Australasians are Not Negroid So Stop Saying It!!
850 words
PumpkinPerson STILL doesn’t want to admit that Australasians aren’t Negroid. No matter how many people, studies or books I cite, he still wants to hold on to this Afrocentric belief of a “large pan-African race“. This is not true. I don’t know how many times I need to type it. Maybe if I type it until my fingers become stubs he will get it?
In fact, Friedlaender et al (2008) agree with me:
Our Structure and tree analyses of the combined microsatellite datasets indicate that Melanesians are quite far removed from Africans, in spite of their superficial similarities in hair form and skin pigmentation [38]. In the initial analysis of the HGDP-CEPH dataset, the placement of the two Melanesian (“Oceanic”) groups was different. There, they split from Eurasia before Asians and Native Americans [39]. This also differed from the result of a genome-wide SNP study [40] on a very small world-wide dataset. The extreme positioning of Melanesians in our tree was not due to our over sampling. Rather, our extensive coverage of Melanesian variation has enabled a clearer resolution of their relationships with populations outside the region.
They cluster nowhere near the vicinity of Africans.
To say that Australasians are Negroid based on phenotypic similarity means the one in question is basically treating race as a “social construct“. Just because two genetically isolated populations look similar doesn’t mean that they are of the same racial grouping.
Since Australoids “look African” as PP claims, would he claim that Middle Eastern people such as the Kalash who look European to be European? I’m sure he would.
But I’ve already quoted Razib Khan as saying:
The final issue is that a lot of the phenotypes that we racially code are recent. This probably explains why groups like the Kalash and Nuristanis can look more like Europeans than South Asians, but they’re genetically more like South Asians.
And when asked the three theories that he thinks falls into the unsupportable category:
“that phylogeny and phenotype track closely. just because you can’t tell the physical difference between two pops (e.g., solomon islanders and sub-saharan africans) they must be phylogenetically close. this is not the case.”
Robert Lindsay gets it and says:
We can also do phenotypes, but the Australoid phenotype is not the same as the African phenotype. There are African phenotypes and Australoid phenotypes, and they plot into separate areas on skull charts with no overlap. On a skull chart, a given skull is either obviously Australoid or obviously Negroid, but in both groups or in an unclear group, and it is always clear which group one is in.
Surface similarities are just that; they mean virtually nothing. In terms of selected DNA, Australoids have selected furthest away from Blacks. As it turns out, features that were selected for in Africa such as non-straight hair, wide noses and dark skin were all adaptive in tropical Australasia also, so these meaningless surface traits were retained.
Are you kidding? You look at an Aborigine and a Nigerian, and to you, they are “just a couple of niggers?” Aborigines do not look like Black people at all. In fact, they do not look like anyone.”
There were 5 principal clusters of CA repeats, formed by people living in 5 of the continental regions of Africa, Europe, East Asia, the Americas, and Australasia. (Wade, 2015: 97) Peoples of the Pacific cluster into their own category. Nicholas Wade reported in 2002:
Scientists studying the DNA of 52 human groups from around the world have concluded that people belong to five principal groups corresponding to the major geographical regions of the world: Africa, Europe, Asia, Melanesia and the Americas.
The study, based on scans of the whole human genome, is the most thorough to look for patterns corresponding to major geographical regions. These regions broadly correspond with popular notions of race, the researchers said in interviews.
This ends it right there. If they even still showed a genotypic resemblance to Africans, they’d still cluster in the vicinity of them. They don’t.
PP then goes on to say that Fst is on “neutral DNA, so they are classifying largely on chronological distance, not genetically preserved phenotype. I’m not saying they’re necessarily wrong, only that we’re talking about two different types of classification systems.” I challenge him to find a study showing that Australoids and Melanesians are anywhere close to Negroids genotypically.
I asked Professor Greg Cochran, co-author of the book The 10,000 Year Explosion with Henry Harpending if Australoids and Melanesians were Negroid and this is what he said:
East Asians, Europeans and ‘Native Americans’ aren’t closely related to Africans either. Just because they “look African” does not mean they are African!
The Kalash people look European, but are they? No. They show similarity to South Asians. They, like Australasians, look similar to other populations because the phenotypes we code are recent. “Phenotypically similar” people are not genotypically similar nor the same racial/ethnic category. I also covered this here last month. Why doesn’t he get it yet?
Stop saying they are Negroid, they are not. They are Melanesian.
