Here’s my goodreads review of the book. As mentioned in the review, the book was overall a slightly disappointing read – but there were some decent quotes included in the book, and I decided that I ought to post a post with some sample quotes here as it would be a relatively easy post to write. Do note while reading this post that the book had a lot of bad quotes, so you should not take the sample quotes I’ve posted below to be representative of the book’s coverage in general.
i. “The aim of science is to seek the simplest explanation of complex facts. We are apt to fall into the error of thinking that the facts are simple because simplicity is the goal of our quest. The guiding motto in the life of every natural philosopher should be “Seek simplicity and distrust it.”” (Alfred North Whitehead)
ii. “Poor data and good reasoning give poor results. Good data and poor reasoning give poor results. Poor data and poor reasoning give rotten results.” (Edmund C. Berkeley)
iii. “By no process of sound reasoning can a conclusion drawn from limited data have more than a limited application.” (J.W. Mellor)
iv. “The energy produced by the breaking down of the atom is a very poor kind of thing. Anyone who expects a source of power from the transformation of these atoms is talking moonshine.” (Ernest Rutherford, 1933).
v. “An experiment is a question which science poses to Nature, and a measurement is the recording of Nature’s answer.” (Max Planck)
vi. “A fact doesn’t have to be understood to be true.” (Heinlein)
vii. “God was invented to explain mystery. God is always invented to explain those things that you do not understand. Now, when you finally discover how something works, you get some laws which you’re taking away from God; you don’t need him anymore. But you need him for the other mysteries. So therefore you leave him to create the universe because we haven’t figured that out yet; you need him for understanding those things which you don’t believe the laws will explain, such as consciousness, or why you only live to a certain length of time – life and death – stuff like that. God is always associated with those things that you do not understand.” (Feynman)
viii. “Hypotheses are the scaffolds which are erected in front of a building and removed when the building is completed. They are indispensable to the worker; but he must not mistake the scaffolding for the building.” (Goethe)
ix. “We are to admit no more cause of natural things than such as are both true and sufficient to explain their appearances.” (Newton)
x. “It is the province of knowledge to speak and it is the privilege of wisdom to listen.” (Oliver Wendell Holmes)
xi. “Light crosses space with the prodigious velocity of 6,000 leagues per second.
La Science Populaire
April 28, 1881″
“A typographical error slipped into our last issue that is important to correct. The speed of light is 76,000 leagues per hour – and not 6,000.
La Science Populaire
May 19, 1881″
“A note correcting a first error appeared in our issue number 68, indicating that the speed of light is 76,000 leagues per hour. Our readers have corrected this new error. The speed of light is approximately 76,000 leagues per second.
La Science Populaire
xii. “All models are wrong but some are useful.” (G. E. P. Box)
xiii. “the downward movement of a mass of gold or lead, or of any other body endowed with weight, is quicker in proportion to its size.” (Aristotle)
xiv. “those whom devotion to abstract discussions has rendered unobservant of the facts are too ready to dogmatize on the basis of a few observations” (-ll-).
xv. “it may properly be asked whether science can be undertaken without taking the risk of skating on the possibly thin ice of supposition. The important thing to know is when one is on the more solid ground of observation and when one is on the ice.” (W. M. O’Neil)
xvi. “If I could remember the names of all these particles, I’d be a botanist.” (Enrico Fermi)
xvii. “Theoretical physicists are accustomed to living in a world which is removed from tangible objects by two levels of abstraction. From tangible atoms we move by one level of abstraction to invisible fields and particles. A second level of abstraction takes us from fields and particles to the symmetry-groups by which fields and particles are related. The superstring theory takes us beyond symmetry-groups to two further levels of abstraction. The third level of abstraction is the interpretation of symmetry-groups in terms of states in ten-dimensional space-time. The fourth level is the world of the superstrings by whose dynamical behavior the states are defined.” (Freeman Dyson)
xviii. “Space tells matter how to move . . . and matter tells space how to curve.” (John Wheeler)
xix. “the universe is not a rigid and inimitable edifice where independent matter is housed in independent space and time; it is an amorphous continuum, without any fixed architecture, plastic and variable, constantly subject to change and distortion. Wherever there is matter and motion, the continuum is disturbed. Just as a fish swimming in the sea agitates the water around it, so a star, a comet, or a galaxy distorts the geometry of the space-time through which it moves.” (Lincoln Barnett)
xx. “most physicists today place the probability of the existence of tachyons only slightly higher than the existence of unicorns” (Nick Herbert).
