Sorry I can’t help, res; I haven’t got his other books. Maybe it’s time I added them to my Christmas list.

Except embryos have totipotent cells which can become any cell in the body and which, therefore means that you can’t ‘estimate the potential’ of a human embryo.

https://notpoliticallycorrect.me/2017/09/16/does-human-potential-lie-in-the-embryo/

https://digest.bps.org.uk/2016/09/12/its-now-possible-in-theory-to-predict-life-success-from-a-genetic-test-at-birth/comment-page-1/#comment-9122

Is anyone aware of a technology that could select individual chromosomes for inclusion into an egg/sperm/early embryo?

Merely selecting amongst 10 embryos for the highest IQ PGS could increase IQ by 1 standard deviation. Using this same technique with more intense selection could perhaps increase intelligence by a few SD.

If one could independently select chromosomes with the most favorable characteristics (selection factor up to 1 in 10~23), then very extreme changes could result using a very low end technology.

Comments?

Note the differences in results for height using the below method (see supplement page 10 etc.) This research has found many fewer SNPs (2000 vs 22,000).

https://www.biorxiv.org/content/biorxiv/early/2017/09/27/194944.full.pdf

Post script.

Some of these same kinds of considerations may also be applicable to infectious diseases. Here is something I find intriguing.

Annu Rev Genomics Hum Genet. 2013;14:215-43. doi: 10.1146/annurev-genom-091212-153448. Epub 2013 May 29.
The genetic theory of infectious diseases: a brief history and selected illustrations.

Casanova JL1, Abel L.

I don’t really see any contradictions between what each of us has said. You bring in the additional question of prognosis – and it is certainly crucial for therapy. I would simply say that the rare vs complex distinction is probably also valid here and that prognosis in the case of complex diseases (many contributing genes) will also remain highly ambiguous and very difficult to ever define clearly purely from gene patterns. As for this statement,

And it’s also rather naive to expect that a genetic explanation of a disease which provided information about the pathways involved would actually turn directly into a treatment. There is a huge leap from one to the other. We have known for some time that certain genes have a significant impact on breast cancer. Do we have a cure yet?

my argument is that for complex diseases it is only when we understand the functional networks that therapy and prognosis will advance strongly. To put this in a slightly different way, maybe we should regard diseases such as cancer as a chronic, semi-stable state in a response landscape that does not react to its environment in the “normal” way (related to some of Weinstein´s suggestions). We then need to understand such states and the transtions to/from these states (which might have many pathways) to make medical progress. Given the different genetic backgrounds of individuals, these states/pathways may show some variation, but presumably disease phenotypes reflect some common underlying features at the systems biology level.

We probably have some common ground when you say this:

It’s just not in any way certain that it’s more genetic information we need to create cures for cancer. The cures, if any, may well come from very different sources.

How useful do you think it is to read “Reckoning with Risk” if I have already read Gigerenzer’s “Calculated risks : how to know when numbers deceive you” and “Gut Feelings”? I have the sense “Calculated risks” overlaps a fair bit with “Reckoning with Risk.”

I think an earlier recommendation of yours (dearieme) might have been part of what motivated me to read one or both of those. Thanks!

You seem to have failed even to understand the point I was making.

With regard to many major diseases, a key medical question is, how many individuals must have a procedure performed to prevent one additional bad outcome?

https://en.wikipedia.org/wiki/Number_needed_to_treat

With regard to prostate cancer, for example, that question arises in the following context (among others): how many individuals with a finding of prostate cancer of a given Gleason score should have their prostates removed? The “safe” thing, of course, is to have them removed in all such findings — but the removal of the prostate is a significant step for a man, not to be undertaken lightly. And, since with the lower Gleason scores, the probability of aggressive cancer is relatively low — perhaps in the lower single digits in many cases — removing all those prostates will be unnecessary in perhaps 95+% of the cases.

This is the reality of the treatment of prostate cancer today.

What would make all the difference? A more accurate estimation of the likelihood that an individual with a finding of a given Gleason score will in fact develop aggressive cancer.

And that is precisely what a genetic prediction, of the sort we see in this paper, might be able to provide us.

The same kind of issue arises in breast cancer, and in many other kinds of diseases. Prediction is more than half of the game.

And it’s also rather naive to expect that a genetic explanation of a disease which provided information about the pathways involved would actually turn directly into a treatment. There is a huge leap from one to the other. We have known for some time that certain genes have a significant impact on breast cancer. Do we have a cure yet?

It’s just not in any way certain that it’s more genetic information we need to create cures for cancer. The cures, if any, may well come from very different sources.

‘Gerd Gigerenzer “Reckoning with riskâ€� is a great read on this topic.’

It’s a tremendous read on many topics. It’s my Book of the Decade for whichever decade I bought it in.

Fair enough.

I disagree. What is it that you propose to screen for? See my answer to candid_observer at #28.

The distinction is the “rare” vs. “complex” disease conundrum again. When the “necessary and sufficient” genes are a handful, finding therapies (even pre-birth genetic modifications) is plausible. When hundreds or thousands of genes contribute to some kind of disease, then a single measure like “propensity to suffer” this disease can be constructed with hundreds if not thousands of different combinations of genes if the statistics of the gene identification was correct. What is it that you then want to monitor as an indicator of disease occurence/progression (the inheritable genes are not changing)? If you then have a reliable indicator of disease, but this involves hundreds of genes (i.e. things like 2 to the power of 100 for just two variants of each gene), what are the chances that some sort of therapy for the particular gene-set of a particular patient is already known? What kind of patient sample sizes will be required to test/verify such therapies for the different patients and how will these be obtained?

The sheer intractability that seems now to be increasingly revealed from GWAS of complex diseases suggests that only the “rare” diseases will really be helped by current GWAS approaches.

The most recent version of this paper at biorxiv: https://www.biorxiv.org/content/early/2017/09/19/190124
has a list of blog posts referencing the paper (including this one).

I am still going through that, but one thing I recommend is taking a look at Rick Hyatt’s comments at: http://marginalrevolution.com/marginalrevolution/2017/09/accurate-genomic-prediction-human-height.html

One of those comments references this paper: https://www.biorxiv.org/content/early/2017/07/07/160291.1
which looks at intelligence and uses a relatively new technique named MTAG (Multi-Trait Analysis of Genome-wide association). I wonder if that will prove generally useful.

Razib has a brief post at: https://gnxp.nofe.me/2017/09/18/release-the-uk-biobank-the-prediction-of-height-edition/
but it contains more enthusiasm than content (am I projecting? ; )

Agreed and well said. Prostate cancer is my go to example in this area (it is actually what I was thinking about when writing my earlier comment, notice the screening intervals–for PSA ; ) because of both the reasons you mention and because screening is currently controversial in the US–primarily for the reasons you describe. Also because there is significant literature in this area and because the controversy seems relatively balanced I think there has been a decent effort to develop good quantitative evidence and arguments.