Agriculture and Evolution: A Reply to The Alternative Hypothesis
2050 words
I love nutrition science. So much so that I read a new book on it every week. The Alternative Hypothesis has a pretty old video on agriculture and evolution. I strongly disagree with his main thesis. I strongly disagree with his denigration of Gary Taubes. Most of all, I strongly disagree with what he says about the East Asian rice eaters because since that video has been made, the carbohydrate/insulin hypothesis of obesity has changed to the insulin hypothesis of obesity.
In the very beginning of the video he brings up Gary Taubes’s research on low-carb diets and how people tend to be healthier than those who eat higher carb diets. He brings up the East Asians who eat a lot of rice. However, it’s clear he doesn’t know that the percent of carbohydrate intake is nowhere near as important as the absolute amount of carbohydrate consumed:
- They consume a fraction of the sugar we do. More sugar consumption leads to greater insulin resistance, more fat creation, less fat breakdown, and more fat accumulation.
- They consume less total glucose, AND the glucose they consume is accompanied by less sugar (and less omega-6 PUFA, if it matters).
- They consume a ratio of omega-6 to omega-3 PUFA that is much lower than we do. This mayfurther reduce any insulin resistance brought on by the glucose they do consume (in smaller doses and with less sugar).
The fact that East Asians didn’t have high rates of diabesity (diabetes and obesity) was a big blow to the carbohydrate insulin hypothesis. However, the East Asian rice paradox is simply explained by low, if non-existent, consumption of refined carbohydrates. Those populations actually consume fewer total carbohydrates than Western diets, and have lower levels of glycemic load as a result. To quote Mark Sisson:
Before recently, Asians ate less refined sugar and used animal fats for cooking. Sugar intake is rising now, of course, and cooking oils made from corn and soybean have largely replaced lard and tallow, but rice in the context of a low-sugar, no-HFCS (remember, the oft-cited 55/45 fructose/glucose breakdown for HFCS is highly misleading and actually quite often incorrect), low-vegetable oil, nose-to-tail nutrient-dense diet is (or was) acceptable. You can’t reduce a food down to its constituent parts and focus on, say, the bit of fructose in a blueberry and then condemn the entire berry because of it. Similarly, you can’t reduce a diet down to a single constituent food and condemn – or praise – it based on that single food. You have to look at the entire picture, and the Asian diet is largely a nutritious one.
These paradoxes where one population seems to disprove a certain hypothesis are pretty easily explainable with the existing data. There are numerous reasons why East Asian rice eaters have lower rates of diabesity. Dr. Jason Fung also explains why:
Wheat, particularly in the modern iteration may be particularly fattening for numerous reasons. The high level of amylopectin means that most of the starch contained in flour is efficiently converted to glucose. This deadly combination of wheat and sugar has been introduced into the Chinese diet. The result is a Chinese diabetes catastrophe. The prevalence of diabetes in China has now even outstripped the USA.
This is the answer to the paradox of the Asian Rice eater puzzle. Why didn’t the Chinese have a diabetes epidemic in 1990 with all their white rice? Well, because they didn’t eat any sugar (fructose), they were not developing insulin resistance. Because they were not snacking all the time, they had periods of low insulin level that helped prevent the development of insulin resistance. So the high rice intake by itself was not enough to cause either of diabetes or obesity.
Then he says that whites intake more total carbs in comparison to blacks and ‘Hispanics’ (1:32 in the video). This is wrong.
Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake. Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.
Diaz et al state in the results of the study:
Dietary differences are seen by ethnicity, with non-Hispanic whites having higherenergy, saturated fat and total fat intake, while Hispanics had higher carbohydrate intake and African-Americans had lower fibre intake.Both African-Americans and Hispanics had higher levels of fasting insulin, demonstrating lower insulin sensitivity in comparison with non-Hispanic whites.
So now that I’ve established that blacks and ‘Hispanics’ consume more total carbohydrates from refined foods, now I’ll show the physiologic effects of insulin.
Insulin inhibits the breakdown of fat in the adipose tissue by inhibiting the lipase that hydrolyzes (the chemical breakdown of a compound due to a reaction with water) the fat out of the cell. Since insulin facilitates the entry of glucose into the cell, when this occurs, the glucose is synthesized into glycerol. Along with the fatty acids in the liver, they both are synthesized into triglycerides in the liver. Due to these mechanisms, insulin is directly involved with the shuttling of more fat into the adipocyte. Since insulin has this effect on fat metabolism in the body, it has a fat-sparing effect. Insulin drives most cells to prefer carbohydrates for energy. Putting it all together, insulin indirectly stimulates the accumulation of fat into the adipose tissue.