I was debating whether to post this, but considering how long it’s been since my last post I decided to do it. A large number of lectures have recently been uploaded by the Institute for Advanced Studies, and despite the fact that most of my ‘blogging-related activities’ these days relate to book reading I have watched a few of those lectures, and so I decided to post a couple of the lectures here:
I liked this lecture. Part II of the lecture in particular, starting around the 38 minute mark, dealt with stuff reasonably closely related to things I’d read about before (‘relatively’…) recently, back when I read Lammer’s text (blog coverage here); so although I didn’t remember the stuff covered in Lammer’s text in too much detail, it was definitely helpful to have worked with this stuff before. However I do believe you can watch the lecture and sort of understand what she’s talking about without knowing a great deal about these topics, at least if you don’t care too much about understanding all the details (I’d note that there are a lot of things going on ‘behind the scenes’ here, and that you can say a lot of stuff about topics closely related to this talk, like outgassing processes and how they relate to things like volcanism as well as e.g. the dynamic interactions between atmospheric molecules and the solar wind taking place in the early stages of stellar evolution). As is always the case for IAS lectures it’s really hard to hear the questions being asked and that’s annoying, but actually I think miss Schilchting is reasonably good at repeating the question or sort of answer them in a way that enables you to gather what’s ‘going on’; at least the fact that you can’t hear the questions is in my opinion a somewhat bigger problem in the lecture below (relatedly you can actually also see where the laser pointer is pointing in this lecture, at least some of the time – you can’t in the lecture below).
As mentioned this one was harder to follow, at least for me.
I hope to find time to blog a bit more in the days to come. One of several reasons why I’ve not blogged more than I have during the last weeks is that I recently realized that if I put in a bit of effort I’d be able to reach 150 books this year (I’m currently at 143 books, but very close to 144), with 50 non-fiction books (I think going for 52 would be a bit too much, but I’m not ruling it out yet – I’m currently at 47 non-fiction books (…but very close to 48)). I should note that I update the book post to which I link above much more often than I update ‘the blog’ in general with new posts. The reason why the ‘read 150 books this year goal’ is relevant is of course that every time I blog a book here on the blog, this takes away a substantial amount of time which I can’t spend actually reading books. Goodreads incidentally have recently made a nice ‘book of the year’ profile where you can see more details about the books I’ve read etc. From that profile I realized that my implicit working goal of reading 100 pages/day over the year has already been met (I’m currently at ~42.000 pages).
“A commonplace argument in contemporary writing on trust is that we would all be better off if we were all more trusting, and therefore we should all trust more […] Current writings commonly focus on trust as somehow the relevant variable in explaining differences across cases of successful cooperation. Typically, however, the crucial variable is the trustworthiness of those who are to be trusted or relied upon. […] It is not trust per se, but trusting the right people that makes for successful relationships and happiness.”
“If we wish to understand the role of trust in society […], we must get beyond the flaccid – and often wrong – assumption that trust is simply good. This supposition must be heavily qualified, because trusting the malevolent or the radically incompetent can be foolish and often even grossly harmful. […] trust only make[s] sense in dealings with those who are or who could be induced to be trustworthy. To trust the untrustworthy can be disastrous.”