A better defined hierarchy of screenings and treatments for prostate cancer would be a valuable addition to medicine. Especially if it could be informed by genetic knowledge.

I think it worth expanding on your (I think implicit) point that it is worth looking at the genetics of prostate cancer virulence separately from the genetics of prostate cancer incidence.

P.S. re: screening intervals: https://www.ncbi.nlm.nih.gov/pubmed/21948815

res, looming large for me is the implications of the current research on those born recently or will soon be born. What changes in the environment will be made to help them be more adaptive citizens?

For example, we might not be far away now from genetic predictors of IQ, EA and other behavioral traits. Will we soon start a genetic based streaming program even at very young ages?

With schizophrenia, what might happen if one were able to disentangle the cognitive impairment from the other symptoms? Might the illness then transform (as the title of the book you noted suggest) into a new way of being without the debilitating consequences as occurs today?

This goes beyond painful investigations. A number of radical procedures depend on estimations of potential aggressive cancer.

Prostate cancer is a good example. The evidence is that a very high proportion of men over, say, age 65 have prostate cancer — perhaps over 50%. This may well show up on a biopsy. But in the vast majority of cases, that cancer is not going to be aggressive, and will simply stay at a low, relatively passive level for perhaps decades.

Question is, do you remove the prostate if you find cancer in a biopsy? There are complicated and disputed protocols used to make this decision. Anything that could add to the reliable prediction of whether the cancer will turn aggressive would be a huge boon, saving lives on the one hand, and unnecessary radical procedures on the other. Obviously further good information from genetics could go a great distance in doing this.

Similar points would apply to breast cancer, of course. And treatment of other cancers and other diseases would likewise profit from such insight.

More targeted screening could be an advantage in a number of dimensions:
– Cost control of screening. That might not be binary (say screen high risk every 2 years, low risk every 5).
– Potentially better screening effectiveness because of higher disease base rates in the population identified. I think this one could be a big deal, but don’t have any idea of the numbers.
– If false positives decrease relative to true positives (previous), net treatment outcomes would probably improve. Would also improve cost control of treatment.
Any more ideas?

Also related:
– At risk individuals might have more incentive to take preemptive measures like modifying their diets.

As you note the potential ability to make connections like disease genetics -> relevant tissues or metabolic pathways -> more targeted drugs
could be valuable.

This could be especially useful for something like schizophrenia which I think is believed to have a number of possible causative factors and to be something of a “group of syndromes with similar symptoms.” I think there is a high likelihood of more targeted drugs being a big improvement there. I would be interested in hearing the thoughts of someone more expert on schizophrenia about this.

Understood. I respect your judgment and discretion.

I find this line of criticism baffling.

Look, if we can predict diseases, with at least some level of accuracy, that can very often be medically useful in and of itself. Suppose we can predict with some reliability someone’s tendency toward colon cancer, or prostate cancer, based on their genes — predictions that would otherwise be impossible. Then we could carefully monitor such cases, and perform diagnostic procedures only on such cases, sparing those with very low susceptibility. It’s entirely possible that a great range of diseases will fall under this rubric, including many forms of cancer.

And of course from a scientific point of view it is often very important to establish that a trait is genetic, and to what degree, especially when the other methods (such as twin studies) are, or are at least are thought to be, methodologically problematic.

Doctor Thompson, I was considering more what happens when there is a large scale genetic database that is ready to be analyzed, such as the UKB. The theory for linear Lasso CS was published 4 years ago. The UKB uploaded results in July and here we are in September already with the first round of results.

I will be especially interested to see how long it will take to recycle the current output back into the UKB. For example, the non-linear analysis and then perhaps additional iterations. The theoretical work has already been done, how long will be required for successive steps of data feedback to occur? All that is needed is to let the supercomputer crunch the numbers. The computing time
is probably minimal. The bureaucratic obstacles are likely much more daunting.

If the UKB database would allow a more open access approach to analysis of the data, then results
could occur almost instantly. The data itself could remain behind a firewall.

res, did you notice that the gigascience article almost entirely neglected to talk about compound heterogeneity? The recent GCDH article had large interction terms for CH. The biggest
interaction was almost largest than the biggest SNP. The giga article focused almost exclusively on epistasis.

I have been worried about the computational explosion that would occur with non-linear terms, though this does not seem to apply. If you extract all the linear SNPs in the first round, then the non-linear interactions especially for the CH ones could be quite modest. {The CH interactions only happen within a given gene. Thus, there might be a high degree of scarcity of such interactions.}

Something that I am puzzling over is how the phase 2 phase boundary might change due to the information derived from step 1. If you eliminate nearly all the noise from the zero SNPs with Lasso
in Step 1 i.e. remove all the red area in the phase diagram, then what would the phase boundary look like in Step 2? Would you then have a firmer boundary?

That is interesting. Have they offered any thoughts on which parts take the most time? Is it mostly HIPAA (or equivalent non-US requirements) compliance?

P.S. Re: MMSE, I don’t have any real knowledge there, but sounds plausible.

res, could use MMSE score to quantitize dementia.
An MMSE GWAS?

Turning a disease into a quantifiable trait might greatly amplify the power of the CS L1 Lasso: you might move n from 100 s back down to 30 s while also benefiting from diseases having fewer non-zero SNPs. infoproc suggested 1000 SNPs for diseases versus perhaps 10,000-40,000 SNPs for traits.

I am sure many in the data processing community must be extremely frustrated by all the data sharing barriers that stand in the way to getting the job done.

If they were to open up access to these data servers there would be a truly massive analysis frenzy. How long will we have to wait for the GCHD for height? Days? Months? Years?

This research is critically important for anyone coping with an inherited illness or concerned about IQ or income inequality .. everyone. It is profoundly immoral for this research to be deliberated hindered.

This could be done in less than a day if there were no barriers. Why don’t they simply open up access to running analysis while keeping the data secure? They could make it a black box in which only the processed results were returned. This could be done on an open sharing basis.

The scientific literature could move from pretty prose to large scale data drops that could then be fed back into the servers for further analysis.

We are still far away from achieving truly open science. There would be this enormous leap forward if the data bureaucrats actually allowed scientists to do their jobs without obstruction.

This might make AD more similar to quantitative traits such as height than a disease.

I think there are many diseases/conditions that share this similarity. See the Liability, Threshold Model: http://www.wikilectures.eu/index.php/Genetic_Liability,_Threshold_Model.

