“A long-held myth regarding development is that as people age, they all become alike. This view is refuted by the third principle of adult development and aging, which asserts that as people age, they become more different from each other rather than more alike. With increasing age, older adults become a more diverse segment of the population in terms of their physical functioning, psychological performance, and conditions of living. In one often-cited study, researchers examined a large number of studies of aging to compare the amount of variability in older versus younger adults (Nelson & Dannefer, 1992). This research established that the variability, or how differently people responded to the measures, was far greater among older adults. Research continues to underscore the notion that individuals continue to become less alike with age. Such findings suggest that diversity becomes an increasingly prominent theme during the adult years, a point we will continue to focus on throughout this book.
The fact that there are increasing differences among adults as they grow older also ties into the importance of experiences in shaping development. As people go through life, their experiences cause them to diverge from others of the same age in more and more ways. You have made the decision to go to college, while others in your age group may have enlisted for military service. You may meet your future spouse in college, while your best friend remains on the dating scene for years. Upon graduation, some may choose to pursue graduate studies as others enter into the workforce. You may or may not choose to start a family, or have already begun the process. With the passage of time, your differing experiences build upon each other to helpmold the person you become. The many possibilities that can stem from the choices you make help to illustrate that the permutations of events in people’s lives are virtually endless. Personal historiesmove in increasingly idiosyncratic directions with each passing day, year, and decade of life.”
I didn’t post this quote when I first blogged Adult Development and Aging mainly because I figured the insight was probably important enough to merit a post of its own, but also because I figured that if they dealt with this aspect in more details later on I’d rather wait until then to handle the specifics. Anyway it’ll be a while until I get to that stuff and I find myself thinking about these things now and then these days. I’m mostly thinking about how this stuff relates to how we form friendships and establish romantic partnerships. As people age it seems to me that they become less likely to meet that ‘someone who’s just right for me’; and not just because of the work of their romantic rivals. Because of the increasing variation in the behaviours, preferences and outcomes perhaps people who are aging gradually realize that it is strategically optimal for them to become more tolerant, more permissive, and so they implicitly gradually implement such strategies to increase their chances – but that’s hardly always the case and to the extent that it is, the process likely involves them making compromises that perhaps would have been unnecessary if the partners in question had met a decade earlier in their lives. (Though I may here underestimate how much work is required to make a relationship last that long.) Path dependence matters a lot when it comes to both friends and relationships. As I’ve underscored before here on the blog a ‘new’ friend is most often introduced by an ‘old’ friend or acquaintance, and most people rely to a very great extent on their existing social network when they want to make adjustments to it. Over time people’s social networks become entrenched; it gets harder to find and keep new friends not only because every potential new friend is competing for your attention with the whole set of friends you already have, but also because the potential new friend becomes increasingly less likely to share your interests or preferences over time, at the very least when compared with the people with whom you frequently interact. Interaction affects preferences and behaviours, for friends, family and partners alike.
Though people in general tend to become more different from each other as they age, I tend to believe that cohabitating partners do not and that they on the other hand tend to become more alike over time. This is of course because they tend to form similar habits, do similar stuff. Another noteworthy dynamic is the ‘I’ve known you a long time and I’ve invested a lot in this relationship at this point, so it doesn’t matter as much to me that you’re not as compatible as I’d like you to be as it would if we’d only just met’. Of course there’s also (hopefully) the frequent feedback from the partner, making you less likely to stray far away from the partner ideal of the other party – such feedback is harder to obtain for people not in a relationship. There’s also the ‘my previous partner/parents/whatever behaved this way (/cheered for the Green team) and so if you don’t behave this way we won’t be compatible’. Politics, religion and similar stuff’s really important, and often people’s opinions about these matters crystallize over time. If crystallization of this kind of stuff takes place over time, it will generally harm outsiders (singles) and benefit insiders (couples); the people in romantic relationships become more alike over time and so they’ll feel a closer bond to each other as time goes by, and the aging single will in the absence of a romantic partner often obtain much of the relevant social feedback from other singles who may not be able to give useful feedback regarding this aspect of life. For example a single aging man may start to think that his religious- or political views cannot possibly matter a great deal to a potential partner because such things do not matter a great deal to the people with whom he usually interacts. It should perhaps also be noted that the potential decreased compatibility of the remaining outsiders with the insiders makes the outside option become less attractive to the insiders (making them less likely to break up with their partners).
About a decade ago I had relatively few problems talking to and interacting with my extended family (cousins, uncles). These days it’s a pain for me to do it for any period of time, and I found myself actively avoiding the presence of some of these people this Christmas. To the extent that I did interact with them I was polite and helpful, but I did avoid them and I did not want to spend time with them. I find myself worried about where I’ll end up in another decade if things do not go well. Or is it ‘if things do go well?’
I got the book as a Christmas present. I’ve never read anything like this and it’s awesome. Absurd. Confusing. Hilarious. I’m close to calling it a must-read. The book certainly does not belong to the categories of: “Books You Needn’t Read”, or “Books That If You Had More Than One Life You Would Certainly Also Read But Unfortunately Your Days Are Numbered”, or “Books That Everybody’s Read So It’s As If You Had Read Them, Too”, though it does probably belong to the category of “Books You Haven’t Read” (all the previous categories are listed in the book; it turns out there are a lot of book categories..). I assume that for me it’ll at some point become a “[Book] Read Long Ago Which It’s Now Time To Reread.”
There are a lot of ‘stories within the story’, and many of the “I’s” (and “you’s”) in the quotes to follow refer to completely different people. I’ve tried to pick out some quotes illustrating just why this book is awesome, funny, absurd, intriguing and original:
i. “You are about to begin reading Italo Calvino’s new novel, If on a winter’s night a traveller. Relax. Concentrate. Dispel every other thought. Let the world around you fade. Best to close the door; the TV is always on in the next room. Tell the others right away, “No, I don’t want to watch TV!” Raise your voice—they won’t hear you otherwise—“I’m reading! I don’t want to be disturbed!” Maybe they haven’t heard you, with all that racket; speak louder, yell: “I’m beginning to read Italo Calvino’s new novel!” Or if you prefer, don’t say anything; just hope they’ll leave you alone.” [The book’s first paragraph…]
ii. “For a couple of pages now you have been reading on, and this would be the time to tell you clearly whether this station where I have got off is a station of the past or a station of today; instead the sentences continue to move in vagueness, grayness, in a kind of no man’s land of experience reduced to the lowest common denominator.”
iii. “You have now read about thirty pages and you’re becoming caught up in the story. At a certain point you remark: “This sentence sounds somehow familiar. In fact, this whole passage reads like something I’ve read before.” […] just when you were beginning to grow truly interested, at this very point the author feels called upon to display one of those virtuoso tricks so customary in modern writing, repeating a paragraph word for word. Did you say paragraph? Why, it’s a whole page; you make the comparison, he hasn’t changed even a comma. And as you continue, what develops? Nothing: the narration is repeated, identical to the pages you have read!
Wait a minute! Look at the page number. Damn! From page 32 you’ve gone back to page 17! What you thought was a stylistic subtlety on the author’s part is simply a printer’s mistake: they have inserted the same pages twice. […]
The next day, as soon as you have a free moment, you run to the bookshop, you enter, holding the book already opened, pointing your finger at a page, as if that alone were enough to make clear the general disarray. “You know what you sold me? … Look here … Just when it was getting interesting …”
The bookseller maintains his composure. “Ah, you too? I’ve had several complaints already. And only this morning I received a form letter from the publisher. You see? ‘In the distribution of the latest works on our list a part of the edition of the volume If on a winter’s night a traveller by Italo Calvino has proved defective and must be withdrawn from circulation. Through an error of the bindery, the printed signatures of that book became mixed with those of another new publication, the Polish novel Outside the town of Malbork by Tazio Bazakbal. […] A Polish novel. Then the book you began reading wasn’t the book you thought but was a Polish novel instead. That is the book you are now so anxious to procure. Don’t let them fool you. Explain clearly the situation. “No, actually I don’t really give a damn about that Calvino any more. I started the Polish one and it’s the Polish one I want to go on with. Do you have this Bazakbal book?”
iv. “”Me? I don’t read books!” Irnerio says.
“What do you read, then?”
“Nothing. I’ve become so accustomed to not reading that I don’t even read what appears before my eyes. It’s not easy: they teach us to read as children, and for the rest of our lives we remain the slaves of all the written stuff they fling in front of us. I may have had to make some effort myself, at first, to learn not to read, but now it comes quite naturally to me.””
v. “I try to follow her, but she doesn’t turn around.
Several paragraphs ensue, bristling with names of generals and deputies, concerned with the shelling and retreats from the front, about schisms and unifications in the parties represented in the Council, punctuated by climatic annotations: downpours, frosts, racing clouds, windstorms. All this, in any case, solely as a frame for my moods […]”
vi. “”You need another sack to stick over his head,” Bernadette said, and once again I had to admit that girl’s intelligence was superior to what you would expect from one of her background.
The trouble was that we couldn’t manage to find another large-size plastic bag. There was only one, for a kitchen garbage can, a small orange sack that could serve very well to conceal his head, but not to conceal the fact that this was a human body contained in one sack, with the head contained in a smaller one.
But the way things were, we couldn’t stay in that basement any longer, we had to get rid of Jojo before daylight, we had already been carrying him around for a couple of hours as if he were alive, a third passenger in my convertible, and we had already attracted the attention of too many people. For instance, those two cops on their bicycles who came over quietly and stopped to look at us as we were about to tip him into the river […] It seems impossible, in a big city like Paris, but you can waste hours looking for the right place to burn up a corpse.”
vii. “What are you like, Other Reader? It is time for this book in the second person to address itself no longer to a general male you, perhaps brother and double of a hypocrite I, but directly to you who appeared already in the second chapter as the Third Person necessary for the novel to be a novel, for something to happen between that male Second Person and the female Third, for something to take form, develop, or deteriorate, according to the phases of human events. Or, rather, to follow the mental models through which we live our human events. Or, rather, to follow the mental models through which we attribute to human events the meanings that allow them to be lived.
This book so far has been careful to leave open to the Reader who is reading the possibility of identifying himself with the Reader who is read: this is why he was not given a name, which would automatically have made him the equivalent of a Third Person, of a character (whereas to you, as Third Person, a name had to be given, Ludmilla), and so he has been kept a pronoun, in the abstract condition of pronouns, suitable for any attribute and any action.”
viii. “I would like all the details that i am writing down to concur in creating the impression of a high-precision mechanism, but at the same time of a succession of dazzles that reflect something that remains out of eyeshot. For this reason I must not neglect to insert every so often, at the points where the plot becomes thickest, some quotation from an ancient text: for example, a passage from the De Magia Naturale of Giovanni Battista della Porta, where he says that the magician—that is, the “minister of Nature”—must know “the reasons that the sight is deceived, the images that are produced under water, and in mirrors made in various forms, which at times dispel images from the mirrors, suspended in the air, and he must know how things done at a distance may be clearly seen.”
ix. “The plan to trap me envisaged that between the Honda motorcycles of my escort and the armoured car in which I rode, three Yamaha motorcycles would interpose themselves, ridden by three false policemen, who would suddenly slam on their brakes before the curve. According to my counterplan, there would instead be three Suzuki motorcycles which would block my Mercedes five hundred meters before, in a fake kidnapping. When I saw myself blocked by three Kawasaki motorcycles at an intersection before the other two, I realized that my counter-plan had been frustrated by a counter-counterplan whose author I did not know.”
x. “In a deck chair, on the terrace of a chalet in the valley, there is a young woman reading. Every day, before starting work, I pause a moment to look at her with the spyglass.”
xi. “I [this is a quote from a chapter in the book including stuff ‘from the diary of Silas Flannery’] have the idea of writing a novel composed only of beginnings of novels. The protagonist could be a Reader who is continually interrupted. The reader buys the new novel A by the author Z. But it is a defective copy, he can’t go beyond the beginning … He returns to the bookshop to have the volume exchanged …I could write it all in the second person: you, Reader … I could also introduce a young lady, the Other Reader, and a counterfeiter-translator, and an old writer who keeps a diary like this diary…”
xii. “at the moment it [a book] doesn’t seem to be available. But if you will be so patient as to wait a week, or two at most, I have an exquisite surprise in store for you. Our informers report that one of our most important banned authors, Anatoly Anatolin, has been working for some time on a version of Bandera’s novel in an Ircanian setting. From other sources we know that Anatolin is about to finish a new novel entitled What story down there awaits its end?, for whose confiscation we have already arranged a surprise police action, so as to prevent the work from entering underground circulation.”
