Healthy Aging Care and Feeding of Mitochondria Fullscript ...€¦ · Mitochondrial function is a key to successful aging Progressive mitochondrial dysfunction is considered a hallmark

7/8/20

1

© American Institute of Integrative Oncology. All rights reserved.www.AIIORE.com

Healthy Aging: Care and Feeding of MitochondriaDr. Nalini Chilkov, L.Ac., O.M.D., [email protected]

1


Mitochondriaca scientist or clinician with a chronic and unusually intense interest in mitochondria

WARNING!!!!!!!

2

http://www.aiiore.com


7/8/20

2


Dr. Nalini Chilkov, L.Ac. OMD, [email protected]

BONUS RESOURCE : Download Dr. Chilkov’s Free

Mitochondrial Metabolism and Healthy Ketogenisis Guide

PLUS, Get Access to Mitochondrial Metabolism, Ketogenic Diets, Fasting and Cancer Webinar

CLICK HERE https://www.aiiore.com/fullscript2020

3


INTRODUCTION

4


https://www.aiiore.com/fullscript2020/


7/8/20

3


All cells, with the exception of red blood cells, contain mitochondria, organelles that produce adenosine triphosphate (ATP), the cellular “energy currency”, from adenosine diphosphate (ADP).

In addition, mitochondria are involved in many other processes within the body such as cell signaling and regulation of cellular metabolism. Mitochondrial energy metabolism is a critical part of cellular health and function, and influences overall health.

Optimal mitochondrial function depends on:

•Quenching of free radicals produced during normal electron transport chain (ETC) activity•Integrity of mitochondrial cell membranes•The transport of critical metabolites, such as fatty acids, into the mitochondria

5


Mitochondrial function is a key to successful aging

Progressive mitochondrial dysfunction is considered a hallmark of aging

Mitochondrial dysfunction leads to chronic diseases with organ involvement and heterogenous clinical manifestations

High energy demanding organs rich in mitochondria includeBrain, Myocardium, Skeletal Muscle, Liver, Kidney

6



7/8/20

4


Our mitochondria are the energy powerhouses of the cell.They could accurately be compared to armored nuclear power plants because they activate and safely contain (when healthy) the intense explosions required to cleave the high-energy bond betweentwo oxygen atoms. These oxygen-cleaving explosions would cause devastating, widespread oxidative damage (akin to a nuclear meltdown) if they occurred anywhere else in the body.

The key point here is that mitochondria are exponentially better at producing ATP… and any physiological process that causes mitochondrial dysfunction can cause widespread cellular energy deficits and fatigue, adversely affecting virtually all organ systems

Raffelock, D.: Mitochondrial dysfunction and physiological depression.Cap 6 in Integrative Therapies for Depression 2016, Greenblatt, JM., BroganK, editors CRC Press, Boca Raton, FL. Pgs 61 – 72.

7


Probability of Mitochondrial

DysfunctionIn Common Signs and

Symptoms of Disease

Mitochondria:Fundamental To Life And Death

Joe Pizzorno, ND.Integ Med Vol 13, No.2

April 2014

8



7/8/20

5


Common Symptoms of Mitochondropathies• Fatigue and Lethargy• Exercise Intolerance• Impaired sensory function (smell, taste, hearing, vison)• Chronic Pain Syndromes• Depression, Lack of Motivation• Cognitive compromise: memory, learning, executive

functions• Hypersensitivity to light, noise, movement• Impaired Detoxification function• Loss of Wellbeing• Loss of Resilience

9


Mitochondrial Function and Immune Response

Mitochondria comprise a key intracellular signaling platform regulating innate immune and inflammatory responses.

