Adolescent Physical Development PDF

Chapter 1: Adolescent Physical Development Learning Objectives: Introduction 1. Summarize the overall physical growth 2. Describe physical development during puberty 3. Define and describe sexual dimorphism in humans 4. Describe adolescent brain development 5. Describe the chang...

Chapter 1: Adolescent Physical Development Learning Objectives: Introduction 1. Summarize the overall physical growth 2. Describe physical development during puberty 3. Define and describe sexual dimorphism in humans 4. Describe adolescent brain development 5. Describe the changes in sleep 6. Identify nutritional concerns 7. Describe common physical health concerns during adolescence. 8. Describe causes of death during adolescence and explain how these differ from those of childhood Physical Growth in Adolescence Age ♂ ♀ % ♂ ♀ % (Year) Height Height Difference Weight Weight Difference 12 58.78 59.64 -1.44% 89.47 92.03 -2.77% 13 61.58 61.94 -0.59% 100.78 101.16 -0.37% 14 64.62 63.18 2.28% 112.71 108.88 3.52% 15 66.98 63.74 5.08% 124.28 114.71 8.34% 16 68.35 64.00 6.79% 134.42 118.69 13.25% 17 69.03 64.14 7.62% 142.34 121.40 17.25% 18 69.37 64.22 8.01% 148.04 123.71 19.67% Table 1-1. Average height and weight for American adolescents (CDC). Puberty begins toward the end of middle childhood when increases in pulsatile hypothalamic GNRH secretion cause FSH and LH to stimulate the gonads to begin secreting sex steroids (see Chapter 2). Sex steroids then cause rapid growth and sexual maturation. These changes begin between 8 and 13 years of age in girls and 9 and 14 in boys (Breehl & Caban, 2022). Humans develop slowly and so sexual maturation is not achieved until 3-5 years after the beginning of the growth spurt. Sexually mature individuals are fertile and able to reproduce. Species that spend a long time as pre-reproductive juveniles can only do so if mortality during this stage is low. There is variability in the timing of puberty in humans and psychologically adverse environments can stimulate earlier puberty in girls and possibly in boys (Bleil et al., 2021; Pham et al., 2022). Undernutrition delays puberty so psychological and physical stressors have opposite effects on the timing of puberty. During the period of rapid growth in 11–18-year-old youths, growth proceeds from the extremities toward the torso, a pattern called distalproximal development. First the 1 hands grow, then the arms, and finally the torso. The overall physical growth spurt results in 10-11 inches of added height and 50 to 75 pounds of increased weight. The head begins to grow sometime after the feet have gone through their period of growth. Growth of the head is preceded by growth of the ears, nose, and lips. The difference in these patterns of growth may result in adolescents appearing awkward and out-of-proportion. A person’s final height is highly correlated with the average of their biologic parents’ height, corrected for sex differences. Final height is 41-71% heritable. Environmental factors act long before puberty as final height correlates only.2 with birth length but.8 with length at age 2. On average, identical twins’ height difference is only 1 inch. There is a secular trend in height such that since the industrial revolution in WEIRD nations people have been growing about an inch taller every decade. Height appears to have leveled off and is not expected to continue to increase. Growth curves reflect the overall health of a child (Rogol et al., 2002). Sex steroids lead to sexual dimorphism in humans meaning physical differences between males and females. By age 18 the average American male is 8% taller and nearly 20% heavier than the average American female (Table 1.1). Because boys and girls are about the same size before puberty, boys must grow more. At age 12 the average boy is 84% of his final height and the average girl is 93% of her final height (Table 1.1). Species Mating Weight Range of Dimorphism in System Dimorphism (M/F) Groups (M/F) Human TBD 1.15 1.09-1.28 Bonobo promiscuous 1.29 Chimpanzee promiscuous 1.36 Gorilla polygyny 2.23 1.63-2.37 Orangutan polygyny 2.37 Gibbon sp. monogamy 1.03 0.91-1.08 Table 1-2. Body weight dimorphism in humans compared to apes. TBD= to be determined in later discussions (Larsen, 2003; Leigh & Shea, 1995; Muller et al., 2020). You might be asking, why are psychologists interested in sexual dimorphism? The reason is that sexual size dimorphism is one indication of a species’ mating system, or the way society organizes mating partnerships. In promiscuous societies females freely choose multiple mates and do not form special bonds with any of them. Polygynous societies are organized into families where one male has multiple females. Individual males and females form long-term bonds in species that practice monogamy. It is unusual for monogamous species to live in extended social groups. Instead, the social unit is the nuclear family and offspring leave once they are sexually mature. Sexual size dimorphism is highest in polygynous and promiscuous species because male competition is high and larger males have an advantage. 