S2 W5 Adolescence Flashcards

1
Q

Sex difference = Puberty = hormones

A

Female = high estrogen and progesterone, low testosterone.
Intersex = variable hormone levels and responsiveness.
Male = higher testosterone and dihydrocortisone.

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2
Q

Puberty

A

a period of rapid physical growth and sexual maturation. The sequence of physical changes is universal, but the timing varies (typically lasting for 3-5 years). Age of onset also varies between 8-15 years

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3
Q

Onset of puberty = Menarche

A

= the term for a cis girl’s first period. It signals that ovulation has begun (although is often irregular for a few years). (= start of reproductive function has begun)

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4
Q

The onset of puberty = Spermarche

A

= the term for a cis boy’s first ejaculation, which signals sperm production has begun. (= start of reproductive function has begun)

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5
Q

Age of onset varies depending on …

A

Sex = girls ahead of boys by months or years.
Genes and ethnicity.
Weight = malnutrition delays puberty, obesity the reverse.
Stress = causes puberty earlier.

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6
Q

Emotions

A

Hormones contribute to the conflict, moodiness, and sexual urges of adolescents, but are not the only cause. Social and cultural reactions to visible body changes also play a large role.

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7
Q

Physical changes = Puberty

A

Skin gets oilier, sweatier, and more acne-prone.
The lymphoid system (tonsils, adenoids) decreases in size. This makes teens less susceptible to asthma and colds.

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8
Q

Status of Gonadal ( testis, ovaries) functions in Children

A

Very low levels of sex hormones: testosterone (T) for boys and estrogens (E) for girls.
Very low levels of GnRH (in the hypothalamus) and FSH/LH (in the anterior pituitary).

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9
Q

Bio trigger for puberty

A

(both boys + girls) = production of gonadotrophin-releasing hormone (GnRH) from the hypothalamus.
GnRH stimulates the pituitary gland which releases a luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
These two hormones signal the female and male sex organs (i.e., the gonads) to release sex-dependent hormones. Different receptors.

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10
Q

Bio sequences of puberty = Primary sex characteristics

A

The parts of the body directly involved in reproduction (e.g., testicles, ovaries, penis, vagina, etc.).

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11
Q

Bio sequence of puberty = Secondary sex characteristics

A

Not necessary for reproduction (e.g., odor, acne, breast development, hair, voice changes).

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12
Q

Maturation of reproductive function

A

is only one of many physiological changes that occur at adolescence. Immaturity is not at the level of the gonads or the anterior pituitary BUT at the level of the BRAIN - primarily, limbic structures and hypothalamus.

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13
Q

the limbic hypothalamic pathways responsible for prepuberty immaturity.

A

Immature gonads transplanted into an adult animal will mature immediately and demonstrate a normal reproductive function.
The pituitary, taken from a prepubescent animal and transplanted into an adult animal, will regulate normal reproductive function.
Alterations/lesions/trauma of the hypothalamus and specific areas in the limbic system (e.g., amygdala, hippocampus) will prevent the prepubertal animal from developing a normal reproductive function. (damaging these areas can cause issues, such as infertility.)

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14
Q

Mental disorders begin in adolescence

A

Kessler et al. (2005) found that 1/2 of all lifetime cases started by the age of 14 years and 3/4 by the age of 24 years.
Anxiety is much higher than all the other groups of disorders. Behavior is the second most prevalent disorder in children/adolescents.
Not all mental health disorders are equal and are of concern in all stages of adolescence (prevalence)

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15
Q

Sexual Dimorphism (Kieling et al. 2024)

A

Anxiety disorders (phobias, separation anxiety) have their onsets either early, mid or late in adolescence. (social aspects to them)
Sexual dimorphism = mood (isolating) disorders are more present in females and more behavioral disorders are present in males. This could be linked to diagnosis and not only prevalence. Similar onset but different prevalence

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16
Q

Substance use disorders

A

Alcohol and drug use/abuse increase with age during adolescence and peaks in early adulthood.
Degenhardt et al. 2008 = alcohol (16-19), Cannabis (18-19), Cocaine (21-24)

17
Q

Nature and Nurture = Alcohol use

A

Dick et al. 2016 = Found a changing degree of genetic and environmental influences across adolescence on alcohol use behavior.
A steady increase in the influence of genetic factors on alcohol use across adolescence. Also, a corresponding decrease in the influence of common environmental factors (Rose et al., 2001a; 2001b).

