Where Science and Faith Converge

Long Life Spans: "Adam Lived 930 Years and Then He Died"

By Hugh Ross - January 1, 2001

by Dr. Hugh Ross, Dr. Fazale ("Fuz") Rana, and Dr. Richard Deem

“Adam lived 930 years and then he died.” The mere assertion that humans could live more than 900 years—as Genesis 5:5 states—seems, for many people, nothing short of absurdity. The mention of long life spans in Genesis 5 hinders these people from openly exploring the Christian faith. Unable to accept 900-year human life spans, skeptics and others view the Bible as unreliable, a book of human myth rather than divine revelation.

This skepticism towards the long life spans of Genesis 5 is understandable. Tremendous advances have been made and will continue to be made in medical science and technology to conquer many dreaded diseases. The Western world has widespread access to health services, and for most Americans, nutrition is not a vital concern. And yet, the average life span in the U.S. is less than 80 years. Over the last century, human life expectancy has increased, but only by a handful of years. In light of these facts, how can the long life spans described in Genesis 5 conceivably be true?  Yet another stumbling block crops up in Genesis 6:3, which declares that God intervened to shorten man’s life span from about 900 to about 120 years. (For a discussion on why God would have allowed man’s long life span only to shorten it later, see The Genesis Question by Hugh Ross.) Even though a maximum life expectancy of about 120 years accords with current data, the abrupt shortening of human life spans creates another hurdle for skeptics. How can this dramatic change in human life spans be scientifically rational?

Recent advances in the biochemistry of aging provide answers to these seemingly intractable problems. Scientists have uncovered several distinct biochemical mechanisms that either cause, or are associated with, senescence (aging). Even subtle changes in cellular chemistry can be responsible for aging, and in some cases, can increase life expectancy by nearly 50%.1, 2  These discoveries point to a number of possible ways that God could have allowed long life spans and then altered human life expectancy––simply by “tweaking” human biochemistry. The recent progress of research in the biochemistry of aging, along with the cosmic radiation caused by the Vela supernova eruption, make the long life spans of Genesis 5 and the decrease of human life spans at the time of the Flood scientifically plausible.3,4 

Reactive Oxygen Species

The free radical theory of aging is one of the leading explanations for senescence.5 Free radicals are chemical entities that possess one or more unshared electrons as part of their structural configurations. Because electrons find stability by forming pairs, the unshared electron(s) of free radicals makes them unstable, highly reactive, and chemically destructive compounds. When a molecule contains an unshared electron it becomes highly reactive because the unshared electron aggressively “seeks out” another electron with which to pair.

Some free radicals produced inside the cell during the normal course of cellular metabolism are derived from molecular oxygen (O2) and are called reactive oxygen species (ROS). 6 Some examples are superoxide (·O2-), the hydroxy free radical (·OH), and hydrogen peroxide (H2O2). Most ROS produced internally and occurring normally in the cell come from the mitochondria—organelles inside the cell that play a central role in harvesting energy.7

According to the free radical theory of aging, the ROS produced in the cell during the natural course of metabolism act randomly and indiscriminately to damage important cell components. For example, in their search for other unshared electrons, ROS attack the molecules that make up the cell’s membrane (lipids), proteins, and DNA.8 Since this damage to cellular components is cumulative, ROS may contribute significantly to the aging process.9

Cells do have mechanisms to counteract many of the harmful effects of ROS. For example, the enzymes superoxide dismutase (SOD) and catalase hunt the free radicals superoxide and hydrogen peroxide, respectively.10 Cells also have additional antioxidants such as glutathione, peroxidase, and vitamins E and C.11 However, these protective systems are insufficient to prevent all the damage caused by ROS over a cell’s lifetime.

