Recently, it has become a craze to demonize hydrogenated vegetable oils, also known as trans fats.
Trans fats are found in most pre-packaged foods, especially anything that contains oils. They are also the main constituent (shortening) of cake frosting (after sugar). And of course, there is margarine, which has become a popular beating stick (no pun intended) of the group of people who seek to vindicate butter and saturated fats (who feel – likely rightfully – that these latter items have been unduly vilified).
The F.D.A. decreed that trans fats should “no longer be ‘generally recognized as safe.’” Why is this so? As explained in a New York Times article:
Partially hydrogenated oils are cheaper than saturated animal fats like butter, and for years were thought to be healthier. They are formed when liquid oil is treated with hydrogen gas and made solid. They became popular in fried and baked goods and in margarine. Crisco, originally marketed in the beginning of the 20th century, was the archetype, although it now contains no trans fat.
But over the years, scientific evidence has shown they are dangerous because they raise the levels of so-called bad cholesterol and can lower the levels of good cholesterol.
Sounds like some awful stuff, right? Their solution:
Banning them completely could prevent 20,000 heart attacks and 7,000 deaths from heart disease each year, the F.D.A. said.
“This is the final slam dunk on the trans fat issue,” said Barry Popkin, a nutrition epidemiologist at the University of North Carolina, Chapel Hill.
So case closed, right?
Well, if you’ve been following along with this series, you’d know I’m going to say not so fast.
How do we know that trans fats are dangerous? As per usual, most of the evidence for the harm posed by trans fats comes from correlations seen in observational studies. As Wikipedia put it:
The major evidence for the effect of trans fat on CHD comes from the Nurses’ Health Study — a cohort study that has been following 120,000 female nurses since its inception in 1976. In this study, Hu and colleagues analyzed data from 900 coronary events from the study’s population during 14 years of followup. He determined that a nurse’s CHD risk roughly doubled (relative risk of 1.94, CI: 1.43 to 2.61) for each 2% increase in trans fat calories consumed (instead of carbohydrate calories). By contrast, it takes more than a 15% increase in saturated fat calories (instead of carbohydrate calories) to produce a similar increase in risk. “The replacement of saturated fat or trans unsaturated fat by cis (unhydrogenated) unsaturated fats was associated with larger reductions in risk than an isocaloric replacement by carbohydrates.” Hu also reports on the benefits of reducing trans fat consumption. Replacing 2% of food energy from trans fat with non-trans unsaturated fats more than halves the risk of CHD (53%). By comparison, replacing a larger 5% of food energy from saturated fat with non-trans unsaturated fats reduces the risk of CHD by 43%.
Another study considered deaths due to CHD, with consumption of trans fats being linked to an increase in mortality, and consumption of polyunsaturated fats being linked to a decrease in mortality.
Medical science, especially that part that gives rise to health prescriptions, unfortunately suffers from an over-reliance on observational studies. These studies only give you correlations. They are incapable of establishing the causal relationship between the phenomena studied. See, again, the words of Gary Taubes:
The shortcomings of observational studies are obvious and should not be controversial. These studies, regardless of their size or number, only indicate associations—providing hypothesis generating data—not causal relations. These hypotheses then have to be rigorously tested. This is the core of the scientific process. Without rigorous experimental tests, we know nothing meaningful about the cause of the disease states we’re studying or about the therapies that might work to ameliorate them. All we have are speculations.
Even more basic, the concern about the effects that trans fats have on cholesterol levels, may be misplaced. The relationship between cholesterol and illness (again, itself gleaned from correlational studies) is hardly as clear cut as it seems. This isn’t even mentioning the fact that statins, drugs used to lower high cholesterol levels, appear to be completely ineffective in reducing mortality in “healthy” subjects. (As well, they may have limited effectiveness for those who do have heart disease).
OK, at this point, you might be thinking that all I have done so far is call into question the evidence on which the assumed dangers of trans fats rests. It’s one thing to point out that the case is not quite as solid as we’d like. That still doesn’t demonstrate that the claim that trans fats are dangerous is wrong. Indeed, you’d be correct on this point. However, now allow me to do you one better:
These graphs show the mortality rates from cardiovascular disease (CVD) in the U.S. over time. As we can see, the present incidence of CVD mortality is considerably lower than it was in the middle of the 20th century.
