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In part II, we will look at the mental gymnastics of someone who is clueless to the data and uses whatever mental gymnastics possible in order to deny the data. Well, shit doesn’t work like that, JayMan. I will review yet more studies on sitting, walking and dieting on mortality as well as behavioral therapy (BT) in regards to obesity. JayMan has removed two of my comments so I assume the discussion is over. Good thing I have a blog so I can respond here; censorship is never cool. JayMan pushes very dangerous things and they need to be nipped in the bud before someone takes this ‘advice’ who could really benefit from lifestyle alterations. Stop giving nutrition advice without credentials! It’s that simple.
JayMan published a new article on ‘The Five Laws of Behavioral Genetics‘ with this little blip:
Indeed, we see this with health and lifestyle: people who exercise more have fewer/later health problems and live longer, so naturally conventional wisdom interprets this to mean that exercise leads to health and longer life, when in reality healthy people are driven to exercise and have better health due to their genes.
So, in JayMan’s world diet and exercise have no substantial impact on health, quality of life and longevity? Too bad the data says otherwise. Take this example:
Take two twins. Lock both of them in a metabolic chamber. Monitor them over their lives and they do not leave the chamber. They are fed different diets (one has a high-carb diet full of processed foods, the other a healthy diet for whatever activity he does); one exercises vigorously/strength trains (not on the same day though!) while the other does nothing and the twin who exercises and eats well doesn’t sit as often as the twin who eats a garbage diet and doesn’t exercise. What will happen?
Jayman then shows me Bouchard et al, (1990) in which a dozen pairs of twins were overfed for three months with each set of twins showing different gains in weight despite being fed the same amount of kcal. He also links to Bouchard et al, 1996 (can’t find the paper; the link on his site is dead) which shows that the twins returned to their pre-experiment weight almost effortlessly. This, of course, I do not deny.
This actually replicates a study done on prisoners in a Vermont prison (Salans, Horton, and Sims, 1971). “The astonishing overeating paradox” is something that’s well worth a look in to. Salans et al had prisoners overeat and also limited their physical activity. They started eating 4000 kcal per day and by the end of the study they were eating about 10000 kcal per day. But something weird happened: their metabolisms revved up by 50 percent in an attempt to get rid of the excess weight. After the study, the prisoners effortlessly returned to their pre-experiment weight—just like the twins in Bouchard et al’s studies.
The finding is nothing new but it’s nice to have replication (on top of the replication that it already had), but that’s not what I was talking about. Of course, being sedentary, eating like shit and not exercising will lead to deleterious health outcomes. The fact of the matter is, the twin in my thought experiment that did not exercise, sat around all day and ate whatever would die way sooner, have a lower quality of life, and more deleterious disease due to the shitty diet while his co-twin would have less since he ate right, exercised and spent less time sitting.
JayMan says, in regards to studies that show that obese people that even do light physical activity show lower all-cause mortality, that “That’s not what large RCTs show.” I know the study that he’s speaking of—the Look AHEAD study (Action for Health and Diabetes) (The Look AHEAD Research Group, 2009). The research group studied the effects of lifestyle interventions in type II diabetics. For one of the groups they gave intensive diet and exercise information, the other they gave only the standard advice. However, the study ended early at 9.3 years because there was no difference between both groups (Pi-Sunyer, 2015). JayMan uses this study as evidence that diet and exercise have no effect on the mortality of type II diabetics; however, in actuality, the results are much more nuanced.
Annuzzi et al (2014) write in their article The results of Look AHEAD do not row against the implementation of lifestyle changes in patients with type 2 diabetes:
The intervention aimed at weight loss by reducing fat calories, and using meal replacements and, eventually, orlistat, likely underemphasizing dietary composition. There is suggestive evidence, in fact, that qualitative changes in dietary composition aiming at higher consumption of foods rich in fiber and with a high vegetable/animal fat ratio favorably influence CV risk in T2D patients.
In conclusion, the Look AHEAD showed substantial health benefits of lifestyle modifications. Prevention of CV events may need higher attention to dietary composition, contributing to stricter control of CV risk factors. As a better health-related quality of life in people with diabetes is an important driver of our clinical decisions, efforts on early implementation of behavioral changes through a multifactorial approach are strongly justified.
They reduced far calories and used meal replacements. This is the trial JayMan is hedging his assertion on. Type II diabetics need a higher fat diet and don’t need the carbs as it will spike their insulin. Eating a higher fat diet will also lower the rate of CVD as well. This trial wasn’t too vigorous in terms of macronutrient composition. This is one of many reasons why type II diabetics discard dieting and exercise just yet.
Even modest weight loss of 5 to 10 percent is associated with significant improvements in cardiovascular disease (CVD) after one year, with larger weight loss showing better improvement (Wing et al, 2011). (Also read the article The Spinning of Look AHEAD.)
Telling diabetics not to eat right and exercise is, clearly, a recipe for disaster. This canard that dieting/exercise doesn’t work to decrease all-cause mortality—especially for diabetics and others who need the lifestyle interventions—is dangerous and a recipe for disaster.
