A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine

Wallace, Douglas C.

doi:10.1146/annurev.genet.39.110304.095751

Cited by 3,185Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsAutophagy in Disease and Therapy

A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine

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Wallace, Douglas C.·2005·Annual Review of Genetics

DOI 10.1146/annurev.genet.39.110304.095751PMC PMC2821041

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Abstract

Life is the interplay between structure and energy, yet the role of energy deficiency in human disease has been poorly explored by modern medicine. Since the mitochondria use oxidative phosphorylation (OXPHOS) to convert dietary calories into usable energy, generating reactive oxygen species (ROS) as a toxic by-product, I hypothesize that mitochondrial dysfunction plays a central role in a wide range of age-related disorders and various forms of cancer. Because mitochondrial DNA (mtDNA) is present in thousands of copies per cell and encodes essential genes for energy production, I propose that the delayed-onset and progressive course of the age-related diseases results from the accumulation of somatic mutations in the mtDNAs of post-mitotic tissues. The tissue-specific manifestations of these diseases may result from the varying energetic roles and needs of the different tissues. The variation in the individual and regional predisposition to degenerative diseases and cancer may result from the interaction of modern dietary caloric intake and ancient mitochondrial genetic polymorphisms. Therefore the mitochondria provide a direct link between our environment and our genes and the mtDNA variants that permitted our forbears to energetically adapt to their ancestral homes are influencing our health today.

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The high metabolic need of the brain cannot be met by glycolytic activity; neurons rely on the tricarboxylic acid cycle and oxidative phosphorylation housed in mitochondria to produce ATP.
“The high metabolic need of the brain cannot be met by glycolytic activity. Rather, neurons rely on the tricarboxylic acid cycle and oxidative phosphorylation housed in mitochondria to produce ATP [72,120].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [120]
The passage on energy-utilizing tissues (section labeled Abstract; no page given) includes the brain and describes mitochondrial ATP production, while another passage describes the mitochondrial TCA cycle and oxidative phosphorylation. The paper does not say that glycolysis cannot meet the brain’s metabolic needs or establish that comparison specifically for neurons. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Mitochondrial oxidative stress is increased by the consumption of excess calories and leads to mitochondrial DNA damage.
“Mitochondrial oxidative stress is increased by the consumption of excess calories and, in turn, it leads to mitochondrial DNA damage [120]”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [120]
The mitochondrial defect in telomere dysfunction becomes increasingly apparent under physiological stress or advanced age.
“this mitochondrial defect in the setting of telomere dysfunction becomes increasingly apparent under conditions of physiological stress or advanced age2.”
From Telomere dysfunction induces metabolic and mitochondrial compromise (2011) · cites this paper as [2]
Aged tissues accumulate mitochondrial DNA mutations that cause respiratory chain deficiency and increased reactive oxygen species.
“Aged tissues show accumulation of mitochondrial DNA (mtDNA) mutations causing respiratory chain deficiency and increased reactive oxygen species (ROS)2,4”
From Telomere dysfunction induces metabolic and mitochondrial compromise (2011) · cites this paper as [2]
Calorie restriction moves the ETC away from a reduced state, lowers ROS production, induces OXPHOS and antioxidant defences, prevents age-related diseases, and increases lifespan.
“By reducing the excess of ingested calories, calorie restriction interventions move the ETC away from a reduced state, lower ROS production, induce OXPHOS and antioxidant defences, prevent age-related diseases and increase lifespan14.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [14]

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Authors: Wallace, D. C.
Affiliations: University of California, Irvine (US)
Corresponding author: Wallace, Douglas C.
ORCID: Wallace, Douglas C.
Venue: Annual Review of Genetics
Publisher: Annual Reviews
Published: 2005-12-01
Volume: 39
Issue: 1
Pages: 359-407
ISSN: 0066-4197 (ISSN-L)
1545-2948
DOI: 10.1146/annurev.genet.39.110304.095751
PMC: PMC2821041
OpenAlex: W2105754268
Cited by: 3,185
References: 259
Citations by year: 2026: 75 · 2025: 108 · 2024: 104 · 2023: 108 · 2022: 121 · 2021: 136 · 2020: 137 · 2019: 137 · 2018: 153 · 2017: 145 · 2016: 163 · 2015: 171 · 2014: 183 · 2013: 204 · 2012: 218
FWCI: 10.65
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Annual Review of Genetics (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (AG-13154, R01AG024373, AG24373, R01AG013154)
National Heart, Lung, and Blood Institute (R01HL064017, HL-64017)
Fogarty International Center (TW01366, R03TW001366)
National Institute of Neurological Disorders and Stroke (NS-21328, R01NS021328, NS41650, R01NS041850)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords: mitochondrial dysfunction, mitochondrial DNA mutations, oxidative phosphorylation, reactive oxygen species, aging, age-related diseases, cancer, degenerative diseases, energy deficiency, evolutionary medicine
MeSH terms: Aging, Energy Metabolism, Humans, Longevity, Metabolic Diseases, Mitochondria, Neoplasms

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A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine

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