The total trans fat consumption, captured by the use of things margarine and shortening, doesn’t quite appear to follow CVD mortality. I’ve put in a separate margarine graph to show that it may appear to follow CVD mortality if looked at in isolation. But when shortening (which is largely trans fat) and oils (which are often hydrogenated) are considered, the pattern becomes highly questionable.
I did find one paper that tried to estimate the actual trans fat consumption over time: The estimates show great variability, including a marked disparity in the early 1990s – which is related to a shift in the measuring system used. The various methods used are described in the paper. Each has only limited accuracy in assessing population-wide average consumption for reasons described in the paper. As well, unfortunately, this doesn’t go far back enough to see if trans fat consumption tracks the mid-century peak in CVD mortality.
In short, despite the professed dangers of trans fats, one of the most basic signs of this danger is missing. If trans fats were primarily behind the incidence of heart disease, then we’d expect rates of CVD incidents to track (likely in a time-lagged fashion) the level of trans fat consumption. However, it’s not at all clear that we see this. However, our understanding of the true level of trans fat consumption is limited by the inherently poor reliability of the methods used to measure it.
At this point, I should point out the work of Fred Kummerow, who has studied the role of trans fat consumption in heart disease and claims that there is a causal link. However, most of Kummerow’s evidence comes from comparison of diseased patients with “healthy” patients (in a surgical setting), autopsies, animal studies, and limited lab cell/tissue analysis. In short, he has little that truly demonstrates a causal link between dietary trans fat consumption and disease. Blood and tissue analysis, of both living and dead human patients, while interesting, is limited in its ability to shed insight into causation. This is because detecting the presence of a substance in the blood or tissues doesn’t necessarily mean it got there through ingestion. That logic is how we got into the trap with cholesterol’s purported role with heart disease. The human body can manufacture a variety of substances. The extent that it does so is heavily under genetic influence. The presence of the chemicals seen in diseased patients could be symptom, not a cause, of the underlying disease.
So if dietary trans fat can’t explain heart disease, what does? The short answer is we don’t know. Contrary to what health experts might lead you to believe, fundamentally, we have no idea what causes heart disease. There are all sorts of hypotheses, but, as we see, all face significant trouble when subjected to scrutiny. Indeed, see here and here for some additional hypotheses and scrutiny of some popular ones.
The former source touches on a very key point: the failure of randomized controlled trials to affect the incidence of heart disease. We’ve already seen the failure of the Look AHEAD trial. Indeed, a slew of clinical trials testing various prescriptions of have netted negative results:
The MR-FIT trial in the USA was the most determined effort to prove the case. This was a massive study in which over 350,000 men at high risk of heart disease were recruited. In one set of participants, cholesterol consumption was cut by 42 percent, saturated fat consumption by 28 percent and total calories by 21 percent. This should have made a noticeable dent in heart disease rates.
But nothing happened. The originators of the MR-FIT trials refer to the results as “disappointing,” and say in their conclusions: “The overall results do not show a beneficial effect on Coronary Heart Disease or total mortality from this multifactor intervention.”
It is not as if this was one negative to set against a whole series of positive trials. In 1998, the Danish doctor Uffe Ravnskov looked at a broader selection of trials: “The crucial test is the controlled, randomised trial. Eight such trials using diet as the only treatment has been performed but neither the number of fatal or non-fatal heart attacks was reduced.” As Ravnskov makes clear, no trial has ever demonstrated benefits from reducing dietary saturated fat. At this point most people might think it was time to pull the plug.
That is even going beyond the issue of the generalizability of results from the Spanish population to non-Spaniards.
This brings us to one thing we do know about heart disease: it is (like all things) heavily influenced by genetics. Indeed, a recent GCTA (Genome-wide Complex Trait Analysis) study that looked at 38,167 individuals from Iceland found that the broad-sense heritability of coronary artery disease is at least 55% (at least in the Icelandic population, that is, of course). That is, heredity is the single largest known factor involved your chances of developing heart disease. (As an aside, the study authors claim that their data show that the shared environment is important source of the variance in these traits, based on the differing heritability measures of more distant relatives. However, if you look closely at their confidence intervals, you’ll see that this conclusion is not warranted.)
