Human Development Paper Due 08/06/2018

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Late Life Human Development Boosting or Buffering Universal Biological Aging

Thorsten Kolling and Monika Knopf

Goethe-University Frankfurt am Main, Germany

GeroPsych, 27 (3), 2014, 103–108

DOI 10.1024/1662-9647/a000108

Abstract. Human development in late life is characterized by a multitude of biological changes, some of which are presumed to occur universally as the result of biological aging factors in a narrow sense, whereas others may have their basis in individual lifestyle. The present paper first describes the various different views of the aging process from a biological perspective (evolutionary, probabilistic, deterministic views) and then outlines how these universal biological changes are boosted or buffered by negative or positive individual lifestyles focusing on recent research using telomere length as a biomarker of aging. We conclude that this perspective on lifestyle-de- pendent differential plasticity of universal biological aging can be used by clinicians to promote healthy aging.

Keywords: biological aging, telomere length, theories of aging, free radicals

Introduction

Biological changes observed in humans with increasing age are significant and comprise a wide range of functions and levels. Not only do we develop wrinkles and gray hair while aging, we also lose muscle bone mass and bone weight, we have a lower metabolic rate, longer reaction times, decreased sexual activity, and experience functional declines in all organs. With aging, there are significant de- creases in a number of biological processes. Compared to a 30-year-old (100% benchmark), a 75-year-old human, for example, has only 92% of the original nerve conduction velocity, 80% brain blood circulation, 70% heart capacity, 40% of maximum physical performance, and 38% taste buds. In line with these decreases in performance we find significant losses in all senses (visual, gustatory, auditory). Because of this largely inevitable and universal biological process of loss of viability and increase in vulnerability with aging, practically any system, tissue, or organ in the human body may eventually fail because of aging. Individ- ual lifestyle and individual life context, however, can boost or buffer these universal biological changes. Psychology, in turn, can provide ideas on how to cope with these age- related losses (e.g., SOC model, Baltes, 1987).

In the present paper, we first discuss the major theories of biological aging, categorizing them into the three broad areas of evolutionary, probabilistic and deterministic aging theories. In the second part, we outline how these universal biological changes are affected by differential negative or positive individual lifestyles or life contexts, focusing on recent research using telomere length as a biomarker of aging.

Evolutionary Aging Theories

From an evolutionary perspective, one major puzzle is why there is an aging process at all, as aging is clearly a disad- vantage to individual life? According to an early theory by Weismann, aging benefits the group, even though it may be detrimental to the individual, a theory known as group selection. After discrediting this theory himself, Weismann then developed a theoretical idea now known as the dispos- able soma theory (Kirkwood, 1997, 2002), stating that the organism separates germ and soma in order to maintain reproductive power due to evolutionary pressure.

Another interesting assumption is that evolution has no mercy on the later human years because a much shorter lifespan in phylogeny means natural selection could not operate on later life. Baltes (1997) argues that the benefits of evolutionary selection reveal a negative age correlation in that the human genome of older adults contains a larger number of deleterious genes and dysfunctional gene ex- pression than in younger adults (Finch, 1990). Because nat- ural selection primarily relies on reproductive fitness, i.e., the transmission of genes during reproductive periods, the first half of life is favored by natural selection. In the sec- ond half of life, negative genetic influences (deleterious and dysfunctional genes) become increasingly manifest. Over a long period of human phylogeny, individuals died before these negative genetic influences could even affect the organism. Neurodegenerative diseases in general and Alzheimer’s disease (AD) in particular represent examples of ailments that typically do not become manifest until after the age of 70. According to Baltes (1997), since old age is

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an evolutionarily relatively young period in individuals’ life, the lifespan of modern humans displays the unfinished evolutionary architecture for the later periods in life.

Stochastic Aging Theories

Stochastic aging theories rely on the core idea that, while individuals age, a significant amount of biological damage is accumulated over time in a random fashion as a by-prod- uct of normal living. These accumulated damages pose an increasing biological threat to the aging individual. The core ideas of stochastic aging are three prominent theories, i.e., the theory of wear and tear, the theory of somatic mu- tation, and the theory of free radicals generation.

