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The male and female height difference seems to be around 1.08 if all cultures are counted from these stats: https://en.wikipedia.org/wiki/Human_height
Can this ratio, 27/25, be explained by genetics and is there any research to explain how genes affect the growth of a man and woman? I assume there are a lot of factors that affect height and it might be very difficult to say if environmental and selective reasons or genetics are behind this factor.
GIANT study reveals a giant number of genes linked to height (October 6th, 2014)
“Height is almost completely determined by genetics, but our earlier studies were only able to explain about 10 percent of this genetic influence.”
There is strong evidence that height is a heritable trait with a strong genetic component. The genetic mechanism could be higher expression of an X-chromosome gene that, expressed in high levels, inhibits cartilage development, perhaps causing lower height. The increased expression seems to be caused by incomplete X inactivation in females. Furthermore, there is differential selection for height between human males and females likely causing the differences we see in modern human populations.
Genetic basis of height
The genetic variants analysed by Wood et al. (2014) account for ~29% of the phenotypic variance and 60% of the heritability of height.
Due to this high heritabilty (and the fact that there are still expected to be more unknown variants affecting height) there most likely is a genetic reason explaining the difference of height in human males and females. Thinking about the nature of this difference is a bit difficult. It is good to know that the trait has a high heritability and therefore a strong genetic component as this allows us to have a look at how natural selection affects height.
Selection on height
Height is a polygenic trait that is under recent and strong natural selection (Field et al., 2016 - preprint) leading to height increase in both human males and females (Fig. 3D in Field et al. (2016)):
What does this tell us in terms of the genetics underlying the height differences in human males and females? First, we have to understand that natural selection (at least mainly) affects individuals, not species. Then, we can understand that natural selection can affect males and females of a species differently. And Field et al. (2016) have shown exactly that for height. In their analyses, you can see that male and female height show (mildly) differing signals of natural selection (Fig. 4C in Field et al. (2016)):
But selection needs heritable genetic variation that allows this differentiation between the sexes. So what is the mechanism?
Genetic mechanism of height differences between human males and females
As pointed out by @tsttst in the comment differences between sexes are usually caused by genes on the X and Y allosomes. There is evidence that the height differences between human males and females are related to the X-chromosome (which also explains some of the missing heritability of the GWAS study by Wood et al. (2014)), reported by Tukiainen et al. (2014). They write
In one of these three associated regions, the region near ITM2A, we observed that there is a sex difference in the genetic effects on height in a manner consistent with a lack of dosage compensation in this locus. Further supporting this observation, ITM2A has been shown to be among those chrX genes where the X chromosome inactivation is incomplete.
They also give a molecular mechanism how this hypothesised increased expression of ITM2A can cause the height difference. They report that the ITM2A gene is involved in cartilage development (van den Plas et al., 2004) and that the height-associated ITM2A variants change expression of the ITM2A protein. This is interesting as increased ITM2A expression in mesenchymal stem cells of adipose tissue seems to inhibit cartilage development (Boeuf et al., 2009). Tukiainen et al. (2014) conclude:
As the allele associated with shorter stature associated with increased expression of ITM2A (sic), this suggests the allelic effect to height could be mediated through the capacity to generate cartilage and bone.
Finally, how can this be interpreted from an evolutionary point of view?
Evolutionary interpretation of height differences in human males and females
Differences in height (but also other traits) between sexes of a species are refered to as sexual dimorphisms. Sexual dimorphism (at least in primates) in height is strongly related to differences in mating behaviour and a sign of aggression and/or dominance-based mating patterns (Wynn and Coolidge (2011, p.82), sorry for that poor referenc link). The counterpart to this is pair-bonding, or in human terms marriage: a primate example is our pretty close relative, the Gibbon, that is (at least socially) monogamous and as expected does not have a height-related sexual dimorphism. Great apes including humans do have this polymorphism even though pair-bonding in humans is widely spread. Therefore, it was not surprising to find a reduction in height dimorphism from Australopithecus over Homo erectus to Homo sapiens (Wynn and Coolidge, 2011, p. 83, see also this, especially the last paragraph of this chapter).
Update on the main source
One of the papers I mainly used for this answer - to illustrate selection on height - was a preprint. It is now published in Science: Field et al. (2016).
