Decay over Time
Bodily decay is gloomy in prospect, but of all human contemplations the most abhorrent is body without mind.
Thomas Jefferson, in a letter to John Adams, August 1, 1816
As we discussed earlier, design laws are those protocols, principles, or laws (e.g., laws of health) on which life is constructed to operate. These are the parameters on which reality operates and exists in all domains of life. One of the design laws involved in aging is the Second Law of Thermodynamics, also known as the Law of Entropy, which in layman’s terms refers to the fact that if energy isn’t put into a system to maintain it and prevent deterioration, the system will slowly decay. Consider walking away from your home or your car and returning twenty years later. If no one did anything to your home or car during the intervening twenty years, in what condition would you find it? It would have decayed. This is a law on how our universe operates: without an influx of energy to maintain order, things slowly become disordered or fall apart—decay.
As we will discuss in chapter 11, our beliefs impact not only our brains but also our physical health, both of which impact aging and the development of dementia. Two grand belief systems, or themes, dominate human thinking—godless evolution and creation by a supreme being (God). Facts, evidence, and life experiences are filtered through these themes. Depending on their underlying belief systems, people draw divergent conclusions when examining the same facts. The purpose of this book is to lead people to healthier lives, which slow the aging process and reduce the risk of dementia. One intervention to accomplish this goal is to identify the design laws (testable parameters) on which life is constructed to operate, to determine which belief system is most consistent with reality (design laws), and to explore whether there are differences in health outcomes based on the belief system held. As we will discover, our beliefs do impact our health and risk of dementia.
The Second Law of Thermodynamics is a testable design law, but what does it have to do with aging and our brains? We can examine the human genome and measure whether the genome is becoming healthier, becoming more complex, and developing enhanced information coding or whether it is slowly decaying, degrading, and deteriorating. Which of the two grand themes, or belief systems, is more consistent with what is actually happening in the human genome and harmonizes with the Second Law of Thermodynamics?
Ancient religious texts describe humanity as originally living in a face-to-face relationship with a Creator God, whose presence was a constant influx of life-sustaining energy. However, when this situation changed and human beings moved out of harmony with their designer, they were told that “dying you will die” (Gen. 2:17 NKJV margin note), meaning if they severed their connection with the source of life-sustaining energy, they would slowly decay and die.
Modern evolutionary theory, taking the opposite view, states that living systems slowly improve, advance, and become more organized with greater complexity without any intelligent-energy input. In other words, evolutionary theory states that systems become more ordered, more organized, and more advanced simply by means of random chance causing mutations and natural selection choosing the most advantageous mutations to reproduce. But any scientist can test this theory and recognize quite quickly that without intelligent input of energy, systems decay. What many well-intentioned evolutionary scientists fail to recognize is that when all systems are decaying, selecting the system with the least decay is not the same as advancing or improving the species. Natural selection occurs, to be sure, but what is actually being selected to survive—species with new genetic complexity and advanced organizational health? No! Natural selection can only select from the environment, and all species on earth are decaying. Thus, natural selection selects those specimens that have the least decay, but they are still degraded from previous generations.
John C. Sanford, PhD, an applied geneticist at Cornell University, provides conclusive scientific evidence that the genome of all living creatures, including human beings, is slowly decaying. In his book Genetic Entropy and the Mystery of the Genome, Dr. Sanford cites articles, research findings, and publications from across the scientific literature documenting that with every generation multiple new genetic mutations enter the human genome. Further, he documents that there has not been one mutation ever found that improves the species or adds genetic information. In other words, every mutation degrades the species.
For those who are not familiar with genetic science, a simple analogy will help. Dr. Sanford rightly points out that the genome is a microscopic library of information waiting to be accessed and put to use. Consider going to your city’s library. The entire library with all its vast information would be analogous to the 3.2 billion molecules found in the twenty-three pairs of chromosomes that make up human DNA. The individual DNA molecules would be all the letters of the alphabet found in the library. Grouping them together they form words. Putting words together forms paragraphs; paragraphs put together form chapters, which would be analogous to individual genes that code for specific products such as hair color, eye color, and the like. The chapters form books, which are analogous to chromosomes, and all the books together (twenty-three pairs of chromosomes) form the library—human DNA.
With this concept in mind, think about what happens if mutations start happening in the books in your library. For example, in one word a single-letter mutation occurs: the word love has the o replaced by an i and now reads as live. This is not the original word; the meaning has changed, yet it is still a “readable” word. But the idea or product of this word is different from the original.
This is analogous to single-point mutations in various human genes, which have been documented in the gene that codes for the enzyme that breaks down a critical brain neurotransmitter (dopamine) involved in attention and focus. This mutation results in different functional outcomes.