A team of pharmacologists recently demonstrated that the aging effects caused by ROS can be largely subverted by augmenting the cell’s native antioxidant defenses by using enzyme mimetics.12 Enzyme mimetics (synthetic compounds that imitate the chemistry of enzymes) catalyze (bring about) the same chemical reactions as the enzymes for which they are named. In other words, enzyme mimetics imitate natural enzymes. For example, SOD/catalase enzyme mimetics catalyze the decomposition of superoxide and hydrogen peroxide. The pharmacologists found that administering SOD/catalase enzyme mimetics to a study group of worms (Caenorhabditis elegans)13 can extend the worms’ average life span by 44% by providing additional defense against the damage that free radicals cause. Not only does the worm study help define the role of ROS in the aging process, it also indicates that human life span could be, and in fact, may be lengthened or shortened by this “pharmacological intervention.”14

Researchers also have been able to extend the life span of fruit flies by about 40% through similar means. Instead of using enzyme mimetics, scientists manipulated the fruit flies’ genes, causing their mitochondria to produce more SOD and catalase. 15 The results were similar.

Further evidence that altering SOD and catalase levels can influence life span comes from recent work by researchers at the University of Texas in Houston. These scientists have shown that by targeting SOD, they may be able to selectively kill cancer cells.16

These new discoveries in ROS suggest that one way God could have designed humanity to live for 900 years and then acted to decrease man’s life expectancy at the time of the Flood would be to make subtle changes in the level of SOD and catalase enzyme expression within cells.

Caloric Restriction

Caloric restriction is one of the approaches that researchers have discovered for extending the life span of certain organisms.17 Selectively reducing food intake (calories) by 30 to 70% can extend life span by up to 40% for a wide range of creatures from yeast to mammals. For years, scientists have thought that caloric restriction extends life expectancy by causing a decrease in metabolic rate, which, in turn, leads to reduced production of ROS.18 Recent studies strongly suggest, however, that caloric restriction yields an increase in life span through a biochemical mechanism distinct from the free-radical mechanism.

Researchers from Massachusetts Institute of Technology (MIT), using yeast as a study organism, recently put in place the final piece of the puzzle to explain that biochemical mechanism. 19, 20 Within chromosomes are genes that code for rRNA. These genes have unique features that, due to normal cellular activity, may cause them to become excised from the chromosome. These excised genes then form individual circular pieces of DNA (called extrachromosomal DNA circles, or ECs) which self-replicate, accumulate, and compete with the yeast’s genome for vital enzymes and other cellular materials. For this reason, ECs are toxic to cells and decrease longevity in yeast.21

The MIT researchers have found that the enzyme Sir2 plays a significant role in reducing the accumulation of ECs, thereby extending the life span of yeast. (Sir2 has been found throughout the biological realm, including in humans.22) It is activated when the energy status of a cell drops off—which would occur under conditions of caloric restriction. 23 When activated, Sir2 causes the chromosomes to become highly condensed and the genes within the chromosomes to be silenced. 24, 25 Because the chromosomes’ genes are silenced, the production of ECs diminishes, resulting in an extension of yeast life span. The results for yeast carry broad implications for the human aging process, since Sir2 has been discovered in humans.

The relationship between gene silencing and aging can be understood through a simple analogy. A car driven normally for thirty years will show signs of significant wear and tear, if it is still functioning. A similar car, however, that is driven only to church on Sundays will remain in mint condition even after thirty years. Likewise, a strand of DNA experiencing normal wear and tear can produce toxic ECs, decreasing life span. The enzyme Sir2, however, silences the genes within a chromosome, limits wear and tear on the DNA, and prevents ECs from forming, thereby extending the life span of yeast.

The work on ROS and caloric restriction correlates with Genesis 1:29-30, where God prescribes a vegetarian diet for pre-Flood humans. A vegetarian diet not only ensures the consumption of high levels of antioxidants, but also prevents the intake of toxins that accumulate in animal flesh. A vegetarian diet also aids with caloric restriction because the consumption of vegetables yields far fewer calories than does the consumption of the equivalent weight of meat. Through a vegetarian diet, God could have used caloric restriction to help extend pre-Flood life spans.