2 When males form coalitions that help them gain mates, size is no longer as much of a factor. For this reason, chimpanzees and bonobos do not have high dimorphism. Monogamy exists in species where males and females are the same size. Notice that size dimorphism in humans is greater than that of monogamous gibbons but less than that of promiscuous chimpanzees and bonobos; and it is much less than that of polygynous gorillas and orangutans (Table 1.2). Sexual dimorphism includes differences in the skeleton, musculature, and body fat. Most of the weight difference is due to more muscle mass in males. Boys are more muscular from childhood onward and girls increase body fat relative to boys after age 10. (The body stores energy as fat because muscle tissue weighs more than fat tissue (3 times more per calorie stored).) Adult men have 150% of the muscle mass of women and twice the number of muscle cells (Rogol et al., 2002). It is important for adolescents to gain bone calcium prior to age 20 because lack of bone mass at that age predicts osteoporosis later in life (Rogol et al., 2002). Body fat in the average teenaged boy is 23% of body weight; the average body fat in teenaged girls is 33%. In addition to larger size, men have muscular, respiratory, and cardiovascular adaptations that give them an advantage in athletic competition (Table 1-3). Characteristic Difference Size Men are 8% taller and 20% heavier than women. Body Composition Women’s bodies have about 40% more fat stores Muscles Muscle mass is 150% greater in men. Men have twice the number of muscle cells. Bone Skeletal maturation is due to estrogen in both sexes. Men have larger bones (Iuliano-Burns et al., 2009). Cardiovascular Men have larger hearts and more red blood cells. Normal red blood cell count is 41-50% for men and 36-48% for women (Hematocrit, n.d.). Lung Function Men have larger lung volumes and more efficient responses to exercise (LoMauro & Aliverti, 2018). Larynx Men have larger larynx and deeper voice. Facial Features Men have larger jawbones, more prominent cheekbones and brow ridge, thinner cheeks and lips (Hu et al., 2018). Table 1-3. Some sexually dimorphic human characteristics. Brain Development During Adolescence The brain is another sexually dimorphic organ in humans, but the details of developmental sex differences are not completely described. Healthy individual males and females also differ widely with respect to the size and structure of the various regions of the brain. Controlling for body size, the average male brain is 9% larger than 3 the average female brain when the brain reaches peak size at 11.5 years for females and 14.5 years for males (Lenroot & Giedd, 2006). Hence the male brain develops more slowly than the female brain. The ventricles or fluid filled spaces within the brain continue to increase into the early 20s and are correspondingly larger in males compared to females. Imaging of the brain reveals areas of grey matter, or clusters of cell bodies, and white matter or tracts of myelinated fibers. Both the outer cerebral cortex and the inner subcortex contain grey and white matter areas. The grey matter of the areas of the cerebral cortex matures at different rates. The parietal lobe reaches peak volume at age 10.2 years for females and 11.8 for males. The frontal grey matter reaches peak volume at age 11 for females and age 12 for males. The last to develop is the temporal lobe which does not reach peak volume until age 16.7 for females and 16.2 for males (Lenroot & Giedd, 2006). After these ages volumes decline because the adolescent brain undergoes the reorganization that makes advanced adult cognition possible (Feinberg & Campbell, 2010). Adolescent brain reorganization involves pruning of synapses along with strengthening of the connections that remain. The adult brain therefore operates more efficiently than the brain of children and adolescents. Increased efficiency means that adult brains use less energy than children’s brains. After adolescence, the brain relies solely on glucose for energy. Whereas the brains of children and teens use ketones for fuel, adult brains only use ketones when glucose levels are low after prolonged fasting (Feinberg & Campbell, 2010). Synaptic pruning and reorganization are accompanied by increases in white matter