Follow-up to: Lifestyle Interventions to Increase Longevity

Abstract

A recent review article by David Gems discusses possible mechanisms by which testosterone and dihydrotestosterone could shorten the life expectancies of human males, and examines previous research on the effects of castration on male survival. However, Gems does not examine how age at castration affects how much castration extends one's life by, which this post does. In general, castration after puberty in males prolongs life to a lesser extent than castration before the onset of puberty.

Additionally, Gems' review does not estimate how long modern-day eunuchs might live relative to intact human males. Two of the other three known studies on the effects of castration on human life expectancies found that, historically, castration prolonged life by more than a decade in the median case. However, some of the life expectancy gains from castration are due to the increased ability of eunuchs to fight off infections. The fact that fewer men die from infections in the 21st century than was the case in previous centuries means that modern-day eunuchs gain fewer years of life from castration than eunuchs gained from castration in the past. As seen from comparing Figure 3b and Figure 4, eunuchs castrated just before the onset of puberty extended their (mean) life expectancies by 11 years in Hamilton & Mestler's study, though modern eunuchs castrated at similar ages might expect to extend their life expectancies by 7 years. 

Introduction

A few relevant studies, such as the study of institutionalized eunuchs by Hamilton & Mestler, the study of Korean eunuchs by Min, Lee, and Park, and the review article by Gems are particularly worth reading or skimming for those interested in this topic. The excel file showing the work behind this post is also available. These documents are supplementary; reading them is not a  prerequisite for reading this post.

This post will examine the proposition that castration of human males (specifically, orchiectomy, the surgical removal of both testicles, but not the penis) either before or after the onset of puberty will extend both their life expectancy, and their lifespan. In light of antagonistic pleiotropy, it a priori makes sense that castration might extend one's life expectancy.

A number of papers have mentioned that the effects of castration on the life expectancy of different types of nonhuman animals don't provide a good model for the effects of castration on the life expectancy of human males. Specifically, "the relationship of gonadal functions to survival seems to involve many variables... individuals, strains, and species may vary in their response to gonadectomy". This leaves only a small number of studies that have much bearing on the question of whether or not orchiectomy extends human life expectancy. While there are some studies on the health effects of chemical and physical castration of (often elderly) modern men with prostate cancer, it seems like having prostate cancer would correlate with having other pathologies. Further, as will be examined later, it seems that orchiectomies performed at early ages have many positive effects on health, whereas orchiectomies performed later in life have fewer positive effects, and may even negatively affect some aspects of health.

After setting aside animal studies and studies of men with prostate cancer, only four papers directly relevant to whether orchiectomy increases the life expectancy of men remain. This is worth stating explicitly, since citing only a fraction of the available research on a given topic can be a fallacy. First, the study by Min, Lee, and Park found that, historically, Korean eunuchs lived 14-19 years longer than intact males from similar social classes in the median case. Secondly, Hamilton and Mestler's study of the effects of orchiectomy on the life expectancies of mentally retarded individuals found that males castrated before puberty lived about 13 years longer than intact men in the median case, and that males castrated after puberty experienced smaller lifespan gains. Thirdly, a letter to Nature by Nieschlag et. al which compared the lifespans of famous castrato singers to the lifespans of other singers from the same era found that orchiectomized male singers lived about as long as intact male singers. Lastly, page four of the review article by David Gems examined all three of these studies, and, after finding methodological issues with the letter to Nature, concluded that the results in these papers were "consistent with the idea that testes are a determinant of the gender gap in human lifespan".

Evidence Regarding Whether or Not Orchiectomy After Puberty Increases Life Expectancy

The only study that examined the effect which age at orchiectomy had on the life expectancy gains from castration in humans was Hamilton and Mestler's study of mentally retarded, institutionalized individuals. Note that the participants in Hamilton & Mestler's study lived shorter lives than non-institutionalized Americans of the same era lived, which could likely be explained by the mentally retarded status of the participants, and the plausibly poor conditions under which participants might have lived. In Figure 4 and Table 10 from Hamilton and Mestler's paper, it is shown that males castrated between 15 and 40 years of age live longer than intact males, but that within this range, earlier castrations added more years to the life expectancy of eunuchs than later castrations did.