The issue is to a large degree the diagnoses are binary though there are exceptions where status is given a quantitative measurement. As you note, age of onset might be useful in general.

P.S. Didn’t really say much new here. More expressing agreement.

res, I think the infoproc site is very descriptive in calling diseases 1-bit sensing.
As you mentioned quantitative traits such as height gives usable information from each
person in the sample to apply to the betas. The problem with diseases is that typically you
have the disease or you don’t. Some risk threshold needs to be crossed before a disease manifest.

I am not completely sure whether the above thinking would necessarily apply in a typical way to Alzheimer’s. By age 90 everyone has Alzheimer pathology. So with AD it is not so much having or not having dementia that is centrally important, but when such impairment emerges. This might make AD more similar to quantitative traits such as height than a disease.

“Out of sample� testing is nothing particularly new.

Of course. But I do think it is the gold standard of validation. Implementing it can be hard (see the contortions involved in reconciling the data sets described in the paper), and for that reason I think even publishing results for it is a good indicator of how seriously the authors take verifying their results. Seeing good out-of-sample results is even better.

I would contend that we need other kinds of measurements (loosely described as highly parallel conventional biology of massive numbers of genes/proteins) rather than ever more GWAS of the present types.

I don’t think the two approaches are exclusive. I agree that integrating new genetic results into the systems biology hierarchy (from rate constants on enzyme reactions to cells to tissues to organisms) is important and should prove to be valuable over time.

Oh, I am in favor of more research, even of more GWAS type studies for “rare” diseases. BUT, I don’t expect that more GWAS is going to be very productive for many medical situations (or complex traits like IQ). Fortunately, it is now sufficiently cheap that we don’t need massive resources for GWAS measurements (access to patients is probably the main bottleneck?) and can increasingly devote resources to other research approaches. I think what I replied to res will give you an idea what I mean:

GWAS style approaches have been spectacularly successful for “rare� diseases because the “necessary and sufficient� criterion involves only a very limited number of genes. I think that by now it is becoming ever clearer that there are many “complex� traits/diseases where simply measuring ever larger cohort sizes is not going to get us much further. As you suggest, “systems biology� in the sense that genes “co-function� in achieving biological states is probably where this has to go. BUT, I would contend that we need other kinds of measurements (loosely described as highly parallel conventional biology of massive numbers of genes/proteins) rather than ever more GWAS of the present types. Just as development of the technology for GWAS was necessary, now we need to concentrate on developing new kinds of technology that measure other things.

“Out of sample” testing is nothing particularly new. In a sense every “parallel” case of different research groups performing “gwas” for the same disease on different data sets is “out of sample” testing. What you like to extol as “out of sample” testing might instead be regarded as the usual scientific requirement that the result can be reproduced by others with independent data collection – as you noted.

GWAS style approaches have been spectacularly successful for “rare” diseases because the “necessary and sufficient” criterion involves only a very limited number of genes. I think that by now it is becoming ever clearer that there are many “complex” traits/diseases where simply measuring ever larger cohort sizes is not going to get us much further. As you suggest, “systems biology” in the sense that genes “co-function” in achieving biological states is probably where this has to go. BUT, I would contend that we need other kinds of measurements (loosely described as highly parallel conventional biology of massive numbers of genes/proteins) rather than ever more GWAS of the present types. Just as development of the technology for GWAS was necessary, now we need to concentrate on developing new kinds of technology that measure other things.

Do we have any sense of how many haploblocks these 20k SNPs represent? Do you have a reference for the number of haploblocks in the European population? Has anyone tried making a haploblock based predictor for height?

I just looked for references to haploblocks and most of what I am seeing is a decade or more old. Given that we know so much more about genetic structure across populations now I am not sure how much to value old references.

One thing I don’t know how to evaluate is how likely CS is to get to actual causal SNPs. In a traditional GWAS there tend to be multiple nearby (in LD disequilibrium) high significance SNPs. I think the CS pressure towards sparseness would help select only one of those SNPs, but is it causal or is it (as you discuss) only representative of a haplotype?

My recollection of my time spent learning about and using L1-regularization was that there were some issues with enforced sparseness at different levels of penalization, especially with correlated variables. I don’t know whether or not that relates to a CS complete solution.

But in this interesting discussion some seemingly informed people don’t think that is a big deal: https://stats.stackexchange.com/questions/30486/when-does-lasso-select-correlated-predictors

P.S. The caption to Figure 5 does offer some support for what you are saying: “Activated SNPs are distributed roughly uniformly throughout the genome.”

P.P.S. One thing I did not pick up on initially was this from the very end of the conclusion:

For case-control data, we find n ∼ 100s (where n means number of cases with equal number controls) is sufficient. Thus, using our methods, analysis of ∼ 100k cases together with a similar number of controls might allow good prediction of highly heritable disease risk, even if the genetic architecture is complex and depends on a thousand or more genetic variants.

I wonder if they are still thinking about those high-IQ case control studies? Or is this more about disease?

It seems odd to me that the necessary sample size for case-control data is ~3x that of broad population data (n ∼ 30s). I would have expected the case-control methodology to be more powerful as suggested by that recent IQ meta-study. Perhaps the relatively low power has to do with looking at fundamentally different problems (e.g. low prevalence disease rather than quantitative traits)?

In my opinion, the talk about SNPs is a bit misleading in this context.
20 000 SNPs is in the same order of magnitude that the number of haploblocks in European population. So they more or less capture the total genetic variability of the population into the model and use it to predict phenotype. It is interesting and certainly useful approach, for example to predict disease risks. But moving from such model to biological explanations – i.e. finding genes that should be manipulated to cure certain symptoms, is a long way.

To “predict� a single simple phenotype such as height, the authors use about 10,000 variables (for a sample size of only 500,000). It seems strange that the authors seem never to tell us how many genes are represented by those 10,000 SNPs

First, do you understand what out of sample testing is? A related technique is described by Dr. Thompson above but not using those words:

the underlying approach is to use large samples of the data to train the learning procedure, and then test the results on samples of 5,000 genotypes which had been held apart for that purpose. In my primitive terms, the sample of discovery is used to generate the best predictor, warts and all, and that is tested on the sample of proof. I like this, because it is pragmatic, not burdened by too many prior assumptions about genes, uses all the data to advantage, and is willing to include weak signals.

I believe this excerpt shows that there were two different techniques being used (i.e. Figure 3 was held out UKBB data as described by Dr. Thompson rather than ARIC data):

Figure (3) shows the correlation between predicted and actual phenotypes in a validation set of 5000 individuals not used in the training optimization described in above – this is shown both for height and heel bone mineral density.

The paper abstract says: “We also use other datasets and SNPs found in earlier GWAS for out-of-sample validation of our results.”

