Sexually Transmitted Diseases (4th edition) (II)
My initial plan was to read the book from cover to cover. Today I realized that the book has more than 2000 pages, and so I probably will not read all of it.
Anyway, some stuff from part 2 (chapters 6-9) of the book, on Social and Psychological Dimensions of Sexuality, which I read today:
ii. “Network epidemiology offers a comprehensive way of thinking about individual sexual behavior and its consequences for STI. Unlike other health-related behaviors (e.g., smoking and seat belts), behaviors that transmit STI directly involve at least two people, and the links either of these persons might have to others. Understanding this process requires moving beyond the standard, individual-centered research paradigm. This has important implications for the analytic framework, data collection, and intervention planning. […] the network perspective changes the way we think about targeting concepts such as “risk groups” and “risk behaviors.” The inadequacy of these concepts became clear as HIV prevalence rose among groups that do not engage in individually risky behavior, for example, monogamous married women.2, 3, 4, 5 By the same token, a group of persons with extremely “risky” individual behavior may have little actual risk of STI exposure if their partners are uninfected, and not linked to the rest of the partnership network. It is not only individuals’ behaviors that define their risk, it is their partners’ behavior and (ultimately) their positions in a network.
The network perspective also changes the way we think about population-level risk factors: the key issue is not simply the mean number of partners but the connectivity of the network, and connectivity can be established even in low density networks. One of the primary ways in which this happens is through concurrent partnerships. Serial monogamy in sexual partnerships creates a highly segmented network with no links between each pair of persons at any moment in time. Relax this constraint, allowing people to have more than one partner concurrently, and the network can become much more connected. The result is a large increase in the potential spread of STI, even at low levels of partnership formation.
Finally, the network perspective changes the way we think about behavior change. Because the relevant behavior occurs in the context of a partnership, individual knowledge, attitudes, and beliefs do not affect behavior directly. Instead, the impact of these individual-level variables is mediated by the relationship between the partners. A young woman who knows that condoms help prevent the sexual spread of HIV may be unable to convince her male partner to use one. It is not her knowledge that is deficient, but her control over joint behavior.
Networks thus determine the level of individual exposure, the population dynamics of spread, and the interactional context that constrains behavioral change. Taking this seriously represents a paradigm shift in the study of STI.”
iii. “Using network analysis, researchers have identified two basic behavioral patterns that have a large impact on the STI transmission network: selective mixing and partnership timing. Selective mixing is about how we choose partners: the population comprises several subgroups and the question is how many partnerships form within and between groups. Partnership timing is about the dynamics of relationships: monogamy requires partnerships to be strictly sequential, concurrency allows a new partnership to begin while an existing partnership is still active. Both are guided by norms that influence individual behavior, which in turn create partnership network structures that leave distinctive signatures on transmission dynamics and prevalence.
Partnership networks also have other structural features that can be important for STI spread. One example is closed cycles, e.g., the triangles and odd-numbered cycles that can emerge in same sex networks, and larger even-numbered cycles for heterosexual networks. Closed cycles have the effect of sequestering an infection and preventing further spread outside the cycle.”
iv. “Age mixing is generally assortative, but shows an asymmetry among heterosexual couples, with males typically older than their female partners. Age is also an attribute that changes over time. The net impact on transmission dynamics depends on whether the STI is curable or incurable. For curable STIs, prevalence will typically peak among youth, since rates of partner change are high in this group and partners are typically of similar ages, so the STI circulates rapidly within group. In the United States, for example, about 70% of all chlamydia cases and 60% of all gonorrhea cases are found among persons 15-24 years of age.48 Age matching will lead to higher prevalence among youth in this case, as it intensifies the spread within this group. Incurable STI, by contrast, will accumulate with years of exposure, so higher prevalence should be found among older groups for these STIs. For example, in the United States, only 11% of persons living with HIV are in the 15-24-year-old age group.55 In this case, assortative age mixing will (all else equal) protect youth by lowering their exposure to higher prevalence older partners.56”
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v. “In the earliest studies of partnership sequencing effects, researchers focused on monogamy and the duration of monogamous partnerships. Long-term monogamous pair formation slows down the rate of disease transmission, as concordant pairs provide no opportunity for spread, and discordant pairs remain together after transmission has occurred. Analytic findings support this intuition: increasing partnership duration raises the number of contacts needed to reach the reproductive threshold, lowers the peak number infected, and increases the time to peak infection.89, 90, 91, 92
Attention then turned to the impact of concurrency, to understand the impact of relaxing the rule of monogamy.93, 94, 95 Concurrency has several consequences that lead to amplified transmission. First, as the earlier research showed, concurrency reduces the time between transmissions: the pathogen is not trapped in a partnership since there is another partner available for immediate subsequent transmission. Second, concurrency removes the protective effect of sequence. Under serial monogamy, earlier partners in the sequence are not exposed to infections that the index case acquires from later partners. Under concurrency, earlier partners lose this protection. In Fig. 7-2, partner 1 is indirectly exposed to partner 2, and partner 3 is exposed to partner 4. Not only does this expose two additional persons, it creates two new potential chains of infection from these persons to others.96 Third, concurrent partnerships link individuals together to create large connected “components” in a network—if you have more than one partner, then your partner may have more than one partner, and so on. Such connected components function like a well-designed road network—they allow a pathogen to travel rapidly and efficiently to many destinations.