Another way God could have altered human life spans is through a gene mutation that mimics caloric restriction. Recent work by investigators from the University of Connecticut identified a mutation in fruit flies that disables a gene involved in metabolism.26, 27 The loss of this gene’s activity makes metabolism less efficient. Inefficiency in metabolism means that the organism can’t extract energy from food very effectively. This limits the energy available and, similar to caloric restriction, leads to longer life spans. Fruit fly life spans doubled as a result of this mutation.

The fruit fly work demonstrates how God could have helped control mankind’s life expectancy by altering the activity of a single gene. Whether He used this method or not, it does represent a simple, viable option.  Interestingly, as highlighted by other work on fruit flies, many organisms seem to be genetically programmed to hasten mortality. Recently, scientists have discovered another single gene mutation that leads to long life spans. Though this gene, called the Methuselah gene, has been shown to extend life spans in fruit flies when mutated, the function of this gene, when not mutated, remains unknown. 28, 29

Telomere Loss

Altering telomerase activity is another way God could have acted to regulate human longevity. Telomerase is an enzyme complex that maintains the length of telomeres—the terminal ends of DNA strands in chromosomes.30 Telomeres maintain chromosome stability. Humans have 23 pairs of chromosomes; one member of each chromosome pair comes from the mother, and the other from the father. Prior to cell division, each chromosome duplicates, and, after cell division, the parent and daughter chromosomes separate from one another.

During DNA replication, telomerase functions to maintain telomere length. Without sufficient telomerase activity, telomeres become successively shorter with each round of cell division. If telomeres disappear, chromosomes lose stability and the cell’s ability to replicate is compromised. Thus, loss of telomerase activity and the disappearance of telomeric DNA is associated with aging.31

Telomere length serves as an indicator of health. Thus, scientists use telomere length to assess the health of cloned animals.32 Researchers have been able to extend life spans by introducing telomerase into cultured human cells that lack telomerase activity.33 Cancer cells, considered to be essentially immortal, possess elevated telomerase activity levels.34 Recent research suggests that the relationship between telomere length and cell longevity is even more complex than previously thought.35, 36 (For example, in an environment where elevated radiation significantly increases cancer cell production, higher telomerase activity may actually shorten, rather than lengthen, life spans.)  God could have changed human life expectancy simply by varying telomerase activity. Alternatively, God may have complemented an increase in radiation levels (see discussion of the Vela supernova event, page XX) with a reduction in telomerase activity so as to minimize human suffering from cancers in the context of shortened life expectancy.

Genome Size

Investigators from Glasgow University in the United Kingdom have recently uncovered a significant relationship between genome size and longevity.37 The term genome refers to the entire DNA makeup of an organism. Genomes consist of genes—which encode the information needed for the cell to make proteins and structural RNA molecules—and of noncoding DNA.

The Glasgow team surveyed 67 bird species and found that larger genome sizes correlate with longer life spans. Birds are ideal models to characterize the effect of genome size on life expectancy because of the substantial data for bird genome size and longevity. Though no clear explanation yet exists for why larger genomes lead to longer lifetimes, the scientists who carried out this study have speculated that larger genomes may slow down the cell cycle (the time between cell divisions). Before a cell cycle can be completed— culminating in cell division—the cell’s DNA must be replicated to produce duplicate copies of the genome. The larger the genome, the longer it takes for DNA replication to occur. This longer replication process results in a longer cell cycle and ultimately leads to longer life spans.

The correlation between genome size and longevity is intriguing in light of the Human Genome Project (HGP). Humans have a large genome—three billion base pairs (genetic letters). However, initial estimates from the HGP indicate that the human genome possesses only 28,000 to 120,000 genes.38 This means that noncoding DNA makes up roughly 97% of the human genome. This prompts speculation, with Genesis 5 and 6 in mind, that quite possibly the large size of the human genome—comprised of a large amount of noncoding DNA—may reflect God’s original purpose for man. God might have designed the large human genome to allow life spans of 900 years. According to this suggestion, the noncoding DNA may have performed a critical function at one time. Perhaps God left the human genome intact at the time of the Flood as He acted through astronomical events and other biochemical changes to limit man’s life expectancy. Then the human genome, as observed today, would be a carryover—and a possible testimony to—the time when God purposed for people to live longer.