Sickness behavior seen in viral infections include cardinal symptoms of Mitochondrial Dysfunction and

Yang Deficiency Syndrome in Chinese Medicine:

• Loss of Energy• Loss of Motivation

• Fatigue and Lethargy• Hypersomnia

• Muscle weakness

10



7/8/20

6


https://ib.bioninja.com.au/higher-level/topic-8-metabolism-cell/untitled/mitochondria.html

11


doi: https://doi.org/10.1371/journal.pbio.3000095.g001

MULTIFUNCTIONAL MITOCHONDRIA

12


https://ib.bioninja.com.au/higher-level/topic-8-metabolism-cell/untitled/mitochondria.html


https://doi.org/10.1371/journal.pbio.3000095.g001

7/8/20

7


MECHANISMS OF MITOCHONDRIAL DYSFUNCTION

13


Mechanisms of Mitochondrial Dysfunction

Triggers• Stress & Upregulated HPA Axis• Environmental Toxins• Malnutrition & Nutrient Depletion• Inflammation • Oxidative Stress:

à Apoptosis & Cell Death

14



7/8/20

8


Mitochondrial Membrane Destruction

• Failure of Kreb’s Cycle, Electron Transport Chain and ATP Production

• Membrane Hyperpermeability and Depolarization• Oxidative Stress• Depletion of NAD• Release of Cytochrome C & Caspase into Cytosol

-> Apoptosis and Cell Death

Triggers à

15


Pharmaceuticals as Mitochondrial Toxins• Inhibit mDNA transcription of Electron Transport Chain

functional proteins

• Inhibit enzymes required for glycolysis and fatty acid beta oxidation

• Produce ROS and Oxidative Stress

• Deplete essential nutrients required for normal mitochondrial function

16



7/8/20

9


Mitochondrial Membrane DestructionMitochondrial Toxins

• Heavy Metals: Fe, Mn, Hg, Pb, Ars

• Plastics, PCB’s

• Pesticides, Herbicides, Glyphosate

• Dichlorobenzene

• Pharmaceuticals

• Mycotoxins

• Lactic Acid

• Ketones

• Lipofuscin

• Glutathione conjugates

• Organic Sulphates

• ROS Oxidative Stress

17


Mitochondrial dysfunction is at the basis of a

constellation of metabolic abnormalities

that significantly contribute to chronic

conditions and diseases.

Translational research : the journal of laboratory and clinical medicine 2013Translating the basic knowledge of mitochondrial functions to metabolic therapy: role of L-carnitine.Santica M Marcovina, Cesare R. Sirtori, +4 authors Hossein Ardehali

18



https://www.semanticscholar.org/paper/Translating-the-basic-knowledge-of-mitochondrial-to-Marcovina-Sirtori/139f16610ed07be74b9dca82d102486d8ae09ff9

https://www.semanticscholar.org/paper/Translating-the-basic-knowledge-of-mitochondrial-to-Marcovina-Sirtori/139f16610ed07be74b9dca82d102486d8ae09ff9

7/8/20

10


HORMESIS and AGING

Hormesis in aging is represented by mild stress-induced stimulation of protective mechanisms in cells and organisms resulting in biologically beneficial effects.

Single or multiple exposure to low doses of otherwise harmful agents, have a variety of anti-aging and longevity extending hormetic effects.

(such as irradiation, food limitation, heat stress, reactive oxygen species and other free radicals )

Review: Hormesis in aging Suresh I.S. Rattan, Ageing Research Reviews 7 (2008) 63–78

19


HOMEOPATHY

Similia Similibus CurenturLike Cures Like

the treatment of disease by minute dosesof natural substances that in a healthy person would

produce symptoms of disease.