In the brain, neurons communicate with each other by releasing chemical signals, called neurotransmitters, into the spaces between neurons, called synapses. Brief puffs of chemicals are released by a neuron that adjacent neurons “see” and respond to. Conceptualize this as being similar to smoke signals. In order to maintain clear communication and prevent “cloudy” and “confused” messages, the brain has multiple mechanisms to clear the synaptic sky between signals. Just imagine how difficult it would be to read smoke signals if the smoke never dissipated between signals.
One mechanism the brain uses to remove neurotransmitters from the synaptic spaces are reuptake pumps that work like little vacuum cleaners to pull the transmitter back into the releasing cell to repackage and reuse for more signaling later. But these pumps don’t get 100 percent of the neurotransmitter, so the brain has enzymes in the synaptic spaces to break down and remove residual neurotransmitters. One of these enzymes is catechol-O-methyltransferase (COMT), and it breaks down the neurotransmitter dopamine. The COMT gene that produces this enzyme is located on chromosome 22. But this gene has had a single-point mutation (one letter has been replaced with another, but it can still be read). Therefore, two genetic forms of the gene can be found: one form with the amino acid valine (Val) at position 108 on the gene; the other with the amino acid methionine (Met) at position 108.
Because of this mutation, the COMT enzyme in individuals with Val instead of Met is more active at body temperature—so active, in fact, it is clearing the dopamine (signal) before it can even be registered. This would be analogous to trying to give smoke signals in high winds; the wind is clearing the smoke so fast no message can be sent. As a result these individuals will have less dopamine available. Signaling between neurons is undermined by this very active form of the enzyme. Memory testing has documented that persons with the Val “letter” in the COMT gene perform worse on short-term memory testing than those with the Met “letter.”1
But our library of information has other more complex products that require more than just single words; they require full sentences. Sometimes mutations occur in which, instead of replacing a single letter, an entire word is deleted or replaced. Imagine reading a sentence that is missing a word. If it is a critical word the meaning may be completely wrong. Your instruction manual should read: “Do not connect the green and red wires.” But your manual is missing the word “not” and reads: “Do connect the green and red wires.” The outcome could be devastating.
Worse still are mutations in which entire sentences (genes) are deleted. In such cases the information simply isn’t there for the body to produce what is needed. An example of this type of mutation is Prader-Willi syndrome, in which seven genes on chromosome 15 are deleted. Fortunately, this disorder is rare, but because such a vast amount of information is lost it is quite severe, and those with it have poor muscle tone, impaired cognitive and sexual development, behavior problems, and often insatiable hunger that leads to obesity.2
Another type of mutation includes repeats in which a gene, or portion thereof, repeats itself multiple times. Consider a book in which one word word word word word word word repeats itself many times. Huntington’s disease is caused by a short three-nucleotide (letter) repeat that occurs multiple times. The gene where this repeat occurs is found on chromosome 4 and produces a protein called huntingtin. The precise function of huntingtin is unclear, but it is important for development and is highly expressed in neurons. When more than thirty-six of these repeats occur, a protein that is toxic to neurons is produced with the sad result manifesting in Huntington’s disease.3
There are also transposons, which are sometimes called jumping genes, in which a gene will move from its proper place to a new location on the chromosome.4 This would be like having a sentence in a book randomly moved to some other place in the book. The impact is widely variable depending on which gene is involved and where it moves.
You can imagine how difficult it would be if you had an instruction manual on how to build an engine, but in the manual there were misspelled words, missing words and sentences, sections with long repeats, and instances where words or sentences were moved from their proper place to random new locations within the manual.
With every human generation more of these mutations occur. This means that the human genome is slowly decaying. Here are the estimated new mutations occurring per generation:
Evolutionary scientists will argue that mutations allow for advantages in certain toxic situations and thus, with an extremely narrow view, argue that such mutations are beneficial and advance the species. A classic example is sickle cell anemia. This condition occurs because of a single-nucleotide polymorphism (one-letter-in-one-word replacement) in the gene that codes for hemoglobin. Hemoglobin is the protein that carries oxygen in the blood. The mutation causes the shape of red blood cells to deform from their smooth, disc-like shapes to ragged, sickle-like shapes.
Because we have two sets of genes, one set from mother and one set from father, a person can have two good genes, one good and one bad gene, or two bad genes. Only those with two bad genes develop full-blown sickle cell anemia. Because those with one copy of the bad gene have been noted to be resistant to malaria, and thereby more likely to survive in malaria-infested areas than those with two good genes, evolutionary biologists often point to this mutation as evidence of how evolution advances the species.
