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Height, Longetivity, and Aging
Humans reach their maximum height at around their mid-20s. It is commonly thought that taller people have better life outcomes, and are in general healthier. Though this misconception stems from misconceptions about the human body. In all reality, shorter people live longer than taller people. (Manlets of the world should be rejoicing; in case anyone is wondering I am 5’10”.) This flies in the face about what people think, and may be counter-intuitive to some but the logic—and data—is sound. I will touch on mortality differences between tall and short people and at the end talk a bit about shrinking with age (and studies that show there is no—or little—decrease in height due to self-reports, the study is flawed).
One reason why the misconception of taller people living longer, healthier lives than shorter people is the correlation between height and IQ—people assume that they are traits that are ‘similar’ in that they become ‘stable’ at adulthood—but one way to explain that relationship is that IQ is correlated with height because higher SES people can afford better food and thus be better nourished. Either way, it is a myth that taller people have lower rates of all-cause mortality.
The truth of the matter is this: smaller bodies live longer lives, and this is seen in the animal kingdom and humans—larger body size independently reduces mortality (Samaras and Elrick, 2002). They discuss numerous lines of evidence—from human to animal studies—and show that smaller bodies have a lower chance of all-cause mortality, the reasoning being (one of the reasons, anyway) that larger bodies have more cells which then would, in turn, be more subject to carcinogens and, obviously, would have higher rates of cancer which would then, too, lower mortality rates. Samaras (2012) also has another paper where the implications are reviewed for this, and other causes are proposed for this observation. Causes are reduced cell damage, lower DNA damage, and lower cancer incidence; with other, hormonal differences, between tall and short people that explain more of the variation between them.
One study found a positive linear correlation between height and cancer mortality. Lee et al (2009) write:
A positive linear association was observed between height and cancer mortality. For each standard deviation greater height, the risk of cancer was increased by 5% (2–8%) and 9% (5–14%) in men and women, respectively.
One study suggests that “variations in adult height (and, by implication, the genetic and other determinants of height) have pleiotropic effects on several major adult-onset diseases” (The Emerging Risk Factors Collaboration, 2012). Taller people also are at greater risk for heart attack (Tamaras, 2013). The cause for this, Tamaras writes, is “including reduced telomere shortening, lower atrial fibrillation, higher heart pumping efficiency, lower DNA damage, lower risk of blood clots, lower left ventricular hypertrophy and superior blood parameters.” Height, though, may be inversely associated with long-term incidence of fatal stroke (Goldbourt and Tanne, 2002). Schmidt et al (2014) conclude: “In conclusion, short stature was a risk factor for ischemic heart disease and premature death, but a protective factor for atrial fibrillation. Stature was not substantially associated with stroke or venous thromboembolism.” Cancer incidence also increases with height (Green et al, 2011). Samaras, Elrick, and Storms (2003) suggest that men live longer than women live longer than men due to the height difference between them, being about 8 percent taller than women but having a 7.9 percent lower life expectancy at birth.
Height at mid-life, too, is a predictor of mortality with shorter people living longer lives (He et al, 2014). There are numerous lines of evidence that shorter people—and people of shorter ethnies, too—live longer lives if they are vertically challenged. One study on patients undergoing maintenance hemodialysis stated that “height was directly associated with all-cause mortality and with mortality due to cardiovascular events, cancer, and infection” (Daugirdas, 2015; Shapiro et al, 2015). Even childhood height is associated with prostate cancer acquisition (Aarestrup et al, 2015). Even men who are both tall and have more adipose tissue (body fat) are more likely to die younger and that greater height was associated with a higher risk of acquiring prostate cancer (Perez-Cornago et al, 2017). Short height is a risk factor for death for hemodyalisis patients (Takenaka et al, 2010). Though there are conflicting papers regarding short height and CHD, many reviews show that shorter people have better health outcomes than taller people.
Sohn (2016) writes:
An additional inch increase in height is related to a hazard ratio of death from all causes that is 2.2% higher for men and 2.5% higher for women. The findings are robust to changing survival distributions, and further analyses indicate that the figures are lower bounds. This relationship is mainly driven by the positive relationship between height and development of cancer. An additional inch increase in height is related to a hazard ratio of death from malignant neoplasms that is 7.1% higher for men and 5.7% higher for women.
It has been widely observed that tall individuals live longer or die later than short ones even when age and other socioeconomic conditions are controlled for. Some researchers challenged this position, but their evidence was largely based on selective samples.
Four additional inches of height in post-menopausal women coincided with an increase in all types of cancer risk by 13 percent (Kabat et al, 2013), while taller people also have less efficient lungs (Leon et al, 1995; Smith et al, 2000). Samaras and Storms (1992) write “Men of height 175.3 cm or less lived an average of 4.95 years longer than those of height over 175.3 cm, while men of height 170.2 cm or less lived 7.46 years longer than those of at least 182.9 cm.”