Do you see why blacks and ‘Hispanics’ are more susceptible to obesity?
Another glaring error he commits is not separating refined carb consumption with natural carb consumption. Refined carbs spike insulin much more than those foods with natural carbohydrates. East Asians do not have a “higher carbohydrate tolerance than Europeans” (2:06 in the video). This one huge error he commits completely discredits his hypothesis.
He then goes on to talk about India’s diabetes rates. But why is it increasing? Because of Western diets. It’s not about a “lower carbohydrate tolerance” as he says at 3:07, it’s about consuming more refined carbohydrates.
Then at 5:05, he says that he’s “solved Gary Taubes’s race problem in regards to diet”. He did nothing of the sort.
I, of course, have no problem with his IQ data. I have a problem with the conclusions he jumps to in regards to carbohydrates and diabetes. He clearly didn’t look at other factors that would explain why East Asians have lower rates of diabesity (which is increasing as they adopt a Western lifestyle… Weird…). The same thing explains it with the Australian Aborigines.
I have absolutely no problem with the second half of his video. My problem is the first half of it–his denigration of Taubes, non-understanding of insulin spikes in comparison to the quality of carbohydrate ingested and not controlling for refined carbs– as it’s clear he didn’t do extensive research into these populations (which Taubes and others have) to show why they don’t have higher rates of diabesity.
What he doesn’t touch on are “obesogenic environments” which is defined as “the sum of influences that the surroundings, opportunities, or conditions of life have on promoting obesity in individuals or populations”. What a huge coincidence that most of the populations he cited today with higher rates of diabesity live in first-world nations, otherwise known as obesogenic environments.
He should have spoken about the Pima Indians and their rates of diabesity. They didn’t have rates of diabesity as high 100 years ago. Why? The introduction of the obesogenic environment. Prisancho (2003) in his study on the Pima and reduced fat oxidation in first-world countries showed how the Pima preferentially burn carbs and not body fat for energy. Fat-burning would account for 9 kcal lost and CHO for 4. Since they preferentially burn carbs for energy and not fat, this shows why they have higher rates of diabesity. It’s not that it’s a genetic susceptibility to burn CHO for energy over fat (there may be a small genetic component, but it doesn’t override the effects of the actual diet). I’ve shown insulin’s role in fat storage above, do you see why the Pima have this diabesity epidemic after the introduction of refined carbohydrates and the obesogenic environment?
Added sugars and salts in foods causes us to want more of those foods. As I alluded to above, food scientists continuously work to find out which combinations of sugar, salt and fat will be more hyperpalatable to us and make us eat them more. Whites nor East Asians have a ‘higher carb tolerance’, they just eat different types of carbs (mostly unrefined, in comparison to blacks and ‘Hispanics’ anyway). If any individual were to overeat on high carb foods they would become diabetic and obese. Whites nor East Asians are exempt from that.
In sum, he didn’t look at where the carbs came from, only total carb intake. Refined carbs and unrefined carbs do different things in the body. The whiter a processed food is, the more it is refined. The more a food is processed, the more its natural nutrients such as fiber are taken out. These low-fat refined foods are one cause of obesity. However, it’s way too complicated to say that only refined carbohydrates cause diabesity.
I strongly recommend he read Taubes’s and Fung’s books. If he did, he wouldn’t have said what he said about Taubes’s theory and completely disregard the absolute total amount of carb intake and not the total amount of carbohydrates ingested.
Race and Body Odor
1600 words
I’m currently reading Nicholas Wade’s A Troublesome Inheritance: Genes, Race and Human History, and it’s an outstanding read. He succinctly puts the science of racial differences so it’s easy for the lay person to understand. I’ve come across a part in the book where he talks about race and body odor. In the past, I’ve gotten into discussions on how and why different races have different body odors. My article Gene Expression by Race is great to get up to speed on the differences I’ve already written on in regards to the races of man.
Robert Lindsay has a good post on race and body odor, but I thought I’d add more information to how and why these differences exist.
East Asians have thicker hair than do Africans and Europeans. The gene, called ‘EDAR‘, is present in both Africans and Europeans, however a different type of this allele is widespread in East Asian populations (Han Chinese, 93 percent; Japan and Thailand about 70 percent and 60 to 90 percent in ‘Native’ Americans [which makes sense since we know that they branched off of Siberians around 10kya]). This allele is called “EDAR-V370A” since the V (valine) and A (alanine) switched on the “370th codon” (Wade, 2015: 88).