throughout adolescence in both females and males. Large growth in myelination of the corpus collosum is seen. This structure consists of 200 million fibers that connect the right and left cerebral cortex (Lenroot & Giedd, 2006). Myelination also makes the adult brain more efficient. One prevailing theory of adolescent brain development asserts that the subcortical structures responsible for reward and emotions develop before the cortical structures that regulate them. There is therefore an imbalance between reason/self-regulation and emotion during adolescence that is similar to the imbalance that occurred years earlier during early childhood. Read more: Adolescent Brain Development, available to all through NCBI or watch the Frontline Documentary: Inside the Teenage Brain. Sleep Changes During Adolescence The synaptic reorganization that occurs during adolescence causes reduced need for sleep (for complete discussion see (Feinberg & Campbell, 2010)). Children’s brains work harder during the day and so children feel sleepy by 8 or 9 PM. When children fall asleep, they experience deep sleep the first half of the night as the brain restores itself. 4 Adenosine accumulation is at least partly responsible for the developmental changes in sleep (Bjorness & Greene, 2009). Neurons produce adenosine when they work hard during the day. With each waking hour more adenosine builds up and causes sleepiness. During deep sleep early in the night the adenosine that accumulated is cleared. As the brain becomes more efficient over the teen years, adenosine does not accumulate as much and so teens do not get tired as early as children. You are likely very familiar with these effects of adenosine because caffeine causes wakefulness by blocking adenosine receptors. Whereas deep sleep occurs early in the night, REM sleep occurs more in the second half of the night. Adolescents and adults retain this overall pattern but because the brain is more efficient, they don’t feel tired as early and they need less deep sleep to clear the adenosine. Therefore, the sleep EEG changes during adolescence. Delta waves that indicate deep sleep change shape and occur less in adults. The sleep EEG changes exactly parallel the age-related reductions in brain volume that accompany synaptic pruning. Adenosine accumulation is one part of “sleep homeostasis” and how quickly a person falls asleep is a marker for this homeostasis. The more sleep deprived a person is, the faster they fall asleep, and the more deep sleep they experience (Carskadon et al., 2004). In addition to mechanisms of sleep homeostasis, diurnal rhythms of certain hormones also contribute to sleep-wake cycle changes during adolescence. Sleep is best when sleep homeostasis mechanisms are in synch with diurnal rhythms of hormones. Jet lag and sleep problems occur when the two are out of synch. Melatonin is a sleep- inducing hormone that is secreted by the pineal gland at night. The suprachiasmatic nucleus of the hypothalamus is the brain’s clock. It receives light information from the retina and then inhibits the secretion of melatonin during the day. At the beginning of adolescence, evening melatonin secretion decreases, and this decrease also contributes to adolescents staying up later (Carskadon et al., 2004). In addition to changes in the melatonin rhythm, adolescents also develop rhythms of cortisol and gonadal steroids. Cortisol, estrogen, and testosterone typically peak in the morning and are lowest in the early evening. Together, hormonal rhythms and increased brain efficiency lead to adolescents staying up later and having a difficult time waking up early in the morning. The adolescents social world also changes such that they may be online and exposed to bright light in the evening and their school day may start earlier than it did when they were younger. As a result, teens in many WEIRD nations are sleep deprived. Adolescents require 8-9 hours of sleep each night. Over the past 30 years the number of adolescents reporting less than 7 hours of sleep each night has increased to over 60% (Keyes et al., 2015). Sleep deprivation may be a factor in driving accidents, substance abuse, weight gain and mood problems (Carskadon et al., 2004). Sleep is also important for memory 5 consolidation and learning. Sleep deprived high school students may have impaired academic performance (Carskadon et al., 2004). Nutrition in Adolescence The rapid growth of adolescents increases the need for total calories, protein, and micronutrients (Table 1-4). Iron deficiency anemia is a common problem for adolescent girls who have increased iron requirements due to menstruation (Das et al., 2017). Calcium needs peak during the stage of maximum bone growth. Obesity