湯偉晉在北投石牌郵局的銀行帳號 & QR code of text - 湯偉晉在北投石牌郵局的帳號_2018-0515_

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2020-07-27
帳號_石牌郵局_湯偉晉_2012_
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戶名
湯偉晉
台北市北投區石牌郵局
郵局的代號
700
存簿的局號
000-2336-029-4402
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Understanding the Functional Medicine Matrix; by Mark Hyman, MD_2019-1227_

Understanding the Functional Medicine Matrix; by Mark Hyman, MD_2019-1227_

 

In Functional Medicine, we take a different perspective of the human body, looking at the interconnectedness between every system. The Functional Medicine matrix is our framework to do that. This is a lens that helps us look at all the body’s systems, symptoms, and risk factors and see the story they tell about why you got sick and how to get better. It connects the dots between all your symptoms. Using a foundation like this matrix, we can see that two people might have the same symptoms with very different root causes or vice versa. The reason Functional Medicine is so powerful is that it looks at the individual; it accounts for the unique subtleties in all of our bodies and where they each need support. Specifically, the matrix works of a series of biological systems we call nodes: defense and repair, energy, biotransformation and elimination, transport, communication, structural integrity, and assimilation. These categories help us do the detective work in an organized way, pin down the problems, and take the most effective treatment route. It also takes a deep look at each patient’s story. This means identifying family history, triggering events, and lifestyle choices that have either mediated or perpetuated their condition. Emotional, spiritual, and mental status are also an equally important part for us to get the full picture. Considering how comprehensive this approach to medicine is, it’s not surprising that studies have found it can improve patient health outcomes and sustain them more so than conventional medical methods. Practicing Functional Medicine and seeing the incredible outcomes my patients have has given me the most meaningful career I could ask for. And I’m not the only one that feels this way.  If you missed last week’s episode of The Doctor’s Farmacy, I sat down with fellow Functional Medicine doctor and my colleague at The UltraWellness Center, George Papanicolaou to talk about how life-changing Functional Medicine has been for us. We discuss what it means to use the Functional Medicine matrix and share some of our favorite patient success stories. Dr. Papanicolaou shares some of his family’s personal health journey— helping his daughter overcome extreme fatigue and healing his own traumatic brain injury—using the power of Functional Medicine. We also dig into the topics of small intestinal bacterial overgrowth, the gut-brain connection, hormonal imbalances, and so much more. I hope you’ll tune in. Wishing you health and happiness, Mark Hyman, MD

Professional medical papers related to cysteine or glutathione;_WJD_2017-1023_V001R01_IR00_

Professional medical papers related to cysteine or glutathione;_WJD_2017-1023_V001R01_IR00_

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Oxidative stress and ageing： is ageing a cysteine deficiency syndrome？ [2005];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569588/

(e) Everybody is likely to experience a cysteine deficiency sooner or later

As everybody beyond the fifth decade of life will experience sooner or later a decrease in muscle function, a decrease in immune function, a decrease in plasma albumin concentration, and/or an increase in TNF-α concentration, it is hypothesized that practically everybody experiences sooner or later an ageing-related deficit in the body cysteine and glutathione reservoirs that warrants cysteine supplementation. This hypothesis implies that ageing may be postponed and frailty be avoided to some extent by supplementation of the ‘paravitamin’ cysteine. It is emphasized, however, that several details still require more systematic investigation. Although substantial negative side effects have not been observed in previous studies on cysteine supplementation, it is felt that the treatment protocols ought to be further improved to achieve maximum safety and efficacy over long periods of time. Properly done, cysteine supplementation can reasonably be expected to improve the quality of life in old age. With the availability of novel cysteine delivery systems with minimum amounts of calories, which are superior to any of the naturally available cysteine sources, it is conceivable that even the maximum human life span may be increased beyond the previous limit.

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Elevation of Glutathione as a Therapeutic Strategy in Alzheimer Disease [2011];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277671/

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Glutathione Synthesis Is Diminished in Patients With Uncontrolled Diabetes and Restored by Dietary Supplementation With Cysteine and Glycine [2010];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005481/

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Crosstalk between cystine and glutathione is critical for the regulation of amino acid signaling pathways and ferroptosis [2016];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.nature.com/articles/srep30033?WT.feed_name=subjects_nutrient-signalling

The ability of cells to sense and respond to nutrient availability is critical for cell survival. It is well-established that essential amino acids are required for the regulation of protein translation and growth. Although cysteine is not considered an essential amino acid, cysteine deficiency is associated with various diseases including metabolic disorders, immune dysfunction, and cancer.