It is worth reproducing Figure 4 from Hamilton & Mestler's article, which shows the survival curves (starting at 40 years of age) of intact males and males castrated at various ages:

One thing about this figure that stands out is that the portion of the survival curve for institutionalized non-castrates shown in this figure is nearly linear. In the present day, intellectually disabled populations have survival curves which look quite different from the one for non-castrates shown in the figure above. For reference, the survival curve for castrated females in Figure 5 of this post has a shape which is comparable to the shape of survival curves for modern first-world populations. It is also remarkable that the tail end of the survival curve for non-castrates in the above figure is fatter than the tails of the survival curves for men castrated after 14 years of age-- it isn't obvious whether or not this difference reflects a real phenomenon. Further, the 3.7 % centenarian rate for Korean eunuchs in the study by Min, Lee, and Park suggests that eunuchs should have a longer (maximum) lifespan than non-castrates, which isn't borne out in Figure 4 from Hamilton & Mestler. This having been said, Figure 4 and Table 10 from Hamilton & Mestler's study show that castration at earlier ages prolongs life more than castration at later ages does.

Below, in Figure 1, the attempted linear fit between median life expectancy versus age at castration given on p. 403 of Hamilton and Mestler's paper is shown. The authors used data from Table 10 of their paper to determine this fit, but did not graph the data or determine an R2 value for this linear fit. The estimated median life expectancy of the non-castrates was 64.7 years-- a reasonable value, given their status as institutionalized mentally retarded men in the early 20th century. Thus, Figure 1 can be used to visualize the fact that even men who were castrated at 30-39 years of age lived longer than non-castrates in the study (p = 0.002). Since the data shown in Figure 1 did not follow a linear trend, additional fits were tried below.

Figure 1. Hamilton & Mestler's Regression of Median Life Expectancy v. Age at Castration

Figure 2. Polynomial Fit for Median Life Expectancy v. Age at Castration

Figure 3. Raw Data and Fits For Interpolation of Mean Life Expectancy v. Age at Castration

Data and fits for the median and mean life expectancies of eunuchs are given in Figures 2 and 3, respectively. The data plotted in sections a and b of Figure 3 could not be reasonably fitted to a curve directly, so sections c and d of Figure 3 show the same data as sections a and b, but plotted on an inverted x axis and successfully fitted to a curve. The polynomial data fits given in all Figures are only intended for use in interpolation.

Effects of Orchiectomy on Mortality from Infectious Diseases and Cardiovascular Mortality

Literature has suggested that castration in human males may promote longer lifespans and higher life expectancies by protecting against infections and cardiovascular events. Much of the evidence for the proposition that castration protects against cardiovascular disease (CVD) comes from basic biology rather than from studies of eunuchs, since Hamilton & Mestler's paper is the only study on eunuchs which attempted to collect data on causes of death in castrated men, and only did so from clinical diagnoses of the primary causes of deaths of eunuchs and intact men between 1940-1964. Still, modern men die of cardiovascular events more often than modern women do, so investigating whether or not castration protects against cardiovascular events is worthwhile.

The authors of the study on Korean eunuchs cite this review as evidence that "male sex hormones reduce the lifespan of men because of their antagonistic role in immune function". Gems' review article also suggests that male sex hormones may act as an immune suppressant. Moreover, in Hamilton & Mestler's study, 27% of eunuchs died of infections, compared to 44% of intact men (p = 0.02), and the mean age of eunuchs dying of infections was 44, compared to 35 for intact men (p = 0.03). However, Table 14 of Hamilton & Mestler's study suggests that castration protects more against deaths from certain kinds of infections, such as tuberculosis, than others. In general, it seems like the claim that castration protects against deaths from infections is true.

On the other hand, the data relevant to whether or not eunuchs die more from CVD than intact men do is muddled at best, and it isn't obvious that castration protects males from CVD by much, if at all. One mostly irrelevant data point is men who have undergone chemical or physical castration after being diagnosed with prostate cancer, as well as hypogonadic men in general; many meta-analyses on the relationship between hypogonadism and frequency of adverse cardiovascular events (and on the effects of hormone replacement therapy on the frequency of adverse cardiovascular events) in men have been done. Men castrated after being diagnosed with prostate cancer tend to have more adverse cardiovascular events than other similarly aged men, but this could be because hypogonadism correlates with being unhealthy, rather than because castration at advanced ages decreases life expectancy.

One poorly done study on Danish eunuchs who were predominantly drawn from the lower class found that these eunuchs did not live as long as men in Denmark did on average, and also found that the standardized mortality ratio for cardiovascular disease-related deaths was higher than the all-cause standardized mortality ratio in eunuchs. However, men in this study were often castrated later in life-- all but one man were castrated after the age of 18, and the average age at castration was 35. As suggested by Figure 2 and Figure 3 above, this means that most of the Danish eunuchs gained appreciably fewer years of life from being castrated than they would have gained if the castrations had been carried out much earlier in their lives. These concerns suggest that this study should not change one's credence in the proposition that castration protects against CVD mortality by much.

Lastly, Hamilton & Mestler's study found that eunuchs dying of cardiovascular disease during or after 1940 lived an average of 51.6 years, while intact males dying of that cause lived an average of 51.1 years. This difference was not found to be significant. However, since not all eunuchs included in the study had died by the time of publication, it is still possible that castration early in life protects against late-life cardiovascular mortality, but not early and mid-life cardiovascular mortality.