I thought I should update the blog even though these days I don’t do a lot of blogging-worthy stuff.
i. A blog I recently discovered: Empirical Zeal. There’s some interesting posts there, for example I liked this one on the state of Indian rural education (though the findings reported are not exactly worthy of celebration).
ii. The acquisition of language by children. From the introduction:
“Imagine that you are faced with the following challenge. You must discover the internal structure of a system that contains tens of thousands of units, all generated from a small set of materials. These units, in turn, can be assembled into an infinite number of combinations. Although only a subset of those combinations is correct, the subset itself is for all practical purposes infinite. Somehow you must converge on the structure of this system to use it to communicate. And you are a very young child.
This system is human language. The units are words, the materials are the small set of sounds from which they are constructed, and the combinations are the sentences into which they can be assembled. Given the complexity of this system, it seems improbable that mere children could discover its underlying structure and use it to communicate. Yet most do so with eagerness and ease, all within the first few years of life.”
It’s actually pretty wild, once you start thinking about it.
iii. The Null Ritual – What You Always Wanted to Know About Significance Testing but Were Afraid to Ask (via Gwern? I no longer remember how I found this.). An excerpt from the article:
“Question 1: What Does a Significant Result Mean?
What a simple question! Who would not know the answer? After all, psychology students spend months sitting through statistics courses, learning about null hypothesis tests (significance tests) and their featured product, the p-value. Just to be sure, consider the following problem (Haller & Krauss, 2002; Oakes, 1986):
Suppose you have a treatment that you suspect may alter performance on a certain task. You compare the means of your control and experimental groups (say, 20 subjects in each sample). Furthermore, suppose you use a simple independent means t-test and your result is signifi cant (t = 2.7, df = 18, p = .01). Please mark each of the statements below as “true” or “false.” False means that the statement does not follow logically from the above premises. Also note that several or none of the statements may be correct.
(1) You have absolutely disproved the null hypothesis (i.e., there is no difference between the population means). ® True False ®
(2) You have found the probability of the null hypothesis being true. ® True False ®
(3) You have absolutely proved your experimental hypothesis (that there is a difference between the population means). ® True False ®
(4) You can deduce the probability of the experimental hypothesis being true. ® True False ®
(5) You know, if you decide to reject the null hypothesis, the probability that you are making the wrong decision. ® True False ®
(6) You have a reliable experimental finding in the sense that if, hypothetically, the experiment were repeated a great number of
times, you would obtain a significant result on 99% of occasions. ® True False ®
Which statements are true? If you want to avoid the I-knew-it-all-along feeling, please answer the six questions yourself before continuing to read. When you are done, consider what a p-value actually is: A p-value is the probability of the observed data (or of more extreme data points), given that the null hypothesis H0 is true, defined in symbols as p(D |H0).Th is defi nition can be rephrased in a more technical form by introducing the statistical model underlying the analysis (Gigerenzer et al., 1989, chap. 3). Let us now see which of the six answers are correct:
Statements 1 and 3: Statement 1 is easily detected as being false. A significance test can never disprove the null hypothesis. Significance tests provide probabilities, not definite proofs. For the same reason, Statement 3, which implies that a significant result could prove the experimental hypothesis, is false. Statements 1 and 3 are instances of the illusion of certainty (Gigerenzer, 2002).
Statements 2 and 4: Recall that a p-value is a probability of data, not of a hypothesis. Despite wishful thinking, p(D |H0) is not the same as p(H0 |D), and a significance test does not and cannot provide a probability for a hypothesis. One cannot conclude from a p-value that a hypothesis has a probability of 1 (Statements 1 and 3) or that it has any other probability (Statements 2 and 4). Therefore, Statements 2 and 4 are false. The statistical toolbox, of course, contains tools that allow estimating probabilities of hypotheses, such as Bayesian statistics (see below). However, null hypothesis testing does not.
Statement 5: The “probability that you are making the wrong decision” is again a probability of a hypothesis. This is because if one rejects the null hypothesis, the only possibility of making a wrong decision is if the null hypothesis is true. In other words, a closer look at Statement 5 reveals that it is about the probability that you will make the wrong decision, that is, that H0 is true. Thus, it makes essentially the same claim as Statement 2 does, and both are incorrect.
Statement 6: Statement 6 amounts to the replication fallacy. Recall that a p-value is the probability of the observed data (or of more extreme data points), given that the null hypothesis is true. Statement 6, however, is about the probability of “significant” data per se, not about the probability of data if the null hypothesis were true. The error in Statement 6 is that p = 1% is taken to imply that such significant data would reappear in 99% of the repetitions. Statement 6 could be made only if one knew that the null hypothesis was true. In formal terms, p(D |H0) is confused with 1 – p(D). The replication fallacy is shared by many, including the editors of top journals. […] To sum up, all six statements are incorrect. Note that all six err in the same direction of wishful thinking: They overestimate what one can conclude from a p-value. […]
We posed the question with the six multiple-choice answers to 44 students of psychology, 39 lecturers and professors of psychology, and 30 statistics teachers […] How many students and teachers noticed that all of the statements were wrong? As Figure 1 shows, none of the students did. […] Ninety percent of the professors and lecturers also had illusions, a proportion almost as high as among their students. Most surprisingly, 80% of the statistics teachers shared illusions with their students.”
The article has much more.
“More than 25% of the U.S. population aged [>65] years has diabetes (1), and the aging of the overall population is a significant driver of the diabetes epidemic. […] The incidence of diabetes increases with age until about age 65 years, after which both incidence and prevalence seem to level off”. I should have known the first number was in that neighbourhood, but somehow I had failed to realize that it was that high; most often prevalence estimates are calculated/reported using the entire population in the denominator, but of course such estimates can be deceiving if you do not think about how they are calculated and I clearly hadn’t. At least 1 in 4 in the above-65 age bracket. That’s a lot of people. The article doesn’t have a lot of data, it’s a ‘consensus report’ handling mostly various treatment guideline suggestions and similar stuff.
v. What is the most uncomfortable situation have you ever been put in- by a guy? Any kind of unwanted flirtation- or something of that nature (Reddit). Lots of really horrible stuff; reading stuff like this makes what might be perceived of as some females’ ‘somewhat overcautious’ behaviour towards members of the opposite sex easier to understand. An example from the link:
“The last stranger-danger moment I will share tonight was at an end-of-midterms party sponsored by the student union at a local bar. I was there with my best friend, and she’s very pretty and very friendly, so we’d very quickly attracted a group of four or five men who were hanging around with us for most of the night. I hadn’t seen any of them before, so I assumed they were students from a different department, and we end up getting a table together and talking for a while. Once my friend mentions that she has a boyfriend, most of them shift their attention to me, though there’s one who still seems interested in her. As I’m talking to them, I find that they’re not students at our university, but that they’re a group of friends visiting from the a couple towns over. Nothing too creepy, so far.
My friend finishes her drink, so the guy she’s talking to goes to buy her another. She’s a little suspicious, so she starts drinking it VERY slowly. Meanwhile, I’m getting distracted talking to one of the guys who works in the same field I’ll be entering soon, and we end up talking for a while about that. He keeps telling me that I’m very beautiful, which I keep brushing off because I knew he was interested in my friend initially, and I was interested in someone else at the time, anyway. Somewhere in the middle of all this, my friend has stopped drinking the drink that was bought for her, and someone asks if she’s going to finish it. She says no.
Eventually, the guy I’m talking to apologizes for his “bad” English, saying that he hasn’t really had to use it since he was in school, which was OVER TEN YEARS AGO. At about the same time, my friend is telling the guy she’s talking to that it’s funny that they decided to visit our city on that particular weekend, because this is a student end-of-midterm party, and he answers, “I know. That’s kind of why we came here.” Someone else asks my friend if she’s going to finish her drink, and she says no, but he can have it if he wants. The drink ‘accidentally’ gets spilled in the process, and she’s signalling me to get the fuck out of there, so I take the opportunity to drag her to the bathroom. I start to notice that she’s acting really fucked up – she can usually drink a ton more than I can, and she’d only had one drink of her own and maybe a third (probably less than that, actually) of the one that guy bought for her. She says she thinks the drink they gave her was drugged, and then she gets sick. I ended up staying the night at her place to keep an eye on her, but I didn’t think to take her to the hospital or anything, so I guess we’ll never know what exactly happened…”
Of course if you’re like me you don’t engage in risky behaviours like drinking with strangers and in that case it doesn’t really matter much if you’re male or female, but then again I’m not like normal people. Most males probably significantly underestimate how risky some of their behaviours – behaviours they would not ever even think of as ‘particularly risky’ – are when a female engages in them. Note that even males that fall into the “I can’t imagine you raising your voice”-category (a female friend said this about me in a conversation I had with her earlier today) are likely to be affected by the behaviours of the (type of) males described in the link; once a female has been through situations like the ones described at the link, she’s less likely to give males the benefit of the doubt and more likely to misinterpret behaviour and the motivations driving behaviour. Reading this stuff has made me believe that the behaviour of ‘overcautious’ females may be better justified and less ‘irrational’ than males tend to think it is.
vi. I haven’t commented on the new DSM-5 – let’s just say I’ve had better things to do. Here’s one take on it (“It’s arcane, contradictory and talks about invisible entities which no-one can really prove. Yes folks, the new psychiatric bible has been finalised.”). The most ‘relevant’ change to me is the fact that they’ll remove the Asperger Syndrome diagnosis, and instead merge it with other autism spectrum disorders. If you’re asking me what I think about that, the answer is that I don’t really care.
vii. Cheetahs on the Edge (via Ed Yong). A must-see:
“Using a Phantom camera filming at 1200 frames per second while zooming beside a sprinting cheetah, the team captured every nuance of the cat’s movement as it reached top speeds of 60+ miles per hour.
The extraordinary footage that follows is a compilation of multiple runs by five cheetahs during three days of filming.”
What (part of) Denmark looks like now:
I’m at my parents’ and will be for the next few days as well.
Today I spent the day offline reading three novels by Colin Dexter; Service for All the Dead, The Dead of Jericho and The Riddle of the Third Mile. I read them in a Danish translation and so I’ve decided not to quote from them here. I read all the Inspector Morse books back in the (7th? 8th grade?), but it’s been a long time so I didn’t remember the plots and I enjoyed rereading these novels.
It’s been a very long time since I last read fiction in Danish, probably at least a couple of years, and today’s experience made me remember that you can actually read a lot of pages in a very short amount of time if the stuff you’re reading is fiction in your native language; a novel like any of these three corresponds, in terms of the time expenditure required, probably to at most a couple of chapters of a decent textbook. I have to say that the “I read 50 books a year” segment just became significantly less impressive to me than it was before.
If you can ever find the opportunity to just take a day out of your life and spend it doing little else but reading stuff you’d like to read, it may be worth considering doing it every now and then.
The first post about the book is here. Below some stuff from chapters 4 and 5, which I liked a lot better than the first ones because they had a lot more data:
“The overall pattern of body weight in adulthood shows an upside-down U-shaped trend reflecting the fact that most people increase in their weight from the 20s until the mid-50s, after which their weight decreases. Most of the weight gain that occurs through the years of middle adulthood is due to an increase in BMI (Ding, Cicuttini, Blizzard, Scott, & Jones, 2007), which is manifested mainly as the accumulation of body fat around the waist and hips (commonly referred to as the ‘‘middle-aged spread’’). The loss of body weight in the later years of adulthood is not, however, due to a loss of this accumulated fat and so does not mean that older adults necessarily become healthier or more fit. Instead, older adults lose pounds because they suffer a reduction of FFM [fat-free mass] due to loss of muscle mass, even if they maintain high levels of activity (Manini et al., 2009).