In fact, a quick return to the age-adjusted incidence of CVD mortality in the U.S. over time shows something interesting:
Assuming that these numbers are trustworthy, (especially for the early 20th century when reliability of cause of death declarations come into question), it seems the total CVD mortality has in fact remained fairly flat throughout for much of the 20th century, only to decline a few decades ago. If we consider “diseases of the heart” alone, we see an interesting rise and fall. What’s up with that?
Allow me to present something else:
These are the top causes of death in the United States since 1900 (from Slate). As we see, prior to the 1930s, the biggest killers were infectious diseases. The increase in modern human lifespan is heavily due to three simple things: improved sanitation, vaccines, and antibiotics. Notice how the incidence of heart disease significantly rises as deaths from infectious diseases fall. This means that the mid-century rise in deaths from heart disease could simply be a result of the fact that more people were living long enough to die from heart disease. Even the age-adjusted rates don’t full account for this factor, because people who lived longer could have systematically more vulnerable to heart disease (heart disease is heritable). The increasing rates of deaths from cancer likely have a similar explanation, and illustrates this process.
It is possible that there was never much we could do about heart disease, aside from getting at better at keeping people alive who’ve already had heart attacks. Unfortunately, it is possible that some people’s bodies are designed in such a way that they develop arterial blockages. The superficial correlations with “lifestyle factors” gleamed from observational studies could be a due to individuals with such a genetic propensity also happening to live certain ways. These factors may have nothing to do with one another causally. Even depression (and by extension, stress), which has been linked to heart disease, may be so linked because of common genetic factors.
With all this talk of genetics, there might be one thing in the environment we might be able to link to heart disease. That thing is smoking (from here):
Smoking rates over time track CVD death rates in the U.S. As well, see this (from Wikipedia):
There appears to be a strong spatial and temporal association between smoking and heart disease. However, that association appears to be primarily due to rates of these things in the Slavic world and the Middle East.
Of course, it’s worth noting that I’ve previously shown that CVD mortality rates can be linked to climate, at least in Europe.
Over the years we’ve been fed all sorts of health advice, different people telling us – preaching to us – what we should do to stay healthy and live as long as possible. It’s becoming increasingly clear that much of it – if not all of it – is bullshit. Indeed, as a result, the health beliefs that most people have today are basically religion. Everyone has their own ideas on how to stay healthy, and little of it is based on any good science (as commenter Sisyphean pointed out). It’s not like we can completely blame folks for this; the advice they’ve been receiving has been confusing and often contradictory, as exemplified by the love-hate-love relationship with butter and saturated fats, and now with trans fats. However, at this point, while I’d agree that, if you want to live as long as you can, it’s good advice to not eat rat poison or go for a stroll into the middle of a busy highway, I can’t vouch for the rest of it. The best advice might just be eat, drink, and be merry – at best, doing what seems to work for you. Least of all, don’t buy what the health experts are pushing until they show you the randomized controlled trials that back them up.
Once again, I’m using Tangerine Dream’s “Cloudburst Flight”, which to me has become a general theme for this series:
The finding of this study seems straightforward – indeed, I was able to say it in a sentence. However, the conclusions we are able to draw from these finding are anything but.
The study looked at sample of 20% of the individuals in the 2006 Canadian census. Unlike previous studies, it has the strength of being able to examine a large, truly random sample.
Previous studies into the matter have claimed to find no significant differences between the children of gay and parents vs. those of straight parents. However, those studies apparently suffered from serious methodological weaknesses. The author of the current study explains:
Generally speaking the literature is characterized by several different types of data bias and small samples that lack any power … Although a proper probability sample is a necessary condition for making any claim about an unknown population, within the same-sex parenting literature researchers have studied only those community members who are convenient to study … Of the fifty-three studies reviewed here, only seven used probability samples. All of the other studies arrived at their samples through means that introduced various levels of bias. Some studies recruited individuals from sperm bank data sources or other types of reproduction technology providers. Other studies used Internet surveys where the respondents were recruited by various methods: parent forums, gay and lesbian web-sites, and online advocacy organizations. Many studies recruited through LGBT events, bookstore and newspaper advertisements, word of mouth, networking, and youth groups. A common method of recruitment was to use a combination of the above methods to form a sample base, and then recruit friends of the base. Still other studies failed to even mention how their samples were arrived at. Each different procedure has a different and unknown source of bias.