Effects of Orchiectomy on Modern Lifespans and Life Expectancy

Some common causes of death in both Hamilton & Mestler's study and the study of Korean eunuchs, such as tuberculosis, are no longer common causes of death. Thus, data from Table 14 in Hamilton & Mestler were used alongside modern actuarial data to crudely predict how long eunuchs castrated in the 21st century might live. The details of the analysis are given in this excel file. The results of this analysis are given below.

Figure 4. Life Expectancy Gains for Modern Eunuchs

 

Table 1. Life Expectancy Gains for Modern Eunuchs

For the most part, the data in Figure 4 and Table 1 are consistent with my holistic understanding of the effects of castration in men. It is hard to say how castration after age 35 would affect life expectancy, as very few eunuchs in Hamilton & Mestler's study were castrated after 35. It's also a shame that about 27% of the eunuchs and intact males who died during 1940-1964 were not listed as having a primary cause of death-- this may have led to an overestimation of the extent to which castration is expected to extend modern eunuch's life expectancies. On the other hand, Min, Lee, and Park found that 3.7% of Korean eunuchs who died between the late 14th to early 20th century were centenarians, "a rate at least 130 times higher than that of present-day developed countries", which suggests that modern eunuchs would likely benefit from increased lifespans.

Effects of Orchiectomy on Health and Physiology

Gems' review article, this article on historical eunuchs, the wikipedia page on castration, and Hamilton & Mestler's study all note certain effects that castration can have on human males.

All castrated males have an increased risk of developing sarcopenia, and becoming overweight. Wilson and Roehrborn note that eunuchs have historically suffered from skeletal problems such as osteoporosis and kyphosis; this is especially true of elderly eunuchs, and eunuchs castrated at earlier ages. Hormone replacement therapy can prevent or deter sarcopenia, osteoporosis and kyphosis. Castration also decreases sex drive, prevents baldness if done early enough in life, and may result in enlarged pituitaries and enlarged breasts. Castration causes the prostate to shrink over time, and if done early enough in life, effectively prevents the development of prostate cancer. Castration also prevents the development of prostatic hyperplasia and testicular cancer.

Men castrated before puberty will develop higher voices, little or no sex drive, and smaller penises.

Effects of Gonadectomy on Human Females

There is very little data relevant to whether or not oophorectomy (castration) of women extends life expectancy or lifespan. Hamilton & Mestler have a small section dedicated to estimating the life expectancy of castrated females based on only 11 female castrates of known fate. They also find the median lifespans of castrated and intact females known to be dead by the end of the study to be equal. Lastly, Hamilton & Mestler find the mean lifespan of institutionalized castrated females known to be dead by the end of the study, 56.2 years, to be significantly greater than the mean lifespan of institutionalized intact females known to be dead by the end of the study, 33.9 years (p < 0.001). The estimated survival curves for all castrated females and all intact females-- not just those known to be dead by the end of the study-- are given in Figure 5.

Figure 5. Survival Curve for Intact and Castrated MR Females

Conclusion and Motivation

Orchiectomy should prolong the lifespans of modern males, especially if done before puberty. While the estimates of life expectancy gains from castration given in Figure 4 and Table 1 aren't perfect, they are my best guesses, and should be interpreted with the correspondingly appropriate level of credence.

My original motivation for writing this post was that I was interested in learning about the different ways in which humans could extend their lifespans and life expectancies. So, while being castrated is one way for males to live longer, quitting smoking and improving one's diet and exercise regimen are better uses of time and energy for people who are just beginning to think about changing their lifestyles in order to live longer.

Thanks to Vaniver, who caught several errors in an earlier draft of this post, and thanks to btrettel for pointing me to a few papers early on. All remaining errors in this post are solely my own.

References

1. Castration. http://en.wikipedia.org/wiki/Castration

2. Antagonistic Peliotrophy Hypothesis. http://en.wikipedia.org/wiki/Antagonistic_pleiotropy_hypothesis

3. Bittles, A. H.; Petterson, B. A.; Sullivan, S. G.; Hussain, R.; Glasson, E. J.; Montgomery, P. D. The influence of intellectual disability on life expectancy. J. Gerontol. A Biol. Sci. Med. Sci. 2002, 57, M470-2.

4. Corona, G.; Maseroli, E.; Rastrelli, G.; Isidori, A. M.; Sforza, A.; Mannucci, E.; Maggi, M. Cardiovascular risk associated with testosterone-boosting medications: a systematic review and meta-analysis. Expert opinion on drug safety 2014, 13, 1327-1351.