That it’s stupid to trust people who cannot be trusted should in my opinion be blatantly obvious, yet somehow to a lot of people it doesn’t seem to be at all obvious; in light of this problem (…I maintain that this is indeed a problem) the above observations are probably among the most important ones included in Hardin’s book. The book includes some strong criticism of much of the current/extant literature on trust. The two most common fields of study within this area of research are game-theoretic ‘trust games’, which according to the author are ill-named as they don’t really seem to be dealing much, if at all, with the topic of trust, and (poor) survey research which asks people questions which are hard to answer and tend to yield answers which are even harder to interpret. I have included below a few concluding remarks from the chapter on these topics:
“Both of the current empirical research programs on trust are largely misguided. The T-games [‘trust-games’], as played […] do not elicit or measure anything resembling ordinary trust relations; and their findings are basically irrelevant to the modeling and assessment of trust and trustworthiness. The only thing that relates the so-called trust game […] to trust is its name, which is wrong and misleading. Survey questions currently in wide use are radically unconstrained. They therefore force subjects to assume the relevant degrees of constraint, such as how costly the risk of failed cooperation would be. […] In sum, therefore, there is relatively little to learn about trust from these two massive research programs. Without returning their protocols to address standard conceptions of trust, they cannot contribute much to understanding trust as we generally know it, and they cannot play a very constructive role in explaining social behavior, institutions, or social and political change. These are distressing conclusions because both these enterprises have been enormous, and in many ways they have been carried out with admirable care.”
There is ‘relatively little to learn about trust from these two massive research programs’, but one to me potentially important observation, hidden away in the notes at the end of the book, is perhaps worth mentioning here: “There is a commonplace claim that trust will beget trustworthiness […] Schotter [as an aside this guy was incidentally the author of the Micro textbook we used in introductory Microeconomics] and Sopher (2006) do not find this to be true in game experiments that they run, while they do find that trustworthiness (cooperativeness in the play of games) does beget trust (or cooperation).”
There were a few parts of the coverage which confused me somewhat until it occurred to me that the author might not have read Boyd and Richerson, or other people who might have familiarized him with their line of thinking and research (once again, you should read Boyd and Richerson).
Moving on, a few remarks on social capital:
“Like other forms of capital and human capital, social capital is not completely fungible but may be specific to certain activities. A given form of social capital that is valuable in facilitating certain actions may be useless or even harmful for others. […] [A] mistake is the tendency to speak of social capital as though it were a particular kind of thing that has generalized value, as money very nearly does […] it[‘s value] must vary in the sense that what is functional in one context may not be in another.”
It is important to keep in mind that trust which leads to increased cooperation can end up leading to both good outcomes and bad:
“Widespread customs and even very local practices of personal networks can impose destructive norms on people, norms that have all of the structural qualities of interpersonal capital. […] in general, social capital has no normative valence […] It is generally about means for doing things, and the things can be hideously bad as well as good, although the literature on social capital focuses almost exclusively on the good things it can enable and it often lauds social capital as itself a wonderful thing to develop […] Community and social capital are not per se good. It is a grand normative fiction of our time to suppose that they are.”
The book has a chapter specifically about trust on the internet which related to the coverage included in Barak et al.‘s book, a publication which I have unfortunately neglected to blog (this book of course goes into a lot more detail). A key point in that chapter is that the internet is not really all that special in terms of these things, in the sense that to the extent that it facilitates coordination etc., it can be used to accomplish beneficial things as well as harmful things – i.e. it’s also neutrally valenced. Barak et al.‘s book has a lot more stuff about how this medium impacts communication and optimal communication strategies etc., which links in quite a bit with trust aspects, but I won’t go into this stuff here and I’m pretty sure I’ve covered related topics before here on the blog, e.g. back when I covered Hargie.
The chapter about terrorism and distrust had some interesting observations. A few quotes:
“We know from varied contexts that people can have a more positive view of individuals from a group than they have of the group.”
“Mere statistical doubt in the likely trustworthiness of the members of some identifiable group can be sufficient to induce distrust of all members of the group with whom one has no personal relationship on which to have established trust. […] This statistical doubt can trump relational considerations and can block the initial risk-taking that might allow for a test of another individual’s trustworthiness by stereotyping that individual as primarily a member of some group. If there are many people with whom one can have a particular beneficial interaction, narrowing the set by excluding certain stereotypes is efficient […] Unfortunately, however, excluding very systematically on the basis of ethnicity or race becomes pervasively destructive of community relations.”