Update August 9, 2017:
Prof. McGill contacted me and would like me to clarify:
“If you read carefully you will see that I did not comment on male-female differences. Any gender connection came from the context that Lou provided. I commented on hip anatomy and function and disease incidence.”
He’s right — all the parts of the article about sex differences came from the author, Lou Schuler, not from McGill’s quotes.
In any case, my comments still apply to anyone who tries to claim that the sex differences in the human bony pelvis mean men HAVE to sit with their legs spread out into other people’s space, giving them a pass on social etiquette. (And yes, such people have come out of the woodwork since I first posted this). I hope readers enjoyed learning about the plasticity (fancy way of saying ability-to-change) of the human skeleton!
Why is infant mortality higher in boys than in girls? A new hypothesis based on preconception environment and evidence from a large sample of twins
Infant mortality is higher in boys than girls in most parts of the world. This has been explained by sex differences in genetic and biological makeup, with boys being biologically weaker and more susceptible to diseases and premature death. At the same time, recent studies have found that numerous preconception or prenatal environmental factors affect the probability of a baby being conceived male or female. I propose that these environmental factors also explain sex differences in mortality. I contribute a new methodology of distinguishing between child biology and preconception environment by comparing male-female differences in mortality across opposite-sex twins, same-sex twins, and all twins. Using a large sample of twins from sub-Saharan Africa, I find that both preconception environment and child biology increase the mortality of male infants, but the effect of biology is substantially smaller than the literature suggests. I also estimate the interacting effects of biology with some intrauterine and external environmental factors, including birth order within a twin pair, social status, and climate. I find that a twin is more likely to be male if he is the firstborn, born to an educated mother, or born in certain climatic conditions. Male firstborns are more likely to survive than female firstborns, but only during the neonatal period. Finally, mortality is not affected by the interactions between biology and climate or between biology and social status.
Why are More Boys Born than Girls?
On average, there are 105 boys born for every 100 girls. Is it purely a genetic tendency or are there environmental factors at play too?
Back in 2008, a study analyzing hundreds of years of family trees, containing information from 556,387 people, suggested that the father&rsquos genes dictate whether he produces sons or daughters. Although no genetic evidence was found, the researchers proposed the idea that men likely carry two different allele types which result in three possible genetic combinations that dictate the ratio of X and Y sperm. Men with the first combination, known as mm, produce more sons. Meanwhile, those with mf produce an equal number of sons and daughters, and those with ff have more daughters (Newcastle University: 2008).
This process may explain why after wartime in many countries, there is a sudden increase in the number of boys born. In the UK for example, after World War I, an extra 2 boys were born for every girl in comparison to the year before it started. This likely happened as men with more sons were more likely to see at least one of their sons return from war than those with fewer sons and more daughters. This could then explain why men who survived the war were more likely to have male children, resulting in the baby-boom (ibid.).
Yet, there may be other reasons for this too. Human conception results in approximately 150 male zygotes for every 100 female zygotes (MinuteEarth: 2014). Accordingly, male fetuses are then more likely to result in miscarriage or be stillborn, than female fetuses. This means that the higher chance of conceiving a male increases the chances of more males being born (Weisskopf: 2004). Moreover, once out of the womb, males are at a higher risk of mortal diseases, and taking life-threatening risks than girls, meaning that fewer men may make it to breeding age. This means that, by the time breeding age is achieved, the ratio of males to females is roughly 1:1.
Adding to this biological factor, in some countries, the ratio of boys to girls may be even higher due to sex-slective abortion. For example, in China, 118 boys are born for every 100 girls, with similar figures also found in the Caucasus as well, an area that also practices female infantacide (Livingston: 2013). This in mind, cultural values may also play a significant role in determining the higher number of males born as a global average, especially when one considers that both China and India taken together (two countries that value male births over female births) make up 36.28% of the world&rsquos population.
To conclude, the higher number of males born than females has many possible reasons. From genetic factors including the possibility of a gender-deciding gene from the father, to a higher ratio of male zygotes present at conception. Cultural factors, such as a preference for male babies, only further encourages this divide.
The key genetic question: Same training, different responses?
The most powerful question, then, in my opinion, based on the above study, is the following thought-experiment:
If you took 470 volunteers from Kenya, and gave them the same training as was given to the 470 in the Bouchard study above, would you find the same range of non-responders to responders? Would you find that 7% of Kenyans improve their VO2max by less than 100ml/min? And would you find that 4% improve by 800ml/min or more?