5. Corona, G.; Rastrelli, G.; Monami, M.; Guay, A.; Buvat, J.; Sforza, A.; Forti, G.; Mannucci, E.; Maggi, M. Hypogonadism as a risk factor for cardiovascular mortality in men: a meta-analytic study. Eur. J. Endocrinol. 2011, 165, 687-701.

6. Gems, D. Evolution of sexually dimorphic longevity in humans. Aging (Albany NY) 2014, 6, 84-91.

7. Hamilton, J. In Duration of Life in Lewis Strain of Rats After Gonadectomy at Birth and at Older Ages; Reproduction & Aging; 1974; pp 116-122.

8. HAMILTON, J. B. Relationship of Castration, Spaying, and Sex to Survival and Duration of Life in Domestic Cats. J. Gerontol. 1965, 20, 96-104.

9. Hamilton, J. B.; Mestler, G. E. Mortality and survival: comparison of eunuchs with intact men and women in a mentally retarded population. J. Gerontol. 1969, 24, 395-411.

10. Jones, C. M.; Boelaert, K. The Endocrinology of Ageing: A Mini-Review. Gerontology 2015, 61, 291-300.

11. Mestler, H. In The Role of Testicular Secretions as Indicated by the Effects of Castration in Man and Studies of Pathological Conditions and the Short Lifespan Associated with Maleness; Pincus, G., Ed.; Recent Progress in Hormone Research; Laurentian Hormone Conference: 1948; pp 257.

12. Min, K.; Lee, C.; Park, H. The lifespan of Korean eunuchs. Current Biology 2012, 22, R792-R793.

13. Nieschlag, E.; Nieschlag, S.; Behre, H. M. Lifespan and testosterone. Nature 1993, 366, 215-215.

14. Roberts, M. L.; Buchanan, K. L.; Evans, M. Testing the immunocompetence handicap hypothesis: a review of the evidence. Anim. Behav. 2004, 68, 227-239.

15. Talbert, G. B.; Hamilton, J. B. Duration of life in Lewis strain of rats after gonadectomy at birth and at older ages. Reproduction & Aging 1974, 116.

16. Wilson, J. D.; Roehrborn, C. Long-term consequences of castration in men: lessons from the Skoptzy and the eunuchs of the Chinese and Ottoman courts. The Journal of Clinical Endocrinology & Metabolism 1999, 84, 4324-4331.

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I think it's generally a good thing to try diet and exercise before having one's manhood removed for a longer life. And according to your data, it wouldn't do most of us much good on account of the fact that a majority, if not all, of the men on this site are already well past puberty. However, this was an interesting journey.

It's convincing to see how consistent all the castration data is, so I was quite surprised when the other day I happened to start reading A History of Life-Extensionism which was just posted online and I learned that one of the reasons for the early medical interest in sex hormones and hormonal treatment for health & life extension was because eunuchs were seen as short-lived, feeble, and stupid and since this was due to a lack of sex hormones, perhaps aging itself is due to a lack (emphasis added):

Brown-Séquard was a foremost authority in endocrinology, having proven specific effects of internal secretions, particularly those of the sex glands. In the widely publicized presentation to the French Biological Society of June 1, 1889, entitled the “Effects in man of subcutaneous injections of freshly prepared liquid from guinea pig and dog testes,”[xciv] [paper] Brown-Séquard announced his first attempts at hormone replacement therapy for rejuvenation, introducing longevity and rejuvenation research as an integral part of scientific discourse, and in fact establishing the field of therapeutic endocrinology.

In that seminal address of 1889,[xcv] Brown-Séquard proceeded from the observation that “true eunuchs are remarkable in their feebleness and their deficit in physical and intellectual activity” and the conviction that “analogous defects are observed in men who abuse coitus or masturbate” to the assumption that “these along with numerous other facts, clearly show that the testicles furnish to the blood, … principles which give energy to the nervous system and probably also to the muscles.” It followed that the supplementation of these deficits by animal sex gland extracts can retard senility. Their almost miraculous reinvigorating effects on his own person were described by Brown-Séquard, ending with a call for further research. (For Brown-Séquard the reinvigoration was not lasting, he died 5 years later, at the age of 77.)

...Perhaps the most ardent follower of Brown-Séquard was Serge (Samuel) Abramovich Voronoff. Born in 1866 near Voronezh, Russia, a son of a wealthy Jewish manufacturer, he immigrated to Paris in 1884 at the age of 18 and became a naturalized French citizen in 1895. (The drive and ability to adapt in the new country must have been strong, as Voronoff was often said to have become “more French than the French.”[cv]) In Rejuvenation by Grafting (1925),[cvi] Voronoff related the history of his method. While serving as a personal physician of the Egyptian viceroy Abbas II, in 1898 he observed the enfeeblement of eunuchs, which led him to believe in the invigorating and rejuvenating power of the sex glands. In 1913, he began experimenting with tissue grafting

(Stambler mentions in the footnotes Hamilton & Mestler's paper as a counterexample, but not the others.)