The wear and tear theory proposes that with usage of the body and over time, cumulative damage occurs within the body leading to death of cells, tissues, organs, and fi- nally, the organism itself. Like components of an artifact, e.g., a car, the body or specific parts thereof wear out from repeated use. This theory sounds perfectly reasonable to the layperson because that is what is also what we observe hap- pening to things around us. As intuitively appealing this theory is, it cannot explain a number of research findings. In mammals, for example, the cellular and molecular basis of the organism is very similar, but there is a wide range of mammal lifespan (100:1 between Argentine desert mice to humans, for example). Even given organisms of similar size, design, activity, and metabolism, we observe signifi- cant differences in their lifespan. Additionally, the wear and tear theory cannot explain, for example, why some spe- cies die immediately after reproduction. Given these exem- plary criticisms, simple deterioration due to wear and tear is not supported by biologists today.

The somatic mutation theory states that stochastic chro- mosomal changes happen during the lifespan due to mis- coding, translation errors, chemical reactions, irradiation, and replication of errors. These mutations change the code sequences of ribonucleic acid (RNA) and deoxyribonucleic acid (DNA), leading to accumulated alterations of a cell if these alterations are not repaired. These nonrepaired alter- ations of cells can alter the genetic sequence of a cell in such a way that cells divide in an unrestrained fashion, leading to tumorgenesis and/or cancer. Mutations occur ei- ther in the expression of the genetic code or the way the code is read without directly changing DNA or RNA. This theoretical view very well explains the finding that tumor- genesis, various forms of cancer, and diseases linked to a weak immune system have an increasing incidence rate in later human years.

The free radical theory, proposed by Harman (1956), suggests that free radicals produced during aerobic respi- ration cause cumulative damage resulting in aging and death. By definition, free radicals are an especially reactive atoms or group of atoms with one or more unpaired elec- trons. Because these unpaired electrons are chemically re-

active, they pose a threat to the aging organisms because of oxidative damage. Free radicals are also discussed as a cause of many human diseases like cancer, AD, cardiac reperfusion abnormalities, kidney disease, and fibrosis (see Sarma, Mellick, & Ghosh, 2010, for a review).

In recent years, free radical production has been concep- tualized as a biomarker in mild cognitive impairment (MCI), a potential transitional phase between normal aging and AD. MCI is described for individuals having a specific but significant memory impairment; their memory perfor- mance pattern lies beyond that expected for age- and edu- cation-matched others (Petersen, Smith, Waring, Ivnik, Tangalos, & Kokmen, 1999). Smith et al. (2010) showed that MCI and preclinical AD patients in contrast to age- matched control patients show elevated levels of oxidative stress measured via redox-active iron. Additionally, a study by Cervellati et al. (2014) demonstrated that oxidative stress was significantly increased in MCI and late-onset AD patients. The authors conclude that, overall, their re- sults suggest oxidative stress might be a precocious feature of MCI and late-onset AD, but that oxidative stress as an early prognostic marker of progression to late onset AD needs further investigations.

Deterministic Aging Theories

In contrast to probabilistic aging theories, deterministic theories presume that aging occurs because of genetically and endogenously programmed processes, e.g., absolute metabolic scope theory (Rubner, 1908) and the cell dou- bling theory (Hayflick, & Moorhead, 1961).

The absolute metabolic scope or rate of living theory, a rather old theory, states that the greater an organism’s rate of oxygen basal, e.g., number of calories or heart beats, the shorter its lifespan (see Speakman, 2007, for a review). Historically speaking, Rubner (1908) compared energy metabolism and the lifespans of five domestic animals (guinea pig, cat, dog, cow, horse) and humans. After mul- tiplying the mass-specific rate of energy expenditure over a maximum lifespan, the resulting data were independent of body size in animals. Variation in expenditure per gram per lifespan was a factor of 1.5 with 50,000-fold differences in body mass. Including humans, the range of variation in expenditure per gram per lifespan was only fivefold. From this reasoning it follows that the total energy expenditure is preset and with increased expenditure, lifespan is neces- sarily decreased.