Aside from the problem of non-random samples, most of the existing parenting studies contain tiny sample sizes. Of the fifty-three studies examined here, only two had sample sizes larger than 500. Much more common were sample sizes between 30-60. The problem with such small sample sizes is that the data cannot generate any power for statistical testing, and low power means there is a small chance of rejecting a false null hypothesis. Hence, the very small sample sizes found in many of these studies creates a bias towards accepting a null hypothesis of ‘‘no effect’’ in child outcomes between same-and opposite-sex households.
OK, so this study “corrects” for these shortcomings by relying on a large, random sample. Still, the rarity of same-sex couples meant that there were few in the sample. Indeed, there are apparently only 423 gay and 969 lesbian families in the entire nation of Canada. Nonetheless, its sample is larger than most such studies.
The study found that children with lesbian “parents” were only 60% as likely to graduate from high school (sons 76%, daughters 45%), while children with gay male “parents” were only 69% as likely (daughters 15%, sons 161%). The disparity remained significant even when certain controls were introduced (such as parental education).
So case closed, right? We can now safely conclude that two opposite-sex parents are important for children’s development, yes? Of course not, not even close.
First of all, despite this study’s improvements over its antecedents, it suffers from a fundamental weakness. It is in essence a classic family study, one that looked at associations within families and then emboldens others to draw conclusions (as illustrated by the title “A Married Mom and Dad Really Do Matter: New Evidence from Canada”) about “family constellation variables.” Yup, there’s your problem: classic confusion of correlation with causation.
You can’t make causal determinations from standard family studies. Even with heterosexual parents, finding associations between parents and their biological children tells you nothing about whether anything about the parents’ rearing of the children had anything to do with what you find, not for the least reason being heredity. Just as finding that substance abusing parents have children that go on to do the same, heredity confounds you at every turn. This is because, as readers should know by now, all human behavioral traits are heritable.
Hence, a key problem is that comparing gay/lesbian parents to straight parents – even when you put in your “controls” – is essentially comparing apples to oranges. I don’t have to tell you that gays and lesbians – particularly the ones that try to live in married/civil union couples are systematically different from straight individuals. A passage from the study illustrates this point:
in the context of gay parenting … avenues through which these households are formed are many and complicated. As noted by Stacey and Biblarz … these families often have experienced a prior divorce, previous heterosexual marriages, intentional pregnancies, co-parenting, donor insemination, adoption, and surragacy.
The biological children of gay and lesbians can hardly considered to be genetically comparable to those of straight individuals, even discounting the sexual orientation itself.
That’s if they’re even their biological children. Here’s another finding of the study:
There are a higher number of visible minority children for gay households (28 % compared to 13 % for common law couples), and a higher number of disabled children (13 % compared to 6 % for opposite sex married parents). This may imply a high number of adopted children in gay households, but interestingly there are no cases of inter-racial same-sex families within the 20 % sample.
I don’t even need to touch the higher fraction of “visible minority” and disabled children in the same-sex parent sample. That’s just icing on the cake at this point.
Having same-sex parents, in and of itself, likely has no impact on children’s development. It would be really strange that if it did, since parenting in general (across the broad range that constitutes “normal” parenting) has no impact on how children turn out. That was the revelation in my first blog post, and it’s a fact that remains underappreciated to this day. This study of gay parents doesn’t change our understanding.
The failure to recognize the broad null effect of nurture (“The Nurture Assumption”) is pervasive even in the HBD community, the people who should of all know better.
Indeed, a recent blog post reciting some quips from Robert Plomin (a foremost behavioral geneticist) rekindled a discredited idea to explain the consistent non-effect of the shared environment term (the fact that there is no correlation between children raised together once you take genes into account) (emphasis in original):
In short, parents think they treat their kids the same… but the kids think the parents treat them differently, and outside observations would support this claim. If anything, the outside observer sees slightly more unequal treatment than the kids themselves do. This indicates that the vast majority of parenting effects would show up in the non-shared environment.
That said, modern study designs have indeed allowed us to decompose the known sources of non-shared environmental influences. Here is the relevant data from the paper:
The proportion of total variance accounted for in outcomes such as adjustment, personality and cognition was 0.01 for family constellation, 0.02 for differential parental behaviour, 0.02 for differential sibling interaction and 0.05 for differential peer or teacher interaction. Moreover, these effects are largely independent and they add up to account for 13% of the total variance. If non-shared environment accounts for ~40% of the variance in these domains, we could say the cup is already more than one quarter full.