This makes me wonder how they could have been so wrong, if all subsequent data indicated long life for eunuchs. I tried to look up Voronoff's Rejuvenation by Grafting & How to restore youth and live longer but they are unavailable online despite existing in Google Books (gee, thanks copyright laws); googling snippets and in other books, quotes indicate he attended the deathbeds of a number of youngish Egyptian eunuchs and far from knowing any centenarian eunuchs much less several like the Koreans, says "I have never known an eunuch to exceed the age of sixty.", describing them as (quoted in Bourke's What it Means to be Human: Reflections from 1791 to the Present)

Voronoff encouraged physiologists to scrutinize the bodies of male eunuchs who could not be classed as 'truly men'. In a visit to Cairo in 1898, Voronoff was 'immensely struck' by the appearance of these eunuchs. They were

long in the leg, with small craniums and smooth, hairless faces. In the majority of instances they are obese, with pendulous cheeks, developed breasts, and enlarged pelves. They look, in fact, like old women, and the resemblance is enhanced by their characteristic high-pitched voices. The muscles are flabby, the walk and movements lethargic, the gums and sclerotics [white of the eye] pallid. They present, in short, all the signs so characteristic of the anaemic, feeble, and flabby organism.

Further evidence for their lack of manly characteristics included their 'slow' intelligence and lack of 'courage and enterprise'.

A Brief History of Bad Medicine implies that these were true eunuchs in the sense that they never experienced puberty and so should have had the maximal benefit:

...had the opportunity to examine some eunuchs - men who had been deliberately castrated at the age of six or seven...Fascinated, Voronoff took the opportunity to examine a large number of eunuchs and affirmed that these characteristics were common to them all. Quite reasonably, he concluded that all these effects were connected with the absence of the testicles...

I have no particular reason to disbelieve Voronoff, and it sounds very much like there was no apparent longevity benefit. So I wonder what the reason for the discrepancy between the modern data and the Asian & Ottoman data, and the Egyptian eunuchs? The main proposed mechanism, better immune system functioning, sounds as if it should give much larger benefits in Egypt than elsewhere, since as part of Africa there are so many infectious diseases there like malaria.

Flabby muscles, lack of courage, etc. are entirely consistent with low (or absent) testosterone. After all, testosterone is the reason why men compete in sports separately from women and are, generally speaking, more aggressive than women.

However general flabbiness does not imply a short life. I wonder if there were social or cultural reasons why Egyptian eunuchs didn't live long.

Hmm. It seems possible that eunuchs could display certain "enfeebled" traits despite living longer. Some of the traits Vornoff described are mentioned by Hamilton and Mestler and the authors of the study on Ottoman and Asian eunuchs. One paper-- I don't remember which, but I can try to find it again if you're interested-- suggested that castrated animals lived longer because of general inantion. I am still curious about the extent to which castration at age 6 or 7 would have different effects on health and lifespan than castration around age 11, though I weakly suspect that 11 is the optimal age to do it at for life expectancy maximization purposes.

It seems possible that eunuchs could display certain "enfeebled" traits despite living longer.

Sure. In fact, they pretty much have to for the original story to make sense: the description of being pudgier, weaker, and more woman-like is common to all descriptions of eunuchs, East or West, including the long-lived ones. No one describes the Korean eunuchs (and future centenarians) as sporting enormous thick beards and holding strongman contests. So if you believe the long-life claims, then you must also believe that the enfeeblement can go along with longer-life.

I quoted those bits mostly to establish that yes, they definitely were physically eunuchs and they weren't simply fakes who bought 'eunuch status' (as I've read a lot of the Chinese court eunuchs were doing towards the end as the system broke down), that they otherwise looked exactly like the long-lived eunuchs elsewhere, and it's not as simple as they were castrated post-puberty because they were before - but Voronoff is emphatic about them not having any apparent longevity benefit to the point where he based his entire anti-aging paradigm on the belief that they have negative longevity.

Why this is, I don't know. The most obvious differentiator between Egypt and the other countries, infectious disease burden, would predict the opposite of what Voronoff claims. So it would seem to be important to find out whether Voronoff was right about the Egyptian eunuchs and if he is, what could possibly be making such an enormous difference in outcomes, since this factor could potentially negate any gains in the modern environment as well and give clues as to what the mechanism is (evidence against the immune hypothesis, evidence for... what?).