One thing to keep in mind here is that people’s stereotypes are often quite accurate. When groups don’t trust each other it’s always a lot of fun to argue about who’s to blame for that state of affairs, but it’s important here to keep in mind that both groups will always have mental models of both the in-group and the out-group (see also the coverage below). Also it should be kept in mind that to the extent that people’s stereotypes are accurate, blaming stereotyping behaviours for the problems of the people who get stereotyped is conceptually equivalent to blaming people for discriminating against untrustworthy people by not trusting people who are not trustworthy. You always come back to the problem that what’s at the heart of the matter is never just trust, but rather trustworthiness. To the extent that the two are related, trust follows trustworthiness, not the other way around.
“There’s a fairly extensive literature on so-called generalized trust, which is trust in the anonymous or general other person, including strangers, whom we might encounter, perhaps with some restrictions on what isues would come under that trust. […] [Generalized trust] is an implausible notion. In any real-world context, I trust some more than others and I trust any given person more about some things than about others and more in some contexts than in others. […] Whereas generalized trust or group-generalized trust makes little or no sense (other than as a claim of optimism), group-generalized distrust in many contexts makes very good sense. If you were Jewish, Gypsy, or gay, you had good reason to distrust all officers of the Nazi state and probably most citizens in Nazi Germany as well. American Indians of the western plains had very good reason to distrust whites. During Milosevic’s wars and pogroms, Serbs, Croatians, and Muslims in then Yugoslavia had increasingly good reasons to distrust most members of the other groups, especially while the latter were acting as groups. […] In all of these cases, distrust is defined by the belief that members of the other groups and their representatives are hostile to one’s interests. Trust relationships between members of these various groups are the unusual cases that require explanation; the relatively group-generalized distrust is easy to understand and justify.”
“In the current circumstances of mostly Arab and Islamic terrorism against israel and the West and much of the rest of the world, it is surely a very tiny fraction of all Arabs and Islamists who are genuinely a threat, but the scale of their threat may make many Israelis and westerners wary of virtually all Arabs and Islamists […] many who are not prospects for taking terrorist action evidently sympathize with and even support these actions”
“When cooperation is organized by communal norms, it can become highly exclusionary, so that only members of the community can have cooperative relations with those in the community. In such a case, the norms of cooperativeness are norms of exclusion […] For many fundamentalist groups, continued loyalty to the group and its beliefs is secured by isolating the group and its members from many other influences so that relations within the community are governed by extensive norms of exclusion. When this happens, it is not only trust relations but also basic beliefs that are constrained. If we encounter no one with contrary beliefs our own beliefs will tend to prevail by inertia and lack of questioning and they will be reinforced by our secluded, exclusionary community. There are many strong, extreme beliefs about religious issues as well as about many other things. […] The two matters for which such staunch loyalty to unquestioned beliefs are politically most important are probably religious and nationalist commitments […] Such beliefs are often maintained by blocking our alternative views and by sanctioning those within the group who stray. […] Narrowing one’s associations to others in an isolated extremist group cripples one’s epistemology by blocking out general questioning of the group’s beliefs […] To an outsider those beliefs might be utterly crazy. Indeed, virtually all strong religious beliefs sound crazy or silly to those who do not share them. […] In some ways, the internet allows individuals and small groups to be quite isolated while nevertheless maintaining substantial contact with others of like mind. Islamic terrorists in the West can be almost completely isolated individually while maintaining nearly instant, frequent contact with other and with groups in the Middle East, Pakistan, or Afghanistan, as well as with groups of other potential terrorists in target nations.”