20



7/8/20

11


Reconsidering the Role of

Mitochondria in Aging

Marta Gonzalez-Freire, et alBiol Sci Med Sci

2015. Nov;70(11):1334-42.doi: 10.1093/gerona/glv070.

21


MitochondriaOxidative StressandMitohormesis

22



7/8/20

12


Mitochondrial DNA (mtDNA)Highly Susceptible to Oxidative Damage:

In close proximity to free radicals in the electron transport chain

Lacks a protein scaffold

Insufficient DNA repair system

Lack of DNA Proteins (Histones)

23


MITOHORMESIS

• High levels of oxidative stress cause macromolecular damage

• Mild-redox agents prevent ROS production, improve mitochondrial function, and delay cellular aging and may prevent/delay mitochondria-driven disorders

• Low levels of ROS enhance an adaptive response of “mitohormesis” activating systemic defense systems, increasing stress resistance, extending life span, promoting longevity and healthy function

Biofactors. 2012 ; 38(2): 158–166. doi:10.1002/biof.197.Mitochondrial pharmacology: Electron transport chain bypass as strategies to treat mitochondrial dysfunction. Hani Atamna

24



7/8/20

13


MitoHormesis

Go, Young-Mi & Jones, Dean. (2017). Redox theory of aging: Implications for health and disease.Clinical Science. 131. 1669-1688. 10.1042/CS20160897

25


MITOCHONDRIAL DYSFUNCTION

Oxidative StressAging

Mitochondria deteriorate with age, losing respiratory

activity, accumulating damage to

their DNA (mtDNA), and producing excessive

amounts of reactive oxygen species (ROS).

Ralph Ryback, M.D.,

CancerImmune compromise

Macular degeneration

26



https://www.psychologytoday.com/us/basics/genetics

https://www.psychologytoday.com/us/experts/ralph-ryback-md

7/8/20

14


NORMAL APOPTOTIC SIGNALLINGin response toINCREASEDOXIDATIVE

STRESS

OXIDATIVE STRESS

CELL DEATH

27


Melatonin and Mitochondrial DysfunctionMelatonin (N-acetyl-5-methoxytryptamine)Neuro-hormone, Neuro-anti-oxidant, Mitochondrial antioxidant

Melatonin scavenges oxygen and nitrogen-based reactants generated in mitochondria

Melatonin mitigates harmful reduction in the mitochondrial membrane potential that may trigger mitochondrial transition pore (MTP) opening and the apoptotic cascade

Mitochondria are implicated in the intrinsic pathway of apoptosis

Melatonin mitigates mitochondrial malfunction.León J, Acuña-Castroviejo D, etalPineal Res. 2005 Jan;38(1):1-9. doi: 10.1111/j.1600-079X.2004.00181.x.PMID: 15617531 Review.

28



https://pubmed.ncbi.nlm.nih.gov/15617531/

7/8/20

15


Melatonin and Mitochondrial Dysfunction• Melatonin promotes mitochondrial homeostasis

• Preserves mitochondrial membrane integrity and function

• Protects against mitochondrial damage due to oxidative stress

• Inhibits cell death by apoptosis and necrosis due to ROS

• Direct scavenger of oxygen and nitrogen reactants

• Stimulates anti-oxidative enzymes

• Increases efficiency of Electron Transport Chain

• Limits electron leakage and free radical generation

• Promotes ATP synthesisLife Sci 2004 Jul 2;75(7):765-90.Melatonin and Mitochondrial FunctionJosefa Leon 1, et alPMID: 15183071 DOI: 10.1016/j.lfs.2004.03.003

29


Alpha-Lipoic-Acid and Mitochondrial Function

Ames BN. Optimal micronutrients delay mitochondrial decay and age-associated diseases.Mech Ageing Dev. 2010;131(7-8):473-479. doi:10.1016/j.mad.2010.04.005

Savitha S, Sivarajan K, Haripriya D, Kokilavani V, Panneerselvam C. Efficacy of levo carnitine and alpha lipoic acid in ameliorating the decline in mitochondrial enzymes during aging.Clin Nutr. 2005;24(5):794-800. doi:10.1016/j.clnu.2005.04.005

Both hydrophilic and lipophilic potent antioxidantIncreases Mitochondrial Glutathione and Vitamin C (Mitochondrial Resuscitation)Increases Mitochondrial Membrane PotentialIncreases ATP Synthesis

We observed that there was an age-dependent decrement in the levels of the TCA cycle enzymes and electron transport chain complexes. Supplementation of L-carnitine (300 mg/kg bw/day) and alpha-lipoic acid (100 mg/kg bw/day) for 30 days brought the activities of these enzymes to almost near normal levels.