Note that this is even more rigorous than Dr. Thompson described (the distinction is using a completely separate dataset (ARIC) for validation rather than a held out subset of the primary dataset (UKBB), I suspect he simplified for explanatory purposes). Here is a more detailed explanation from the paper:

For height we tested out-of-sample validity by building a predictor model using SNPs whose state is available for both UKBB individuals (via imputation) and on Atherosclerosis Risk in Communities Study (ARIC) [18] individuals (the latter is a US sample). This SNP set differs from the one used above, and is somewhat more restricted due to the different genotyping arrays used by UKBB and ARIC. Training was done on UKBB data and out-of-sample validity tested on ARIC data. A ∼5% decrease in maximum correlation results from the restriction of SNPs and limitations of imputation: the correlation fell to ∼0.58 (from 0.61) while testing within the UKBB. On ARIC participants the correlation drops further by ∼7%, with a maximum correlation of ∼0.54. Only this latter decrease in predictive power is really due to out-of-sample effects. It is plausible that if ARIC participants
were genotyped on the same array as the UKBB training set there would only be a ∼7% difference in predictor performance. An ARIC scatterplot analogous to Figure (4) is shown in the Supplement. Most ARIC individuals have actual height within 4 cm or less of predicted height.

and

For out-of-sample validation of height, we extracted SNPs which survived the prior quality control measures, and are also present in a second dataset from the Atherosclerosis Risk in Communities Study (ARIC) [18]. This resulted in a total of 632,155 SNPs and 464,192 samples.

More on out-of-sample testing at http://ec.europa.eu/eurostat/statistics-explained/index.php/Glossary:In-sample_vs._out-of-sample_forecasts

I believe out-of-sample testing on a completely separate data set can be considered the gold standard of verification by the original researchers. Even better is having a separate group do that with more data sets. Hopefully that will also happen.

Regarding your genes point, I agree that is disappointing. The authors did not dig into the biology much. The 2014 height GWAS I linked in another thread: http://neurogenetics.qimrberghofer.edu.au/papers/Wood2014NatGenet.pdf
IMHO serves as a good model for some possible analyses to perform. Hopefully some hard core systems biologists will join the existing collaboration. One notable characteristic of the recent paper is just how few authors there are compared to many current GWAS papers.

Sorry, rats not mice.

Amino Acids. 2010 May;38(5):1561-9. doi: 10.1007/s00726-009-0369-x. Epub 2009 Nov 5.
Evidence for the involvement of D-aspartic acid in learning and memory of rat.
Topo E, Soricelli A, Di Maio A, D’Aniello E, Di Fiore MM, D’Aniello A.
Abstract
D-Aspartic acid (D-Asp) is an endogenous amino acid present in neuroendocrine systems. Here, we report evidence that D-Asp in the rat is involved in learning and memory processes. Oral administration of sodium D-aspartate (40 mM) for 12-16 days improved the rats’ cognitive capability to find a hidden platform in the Morris water maze system. Two sessions per day for three consecutive days were performed in two groups of 12 rats. One group was treated with Na-D-aspartate and the other with control. A significant increase in the cognitive effect was observed in the treated group compared to controls (two-way ANOVA with repeated measurements: F ((2, 105)) = 57.29; P value < 0.001). Five further sessions of repeated training, involving a change in platform location, also displayed a significant treatment effect [F ((2, 84)) = 27.62; P value < 0.001]. In the hippocampus of treated rats, D-Asp increased by about 2.7-fold compared to controls (82.5 +/- 10.0 vs. the 30.6 +/- 5.4 ng/g tissue; P < 0.0001). Moreover, 20 randomly selected rats possessing relatively high endogenous concentrations of D-Asp in the hippocampus were much faster in reaching the hidden platform, an event suggesting that their enhanced cognitive capability was functionally related to the high levels of D-Asp. The correlation coefficient calculated in the 20 rats was R = -0.916 with a df of 18; P < 0.001. In conclusion, this study provides corroborating evidence that D-aspartic acid plays an important role in the modulation of learning and memory.

Genes tell the body to make more or less of specific molecules. Figure out what those molecules are and you can “hack” intelligence without DNA changes. For instance, mice either 1) given aspartic acid or 2) who had higher endogenous (i.e., naturally occurring due most likely to genetics) aspartic acid in their brains had better working memory. (Interestingly for those looking at intelligence in populations, East Asians and seafood consumers appear to be the ones getting the highest aspartic acid in their diets).

“Is there any real medical utility to knowing that several thousand genes may influence whether any given patient has been susceptible since birth to “inheritedâ€� Alzheimers? Is it likely that knowing several thousand genes may have (mostly very small) contributions to Alzheimers will help in producing therapies?”

Yeah, why bother doing research if you have the magical ability to tell in advance that it can’t do any good?

Still not very convincing and not very useful.

To “predict” a single simple phenotype such as height, the authors use about 10,000 variables (for a sample size of only 500,000). It seems strange that the authors seem never to tell us how many genes are represented by those 10,000 SNPs, but Fig. 5 does seem to show that they are (randomly?) distributed across most of the genome, i.e. the number of genes is presumably also in the many thousands.

Lets give the authors the benefit of the doubt and imagine that this “success” applies to a complex disease such as Alzheimers (as they suggest). Is there any real medical utility to knowing that several thousand genes may influence whether any given patient has been susceptible since birth to “inherited” Alzheimers? Is it likely that knowing several thousand genes may have (mostly very small) contributions to Alzheimers will help in producing therapies?

Finally, isn’t this kind of “analysis” actually subject to many unverified assumptions? For example, assume that “nurture” does have a significant role in adult height (highly likely since humans have NOT been mutating fast enough to produce the substantial increases in height observed over the last few generations). This would mean that the whole analysis set (500,000) is distorted by unknown and uncontrolled factors.

This article seems to be another nail in the coffin of present GWAS-style approaches.

My suspicion regarding male interest in female homosexuality is that it’s at least partially rooted in an aversion to male homosexuality. It allows men to watch female sexuality without having to watch another man.

Crap. I just realized that you said you don’t want any more comments on male homosexuality. My bad.

This was from your Twitter in relation to the Guardian article on ‘Born that Way’:

http://www.ncbi.nlm.nih.gov/pubmed/10743878

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=9625997&fulltextType=RA&fileId=S0033291714002451

This is the newest one that points Xq28 as the cause for same-sex attraction in men.

http://www.ncbi.nlm.nih.gov/pubmed/7581447?dopt=Abstract

What I noticed in that Guardian article is that, for one, most of the studies were old or had conflicting results, and the newest one, from May, measures only 900 gay men.