This is an excellent book. I decided to include in this post the entire book description included on goodreads, even if it’s somewhat long, because I thought the description gave a good overview of the topics covered in this book:
“Providing the most up-to-date research and current clinical knowledge of diabetic bone disease and the challenges still facing the research and clinical care communities, this book unites insights from endocrinology and orthopedics to create a truly unique text. The first part covers clinical and pre-clinical applications and research. The first two chapters present the clinical and epidemiological data about diabetic bone disease, evaluated and reviewed for type 1 and type 2, respectively. This is followed by discussions of how the propensity to fracture in diabetic bone disease can impact fracture risk assessments and how it can be adjusted for using current clinically relevant fracture risk models. A comprehensive overview of orthopedic complications observed in diabetes is next, as well as a focus on the consequences of diabetes on periodontal disease. Other topics include the utility of skeletal biomarkers in assessing diabetic bone disease, how drugs used to treat diabetes may also have skeletal consequences, and the possibility that diabetes may fundamentally impact early progenitor cells of various bone lineages and thus globally impact bone. The second part covers biomechanics and bone quality in diabetes: how diabetes ultimately may impact the architecture, integrity, and quality of bone. Utilizing the expertise of top researcher and clinicians in diabetic bone disease in one comprehensive text, this volume will be a useful and thought-provoking resource for endocrinologists and orthopedic surgeons alike.”
I would note that the book is also a useful and thought-provoking resource if you’re just a random diabetic who happens to know enough about medicine and related topics to make sense of a book like this one – i.e. if you’re someone like me. A few related observations from the book’s preface:
“Historically, most attention has been focused on four major complications known to afflict many individuals with T1DM and T2DM: retinopathy, neuropathy, nephropathy, and cardiovascular disease. However, epidemiological data now show that other tissues and organs may be significantly impacted by the diabetic state—and the skeletal system is now emerging as a primary target of diabetes-mediated damage (i.e., diabetic bone disease).
Studies have demonstrated that osteopenia and osteoporosis may be frequent complications of T1D, both in children and adults, and that T1D is associated with decreased bone density and increased fracture risk. In contrast to T1D, T2D has typically not been associated with osteopenia or osteoporosis and, in fact, has been more often associated with increased BMD [bone mineral density]. However, newer data show that bone quality and bone microarchitecture may be compromised in both conditions, suggesting that underlying mechanisms related to increased risk to fracture may be contributory to both forms of diabetes.
In this volume, we provide the reader with up-to-date information about what is currently known about diabetic bone disease and what are the challenges still facing the research and clinical care communities.”
This was a topic about which I knew next to nothing, and one of emotional responses I had early on to some of the coverage in the book was to think along the lines of: ‘Ah, type 1 diabetes, the gift that keeps on giving…’ or perhaps: ‘How was I not told this???’ It reminded me a bit of how I felt back when I realized some years ago that my diabetes was probably also messing with my lungs, without me knowing about it and despite nobody having told me anything about that (for details on that topic, see e.g. this paper). As far as I can remember, bone health has never come up during conversations I have had over the years in the past with endocrinologists or diabetes nurses, nor has it ever been discussed in detail in publications I’ve read on diabetes-related topics; the closest I’ve got has probably been remarks about individuals developing diabetics during childhood being slightly shorter than non-diabetics on average, due to (non-specific) disease-related adverse effects on growth during childhood. Relevant mechanisms have not been discussed in any detail, and actually what I had read on the topic of diabetes and growth had basically lead me to believe that a slight growth disadvantage was really all there was to this topic, as a potential interaction between diabetes status and osteoporosis risk was never touched upon in these publications. To give a great illustrative example, Sperling et al.‘s comprehensive textbook (~600 pages) about type 1 diabetes includes exactly 3 hits for osteoporosis in the text, all of which relate to very specific subtopics and none of which even remotely relate to the highly increased risk of fractures which type 1 diabetes in particular confers – the authors of that text clearly had no idea that type 1 diabetes dramatically increases the risk of fractures and poor bone health; there are zero indications to the contrary. It’s probably not uncommon to see important information in textbooks which people forget about in clinical practice (perhaps because the people working in clinical practice read different textbooks, in which this information was not included…), but it’s certainly less common to see important information not included in textbooks because the textbook authors simply don’t know about them. It seems highly likely to me that a lot of health care providers involved in diabetes care currently do not know anything about the topics discussed in this publication; I hope this state of affairs will change in the future.