I would hypothesize that the whole curve would be shifted way over to the right – there would of course be low and high responders. But the lower responders in the Kenyan sample, would, I suspect, be fewer and perhaps would improve by 200ml/min, not 100ml/min. As for high responders, instead of finding only a few who improve by 40%, you may find many more. This would be the indication of a genetic advantage – not that every single person is superior, but that within a given population (470 people in this case), you are more likely to find the physiological characteristics of a champion athlete in one group than in another.
And as soon as you super-impose the opportunity, the competitive environment, the altitude, the diet, the psychology, the culture and belief, the lifestyle, then you have the recipe for a distance champion – Kenya succeeds not because they have these factors, but because they apply these factors to an exceptional genetic pool.
Jamaica has the same scenario for speed, I would hypothesize: a concentrated group of individuals who possess the necessary physiological attributes to run fast, and to respond enormously to power and sprint training. Then onto that, you add the history, the role-models like Usain Bolt, the school competition, the excellent coaching, the culture of the island, and the result is the perfect mix to produce athletes who may well go on to win half a dozen Olympic gold medals.
In Genetics, It’s Always International Women’s Day
We’ve seen, over the past year, that men have contracted COVID-19 at almost twice the rate of women. Is this just a coincidence, is there some cultural or behavioral reason, or is there something more medically profound at play?
According to our guest on this week’s WhoWhatWhy podcast, Dr. Sharon Moalem, M.D., Ph.D., women have a clear, genetically-based survival advantage. It begins immediately upon birth, and has been confirmed in every corner of the world.
According to Moalem, the cause is two-fold: it’s a case of male biological fragility coupled with the superiority of the female immune system. COVID-19 has brought all of this into bold relief.
While medical testing and drug research have historically failed to fully take into account the power of two X chromosomes (XX versus the male XY), we are now learning that the dosing, side effects, and efficacy of many drugs should be based on the gender of the patient. According to Moalem, even the COVID-19 vaccines should have been dosed differently for men and women, and we should have expected different reactions to the shot.
Moalem explains that gender differences have applications in the treatment of virtually every disease, from vision problems to colds to cancer. Indeed, gender differences may give rise to the ultimate customization of medicine, with men being recognized as clearly “the weaker sex” when it comes to survival.
Click HERE to Download Mp3
Genetics: The Study of Heredity
Read this article to learn about the genetics:- the study of heredity. It is appropriately regarded as the science that explains the similarities and differences among the related organisms.
The Blood Theory of Inheritance in Humans:
For many centuries, it was customary to explain inheritance in humans through blood theory. People used to believe that the children received blood from their parents, and it was the union of blood that led to the blending of characteristics.
That is how the terms ‘blood relations’, ‘blood will tell’, and ‘blood is thicker than water’ came into existence. They are still used, despite the fact that blood is no more involved in inheritance.
With the advances in genetics, the more appropriate terms should be as follows:
I. Gene relations in place of blood relations.
II. Genes will tell instead of blood will tell.
Brief History and Development of Genetics:
Genetics is relatively young, not even 150 years. The blood theory of inheritance was questioned in 1850s, based on the fact that the semen contained no blood. Thus, blood was not being transferred to the offspring. Then the big question was what was the hereditary substance.
It was in 1866, an Austrian monk named Gregor Johann Mendel, for the first time reported the fundamental laws of inheritance. He conducted several experiments on the breeding patterns of pea plants. Mendel put forth the theory of transmissible factors which states that inheritance is controlled by certain factors passed from parents to offspring’s. His results were published in 1866 in an obscure journal Proceedings of the Society of Natural Sciences.
For about 35 years, the observations made by Mendel went unnoticed, and were almost forgotten. Two European botanists (Correns and Hugo de Vries) in 1900, independently and simultaneously rediscovered the theories of Mendel. The year 1900 is important as it marks the beginning the modern era of genetics.
The origin of the word gene:
In the early years of twentieth century, it was believed that the Mendel’s inheritance factors are very closely related to chromosomes (literally coloured bodies) of the cells. It was in 1920s, the term gene (derived from a Greek word gennan meaning to produce) was introduced by Willard Johannsen. Thus, gene replaced the earlier terms inheritance factor or inheritance unit.