is the most important health problem for adolescents; about 22% of teens are obese and an additional 10% are overweight (Shay et al., 2013). The obesity prevalence is 26.2% for Hispanic, 24.8% for non-Hispanic Black, 16.6% for non-Hispanic White, and 9.0% for non-Hispanic Asian teens (Childhood Obesity Facts | Overweight & Obesity | CDC, 2022). The prevalence of obesity in teens has tripled since 1965 when only 7% of teens were obese (Overweight & Obesity Statistics | NIDDK, n.d.). Less than 1% of teens eat a healthy diet (Shay et al., 2013). Only 44% of girls and 67% of boys are sufficiently active (Shay et al., 2013). Poor nutrition, lack of exercise and sleep deprivation all contribute to mental health issues in teens and can be a focus of wellness counseling using cognitive behavioral methods (Hoying et al., 2016). Females Males Ages 9-13 14-18 19-30 9-13 14-18 19-30 Energy (kcal/day) 2071 2368 2403 2279 3152 3067 Protein (g/day) 34 46 46 34 52 56 Fiber (g/day) 26 28 25 31 38 38 Calcium (mg/day) 1300 1300 1000 1300 1300 1000 Iron (mg/day) 8 15 18 8 11 8 Table 1-4. Nutritional requirements for early and late adolescence and early adulthood (Das et al., 2017). Adolescent Health Conditions Studies in WEIRD nations report that 20-30% of teens have a medical issue that lasts longer than six months. In 10-13% of teenagers this chronic condition substantially limits their daily life or requires close medical supervision (Yeo & Sawyer, 2005). Mental health conditions are more significant to teen health than physical conditions, but individuals with poor physical health are at higher risk for mental health problems. Other than being overweight, most adolescents are in good physical health. The negative health effects of inactivity, overweight, and obesity do not manifest in most individuals until middle adulthood. Prevention efforts directed at teens aim to prevent problems later in life (Shay et al., 2013). Unfortunately, many teens have a difficult time planning for their future health because they feel invincible and are more 6 concerned with immediate rewards. Other than obesity, asthma is the most prevalent chronic medical problem in teens (Table 1-5). The high rate of musculoskeletal conditions is due to injuries (Defranco et al., 2009). Condition Prevalence (per 1000) Any mental health condition 367 Asthma 100 Musculoskeletal conditions: 41 Skin conditions 32 Ear or hearing problems 18 Cerebral palsy 15 Epilepsy 4 Diabetes Type 1 2 Diabetes Type 2 2 Cystic fibrosis 0.1 Table 1-5. Prevalence of chronic health conditions (> 3-6 months) in adolescents (Merikangas et al., 2009; Yeo & Sawyer, 2005). Acne Nearly all teens have acne at some point, about half have more persistent acne and 11% have moderate to severe acne that can negatively impact their mental health (Arora et al., 2011; Smithard et al., 2001). The psychological fallout includes much higher rates of clinical depression, anxiety, anger, suicidal thoughts, and even suicide (Arora et al., 2011). Although multiple factors such as testosterone and progesterone levels, contribute to acne development, chronic inflammation is an important mechanism. A bacterium that infects the oil glands, Propionibacterium acnes triggers the inflammation and gonadal steroids increase oil production that encourages this infection (Arora et al., 2011). In some teens, vitamin D deficiency increases the chronic inflammation and vitamin D supplements improve the condition (Lim et al., 2016). 7  Adolescent Mortality “The many biological and socio-psychological changes that adolescents experience contribute to an observed health paradox: adolescence is one of the healthiest times in an individual's life as physical strength and cognitive reasoning capabilities rapidly mature, yet mortality rates in adolescence are 200% greater than in childhood” (Gilbert, 2012, emphasis added). Death rates are low during middle childhood and begin to rise for adolescents after puberty. Death rates for males at age 19 are 6.75 times higher than for age 12. Death rates for females at age 19 are 3.29 times higher than at age 12 (Products - Data Briefs - Number 37 - May 2010, 2019). Between 1999 and 2006, the leading cause of death for teens was accidents (48% of deaths). Most accidents involved motor vehicles (73%); the rest were poisoning including drug overdose (7%), drowning (5%), firearms (2%) and other (15%). After accidents, deaths were from homicide (13%), suicide (11%), cancer (6%) and heart disease (3%). From 1999-2006 there were 49.5 deaths per 100,000 adolescents. In 2020 the top causes of death remained the same, however the death rate rose to 58.6 per 100,000. In 2020 COVID-19 was the 8th leading cause of death for teenagers. There were also 38 deaths due to pregnancy in teenage girls. Black males have the highest death rate and nearly all the excess deaths in this group are due to homicide. Note that mental health issues and risky behavior are the reason for the increased death rate in adolescents compared to children just prior to puberty. Figure 1-1. Death rates from 1999-2006 for youths aged 12-19 years. 