Parent-child interaction was the Occam’s Butterknife way for developmental psychologists to rescue parenting after studies failed to turn up evidence for its effects. Judith Rich Harris and Steven Pinker both long since dispatched this idea, as I explained:
It requires that there are no across the board differences from one set of parents to another. To see why, imagine parents did have some effect. Even if there were differences in the exact treatment each child received, there are going to be systematic similarities with the way each set of parents treat all their children. If such an effect existed, it would turn up in the shared environment, since kids growing up together would be impacted by these across the board similarities. But the shared environment influence is in fact negligible.
It requires perfect crossover interaction. Let’s say you assume that parental effects – whatever their across the board similarity for a given set of parents – had totally idiosyncratic effects on children. Then in order to explain the null effect of the shared environment, the sum of these effects on children’s traits had to be exactly zero. Any number of children exhibiting one sort of effect would have to be balanced by an equal number of children exhibiting the exact opposite effect. That is a rather large stretch.
Occam’s razor and….
The notion that parental influences exist, but the factors that vary among parents in how they treat their children across the board must either have no consistent effect or must perfectly cancel across children such that it gives the appearance in the data that it has no effect at all requires us to entertain many more causal entities that the simpler idea that they just have no effect at all.
Of course, it gets worse for parenting, thanks to studies into the effects of birth order:
In any case, there is additional trouble for the idea of significant parental impact: it has to contend with the absence of birth order effects. Thorough analysis has failed to find any systematic differences in children due to birth order. Birth order is one case of systematic, non-genetic differences in the home environment of children. It’s hard to reconcile the existence of parental effects with the failure to find anything when looking at a reliable systematic difference in the parental environment.
Parenting is simply less important than most people think. But as with the issue with health and obesity, even individuals who understand the pervasiveness of nature and the apparent stochasticity of what we call “environment” like to believe there is some way they can exert control (see locus of control, courtesy Richard Harper).
To be fair to parenting, over at my comment at the blog I left the current unknowns about parenting:
Now, to be completely fair to parenting, some commenters on the matter, such as Steve Sailer, posit that parental effects are largely unimportant when looking at higher-SES, Western parents. The difference from one set of middle-class Western parents to another set may not matter much, but the difference might matter if we compared White Western parents to say poorer Latin American parents. On that we have to say the data don’t yet rule such a difference out. My own suspicion is that even in those cases, we will find that the difference – if any – stems from environmental impacts that only act in a negative way; e.g., we know that childhood malnourishment can stunt IQ, but nutrition beyond what’s adequate won’t raise IQ. In the same way, children from poorer families might miss out on critical developmental inputs. As well, they may miss out on key opportunities to achieve, which itself is perhaps more a function of the outside the home environment in which these poor children happen to dwell.
Only further research with non-Western, non-White samples can hope to answer this question. In either case, for now, the message is clear, parenting matters a lot less than society merits it, be those parents married, unmarried, straight, gay or lesbian.
As for the song for this post, while this song doesn’t have much to do with the subject, for some reason, it seems to me to fit:
Roosh V, a pick-up artist, and one of the foremost voices in the “manosphere” – especially its reactionary wing, has been getting some attention lately. This past evening, ABC’s 20/20 featured an exposé into the “manosphere”, the world of men who make an effort to improve their romantic/sexual success with women and discuss their frustrations with such.
The “manosphere”/”Game” world overlaps to a degree with the HBD-sphere. Many of its adherents and key voices are individuals with reactionary/paleoconservative ideology (one which I – as a fairly unique Left-leaning HBD’er – do not share), as is the case with the overarching community that includes HBD. And like the HBD-sphere, it has its own conventional wisdom that may not necessarily adhere to facts. RooshV recently posted a list of “Community beliefs”, encapsulating some of this community wisdom in one place. In this post I will do a quick analysis of these beliefs to see how well they hold up to the facts.
Here are the stated “Community Beliefs.” Let’s break them down one by one:
1. Men and women are genetically different, both physically and mentally. Sex roles evolved in all animals. Humans are not exempt.
True. Indeed, that men and women are genetically different is in fact tautological: it is this genetic difference (XY vs. XX chromosomes) that defines male vs. female. But, in the sense that this genetic difference entails biological mental differences, this is correct (see my page HBD Fundamentals: On biological sex differences).