18
Q

Substance + psychosis

A

Substance use can increase risk of psychosis.
Bourque et al. 2017 = suggest that becoming a more regular marijuana user during adolescence is associated with an increased risk of psychotic symptoms (not necessarily psychosis!).
In healthy humans, cannabis and its principal psychoactive component (Tetrahydrocannabinol [THC]), can produce transient, dose-dependent, psychotic symptoms as well as cognitive effects.

19
Q

Substance use and brain

A

= Exposure to cannabinoids in adolescence results in structural brain changes and impaired synaptic plasticity, impacting front-limbic systems that are critically involved in higher brain functions.
= THC concentrations, other environmental factors, and genetic predisposition likely play a role in the strength of the risk cannabis poses to the user.

20
Q

Models of adolescents = historical perspectives

A

G. Stanley Hall viewed adolescence as a “period of inevitable turmoil” that takes place during the transition from childhood to adulthood. Particularly focused on aggression and crime.
Proposed the ‘Storm and Stress Model’ of adolescence (1904).

21
Q

Storm and Stress Model’ of Adolescence (G.Stanley Hall, 1904)

A

= considers evolutionary, hormonal, and environmental factors (e.g., life stressors).
= Human development reflection of the evolutionary development the species went through. From “animalistic” => “civilized”.
= the earlier maturation of the “primitive” (i.e., subcortical) areas of the brain in comparison to the “higher functioning” (i.e., prefrontal cortex) areas.

22
Q

Dual systems models Maturational imbalance model (Casey et al, 2008)

A

Suggests that there is an imbalance between systems that mature early in development (i.e.supcortical regions, ) and systems that are late to mature (i.e., cortical regions). This imbalance gives rise to adolescent-specific behaviors – such as a greater propensity to take risks (Casey, 2015).

23
Q

Social Emotional Processing

A

Ventral striatum (VS) = is responsible for the salience of behavior and motivation.
Amygdala (AMY) = responsible for emotion processing and fear responses.
Prefrontal cortex (PFC) + anterior cingulate cortex (ACC) = responsible for executive function, behavioral control, and decision making.

24
Q

Maturational imbalance model

A

Model for enhanced ‘affective and incentive-based’ behavior in adolescence.
Early maturation of subcortical regions such as the amygdala and ventral striatum (top line) and late maturation of prefrontal cortical regions (bottom line).
Predicts a nonlinear enhancement in affectively driven (i.e., emotion-driven) behavior during adolescence.

25
Q

Adolescents response to taste ( sensation seeking, reward sensitivity)
Galvan and McGlennan, 2013

A

Tested 2 groups on their response to taste: 15 adolescents (13-17Y) and 15 adults (23-25); Exposed to 2 different types of stimuli: Appetitive - sucrose water. Aversive - salt water
Adolescents rate sucrose more positively and salt more negatively than adults.
Ventral striatum = more activated by sucrose water in adolescents than in adults.
Caudate = more activated by salt water in adolescents than in adults.
Insula = more activated by salt water in adults than in adolescents.

26
Q

Adolescents response to faces

A

Hare et al. (2008) = 3 groups on their responses to emotive faces: 12 children (7-12Y). 24 adolescents (13-18Y) 24 adults (19-32Y). with fearful, happy, and calm facial expressions as targets and nontargets.
Greater amygdala activation (definitely in negative response)

27
Q

Risk-taking in adolescents

A

Chein et al. 2011 = Randomly assigned late adolescents (ages 18 and 19) to complete a series of tasks either alone or in the presence of two same-age, same-sex peers. Risk-taking propensity was assessed using the Stoplight game.
Performed more risky decisions when with peers (peer pressure) and had more numbers of crashes with peers.

28
Q

Dichotomous frameworks

A

competing cognitive control and emotive systems.
Dual systems accounts: behavior breaks down when emotional systems win out over less mature cognitive control systems: rewards vs control systems. Doesn’t account for the complexities and temporal time course of emotionally driven behaviors.

29
Q

The imbalance models

A

circuit-based account of the complex nonlinear ways in which emotion reactivity/regulation change with age. Changes in behavior during adolescence concise with developmental changes across system with fine-tuning of connections within subcortical limbic circuits, then between cortical prefrontal and limbic circuits and subsequently between corticocortical circuits