At the other end of the spectrum, some older adults continue to gain weight to the point of developing a BMI that places them in the overweight or obese categories. Between the mid-1990s and mid-2000s, the percent of older adults classified as overweight increased from 60 to 69% and as obese from 22 to 31% (Houston, Nicklas, & Zizza, 2009). […]
You are able to move around in your environment due to the actions of the structures that support this movement, including the bones, joints, tendons, and ligaments that connect the muscles to the bones, and the muscles that control flexion and extension. In the average person, all these structures undergo age-related changes that compromise their ability to function effectively. Beginning in the 40s (or earlier in the case of injury), each component of mobility undergoes significant age-related losses. Consequently, a gradual reduction of walking speed occurs (Shumway-Cook et al., 2007). […] The adult years are characterized by a progressive age-related loss of muscle tissue, a process known as sarcopenia. There is a reduction in the number and size of muscle fibers, especially the fast-twitch fibers involved in speed and strength. As indicated by research from cross-sectional studies, muscle strength (as measured by maximum force) reaches a peak in the 20s and 30s, remains at a plateau until the 40s to 50s, and then declines at a faster rate of 12 to 15% per decade (Kostka, 2005), with more pronounced decreases, at least cross-sectionally, for men. Muscular endurance (as measured by isometric strength) is, however, generally maintained throughout adulthood (Lavender & Nosaka, 2007). […] The loss of muscle mass brings with it a set of negative consequences including increased risk of falling, limitations in mobility, and reduced quality of everyday life. Unfortunately, sarcopenia can become part of a vicious cycle because the greater the loss of muscle mass, the greater the difficulty in undertaking exercise, causing an exacerbation of muscle loss and further weakening (Lang et al., 2009). […]
Bone is living tissue that constantly reconstructs itself through a process of bone remodeling in which old cells are destroyed and replaced by new cells. The general pattern of bone development in adulthood involves an increase in the rate of bone destruction compared to renewal and greater porosity of the calcium matrix, leading to loss of bone mineral content. […] Estimates of the decrease in bone mineral content over adulthood are about .5% per year for men and 1% per year for women (Emaus, Berntsen, Joakimsen, & Fonnebo, 2006). Further weakening occurs due to microcracks that develop in response to stress placed on the bones (Diab, Condon, Burr, & Vashishth, 2006). Part of the older bone’s increased susceptibility to fracture can be accounted for by a loss of collagen, which reduces the bone’s flexibility when pressure is put upon it (Saito & Marumo, 2009). […]
Cardiovascular efficiency is indexed by aerobic capacity, the maximum amount of oxygen that can be delivered through the blood, and cardiac output, the amount of blood that the heart pumps perminute. Both indices decline consistently at a rate of about 10% per decade from age 25 and up so that the average 65-year-old has 40% lower cardiovascular efficiency than the young adult (Betik & Hepple, 2008). The decline is more pronounced in males than females (Goldspink et al., 2009). Maximum heart rate, the heart rate achieved at the point of maximum oxygen consumption, also shows a linear decrease across the years of adulthood. Declines in aerobic capacity occur even in highly trained athletes, but those who continue to exercise at a high level of intensitymaintain their aerobic capacity longer than non-athletes (Tanaka&Seals, 2003). […] With regard to aerobic functioning, exercise is one of the best ways you can slow down the rate of your body’s aging process. […]
Approximately 30% of all adults 65 and older suffer from urge incontinence, a form of urinary incontinence in which the individual experiences a sudden need to urinate, and often results in urine leakage. Stress incontinence involves loss of urine experienced during exertion. The prevalence of daily incontinence ranges from 12% in women 60 to 64 years old to 21% in women 85 years old or older […] A variety of treatments are available to counteract incontinence, but because people often mistakenly assume that bladder dysfunction is a normal part of aging, they are less likely to seek active treatment. In one study of more than 7.2 million patients diagnosed with overactive bladder, 76% went untreated (Helfand, Evans,&McVary, 2009). Medications such as tolderodine (Detrol LA) are becoming increasingly available to help control bladder problems. […]
Although men do not experience a loss of sexual function comparable to the menopause (despite what you might hear about the ‘‘male menopause’’), men undergo andropause, which refers to age-related declines in the male sex hormone testosterone. The decline in testosterone is equal to 1% per year after the age of 40, a decrease observed in longitudinal as well as cross-sectional studies (Feldman et al., 2002). The term ‘‘late-onset hypogonadism’’ or ‘‘age-associated hypogonadism’’ has begun to replace the term andropause, although all three terms are currently in use. […] Erectile dysfunction (ED), a condition in which a man is unable to achieve an erection sustainable for intercourse, is estimated to increase with age in adulthood, from a rate of 31% among men 57–65 to 44% of those 65 and older. ED is related to health problems in older men, including metabolic syndrome (Borges et al., 2009). […]
Normal aging seems to have major effects on the prefrontal cortex, the area of the brain most involved in planning and the encoding of information into long-term memory, as well as in the temporal cortex, involved in auditory processing (Fjell et al., 2009). The hippocampus, the structure in the brain responsible for consolidating memories, becomes smaller with increasing age, although this decline is more pronounced in abnormal aging such as in Alzheimer’s disease (Zhang et al., 2010). […]
Most people require some form of corrective lenses by the time they reach their 50s or 60s. Presbyopia, or loss of the ability to focus vision on near objects, is the primary culprit for the need for reading glasses, and is the visual change that most affects people in midlife and beyond.
Presbyopia is caused by a thickening and hardening of the lens, the focusing mechanism of the eye (Sharma & Santhoshkumar, 2009). As a result, the lens cannot adapt its shape when needed to see objects up close to the face. By the age of 50, presbyopia affects the entire population. Treatment for the cause of presbyopia does not exist, and although bifocals were the only correction since the time of Benjamin Franklin (who invented them) newer multifocal contact lenses are increasingly becoming available on the market (Woods, Woods, & Fonn, 2009). Though you cannot cure presbyopia, you may be able to alter its onset because lifestyle habits seem to affect the rate at which the presbyopic aging process occurs. For example, smoking accelerates the aging of the lens (Kessel, Jorgensen, Glumer, & Larsen, 2006).
Older adults are also likely to experience the loss of visual acuity, or the ability to see details at a distance. The level of acuity in an 85-yearold individual is approximately 80% less than that of a person in their 40s. […]
Loss of balance is one of the main factors responsible for falls in older adults (Dickin, Brown, & Doan, 2006). In 2007 alone, more than 15,800 people 65 and older were known to have died directly from injuries related to falls (Kung, Hoyert, Xu, & Murphy, 2008); 1.8 million were treated in emergency departments for fall-related nonfatal injuries, and about 460,000 of these people were hospitalized (Stevens, Ryan, & Kresnow, 2006). […]
Smell and taste belong to the chemical sensing system referred to as chemosensation. The sensory receptors in these systems are triggered when molecules released by certain substances stimulate special cells in the nose, mouth, or throat. Despite the fact that the olfactory receptors constantly replace themselves, the area of the olfactory epithelium shrinks with age, and ultimately the total number of receptors becomes reduced throughout the adult years. At birth, the olfactory epithelium covers a wide area of the upper nasal cavities, but by the 20s and 30s, its area has started to shrink noticeably.
Approximately one third of all older adults suffer some form of olfactory impairment (Shu et al., 2009) with almost half of those 80 years and older having virtually no ability to smell at all (Lafreniere & Mann, 2009). The loss of olfactory receptors reflects intrinsic changes associated with the aging process, as well as damage caused by disease, injury, and exposure to toxins. Research suggests that these environmental toxins may play a larger role in olfactory impairment than changes due to the aging process. […]
A sedentary lifestyle is the first major risk factor for heart disease. The relationship between leisure activity and heart disease is well established (Yung et al., 2009), with estimates ranging from a 24% reduction in the risk of myocardial infarction among non-strenuous exercisers to a 47% reduced risk among individuals engaging in a regular pattern of strenuous exercise (Lovasi et al., 2007). As it happens, the majority of adults at highest risk for heart disease (i.e., those 75 and older) are the least likely to exercise. Only about 36% of people 65 to 74 and 16% of those 75 and older engage in vigorous leisure activity (National Health Interview Survey, 2009). […] Approximately one fifth of all adults in the United States are current smokers. The rates of current smokers decrease across age groups of adults to 10% of those 65 and older (National Health Interview Survey, 2009). […]
In 2009, it was estimated that nearly 1.5 million Americans received a diagnosis of cancer (not including skin cancer or noninvasive cancers) and that about 10.5 million are living with the disease. The lifetime risk of developing cancer is about 1 in 2 for men and 1 in 3 for women (American Cancer Society, 2009). […] All cancer is genetically caused in the sense that it reflects damage to the genes that control cell replication. […this is actually, I think, a very good way to put it.] […]
A nationwide study of over 900,000 adults in the United States who were studied prospectively (before they had cancer) from 1982 to 1998 played an important role in identifying the role of diet. During this period of time, there were more than 57,000 deaths within the sample from cancer. The people with the highest BMIs had death rates from cancer that were 52% higher for men and 62% higher for women compared with men and women of normal BMI. The types of cancer associated with higher BMIs included cancer of the esophagus, colon and rectum, liver, gallbladder, pancreas, and kidney. Significant trends of increasing risk with higher BMIs were observed for death from cancers of the stomach and prostate in men and for death from cancers of the breast, uterus, cervix, and ovary in women (Calle, Rodriguez, Walker-Thurmond, & Thun, 2003). We can conclude from this research that maintaining a low BMI is a critical preventive step in lowering your risk of cancer.
In addition to BMI, eating specific foods seems to play a role in cancer prevention. Stomach cancer is more common in parts of the world—such as Japan, Korea, parts of Eastern Europe, and Latin America—in which people eat foods that are preserved by drying, smoking, salting, or pickling. By contrast, fresh foods, especially fresh fruits and vegetables, may help protect against stomach cancer. Similarly, the risk of developing colon cancer is thought to be higher in people whose diet is high in fat, low in fruits and vegetables, and low in highfiber foods such as whole-grain breads and cereals. […]
It is estimated that 8 million women and 2 million men in the United States suffer from osteoporosis (Sweet, Sweet, Jeremiah, & Galazka, 2009). Women are at higher risk than men because they have lower bone mass in general but nevertheless, osteoporosis is a significant health problem in men. Rates of osteoporosis-related bone fracture are equivalent to the rates of myocardial infarction (Binkley, 2009). Women vary by race and ethnicity in their risk of developing osteoporosis; White and Asian women have the highest risk, whereas Blacks and Hispanics the lowest. In addition, women who have small bone structures and are underweight have a higher risk for osteoporosis than heavier women. […]
According to the World Health Organization, the number of people suffering from diabetes worldwide is approximately 171 million in 2010, a number that will double by 2030. […]
Approximately 20% of cases of dementia are due to cerebrovascular disease (Knopman, 2007). […] In vascular dementia, progressive loss of cognitive functioning occurs as the result of damage to the arteries supplying the brain. Dementia can follow a stroke, in which case it is called acute onset vascular dementia, but the most common form of vascular dementia is multi-infarct dementia or MID, caused by transient ischemic attacks. In this case, a number of minor strokes (‘‘infarcts’’) occur in which blood flow to the brain is interrupted by a clogged or burst artery. Each infarct is too small to be noticed, but over time, the progressive damage caused by the infarcts leads the individual to lose cognitive abilities. There are important differences between MID and Alzheimer’s disease. The development of MID tends to be more rapid than Alzheimer’s disease, and personality changes are less pronounced. The higher the number of infarcts, the greater the decline in cognitive functioning (Saczynski et al., 2009). […]
People who develop Parkinson’s disease show a variety of motor disturbances, including tremors (shaking at rest), speech impediments, slowing of movement, muscular rigidity, shuffling gait, and postural instability or the inability to maintain balance. Dementia can develop during the later stages of the disease, and some people with Alzheimer’s disease develop symptoms of Parkinson’s disease. Patients typically survive 10 to 15 years after symptoms appear.”