Chemical basis of heredity:
There was a controversy for quite some time on the chemical basis of inheritance. There were two groups—the protein supporters and DNA supporters. It was in 1944, Avery and his associates presented convincing evidence that the chemical basis of heredity lies in DNA, and not in protein. Thus, DMA was finally identified as the genetic material. Its structure was elucidated in 1952 by Watson and Crick.
Basic Principles of Heredity in Humans:
The understanding of how genetic characteristics are passed on from one generation to the next is based on the principles developed by Mendel. As we know now, the human genome is organized into a diploid (2n) set of 46 chromosomes. They exist as 22 pairs of autosomes and one pair of sex chromosomes (XX/XY). During the course of meiosis, the chromosome number becomes haploid (n). Thus, haploid male and female gametes — sperm and oocyte respectively, are formed.
On fertilization of the oocyte by the sperm, the diploid status is restored. This becomes possible as the zygote receives one member of each chromosome pair from the father, and the other from the mother. As regards the sex chromosomes, the males have X and Y, while the females have XX. The sex of the child is determined by the father.
Monogenic and Polygenic Traits:
The genetic traits or characters are controlled by single genes or multiple genes. The changes in genes are associated with genetic diseases.
These are the single gene disease traits due to alterations in the corresponding gene e.g. Sickle-cell anemia, phenylketonuria. Inheritance of monogenic disorders usually follows the Mendelian pattern of inheritance.
The genetic traits conferred by more than on gene (i.e multiple genes), and the disorders associated with them are very important e.g. height, weight, skin colours, academic performance, blood pressure, aggressiveness, length of life.
Patterns of Inheritance:
The heredity is transmitted from parent to offspring as individual characters controlled by genes. The genes are linearly distributed on chromosomes at fixed positions called loci. A gene may have different forms referred to as alleles. Usually one allele is transferred from the father, and the other from the mother.
The allele is regarded as dominant if the trait is exhibited due to its presence. On the other hand, the allele is said to be recessive if its effect is masked by a dominant allele. The individuals are said to be homozygous if both the alleles are the same. When the alleles are different they are said to be heterozygous.
The pattern of inheritance of monogenic traits may occur in the following ways (Fig. 69.1).
1. Autosomal dominant inheritance:
A normal allele may be designated as a while an autosomal dominant disease allele as A (Fig. 69.1 A). The male with Aa genotype is an affected one while the female with aa is normal. Half of the genes from the affected male will carry the disease allele.
On mating, the male and female gametes are mixed in different combinations. The result is that half of the children will be heterozygous (Aa) and have the disease. Example of autosomal dominant inherited diseases are familial hypercholesterolemia, β-thalassemia, breast cancer genes.
2. Autosomal recessive inheritance:
In this case, the normal allele is designated as B while the disease-causing one is a (Fig. 69.1 B). The gametes of carrier male and carrier female (both with genotype Bb) get mixed. For these heterozygous carrier parents, there is one fourth chance of having an affected child. Cystic fibrosis, sickle-cell anemia and phenylketonuria are some good examples of autosomal recessive disorders.
3. Sex (X)-linked inheritance:
In the Fig. 69.1 C, sex-linked pattern of inheritance is depicted. A normal male (XY) and a carrier female (X C Y) will produce children wherein, half of the male children are affected while no female children is affected. This is due to the fact that the male children possess only one X chromosome, and there is no dominant allele to mark its effects (as is the case with females). Colour blindness and hemophilia are good examples of X-linked diseases.
A selected list of genetic disorders (monogenic traits) due to autosomal and sex-linked inheritance in humans is given in Table 69.1.
Genetic Diseases in Humans:
The pattern of inheritance and monogenic traits along with some of the associated disorders are described above (Table 69.1). Besides gene mutations, chromosomal abnormalities (aberrations) also result in genetic diseases.
The presence of abnormal number of chromosomes within the cells is referred to as aneuploidy. The most common aneuploid condition is trisomy in which three copies of a particular chromosome are present in a cell instead of the normal two e.g. trisomy-21 causing Down’s syndrome-, trisomy-18 that results in Edward’s syndrome. These are the examples of autosomal aneuploidy. In case of sex-linked aneuploidy, the sex chromosomes occur as three copies, e.g. phenotypically male causing Klinefelter’s syndrome has XXY trisomy-X is phenotically a female with XXX.
Selected examples of chromosomal disorders along the with the syndromes and their characteristic features are given in Table 69.2.
