应激。

研究发现,低钠和低果糖饮食八周后,线粒体DNA在白细胞中的数量增加了70倍。

Transcripts

play00:04

foreign

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Dr David Perlmutter here we're going to

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talk about mitochondria today

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mitochondria you know the energy

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producers the powerhouses within every

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cell brain cells may have as many as a

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thousand mitochondria in each Neuron a

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mitochondria are seen diffusely

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throughout the body in virtually all of

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our cells interestingly not in our red

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blood cells but certainly in our white

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blood cells and having good

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mitochondrial function and numbers

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within our white blood cells is an

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important player as it relates to a

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proper effective immune function and

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keeping inflammation in Balance we know

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that mitochondrial dysfunction or

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problems with the mitochondria is

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something that's at the the core of some

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of our most pervasive issues like cancer

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and coronary artery disease

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cardiovascular disease in general and

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certainly as it relates to the brain and

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things like dementia the brain is a very

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energy hungry or organ the brain weighs

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what three to five percent of the total

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body weight and yet at rest may be

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consuming as much as 25 percent of the

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caloric expenditure of the entire body

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so the brain does use a lot of energy

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and as such it is highly dependent upon

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functionality of the mitochondria so the

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question that becomes how can we enhance

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mitochondrial biogenesis what a great

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term that is it simply means what can we

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do to increase the number of

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mitochondria that are available for

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energy production and one of the

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simplest measurements that can be done

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to look at mitochondria involves looking

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at the levels of mitochondria within the

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red blood cells it's a simple blood draw

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and then you evaluate actually the DNA

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mitochondrial DNA which is different

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from the normal cellular DNA that lives

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in the white blood cells that gives you

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an indication as to how many

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mitochondria are present within our

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white blood cells and it does serve as a

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surrogate marker for us to make

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Assessments in terms of what

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mitochondria are doing throughout the

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rest of the body

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so as it turns out there is research

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that demonstrates

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that we can in fact increase our

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mitochondrial density in this case

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measured in the white blood cells and

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this was an interesting study that

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looked at the effect of a low fructose

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and low sodium diet on the DNA that was

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measured of mitochondria in white blood

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cells in human subjects and again it's

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really very important at least in this

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study they recognize the importance of

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dysfunction or problems with the

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mitochondria as being a major risk

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factor in things like obesity diabetes

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and hypertension and because it is

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related to obesity diabetes and

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hypertension we then know that it is

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related to the downstream issues that

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are consequences of obesity and diabetes

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and hypertension things like coronary

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artery disease Alzheimer's disease and

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even cancer are the downstream

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manifestations or bro brought about when

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these mechanisms are activated so we've

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connected some dots then between

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mitochondrial dysfunction and some of

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the most important degenerative

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conditions on the planet things like

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heart disease and cancer and stroke for

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example and certainly Alzheimer's

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disease so I'd like to consider the

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statement however from a different

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perspective from the perspective of down

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regulating mitochondria making

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mitochondria less functional and how

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that may have acted as what we call a

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survival mechanism so when we have high

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levels of fructose and or high levels of

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sodium in the diet it really primes the

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body or at least the bodies of our

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ancestors for survival

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by down regulating or making less

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functional the mitochondria why because

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when mitochondria are less functional we

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have less energy utilization and that

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can be a really powerful Advantage when

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there's not a lot of food around so if

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the mitochondria are not burning as much

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energy it might allow survival when the

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very energy that it would burn is less

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abundant and in addition we know that

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when mitochondrial function is

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compromised it leads to the generation

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of fat and that of course can be a

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survival mechanism now let's look at the

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nuts and bolts of the study it looked at

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36 overweight

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pre-hypertensive adults and put them on

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either a low sodium defined as less than

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or equal to six grams a day or an

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isocaloric meaning the same number of

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calories low sodium and low fructose

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meaning less than 20 grams a day of the

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fructose diet and followed these

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individuals for eight weeks and compared