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Zinc-Binding Cysteines: Diverse Functions and Structural Motifs [2014];_WJD_2017-1016_V001R01_IR93_

Source (資訊來源):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101490/

Info cited on 2017-10-16-WD1 (資訊引用於 中華民國106年10月16日) by 湯偉晉 (WeiJin Tang)

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Cysteine residues are known to perform essential functions within proteins, including binding to various metal ions. In particular, cysteine residues can display high affinity toward zinc ions (Zn2+), and these resulting Zn2+-cysteine complexes are critical mediators of protein structure, catalysis and regulation.

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Glutathione： a molecular whistleblower for Alzheimer’s disease [2015];_WJD_2017-1013_V001R01_IR93_

Source (資訊來源):

https://atlasofscience.org/glutathione-a-molecular-whistleblower-for-alzheimers-disease/

Info cited on 2017-10-13-WD5 (資訊引用於 中華民國106年10月13日) by 湯偉晉 (WeiJin Tang)

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Depletion of reduced glutathione, ascorbic acid, vitamin E and antioxidant defence enzymes in a healing cutaneous wound. [1997];_WJD_2017-1023_V001R01_IR92_

Source (資訊來源):

https://www.ncbi.nlm.nih.gov/pubmed/9257121

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DNA recognition by Cys2His2 zinc finger proteins. [2000];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.ncbi.nlm.nih.gov/pubmed/10940247/

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Endogenous Glutathione Conjugates： Occurrence and Biological Functions [1998];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

http://pharmrev.aspetjournals.org/content/50/3/335

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The role of glutathione in copper metabolism and toxicity. [1989];_WJD_2017-1023_V001R01_IR92_

Source (資訊來源):

http://www.jbc.org/content/264/10/5598.full.pdf

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Central nervous system uptake of intranasal glutathione in Parkinson’s disease [2016];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.nature.com/articles/npjparkd20162

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Neuroprotection against neuroblastoma cell death induced by depletion of mitochondrial glutathione [2013];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

http://pubmedcentralcanada.ca/pmcc/articles/PMC3645366/

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Mitochondrial glutathione pool is vital in protecting cells against oxidative stress as the majority of the cellular reactive oxygen species are generated in mitochondria. Oxidative stress is implicated as a causative factor in neuronal death in neurodegenerative disorders. We hypothesized that depletion of mitochondrial glutathione leads to mitochondrial dysfunction and apoptotic death of SK-N-SH (human neuroblastoma) cells and investigated the neuroprotective strategies against GSH depletion.

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Our data suggest that depletion of mitochondrial glutathione leads to mitochondrial dysfunction and apoptosis. The study indicates that preventing mitochondrial glutathione depletion could become a novel strategy for the development of neuroprotective therapeutics in neurodegenerative disorders.

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Glutathione as a Redox Biomarker in Mitochondrial Disease—Implications for Therapy [2017];_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

http://www.mdpi.com/2077-0383/6/5/50/htm

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2017-10-23

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Glutathione in Parkinson's Disease [2016]; Ph.D. dissertation, University of Washington_WJD_2017-1023_V001R01_IR93_

Source (資訊來源):

https://www.google.com.tw/url?sa=t&rct=j&q=&esrc=s&source=web&cd=6&ved=0ahUKEwjb5dCVhobXAhXCJJQKHR2zBZgQFghPMAU&url=https%3A%2F%2Fdigital.lib.washington.edu%2Fresearchworks%2Fbitstream%2Fhandle%2F1773%2F36458%2FMischley_washington_0250E_15659.pdf&usg=AOvVaw0p5rvyvaXtStxbVseWRUth

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知識性的教材_湯偉晉_2016-0815_{服用 智慧風華 時，應該遵守的一般性原則。}_V001R01_

知識性的教材_湯偉晉_2016-0815_{服用 智慧風華 時，應該遵守的一般性原則。}_V001R01_

西元2016年8月15日星期一

服用 智慧風華 時，應該遵守的一般性原則。

如果你的身體偏離正常的情況已經比較遠了，那麼在開始服用 智慧風華 的時候，最初的劑量不可以立刻就用很高的劑量，要逐漸緩慢地上升。例如從每天一顆開始，兩個禮拜之後再升高到兩顆。最高可以升高到4顆，也就是正常建議劑量的兩倍劑量。