As also noted in the comments above, the relationship between diabetes and bone health is complicated and interacts with type; type 1 seems to be much worse for the bones than is type 2, and the relationship between in particular type 2 diabetes and bone health is not at all simple. Type 2 diabetics tend to have both some elevated non-diabetes-related risk factors for fractures (in one chapter the authors thus list in that category obesity, reduced muscle quality, poor balance, and falls – e.g. but not only hypoglycemia-related) and some diabetes-specific risk factors ((/very) poor glycemic control probably increases risk (but see also below), duration of disease increases risk, medications – e.g. the thiazolidinedione drug class used to treat type 2 diabetes), but these don’t fully account for the increased risk.
Most of the standard metrics used to assess fracture risk, such as FRAX, do not take diabetes status into account, which is a problem – “studies indicate that FRAX systematically underestimates fracture risk in patients with T2DM” (this problem is not just related to FRAX, thus elsewhere in the publication it is noted more generally that: “fracture prediction tools underestimate fracture risk in diabetes”). The only one of the widely used risk assessment tools which does take diabetes status into account is the QFracture tool, but this tool “has not been specifically evaluated with regard to calibration in individuals with diabetes”; so there is a lot of uncertainty here. This state of affairs is of course hardly ideal, especially not considering how the number of type 2 diabetics is projected to increase over time in the years to come. It is worth keeping in mind that the total population prevalence of type 2 can be deceiving people here into thinking this is less of a problem than it really is, as most people at increased risk of fractures are old people, and type 2 incidence/prevalence increases with age: “Type 2 diabetes affects over 25 % of older adults in the United States, including diagnosed and undiagnosed cases .” The hip fracture estimates included in Vestergaard’s meta-review discussed below indicate a relative risk of hip-fracture of ~1.4 in the type 2 diabetic sub-population, and if you multiply that number by the 25% prevalence among elderly people in the US, that’s more than a third of all fractures in older adults. That’s a lot of people, and a lot of risk not well accounted for.
A problem related to the above observations in the context of type 2 diabetes (and most of the research that has been done in this area has been done on type 2 diabetes, for reasons which should be obvious (“type 1 diabetes mellitus (T1D) accounts for <10 % of all diabetes […] In the USA, prevalence of T1D has recently been estimated at 1 in every 433 youth <20 years of age”)) is that dual-energy X-ray absorptiometry (DXA), a standard way to measure bone mineral density also used to diagnose osteoporosis, does not ‘pick up on’ the excess risk associated with T2DM; in type 2 individuals risk is elevated even when taking DXA measurements into account (this fact may actually be one argument why the QFracture tool may not be bad at all to apply to people in this patient subgroup; QFracture does not include DXA numbers, and if a substantial proportion of the risk is unrelated to the DXA estimates in type 2 anyway then maybe they’re not that important to include). The arguably poor performance of DXA in the context of fracture risk in type 2 diabetes have lead to the development of other tools which might be better at assessing risk in this patient population, and the authors of some of the later chapters of the book talk in some detail about these tools and the results derived from related studies using these tools. It should perhaps be noted in the context of DXA and bone mineral density numbers that one of the clear differences between type 1 and type 2 here is that bone mineral density tends to be decreased in type 1 diabetes, whereas it’s usually if anything increased in type 2 (but the increased, or at least not lowered, bone mineral density in type 2 does not translate into a lower risk of fracture; risk is still elevated, which is what is surprising and not easy to fully account for).
An interesting aspect of the coverage was that the relationship between glycemic control and bone health seems to not be completely clear; to me the coverage of this topic throughout the various chapters (many chapters cover closely related topics and there’s some coverage overlap, but I didn’t mind this at all) reminded much more of the typical coverage you see in publications discussing how the risk of macrovascular complications relate to glycemic control (…’it’s complicated’) than it reminded me of how the risk of microvascular complications relate to glycemic control (…’hyperglycemia increases risk and there’s a dose-response relationship between complication risk and the level of hyperglycemia’). One problem is that low Hba1c may increase the fall risk because of an increased risk of hypoglycemic episodes, increasing risk at the lower end of the spectrum.