30


https://pubmed.ncbi.nlm.nih.gov/%3Fterm=Leon+J&cauthor_id=15183071

https://pubmed.ncbi.nlm.nih.gov/15183071/

https://doi.org/10.1016/j.lfs.2004.03.003


7/8/20

16


Mitochondrial Dynamics

Mitochondrial Biogenesis

FissionFusionMitophagy

31


Mitochondrial Remodeling and Recycling:

Fission: Coordinated with DNA replication-> duplication and biogenesisStimulated by fuel and nutrient excess

Fusion: Mitochondria become interconnected . Damaged mitochondria acquire undamaged genetic material and maintain functionalityTriggered by nutrient deficiency

AGING is associated with upregulated fusion and inhibition of mitogenesis Cancer, Cardiovascular Disease, Neurodegenerative Disease

32



7/8/20

17


Mitochondrial Recycling

33


MITOPHAGY and AGE- RELATED PATHOLOGIES

Mitophagy: An

Emerging Role in

Aging and Age-

Associated Diseases

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7113588/pdf/fcell-08-00200.pdf

34





7/8/20

18


mTOR ( mammalian target of rapamycin) and AMPK (adenosine monophosphate activated

protein kinase) Control MitophagyMitophagy guarantees cell survival Mitophagy is the selective degradation of mitochondria by autophagyMitophagy has a key function in delaying aging and age-related disorders such as neurodegenerative disorders, cardiovascular pathologies, and cancer.Down-regulation of mTOR stimulates mitophagy

Autophagy is the natural, regulated mechanism of the cell that removes unnecessary or dysfunctional components. It allows the orderly degradation and recycling of cellular components. It is an an “Intracellular Recycling System”Upregulation of AMPK activates mitogenesis, oxidative metabolismOxidative Phosphorylation, Electron Transport Chain and resistance to oxidative stress

35


mTOR Inhibition, AMPK Promotion and Natural CompoundsmTOR Inhibition

CurcuminResveratrolQuercetinHonokiolRapamycinMetforminFastingCalorie Restriction

Jason Fung MDhttps://thefastingmethod.com/fasting-and-autophagy-mtor-autophagy-1/

AMPK Promotion

EGCG (Green Tea)ResveratrolGinsenoside Rg3Momordica charantia(Bitter Melon)Salicylic Acid(Willow bark)Indole-3-Carbinol+DIMTHC (Cannabis sat)Silibinin (Milk Thistle)Nicotinamide ribosideMetformin

Decreased Carcinogenesis

36



https://thefastingmethod.com/fasting-and-autophagy-mtor-autophagy-1/

https://thefastingmethod.com/fasting-and-autophagy-mtor-autophagy-1/

7/8/20

19


MITOGENESIS and Impaired in Aging

There must be a balance between mitophagy and mitogenesis

Transcriptional regulator PGC-1a stimulates mitochondrial biogenesisPGC-1a activity declines with age

PGC-1a interacts with NRF2 which controls response to oxidative stress

Decline in PGC-1a and NRF2 expression leads to increased apoptosis,mitophagy, decreased mitogenesis and increased damage by ROS

These processes are linked to sarcopenia and frailty in aging

37


Reconsidering the Role of Mitochondria in

Aging

Marta Gonzalez-Freire, Rafael De Cabo, Michel Bernier, Steven J. Sollott, Elisa Fabbri, Placido Navas, Luigi Ferrucci

J Gerontol A Biol Sci Med Sci2015. Nov;70(11):1334-42.doi:

10.1093/gerona/glv070.