A second example for deterministic theories, the genetic clock theory, states that some genes keep track of the body’s progress and control the age at which certain events occur. This is known as the Hayflick limit. This limit suggests that the replicative capacity of normal human fibroblasts in cul- ture was not infinite, but that proliferation only continued for about 40–50 fibroblast population doublings. Then, cells subsequently revealed senescence and eventually died

104 T. Kolling & M. Knopf: Late Life Human Development

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(see Bekaert, De Meyer, & van Oostveldt, 2005, for a re- view). As hypothesized by Olovnikov (1971), this is due to a length reduction of telomeres, i.e., the nucleoprotein structures that cap the ends of eukaryotic chromosomes composed of repetitive nucleotide sequences serving to sta- bilize the chromosome and protecting it from deterioration or fuzzy fusion with other chromosomes, with each new cell division. Since these groundbreaking findings, empir- ical evidence has amassed for this telomere-based mitotic clock. It was demonstrated, for example, that the number of fibroblast population doublings (PDs) in different spe- cies is associated with the maximum lifespan of the respec- tive species. In mice, for example, the number of PDs lies at around 14–28, whereas chicken have around 11–35, hu- mans about 40–60 and Galapagos turtles between 90 and 125.

Research on the associations between telomere length (TL) as a predictive biomarker of mortality is still contro- versial, with some studies showing relations between tele- more length and mortality and others not replicating this relationship (see Bischoff et al., 2006; Cawthon, Smith, O’Brien, Sivatchenko, & Kerber, 2003). Especially in the oldest old, associations between telomere length with mor- bidity and mortality are not apparent (Martin-Ruiz, Gus- sekloo, Heemst, Zglinicki, & Westendorp, 2005).

Research has also demonstrated that telomere length is a risk factor for a number of age-related diseases, including associations with cardiovascular disease (Bekaert et al., 2007), type 2 diabetes mellitus (Zee, Castonguay, Barton, Germer, & Martin, 2010), vascular dementia (von Zglinicki et al., 2000) and AD (Panossian et al., 2003; Thomas, O’Callaghan, & Fenech, 2008).

Interestingly, in the human progeroid syndrome (HPS), i.e., the Werner, Cockyane and Hutchinson-Gilford syn- dromes (Martin & Oshima, 2000) the number of population doublings is also significantly reduced. HPS is a very sel- dom clinical case of accelerated aging that is rooted in ge- netic alterations (mutations in LMNA gene). Characteris- tics of Werner syndrome, for example, are shortness of stat- ure and a characteristic habitus (thin extremities with stocky trunk), graying of the hair, premature baldness, patches of apparently stiffened skin, particularly in the face and lower extremities, trophic ulcers of the legs, juvenile cataracts, hypogonadism tendency to diabetes, calcifica- tion of blood vessels, osteoporosis, metastatic calcifica- tions; and tendency to occur in siblings (Thannhauser, 1945).

From a neuropsychological viewpoint, a Scottish study using the Lothian Birth Cohort of 1921 showed that mean peripheral blood leukocyte telomere length at age 79 years of age was associated with psychological verbal fluency tests before and after adjustment for mental ability at age 11 (Harris et al., 2006). In a study with nondemented stroke survivors, longer telomeres at baseline were associated with reduced risk for death and dementia and less reduction in Mini-Mental State Examination score (Martin-Ruiz et al., 2006). In a large study with 2,734 nondemented elders,

Yaffe et al. (2011) measured the cognitive performance lev- el with the modified Mini-Mental State Examination (MMSE) and the Digit Symbol Substitution Test (DSST) repeatedly over 7 years. The authors report that, at baseline, longer telomere length was associated with better DSST scores but not for change in score. However, 7-year MMSE change scores were less severe among those with longer telomere length. Findings were similar after multivariable adjustment for age, sex, race, education, and baseline score. To sum up, TL is increasingly used as a molecular biomark- er to describe age-related diseases and neuropsychological performance.