Alternatively, the human genome may have been even larger before the Flood.  Given their relatively large body size and high level of activity, humans live considerably longer than members of other species. This combination of size and activity level may in itself explain humans’ large genome size, but the pre-Flood life spans may have required an even larger genome.

Vela Supernova

A major astronomical event provides a partial explanation for how God may have acted to reduce the long pre-Flood human life spans. Cosmic radiation is one of the main factors that limits human life expectancy. The cosmic radiation coming down to Earth has not been uniform through time, and in fact, most of the deadliest cosmic radiation Earth experiences comes from a fairly recent and nearby (1,300 light years away) event, the Vela supernova. (A supernova is a rare celestial phenomenon, the explosion of most of the material in a star.) About 20,000 to 30,000 years ago (roughly the time of the Genesis flood), the Vela supernova erupted.39, 40

Prior to the Vela supernova, only a fraction of the current level of deadly cosmic radiation bathed the Earth. Under these lower radiation conditions (coupled with complementary biochemical adjustments) life spans of up to 900 years might have been possible. Scientists do acknowledge that this higher-level radiation silently bombarding the Earth since Vela plays a significant role in limiting life expectancy. Moreover, a significant radiation event such as Vela would explain the mathematical curve—the gradual, exponential reduction in life spans from about 900 to 120 years—reported in Genesis 11.

Assessing Scientific Plausibility

Advances in the biology and biochemistry of aging have been remarkable, and, at the same time, they reveal that the aging process is, indeed, complex. Much remains to be learned and discovered about it. Recent discoveries do clearly indicate that aging can result from subtlety changes in the invisible realm of cosmic radiation and cellular chemistry. Given the subtly of these changes, investigators are gaining some hope and confidence that in the near future they will be able to slow the human aging process through drug treatment and dietary alteration.

Scientists’ success in altering the life span of selected organisms (such as worms, yeast, and fruit flies) and their emerging ability to increase human life expectancy through biochemical manipulation lend scientific plausibility to the long life spans recorded in Genesis 5. If humans with their limited knowledge and power can alter life spans, how much more so can God? He could have used any of four (or more) subtle alterations in human biochemistry to allow for long life spans. He could have used the Vela supernova or other astronomical events, in combination with complementary biochemical changes, to shorten human longevity.

Exactly how God altered human life spans no one knows. However, recent discoveries in the biochemistry of aging continue to build the case for the reliability of Scripture—specifically of Genesis 5 and 6. Researchers stand on the threshold of additional breakthroughs in understanding the aging process. Further advances are anticipated in the endocrinology and hormonal control of aging, and in deciphering Werner’s syndrome (a disorder that leads to premature aging).41-44 One can look forward to these and other discoveries in the biochemistry of aging with the confidence that they will continue to lend credibility to the biblical record.