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them to controls and it looked at the

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measurement of how much DNA related to

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mitochondria was seen in the blood test

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which looked at the white blood cells in

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a normal blood test and the study went

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on for an eight week period of time

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again comparing a low sodium diet

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to a low sodium and low fructose diet

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and what did they find

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they found that with time just putting

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them on a low sodium diet led to a at

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week eight you see in the amber color

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already the mitochondrial DNA is

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starting to tick up and when you compare

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that on in week eight to being on low

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sodium and cutting down the fructose to

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20 grams a day a dramatic increase a 70

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fold increase in the mitochondrial DNA

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basically the number of mitochondria in

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the white blood cells that are present

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now because we're sending less alarm

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signals to our bodies to make fat store

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fat and to ratchet down mitochondrial

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function now the authors of the study

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proposed a mechanism and that is that

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the mechanism for protection

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could relate in other words how did it

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protect against damaging uh the

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mitochondria to decreasing oxidative

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stress as changes in oxidants parallel

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the changes in mitochondrial density

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what does that mean higher levels of

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oxidative stress threaten the viability

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the life the number of mitochondria when

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you put people on a low sodium low

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fructose diet you're putting them on a

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lower threat a lower oxidative stress

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level as it relates to their

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mitochondria so more mitochondria are

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created and these mitochondria survive

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that's what we want what they noted in

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the low sodium low fructose group this

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gets a little technical but they loaded

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that they noted that the level of

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something called dnph

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dinitrophenylhydrazine was decreased by

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52 percent now that sounds pretty

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scientific let me tell you what that

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means that's a marker of oxidative

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stress that's a marker of the damaging

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action of chemicals called free radicals

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it's the reason we take antioxidants in

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addition and that number went down quite

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dramatically the uric acid level went

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down by 22 percent in people who are on

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a low sodium low fructose diet why might

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that be well fructose directly raises

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uric acid and sodium raises uric acid a

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little bit indirectly because it

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increases the conversion of glucose into

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fructose which then raises uric acid

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that's called the polyol pathway so this

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is really quite a fascinating study that

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demonstrates by lowering sodium and

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reducing fructose consumption there is a

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dramatic effect upon the number of

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mitochondria and therefore mitochondrial

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function as we see with less oxidative

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stress demonstrated by the reduction in

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the dnph

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that was an interesting study wasn't it

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showed that low sodium and a low

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fructose diet combined after the eight

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weeks was associated with a dramatic

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increase in mitochondrial density as

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measured Again by the amount of

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mitochondrial DNA that was found in the

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white blood cells again a surrogate

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marker basically for DNA of the

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mitochondria throughout the body and

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therefore mitochondria throughout the

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body we want to do what we can to help

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our mitochondria work help them

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repopulate help them regrow enhance what

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I mentioned earlier called mitochondrial

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biogenesis meaning the growth of new

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mitochondria and at the same time rid

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our bodies of defective mitochondria

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which is something called

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mitophagy part of what the broader term

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autophagy and here we've learned that a

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low sodium low fructose diet is really

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effective in doing that and I think you

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know the area that is United by low

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fructose in low sodium the mechanism

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that they share is of course this

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Downstream production of uric acid so we

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are Upstream of uric acid we know that

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uric acid is a an instigator of

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oxidative stress can damage mitochondria

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can compromise cellular function can

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increase inflammation can compromise

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nitric oxide therefore lead to poor

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blood supply and at the same time a

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compromises insulin sensitivity so the

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downstream effects of higher levels of

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sodium in the diet and higher levels of

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fructose in the diet is an elevation of

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the uric acid and this was a a very

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dramatic demonstration a 70 fold

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increase in after eight weeks of the

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mitochondrial DNA in the white blood

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cells very interesting information and I

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think for many of you this will be quite

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thought provoking hope you enjoyed our

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time together today I did thanks for

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joining me I'm Dr David Perlmutter bye

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for now

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