It reminds me of a gay scientist that was overjoyed with the ‘presence’ of a gay gene, yet he said that they hadn’t actually found it yet. He said that they needed more money. I wouldn’t say science for the gay gene is ‘on the right track’. Hell, they dropped it in 2005 and again in 2009.

I have a hard time believing that such a dangerous and unhealthy lifestyle could be /that/ heritable. Homophobia is more present than homosexuality. Obviously, one is celebrated, the other condemned.

Thoughts?

Might this big news also have relevance to atypical orientations, pathogens, immune responses?

http://neurosciencenews.com/lymphatic-system-brain-neurobiology-2080/

Conservatives are more r typed.

I remember reading something of yours about how liberals aren’t breeding but conservatives are.

Here is a questions for you.

Are SJW’s (social-justice warriors) breeding?

I probably should post this on a male homosexuality thread, but it’ll do here. You can pass it along to those who snicker at or are dismissive of the pathogen theory. Many such people claim we’d *know by now* if it were the result of a bug, many want an other-than-Cochran source. It’s not about homosexuality, but it’s a good, quick read for those who should be thinking about all kinds of behavioral outcomes caused by viruses.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782954/

“They found that both are highly heritable (primarily driven by additive genetic factors), but what’s more, high facial masculinity in men led to high facial masculinity in their sisters, decreasing these women’s attractiveness.”
thats probably the same mechanism which makes that men / women of some races are on average more or less attractive than men / women of other races

It’ll be interesting to see how those research programs address allegations of publication bias (etc.). Having said that, there was a recent response to various criticisms, including publication bias:

http://www.sscnet.ucla.edu/comm/haselton/unify_uploads/files/Gildersleeve,%20Haselton,%20Fales%20(2014)%20reply%20to%20Wood%20et%20al.,%20Harris%20et%20al.%20psych%20bull%20.pdf

Ever noticed how artists draw female villains? They are given long noses and chiseled features with long pointed jaws. Witches are a great example. Similarly male villains are often drawn with smaller jaws and more feminine features. The goatee is often worn as compensation for a weak chin and has become a short hand for evil. Humans have long known intuitively that we differ, that some men are less physical and more emotional and some women are less emotional and more physical. Of course it’s also natural that the more common forms treat their counter parts with contempt. Nothing is more predictable than the cerebral young male with a small chin, an even digit ratio and a burning hatred for those knuckle dragging philistines who pick on him. But I do wonder why the masculine females tend to blame men for their problems rather than the other girls who made them feel bad for not caring about makeup and getting a boyfriend.

The notion that male celebrities viewed as most attractive by women are particularly masculine is quite debatable. I just looked at one such list, and by my lights only a small number of the top 25 on the list seemed masculine (e.g., Hugh Jackman, George Clooney).

At any rate, there’s a lot of evidence that masculinized men with testosterone-laden bodily and facial features, and inter-sexually competitive, socially dominant personalities, become attractive to women in the fertile (follicular) phase of the menstrual cycle. This effect is strongest among women with boyfriends/husbands who are especially lacking in such masculine traits (what the manosphere guys would call ‘beta males’), and it dissipates or disappears completely when they are in their infertile, luteal phase, where they instead prefer more feminized, ‘good dad’/’good provider’ men. Also, more attractive women tend to be most attracted on average to masculine men throughout their ovulatory cycle.

These kinds of phenomena have the hallmarks of being a psychological adaptation in women, namely for selective sire choice (viz., good genes for offspring) in certain contexts. In other words, a strong case can be made that the systematic, multi-layered empirical patterns observed are best explained as the result of a cognitive adaptation in women. Granted, such fantasies about and desires for men with good genes traits should be put in proper context: it’s not to say that all women suddenly become obligate raging whores during their fertile window and seek out men with good genes for intercourse; this is more of an ‘at-the-margins’ phenomenon. And supposedly many factors play into the cost-benefit analysis of whether a particular woman actually ends up acting on those desires. Another thing to keep in mind is that, by hypothesis, less attractive women are less able to secure long-term commitment from good genes males; so such women might instead opt to secure commitment from a man of lesser genetic quality, then cuckold him and secure better genes via a dalliance with a man in possession of good genes.

The general empirical patterns have also been found in at least a couple of traditional small-scale societies – so it does not appear to be merely an artefact of the evolved human cognitive architecture interfacing with modern ‘WEIRD’ conditions.

This stuff is pretty well documented in the evolutionary psychology literature on mating.

A short overview can be found here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2394562/pdf/rspb20071425.pdf

This book is a longer, in-depth analysis:
https://global.oup.com/academic/product/the-evolutionary-biology-of-human-female-sexuality-9780195340990?cc=ca&lang=en&#038;

“Why are men regarded as being attractive also fairly masculine in appearance (I know people are can think of counter-examples like Bieber and Di Caprio)? Is it just a byproduct of higher testosterone, some kind of signal of fighting abilities”

Imagine a standing start where women were attracted to male traits on a purely random basis then the male traits that would be selected for would be those that led to higher reproduction and survival of the various females. So in a violent environment women randomly attracted to those male traits which signaled a high capacity for violence might have more surviving kids so attraction to those traits would spread.

If the environment changed and other traits began to confer that advantage then over time women attracted to those other traits would be selected for instead so the weighted basket of traits that women were attracted to would change over time with the environment e.g. from being attracted to 80% thug to only being attracted to 20% thug.

Say there were two broad categories of sexual attraction 1) visual and 2) behavioral and they were weighted differently between men and women such that

men: 2/3 visual, 1/3 behavioral
woman: 1/3 visual, 2/3 behavioral

then something that only effected the visual component would have a differential effect, for the sake of argument say

men: 2/3 gay, 1/3 bisexual
women: 1/3 lesbian, 2/3 bisexual

(and vice versa for the behavioral component)

if there were two components (visual and behavioral) and they could be misaligned independently the four categories created would be

visually female, behaviorally female
visually female, behaviorally male
visually male, behaviorally female
visually male, behaviorally male

what ever real fighting experience you think you have is not real. I know guys like you, all talk. Real guys don’t talk about this stuff. It’s the equivalent of announcing you have a huge rooster.

More projection. You are simply ignorant and lack experience and falling back on “I’m a real fighter” internet bravado.

Real professionals will analyze what works and what does not in a dispassionate manner and avoid sweeping generalizations.

You know how I know I’ve been in real fights? Of all the brawls I had growing up, about half the time I caught beatings. And in most of those cases, it was several black kids stomping me while I was in fetal position (after I tagged the first one or two and then was mobbed). If you get into enough real fights, that will happen.

You wrote:

I’ve only been roundhoused once in the face while sparring and tkd was not part of my opponent’s training.