因為智慧風華的成分都是身體本來就需要的營養素，所以每天兩倍的劑量也是很安全的。

每天需要補充幾顆，其實是供給和需求的問題。每一個人當下的情況不同，也因此每一個人需要的劑量也不盡相同，實際的需求甚至會隨著身體當時的狀況而改變。所以服用智慧風華的人，應該要養成觀察自己身體的習慣。這樣才能夠更精確地知道，自己每天大約需要服用幾顆智慧風華。我們努力的目標是，希望紅血球內部的穀胱甘肽之濃度，不要隨著年齡的增長而一直下降。因為紅血球內部的穀胱甘肽 會隨著年齡的增長而逐漸下降，是一種非常普遍的現象。這一個事實也解釋了，為什麼每一個人都會老，都會死。從科學上我們已經非常清楚地知道，當一個細胞內部的穀胱甘肽之濃度一直在下降的時候，本來就存在細胞中的 細胞凋亡(apoptosis) 的機制就會被啟動。也就是說，這一個細胞就會試著開始自我毀滅，以便不要讓自己成為附近其他細胞的負擔。試著把穀胱甘肽的濃度維持在年輕細胞的水平，是一件很重要的事情。

如果你的情況是屬於，會有生命危險的情況，也就是說你的健康情況非常糟。在這種情況下，最好要事先跟我諮詢一下。因為在這樣的情況之下，你很有可能也需要同時搭配其他的營養素。

智慧風華所提供的營養素，是在營養金字塔最底層的東西。但是想要維持身體的健康，每一個層次的營養素都是需要的。當然每一種營養素所需要補充的量，並不見得相同。同樣地，需要補充哪一種營養素的時機，也往往不一樣，必須要斟酌身體當時的狀況而定。

智慧風華 裡面的 半胱胺酸 是構成蛋白質、抗體，以及 穀胱甘肽 的主要原料。因此它在維護身體健康上，扮演著非常重要的角色。透過穀胱甘肽、蛋白質以及抗體，分別在不同層次的運作，半胱胺酸深遠地影響著，人類的身體在各個方面的健康。

湯偉晉 親筆寫於
中華民國105年8月15日
星期一台北時間上午11點25分

備註：
智慧風華膠囊的另外兩種成分也是非常重要，但是限於篇幅就不在此詳述了。

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知識性的教材_湯偉晉_2016-0815_{服用 智慧風華 時，應該遵守的一般性原則。}_V001R01_IR90_.png




知識性的教材_湯偉晉_2016-0815_{服用 智慧風華 時，應該遵守的一般性原則。}_V001R01_IR90_.png

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Estrogen's Role in Cancer [2003](IR93); oxidative stress, oxygen

Estrogen's Role in Cancer [2003](IR93); oxidative stress, oxygen

Oxidative activation of antioxidant defence [2005](IR93); Germany; glutathione, cysteine, rely on a powerful sulfur redox chemistry - The parallel GSH- and thioredoxin (Trx)-centred antioxidant pathways

Oxidative activation of antioxidant defence [2005](IR93); Germany; glutathione, cysteine, rely on a powerful sulfur redox chemistry - cover page.png

Oxidative activation of antioxidant defence [2005](IR93); Germany; glutathione, cysteine, rely on a powerful sulfur redox chemistry - The parallel GSH- and thioredoxin (Trx)-centred antioxidant pathways.png

Oxidative activation of antioxidant defence [2005](IR93); Germany; glutathione, cysteine, rely on a powerful sulfur redox chemistry - Oxidation states of cysteine during oxidative modification.png

Oxidation states of cysteine during oxidative modification

Figure saved by WeiJin Tang (湯偉晉) on [2015-08-11]

Glutathione Synthesis Is Diminished in Patients With Uncontrolled Diabetes and Restored by Dietary Supplementation With Cysteine and Glycine [2010](IR93)

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(Memo Item created on February 12, 2013 01:29 PM)
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Glutathione Synthesis Is Diminished in Patients With Uncontrolled Diabetes and Restored by Dietary Supplementation With Cysteine and Glycine [2010](IR93) - full text

http://care.diabetesjournals.org/content/34/1/162.full
http://www.ncbi.nlm.nih.gov/pubmed/20929994