East Asians who carry this allele have thick and shiny hair. However, correlation is not causation, blah blah blah. So researchers genetically modified a strain of mice whose EDAR gene was converted into the form that East Asians carry. The results were shocking. The mice with the East Asian EDAR variant had thicker fur, and more eccrine glands in their footpads. Sweat glands come in two forms–eccrine glands which secrete water to cool the body and apocrine glands which secrete proteins and hormones (Wade, 2015: 89). Looking at the Chinese, we can see that they do carry significantly more eccrine glands!! Moreover, the mice also had smaller breasts. If East Asians had this EDAR variant then, logically speaking, they would have smaller breasts and what do you know: they do! This is, most likely, the reason why East Asians have smaller breasts than Africans and Europeans.
Another prominent effect of the EDAR variant that East Asians carry is the proclivity for shoveled teeth. When viewed from the back, East Asian teeth look ‘shovel-shaped’. The reason that this single gene is able to effect a lot of the phenotype is because this gene is active early in development. “EDAR has a great influence on the body because it’s switched on so early in embryonic development and helps shape organs such as the skin, teeth, hair and breasts” (Wade, 2015: 89).
Why does this singular gene have so many effects? One posited reason is thick hair and small breasts were admired by men (and thick hair for women) and this is what drove the selection (sexual selection). Another possibility, says Wade “is that many or all of the effects of EDAR-V370A were advantageous at one time or another, and that natural selection favored each in turn” (Wade, 2015: 90).
Turning our attention to Africans, they have more eccrine sweat glands, and, in comparison to East Asians, Africans have wider pores in their skin. Due to this, blacks have a stronger scent when sweating than East Asians. Conversely, East Asians have smaller pores.
I no longer have access to the source of this next quote, however, I have parts of the text saved:
There are fewer apocrine glands in Orientals and Native American Indians than in Blacks and Whites. Apocrine glands excrete fat and protein along with water (Poirier et al p 567).
The amount of chloride excreted by sweat glands varies by race: Blacks have more chloride in sweat than do whites. Acclimatized Whites excrete less chloride than unacclimatized whites– a useful adaptation (text 452). Water loss can be considerable: in extreme temperatures young males can loose 4 liters per hour. Thus, human ancestors in tropics must have always had ready access to water (see Overfield for many details).
So since apocrine sweat glands excrete more fats and proteins along with water, this explains why the two races differ in smell in comparison to East Asians. It also makes sense that ‘Native’ Americans would have fewer apocrine glands than Caucasians and Africans since they split off of East Asians around 10-15 kya. You can also see that blacks have more chloride in their sweat. Now, I’ve never encountered this myself, but I’ve seen numerous people say that blacks smell worse than whites or East Asians. This does have a biological basis, and it has to do with pore size, pore type and amount of chloride excreted by the sweat glands.
Of course, like with a lot of traits (not all), whites fall in the middle.
“Almost all Europeans have and all Africans have the wet earwax allele of the ABCC11 gene. The sharp differentiation of the two alleles implies a strong selection pressure.” (Wade, 2015: 90) The function of earwax is to prevent bugs from flying in the ear. Obviously, if the wax is wet (like Africans and Caucasians), the bug won’t be able to get too far into the ear before it gets stopped by the wet earwax. And as luck would have it, the two alleles of the ABCC11 gene are involved in the apocrine sweat glands (Wade, 2015: 90).
The apocrine sweat glands, unlike the eccrine glands, are restricted to the nipples, eyelids, armpits and other special areas on the body. These glands make slightly oil secretions, the specialty of which is to secrete earwax. The glands are odorless, but begin to cause a smell after bacteria begins decomposing dead skin cells(Wade, 2015: 90-91).
East Asians, having the dry earwax allele produce fewer excretions from their apocrine glands and, thusly, have less body odor. “Among people spending many months in confined spaces to escape the cold, lack of body odor would have been an attractive trait and one perhaps favored by sexual selection.” (Wade, 2015: 91) I love this!! It makes so much sense. East Asians were already selected for smaller sweat glands which, along with their dry earwax, produce less of a strong smell when they are perspiring.
Wade further goes into the earwax/body odor relationship and states that the dry earwax allele is almost universal in north China “but yields to the wet allele toward the south.” (Wade, 2015: 91) Most, but not all East Asians have the dry earwax allele, as well as the EDAR-V370A allele.