People who utter things like this, on the other hand, have not been in enough fights. I’ve been knocked down by in all manners of ways (punches, kicks, 2�4, baseball bat, plumbing pipe). If you fight enough, you get beaten with everything. I’ve also been stabbed. Not fun at all.

You are either a fighter or you’re not. Training will not make a non fighter a fighter

I generally avoid cursing, but that is a crock of shit.

Gene Yu, former Green Beret captain with multiple combat tours, talks about how he was not a “natural fighter” and got knocked out in his first West Point PE boxing class (he spent the next two days at a hospital) and developed a fear of getting his ass kicked. In an effort to overcome this, he took boxing classes at the AKA (he’s from Cupertino) from a serious professional trainer who taped him and analyzed his techniques for him, and also had him spar serious boxers. Yu went on to become a fearsome boxer and became the West Point intramural champion and earned a starting spot on the West Point varsity boxing team (which features some of the top amateur boxers in the country) and went on to dominate his opponents until an elbow injury ended his amateur boxing career.

Captain Yu also talks about how untrained vs. trained men behave in battle. His view is that there is no such thing as “tough” vs. “not tough” or fighter vs. non-fighter. There is only the difference between properly trained and untrained. Properly trained men do not fear combat, because they know what they are capable of and what they can do. Untrained men panic at the first adversity, because they do not know what to do and become mentally paralyzed.

Bas Rutten, a noted MMA champion and trainer, talks about how to train “normal” folks who fear getting hit and turn them into MMA fighters – he has them stand with their backs to the wall (so they can’t retreat) and start with 10-20% strength punches and get them used to not flinching and closing their eyes when they face a barrage of punches. Gradually, Rutten increases the intensity of the strikes. After a while, most of the trainees stop flinching at the full-strength punches. You do not fear what you know. That’s what proper training does for you.

Michael said, “It just means human sexual attraction is complex and it is easy for nature to ‘get it wrong’ — unlike insects that use pheromones.”

Sounds as if you haven’t been following the decades’ worth of work on mice and olfaction.

@ Staffan

Most of them were pretty chiseled at one point or another except for Johnny Depp (arguably) and Jude Law.

Don’t need luck. Manners, don’t need those either. I’d feel sorry for you if I could feel anything. Ignorance is bliss for buds like you.
The question is not silly. In a hand to hand fight with no rules who would win all other things being equal: fighter using more combative techniques such as muay Thai or more sports oriented techniques such as tkd?

Styles don’t matter but the fighter and his training. You are either a fighter or you’re not. Training will not make a non fighter a fighter just like taking art classes will not make a person an artist. If the training does not consist of practical combative techniques than the fighter is at gross disadvantage. Is that clear? Consequently you may have been in combat overseas and taken martial arts classes but you’re not a fighter. How do I know?

what ever real fighting experience you think you have is not real. I know guys like you, all talk. Real guys don’t talk about this stuff. It’s the equivalent of announcing you have a huge rooster.

You’re deluded if you think you can keep protect yourself from a trained fighter. Pray that righteous men are stronger than evil men. That’s the only thing that keeps society safe in practical terms. All your attempts at self defense training are just attempts to maintain the illusion of control over the ability of others to hurt you.

Yes, no one knows what the relevant changes are. But we have a pretty good idea of what the relevant changes are NOT.

Macronutrient consumption in Americans has remained relatively stable over the past 100 years. So it isn’t sugar, and it isn’t carbs, and it isn’t fat. Processed food has been a staple in the Western diet since the late 19th century.

We have no evidence that peer groups have an effect. Oh but we do. We just don’t have any solid scientific evidence, probably because of lack of interest. Absence of evidence isn’t….you know.

While the following points do not have solid research backing them up, that is no reason to discount them. Indeed I await the day when research is done to support these points. Anecdotal evidence function as leads for research.

1) Asians who come to America complain about becoming fatter. They may not converge with white American norms, but they become fatter. They have even coined a term for this – its become expected. 3rd generation Asian Americans do NOT perfectly share a common culture with American whites (the “tiger mother” thing should make this sufficiently clear) and ARE fatter than Asians in Asia even if not as fat as white Americans.

2) Europeans who come to America complain about becoming fatter. This is particularly true of the French, but all Europeans experience this. I have been the the Ukraine – Ukrainian immigrants to America are significantly fatter.

3) Without any big change in diet or eating habits, Americans became after only after the 1970s. Social values changed dramatically at exactly this time. Why social values changed at this time we don’t know, but to dis-claim any link between the two phenomena, in the absence of any serious change in dietary habits or the food environment, seems like willful closing of one’s eyes. Moreover, the nature of the change in social values seems calculated to promote weight gain – the change was all in the direction of loosening of standards and discipline, and a shift away from judgementalism and shaming. In the absence of a society-wide return to judgementalism, isolated cases of fat-shaming are unlikely to have any effect.

4) My personal experience. I grew up thin outside of America, and have been fat in America from age 12 till 22. I accepted it as fate. At 22 I moved to East Asia and spent the following decade there and in Europe. Within 6 months of arriving in Asia I lost about 30 pounds. I remember exactly my thought process – I was deeply unsettled by the contrast between my body and everyone else’s. It bothered me. A lot.

5) I returned to America and settled in suburban California, where everyone was overweight. Within 6 months I had gained 20 pounds and stayed that way for 2 years despite efforts to reverse it. After that, I moved to New York, where people are much thinner and dress much better, and I joined social circles where the expectation to be thin and well dressed was the default. Within 6 months I had lost 30 pounds.

Its pretty conclusive to me, personally, that fatness is social and depends on peer group.

I agree with you that America being what it is, it is impossible for most people to lose weight by dieting. I know that if I myself moved to the suburbs I would probably gain weight. A person can lose weight if he has a strong motivation for doing so – i.e the pleasure of being thin outweighs the pleasure of eating – but currently most American social environments don’t provide this motivation. However, when the motivation is there, being thin is almost effortless. One can’t change one’s social circle just to lose weight, but if it happens, most people will almost effortlessly find the motivation to do so.

Its a simple hedonic calculation – if the displeasure of being fat outweigh the pleasures of eating food, you’ll lose weight. Only certain social environments can make being fat worse than the pleasure of food.

One would think health warnings might do the trick, but for most people it seems to be inadequate. Possible health effects in the distant future seem not to outweigh the pleasure of food here and now. But social effects right now seem capable of doing so.

“…most of the male celebrities considered most attractive by females (adult ones at least) have stereotypically chiseled jaws and muscled physiques.”

http://www.people.com/people/package/gallery/0,,20315920_20154495,00.html#30229116

Suppose we were studying female left-hander-sexual behaviour (females who have had sex with someone who is left handed). If we looked at a table of their number of sexual partners we would notice that they were quite promiscuous. For example, we would expect that females with 2 lifetime sexual partners would be a little less than twice as likely to have had a left-hander-sexual experience than those with 1 lifetime sexual partner.