  • Base pairs: The specific association between two sub unit groups on opposite strands of aligned DNA molecules. They serve as the most fundamental unit of genetic information. Base pairs are the alphabet of the genetic language. Genetic information is formed by the specific sequences of base pairs in a DNA molecule.
  • Caenorhabditis elegans: A commonly occurring worm, specifically a nematode, used as an experimental system to study biochemical and biological processes in complex multicellular animals.
  • Caloric restriction: A method to extend life spans of model organisms that involves a dramatic reduction in food intake.
  • Catalase: An enzyme that converts hydrogen peroxide into water. This enzyme is part of the cell’s antioxidant defense system.
  • Cell cycle: The repeated and ordered sequence of events in which a cell grows and prepares for cell division. The cell cycle both begins and culminates with cell division.
  • Cellular metabolism: The collection of chemical reactions and processes occurring inside cells.
  • DNA (deoxyribonucleic acid): A complex chain-like molecule formed by linking, in a head-to-tail fashion, smaller molecules. The sequence of small molecules that form DNA chains contains information needed to direct the production of the cell’s proteins.
  • Endocrinology: The scientific discipline that studies the internal secretions produced by endocrine glands and the glands themselves. Also of interest is the physiological effect of the secretions with respect to the whole organism as well as pathologies associated with the endocrine system.
  • Extrachromosomal circles (ECs): Small circular pieces of DNA produced as a by-product of specific enzymes operating on tandemly repeated rRNA genes. The presence of extrachromosomal circles in yeast has been correlated with aging.
  • Free radical: Any chemical entity with an unpaired electron as part of its electronic configuration.
  • Genome: The entire DNA makeup of an organism including genes and non-coding DNA.
  • Glutathione: A compound found inside the cell that participates in the cell’s antioxidant defense system.
  • Human Genome Project: An international project involving a large number of laboratories with the goal of determining the complete DNA sequence of the human genome and characterizing the human genome’s functional organization.
  • Mitochondria: Organelles inside cells that “produce” energy for cellular use.
  • Organelles: Membrane-bound structures inside cells that carry out specialized functions.
  • Peroxidase: An enzyme that serves as part of the cell’s antioxidant defense system.
  • Reactive oxygen species: Unstable, highly reactive compounds chemically derived from molecular oxygen.
  • Senescence (aging): Growing old. The time-related loss of physiological functions needed for survival and reproduction.
  • Sir2: A protein whose activity leads to gene silencing during caloric restriction.
  • Supernova: A star that suddenly bursts into very great brilliance as a result of its blowing up; it is orders of magnitude brighter than a nova.
  • Superoxide dismutase: An enzyme that converts the superoxide ion (·O2¯) into hydrogen peroxide. This enzyme is part of the cellular antioxidant defense system.
  • Telomeres: Repetitive sequences of DNA located at the terminal or “tip” ends of chromosomes. Telomores maintain the stability of chromosomes.
  • Werner’s syndrome: A genetic disorder, also called progeria of the adult, that is characterized by a normal childhood, a cessation of growth in teenage years and a premature aging in the late teen/early adult years.
  1. Simon Melov et al., “Extension of Life Span with Superoxide Dismutase/Catalase Mimetics,” Science 289 (2000), 1567-69.
  2. Judith Campisi, “Aging, Chromatin, and Food Restriction—Connecting the Dots,” Science 289 (2000), 2062-63.
  3. “Science Switched Sides: Part 1,” Facts for Faith 1 (Q1 2000), 29.
  4. Hugh Ross, The Genesis Question: Scientific Advances and the Accuracy of Genesis (Colorado Springs: NavPress, 1998), 119-21.
  5. Toren Finkel and Nikki J. Holbrook, “Oxidants, Oxidative Stress and the Biology of Aging,” Nature 408 (2000), 239-47.