Lastly, regarding height and mortality, Turchin et al (2012) write “We show that frequencies of alleles associated with increased height, both at known loci and genome wide, are systematically elevated in Northern Europeans compared with Southern Europeans.” This makes sense, because Southern European populations live longer (and have fewer maladies) than Northern European populations:
Compared with northern Europeans, shorter southern Europeans had substantially lower death rates from CHD and all causes.2 Greeks and Italians in Australia live about 4 years longer than the taller host population … (Samaras and Elrick, 2002)
So we have some data that doesn’t follow the trend of taller people living shorter lives due to maladies they acquire due to their height, but most of the data points in the direction that taller people live shorter lives, higher rates of cancer, lower heart pumping efficiency (the heart needs to pump more blood through a bigger body) etc. It makes logical sense that a shorter body would have fewer maladies, and would have higher heart pumping efficiency, lower atrial fibrillation, lower DNA damage, lower risk of blood clotting (duh) when compared to taller people. So it seems that, if you’re a normal American man, then if you want to live a good, long life then you’d want to be shorther, rather than taller.
Lastly, do we truly shrink as we age? Steve Hsu has an article on this matter, citing Birrell et al (2005) which is a longitudinal study in Newcastle, England which began in 1947. The children were measured when full height was expected to be acheived, which is about 22 years of age. They were then followed up at age 50. Birrell et al (2005) write:
Height loss was reported by 57 study members (15%, median height loss: 2.5 cm), with nine reporting height loss of >3.5 cm. However, of the 24 subjects reporting height loss for whom true height loss from age 22 could be calculated, assuming equivalence of heights within 0.5 cm, 7 had gained height, 9 were unchanged and only 8 had lost height. There was a poor correlation between self-reported and true height loss (r=0.28) (Fig. 1).
In this population, self-reported height was off the mark, and it seems like Hsu takes this conclusion further than he should, writing “Apparently people don’t shrink quite as much with age as they think they do.” No no no. This study is not good. We begin shrinking at around age 30:
Men gradually lose an inch between the ages of 30 to 70, and women can lose about two inches. After the age of 80, it’s possible for both men and women to lose another inch.
The conclusion from Hsu on that study is not warranted. To see this, we can look at Sorkin, Muller, and Andres (1999) who write:
For both sexes, height loss began at about age 30 years and accelerated with increasing age. Cumulative height loss from age 30 to 70 years averaged about 3 cm for men and 5 cm for women; by age 80 years, it increased to 5 cm for men and 8 cm for women. This degree of height loss would account for an “artifactual” increase in body mass index of approximately 0.7 kg/m2 for men and 1.6 kg/m2 for women by age 70 years that increases to 1.4 and 2.6 kg/m2, respectively, by age 80 years.
So, it seems that Hsu’s conclusion is wrong. We do shrink with age for myriad reasons, including discs between the vertebrae and spine decompress and dehydrate, the aging spine becomes more curved due to loss of bone density, and loss of torso muscle could contribute to the differing posture. Either way, these are preventable, but some height decrease will be notable for most people. Either way, Hsu doesn’t know what he’s talking about here.
In conclusion, while there is some conflicting data on whether tall or short people have lower all-cause mortality, the data seems to point to the fact that shorter people live longer due since they have lower atrial fibrillation, higher heart pumping efficiency, low DNA damage, lower risk for blood clots (since the blood doesn’t have to travel too far in shorter people), along with superior blood parameters etc. With the exception of a few diseases, shorter people do have a higher quality of life and higher lung efficiency. We do get shorter as we age—though with the right diet we can ameliroate some of those effects (for instance keeping calcium high). There are many reasons why we shrink due to age, and the study that Hsu cited isn’t good compared to the other data we have in the literature on this phenomenon. All in all, shorter people live longer for myriad reasons and we do shrink as we age, contrary to Steve Hsu’s claims.
Height and IQ Genes
Genes account for about 80 percent of the variation in height and IQ, with both height and IQ correlating at .2. Therefore, genes must contribute largely to population variances in height. However, finding certain genes that contribute largely to these two traits is a problem, largely because both traits are polygenic in nature. Recent research has shown that most—or all–genes are height genes. If this is the case, are most—or all—genes IQ genes?
Height is around 80-90 percent heritable (Peeters et al, 2009). What this means is that the difference between the tallest and shortest 5 percent of the population is 11 inches, with 10 inches being accounted for by genes and 1 inch being accounted for by environment (Heine, 2017: 30). The gene that contributes the most to human height has been found to give 1/6th of an inch (Weedon et al, 2007). However, a recent meta-analysis shows that certain rare alleles give as much as 8/10ths of an inch (Hirschhorn, Deloukas, and Lettre, 2017). Furthermore, thousands of gene variants combined explain about 50 percent of human height (Yang et al, 2010). Yang et al (2010) also found 294,831 SNPs related to people’s height, which is—more or less—12 times the number of genes in our genome (Heine, 2017: 30; the number of genes in our genome is in the range of 19,000-20,000; Ezkurdia et al, 2014). Another meta-analysis found that 697 genetic variants explain about 20 percent of the genetic variation (Wood et al, 2014). Furthermore, according to geneticist David Goldstein, “most genes are height genes” (Goldstein, 2009).