To what extent does the apparent promiscuity of females who have had sex with females reflect a similar, more hits on random humans therefore more likely to hit (on) a female, situation.

http://www.genengnews.com/gen-news-highlights/brain-gender-altered-by-lifting-epigenetic-repression/81251103/

http://medicalxpress.com/news/2015-03-female-mammalian-phenotype-results-repression.html

Jayman, we’ve known for several years that the rodent brain has two functional circuits, male/female, and that pheromonal cues are processed differently by the female and male brains, resulting in all kinds of different behaviors, all the way from parental behaviors to reproductive behaviors but not until recently have we understood how the brain became either female or male.

The latest research is pretty exciting. The male-female differentiation of the pre-optic area doesn’t take place as early as was once thought. In fact, it happens pretty late in gestation, perinatally, and evidently continues post-natally as well. The area is heavily methlylated in the undifferentiated POA until a hormone release from the gonads masculinizes the male brain by removing the methyl groups from many genes, allowing expression resulting in typical male reproductive behaviors. Repressing this unsilencing maintains the default female brain.

Perhaps this gets us closer to understanding how male homosexuality (and even female homosexuality) might come about. Maybe it can even explain why some male homosexuals are so much more effeminate than others, with a low number of unsilenced genes resulting in a less feminine gay male and a high number of unsilenced genes resulting in a more effeminate gay male.

Especially interesting to me in light of our many discussions of the likelihood of a pathogenic cause is the following observation by the research team:

“Intriguingly, the latest study also found that inflammatory immune cells known as microglia appear to play a role in masculinization, in part through their production of prostaglandins, a neurochemical normally associated with illness. In recent years, scientists have increasingly realized that the immune system is integral to the development of the brain;”

Very interesting. (Isn’t it also true that the male immune system is not quite as effective as the female’s? Perhaps that explains the higher prevalence of male homosexuality.)

Scientists have conducted experiments with serotonin receptor-knockout mice. If I recall correctly they became hypersexual and indiscriminately mounted other mice of both sexes. I don’t whether such a mechanism has any bearing on bisexuality in humans, female or male. But I do wonder whether there is some kind of link between bisexuality and hypersexuality, promiscuity, and very high sex drive in humans.

More masculine women => higher sex drives => being less picky
or
More masculine women => higher sex drive and attraction to females ?

Socially, “bisexual” may be a more acceptable way of signalling or thinking about “promiscuous”.

I recall from my college days a great deal of anger directed by “true lesbians” and “true bisexuals” against “cuddle girls” and the like who “claim” to be gay or bi in social situations in order to pick up men. There were even accusations of “cultural appropriation”–yes, of “straights appropriating gay culture”, to which I very confusedly responded that I thought gay was an orientation, not a culture. The ultimate irony was that the “true lesbians” and “true bisexuals” making these claims were themselves primarily engaged in hetero-relationships during the time I knew them.

As someone who has only ever had two significant relationships in her life, the idea of trying to suss out such tiny variations in attraction seems rather pointless.

Being left-handed has very little impact on the number of children one has.

Being unattracted to the opposite sex can have a big impact on the number of children one has.

Ergo, one of these things is likely to be strongly selected against.

Looking at the data, it looks like SSA is just a side effect of promiscuity. Promiscuous people just aren’t all that picky.

Women who aren’t seeking out dozens of partners simply pick the partner they like best and stick with them. Such women might find other women just as attractive as “non-hetero” women do, but not bother mentioning it because they have no need for more partners.

“Doesn’t matter. The only way for them to be preserved in this scenario is a complete lack of additive effect (which is implausible). All such alleles would quickly go to zero over evolutionary time.”

Lots of genes have slight negative effects. They haven’t all vanished.

“The difference here is that long distance migration is inherently difficult and dangerous. F$, not so much. ”

A million articles on game blogs would beg to differ. These blogs would not exist if it were that easy.

Jayman — great to get you in real time!

“What do you think happens to any such genes that cause such malfunction in attraction in humans? Iterate it over time. ”

Obviously if there were just one gene or two genes involved, their rate of incidence would go toward zero quickly. On the other hand, if it is a complex behavior that involves many genes, this would not necessarily be so.

Failing to migrate is highly maladaptive and leads to death, nature can never completely select it out. Every generation, a substantial portion of birds screw it up.

“The low heritability and evolutionary contradiction of male homosexuality necessitates the pathogenic explanation. ”

Not true. It just means human sexual attraction is complex and it is easy for nature to ‘get it wrong’ — unlike insects that use pheromones.

If 10% of birds get confused and don’t migrate to where they are supposed to each year, it does not mean that there is a pathogen. It just means that migration has a high failure rate because it is a complex behavior. Lots of things can go wrong.

Ah, I’d read the discussion over at Cochran’s but failed to read your much more illuminating post and comments discussion. Interesting stuff.

Why does homosexuality have to be anything more than a variety of minor developmental errors that are inevitable with something as ludicrously complex as the human brain and sexual/reproductive behavior in particular? About 10% of people are left-handed and my understanding is that it’s pretty much just an error in development. Everyone is supposed to be right handed but sometimes something goes wrong. Can’t homosexuality be something similar? There’s fewer homosexuals than left-handers but then homosexuality is more harmful to your reproductive chances so there’d be selection to make it less common — but no amount of selection can completely eliminate simple developmental error, can it?

Great post Jayman, thanks. Good to have you back.

“A British survey (Mercer et al, 2013) finds that among the youngest cohorts of women (ages 16-34), as much as 19% claim to have sexual contact with another woman”

But according to that data, less than 50% of these actually involved ‘genital contact’. I would class those as the genuine lesbians. The rest might be just ‘bi-curious’, or might have kissed and fondled a female friend in a nightclub to attract some male attention?

Hey Jayman,

I have a newb question here. Why are men regarded as being attractive also fairly masculine in appearance (I know people are can think of counter-examples like Bieber and Di Caprio)? Is it just a byproduct of higher testosterone, some kind of signal of fighting abilities, or did masculine traits actively evolve through sexual selection? You claim in this post that masculine looks are mostly orthogonal to male attractiveness but this doesn’t make sense to me since most of the male celebrities considered most attractive by females (adult ones at least) have stereotypically chiseled jaws and muscled physiques.

WHOA! First on the first Jayman post in a long time.

Haven’t read it yet, but will do soon. Especially since it’s about lesbians, what a great topic.

Round house me or one in general?