  6. Sandeep Raha and Brian H. Robinson, “Mitochondria, Oxygen Free-Radicals, Disease and Ageing,” Trends in Biochemistry 25 (2000): 502-08.
  7. Raha and Robinson, 502-08.
  8. Robert Arking, The Biology of Aging, 2d ed. (Sunderland, MA: Sinauer Associates, 1998), 398-414.
  9. Finkel and Holbrook, 239-47.
  10. Lubert Stryer, Biochemistry, 3d ed. (New York: W. H. Freeman, 1988), 422.
  11. Arking, 401-03.
  12. Melov et al., 1567-69.
  13. Oddly enough, the model systems used to study aging, yeast, nematodes, and fruit flies accurately reflect the mechanisms leading to senescence in humans. This stems from the fundamental unity of biochemistry among eukaryotic organisms (single and multicellular organisms comprised of complex cells—cells possessing a nucleus and internal membrane structures).
  14. Melov et al., 1567-69.
  15. Raha and Robinson, 502-08.
  16. Peng Huang et al., “Superoxide Dismutase as a Target for the Selective Killing of Cancer Cells,” Science 407 (2000), 390-95.
  17. Arking, 313-27.
  18. Leonard Guarente and Cynthia Kenyon, “Genetic Pathways that Regulate Ageing in Model Organisms,” Nature 408 (2000), 255-62.
  19. Su-Ju Lin et al., “Requirement of NAD and SIR2 for Life Span Extension by Calorie Restriction in Saccharomyces cerevisiae,” Science 289 (2000), 2126-28.
  20. Campisi, 2062-63.
  21. David A. Sinclair and Leonard Guarente, “Extrachromosomal rDNA Circles—A Cause of Aging in Yeast,” Cell 91 (1997), 1033-42.
  22. Jeffrey S. Smith et al., “A Phylogenetically Conserved NAD+-Dependent Protein Deacetylase Activity in the Sir2 Protein Family,” Proceedings of the National Academy of Sciences, USA 97 (2000): 6658-63.
  23. Su-Ju Lin et al., 2126-28.
  24. Shin-ichiro Imai et al., “Transcriptional Silencing and Longevity Protein SIR2 is an NAD-Dependent Histone Deacetylase,” Nature 403 (2000), 795-800.
  25. Joseph Landry et al., “The Silencing Protein Sir2 and Its Homologs are NAD-Dependent Protein Deacetylases,” Proceedings of the National Academy of Sciences, USA 97 (2000): 5807-11.
  26. Elizabeth Pennisi, “Old Flies May Hold Secrets of Aging,” Science 290 (2000), 2048.
  27. Blanka Rogina et al., “Extended Life Span Conferred by Contransporter Gene Mutations in Drosophila,” Science 290 (2000), 2137-40.
  28. Elizabeth Pennisi, “Single Gene Controls Fruit Fly Life Span,” Science 282 (1998), 856.
  29. Yi-Jyun Lin et al., “Extended Life Span and Stress Resistance in Drosophila Mutant methuselah,” Science 282 (1998), 943-46.
  30. Alan G. Atherly, Jack R. Girton and John F. McDonald, The Science of Genetics (Fort Worth: Saunders College, 1999), 302-03.
  31. Arking, 460-64.
  32. For example see: Teruhiko Wakayama et al., “Cloning of Mice to Six Generations,” Nature 407 (2000), 318-19.
  33. Andrea G. Bodnar et al., “Extension of Life-Span by Production of Telomerase into Normal Human Cells,” Science 279 (1998), 349-52.
  34. Douglas Hanahan, “Benefits of Bad Telomeres,” Nature 406 (2000), 573-74.
  35. Steven E. Artandi et al., “Telomere Dysfunction Promotes Non-Reciprocal Translocations and Epithelial Concerns in Mice,” Nature 406 (2000), 641-45.
  36. Elizabeth H. Blackburn, “Telomere States and Cell Fates,” Nature 408 (2000), 53-56.
  37. Pat Monaghan and Neil B. Metcalfe, “Genome Size and Longevity,” Trends in Genetics 16 (2000), 331-32.
  38. Elizabeth Pennisi, “And the Gene Number Is …?” Science 288 (2000), 1146-47.
  39. B. Aschenback et al., “Discovery of Explosion Fragments Outside the Vela Supernova Remnant Shock-Wave Boundary,” Nature 373 (1995), 588.
  40. A. G. Lyne et al., “Very Low Braking Index for the Vela Pulsar,” Nature 381 (1996), 497-589.
  41. Koutarou D. Kimura et al., “ daf-2, an Insulin Receptor-Like Gene that Regulates Longevity and Diapause in Caenorhabditis elegans,Science 277 (1997), 942-45.
  42. Kui Lin et al., “daf-16: an HNF-3/forkhead Family Member That Can Function to Double the Life-Span of Caenorhabditis elegans,” Science 278 (1997), 1319-22.
  43. Catherine A. Wolkow et al., “Regulation of C. elegans Life-Span by Insulinlike Signaling in the Nervous System,” Science 290 (2000), 147-50.
  44. Junko Oshima, “The Werner Syndrome Protein: An Update,” Bioessays 22 (2000): 894-901.

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