“Everyone ages. This very fact should be enough to draw you into the subject matter of this course, whether you are the student or the instructor. Yet, for many people, it is difficult to imagine the future in 50, 40, or even 10 years from now. The goal of our book is to help you imagine your future and the future of your family, your friends, and your society. We have brought together the latest scientific findings about aging with a more personal approach to encourage you to take this imaginative journey into your future. […]
Our goal is to engage you by presenting you with information that is of both personal and professional interest. We will explore the variety of ways individuals can affect their own aging process, such as through incorporating behaviors and activities designed to maintain high levels of functioning well into the later decades of life.”
From the introduction and first part of chapter 1 of the book. I thought the subject would be interesting to read about, and apparently this is the kind of stuff that’s available. I’m not super impressed at this point as there’s a lot of ‘talk’ included in the first chapters of the book – they tend to use many words to say very little. And quite a bit of the talk stuff is just unscientific theorizing without data. But there’s some interesting stuff here as well. Below some stuff from the first 3 chapters (click to view figures in a higher resolution):
“In 1900, the number of Americans over the age of 65 years made up about 4% of the population […] People 65 and older now represent 12.3% of the total U.S. population […] In 1990, an estimated 37,306 people over the age of 100 lived in the United States. By 2004 this number increased 73% to 64,658, and by 2050 there will be over 1.1 million of these exceptionally aged individuals.”
“Women over the age of 65 currently outnumber men, amounting to approximately 58% of the total over-65 population [in the US]. […] In 2010, there were 531 million people worldwide over the age of 65. Predictions suggest that this number will triple to 1.53 billion by the year 2050 (U.S. Bureau of the Census, 2010c). China currently has the largest number of older adults (106 million), but Japan has the highest percentage of people 65 and older (20%) (Kinsella & He, 2009). […]
“The most compelling attempts to explain aging through genetics are based on the principle of replicative senescence, or the loss of the ability of cells to reproduce. Scientists have long known that there are a finite number of times (about 50) that normal human cells can proliferate in culture before they become terminally incapable of further division (Hayflick, 1994).
Until relatively recently, scientists did not know why cells had a limited number of divisions. It was only when the technology needed to look closely at the chromosome developed that researchers uncovered some of the mystery behind this process.
As we saw in Figure 2.6, the chromosome is made up largely of DNA. However, at either end of the chromosomes are telomeres, repeating sequences of proteins that contain no genetic information (see Figure 2.8). The primary function of the telomere is to protect the chromosome from damage. With each cell division, the telomeres become shorter, ultimately altering patterns of gene expression affecting the functioning of the cell and the organ system in which it operates. Once telomeres shorten to the point of no longer being able to protect the chromosome, adjacent chromosomes fuse, the cell cycle is halted, and ultimately the cell dies (Shin, Hong, Solomon, & Lee, 2006). Evidence linking telomere length to mortality in humans suggests that the telomeres may ultimately hold the key to understanding the aging process (Cluett & Melzer, 2009).
However, biology does not completely explain the loss of telomeres over the course of life. Supporting the idea of biopsychosocial interactions in development, researchers have linked telomere length to social factors. Analyzing blood samples from more than 1,500 female twins, researchers in the United Kingdom determined that telomere length was shorter in women from lower socioeconomic classes (Cherkas et al., 2006). There was a difference of seven ‘‘biological years’’ (measured in terms of telomeres) between twins with manual jobs and their co-twins in higher-ranking occupations. The researchers attributed this difference to the stress of being in a lower-level occupation in which people have less control over their day-to-day activities. Body mass index, smoking, and lack of exercise were additional factors influencing telomere length. A subsequent study on this sample provided further research of the important role of lifestyle factors. Even after the researchers adjusted for such factors as age, socioeconomic status, smoking, and body mass index, people who engaged in higher levels of physical activity had longer telomeres than those who did not (Cherkas et al., 2008). […]
Random error theories are based on the assumption that aging reflects unplanned changes in an organism over time. The wear and tear theory of aging is one that many people implicitly refer to when they say they feel that they are ‘‘falling apart’’ as they get older. According to this view, the body, like a car, acquires more and more damage as it is exposed to daily wear and tear from weather, use, accidents, and mechanical insults. Programmed aging theories, in contrast, would suggest that the car was not ‘‘built to last,’’ but rather was meant to deteriorate over time in a systematic fashion. […]
The free radical theory, or oxidative stress theory (Sohal, 2002), focuses on a set of unstable compounds known as free radicals, produced when certain molecules in cells react with oxygen. The primary goal of a free radical is to seek out and bind to other molecules. When this occurs, the molecule attacked by the free radical loses functioning. Although oxidation caused by free radicals is a process associated with increasing age, researchers have questioned the utility of this approach as a general theory of aging (Perez et al., 2009).”
Chapter 3 has some stuff on problems with making causal claims in this area of research and some stuff on longitudinal studies and cross-sectional studies in this area, including pros and cons of the two types of studies. After they’ve covered this stuff they note that:
“considerable progress in some areas of research has been made through the application of sequential designs. These designs consist of different combinations of the variables age, cohort, and time of measurement. Simply put, a sequential design involves a ‘‘sequence’’ of studies, such as a cross-sectional study carried out twice (two sequences) over a span of 10 years. The sequential nature of these designs is what makes them superior to the truly descriptive designs conducted on one sample, followed over time (longitudinal design) or on different-aged samples, tested on one occasion (cross-sectional design). Not only do sequential studies automatically provide an element of replication, but when they are carried out as intended, statistical analyses can permit remarkably strong inferences to be drawn about the effect of age as distinct from cohort or time of measurement.”
Much of the stuff covered in chapter 3 on research methods should be known stuff to people reading a blog like this, because aging research isn’t that different from other types of research. I skimmed over some of this stuff because much of it is (a wordier and less formalized way to deal with) known stuff from introductionary statistics classes in my past.
My first post about the book can be found here. In this post I’ll talk a little bit the chapters 4-5, which deal with infectious diseases and neoplasia.
When reading chapter 4 – on infectious diseases – it was a great help to have read chapter 3 first – that chapter had a lot of stuff on how the body defends itself against the kind of stuff they talk about in chapter 4, and even though they recap a bit of that stuff in chapter 4 it’s probably smart to read those two chapters in the order they appear in the book. I did not find chapter 4 particularly hard to read, in part probably because this stuff is closely related to the microbiology stuff I read in the past, which dealt in much more detail with the microorganisms causing these diseases. There’s a lot of important concepts covered: transmission mechanisms; factors impacting disease susceptibility; the normal microbial flora and how it relates to this topic at hand; constitutive defences the body (‘defence mechanisms which do not require prior contact with the microorganism – such as physical and chemical barriers to colonization, inflammatory response, the complement system, and phagocytosis); disease progression (to cause disease all microorganisms must go through four stages: they must encounter the host, gain entry, multiply and spread, and cause host tissue injury. The course of an infection may vary from asymptomatic to life threatening; an important distinction is between acute (and sub-acute) and chronic infections). Chronic infection is not the only outcome of a long-term colonization; an individual may also enter a carrier state, or the infection may become latent until reactivation.).
After the ‘general stuff’ has been covered in chapter 4, they deal with the pathophysiology of some examples of infectious diseases; infective endocarditis (bacterial or fungal infection of the interior of the heart), meningitis, pneumonia, infectious diarrhea, and sepsis/sepsis syndrome/septic shock. I’ll not go into much detail about these diseases, but I should probably note here that the names we use to describe infectious diseases like these may cause people to misunderstand how they work: To be clear, there isn’t just one ‘endocarditis bacterium’ or a specific ‘meningitis bacterium’. When specific sites/organ systems are invaded by microorganisms which spread and cause tissue damage (damage which can be caused both by the toxins released by the invading microorganisms and by the host response to the invasion), we have a name for that – but many different microorganisms may cause symptoms by invading the specific site or organ system in question, though some are more likely to affect specific sites than others. Sometimes the names of the microorganisms may even add to this confusion; for example one of the most common causes of bacterial meningitis (infection of the meninges) in children aged 2 months to 15 years is H Influenzae (which kind of sounds like, well…).
Chapter 5 deals with neoplasia. If you dont’ feel like reading this stuff, at least read Mukherjee. The chapter deals briefly with colon carcinoma as an example of an epithelial neoplasia; this stuff from Khan Academy is another great resource on this subject – it also deals a bit with cancer development more generally, and it’s a lot more accessible than is this chapter.
Anyway, the chapter… It starts out with a bit of a downer: “The recognition of overt malignancy by physical examination or imaging requires the presence in the body of about 1 billion malignant cells.” It goes on to note that: “A preclinical phase may sometimes be recognized” but even so, “More commonly, the preclinical phase goes undetected until invasive cancer, occasionally with regional or distant metastases, is already present.” That’s the way it is. The chapter then goes on to talk about many of the same things Mukherjee covers in the latter half of his book, like the role of tumor suppressor genes and oncogenes, the role of environmental triggers (carcinogens), inheritance, … In the field of oncology there seems to be a big focus on the role of genetic changes taking place in the cell(s), and: “A paradigm for sequential genetic alterations has been proposed as a necessary set of events leading to tumorigenesis.” Mukherjee also has more on this, if you’re interested. There are a lot of oncogenes and tumor suppressor genes that play a role in human cancers. In terms of the phenotypic changes they cause, this table is relevant (click to view full size):
A good related quote from the first part of the chapter:
“Molecular and cellular changes in tumor cells are, in a sense, a modification of normal physiology that benefits their growth and spread. The initial alterations may be “preprogrammed” in rare inherited malignancies, or they may be acquired as a consequence of mutations brought about by environmental exposure or occuring by chance during normal cell division. In a process akin to evolution, albeit in a fast time frame, additional genetic changes occur that favor further growth, invasion, and spread. Evasion of the host’s immune system, enhanced proliferative and invasive potential, and resistance to therapy are examples of early, middle, and late changes in the progression of neoplasia.”
The simple way to think about cancer is this: Cancer cells outcompete the surrounding cells because they’re better at growing and spreading, and they cause disease because the reason why they’re better at growing and spreading is that they’re no longer doing what they’re supposed to be doing, and because they’re taking up space and nutrients from the cells that still do their jobs.
The chapter also has some stuff on breast cancer and talks a bit about the BRCA mutations. After that they talk about mesenchymal, neuroendocrine and germ cell neoplasias, which are types of neoplasias the pathophysiology of which “can be described in terms of the embryonic tissue of origin.” The examples they include are carcinoid tumors, testicular cancer, and sarcomas. Again the naming of these diseases may be a bit confusing – tissue will often migrate during development and you can actually end up with, say, a testicular neoplasm which is not located anywhere near your testes (for example, the testicular tissue may have migrated to your chest..). Then they cover hematologic neoplasms (blood, bone marrow, or lymph nodes), and here they’ve included some stuff on lymphomas (“uncontrolled proliferation and potential dissemination of lymphocytes“) and AML, a type of leukemia (Mukherjee has a lot more stuff on that). I found it surprising that they did not spend more time on the last part, the systemic effects of neoplasia – basically they only spend one page on that stuff, though they do also include a few tables to illustrate these aspects of the diseases. I’ve included one of the figures below (click to view in a higher resolution):
Indirect systemic effects of cancer which are not caused by the local presence of cancer cells are what’s called pareneoplastic syndromes.
(1686 and 2538 views? Seriously???)
i. Huia (featured).