Don’t get all worked up there, fellah. It was a generic statement – that there are some superb TKD practitioners who eat snakes and are all-around bad asses.

Styles matter when they pigeon hole practicality for showmanship.

I don’t now many serious martial artists who only train in one style, a tendency that has only grown since the explosion of MMA. All the men of the 707th Special Mission Bn of the ROK I worked with were trained in TKD, Judo, Hapkido, and military combatives.

Don’t get your Kim Chi (pun intended) in a bunch because tkd is sports and asthetically oriented versus Muay Thai or combative karate which though competitive is more practical. Ask your self this: if you pick a hundred random average Muay Thai fighters and put them against the same random amount of tkd dancers, who would win overall?

There is no such thing as “combative Karate.” There are several different major schools such as Shotokan (whence TKD originates), Kyokushin (founded by a ethnic Korean in Japan), Goju-Ryu, etc., all with different emphases and rules. Lately, I’ve become enamored with Shotokan (here is an excellent analytical piece about Shotokan’s strengths and weaknesses as it relates to MMA: http://fightland.vice.com/blog/lyoto-machida-the-double-edged-sword-of-competition-karate).

And I don’t do the juvenile, “my Kung Fu is stronger than your Kung Fu” routine. Even your question of “Muay Thai vs. TKD” is silly… mainly because you neglect the crucial element: under what rules? Or are we talking about a street fight or military urban combat? In the last case, the Black Berets would simply mow down the Muay Thai fighters with small arms fire and move on.

*ALL* martial arts are sports, with varying levels of restrictions and rules. Otherwise practitioners and competitors wouldn’t survive. And because these rules incentivize a given stylists’ training and practice, rules dictate “who wins.” MT boxers would lose to TKD folks under TKD rules. TKD people would be murdered by Thai boxers at Lumpini Stadium. As for who has done better in MMA, the records are mixed (notable TKD-based fighters include Chan Sung Jung, Anthony Pettis, and Benson Henderson, etc. and of course there are many who have incorporated Muay Thai techniques and training). But I do not know a single TKD or Muay Thai purist who has survived even the minor league-level promotions.

And of course because TKD is “practiced” by a far larger number of people than MT, people who train in the latter are more likely to be “hardcore” than the former *in general.* You can’t compare athletes doing BJJ and Muay Thai (as I have done in the past 15 years) with women and children doing their cardio-Karate routine at the nearest TKD McDojo.

As I wrote before, there are excellent techniques I learned from every system I have trained (e.g. knife and stick fighting in Kali – show me that Thai fighter and I’ll shank him about 20 times before he knew what struck him). From what little I trained in TKD, I learned quite a bit about non-telegraphed kicks, as another example. From Muay Thai, I learned much about elbows and knees in the clinch, generating power with cut kicks, etc., from Judo and Sambo, lots of throws and trip and arm locks, etc., from Aikido gun-retention and draw-prevention. You get the point.

Like many martial artistists you like to think that training in martial arts makes you able to fight because you studied the techniques.

I grew up brawling with blacks kids in NYC (who preyed on my white and Asian friends). I didn’t train in martial arts, boxing, and wrestling as an academic exercise.

As an adult, I’ve been in combat overseas. Although the military now stresses combatives to inculcate an aggressive “fighting spirit” and to teach some last ditch self-defense, unarmed techniques in general are of extremely low utility in real combat where infantrymen, armored vehicles, gunships, arty, and even improvised explosives clash. Heck, everyone carries sidearms, but the average GI now gets a tiny amount of pistol training because it’s not considered high priority (if the fight has gone to handguns, things have gone very, very wrong).

chinaman… You’re an irritable little man despite your height.

Judging from how prickly you’ve taken my rather mild critique and your utter lack of manners, I’d say “projection” about covers it.

Good luck to you.

Round house me or one in general? In a sucker punch situation or sparring? I’ve only been roundhoused once in the face while sparring and tkd was not part of my opponent’s training. Styles matter when they pigeon hole practicality for showmanship.

Fighting is fighting. Some styles or schools focus on fighting others focus on sport or asthetics. Don’t get your Kim Chi (pun intended) in a bunch because tkd is sports and asthetically oriented versus Muay Thai or combative karate which though competitive is more practical. Ask your self this: if you pick a hundred random average Muay Thai fighters and put them against the same random amount of tkd dancers, who would win overall? You know the answer. Why this fact upsets you I can guess. Like many martial artistists you like to think that training in martial arts makes you able to fight because you studied the techniques. Studying fighting techniques or basketball techniques does not make a good or competent fighter or player. One either has the latent ability and improves on that or lacks the ability and only improves their body mechanics.

You’re an irritable little man despite your height. I dont know if your roundhouse to the face comment was a cheap attempt at an insult but it seems like it. I don’t respond to insults. Threats are another story. Tell your tkd pals to go for the sucker punch unless their arms grew from their shoulders. That may give them a chance. I won’t react with more force than needed. Speed, strength, and real time reaction has taught me patience and mercy, and no one taught me speed, strength, the ability to think in real time. Those things fighters are gifted with and improve with training. one should be careful who they approach recklessly. There are no rules or referees in real combat.

Good day twink,

Rene de la bataille

6 foot 2?

The only two places I lived/visited where I felt short were Iowa and the Netherlands. But I am not the tallest East Asian I know, by far.

What combat sports do you practice tae kwon do, or something more practical like boxing or knock down sparring karate?

I started with Judo and boxing since childhood (I trained with Olympic athletes in both fields for many years). I’ve trained in Brazilian Jujitsu, Muay Thai, and military combatives for the past fifteen years or so, but have begun to reduce my Muay Thai training (really rough on the joints as I get older, and striking in general is very high impact/bad for my repeat-concussed brain), and have found renewed interest in Shotokan Karate of late (I’ve become a huge fan of Shotokan’s emphasis on footwork, timing, and distance recently and am very infatuated with the “Shotokan Blitz”).

Over the years I have dabbled in and tried Aikido/Aiki Bujutsu (for disarms and compliance techniques), JKD Concepts, Sambo, Krav Maga, and Filipino Martial Arts (mostly for knife fighting). I also wrestled in high school. I did a little bit of Tae Kwon Do and Kyokushin Karate, but didn’t stick.

As for Tae Kwon Do and practicality, I’ve met some Black Berets in ROK who will roundhouse kick you in your face before you can blink. Don’t confuse serious people with the women and children playing at “McDojos.” It’s the men, their skill sets, and the specific situations that matter, not “styles.” A lot of people make fun of Aikido (“Grab this arm… no, the other one”) for being impractical, but such people have not carried weapons and have done disarms and retentions.

While the ratio of bullshit to useful varies for a number of different reasons, I’ve learned very useful things in every combat sport I tried.