For a final point, it is assumed that all races have roughly the same skin structure. HOWEVER, morphological differences exist between the races. To quote Ruche and Cesarini (1992):
Under the microscope skin structure is roughly the same in all races, but morphological differences exist, particularly within the epidermis, with potential practical consequences. In comparison with white skin, the black skin stratum corneum is equal in thickness but more compact: about twenty cell layers are observed in blacks versus sixteen layers in whites. The lipid content of black epidermis is also somewhat higher, and this perhaps explains the greater cellular cohesion, hence the difficulty in stripping off the black horny layer. These findings could also explain a slightly inferior permeability of black skin to certain chemicals. The hair of blacks in naturally more brittle and more susceptible to breakage and spontaneous knotting than that of whites. The kinky or wooly form of black hair, the weak intercellular cohesion between cortical cells and the specific hair grooming practices among black people account for these effects. The higher electrical resistance of black skin suggests that the black epidermis would be less hydrated than white epidermis. Anatomically, the amount of sweat glands in black and white skins is identical and varies with climatic changes but not with racial factors. Likewise, sweating is thought to be similar in both races, taking into account the contradictory results from studies, but black subjects withstand humid heat better while whites cope better with dry heat.
So racial factors have no bearing on this, but climatic changes do. Generally, Africans come from humid climates nearer to the equator while Europeans come from cooler places farther from the equator. So we can say that, technically, there is a racial variation between the two.
And from this website on body odor:
Excessive sweating is a more common problem for Caucasians and Africans, who tend to have more hair follicles to which the apocrine glands are attached. East Asian people appear to have less and smaller apocrine glands, which explains why they might not need to use deodorants as often as populations of Africa and Europe (see paragraph below). As a matter of fact the deodorant/antiperspirant market in Asia is much smaller than in the western world. Surely, though, there may be many exceptions since body odour is obviously influenced by many factors, for example by one’s personal diet (spicy asiatic food etc.).
Below this section, the article talks about earwax and body odor, which I have covered above.
Differing allele frequencies between the races of man produce differing phenotypes based on where that groups’ ancestors evolved. Changes in certain alleles and not in others clearly led to differences in phenotype that did not occur because the environment was different between the races. These pheno and genotypic differences *prove the existence of race*, along with modern-day genomic testing. The fact that the races differ, albeit subtly, on numerous traits proves the existence of race, population, whatever you want to call it. It doesn’t change race’s reality.
If you have not read it, buy it!!! You’ll be a better and sharper race-realist as Nicholas Wade is an outstanding researcher and can explain complex concepts very simply.
The Rise of Bipedalism
1350 words
What caused the rise of bipedalism? The need for food? Tools? Advantage of seeing over tall grass? There are many posited reasons why bipedalism evolved in humans, but there’s no way to really know how this occurred. However, we can infer what caused bipedalism from what was occurring around the time that humans and chimps split.
There is no way for us to know exactly how and why bipedalism evolved in humans, but we can make inferences based on what we know was occurring around the time that humans and chimpanzees split. At that time, there was a major climate shift occurring. To better understand how the rise of bipedalism occurred, we have to have a better understanding of the elusive Last Common Ancestor (LCA) between humans and apes.
Since the elusive LCA lived in an African rainforest as Darwin inferred, all traces of the LCA probably rotted away on the forest floor. Since gorillas and chimps walk on their knuckles, the LCA of chimps and gorillas must have knuckle-walked as well (Lieberman, 2013: 36). So the LCA of the two must have been similar to them. Using this same logic, we can say the same about the human/chimpanzee LCA.
Looking at chimps and gorillas when they walk on two legs, you can see that they lurch forward, while humans don’t do so. When you look at how chimps walk, for instance, they have their legs far apart and their body sways from side-to-side like a drunk human. Conversely, when a human walks, they imperceptibly sway their torsos meaning we can expend more energy moving forward than stabilizing the upper body. The large bone that makes up the pelvis, the illium, is tall and faces backward in apes but sideways in humans. This was crucial for the rise of bipedalism in humans as it allowed the small gluteal muscles on the side of the hip to stabilize the upper body over each leg while walking when only one leg is on the ground.
Of course another important adaption for bipedal walking is an S-shaped spine.Apes, like other quadrupeds, have spines that slightly curve forward, so when standing upright, their bodies tilt naturally forward. Due to this, when standing upright, an apes’ torso is positioned unstably in front of its hips. In contrast to an apes’ spine, human spines have two pairs of curves. The lower curve in the lumbar is made possible by having more vertebrae than apes (5 for humans, 3 or 4 for apes). Several of these vertebrae have a wedge shape in which the top and bottom surfaces are not parallel. Just like architects use wedge-shaped stones to make arches, the wedge-shaped vertebrae curve the lower spine inward above the pelvis positioning the torso stably above the hips. Human chest and neck vertebrae make another softer curve at the top of the spine which orients the head downward.