38



7/8/20

20


ENHANCING MITOCHONDRIAL BIOGENESIS

Pyrilloquinone (PQQ)Activates PGC-1aWater soluble enzyme cofactorAntioxidant, neuroprotective, cardioprotectiveParsley, green tea, green peppers, kiwi, papaya

Rhodiola rosea (Hong Jing Tian)Enhances Lymphocyte MitogenesisActivates synthesis of ATP in mitochondriaPotent antioxidant, anti-inflammatoryNeuroprotective, Cardioprotective

39


Caloric Restriction, Caloric Restriction Mimicry,Mitophagy and Mitogenesis

Caloric RestrictionCoordinates Turnover(Autophagy and Mitophagy) AND MitogenesisCaloric Restriction Mimetics• Aspirin• Resveratrol• Urolithin A*• NADH• Rapamycin (inhibits mTOR)

Increasing evidence shows that mitophagy (by removing damaged mitochondria)is significantly involved in

counterbalancing age-related pathological conditions .

Thus, chronic stimulation of mitochondrial turnover

by enhancing mitophagy is a promising approach

to delay age-related diseases and to extend health- and

lifespan.*Urolithin A is a metabolite compound resulting from the transformation of ellagitannins (strawberries, raspberries, walnuts, pomegranate) by the gut bacteria.

Mitophagy: An Emerging Role in Aging and Age-Associated DiseasesFront Cell Dev Biol 2020 Mar 26;8:200. doi: 10.3389/fcell.2020.00200.

40



7/8/20

21


Every Morning. I think about going

for a long walk.

At least my brain is getting some

exercise

41


Exercise & Mitogenesis

Moderate Intensity Exercise stimulates mitogenesisA combination of aerobic and anaerobic exercise is most effective

Lumini JA, Magalhães J, Oliveira PJ, Ascensão A. Beneficial effects of exercise on muscle mitochondrial function in diabetes mellitus. Sports Med. 2008;38(9):735-750. doi:10.2165/00007256-200838090-00003

There is evidence that chronic exercise and lifestyle interventions reverse impairments in mitochondrial density and size, in the activity of respiratory chain complexes and in cardiolipin content

42



7/8/20

22


MITOCHONDRIAL PROTEOSTASIS

ProteinMisfolding

43


Mitochondrial Proteostasis and AgingMany age related neurodegenerative diseases such as

Parkinson’s and Alzheimers and degenerative Cardiac Amyloidosis involve

accumulation of misfolded proteins in the endoplasmic reticulum and the mitochondria

Impairment of the ubiquitin-proteasome system is associated, protein oxidative damage

and an imbalance of proteostasisMitochondrial-Specific Unfolded Protein Response (MUPR)

is a mechanism that attempts to restore proteostasis

44



7/8/20

23


Augmenting mitochondrial stress signaling by Enhancing NAD+ Levels may

Activate the Mitochondrial-Specific Unfolded Protein Response (MUPR)

and promote longevityNicotinamide Ribonucleoside

Stablized Oral NADH and IV NADH

(more effective combined with Resveratrol)

45


MITOCHONDRIAL MEMBRANE LIPID COMPOSITION

46



7/8/20

24


Phospholipids are the constituents of the inner and outer mitochondrial membranesMitochondrial Associated Membranes of the endoplasmic reticulum and mitochondria contain important signaling site for apoptosis, autophagy, Ca++ transport, inflammation, lipid synthesis and multiple mitochondrial functions

Cardiolipin is a phospholipid exclusively found in the inner mitochondrial membraneand plays an important role in the organization and assembly of the Electron Transport Chain

Alteration of Electron Transport Chain assembly due to aging is associated with loss of Glutathione, cardiac failure and chronic fatigue

47


MEMBRANE LIPID REPLACEMENT THERAPY plus antioxidants & co-factors

Reduces age-related functional damage to mitochondrial membranes AND

Reduces adverse effects of oxidative chemotherapeutic agentsLipid Replacement Therapy

the use of functional oral supplements containing cell membrane phospholipids and antioxidants, has been used to replace damaged, usually oxidized, membrane glycerophospholipids that accumulate

during aging and in various clinical conditions in order to restore cellular function