2. Women are sluts if they sleep around, but men are not. This fact is due to the biological differences in gender.
True with caveats. As Eliot Spitzer, Anthony Weiner, John Edwards, and Arnold Schwarzenegger could tell you, it’s not like our society gives a pass to philandering men. That said, promiscuous women are looked down upon more than promiscuous men for one simple reason: paternal uncertainty. Unlike women, men have no way (prior to DNA testing, anyway) to guarantee that a child they have putatively fathered is in fact theirs. Human males invest in their children, but any investment in a non-biological child is wasted, evolutionarily. As such, female fidelity became a valued trait, since it increases the chances that any children born to a woman’s mate are in fact biologically his.
3. Men will opt out of monogamy and reproduction if there are no incentives to engage in them.
Muddled. In the absolute sense (all men), it’s clearly nonsense. In the particular sense (some men), it’s unclear. For one, which men? How big a fraction of all men are we talking about? In which societies (“different peoples is different”)? But the most confused bit the claim “no incentives.” What would it mean for men to have “no incentives” to engage in monogamy or reproduction? Are biological drives not incentives? Men are continuing to marry and have children. Indeed, the most monogamous men may be having the most children.
If taken in the weaker sense, that some men will forgo monogamous mating if given the option, this may be partially true. We do have some evidence that effective sex ratios impact male/female mating behavior. Particularly, when there is an excess of single females relative to single men, men become less likely to commit and exhibit greater preference for short-term mating. Females may adjust their behaviors accordingly, as perhaps Latvian women have.
4. Past traditions and rituals that evolved alongside humanity served a net benefit to the family unit.
Muddled. Whose traditions and whose family units are we talking about?
Even if we restrict ourselves to Europe and the Near East, a whole slew of “family units” and accompanying traditions evolved:
As documented by Emmanuel Todd (discussed further by HBD Chick and by Craig Willy), even in fairly recent history, humans have invented all sorts of family arrangements. Each may have been a response to the circumstances each group faced in their various environs, or they may be a reflection of the underlying traits of these peoples, or both. As we can see, what constitutes the “family unit” has varied greatly across various human societies.
5. Testosterone is [one of] the biological cause[s] for masculinity. Environmental changes that reduce the hormone’s concentration in men will cause them to be weaker and more feminine.
True, as corrected. While testosterone is the most well-known and arguably primary androgen, it’s not the only one nor is it the only one which is important. The other androgens, which “are of equal importance in male development,” include:
- Dehydroepiandrosterone (DHEA)
- Androstenedione (Andro)
- Dihydrotestosterone (DHT)
Testosterone, or even the other androgens, aren’t quite the “things” that makes males male. Testosterone is found in women, for example. Further, while testosterone levels do indeed fluctuate in men in response to the environment, and while testosterone supplementation does alter male behavior, male-typical behavior cannot be simply reduced to the presence of testosterone. Giving a woman testosterone or other androgens will affect her behavior, but it won’t be enough to turn her into a man (see belief #1).
6. A woman’s [mate] value is mainly determined by her fertility and beauty. A man’s [mate] value is mainly determined by his resources, intellect, and character.
True (as corrected) with caveats. First, even when corrected, it’s an oversimplification. “Mainly” is too strong of a word. Health is an important quality in both sexes. Intelligence is valuable for women as well men, as is a woman’s character (particularly her fidelity – see belief #2).
7. Elimination of traditional gender roles and the promotion of unlimited mating choice in women unleashes their promiscuity and other negative behaviors that block family formation.
Sort of. As discussed in the posts by Peter Frost linked under belief #3, unbalanced sex ratios can often lead to later marriage and more preference towards short-term mating. To the extent that this now occurs, we like to think that this is a modern phenomenon. But, as M.G. once discussed, a similar period occurred in America before – incidentally during of a time of great societal inequality and national strife in the turbulent Interwar years.
Further still, despite the loosening of sexual mores, as Frost noted, there are racial constraints on how much it can change. Despite whatever prevailing trends, family formation is going to remain the norm among slower life-history groups, like Europeans. Family formation may be less common among say Blacks, who have traditionally had unstable polygynous pairings.
8. Socialism, feminism, and cultural Marxism cause societies to decline because they destroy the family unit, decrease the fertility rate, and require large entitlements that impoverish the state.