I also don't think I've seen Egyptian eunuchs ever come up before in the previous papers or discussions I read about castration and life expectancy, so further research on this could be useful. (Unfortunately, Egypt is in a lot of turmoil now and you'd probably need to read Egyptian Arabic or French if you wanted to do original research on the ground; it's too much to hope for that there might be big registries of Egyptian eunuchs in English with data on lifespans.)

In any case, thanks for mentioning the case of Egyptian eunuchs. It's plausible that Lumifer's suggestion, that social or cultural causes may be behind the shorter lifespans of Egyptian eunuchs, accounts for this effect, but I obviously can't say either way, not having looked into the matter of Egyptian eunuchs myself.

It is worth mentioning that Hamilton and Mestler didn't think that African American eunuchs gained as many years of life from castration as white eunuchs did. I basically ignored the data on African American eunuchs from Hamilton and Mestler in the above post. In fact, I don't have much of an intuition regarding how race might affect the number of years of life gained from health/medical interventions at all.

It is worth mentioning that Hamilton and Mestler didn't think that African American eunuchs gained as many years of life from castration as white eunuchs did. I basically ignored the data on African American eunuchs from Hamilton and Mestler in the above post.

Oh, I thought you covered all the eunuchs... If you left out poorer-performing eunuch groups, that tends to undermine the case. Unless one wanted to argue that Africans didn't benefit and so through all the African admixture, Egyptian ones might not benefit either. That would be somewhat plausible. There are consistent differences in lifespan between races, after all.

One more thing is that evidently castration had a low survival rate. That makes long life conditional not only on having been castrated, but on on having been castrated and surviving it.

If there were such a mortality bias where the procedure kills the weaker, then unless native Egyptian surgical skills in the late 1800s are much better than Chinese surgical skills, I would again expect that to produce excess longevity in Egyptian eunuchs and not the Chinese/Korean eunuchs (which is the opposite of what we seem to observe).

That was a general point about eunuch longevity studies, not specifically about the Egyptian ones. I expect the techniques in Egypt and China to have beeen similar.

I expect that the survival rate should be incredibly close to 100%, if one goes to a surgeon rather than cutting himself. The number of years of life one should expect to lose from dying during an orchiectomy times the probability of death occurring then is going to be hundreds of times less then the expected number of years even a 30-year old would gain from castration.

The survival rate is close to 100% now. However the data that you rely on comes from previous centuries when the survival rate was low. Thus your data set has a literal survival bias.

Since lots of eunuchs reached positions of power, and because of the strong correlation between intelligence and health, I wonder if castration increases intelligence.

Beware social confounders.

Eunuchs couldn't sire children to leave wealth and titles to and could not marry into wealthy and powerful families. This means that intact men who were in positions of power because they came from powerful families were more likely to give important offices to eunuchs since they did not have to fear that eunuchs would become a long-term threat to their own or their family status.

Yes, this was standard practice in the ERE.

Interesting idea! The idea of castration increasing intelligence didn't come up at all during my research, so I don't really know.

I expect that historical eunuchs would have been more intelligent than their contemporaries to the extent that castration protected against infectious diseases which caused mental impairment (such as ergotism, i.e. fungal food poisoning). At the same time, it might be that eunuchs mainly acquired positions of power due to cultural reasons.

Sorry to be a terrible pedant, but isn't it 'orchiectomy' rather that 'oriechtomy'?

That's right; fixed.

Epistemic status of this comment: tentative.

It’s interesting that the eunuchs studied by Min, Lee, and Park, who died before and around 1805, seem to have outlived their contemporaries by a greater number of years than eunuchs studied by Hamilton and Mestler, who were born between 1871 and 1932, outlived contemporary institutionalized intact males by. Further, my post argues that eunuchs in the 21st century will outlive contemporary intact men by less than eunuchs in Hamilton & Mestler outlived their own intact counterparts.

This is interesting because it suggests that the causes of death which contribute to eunuchs having longer life expectancies than intact men have are, weighted by how much they so contribute, also more likely than not to be causes of death which have contributed more to historical men having lower life expectancies than men in the 21st century have. It’s as if some historical causes of death, like tuberculosis, weakly tend to be fundamentally easier to do work on than others, in that they can be successfully approached from multiple angles if they can be successfully approached at all.

Longevity is one thing, but quality of life is another. As a transgender man, I found that life wasn't worth living without testosterone. I'm sure that cisgender men with orchiectomy-induced testosterone deficiencies would feel similarly crappy.

Fluttershy:

I'm really sorry about that fanfic, okay?

Phil, you're a great author, and I don't think that you need to be sorry for writing that fanfic. In case saying sorry satisfies some of your values, though, I accept your apology on behalf of Fluttershy from FiM.