Individual Lifestyle and Life-Context Components

The main idea here is that the universal and largely inevi- table biological damages discussed so far are buffered or boosted by differential individual lifestyle and individual life context. We exemplify this rationale with recent re- search on the relationships between TL and negative (drinking, smoking, obesity, mood disorders) or positive (exercising, behavioral interventions like meditation) indi- vidual lifestyles and life-contexts.

Chronic alcohol consumption, for example, can result in premature and/or exaggerated aging (e.g., Spencer, & Hutchinson, 1999). Drinking over extended periods of time (alcoholism) demonstrably leads to alcohol-induced oxida- tive stress and free radical damage as alcohol (1) changes the cell’s NAD+/NADH ratio, i.e., a ratio reflecting meta- bolic activities and cell health as a result of alcohol metab- olism, (2) damages mitochondria, (3) has negative effects on cell structure, (4) alcohol-induced oxygen deficiency (i.e., hypoxia) in tissues, (5) effects on the immune system, among others (for a review, see Wu & Cederbaum, 2003). Although this hypothesis that alcohol accelerates biologi- cal processes related to aging is well known, how exactly alcohol drinking accelerates aging processes is not well un- derstood. Pavanello et al. (2011) were the first to compare alcohol abusers and social drinkers with respect to telomere length (TL). They found significantly reduced TL after ad- justing for age, smoking, BMI, diet, job at elevated risk of accident, and genotoxic exposures.

Negative effects of smoking and obesity have also been shown in recent years using TL as a biological indicator of aging. A recent study (Valdes et al., 2005) with smoking and obese women between ages 18–76 years demonstrated that TL decreased steadily (27 basepairs per year). In obese women, telomeres were significantly shorter than in the lean control women. Smoking also significantly reduced telomere length, though length reduction was dependent on dose (i.e., packs smoked per year). This finding indicates that smoking and obesity accelerate human aging: Accord- ing to the authors, smoking corresponds on average to 4–6

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years of aging (smoking a pack a day over 40 years corre- sponds to 4–7 years). Other studies also showed the nega- tive effects of obesity on TL. Interestingly, in an interven- tion study (García-Calzón et al., 2014) with obese subjects (55–80 years) it was demonstrated that TL increases after a 5-year Mediterranean diet intervention. This finding was replicated in a sample with obese adolescents (García-Cal- zón et al., 2014).

In a study with 44 individuals with mood disorders and 44 nonpsychiatrically ill age-matched control persons, Si- mon et al. (2006) demonstrated that telomere length was significantly shorter in mood disorder patients with tele- more length reduction representing as much as 10 years of accelerated aging. Stress as a negative factor also predicted the probability of having short telomeres in a sample of healthy postmenopausal women (Puterman et al., 2010). In a number of other studies, the effects of (chronic) stress on telomere length were also reported (Choi, Fauce, & Effros, 2008; Epel et al., 2004; Epel et al., 2006).

In the study by Puterman et al. (2010) exercising, how- ever, was identified as a prevention factor. Logistic regres- sion analyses indicated a significant moderating effect of exercise in that a 1-unit increase on the Perceived Stress Scale among nonexercisers was related to a 15-fold in- crease in the odds of having short telomeres, whereas among exercisers perceived stress was unrelated to TL. In line with these findings, Cherkas et al. (2008) demonstrated that in an age-mixed twin sample telomere length was pos- itively associated with increasing physical activity level in leisure time even after controlling for age, sex, body mass index, smoking, socioeconomic status, and physical activ- ity at work. A number of other studies also demonstrated the positive effects of exercising on telomere length, not only in aging individuals (Krauss et al., 2011; LaRocca, Seals, & Pierce, 2010), but also in adolescents (Zhu et al., 2011).