The book has a lot of stuff about the specifics of what might be going on at the cellular level and so on, but I won’t talk much about that here even if I found it interesting (it would take a lot of time to go over the details here); one key point to take take away from that part of the coverage should however be mentioned here, and that is that that stuff thoroughly convinced me that there’s no way the increased fracture risks observed in the various epidemiological studies presented at the beginning of the publication are flukes. There are good reasons to think that diabetes may be bad for the bones, quite aside from the reason that they seem to break their bones more often than other people do.
I have included some data and key observations from the book below. As the post is rather long I decided to highlight/bold a few of the most important observations (they’re not bolded in the book).
“In patients with T1D, an increased incidence of osteopenia and osteoporosis has been recognized for over three decades [10–14], occurring not only in adults, but in children as well [15–17]. Many more recent studies have since validated these early findings, demonstrating a reduced bone mineral density (BMD) in T1D [18–22]. Clinical factors associated with lower bone density include: male gender […]; longer duration of disease […]; younger age at diagnosis […]; lower endogenous insulin or C-peptide levels ; low body mass index (BMI) […]; and possibly the presence of chronic diabetes comorbidities or associated autoimmunity . Some studies also suggest that greater longitudinal decrements in BMD occur over time in males . […] In most studies, poor glycemic control does not seem to be strongly associated with a reduced BMD [18–20, 22, 23, 30, 31] […] T1D is […] associated with an increased risk for fracture, higher than the risk in type 2 diabetes (T2D)”
“among risk factors for hip fracture in >33,000 middle-aged adults in Sweden (~25–60 years), the strongest risk factor for both women […] and men […] was diabetes , suggesting that the presence of diabetes was a major risk determinant for this age group. Similar findings had been reported years before in middle-aged Norwegian women and men […] Together, [studies conducted during the last 15 years on type 1 diabetics] demonstrate an unequivocally increased fracture risk at the hip [compared to non-diabetic controls], with most demonstrating a six to ninefold increase in relative risk. […] type I DM patients have hip fractures at a younger age on average, with a mean of 43 for women and 41 for men in one study. Almost 7 % of people with type I DM can be expected to have sustained a hip fracture by age 65  […] Patients with DM and hip fracture are at a higher risk of mortality than patients without DM, with 1-year rates as high as 32 % vs. 13 % of nondiabetic patients […] Though only a very few studies have examined fracture risk at other skeletal sites [51, 54], an increased risk for vertebral fracture is also a consistent finding in studies that have quantified this. […] in one study, an approximate threefold increase in risk for all non-vertebral fractures was reported in men with T1D”.
“studies […] suggest that cumulative changes in bone architecture are beginning early in childhood, particularly in those diagnosed with T1D at very young ages . Compared with nondiabetic children, reductions in BMD [68, 74–78] and bone size, specifically total cross-sectional area (CSA) [73, 79] and cortical area [15, 80], are relatively consistent findings. […] As a whole, […] studies suggest that systemic markers of bone formation in T1D are generally indicative of a condition in which bone formation is reduced. […] Taken together, it would appear that T1D is characterized best as a state of inappropriately lowered bone turnover which exists in conjunction with relative osteoblast dysfunction  and, hence, low bone formation […] serum AGE concentrations are clearly elevated in T1D during childhood , even during preschool and prepubertal years […] skin AGEs […] are increased in children with both T1D and T2D, to the extent that “approximately 4–6 years of diabetes exposure in some children may be sufficient to increase skin AGEs to levels that would naturally accumulate only after ~25 years of chronological aging””.
“diabetic bone has a greater propensity for fracture than is predicted by BMD […] A role for the skeletal accumulation of advanced glycation end products […], chronic hyperglycemia , oxidative stress , and microarchitectural bone defects  have all been proposed, and it is expected that the pathological mechanisms leading to bone fragility in T1D are multifactorial […] Beyond fragility fractures, other skeletal complications also occur disproportionately in persons with T1D, including fracture-healing complications (nonunion, malunion) , Charcot osteoarthropathy , osteomyelitis, and diabetic foot syndrome.”