What they looked like:
“Even though the Huia is frequently mentioned in biology and ornithology textbooks because of this striking dimorphism, not much is known about its biology; it was little studied before it was driven to extinction. The Huia is one of New Zealand’s best known extinct birds because of its bill shape, its sheer beauty and special place in Māori culture and oral tradition. […]
The Huia was found throughout the North Island before humans arrived in New Zealand. The Māori arrived around 800 years ago, and by the arrival of European settlers in the 1840s, habitat destruction and hunting had reduced the bird’s range to the southern North Island. However, Māori hunting pressures on the Huia were limited to some extent by traditional protocols. The hunting season was from May to July when the bird’s plumage was in prime condition, while a rāhui (hunting ban) was enforced in spring and summer. It was not until European settlement that the Huia’s numbers began to decline severely, due mainly to two well-documented factors: widespread deforestation and overhunting. […]
Habitat destruction and the predations of introduced species were problems faced by all New Zealand birds, but in addition the Huia faced massive pressure from hunting. Due to its pronounced sexual dimorphism and its beauty, Huia were sought after as mounted specimens by wealthy collectors in Europe and by museums all over the world. These individuals and institutions were willing to pay large sums of money for good specimens, and the overseas demand created a strong financial incentive for hunters in New Zealand.”
ii. British colonization of the Americas. Not very detailed, but this article is a good place to start if one wants to read about the various colonies; it has a lot of links.
iii. Iron Dome.
“Iron Dome (Hebrew: כִּפַּת בַּרְזֶל, kipat barzel) also known as “Iron Cap“ is a mobile all-weather air defense system developed by Rafael Advanced Defense Systems. It is a missile system designed to intercept and destroy short-range rockets and artillery shells fired from distances of 4 to 70 kilometers away and whose trajectory would take them to a populated area. […] The system, created as a defensive countermeasure to the rocket threat against Israel‘s civilian population on its northern and southern borders, uses technology first employed in Rafael’s SPYDER system. Iron Dome was declared operational and initially deployed on 27 March 2011 near Beersheba. On 7 April 2011, the system successfully intercepted a Grad rocket launched from Gaza for the first time. On 10 March 2012, The Jerusalem Post reported that the system shot down 90% of rockets launched from Gaza that would have landed in populated areas. By November 2012, it had intercepted 400+ rockets. Based on this success, Defense reporter Mark Thompson estimates that Iron Dome is the most effective and most tested missile shield in existence.
The Iron Dome system is also effective against aircraft up to an altitude of 32,800 ft (10,000 m). […]
During the 2006 Second Lebanon War, approximately 4,000 Hezbollah-fired rockets (the great majority of which were short-range Katyusha rockets) landed in northern Israel, including on Haifa, the country’s third largest city. The massive rocket barrage killed 44 Israeli civilians and caused some 250,000 Israeli citizens to evacuate and relocate to other parts of Israel while an estimated 1,000,000 Israelis were confined in or near shelters during the conflict.
To the south, more than 4,000 rockets and 4,000 mortar bombs were fired into Israel from Gaza between 2000 and 2008, principally by Hamas. Almost all of the rockets fired were Qassams launched by 122 mm Grad launchers smuggled into the Gaza Strip, giving longer range than other launch methods. Nearly 1,000,000 Israelis living in the south are within rocket range, posing a serious security threat to the country and its citizens.
In November 2012, during Operation Pillar of Defense, the Iron Dome’s effectiveness was estimated by Israeli officials at between 75 and 95 percent. According to Israeli officials, of the approximately 1,000 missiles and rockets fired into Israel by Hamas from the beginning of Operation Pillar of Defense up to November 17, 2012, Iron Dome identified two thirds as not posing a threat and intercepted 90 percent of the remaining 300. During this period the only Israeli casualties were three individuals killed in missile attacks after a malfunction of the Iron Dome system.
In comparison with other air defense systems, the effectiveness rate of Iron Dome is very high.”
iv. Evolution of cetaceans (whales and dolphins). They’re a lot ‘younger’ than I thought.
This is an actual (composite) picture of a robot on another planet. At this moment it is walking around doing scientific experiments. On another planet. I’ll say it again: Living in the 21st century is awesome.
vi. Halting Problem.
“In computability theory, the halting problem can be stated as follows: “Given a description of an arbitrary computer program, decide whether the program finishes running or continues to run forever“. This is equivalent to the problem of deciding, given a program and an input, whether the program will eventually halt when run with that input, or will run forever.
Alan Turing proved in 1936 that a general algorithm to solve the halting problem for all possible program-input pairs cannot exist. A key part of the proof was a mathematical definition of a computer and program, what became known as a Turing machine; the halting problem is undecidable over Turing machines. It is one of the first examples of a decision problem. […]
The halting problem is a decision problem about properties of computer programs on a fixed Turing-complete model of computation, i.e. all programs that can be written in some given programming language that is general enough to be equivalent to a Turing machine. The problem is to determine, given a program and an input to the program, whether the program will eventually halt when run with that input. In this abstract framework, there are no resource limitations on the amount of memory or time required for the program’s execution; it can take arbitrarily long, and use arbitrarily much storage space, before halting. The question is simply whether the given program will ever halt on a particular input. […]
One approach to the problem might be to run the program for some number of steps and check if it halts. But if the program does not halt, it is unknown whether the program will eventually halt or run forever.
Turing proved there cannot exist an algorithm which will always correctly decide whether, for a given arbitrary program and its input, determine the program halts when run with that input; the essence of Turing’s proof is that any such algorithm can be made to contradict itself, and therefore cannot be correct. […]
The halting problem is historically important because it was one of the first problems to be proved undecidable.”
vii. Fetal Alcohol Syndrome.
Fetal alcohol syndrome (FAS) is a pattern of mental and physical defects that can develop in a fetus in association with high levels of alcohol consumption during pregnancy. […]
Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damage neurons and brain structures, which can result in psychological or behavioral problems, and cause other physical damage. Surveys found that in the United States, 10–15% of pregnant women report having recently drunk alcohol, and up to 30% drink alcohol at some point during pregnancy.
The main effect of FAS is permanent central nervous system damage, especially to the brain. Developing brain cells and structures can be malformed or have development interrupted by prenatal alcohol exposure; this can create an array of primary cognitive and functional disabilities (including poor memory, attention deficits, impulsive behavior, and poor cause-effect reasoning) as well as secondary disabilities (for example, predispositions to mental health problems and drug addiction). Alcohol exposure presents a risk of fetal brain damage at any point during a pregnancy, since brain development is ongoing throughout pregnancy.
Fetal alcohol exposure is the leading known cause of mental retardation in the Western world. In the United States and Europe, the FAS prevalence rate is estimated to be between 0.2-2 in every 1000 live births. FAS should not be confused with Fetal Alcohol Spectrum Disorders (FASD), a condition which describes a continuum of permanent birth defects caused by maternal consumption of alcohol during pregnancy, which includes FAS, as well as other disorders, and which affects about 1% of live births in the US. The lifetime medical and social costs of FAS are estimated to be as high as US$800,000 per child born with the disorder.”
That’s a US estimate, but I think a Danish one would be within the same order of magnitude. Imagine how the incentives of expectant mothers would change if we fined females who gave birth to a child with FAS, letting the fine be some fraction of the total estimated social costs. And remind me again why we do not do this?
i. “A friend in power is a friend lost.” (Henry Brooks Adams)
ii. “He knows nothing; and he thinks he knows everything. That points clearly to a political career.” (George Bernard Shaw)
iii. “Those have most power to hurt us that we love.” (Francis Beaumont / John Fletcher)
iv. “It doesn’t much signify whom one marries, for one is sure to find next morning that it was someone else.” (Samuel Rogers)
v. “Teaching physics without calculus or research psychology without statistics is teaching about science rather than teaching science.” (Victoria Hart)
vi. The problem with separating science and math is that science NEEDS math. Math, however, does not need science.” (-ll-)
vii. “Seek not to know who said this or that, but take note of what has been said.” (Thomas á Kempis)
viii. “What time he can spare from the adornment of his person he devotes to the neglect of his duties.” (William Hepworth Thompson)
ix. “Men talk of killing time, while time quietly kills them.” (Dion Boucicault)
x. “No people do so much harm as those who go about doing good.” (Mandell Creighton)
xi. “To find a friend one must close one eye. To keep him—two.” (Norman Douglas)
xii. “Science is special because there is no ancient wisdom. The ancients were fools, by and large. I mean no disrespect, but if you wish to design a rifle by Aristotelian principles, or treat an illness via the Galenic system, you are a fool, following foolishness. Science is the true ladder to heaven, anyone who has practiced it can not be help be amazed by its miraculous powers of prediction. […] Knowledge is hard. We, as individual humans are stupid. Science is sloppy and noisy. But science got us to the moon, and science gave is antibiotics.” (Razib Khan)
xiii. All political persuasions are a mix of norms and assumptions about the way the world is arranged. When you make false assertion about the nature of things, you will make worthless inferences. […] Note that any assumption of what is does not here necessarily entail what ought to be. But it is much easier to achieve an ought if you accurately characterize the is.” (-ll-)
xiv. “In every adversity of fortune, to have been happy is the most unhappy kind of misfortune.” (Anicius Manlius Severinus Boethius)
xv. “Everyone believes very easily whatever they fear or desire.” (Jean de La Fontaine)
xvi. “Our destiny is frequently met in the very paths we take to avoid it.” (-ll-)
xvii. “It is the common vice of all, in old age, to be too intent upon our interests.” (Terence)
I decided to give the book a shot. I didn’t manage to get all that far (~50 pages). Some quotes:
“Consider this excerpt from Barack Obama’s victory speech to supporters after winning the 2008 US Presidential election in which he attempts to temper the sense of euphoria at his success, and to remind Americans that they should not squander the opportunity for significant change and to build a better future for their children. Obama uses some remarkably effective rhetoric for a good cause, as he had done throughout his campaign, and he might well be admired as a talented rhetorician.” […]
“Morality requires us to consider the consequences of our actions and, since speech and writing are types of action, natural (though irrational) responses to what we say and write must sometimes be taken into account in deciding what we ought to say. We should not say what is false, but that a proposition is true is not always enough to justify expressing it.” […]
“Appeal to fear (also known as scare tactics)
This is the tactic of trying to elicit a fear in one’s readers or listeners in order to influence their behaviour or attitudes. A frequent example of the appeal to fear occurs in discussions about immigration into wealthy countries. Many politicians and other opinion-formers use the tactic of eliciting citizens’ fears of economic destitution and cultural demise by constructing deliberately exaggerated images of ‘waves of immigrants’2 entering a country illegally and generally living a life better than that they deserve; taking jobs, education, health care and state benefits to which they have no rightful entitlement and thereby making Mr and Ms Average Citizen worse off. This familiar scare tactic (that almost certainly also makes appeal to some people’s racist attitudes) is often used by politicians to persuade people to support draconian immigration policies and infringements of people’s civil rights, and to demonstrate that support by voting for them at election time. But no reason has been given for the belief that disaster would result if such extreme policies were not enacted. Instead, it is hoped that describing these disastrous scenarios will alarm people so severely as to disturb their reason, prompting the confused supposition that the disastrousness of the worst possible scenario should be matched by the severity of the preventive measures taken.”
I was close to stopping reading at this point. I’d been close to just putting the book away already when I saw that they included some – and said relatively nice things about – political waffle by Obama in the first chapter. But there were a few new concepts and distinctions introduced along the way in the book and some of this stuff I hadn’t dealt with in a while, and besides I thought that between-the-lines politicizing was a strange reason for giving up on a book on critical thinking. So I read on…:
“The ploy of equivocation also occurs when someone attempts to mislead with statistics by saying something that is true, but which they expect their audience to understand according to an interpretation that is false. The following example of attempting to mislead with statistics, which comes from a speech by George W. Bush, also includes an equivocation on the meaning of ‘average’:
These tax reductions will bring real and immediate benefits to middle-income Americans. Ninety-two million Americans will keep an average of $1,083 more of their own money.
This claim sounds like the average American will get a little over $1,000. But hang on. Ninety-two million is the number of Americans who pay income tax. One might understand Bush, as his speechwriters intend one to, as saying that the tax bill of the average American will reduce by $1,083. But if ‘average American’ means ‘American with average income’, then Bush’s claim is false. What is true is that $1,083 is the average tax reduction under the new plan. But that’s because the highest earners save hundreds of thousands (similarly, if Bill Gates is in the room along with ten call-centre workers, then the average net worth is still in the billions). The American with average income still only gets a few hundred dollars relief.”