Concurrency increases the speed of STI transmission through a population. […] a substantial number of studies have examined concurrency, and in general the findings have confirmed its importance for STI transmission.”
vi. “Given the high prevalence of HIV among MSM [men who have sex with men, US] in many large cities, averaging about 25% in the United States but ranging by city from 18 to 40%,66 HIV infection per se has become a very salient issue for MSM partnerships. The likelihood of being in a partnership, albeit of short or long duration, with someone having HIV infection is much more likely for MSM than it is for heterosexuals. This makes discussion of HIV status a particularly important dynamic for MSM within their partnerships. Disclosure of HIV status remains a challenge for HIV-positive MSM; among those reporting unprotected sex, almost half67,68 reported not disclosing their HIV status to prospective sex partners prior to having unprotected sex, and even fewer report disclosing within their casual partnerships.69 Within more intimate partnerships there is a tension between facing fear of rejection from a partner and wanting to share the information with that partner, often resulting in a delay of the discussion. 70”
vii. “Hart23 has argued not only that there is increasing recognition of venereal disease as a behavioral disease, but that psychological variables implicated in venereal disease may be primarily related to the personality of the individual. He reported for his heterosexual sample that an increase in extroversion, and to a lesser extent neuroticism as measured by the Eysenck Personality Inventory,24 were associated with increased STI. Similar findings are reported by other researchers: Eysenck found that extroverts will have intercourse earlier, more frequently, with more different partners and in more different positions than introverts: they will also engage in more varied sexual behavior outside intercourse and engage in longer foreplay.25 […]
Eysenck25 found that high psychoticism scorers (those who tend to be isolated, affectless, and aggressive) were also more sexually curious, more accepting of premarital sex, more promiscuous, and more hostile. Extroverts scored as more promiscuous and less sexually nervous, while high scorers on the neuroticism scale had significantly lower scores on sexual satisfaction and significantly higher scores on excitement, nervousness, sexual hostility, sexual guilt, and sexual inhibition.
The association between romantic love, conceptualized as a possibly biologically programmed urge to fall in love, that intellectually blinds the individual, and STD acquisition, is reviewed by Goldmeier and Richardson.35 They see romantic love as akin to an obsessional condition in which euphoric mental states override the rational aspects of a decision to have sex or safer sex. Goldmeier and Richardson note research36 shows that people “in love” differed from controls in having reduced serotonin transporter sites (measured in platelets, and perhaps reflecting a putative “altered serotonergic tone,”) and that being “in love” is associated with raised cortisol levels until the initial throes of love dissipate in 12-24 months. They argue that these data support the contention that romantic love produces a “deterministic and nonlogical response to have sex and thus acquire an STI” and that biological states produced by being “in love” may drive some STI-related risk behaviors.”
viii. “There is a large literature on the response to genital herpes infection, reviewed by Longo and Koehn.69 […] For people who have had genital herpes for less than a year, negative life events, depression, anxiety, anger, and social alienation predict herpes simplex virus (HSV) recurrences; after a year, high levels of depression and low self-esteem are consistently associated with more frequent HSV recurrences. It is important to note that responses to infection may lead to these states, thus setting up a cycle of response and recurrence. […] Carney et al.,71 in a longitudinal study, found that the first episode of genital herpes had a substantially negative psychological impact, with over 60% meeting screening criteria for being a psychiatric case as measured by the General Health Questionnaire. However, two-thirds of these became noncases if there were no recurrences of disease: if there were recurrences, the level of psychiatric case classification stayed high. A clinical study72 found that the majority of people with genital HSV report that infection made them less capable of physical warmth and intimacy, enjoy sex less, and feel less sexually desirable. This extended outside sexual contacts: all reported that work performance was also hampered. A majority reported disturbance of affect, feeling that genital HSV is incompatible with happiness, and feeling pessimistic about the future course of the illness. Depression was also reported by 84%. Sexual dysfunctions including reduced interest, reduced ability to achieve orgasm, avoidance of intimacy, and reduced enjoyment of sex, as well as feeling repugnant to others […]
Psychological complications of HIV infection may be exogenous or endogenous. Exogenous complications arise from the psychosocial stresses resulting from negative societal and interpersonal reactions to AIDS. Faulstich87 notes that the “worried well” (whether infected or not) may exhibit generalized anxiety and panic attacks, along with excessive somatic preoccupation and fear of the disease. On diagnosis of HIV infection or AIDS, individuals may exhibit disbelief and denial, followed by depressive and anxiety symptoms. Emotional distress may commonly lead to adjustment disorders with depressed mood or major depression. Recurrent psychological themes include uncertainty about disease progression, social isolation (imposed or adopted), dealing with terminal illness, and guilt or blame over lifestyle. Suicidal ideation may be present. The advent of HAART may have lowered the intensity of the psychological impact of HIV infection in places where HAART is accessible, as can medical feedback about success or failure of treatment regimens.88
Endogenous complications result from the neuropsychiatric sequelae of HIV infection, either from the direct effect of HIV infection, on the central nervous system (CNS), opportunistic CNS infections, or CNS neoplasia. Up to half of patients with AIDS in the absence of HAART may present signs and symptoms of CNS infection, including subacute encephalitis characterized by malaise, social withdrawal, lethargy, and reduced sexual drive (these may also be signs and symptoms of depressed mood, or of systemic disease).
Subsequently, signs of progressive dementia may appear. Neuropsychiatric deficits resulting from HIV may typically involve impaired language, memory and integrative abilities, and occasionally depressed mood, and their insidious onset makes it important to maintain a high index of suspicion that psychological symptoms may indicate onset of CNS involvement. Although rarer, tertiary syphilis may also involve the CNS and include psychological symptoms. […]
Nilsson Schönnesson and Ross90 found that psychological adaptation occurs but as the disease enters each new phase (asymptomatic, mild symptomatic, severe, and terminal), psychologic symptoms reoccur. Mood states in the asymptomatic and mild symptomatic phase typically included anger, whereas disappointment, sense of violation, and feelings of aloneness characterized the terminal phase, with powerlessness and helplessness being expressed in all phases.”
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