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Published online before print October 7, 2010, doi: 10.2337/dc10-1006 Diabetes Care January 2011 vol. 34 no. 1 162-167

Glutathione Synthesis Is Diminished in Patients With Uncontrolled Diabetes and Restored by Dietary Supplementation With Cysteine and Glycine

Rajagopal V. Sekhar, MD1,2, Siripoom V. McKay, MD3,4, Sanjeet G. Patel, MD1,2, Anuradha P. Guthikonda, MD1,2, Vasumathi T. Reddy, PHD1,2, Ashok Balasubramanyam, MD1,2 and
Farook Jahoor, PHD3,4

- Author Affiliations

1Translational Metabolism Unit, Baylor College of Medicine, Houston, Texas; 2Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, Texas; 3Department of Pediatrics, Baylor College of Medicine, Houston, Texas; 4Children's Nutrition Research Center, Agriculture Research Service, U.S. Department of Agriculture, Baylor College of Medicine, Houston, Texas. Corresponding author: Rajagopal V. Sekhar, rsekhar@bcm.edu.

Abstract

OBJECTIVE
Sustained hyperglycemia (高血糖血症) is associated with low cellular levels of the antioxidant glutathione (GSH), which leads to tissue damage attributed to oxidative stress. We tested the hypothesis that diminished GSH in adult patients with uncontrolled type 2 diabetes is attributed to decreased synthesis and measured the effect of dietary supplementation with its precursors cysteine and glycine on GSH synthesis rate and oxidative stress.

RESEARCH DESIGN AND METHODS
We infused 12 diabetic patients and 12 nondiabetic control subjects with [2H2]-glycine to measure GSH synthesis. We also measured intracellular GSH concentrations, reactive oxygen metabolites, and lipid peroxides. Diabetic patients were restudied after 2 weeks of dietary supplementation with the GSH precursors cysteine and glycine.

RESULTS
Compared with control subjects, diabetic subjects had significantly higher fasting glucose (5.0 ± 0.1 vs. 10.7 ± 0.5 mmol/l; P < 0.001), lower erythrocyte concentrations of glycine (514.7 ± 33.1 vs. 403.2 ± 18.2 μmol/l; P < 0.01), and cysteine (25.2 ± 1.5 vs. 17.8 ± 1.5 μmol/l; P < 0.01); lower concentrations of GSH (6.75 ± 0.47 vs. 1.65 ± 0.16 μmol/g Hb; P < 0.001); diminished fractional (79.21 ± 5.75 vs. 44.86 ± 2.87%/day; P < 0.001) and absolute (5.26 ± 0.61 vs. 0.74 ± 0.10 μmol/g Hb/day; P < 0.001) GSH synthesis rates; and higher reactive oxygen metabolites (286 ± 10 vs. 403 ± 11 Carratelli units [UCarr]; P < 0.001) and lipid peroxides (2.6 ± 0.4 vs. 10.8 ± 1.2 pg/ml; P < 0.001). Following dietary supplementation in diabetic subjects, GSH synthesis and concentrations increased significantly and plasma oxidative stress and lipid peroxides decreased significantly.

CONCLUSIONS
Patients with uncontrolled type 2 diabetes have severely deficient synthesis of glutathione attributed to limited precursor availability. Dietary supplementation with GSH precursor amino acids can restore GSH synthesis and lower oxidative stress and oxidant damage in the face of persistent hyperglycemia (高血糖血症).