And I just got so annoyed at this point that I decided to stop reading after I’d finished the chapter (chapter 2). This is not the way to write a book like this.
“…it’s just a matter of estimating the hazard functions…”
Or something like that. The words in the post title the instructor actually said, but I believe his voice sort of trailed off as he finished the sentence. All the stuff above is from today’s lecture notes, click to enlarge. The quote is from the last part of the lecture, after he’d gone through that stuff.
In the last slide, it should “of course” be ‘Oaxaca Blinder decomposition’, rather than ‘Oaxaca-Bilder’.
I like it so far.
If you’ve never opened a textbook about medicine, genetics, microbiology or similar stuff before in your life, it’ll probably be too technical for you to benefit much from it; I’d certainly have had an easier time reading chapter two on genetic diseases if I’d had a stronger background in biochemistry, and it’s not like this is a topic I’ve never dealt with before. Chapter 3, on disorders of the immune system, was even worse than chapter two. Microbiology, which is somewhat related to the field of immunology, is also a subject I’ve read about in the past, however that reading has been much more ‘fragmented’ and less systematic than has my reading of e.g. the genetics literature (which is itself rather scattered and unsystematic, compared to my reading of the diabetes literature…). So even though while reading the immunology part I seemed to remember both having seen some of this stuff before in the textbooks as well as having touched upon some of the themes on Khan Academy and Wikipedia, I found some of this stuff quite hard to read and understand. In the genetics section, it helped a lot to be familiar with a lot of the key concepts (‘fitness’, ‘linkage disequilibria’, ‘stages of meiosis’, ‘genotype/phenotype’, ‘Mendelian inheritance’, ‘mutation and drift’, ‘fixation’, …) – I had no such systematic knowledge to rely on when reading about the immunology stuff.
All that said, there’s a lot of good stuff in this book and when you’re not reading a book like this in order to pass an exam you’re not as worried about missing some details – I don’t plan on understanding everything in this book and I feel fine about ‘mentally skipping sections’ which are very technical (meaning reading the words but not fully understanding what the words mean). It doesn’t seem likely to me that the added understanding I’d get from ‘looking up everything’ would add enough to my understanding of the material to justify the costs. I want to enjoy reading this, so I’ll read all the stuff but I won’t look up all the unknown stuff.
As can probably be inferred from the above comments, the book is much more technical than the sexual diseases book I covered a few days ago. I decided to include below a few examples of what this means by quoting a couple of passages from chapter three, on disorders of the immune system:
“Activated macrophages secrete proteolytic enzymes, active metabolites of oxygen (including superoxide anion and other oxygen radicals), arachidonic acid metabolites, cyclic adenosine monophosphate (cAMP), and cytokines such as interleukin-I (IL-I), IL-6, tumor necrosis factor (TNF), and IL-8, among others. Many tissue-specific cells are of macrophage lineage and function to process and present antigen (Langerhans’ cells, oligodendrocytes, etc.).” […]
“Polymorphonuclear leukocytes (neutrophils) (PMNs) are granulocytic cells that originate in the bone marrow and circulate in blood and tissue. Their primary function is antigen-nonspecific phagocytosis and destruction of foreign particles and organisms. The precency of Feγ receptors on the surface of neutrophils also facilitates the clearance of opsonized microbes through the reticuloendothelial system.” […]
“in the airway inflammatory response in asthma, eosinophil-derived mediators of inflammation, including major basic protein (MBP), eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP) and lysophospholipase (LPL) are toxic to respiratory epithelium.”
Of course it’s not all like this but if you’re not okay with not always knowing more or less completely what’s going on, you should probably stay away from this book.
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”
(click to view full size)
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.”
…by King Holmes, P. Sparling, Walter Stamm, Peter Piot, Judith Wasserheit, Lawrence Corey, Myron Cohen (…and many others: “This edition welcomes new editors Myron Cohen, Larry Corey, and Heather Watts, and 119 new authors”).
I thought that since I brought up my recent doctor’s appointment (not STD-related in any way…) in my last post, I should update you on that stuff here before getting to the book blogging. It was good news all around: There was nothing unusual about the EKG, I do not have microalbuminuria and my Hba-1c was 0.070 (/53) [relevant link to Danish readers]. HDL cholesterol was higher- and LDL and total cholesterol levels, as well as triglycerides, were much lower than required, and the BP was 123/82. I’m always a little concerned about the BP values because they’re sort of the ‘weakest link’ when it comes to my regular test results, but it’s nowhere near high enough to justify any kind of pharmacological intervention at this point.
Back to the book: I’ve read roughly the first 100 pages (Introduction and Overview as well as Part 1 – i.e. the first 5 chapters), and I like it so far. Some good stuff from the first part of the book:
1. “The prevalence, of persistent vaginal and cervical infections are remarkably high in young women; and the incidence, and prevalence, of the chronic STIs are exceptionally high in adults, with seroprevalence increasing steadily with advancing age for infections caused by HIV, syphilis, hepatitis B, and especially, HSV-2 and the genital types of HPV. It is therefore, undoubtedly true that a very large proportion of patients seen by clinicians of all disciplines—perhaps the majority of all adults in the world—have one or more STIs.”
2. “Cohort studies demonstrate condom effectiveness against STI acquisition, not only vs. HIV, but also vs. HSV, gonorrhea, and chlamydial and vaginal infections, and specifically against HPV infection—refuting earlier concerns that condoms did not prevent HPV acquisition.” (that condoms do seem to offer protection against HPV was news to me. Later on in the book the protection offered is made more explicit: “Even for human papilloma virus, which can be transmitted without exposure of mucosal surfaces, condoms have been found to reduce the risk of acquisition by 70%.28“)
3. One major effect of the introduction of penicillin […] was loss of public health interest in STD control. Public spending on STD control declined throughout the world, and these diseases became a low priority.24 For example, India developed the capacity to manufacture its own penicillin in 1954, after which the state governments of India turned their attention to other health problems.40
One significant exception to this trend was China. Partly because the Chinese had blamed STDs on foreign occupation of China and foreign cultural decadence, the Communist government adopted STD control as one of its major policy initiatives immediately after its 1949 political victory. In a campaign that included widespread public relations efforts through plays, radio programs, and small discussion groups, the government undertook a massive screening and treatment program including vocational rehabilitation for former female sex workers. By 1964, the government claimed to have eliminated STDs, a statement that is impossible to verify but widely accepted as a general indication of a very low Chinese prevalence rate. The long-term effects of the campaign are, however, less clear. Because STDs were represented as a social evil and sign of decadence, Chinese patients tried to avoid public hospitals, which charged STD patients to punish them for their having acquired these diseases. Social stigma became a major problem. Furthermore, the medical specialty of venereology was no longer practiced and taught after 1960s. With the liberalization of employment policies in 1989 and the subsequent development of an enormous migrant labor population (between 50 and 120 million people), rates of STDs began to increase, with insufficient medical resources and ability to respond.41”
4.”Historically, prevention is the neglected aspect of STD control programs. Moral reformers have often asserted their control over prevention efforts by defining STD prevention as a problem of morality. Whether led by church groups themselves or by charitable organizations, these efforts focused on fear-based messages about the consequences of immorality (death, disfigurement, infertility, shame) along with representations of happy family life with abundant, healthy offspring as a consequence of correct moral choices..24
This approach seldom focused on the structural factors which influence sexual behavior, such as long-term labor migration which keeps spouses separated, population displacement, and lack of economic opportunities for young females. […] Not until the threat of HIV/AIDS emerged during the 1980s, when a fatal STD with no cure threatened the lives of millions, did governments begin to invest substantial resources into systematically studying behavioral science approaches to changing behavior.”
5. “STI/HIV are not spread randomly. Unprotected sex with an infected partner is by far the most important risk factor for STI/HIV infection.1,9 This in turn is influenced by prevalence and distribution of infection in a population, as well as the behavior of an individual and his/her partners.
Economic deprivation, low education, economic inequality, and economically driven migration and mobility have all been found to be associated with the risk of STI/HIV infection.10, 11, 12 […] processes associated with development such as increases in disposable income and increases in mobility among certain groups and not others are associated with increased risk.10,18 Professions involving high mobility and extended periods away from families, such as migrant labor, serving in the military, driving trucks, or working as sailors are also associated with augmented risk.”
6. “The primary mechanism through which STI contribute to mortality is through mortality associated with HIV. And with an estimated median survival time, a little above 9 years from HIV infection to death in developing countries in the absence of antiretroviral therapy, HIV has had a dramatic impact on adult mortality.25,37 [I’ve written about these numbers before here on the blog, but the 9 year time frame was news to me. Note that it’s age-dependant: “most infected [at birth or as a result of breast-feeding] children, in absence of antiretroviral therapy, will develop AIDS and die before their fifth birthday”. There’s a lot more in the book about this stuff if you’re interested.] […]
7. “Data on cost-effectiveness [of interventions] are extremely limited and a function of the scarcity of both effectiveness and cost data. The best available data are for health facility-based interventions such as syndromic STI management, screening of blood for transfusion, and prevention of MTCT. The data on cost-effectiveness of behavioral, community, and structural interventions are far weaker. […] the position taken in the current chapter is that estimates of the cost-effectiveness of STI interventions are highly variable, reflecting both the great heterogeneity in environments as well as the great heterogeneity in the efficiency of service delivery:
The health benefit in terms of numbers of disability-adjusted, discounted, healthy life years saved by curing or preventing a case of syphilis varies from 3 years in a person who has ceased all sexual activity to as many as 161 years in a sex worker with two partners a day. The cost of treating that prostitute for syphilis varies from US$ 5 to US$ 100. Thus the cost per disability adjusted life year (DALY) of syphilis treatment can range from 100/3 or US$ 33 per DALY to 5/161 or less than a US$ 0.05 per DALY. As we learn more about the complexities of delivering STI treatment services and take into account the diversity of risk behavior, the ease with which STI interventions can be ascribed a simple cost-effectiveness ratio has declined. […]
Almost by definition, there is more to be gained by changing the behavior of people with high levels of risk behavior than by changing that of an equivalent number of people with lower levels of risk behavior. However, the difference in the effectiveness between the two falls as epidemics become more generalized, such that in heavily affected countries prevention interventions are likely to become extremely cost-effective even when targeted to individuals with relatively low levels of risk behavior. Consequently, countries with low-level and concentrated epidemics should emphasize interventions that are targeted to individuals at especially high risk of becoming infected or transmitting the virus, whereas countries with generalized epidemics should also invest heavily in interventions that target entire populations or population subgroups. Thus, any determination of the likely effectiveness and cost-effectiveness of specific interventions in particular circumstances requires an accurate understanding of the stage and nature of the national epidemic.”
8. “The natural history of an infection is the relationship between that infection and disease and associated patterns of infectiousness. In understanding this natural history, individuals can be divided between mutually exclusive categories and the flows between them illustrated schematically in flow diagrams. Figure 3-1 shows the assumptions frequently made about a range of the key STIs in such flow diagrams.”
(click to view full size)
9. “Those with many sexual partners can drive the incidence of an STI in the population and have been described as a “core group”.48 Axiomatically, for a sexually transmitted disease (STD) to exist there must be individuals with sufficient sexual partners to transmit infection to more than one other person.49 If interventions could reliably prevent infection in these individuals, the STI could be eliminated. Studies of risk behaviors and the distribution of STIs have attempted to identify the characteristics of those within the core group as a target for interventions. […]
The lower the incidence of an STI in a population, the more it will be concentrated in those with higher risk behaviors. If the behaviors placing individuals at risk are similar then those most at risk of one STI would be the same as those most at risk of another infection. We would expect infections with a higher combined transmission probability and duration to not only be more widespread, but to also be found in those with STIs with a lower combined reproductive potential.52 If this is not the case as has been suggested in some observations,53 potential explanations include the acquisition of immunity against one infection, different likelihoods of receiving treatment, and different risk behaviors placing individuals at risk. […]
The choice of sexual partners of an individual will have a large influence on whether or not they are exposed to someone infected. The choice of sexual partners will depend upon the contexts in which potential couples meet, for instance, schools, church groups, beer halls, and family gatherings and how they relate. Studies show that individuals tend to choose sexual partners, particularly spouses, who are similar with respect to social and demographic variables such as age, education and income.47,49 Such a choice will lead to assortative (like-with-like) sexual mixing within the population with respect to the specific variables. […] Assortative mixing restricts the spread of STIs but helps maintain chains of infection within high-risk groups. Thus if mixing were assortative, an STI would be more likely to invade rapidly and persist within a population but would also be less likely to spread widely. In contrast, random mixing would spread infection from high- to low-risk individuals who are dead ends for the infection.”