Author of the book DNA is not Destiny and cultural and social psychologist Steven J. Heine writes:
“This means if you wanted to genetically engineer a designer baby who you would like to grow up to be tall, you would have to make almost 300,000 genetic alterations to the genome and you still would only be half way there. When the genetic evidence suggests that almost all genes are related to height, then in a way, we learn close to nothing about the genetic basis of height.” (Heine, 2017: 30)
Hirschhorn, Deloukas, and Lettre, (2017) found 83 rare and low-frequency genes that explain 1.7 percent of the adult heritability of height, along with newly identified and novel variants that explained 2.4 percent, “and all independent variants, known and novel together explained 27.4% of heritability. By comparison, the 697 known height SNPs explain 23.3% of height heritability in the same dataset (vs. 4.1% by the new height variants identified in this ExomeChip study)” (pg 7). So 27.4 percent of the variance is explained by known common variants and these new variants discovered.
Americans who drink more milk are, on average, half an inch taller than Americans who don’t recall drinking as much milk, even after controlling for race, income, and education (Wiley, 2005). This shows the importance milk has on skeletal muscle growth. This increase has even been noticed in Japan, where they increased their milk intake using school lunch programs (Takahasi, 1984), which increased their height by 4 inches (Funatogawa et al, 2009).
We also grow more in the spring and summer than in the fall and winter. This is due to ultraviolet radiation from the sun’s rays that synthesize some of the vitamin D we drink that is in the cow’s milk. Clearly, environmental factors (UV rays, milk consumption, overall nutrition, etc) all have a part to play in human height variation (Heine, 2017: 30). However, if all genes may be height genes, may all genes be IQ genes?
In regards to IQ, 3 genetic variants explain .3 IQ points (Rietvald et al, 2014):
After adjusting the estimated effect sizes of the SNPs (each R2 ∼ 0.0006) for the winner’s curse, we estimate each as R2 ∼ 0.0002 (SI Appendix), or in terms of coefficient magnitude, each additional reference allele for each SNP is associated with an ∼0.02 SD increase in cognitive performance [or 0.3 points on the typical intelligence quotient (IQ) scale].
This is the gene with the highest known effect that we currently know of. No “but undiscovered X means Y!!”, because science isn’t based on ‘what ifs’.
To predict one’s intelligence, you would need all genes on an SNP chip—which contains about 500,000 SNPs—to be able to predict half of the individual variation in IQ (Davies et al, 2011; Chabris et al, 2012; Heine, 2017: 175). Just as is the case with height, it seems that it’s possible that most—if not all—genes are IQ genes.
So, clearly, intelligence is highly polygenic, and, contrary to what Plomin says, it’s doubtful that we’ll be able to genotype one to guesstimate their intelligence level.
This is because you need more than 500,000 SNPs on a gene chip and even still, that would only explain half of the variance. So it’s reasonable to assume—as is the case with height—that all genes are IQ genes.
Chabris et al (2012) write:
One SNP, rs2760118 in SSADH (also known as ALDH5A1), exhibited a nominally significant association with g (t = 2.01, p = .04), but this association did not survive a Bonferroni correction. The mean g values (transformed to the IQ scale) by genotype for this SNP were 98.3, 99.7, and 100.6 for genotypes TT, TC, and CC respectively.
So it seems that all genes are height genes and all genes could possibly be IQ genes (that is, having a small effect). If most genes are height genes, and height is linked to IQ, then most genes should be IQ genes as well. Therefore, it is plausible that all genes are IQ genes.
Finally, I need to talk about the study that everyone is talking about, the study that found 52 new genes for intelligence (Sniekers et al, 2017). However, Razib Khan cautions: “My plain words are this: do not trust, and always verify“. A Google search for “gene found for” brings up 26,300,000 hits. As can be seen with the study that was published the other day on the supposed ‘new hominin’ found in Europe, science journalists use fancy and catchy headlines. “Genes for ___ and ___” is a bad way to put it—few traits are caused by a single gene, and most traits are highly polygenic, height and IQ included.
Do I think we’ll disentangle the intricacies involved with height and IQ? One day. But since at the moment, 500,000 SNPs need to be loaded on a gene chip to explain half of the variation in individual IQ.
Since most—or all—genes are related to height and the same may be so for IQ, we don’t really learn anything knowing the genes that control for these two traits. In regards to Heine’s (2017) example of genetic engineering 300,000 SNPs for height and you’d only be halfway there, I’d assume the same would be true for IQ. Both traits are highly polygenic, with thousands of genes controlling these traits. Genetic engineering a human for high intelligence or height looks to be a long shot—at least until far into the future.