Diabetes is the leading worldwide cause of blindness (失明), end-stage renal disease (終末期腎臟疾病), and amputations (截肢). Diabetes also is associated with an elevated risk of macrovascular complications including myocardial ischemia and strokes. Although multiple pathways are involved in mediating tissue damage, including the polyol pathway, advanced glycation end product formation, protein kinase C activation, and the hexosamine pathway, a common feature is increased oxidative stress marked by elevated levels of reactive oxygen species (ROS) (1). The ability of a cell to resist damage caused by oxidative stress is determined by the capacity of an array of antioxidant defense systems, among which reduced glutathione (GSH) is the most ubiquitous and abundantly available within human cells. GSH is a tripeptide synthesized from glutamate, cysteine, and glycine in two steps catalyzed by γ-l-glutamyl-l-cysteine:glycine ligase and glutathione synthetase. Diabetes is associated with decreased cellular glutathione concentrations (2–5), but the cause of GSH deficiency currently is unknown. Oxidative stress and ROS formation are markedly increased by uncontrolled hyperglycemia (高血糖血症) (2,6); conversely, lowering blood glucose concentrations lowers oxidative stress (7,8). Decreased oxidative stress could be an important mechanism whereby glycemic control diminishes the incidence of diabetic microvascular complications (9,10). However, there are practical limitations to blunting oxidative stress through glycemic control alone, despite strenuous attempts to implement evidence-based guidelines, a majority of patients are unable to achieve the glycemic goals (e.g., A1C <7 advocated="" american="" and="" as="" association="" blindness="" by="" cause="" clear="" complications="" consequently="" control="" despite="" diabetes="" excellent="" for="" glycemic="" landmark="" leading="" message="" need="" of="" prospective="" regarding="" remains="" span="" study="" such="" the="" trial="" trials="" uk="">失明), renal failure, and amputations (截肢). There is an urgent need for novel strategies to reduce the rate of diabetes complications in patients unable to achieve stable glycemic control. We therefore investigated whether oxidative stress associated with low levels of GSH could be ameliorated through the alternative strategy of increasing cellular GSH levels in diabetic patients with uncontrolled hyperglycemia (高血糖血症). Because circulating concentrations of a protein depend on the balance between its rates of production and consumption, we hypothesized that GSH deficiency in uncontrolled diabetes occurs because of diminished synthesis. We further hypothesized that short-term dietary supplementation of two key amino acid precursors of GSH, glycine and cysteine, would increase intracellular GSH synthesis and concentrations and thus lower oxidative stress, despite continuing hyperglycemia (高血糖血症). To test these hypotheses, we used stable isotope (同位素) methods to compare GSH synthesis rates and concentrations within erythrocytes, as well as plasma markers of oxidant damage, in adult patients with poorly controlled type 2 diabetes matched to nondiabetic control subjects. The diabetic patients were studied before and after 14 days of dietary supplementation with cysteine and glycine.

RESEARCH DESIGN AND METHODS

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教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}[2013-10-26-WD6]

教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}[2012-10-26-WD5]

教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}

演講的題目:
生老病死的秘密 - 從科學的觀點切入
The Secret of Life and Death – A Scientific Approach

引言人的姓名:
余儀呈 醫師先生, 芝山診所, 台北市士林區天母生活圈, 前台北榮民總醫院 家庭醫學科 主治醫師

主講人的姓名:
湯偉晉 先生, 總經理, 湯生科技股份有限公司
國際扶輪3520地區台北永康扶輪社推薦的主講人

演講當天的日期和時間:
西元 2012-10-26 星期六 下午2點~下午4點

地點:
芝山生活家 (芝山診所的舊址)

芝山生活家的電話:
(02) 2836-9493 (星期一公休)

芝山生活家的地址:
台北市德行東路203巷2號

備註:
因為座位有限，所以如果您想參加，請務必事先預約報名。謝謝！

New test for mysterious metabolic diseases developed at Stanford/Packard [2009](IR91); FNKWs{glutathione, Stanford university}

New test for mysterious metabolic diseases developed at Stanford/Packard [2009](IR91); FNKWs{glutathione, Stanford university}

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(Memo Item created on July 10, 2013 02:53 PM)
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New test for mysterious metabolic diseases developed at Stanford/Packard [2009](IR91); FNKWs{glutathione, Stanford university}

http://med.stanford.edu/news_releases/2009/february/enns.html
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FEB. 9, 2009

PRINT MEDIA CONTACT
Erin Digitale | Tel (650) 724-9175
digitale@stanford.edu        BROADCAST MEDIA CONTACT
Robert Dicks | Tel (650) 497-8364
rdicks@lpch.org      
New test for mysterious metabolic diseases developed at Stanford/Packard
  4 212
BY ERIN DIGITALE

Related News

» Metabolic disorder found treatable, researcher says
» New Packard laboratory speeds diagnosis, treatment of genetic defects
STANFORD, Calif. —Scientists at Stanford University School of Medicine have devised a much-needed way to monitor and find treatments for a mysterious and devastating group of metabolic diseases that arise from mutations in cells' fuel-burning mechanism.