I was previously aware that e.g. thinking of yourself as a pony who trys new things makes you more likely to try new things in the future, though reading your story helped me grasp that on a deeper, more emotional level than I had before. In fact, I think that by choosing "Fluttershy" as my username on LessWrong, I inadvertently nudged myself to eventually become both kinder and more shy than I would have become if I had chosen a different username.

Note to the FiMFiction crowd: I've made an account here.

I was kidding. I found it very funny to see a politely-written article by Fluttershy about castrating males.

I'm not interested in castration itself for life-extension. I wouldn't do it, I'm too old anyway, and I wouldn't do it to anybody else, particularly not a 10-year old. Besides, somebody who's 10 years old today will probably live into the 22nd century, and they'll come up with something better than castration.

It is interesting if it causes life-extension. We'd like to know how it does. But I suspect we already do.

There are 2 large, opposing pathways in every cell of every multicellular animal and more things besides, from yeast all the way to humans, the TOR and FOXO pathways. TOR stands for Target Of Rapamycin. It's the thing rapamycin inhibits. FOXO stands for Forkhead box class O. A forkhead box is a transcription gene, one that, when transcribed, causes other genes to be (or not be) transcribed.

mTOR causes growth, cell proliferation, stem cell differentiation, cell cycle promotion, muscle growth, bone growth, wound healing. It also increases DNA damage, diabetes, cancer, and just about every other major cause of aging.

FOXO up-regulation causes DNA repair, restoration of insulin response, apoptosis (cancer suppression), mitochondrial biogenesis, and a wide variety of cell protectant effects.

Every known mechanism of life-extension activates FOXO and suppresses TOR. Rapamycin, resveratrol, caloric restriction, exercise, nearly every genetic mutation that extends life, and, yes, castration.

So it's probably better to take rapamycin.

Stupid question: if you think that huge improvements in medicine and radical life extension are just around the corner, should you castrate yourself or your children to increase your chances to survive up to that point in order to uncastrate yourself later with the help of new improved medicine? Potentially high rewards strategy, even if it's very risky.

I don't think now is the window when that's relevant, because you would have to put the takeoff decade at ~2080. If it's later, then castration isn't enough to get you there, and if it's earlier, castration slightly increases your chances of getting there but doesn't shift the median outcome much.

If you put the takeoff decade at, say, 2050 (which seems closer to 'right around the corner' to me), then the time to have been castrated would have been ~1980-1990.

(I'm assuming we're talking about castrating 10 year olds; I doubt it's worth it for anyone older.)

I'm assuming we're talking about castrating 10 year olds

And LessWrong jumps the shark.

or your children

I am pretty sure this will land you in jail which will reduce your life expectancy quite dramatically.

So, there's growing acceptance of using drugs to prevent puberty in prepubescents who are transgender, because it makes it easier to transition later. It seems likely one could piggyback on that and get a son up to 18 without going through puberty, at which point they should be able to legally approve of their castration.

and get a son up to 18 without going through puberty

If the son is not transgender, I would be willing to stick an "abuse" label onto that. This is taking a (presumably) normal human being and fucking him up in a pretty major way.

If the son is not transgender,

Possibly TMI:

I don't consider myself transgender, but I have been wishing this had been done to me pretty much since I was 12.

The main thing I learned from this article is that everything I thought I knew about castration holds up under Lesswrongian analysis, including the part where I completely missed the opportunity and would probably be more likely to die early were I castrated now. There would still be some advantages, but it seems too late to be worth it.

You did specify "presumably normal", though. Presumably, I am far from normal.

I'm assuming that this is done with their understanding and consent, to the extent that is possible. (I don't think it's advisable, for a handful of reasons, but I think legal difficulties are a minor impediment at best.)

this is done with their understanding and consent, to the extent that is possible.

I don't think the possible extent is sufficient.

I think legal difficulties are a minor impediment at best

The original case to which I replied involved a straightforward castration, not delaying puberty. The "legal difficulties" might be a minor impediment, but are likely to have major consequences.

(I don't think it's advisable, for a handful of reasons, [...])

I agree, even though I'm effectively punishing my past self in doing so.