“In orthopaedics, patients with diabetes have a number of associated disorders, and these present a challenge as many have an increased hospital stay, higher risk of infection, and higher risk of complications after orthopaedic treatment. The orthopaedic-related problems in diabetes are varied, and the true causal links between diabetes and the disorders are largely unknown. […] The incidence of trigger finger [/stenosing tenosynovitis] is 7–20 % of patients with diabetes comparing to only about 1–2 % in nondiabetic patients […] The prevalence of [carpal tunnel syndrome, CTS] in patients with diabetes has been estimated at 11–30 % [130, 133, 153, 156], and is dependent on the duration of diabetes. […] Type I DM patients have a high prevalence of CTS with increasing duration of disease, up to 85 % after 54 years of DM. However the prevalence does not seem to be associated with glycemic control”
“Diabetes increases the severity and risk of periodontitis, the most common lytic disease of bone and a frequent complication of diabetes […] The risk of periodontitis is increased approximately 2–4 times in diabetic versus nondiabetic subjects [4, 47]. In one study, periodontitis was found in 60 % of T1DM patients compared to 15 % without diabetes . Patients with diabetes are at higher risk of severe periodontitis compared with nondiabetic subjects […] There is a direct link between persistent hyperglycemia, an exaggerated inflammatory response to periodontal pathogens and periodontal bone loss”.
“Because diabetic bone disease in type 1 diabetes represents a deficit in osteoblast function and bone formation, antiresorptive therapies for osteoporosis (e.g., bisphosphonates, denosumab) may be ineffective in this form of secondary osteoporosis […] Calcium and vitamin D supplementation […] is considered standard-of-care for osteoporosis treatment . Nonetheless, 1 year of calcitriol supplementation in young adults with recent-onset T1D did not significantly change circulating markers of bone turnover […] very little information from comparative effectiveness studies is available on the treatment of osteoporosis in T1D.”
Type 2 does not increase risk nearly as much as does type 1:
“In 2007 Vestergaard published a meta-analysis of hip fracture results that included eight studies and reported an age-adjusted summary relative risk for hip fracture of 1.38 (1.25–1.53), comparing those with and without T2D . This increase in fracture risk with T2D occurred in spite of higher bone density in those with T2D. […] Most [15–21], but not all [22, 23], subsequent studies have reported increased rates of hip fracture with T2D in age-adjusted models. […] Evidence that more frequent falls do not fully account for increased fracture risk with T2D […], combined with evidence from rodent models , has led to the conclusion that diabetic bone is more fragile for a given BMD. Understanding the aspects of bone that are affected by diabetes and that result in fragile bone has been an important focus of research on diabetes and skeletal health.”
“The effect of glycemic control on fracture risk, BMD, and falls remains poorly understood and controversial.”
“Diabetic patients with multiple complications appear to be at higher risk of fracture, but results are mixed for the association between specific complications and fracture.”
“Our current understanding of the pathogenesis of skeletal fragility in [type 2] diabetes suggests a working model […], whereby poor glucose control in patients with T2DM leads to increases in AGEs that have negative effects on osteoblasts, which in turn causes a reduction in bone formation. This defect in bone formation subsequently results in low bone turnover in T2DM patients, which prolongs the lifespan of type I collagen in bone, thereby leaving it particularly vulnerable to damage from increased AGEs. Ultimately, this creates a “vicious cycle” that may contribute to reduced bone quality and increased fracture risk in patients with T2DM.”
As for an overall assessment of the book, I gave the book five stars on goodreads, because it’s basically to a significant extent written the way I’d like Springer publications like this one to be written. The language in one chapter (out of 11) was slightly sub-optimal, but aside from that chapter every single chapter was in my opinion well written, some of them very well written. Frequent discussions of the results of meta-analyses were included in the book. The authors seemed in general to be aware of potential problems with specific interpretations and to me seemed cautious about drawing strong conclusions from the data they had at hand; in terms of the analytical level of the coverage the publication for example included comments about problems with confounding by indication in cross section analyses. There were a couple of places in one of the later chapters where it was slightly difficult for me to figure out ‘what was going on’, but the coverage included in the next chapter of the book clarified these issues; I was not willing to subtract a star because of that.