Mitochondrial disorders can cause organ failure, seizures, stroke-like episodes and premature death. The diseases—more than three dozen in total—arise from genetic errors of the mitochondria, the cell structures that process oxygen and turn food molecules into useable energy. Mitochondrial disorders affect one in 4,000 kids and one in 8,500 adults. They are difficult to diagnose, and no treatments or cures exist.

But that could soon change. A team at Stanford and Lucile Packard Children's Hospital has discovered a biological marker they can use to monitor the diseases. The finding will enable researchers to hunt for treatments and help physicians check patients' status before health crises erupt. The research was published online Feb. 9 in the Proceedings of the National Academy of Sciences.

"When a car engine doesn't work right, it smokes," said senior study author Greg Enns, MB, ChB, who is professor of pediatrics at Stanford University School of Medicine and director of the biochemical genetics program at Packard. "What we looked for is, in essence, biochemical smoke."

Like a car engine, when mitochondria are not burning fuel cleanly, they kick out nasty gunk. Defective mitochondria produce large quantities of oxygen free radicals—highly reactive molecules that damage DNA and cell structures. Comparing patients who have a mitochondrial disorder with healthy people in the control group, Enns' team searched for signs that free radicals overtax patients' natural antioxidant defense systems. And they found it.

"Even when these patients are coming into the clinic looking pretty healthy, they have evidence of extra metabolic stress," Enns said, noting the findings were surprising because none of the patients were in the midst of a health crisis such as organ failure when blood samples were taken. It is the first time such signs have been uniformly shown in the blood of patients across a wide range of mitochondrial disorders, he added.

The team saw that levels of glutathione, the body's primary antioxidant, were significantly reduced in white blood cells from the 20 mitochondrial disease patients in the study. The observation means patients' antioxidant defenses were indeed depleted. Glutathione was also diminished in nine patients with organic acidemias, another group of metabolic diseases that researchers think may be associated with aberrant mitochondrial function.

A second finding gave the researchers a big hint about where to hunt for treatments. Patients taking antioxidant supplements did not have depleted glutathione, they found. Scientists have long suspected antioxidants such as vitamin C and vitamin E might help patients with mitochondrial disease or organic acidemias, and doctors sometimes suggest the supplements to their patients. But no one has been able to test whether they work.

"As a clinician, one of the most frustrating things has been not being sure if supplements are doing any good," said Enns. "Now we're able to take a baseline blood reading and see 'before' and 'after' snapshots."

William Craigen, MD, PhD, the director of the metabolic clinic at Texas Children's Hospital, called this finding "the beginning of insight into the mechanisms of mitochondrial disease." Craigen, who is also medical director for the mitochondrial diagnostic lab at Baylor College of Medicine, was not involved in the Stanford study. "This new research provides an opportunity to start treating a heterogeneous group of diseases in a single fashion, with a simple and easy-to-administer treatment, potentially improving patients' long-term outcomes," he added.

Glutathione measurements could also help diagnose patients, Enns said, by giving physicians a clear indication that something is awry in the mitochondria. Genetic and molecular tests have already led to increases in the number of diagnoses, but the diagnosis is still difficult to pin down.

The method Enns' team used to measure glutathione, called high-dimensional flow cytometry, has limitations: it requires very fresh blood samples, uses expensive equipment only available in research labs, and provides relative rather than absolute glutathione measurements. Now that the team knows what metabolic change to look for, they're working to develop a more broadly applicable measurement technique.

And glutathione measurements could help scientists unravel other disease mysteries, too. "You name the disease, you can postulate mitochondrial involvement," Enns said. "It's been proposed for everything from poor vision to hearing loss, kidney disease, liver disease, autism spectrum disorders, diabetes, Alzheimer disease, cancers. Our work could lead to research on therapies for a broad range of disorders."

Enns collaborated with research associate Kondala Atkuri, PhD; associate professor of pathology Tina Cowan, PhD; professor emeritus of genetics Leonard Herzenberg, PhD; and research professor of genetics Leonore Herzenberg, PhD, who is also a member of the Stanford Cancer Center. The Herzenbergs have a financial interest in BioAdvantex, a company whose dietary supplement, PharmaNAC, is intended to increase glutathione levels. The study was funded by grants from the United Mitochondrial Disease Foundation, the Lucile Packard Children's Hospital Pediatric Health Research Fund and the Arline and Pete Harman Scholarship.

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The Stanford University School of Medicine consistently ranks among the nation's top 10 medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
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