The countries with the most “socialist” policies in place also have the highest fertility rates. Now before any of you criticize the NW Euro fertility rates being driven by non-European immigrants, in all the more fecund NW Euro countries, native fertility rates are 1.7 children/child-bearing woman or higher. Fertility rates are lower – indeed much lower – in the less feminist, less socialist Southern and Eastern European countries.
Even the other aspect of fertility that (rightly) concerns people – eugenic fertility – may be best achieved with “socialist” policies (as I’ve previously explained). These include programs to help working mothers, such as state supported day care and paid maternity leave. (Though of course, even these cannot completely compensate for basic effective cost of living – which, in the developed world, is the main driver of fertility rates.) Many in the right-wing corners of the manosphere wish for a return to the pre-sexual revolution days. That is simply not going to happen. Women in the West aren’t going to completely abandon education and careers – that’s here to stay. The best ways to encourage eugenic fertility is to reduce the conflict between education/work and family for high-IQ women. I will take up this issue again in a future post.
As with the HBD community, the manosphere circulates truths not necessarily known to the mainstream world, but it also propagates a fair amount of rubbish. As I do with HBD and the human sciences in general, I try to seek out the truth of the matter, and set the record straight whenever I can.
Some food for thought:
People who follow me know that I stress the three laws of behavioral genetics, starting with the all-important First Law, all human behavioral traits are heritable.
OK, but that established, most people aren’t necessarily interested in heritability per se; they want to know about changeability. Can the trait in question be changed? Sure, there are non-genetic inputs to physical and behavioral traits, including “environmental” ones (note that I distinguish “non-genetic” from “environmental”). And indeed, human traits can certainly be affected by global and local environmental forces (again, notice that I distinguish the two).
That said, that doesn’t necessarily mean we can shape traits to be what we want them to be, even if we limit our target range. See this series of insightful tweets from Sam S/”misdreavus”, a regular commenter at HBD blogs who frequents Cochran’s & Harpending’s in particular. “misdreavus” is definitely one of the greatest – if not the greatest HBD commenter who doesn’t yet have his own blog (a title I would have given to Jason Malloy before he started blogging over at Human Varieties):
A common error by ppl who are ignorant of quantitative genetics is conflating phenotypic plasticity with sources of environmental *variance*
For example, avg. height among European populations has increased by several cm since the Victorian era. Of course, height is plastic.
That hardly proves that my 5’4″ male friend could have increased his height by several inches if he had only had the *willpower* to do so.
Just about every single phenotype for which there exists variation in the human species is plastic. This is trivial information. (1/2)
Modify the environment enough and you can drastically change just about *everything* – even skin color. Google “argyria” (2/2)
The lesson to take home from this? Yes, Americans were a less obese 60 years ago than they are today. IQ tests have been renormed, as well.
Heritability estimates alone say little about phenotypic plasticity. A trait can have a heritability of 100% can be *very* plastic.
But they do impose strict limits on how much phenotypic change in possible by rearranging environments that are major sources of variation.
As for obesity, we know it has a high heritability. Sure there is an environmental component to it as well, but currently few major (1/2)
sources of variation. Parenting, access to “healthy” foods, peer influence, etc turn out to matter little once you control for (2/2)
The message to take home from all this? Shaming fat people doesn’t work. Shaming their parents doesn’t work. Mocking them doesn’t (1/2)
work. Encouraging them to go on diets doesn’t work. If it *did* work surely there would be a study by now that demonstrates that it (2/2)
And please don’t speak to a nebulous, “ghost in the machine” entity called “willpower” to excuse away the impact of heredity on obesity.
Good points. Expect more on the topic in the future.
My posts on free will:
Another map of the American nations:
This is where the states stand on Obamacare’s expansion of Medicaid. As you can see, it’s far from universally embraced. Now let’s compare that to this map:
And for that matter, this map:
Most of the usual suspects. Most prominent among those who reject the Medicaid expansion are those in the Deep South/Tidewater. By contrast, much of Yankeedom, the Midlands, and the Left Coast have embraced it openly, as expected.
Interestingly, much of Greater Appalachia has embraced the Medicaid expansion as well. This highlights a very important aspect of the healthcare discussion, as with socialist ideals in general: the importance of homogeneity.