10. “The basic reproductive number (R0) is a measure of the potential for the spread of an infection and can be defined for STIs as the average number of infections caused by one infectious individual entering an entirely susceptible population.69 The key components determining the value of the basic reproductive number are those discussed above: the transmission likelihood (β), the contact rate (c ) and the duration of infectiousness (D), with, in a simple, illustrative model, the product of these three being the basic reproductive number: R0 = βcD.69 The value of R0 determines: the chances of an epidemic when an infection enters a population; the rate of spread of the epidemic; the endemic level of infection, and the effort required to bring the infection under control. An important distinction has to be drawn between the basic reproductive number, R0, which measures the potential for spread in a naive population, and the effective reproductive number, Rt, which changes depending on the experience of infection in the population.70 This effective reproductive number is the number of new infections caused by an average infection at a given time, t, which at time zero equals the basic reproductive number. Once some contacts are already infected or immune, the effective reproductive number is reduced and is the product of the basic reproductive number and the fraction of contacts remaining susceptible. When an infection successfully invades a population its prevalence will initially grow exponentially, until it saturates and the effective reproductive number falls. […] the greater the value of R0, the higher predicted prevalence of infection and immunity. In the case of STIs, where there is heterogeneity of risk, contacts are concentrated in a small fraction of the population and infection saturates long before it would in a homogenous population. […]
The pattern of spread of the epidemic and its subsequent progress to an endemic level depends upon the duration of infection and the role of acquired immunity […] For a short-lived infection with no acquired immunity, such as gonorrhea, we can expect a steady state to be reached quickly. If death or acquired immunity reduces the susceptible pool, the prevalence of infection can fall until the resupply of susceptibles through newly susceptible individuals entering the population either balances the losses or builds up over time to cause new epidemics. The associated declines in prevalence could be confused for the impact of interventions but are the natural course of the epidemic. In the case of syphilis, acquired or concomitant immunity can explain the long-term cycles in incidence observed in US case reports.10 In the case of HIV, declines in prevalence can reflect earlier declines in incidence caused by saturation.73″
11. “To reduce the incidence of STI infection interventions must alter the reproductive potential of the infection. Shortening the infectious period, reducing the contact rate, or reducing the transmission probability, all reduce the basic reproductive number of infection, while introducing artificial immunity through vaccination would reduce the proportion of the population susceptible and thereby reduce the effective reproductive number. Reducing the basic reproductive number has a nonlinear impact on the endemic prevalence of infection […] heterogeneity in risk plays a key role in the epidemiology of STIs. In populations with a distribution of risk, small reductions in risk can have a large impact in a lower risk group while having little impact in higher risk groups.75 Thus, initially interventions can have a large impact, but as their intensity is increased it generates diminishing returns, as infection is removed from low-risk sections of the population and becomes more concentrated. […]
The relative success of different STIs is likely to have changed in response to treatment, with chancroid, syphilis, and gonorrhea becoming relatively less common if their symptoms are more likely to receive attention. Similarly within microbial populations, treatment is likely to provide a selective advantage to organisms that generate negligible symptoms, more so than organisms that have partial drug resistance. Over time, we might expect the pathogenicity of curable STIs to decline unless there is a correlation between symptoms and transmissibility, which is hypothetically likely if disease is associated with larger bacterial colonies and transmission depends upon the infectious dose of bacteria. However, if interventions through screening target both asymptomatic and symptomatic infections, then selection is likely to favor organisms that transmit more readily, with a concomitant shorter duration of infection in the absence of treatment.77 Similarly, drug resistance becomes a better adaptive strategy if both symptomatic and asymptomatic infections are rapidly treated through active screening.”
12. “An estimated 1.9 million people (1.3-2.6 million) are living with HIV in North America and in Western and Central Europe.
In high-income countries, where the great majority of people who need antiretroviral treatment do have access to it, people living with HIV are staying healthy and surviving longer than infected people elsewhere. Widespread access to life-extending antiretroviral treatment kept the number of AIDS deaths at between 19,000 and 42,000 in 2005. However, prevention efforts are not keeping pace with the changing epidemics in several countries. Sex between men is the most common route of infection in Australia, Canada, Denmark, Germany, Greece, and the United States. Patterns of HIV transmission are changing with an increasing proportion of people becoming infected through unprotected heterosexual intercourse. In Belgium, Norway, and the UK, the increase in heterosexually transmitted infections is dominated by people from countries with generalized epidemics, predominantly sub-Saharan Africa. In the United States, about half of newly reported infections are among African Americans who represent 12% of the population. […] Drug injecting accounted for more than 10% of all reported HIV infections in Western Europe in 2002 (in Portugal it was responsible for over 50% of cases). In Canada and the United States, about 25% of HIV infections are attributed to drug injecting.”
13. “The incidence, prevalence, and population distribution of sexually transmitted infections (STIs) are largely determined by the complex interplay of dynamically changing demographic, economic, social, and behavioral forces and the response of the health system to emergent STI morbidity patterns. Over the past 3 decades, overall incidence and prevalence of bacterial STI, in particular gonorrhea, syphilis, chancroid, and chlamydial infections have declined in the United States, Western Europe, and many developing countries, to their lowest levels since World War II. Declines in bacterial STI in developing countries are attributed to the widespread implementation of syndromic management and to a large-scale shift to safer sexual behaviors in response to the HIV epidemic. Despite such remarkable declines, rates of some bacterial STI are still high and/or increasing in some subpopulations […] During the past decade prevalences of viral STI, particularly genital herpes infections (HSV), appear to have increased in many countries […] Diagnosis, management, and control of viral STIs have changed drastically over the past decade. The introduction of new diagnostic technologies has increased recognition of viral STI, improved sensitivity in identification of bacterial STI, and expanded the repertoire of usable specimens. The use of urine and vaginal swabs has greatly expanded coverage of screening services and has led to the availability of true population-based estimates of the prevalences of STIs.1 […] In all societies, for many reasons discussed in this chapter, STIs tend to concentrate in certain populations including urban, poor, and minority populations, with highest rates among sexually active adolescent females followed by adolescent and young adult men. This pattern is particularly pronounced in western industrialized countries where effective prevention and control efforts result in concentrated STI morbidity. During the past decade commercial sex has become an increasingly important factor in STI transmission6,7 in many areas of the world including the United States and Western Europe.”
14. “Trajectories whereby STI epidemics evolve differ for different types of population-pathogen interactions.30, 31, 32 Whereas highly infectious, short duration bacterial STIs—for instance, gonorrhea—depend on the presence of core groups marked by multiple sex partnerships (often of short duration) for their spread, less infectious, long duration viral STIs—for example, herpes simplex virus (HSV) or human papillomavirus (HPV) infections—are less dependent on multiple partnerships of short duration or on short gaps between partnerships. Thus, the pattern of spatial and population distribution of various STIs differs markedly. Syphilis and gonorrhea tend to be concentrated in individuals with multiple partnerships and in populations with highly connected sexual networks; whereas genital chlamydial infections, genital herpes, and genital HPV infections are much more ecumenically, widely distributed across the entire population.33
15. “The most recent updated estimates for prevalence and incidence of STIs globally are provided by the WHO.47 These estimates suggest that of 340 million new cases of gonorrhea, syphilis, chlamydial infection, chancroid, and trichomoniasis STIs in 1999 under 10% occurred in North America and Western Europe; over 90% of new infections were in developing countries (Table 5-1). In 1999, the overall estimated number of new cases of chlamydia, gonorrhea, and syphilis infections among 15-49-year-old men and women totaled over 166 million with close to 92 million cases of chlamydial infection, 62.35 million cases of gonorrhea, and 11.76 million cases of syphilis (Table 5-2). In addition, there were an estimated 173.46 million cases of trichomoniasis.
In developing countries, passive surveillance of STI morbidity is particularly inadequate. However, in recent years the epidemiology of STIs in sub-Saharan Africa is better defined based on large population-based prevalence surveys. The results of these surveys have confirmed the high prevalences of STIs even in rural populations, for example, syphilis (5-10% of adults infected), vaginal trichomoniasis (20-30% of women), and bacterial vaginosis (up to 50% of women). Syphilis has been estimated to cause 490,000 stillbirths and neonatal deaths per year in Africa—a figure similar to the number of children dying of HIV/AIDS worldwide.48
16. “Data on gonococcal antimicrobial resistance across the EU are not comprehensive. Plasmid-mediated resistance to penicillin and tetracycline had increased in Europe during the early 1990s. Sporadic resistance to fluoroquinolones was also documented in the early 1990s, mainly imported from South East Asia.52 […] Recently, increases in fluoroquinolone resistance have been reported in many countries in Europe. In Denmark, the laboratory-confirmed percentage of gonococci with fluoroquinolone resistance increased from 0% to 27% in 1999, 17% of the strains were resistant to both penicillin and fluoroquinolones.52 […] By early 2004, fluoroquinolones were no longer recommended in the United States as first-line treatment for MSM, and by early 2007, were no longer recommended as first-line treatment of gonorrhea in any group.86
17. “Chlamydia trachomatis is still the most prevalent sexually transmitted bacterial infection in North America and Europe.52,54 It is difficult to describe temporal trends in the incidence of chlamydial infection because of the large proportion of asymptomatic infections; the increasing use of increasingly sensitive diagnostic tests, with expansion of chlamydia screening activities in Europe and the United States; the increased emphasis on case reporting by providers; and the improvements in the information systems for reporting. In many European countries, case reporting of genital chlamydial infections is not mandatory; consequently, relatively little information is available from national surveillance sources. […]
In a recent study,122 U.S. women aged 14-49 participating in the National Health and Examination Survey (NHANES) cycles 2001-2004 provided self-collected vaginal swabs; vaginal fluids extracted from the swabs were evaluated for Trichomonas vaginalis using polymerase chain reaction (PCR). The overall prevalence of T. vaginalis was 3.1%; it was highest among non-Hispanic blacks (13.3%) and lower among Mexican Americans (1.8%) and non-Hispanic whites (1.3%). […]
Viral STIs are not notifiable in most European countries and relatively limited temporal trend data have been published.52 Genital HSV infection is the most common ulcerative STI in the UK and the United States. However, many patients with genital herpes do not perceive or recognize symptoms of the infection, and clinical case-reports grossly underrepresent the true incidence of genital herpes as reflected by serologic testing for antibody to HSV-2. […] HSV-2 prevalence appears to be higher in Northern Europe and in North America than in Western and Southern Europe. The highest prevalence of HSV-2 infection was found among women in Greenland, reaching 57% among 20-26-year olds and 74% in 25-39-year olds. In Scandinavia, HSV-2 prevalence was relatively higher than in other areas of Europe—15-35% among women between 25 and 35 years of age.124 […] The most recent data on HSV-2 seroprevalence in the United States were collected in a stratified random sample of the United States population through the NHANES during 1988 through 1994 and 1999 through 2004.126 Persons between ages 14 and 49 were included in the analyses. The overall age-adjusted HSV-2 seroprevalence was to 21.0% in the period 1988-1994, decreasing to 17.0% in 1999-2004, representing a relative decline of 19% between the two surveys. […] The seroprevalence of HSV-1 also decreased from 62% to 57.7% between the two surveys—a relative decrease of 6.9%. […]
Genital HPV infections are the most prevalent STIs in the United States and in the world. HPV infections other than those causing genital warts (usually types 6 and 11) are nearly always subclinical, not recognized by the infected individual. By screening for HPV DNA every 3 months, using PCR amplification tests, the cumulative incidence of genital HPV infections in one study was 43% over a 3-year period in one study of sexually active female University students127 and 32% over a 2-year period in another.128 […] A recent pooled analysis showed the age standardized prevalence of all types of HPV infection to vary 20-fold among different regions of the world.130 The prevalence of high risk types of the virus was 18% in sub-Saharan Africa, 5% in Asia, 10% in South America, and 4% in Europe. The prevalence of HPV infection is highest among young women and appears to drop-off with increasing age.131 […] Risk factors for HPV infection include increased number of sex partners, increased number of male partners’ lifetime partners, a short-time interval between meeting a partner and engaging in sexual intercourse, increased age difference between partners, and current smoking.128 […] Based on these preliminary findings from cohort studies, and together with data from national surveys of sexual behavior […] it is not unlikely that the majority of adults in the United States, perhaps three-quarters, have been infected with one or more types of genital HPV.”