Lipid Replacement Therapy: A natural medicine approach to replacing damaged lipids in cellular membranes and organelles and restoring function. Garth L.Nicolson, Michael E.Ash. https://doi.org/10.1016/j.bbamem.2013.11.010

48



https://www.sciencedirect.com/science/article/pii/S0005273613004070

https://doi.org/10.1016/j.bbamem.2013.11.010

7/8/20

25


MEMBRANE LIPID REPLACEMENT THERAPY plus antioxidants & co-factors

Mitohondrial CO FACTORS

CoQ10Vitamin EAlpha Lipoic Acida-Ketoglutaric AcidL-CarnitineMethyl B complex vitaminsPantothenic acidZincSeleniumManganeseMagnesiumNADHNicotinamide Ribonucleoside

MEMBRANE LIPIDS

ORAL Omega 3 Fatty Acids 2-4g + /dayEPA-DHA

ORAL Phospholipids 600-1200mg+ bidPhosphatidyl CholineGlycerophosphocholinePhosphatidyl serine

IV Phospholipids Phosphatidyl Choline2 grams/day

Lipid Replacement Therapy: A natural medicine approach to replacing damaged lipids in cellular membranes and organelles and restoring function. Garth L.Nicolson, Michael E.Ash. https://doi.org/10.1016/j.bbamem.2013.11.010

49


Lipid Replacement Therapy:

A natural medicine approach to replacing

damaged lipids in cellular membranes and organelles and restoring function.

Garth L.Nicolson,

Michael E.Ash.


50







7/8/20

26


ELECTRON TRANSPORT CHAIN EFFICIENCY

51


Essential Nutrients

for ATP

Production

52



7/8/20

27


L-Carnitine, Fatty Acid Oxidation and Transport

Kumaran S, Subathra M, Balu M, Panneerselvam C. Age-associated decreased activities of mitochondrial electron transport chain complexes in heart and skeletal muscle: role of L-carnitine. Chem Biol Interact. 2004;148(1-2):11-18. doi:10.1016/j.cbi.2003.10.010

• Carnitine is a naturally occurring hydrophilic amino acid derivative, produced endogenously in the kidneys and liver and derived from meat and dairy products in the diet.• It plays an essential role in the transfer of long-chain fatty acids into the

mitochondria for beta-oxidation• Essential for mitochondrial energy production• Deficiency may contribute to fatigue

53


CoQ10 (Ubiquinone) and Mitochondrial Electron Transportreduced form = UbiquinolCoQ10 is a lipophilic molecule critical for the transport of electrons in themitochondrial respiratory chain. (along with Lipoic Acid)

The most widely used co-factor in treating mitochondrial diseases

Effects gene expression and cell signaling and cellular metabolism

Functions as an anti-oxidant in cell membranes

Reduces Lactic Acid

54



7/8/20

28


INTERVENTIONS

55


MitochondriaFundamental

ToLife And

Death

Joe Pizzorno, ND.

Integ Med Vol 13, No.2April 2014

56



7/8/20

29


MitochondrialMetabolism

And Energy

Production

NUTRIENTCO-FACTORS


And Energy

Production

NUTRIENTCO-FACTORS


And Energy

Production

NUTRIENTCO-FACTORS

Diet Must Be Replete in

• Amino Acids• Fatty Acids• Methly B- Complex Vitamins• Magnesium• Phytophenols

57


Dietary Interventions

• Intermittent Fasting• Plant Based & Phytochemical Rich• Glutathione Rich • Anti-Inflammatory• Replete in protein and micronutrients• Promote normal glycemic control• Food Preparation and Storage (reduce oxidants, molds,mito-toxins)• Avoid fried foods, blackened foods, red meat, iron rich foods,• Avoid Cooking and Storage with Copper, Aluminum, Cast Iron, Plastics