This is a beautiful example of missing the forest for the trees—missing the larger reality by focusing on a less-significant fact. It is true that those with one copy of the bad sickle cell gene are more likely to survive in malaria-ridden environments. Thus, they are more likely to pass their genes along and thereby continue the existence of this mutation. However, this mutation does not add information to the human genome, nor does it result in stronger and healthier humans with greater life expectancy. Further, this single mutation, which confers advantage in surviving malaria, does not prevent the multiplicity of other damaging DNA mutations from occurring with every generation. So regardless of whether one survives malaria, their genome has been degraded by a minimum of one thousand new damaging mutations.
Does natural selection occur? Absolutely, but what evolutionary biologists remain blinded to is that every genetic option is degrading, regardless of which individual is selected to survive!
At age sixty-five a person will have six thousand point mutations in their DNA that were not there when they were born. The human genome is slowly decaying, and this decay is one factor in aging.
Genetic Mutation and Aging
While genetic mutations can happen spontaneously, there are many environmental factors that cause mutations and thus cause genetic decay and accelerate aging. To the degree we can avoid or reduce exposure to these factors, we can slow the aging process and reduce our risk of dementia. Environmental factors that cause mutations are called mutagens, and they can be physical, chemical, or biological.
Physical mutagens are ionizing radiation such as gamma and alpha particles and X-rays. These particles physically damage the DNA, causing mutations. The most common sources are Cobalt-60 and Cesium-137. Cobalt-60 is a by-product of nuclear reactors and is used in medical radiation therapy, to irradiate food in order to kill pests, and in some industrial applications. Cesium-137 is also a by-product of nuclear reactors and can be used in medical radiation therapy and some industrial applications. Obviously, we would want to avoid exposure to such particles. Get X-rays only when medically necessary. If working in the medical field and exposed to X-ray equipment, always wear lead aprons and other protective equipment. If working with medical radioactive material, always follow handling procedures and wear radiation detectors.
The other major source of physical mutagens is ultraviolet radiation, which is in sunlight and is a major contributing factor to skin cancers. It is this wavelength of light that sunscreens are designed to block. In regard to aging most of us have seen individuals who have had excessive sun exposure throughout life; their skin is more damaged and aged than that of persons with less sun exposure. That is because of the greater damage occurring to the DNA (and other molecules) in their skin cells, which accelerates decay and aging. We can reduce risk by limiting sun exposure and by using sunscreen when in the sun.
Chemical mutagens, which are chemicals that can mutate our DNA, include reactive oxygen species (ROS) (which we will explore in detail in a later chapter) and polycyclic aromatic hydrocarbons (PAH). PAH can be found in abundance in fossil fuels (oil and coal), meat cooked at high temperatures such as grilling and charring, and tobacco smoke.6 These PAH molecules have been shown to increase various types of cancer.7 They can also alter genetic expression and brain development in children and increase cognitive and behavior problems in children whose mothers breathed high amounts of PAH (air pollution from burning fossil fuels) while pregnant with them.8 Other chemical mutagens include arsenic, cadmium, chromium, and nickel.9 Keeping our environment clean, reducing air pollution, avoiding tobacco smoke, and not eating meats charred or grilled will reduce exposure to these damaging compounds and thereby slow aging and reduce both cancer and dementia risk.
Biological mutagens include certain viruses and bacteria, as well as the transposons we discussed earlier. One example of this is the human papillomavirus (HPV), which is sexually transmitted and known to cause a variety of cancers. HPV infection causes a cascade of responses in the body, resulting in gene mutations that contribute to various cancers, such as cervical cancer.10 Fortunately, vaccines are now available to prevent HPV infection.
As we wind up our chapter on human genetics and aging, we need to discuss telomeres and aging. Telomeres are critical in cellular replication. As cells are damaged or just wear out with age, they need to be replaced. The way the body does this is by one cell copying itself to make another or by progenitor cells (factory cells) making new cells. But in order for the new cell to have all the abilities and functionality of the parent cell, it needs its own copy of the library of information (chromosomes). When a cell divides (mitosis), it copies its chromosomes so that both cells will have a complete set of genetic information. The telomeres are the end caps on each chromosome. Consider them like the plastic caps on your shoelaces. They keep the genetic material together and organized and prevent unraveling. But the length of these end caps is critical in determining the ability of the cell to replicate. If they get too short the cell can no longer copy itself or make new cells.
In the 1970s it was discovered that when cells replicated, the telomere end caps didn’t fully replicate. In fact, they shortened with each replication. If the telomeres get too short the cell can no longer divide. If cells can’t divide, they can’t replace damaged and worn-out cells and thus aging occurs. The results are readily seen when one compares the skin of an elderly person with that of a child. If both experience a similar superficial cut the child will heal quickly, but the older person’s skin will struggle to heal. One factor is that the shorter telomeres in the elderly person make it harder for their cells to reproduce and close the wound.