I would like there to be a mechanism for making this possible, but it just seems too dangerous; even the idea of delaying puberty until the age of consent doesn't work, because apparently this path can have permanent side-effects as well.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8260231/

BTW for anyone who knows me, this post is probably my favorite article on ALL OF LESSWRONG

 


Among invertebrates, birds and mammals, experimental paradigms that limit reproductive investment also cause lifespan extension [232]. Hypothetically, the need for repairing and preventing damage to the germline dominates resource allocation strategies, while the somatic tissues age and deteriorate [112]. In support of such theories, modulations of reproduction that eliminate germ cells in C. elegans and D. melanogaster provide effective mechanisms for extending lifespan [232-234], phenotypes that may be caused by heightened resource availability and proteome stability within the post-mitotic soma [17, 235]. Inhibiting germline proliferation delays the onset of PolyQ-dependent aggregation and toxicity [235]. Proteasome activity and RPN-6 protein levels are increased in germline-lacking worms [17]. In these long-lived animals, increased proteasome activity, rpn-6 expression and longevity are modulated by DAF-16 [17]. Similar to these long-lived worms, FOXO4 is necessary for increased proteasome activity and PSMD11/Rpn6 levels in immortal hESCs [28, 236]. Interestingly, it has been recently reported that DNA damage in germ cells of C. elegans induce a systemic response that protects somatic tissues by increasing their proteasome activity [237].

Possibly slightly relevant

[-][anonymous]9y10

So, while being castrated is one way for males to live longer, quitting smoking and improving one's diet and exercise regimen are better uses of time and energy for people who are just beginning to think about changing their lifestyles in order to live longer.

Oh bugger. And here I am, not smoking, barely drinking, exercising with reasonable regularity, and only having a little bit of a bad-food habit.

Good job. Why hasn't this been published in a journal?

Thanks; this comment made me happy. Part of the answer is that I generally have low self-esteem, which negatively affects my perception of the quality of certain things that I have written. Another part of the answer was that I wrote this with the very specific goal of estimating values of the "years of life added vs. age at castration" curve at different points in mind, which seems much more narrow than the goal of doing basic science work, which is most of what journals publish.

Additionally, many journals have publication fees, which I would have to pay out of pocket. Others charge readers access fees; I'd rather people be able to access my work freely. As things currently stand, I might still be able to mention this work during interviews as an example of a time when I noticed others didn't seem to be working on a certain problem and took action myself, if the interviewer didn't seem to be prejudiced against transhumanist or LGBT folks.

[-][anonymous]9y20

At the very least, it seems like you could get this published as a guest post on a popular life extension blog.

[-][anonymous]9y10

More object-level question: sorry for not spotting it due to academic voice, but did you do enough original research on your own here to make the analysis publishable? Or could you maybe submit it as a student project, if you're still in school?

Thanks for the suggestion. I'm guessing that I probably did enough research that I could have at least published this as a letter to a journal, instead of as a full-fledged publication. I'm no longer a student.

I find it interesting that you both are underconfident and realize you are underconfident. Have you tried adjusting for underconfidence like you would any other cognitive bias? (At least you need not adjust for overconfidence!)

(At least you need not adjust for overconfidence!)

Someone thinking they are underconfident does not prove they are not overconfident.

I don't have much social confidence, but social confidence need not be related to credence calibration. I still end up giving somewhat overconfident answers on CFAR's credence calibration game, despite being shy. My above comment could have been clearer: the bit about "my perception of the quality of certain things that I have written" has more to do with my self-worth, and less to do with my ability to judge the quality of my own writing.

Oh, I think I see. Confidence is a feeling, while credence is a belief.

Arxiv. Lots of journals are open access these days.

I'm not sure where a preprint on castration & longevity would fit on the arXiv...I'd try bioRxiv or the Social Science Research Network.

Yes, you are right, re: venues. Thanks!

many journals have publication fees, which I would have to pay out of pocket. Others charge readers access fees

A short summary of what is wrong with science, as done today. :(

Possible solution: Create an "amateur science foundation" which would review articles for free, and if they are good, would publish them in open-access journals. (To prevent flooding by crackpots, if a person submits an obviously stupid article, they get a warning, and after three warnings they are blacklisted.)

Alternatively, the site could let the users determine what it good. Users could "like" or "dislike" articles, and these likes and dislikes would affect the reputation of the publisher. The higher the publisher's reputation, the more likes, and the fewer dislikes and article has, the higher rank the article would get when being searched for, and articles with sufficiently low rankings would be hidden. Think Stack Exchange for science.

It could be expanded in many ways, for example by weighing likes and dislikes by high-status users more heavily than low-status ones, or by using numeric ratings instead.

I'm considering taking anti-androgens, but I'm not sure what effect this would have on lifespan.

Would anti-androgen use have similar effects on lifespan as castration? I know both anti-androgens and castration cause decreased testosterone production, but I know almost nothing about this sort of thing, so I don't know if this is relevant.

Anti-androgens are much easier to attain than castration. According to this, "WPATH Standards of Care no longer encourage therapy as a requirement to access hormones".

Also, according to the article I linked, "Your body needs sex hormones – estrogen or testosterone – primarily for bone health but for a myriad other reasons as well." Hormone replacement therapy has potentially dangerous side-effects, though. Do you know if this would outweigh the benefits of castration or anti-androgen use?

I don't think LW is a good place to get medical advice.