The final skeletal difference that allowed for bipedalism is the human feet. As we walk, we land first on the heel then as the rest of the foot makes contact with the ground we stiffen the foot’s arch which enables us to push the body upward and forward mostly with the big toe. The shape of our feet is due to the shape of the foot’s bones as well as numerous bones and ligaments that secure the bones in place.
Since it’s impossible to know exactly what selected for bipedalism, we have to make inferences. But most evidence supports the idea that regularly standing upright and walking made it easier for early humans to find food more effectively due to the scarcity of food due to the climate shift that was occurring at the time that humans and chimps diverged (Lieberman, 2013: 40).
We don’t know what the LCA looked like nor how it lived or moved, but by making inferences to what we know, we can say that it was big. The LCA probably was most likely a fruit eater as well. So some walking on two legs would help it find food better.
Another reason why bipedalism got selected for was because walking on two legs conserved energy while traveling. The LCA most likely walked on its knuckles which expends more energy. Human walking conserves 75 percent more energy than walking on all fours. (Lieberman, 2013: 42) Basically, we could walk further with using less energy. I don’t even need to say what that means.
As one might expect, other selective pressures are hypothesized to have favored bipedalism in the first hominins. Additional suggested advantages of being upright include improved abilities to make and use tools, to see over tall grass, to wade across streams, and even to swim. None of these hypotheses bear up under scrutiny. The oldest stone tools appear millions of years after bipedalism evolved.(Lieberman, 2013: 43)
The best evidence we have suggests that bipedalism evolved during the climate change so early hominins could acquire ‘fallback foods’ like fibrous plant roots and the like. At the time of the climate change as chimps and humans split, food became harder to find and so early Man needed to subsist on fibrous plant roots. Smaller canines were critical here, and this is seen in the dental records we have from this time.
Stone tools appear millions of years after bipedalism evolved. Bipedalism evolved, in my opinion, as a postural adaptation as well as to better find these ‘fallback foods’ when early Man couldn’t eat his regular diet.
Bipedalism didn’t occur to get us on our feet to free our hands. Rather, it occurred so we could forage more efficiently and expend less energy as bipedal walking expends 75 percent more energy than knuckle walking (as the LCA is thought to have walked).
Consider lumbar regions. In any population of chimps, you’d find that about half of them have three lumbar vertebrae, the other half have four, and a very tiny number have five, thanks to heritable genetic variations. If having five lumbar vertebrae gave some apes a few million years ago a slight advantage when standing and walking, they would have been more likely to pass that variation off to their offspring. The same selective processes must have applied to other features that must have improved the LCA’s ability to be bipedal, such as how wedged its lumbar vetebrae were, the orientation of its hips , and the stiffness of its feet (Lieberman, 2013: 45).
A drawback of becoming bipedal is coping with pregnancy. As any pregnant woman tells you, the further she is in her term, the harder it becomes to stand upright. This requires the mother to contract her back muscles more or lean backward, which shifts her center of mass back over her hips. Though this pose saves energy, it places extra stress on the lumbar vertebrae of the lower back as the vertebrae attempt to slide away from one another. Thus, back pain is common in mothers. However, we can see how natural selection helped human mothers by increasing the number of wedged vertebrae, over which women arch their lower spines: three in females versus two in males (Lieberman, 2013: 46). The extra curving from the vertebrae reduces the sheer force on the spine.
Another disadvantage of becoming bipedal is speed. According to Lieberman, early humans’ inability to gallop limited our early ancestors to being about half as fast as a typical ape when sprinting (Lieberman, 2013: 46). Two limbs are also much less stable than four which makes it harder to make sharp turns when running. Another thing that bipedalism hindered was climbing up trees. It’s much easier and faster to climb up trees as a quadruped than biped. Becoming bipedal also lead to the ailments we have today such as ankle, back, and knee problems.
We can never really know exactly how and why bipedalism evolved. However, we have enough information on how ancient human ancestors lived and walked to make inferences on how and why bipedalism evolved. With a basic understanding of kinesiology, one can begin to know how and why bipedalism evolved in humans. Clearly, it was way more advantageous for our early ancestors to become bipeds than stay quadrapeds.
NotPoliticallyCorrect 
They are not closely related to Africans.