58



7/8/20

30


Interventions

Identify and Eliminate Toxic Exposuresat home and work and leisure activities

• Recreational and Pharmaceutical Drugs• Environmental toxins: • Polluted Air, Water, Soil• Electromagnetic exposures• Herbicides Pesticides, Fungicides• Heavy Metals (Hg-Ag Amalgams), Pb, Ar, Al, Mn, Cd• Cosmetics and Body Care Products• Sources of Oxidative Stress: Smoking, Sun Exposure, Excess

Exercise• Polyaromatic Hydrocarbons

59


Oxid Med Cell Longev. 2015; 2015: 408927.Mitochondria-Targeted Protective Compounds in Parkinson’s and Alzheimer’s DiseasesPublished online 2015 Apr 29. doi: 10.1155/2015/408927

60



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429198/

https://dx.doi.org/10.1155%252F2015%252F408927

7/8/20

31


Mitochondria-Targeted Protective Compounds in Parkinson’s and Alzheimer’s Diseases

Oxid Med Cell Longev. 2015; 2015: 408927.Published online 2015 Apr 29. doi: 10.1155/2015/408927

MitoquinonemesylateLipoic AcidAscorbic Acid NicotinamideN-Acety CysteineGlutathioneAcety-L-Carnitine

Melatonin17-b EstradiolResveratrolThymoquinoneCaffeinePuerarinEGCG

61


Promoting Mitochondrial Function:Nutriceuticals and Phytochemicals• CoQ10 – rate-limiting nutritional factor in the electron transport chain • Alpha Lipoic Acid – cofactor in multi-enzyme complexes that catalyzes oxidative decarboxylation dehydrogenase complex

• Pantethine – necessary to shuttle fats from the blood stream across the cellular membrane for cell entry • L-Carnitine – necessary to shuttle those same fats across the mitochondrial membranes for burning

62


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429198/

https://dx.doi.org/10.1155%252F2015%252F408927


7/8/20

32


Promoting Mitochondrial Function:Nutriceuticals and Phytochemicals

• B Vitamins, Magnesium and Manganese – required as Krebs cycle enzyme cofactors• Malic and Succinic Acids - for refilling of key Krebs cycle intermediates • Creatine - to support additional energy production • Trans-Resveratrol and Curcumin Induce mitochondrial biogenesis through SIRT1 gene signaling and PGC-1-alpha induction, slowing the aging process.• Ribose – a nucleotide repleter and direct cellular energy source

63


Dr. Nalini Chilkov, L.Ac. OMD, [email protected]

BONUS RESOURCE : Download Dr. Chilkov’s Free

Mitochondrial Metabolism and Healthy Ketogenisis Guide

PLUS, Get Access to Mitochondrial Metabolism, Ketogenic Diets, Fasting and Cancer Webinar

CLICK HERE https://www.aiiore.com/fullscript2020

64



https://www.aiiore.com/fullscript2020/

7/8/20

33

THIS INFORMATION IS PROVIDED FOR THE USE OF PHYSICIANS AND OTHER LICENSED

HEALTH CARE PRACTITIONERS ONLY. THIS INFORMATION IS INTENDED FOR PHYSICIANS

AND OTHER LICENSED HEALTH CARE PROVIDERS TO USE AS A BASIS FOR DETERMINING

WHETHER OR NOT TO RECOMMEND SUPPORT OR PRODUCTS TO THEIR PATIENTS. THIS

MEDICAL AND SCIENTIFIC INFORMATION IS NOT FOR USE BY CONSUMERS. THE DIETARY

SUPPLEMENTS ARE NOT INTENDED FOR USE BY CONSUMERS AS A MEANS TO CURE,

TREAT, PREVENT, DIAGNOSE, OR MITIGATE ANY DISEASE OR OTHER MEDICAL CONDITION.


65


Documents

Healthy Aging Care and Feeding of Mitochondria Fullscript ...€¦ · Mitochondrial function is a key to successful aging Progressive mitochondrial dysfunction is considered a hallmark