18. “Worldwide, more men than women report multiple partnerships except in some industrialized countries, where the proportions of men and women who report multiple partnerships are similar.10 The mean age difference between married men and women is lower in industrialized countries (1.9 in Australia and 2.2 in United States) than in developing countries; data are not available on age differences between sex partners. According to a recent review153 of estimates of lifetime, prevalence of men having had sexual intercourse with other men is lower in industrialized countries (6% in the UK and 5% in France) than in most other regions of the world. Rates of condom use are generally higher in industrialized countries than in developing countries, especially in women.10 The increase in condom use in recent years has also often been more substantial in industrialized countries; the only exception to this pattern is France where women have reported declining condom use in more recent years.”
19. “Historically, the predominant focus of STI epidemiology has been on the attributes and behaviors of individuals, and on the risk of acquiring, rather than of transmitting infection. This approach is consistent with the approaches of clinical medicine, chronic disease epidemiology, and psychology. However, when considered as the “sole” or “main” focus, it appears to be inconsistent with STI transmission dynamics190 and it has been increasingly challenged in recent years. The new paradigm includes at least three principles: that one person’s health outcome is highly dependent on other person’s health outcomes;191,192 that transmission of infection and its prevention is at least as important and perhaps more important than acquisition of infection and its prevention—thus focusing attention on infected individuals and the role they play in the spread of infection; that characteristics of sex partners and partner selection processes are an important component of risk determination—thereby focusing on behaviors of sex partners as well.186
20. “The inadequacy of the STD health service infrastructure and the resulting preventable increment in duration of infectiousness is a major reason why the United States has the highest rates of STIs among developed countries.”
21. “In the light of all these considerations, it is obvious that in evaluating behavioral interventions to prevent STIs, and HIV, data from randomized controlled trials are particularly important, the choice of outcome measure is critical, and the outcome measure of choice is the appropriate biomedical measure of the STI or STIs of interest.264,270
Most evaluations of behavioral interventions to date have employed less rigorous study designs and behavioral outcome measures. A systematic review of computerized abstracts from International AIDS conferences between 1989 and 1992 showed that only 10 of 15,946 abstracts reported on randomized controlled trials of behavioral interventions.264 Two subsequent critical reviews of behavioral interventions in general and behavioral interventions for young people reported similar findings.271,272 These reviews also indicated that many behavioral intervention studies focused only on determinants of behavior such as knowledge, beliefs, and attitudes as outcome measures. […] In the past 2 decades a number of behavioral intervention trials have been conducted including those mentioned above. Many of these studies showed efficacy in reducing risky behaviors, and a smaller number showed efficacy in reducing incidence of bacterial STI in study subjects. Interestingly, to date, no cluster randomized trial of behavioral interventions (where at least one arm of the study represented a behavioral intervention) has showed significant impact at the population level.”
I don’t like when the blog isn’t updated for several days, so here are some links to stuff I’ve encountered on the internet in the recent past:
i. Diabetic Autonomic Neuropathy. An overview article which covers a lot of ground; it has approximately 1000 citations and I believe it’s one of the most read articles published in Diabetes Care, a journal you incidentally should know about if you’re diabetic or are interested in diabetes.
ii. Also diabetes-related and closely related to the above paper: The EKG in Diabetes Mellitus. This article is particularly relevant to me because I had an EKG last week and will be told the results of it tomorrow where I have a doctor’s appointment – reading stuff like this first makes it easier to ask the right questions. I jokingly explained to a friend yesterday that if the results of that test come out a specific way, it will be much easier for me to make pension plans (meaning I’d most likely be dead long before the official retirement age – naturally I do not hope for that outcome to happen). I’ll also learn the results of the standard Hba-1c blood test – which is measured 3-4 times a year – as well as the annual urin-sample analysis to check for microalbuminuria (kidney damage). Also, cholesterol levels and triglycerides. So I’ll learn more from this check-up than I usually do. I hope everything is fine but there’s a reason why they perform tests like these; I have no way of knowing myself if there’s a problem here.
Anyway, a few quotes from the paper:
“Fibrotic changes, especially in the basal area of the left ventricle, have frequently been observed in diabetic patients, even when cardiac involvement is clinically not yet evident. […] The EURODIAB Insulin-Dependent Diabetes Mellitus Complications Study (EURODIAB IDDM)9 investigated 3250 type 1 diabetes patients with an average diabetes duration of >30 years; the prevalence of left ventricular hypertrophy was found to be 3 times greater than that reported in the general population of similar age. […] Baroreflex dysfunction and disturbed heart rate variability are the most commonly used methods to assess CAN [Cardiovascular autonomic neuropathy, US]. […]
Ong et al14 found the QTc to be shorter if patients had signs of neuropathy, although these patients’ heart rate was higher and their circadian patterns seemed to be preserved. Valensi et al15 found an unchanged QTc in mild neuropathy, although the circadian day/night QTc pattern was reversed. Pappachan et al16 expressed the view that the QTc interval can be used to diagnose CAN with reasonable sensitivity, specificity, and positive predictive value. Grossmann et al17 observed a prolonged QTc only in diabetic patients with CAN; late potentials were not recorded in any of these patients with CAN. CAN patients with prolonged variability in QTc, QT, or both had high incidence of sudden death.18 […]
Myocardial ischemia is more often painless in patients with diabetes mellitus.19 Resting ECG abnormalities20 as well as cardiac autonomic dysfunction21 were found to be predictors of silent ischemia in asymptomatic persons with T1D.
In otherwise healthy diabetic men during an average follow-up of 16 years, an abnormal and even an equivocal exercise ECG response was associated with a statistically significant high risk for all-cause and cardiac mortality and morbidity, independently of physical fitness and other traditional risk factors; fit men had a higher survival rate than did unfit men.22 [One more reason why I shouldn’t have that much trouble motivating myself to stay in shape.] […]
The early stage of diabetic cardiomyopathy may already be associated with a range of metabolic abnormalities and even with abnormalities in diastolic function. Frequently, no structural cardiac abnormalities can be identified at this stage; the often subtle ECG alterations may be our only way to diagnose early diabetic cardiomyopathy. […]
Even early in the course of diabetes mellitus, ECG alterations such as sinus tachycardia, long QTc, QT dispersion, changes in heart rate variability, ST-T changes, and left ventricular hypertrophy may be observed. ECG alterations help evaluate cardiac autonomic neuropathy and detect signs of myocardial ischemia even in asymptomatic patients. Prolonged myocardial fibrosis leads to diabetic cardiomyopathy, with peculiar ECG presentation. Electrocardiographic changes are already present in fetuses, children, and adolescents. The resting ECG, frequently complemented by exercise ECG, assists in cardiac screening of diabetic individuals and helps detect silent ischemia, assess prognosis, and predict mortality”
iii. Boredom Proneness: Its Relationship to Psychological- and Physical-Health Symptoms, by Sommers and Vodanovich.
“The relationship between boredom proneness and health-symptom reporting was examined. Undergraduate students (N 5 200) completed the Boredom Proneness Scale and the Hopkins Symptom Checklist. A multiple analysis of covariance indicated that individuals with high boredomproneness total scores reported significantly higher ratings on all five subscales of the Hopkins Symptom Checklist (Obsessive–Compulsive, Somatization, Anxiety, Interpersonal Sensitivity, and Depression). The results suggest that boredom proneness may be an important element to consider when assessing symptom reporting. Implications for determining the effects of boredom proneness on psychological- and physical-health symptoms, as well as the application in clinical settings, are discussed.”
I had no idea there was such a thing as a ‘Boredom Proneness Scale’! I found the literature overview in the beginning of the paper much more interesting than the study itself (one word: WEIRD). Judging from the reported results there, if you’re bored a lot and/or have a really boring job you may be well advised to do something about that – because being bored is associated with a lot of bad stuff:
“To date, the work on boredom proneness has focused on its association with negative affect, as well as problems in academic and work settings. For instance, significant positive relationships have been found between the tendency to experience boredom and depression, anxiety, hostility, anger, loneliness, and hopelessness (e.g., Ahmed, 1990; Farmer & Sundberg, 1986; Rupp & Vodanovich, 1997; Vodanovich, Verner, & Gilbride,
1991; Watt & Davis, 1991). Other researchers have reported boredom proneness to be related significantly to lower educational achievement, truancy rate, and poor work performance (e.g., Branton, 1970; Drory, 1982; Gardell, 1971; Maroldo, 1986; O’Hanlon, 1981; Robinson, 1975; Smith, 1981).
Limited work, however, has been devoted to investigating the association between boredom and psychological- and physical-health symptoms. Evidence for such a relationship can be inferred from studies reporting significant, positive correlations between boredom and substance abuse and eating disorders (e.g., Abramson & Stinson, 1977; Ganley, 1989; Johnston & O’Malley, 1986; Martin, 1989; Pascale & Sylvester, 1988).
Other researchers have established a connection between boredom and detrimental health effects in organizational settings. For instance, Smith, Cohen, and Stammerjohn (1981) found that workers in monotonous jobs reported more visual, musculoskeletal, and emotional-health complaints than those performing non-monotonous work. Samilova (1971) found that female Russian workers employed in repetitive tasks experienced higher incidence of health problems, including gastritis, peripheral neurological disorders, and joint, tendon, muscle, and cardiovascular disease, than workers in less-repetitive jobs. Ferguson (1973) found that telegraphists who complained of task monotony indicated a greater occurrence of physical-health problems, such as asthma, bronchitis, trunk myalgia, and hand tremors, as compared to other workers in less-monotonous positions.”
iv. Ideology, Motivated Reasoning, and Cognitive Reflection: An Experimental Study. I haven’t actually gotten around to reading this yet, but I bookmarked it for a reason; I probably will later during the week.
v. Media Use Among White, Black, Hispanic, and Asian American Children, by Rideout, Lauricella and Wartella. I’ve written about that stuff before but I haven’t written about this data. It’s survey data so it should be taken with a grain of salt. Even if it is, however, I think there’s some interesting information here. Some stuff from the report:
“Historically, scholars have been aware of differences in the amount of time that White and minority children spend with media, especially TV. But last year’s Generation M2 study indicated a large increase in the amount of time both Black and Hispanic youth are spending with media, to the point where they are consuming an average of 13 hours worth of media content a day (12:59 for Blacks and 13:00 for Hispanics), compared with about eight and a half hours (8:36) for White youth, a difference of about four and a half hours a day.” [my emphasis] […]
The biggest differences are in the amount of time spent with a TV (a difference of about one to two hours of TV a day between White and minority youth), music (a difference of about an hour a day), computers (up to an hour and a half difference), and video games (from 30 to 40 minutes difference).”
Here’s the ‘big picture’, click to view full size:
vi. I really, truly dislike (and that’s putting it mildly) the new format for the discover magazine blogs, but I really liked this post by Razib Khan. Then again it was posted before the switch. I like a lot of his stuff so I tend not to link to individual posts (I’d have to link to a lot of stuff…) but I figure I should remind you now and then that you should be reading his blog. Even if the new format sucks.