8  References Adolescents and STDs | Sexually Transmitted Diseases | CDC. (2022, June 30). https://www.cdc.gov/std/life-stages-populations/stdfact-teens.htm Breehl, L., & Caban, O. (2022). Physiology, Puberty. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK534827/ Congenital adrenal hyperplasia: MedlinePlus Medical Encyclopedia. (n.d.). Retrieved February 18, 2023, from https://medlineplus.gov/ency/article/000411.htm Dunger, D. B., Ahmed, M. L., & Ong, K. K. (2006). Early and late weight gain and the timing of puberty. Molecular and Cellular Endocrinology, 254–255, 140–145. https://doi.org/10.1016/j.mce.2006.04.003 Fisher, W. A., White, L. A., Byrne, D., & Kelley, K. (1988). Erotophobia-Erotophilia as a Dimension of Personality. The Journal of Sex Research, 25(1), 123–151. Friedman, M. S., Silvestre, A. J., Gold, M. A., Markovic, N., Savin-Williams, R. C., Huggins, J., & Sell, R. L. (2004). Adolescents define sexual orientation and suggest ways to measure it. Journal of Adolescence, 27(3), 303–317. https://doi.org/10.1016/j.adolescence.2004.03.006 Gangestad, S. W., & Simpson, J. A. (2000). The evolution of human mating: Trade-offs and strategic pluralism. Behavioral and Brain Sciences, 23(04), 573–587. Gilbert, K. E. (2012). The neglected role of positive emotion in adolescent psychopathology. Clinical Psychology Review, 32(6), 467–481. https://doi.org/10.1016/j.cpr.2012.05.005 Heron, J., Low, N., Lewis, G., Macleod, J., Ness, A., & Waylen, A. (2015). Social Factors Associated with Readiness for Sexual Activity in Adolescents: A Population- Based Cohort Study. Archives of Sexual Behavior, 44(3), 669–678. https://doi.org/10.1007/s10508-013-0162-5 Hoyt, L. T., Niu, L., Pachucki, M. C., & Chaku, N. (2020). Timing of puberty in boys and girls: Implications for population health. SSM - Population Health, 10, 100549. https://doi.org/10.1016/j.ssmph.2020.100549 Klinefelter syndrome: MedlinePlus Genetics. (n.d.). Retrieved February 18, 2023, from https://medlineplus.gov/genetics/condition/klinefelter-syndrome/ Liu, G., Hariri, S., Bradley, H., Gottlieb, S. L., Leichliter, J. S., & Markowitz, L. E. (2015). Trends and Patterns of Sexual Behaviors Among Adolescents and Adults Aged 14 to 59 9 Years, United States. Sexually Transmitted Diseases, 42(1), 20–26. https://doi.org/10.1097/OLQ.0000000000000231 Mallet, P., & Kindelberger, C. (2018). Adolescents’ sociosexual orientation is related to attachment to their same-sex parent. Personality and Individual Differences, 126, 7–11. Pasquino, A. M., Passeri, F., Pucarelli, I., Segni, M., & Municchi, G. (1997). Spontaneous pubertal development in Turner’s syndrome. Italian Study Group for Turner’s Syndrome. The Journal of Clinical Endocrinology and Metabolism, 82(6), 1810–1813. https://doi.org/10.1210/jcem.82.6.3970 Savin-Williams, R. C., & Ream, G. L. (2007). Prevalence and stability of sexual orientation components during adolescence and young adulthood. Archives of Sexual Behavior, 36, 385–394. Sell, R. L. (1997). Defining and Measuring Sexual Orientation: A Review. Archives of Sexual Behavior, 26(6), 643–658. https://doi.org/10.1023/A:1024528427013 Skinner, S. R., Robinson, M., Smith, M. A., Robbins, S. C. C., Mattes, E., Cannon, J., Rosenthal, S. L., Marino, J. L., Hickey, M., & Doherty, D. A. (2015). Childhood Behavior Problems and Age at First Sexual Intercourse: A Prospective Birth Cohort Study. Pediatrics, 135(2), 255–263. https://doi.org/10.1542/peds.2014-1579 Steensma, T. D., Kreukels, B. P. C., de Vries, A. L. C., & Cohen-Kettenis, P. T. (2013). Gender identity development in adolescence. Hormones and Behavior, 64(2), 288–297. https://doi.org/10.1016/j.yhbeh.2013.02.020 Twenge, J. M., Sherman, R. A., & Wells, B. E. (2016). Changes in American Adults’ Reported Same-Sex Sexual Experiences and Attitudes, 1973–2014. Archives of Sexual Behavior, 45(7), 1713–1730. https://doi.org/10.1007/s10508-016-0769-4 Wiepjes, C. M., Nota, N. M., de Blok, C. J. M., Klaver, M., de Vries, A. L. C., Wensing- Kruger, S. A., de Jongh, R. T., Bouman, M.-B., Steensma, T. D., Cohen-Kettenis, P., Gooren, L. J. G., Kreukels, B. P. C., & den Heijer, M. (2018). The Amsterdam Cohort of Gender Dysphoria Study (1972-2015): Trends in Prevalence, Treatment, and Regrets. The Journal of Sexual Medicine, 15(4), 582–590. https://doi.org/10.1016/j.jsxm.2018.01.016 10