The telomeres of an infant contain approximately eight thousand base pairs. By age thirty-five the telomeres contain thirty-five hundred base pairs and by age sixty-five, only fifteen hundred.11 Recent research has documented that individuals with mood disorders as well as children who have been institutionalized have shorter telomeres than healthy control subjects. Further, hostility and negative emotions can shorten telomeres.
Scientists have recently documented that telomere length may be able to predict remaining life span. Lawrence Honig, MD, PhD, a professor of neurology at Columbia University, and his colleagues studied 1,978 people ranging from 66 to 101 years of age, with the average age of 78, from multiethnic backgrounds (African American, Hispanic, and white). They discovered that men in general had shorter telomeres than women, those with shorter telomeres died at an earlier age, and shorter telomeres were associated with developing Alzheimer’s dementia.12 However, men do not appear to have shorter telomeres at birth; instead, their telomeres shorten more rapidly throughout life.13 This suggests that the modifiable factors listed below are likely playing a significant role in the gender differences seen later in life. Interestingly, researchers also noted a wide range of telomere lengths across the age range, meaning age itself didn’t predict the length of one’s telomeres but telomere length did predict how much longer one could expect to live.
One factor that did impact telomere length was paternal age (age of the father) at the time of conception; the older the father at the time of conception the longer the telomeres in his children, both sons and daughters. Older age of the mother had either no impact or a negative effect on telomere length. The longer telomeres also seemed to pass down to the grandchildren of the older father—and if the son was older when his children were conceived this added further lengthening effects to his children’s telomeres.14 And the longer telomeres at birth did translate to living longer lives.15 What seems to be happening is that genetics accounts for about 80 percent of telomere length and environment affects about 20 percent of telomere length.
Factors that have been noted to accelerate the shortening of telomeres include childhood adversity,16 mood disorders, relationship conflicts and negative mental attitudes, and hostility. Factors that have been associated with lengthening telomeres include plant-based diet, stress reduction and meditation, and physical exercise.17 Therefore, interventions that bring conflict resolution, resolve internal stress (such as forgiving those who have wronged us), and allow avoidance of activities that increase stress (cheating on one’s spouse, embezzling from an employer, falsifying an insurance claim, etc.) will have a positive impact on telomere length—as well as reduce many other damaging stress-related processes within the body. Additionally, our worldview impacts our mental stress level.
As we will document in later chapters, stress reduction and meditation are directly connected to our belief systems. Belief systems that enhance reasoning, thinking, and evaluation of evidence and that include a benevolent God are the healthiest. Belief systems with no God but that promote reasoning, thinking, evaluation of evidence, and a benevolent mindset toward others are the next healthiest. But belief systems with authoritarian gods that undermine thinking, reasoning, and evaluation of evidence and incite fear by focusing on rule keeping and punishment for rule breaking are unhealthy, accelerate aging, and increase the risk of dementia. Thus, our worldview is directly connected to our life practices, stress management, and mode of relating to others and can contribute to both aging and dementia risk. We will explore specific reasons and evidences for this in later chapters. At this point, my goal is for the reader to be willing to think, evaluate evidence, and consider different viewpoints but only make a change in belief when fully persuaded by the weight of evidence.
As was mentioned, one factor that lengthens telomeres is a healthy diet. A recent study of more than thirty-six hundred adults found that doubling the amount of carotenoids (antioxidant molecules that give plants color) in the diet lengthened telomeres 2 percent. And those in the study with the highest levels of carotenoids had telomeres 5–8 percent longer!18 Foods high in carotenoids include carrots, sweet potatoes, tomatoes, and green leafy vegetables. Not surprisingly, a study by Dean Ornish published in Lancet Oncology in 2013 found that a lifestyle change to a plant-based diet resulted in increased activity in telomerase (the enzyme that lengthens telomeres).19
One study on exercise and telomere length found slightly contradictory results. It found that not all exercise lengthened telomeres, but standing several hours a day did. Another way to interpret the data is that long-term sitting or a significantly sedentary lifestyle shortens telomeres.20
Clearly, telomere length is involved in cellular reproduction and thereby the ability to maintain youth and vitality. But unrestrained telomere lengthening is not the answer. At least one study has documented that many human cancers occur because of unrestrained telomere lengthening, which results in unregulated cellular reproduction—that is, cancer.21
Our goal, then, is not unregulated telomere growth but to make lifestyle choices that reduce or delay telomere shortening and promote telomere health and length. It is striking to note that the Bible is not only more consistent with the science of genetic entropy but also connects relationship health and childhood peace with longer life (Exod. 20:12)—something science has now proven to be true.
LEARNING POINTS
ACTION PLAN: THINGS TO DO