Studies using behavioral interventions also demonstrat- ed positive effects on telomere length. In one study, for example, loving-kindness meditation, i.e., a practice de- rived from the Buddhist tradition which utilizes a focus on unselfish kindness and warmth toward all people, was as- sociated with longer telomeres in women (Hoge et al., 2013). Although the study was limited by its small sample size, it nonetheless demonstrates that specific behavioral interventions do have effects on telomere length. Addition- ally, a study in a sample of women with breast cancer using mindfulness-based stress reduction (MBSR) also demon- strated that a short-term MBSR intervention (six weekly sessions) increased telomerase activity but not telomere length (Lengacher et al., 2014).

Last but not least, life context may also influence bio- logical aging operationalized via TL. Life context is mostly operationalized using socioeconomic status in studies with TL as biomarker. How socioeconomic status affects aging on a biological level is still largely unclear, and conflicting results have been found. Whereas Adams et al. (2007) found no association between TL and socioeconomic status

(SES), a number of other studies (e.g., Cherkas et al., 2006) as well as a recent meta-analysis (Robertson et al., 2013) showed some rather low relations between SES and TL.

Conclusions

Summing up the above-mentioned universal biological the- ories of aging and the differential effects of individual life- style and context, we conclude that, first, the different bi- ological views of human aging sketched in the present ar- ticle reveal that biological aging is a largely inevitable process confronting every individual with an increasing amount of physiological challenges and the increasing risk of developing a variety of diseases. As Paul Baltes in an award address to the American Psychological Association put it: “Evolution and biology are not good friends of old age” (Baltes, 1997, p. 368). Or even more radically as in the famous quote by Bette Davis, “Old age ain’t no place for sissies.”

Second, the review of biological aging theories (evolu- tional, deterministic, probabilistic) also indicates that, out of biological research endeavors to describe aging process- es, telomere length has emerged as a very important bio- logical psycho-biomarker of aging (see also Epel, 2009). The research on telomere length described shows that TL is a potential powerful marker from both a clinical and neu- ropsychological perspective.

Third, the findings on how individual lifestyle or life context affects the biological aging processes show that, although the universal lifespan and aging process affect ev- ery individual, a significant plasticity is found in biological aging. This is demonstrated by an emerging field of re- search using TL as psycho-biomarker indicating that neg- ative lifestyle components (e.g., drinking, smoking, chron- ic stress) shorten telomeres, and that positive lifestyle com- ponents (e.g., exercising, healthy diets, behavioral interventions such as meditation) can in fact decelerate the shortening of telomeres with aging.

Future research, however, needs to disentangle the rela- tionships between biological changes, diseases, and psy- chological components (lifestyle) more clearly than previ- ously accomplished (see also Mather, Jorm, Parslow, & Christensen, 2011, for a comprehensive review). For exam- ple, longitudinal multilevel studies using moderator and mediator techniques and experimental research designs might answer open questions on lifespan development of telomere length.

From an applied perspective, the reviewed findings on universal biological aging processes and differential plas- ticity are also an important message for clinicians (e.g., psychiatrists, psychotherapists) as this plasticity of biolog- ical aging can provide new scientific arguments to promote healthy lifestyles in an aging population.

Last but not least, from a psychological point of view, it is important to develop ideas about how older people can

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cope with significant physical decrements that are becom- ing inevitably more severe with increasing age, even given healthy lifestyles. The SOC model (e.g., Baltes, 1997), for example, presents psychological ideas on how an individ- ual may psychologically handle such age-related losses. In addition, age-sensitive living contexts are required allow- ing older individuals to live her/his latest years in autonomy and dignity.

Declaration of Conflicts of Interest

The authors declare that no conflicts of interest exist.

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Manuscript submitted: 30 May 2014 Manuscript accepted after revision: 16 June 2014

Dr. Thorsten Kolling

Department of Psychology Goethe-University Frankfurt Grüneburgplatz 1 60323 Frankfurt am Main Germany [email protected]

108 T. Kolling & M. Knopf: Late Life Human Development

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