A few recent articles have correctly noted that the Deep South’s opposition to Obamacare stems from simmering racism. More accurately (though not by much), I’d say it stems from clannish peoples not wanting share the spoils of the commonweal with those outside the “tribe”:
Before he was disgraced into resigning his presidency over the Watergate burglary scandal, Richard Nixon had successfully engineered an even more odious plot known as his Southern Strategy. The trick was devilishly simple: Appeal to the persistent racist inclination of Southern whites by abandoning the Republican Party’s historic association with civil rights and demonizing the black victims of the South’s history of segregation.
That same divisive strategy is at work in the Republican rejection of the Affordable Care Act. GOP governors are largely in control of the 26 states, including all but Arkansas in the South, that have refused to implement the act’s provision for an expansion of Medicaid to cover the millions of American working poor who earn too much to qualify for the program now. A New York Times analysis of census data concludes that as a result of the Republican governors’ resistance, “A sweeping national effort to extend health coverage to millions of Americans will leave out two-thirds of the poor blacks and single mothers and more than half of the low-wage workers who do not have insurance, the very kinds of people that the program was intended to help. …”
Also this piece from Paul Krugman – The War On The Poor Is A War On You-Know-Who:
What the report makes clear is that the current Republican obsession with attacking programs that benefit Americans in need, ranging from food stamps to Obamacare, isn’t about some philosophical commitment to small government, still less worries about incentive effects and implicit marginal tax rates. It’s about anxiety over a changing America — the multiracial, multicultural society we’re becoming — and anger that Democrats are taking Their Money and giving it to Those People. In other words, it’s still race after all these years.
Of course, in Krugman’s case, he’s unsurprisingly blind to the deleterious effects the demographic change he extols will have, but he is spot on about conservative White opposition to social welfare programs.
As HBD Chick put it (on her post liberal (white) guilt as altruistic punishment):
i said: “…lady a is ok with contributing to the commonweal, but lady b (and her man, bubba) are not (even though, at the same time, they might be VERY ok with TAKING from the common pot!).”
for the record, i think this is one of the fundamental problems with “lady b”/clannish societies, and that is that, while they generally do not want to contribute to the common pool (to varying degrees), they are VERY happy to TAKE from the common pool as much as possible to the benefit of themselves and their extended family members.
The clannish elements of British American society, the descendants of the Cavaliers and the Ulster Scots, are indifferent to contributing a common pot, and they are certainly uncomfortable about anything they contribute to the common pot going to non-kin, especially people who aren’t even of the same race.
The denizens of the Deep South/Tidewater live in states with large Black minorities. Deep Southern Whites correctly see their funds being redistributed from themselves to non-Whites, particularly Blacks. Hence, they oppose it.
Which brings me to Greater Appalachia. The Appalachian states that accept the Medicaid expansion are largely homogeneously Scotch-Irish. Further still, they would certainly be on the receiving end of tax revenue from Obamacare. Hence, they are more receptive to the Medicaid expansion, perhaps correctly reasoning that they stand to gain from its implementation (at least within-state).
Interestingly, the Far West is a bit topsy-turvy from what we’d expect. The northern more homogenous Far Western states oppose the Medicaid expansion, while the ones that contain “El Norte” embrace it. In the former case, I suspect that the rugged individualism of the Far Westerners overrides their recognition that they’d (largely) stand to gain from Obamacare. However, Montana did set up its own single-payer universal health care system ahead of Obamacare. This may exemplify the sentiment in somewhat clannish peoples: commonweal, but only for those in the tribe.
On that note, to be fair to the progenitors of the nations of the Old North, both the descendants of the Puritans and the descendants of the Quakers are likely minorities in their respective nations – the latter certainly so (since they were since the beginning). I suspect that the purer Yankee and Quaker elements would, if left to their own devices, set up their own – internal – universal health care system, much as Vermont has. They favor the commonweal – within group. Both the Puritans and the Quakers were “in-betweeners”, and may not have favored complete universalism.
As for here in Yankee/New French Maine, we’re unfortunately stuck with the brilliance of our esteemed French-Canadian Governor Paul LePage. He vehemently opposes the Medicaid expansion here. Perhaps this may have something to do with his New French origin. The French Canadians seem to have either picked up some clannish elements here in America or perhaps brought these traits with them, owing to their regional origin in France (see also Maps of the American Nations).
In either case, it is clear that the American nations persists, and perhaps, as John Derbyshire recently put it, “The War Between the States goes on,” where one battlefield (out of many) is healthcare.
See also: The Audacious Epigone: Endovelicus