Eugenics is a science of improving human race based on genetics. Improving the traits of plants and animals through breeding programmes has been in practice for centuries. Eugenics is a highly controversial subject due to social, ethical, and political reasons. The proponents of eugenics argue that people with desirable and good traits (good blood) should reproduce while those with undesirable characters (bad blood) should not.
The advocates of eugenics, however, do not force any policy, but they try to convince the people to perform their duty voluntarily. The object of eugenics is to limit the production of people who are unfit to live in the society.
Eugenics in Nazi Germany:
Germany developed its own eugenic programme during 1930s. A law on eugenic sterilization was passed in 1933. In a span of three years, compulsory sterilization was done on about 250,000 people, who allegedly suffered from hereditary disabilities, feeble mindedness, epilepsy, schizophrenia, blindness, physical deformities, and drug or alcohol addition. The German Government committed many atrocities in the name of racial purity. Other countries however do not support this kind of eugenics.
What is the male vs. female adolescent growth rate?
Until puberty starts, at around the age of 10, there isn't much difference in growth rate between boys and girls about two inches (5 centimeters) per year. Growth rates change during puberty, when hormones start the process of physical changes in teens, which occur at different individual rates and at different ages within their gender group. Growth continues for one or two years during puberty, but males and females develop at different rates.
The onset of puberty in girls usually starts at around the age of 10. Girls on the average start their growth spurt between the ages of 10 and 14, about a year before boys. This is the reason girls are often taller than boys of the same age in early adolescence. The growth spurt in girls is also shorter than in boys. Before girls start menstruating they have already reached close to their maximum height. The period of intense growth occurs from 6 to 12 months before menstruation begins. In females, the growth in height during puberty is accompanied by an increase in hip width.
The average boy starts his growth spurt at the age of 12, and it is much more dramatic. Boys can grow four inches (10 cm) per year, but the most intense period of growth only lasts for a few months. At the end of puberty, boys are usually about five inches (13 cm) taller than girls on the average. The peak of growth is generally two years after puberty begins. In boys, the muscles also develop at this time. Genetics play a big part in growth patterns. Children usually stay in the same growth percentile over the years, which is an indication of normal individual growth rate.
How Beekeepers Can Hurt the Bee Population
As beekeepers we like to think we're helping the bee population and, therefore, the planet. However, an increasing number of beekeepers does not in itself mean the situation is improved. Without awareness, it may in fact be harmful.
As we have seen, genetic diversity is important for any species. And yet it's not uncommon for beekeepers - commercial or otherwise - to raise many queens from a single genetic line. This greatly constrains genetic diversity and, over time, leaves the population vulnerable to the wrong disease at the wrong time, with the potential to devastate the population.
For a deeper look at this topic here's a lecture by Debbie Delaney at the National Honey Show.
5 comments on “Honey Bee Genetics”
Question. I'm into my second year of bee keeping here in So. Cal. I have an issue with highly aggressive bees. All my bees are from feral sources ie: cutouts, trap-outs and the majority from swarms. If these traits originated from Africanized gene lines, what is the greater source of these traits? Queen or Drones? Does requeening have as much an impact if the drones are still in the equation or is it a longer term effort of re-queening to gentle the colonies? Your opinions would be appreciated.
This is really not an answer to your question but I also keep wild bees in southern California. The wild bees exhibit a range of behavior, from docile to aggressive. If I get a hive that is aggressive, I kill it. I don't want to deal with them and I don't want their genes going out into the wild gene pool.
My definition of aggressive is that the bees follow you when you leave the bee yard and won't leave you alone. Docile bees leave you fairly quickly when you leave the bee yard. Don't put up with aggressive bees. There are a lot of swarms and cutouts available in our area to replace an aggressive hive.
A queen has 32 chromosomes, 16 from her mother (queen) and 16 from her father (drone).
When the queen "splits" her 32 chromosomes into 16 to lay a drone egg, which 16 chromosomes is she passing to the drone? Is she passing her mother's? Or her father's? Or some combination?
A random combination of the DNA she inherited from both parents.
The feeding of royal jelly does not trigger the change of cast from worker to queen. Bee worker larvae fed royal jelly in a laboratory only become poorly fed workers. It is thought that other substances fed to the queen larvae by hundreds of bees turn off the development of a worker allowing a queen to develop.