Intentional weight loss needs to be separated from intentional weight loss as to better study the effects of both variables. Kritchevsky et al (2015) meta-analyzed 15 RCTs that “reported mortality data either as an endpoint or as an adverse event, including study designs where participants were randomized to weight loss or non-weight loss, or weight loss plus a co-intervention (e.g. weight loss plus exercise) or the weight stable co-intervention (i.e. exercise alone).” They conclude that the risk for all-cause mortality in obese people who intentionally lose weight is 15 percent lower than people not assigned to lose weight.
This study replicates a meta-analysis by Harrington, Gibson, and Cottrell (2009) on the benefits of weight loss and all-cause mortality. They noted that in unhealthy adults, weight loss accounted for a 13 percent decrease in all-cause mortality increase while in the obese this accounted for a 16 percent decrease. Of course, since the weights were self-reported and there are problems with self-reports of weight (Mann et al, 2007), then that is something that a skeptic can rightfully bring up. However, it would not be a problem since this would imply that they weighed the same/gained more weight yet had a decrease in all-cause mortality.
Even light physical activity is associated with a decrease in all-cause mortality. People who go from light activity, 2.5 hours a week of moderate physical intensity compared to no activity, show a 19 percent decrease in all-cause mortality while people who did 7 hours a week of moderate activity showed a 24 percent decrease in all-cause mortality (Woodcock et al, 2011). Even something as simple as walking is associated with lower incidence of all-cause mortality, with the largest effect being seen in individuals who went from no activity to light walking. Walking is inversely associated with disease incidence (Harner and Chida, 2008) but their analysis indicated publication bias so further study is needed. Nevertheless, the results line up with what is already known—that low-to-moderate exercise is associated with lower all-cause mortality (as seen in Woodcock et al, 2011).
What is needed to change habits/behavior is behavioral therapy (BT) (Jacob and Isaac, 2012; Buttren, Webb, and Waddren, 2012; Wilfley, Kolko, and Kaas, 2012; ). BT can also be used to increase adherence to exercise (Grave et al, 2011). BT has been shown to have great outcomes in the behaviors of obese people, and even if no weight loss/5-10 percent weight loss is seen (from Wing and Hill, 2001), better habits can be developed, and along with ‘training’ hunger hormones with lifestyle changes such as fasting, people can achieve better health and longevity—despite what naysayers may say. Though I am aware that outside of clinics/facilities, BT does not have a good track record (Foster, Makris, and Bailer, 2005). However, BT is the most studied and effective intervention in managing obesity at present (Levy et al, 2007). This is why people need to join gyms and exercise around people—they will get encouragement and can talk to others about their difficulties. Though, people like JayMan who have no personal experience doing this would not understand this.
In regards to dieting, the effect of macronutrient composition on blood markers is well known. Type II diabetics need to eat a certain diet to manage their insulin/blood sugar, and doing the opposite of those recommendations will lead to disaster.
Low-carb ketogenic diets are best for type II diabetics. There are benefits to having ketones circulating in the blood, which include (but are not limited to): weight loss, improved HbA1c levels, reduced rate of kidney disease/damage, cardiac benefits, reversing non-alcoholic fatty liver, elevated insulin, and abnormal levels of cholesterol in the blood (Westman et al, 2008; Azar, Beydoun, and Albadri, 2016; Noakes and Windt, 2016; Saslow et al, 2017). These benefits, of course, carry over to the general non-diabetic population as well.
Of course, JayMan has reservations about these studies wanting to see follow-ups—but the fact of the matter is this: dieting and eating right is associated with good blood markers, exactly what type II diabetics want. In regards to food cravings, read this relevant article by Dr. Jason Fung: Food Cravings. Contrary to JayMan’s beliefs, it’s 100 percent possible to manage food cravings and hunger. The hormone ghrelin mediates hunger. There are variations in ghrelin every day (Natalucci et al, 2005) and so if you’re feeling hungry if you wait a bit it will pass. This study lines up with most people’s personal experience in regards to hunger. One would have to have an understanding of how the brain regulates appetite to know this, though.
JayMan also cannot answer simple yes or no questions such as: Are you saying that people should not watch what they eat and should not make an effort to eat higher-quality foods? I don’t know why he is so anti-physical activity. As if it’s so bad to get up, stop sitting so much and do some exercise! People with more muscle mass and higher strength levels live longer (Ruiz et al, 2008). This anti-physical activity crusade makes absolutely no sense at all given the data. If I were to stop eating well and strength training, along with becoming a couch potato, would my chance of dying early from a slew of maladies decrease? Anyone who uses basic logic would be able to infer that the answer is yes.
I also need to address JayMan’s last comment to me which he censored:
No intervention shows that lifestyle changes extend life – or even improve health. Even if they did, their generalizability would depend on their actual prescription. In any case, the point is moot, since they don’t even show such improvements in the first place.
You’re only saying that because you’re literally hand waving away data. It’s clear that going from no exercise to some exercise will decrease all-cause mortality. I’m sorry that you have a problem reading and understanding things that you don’t agree with, but this is reality. You don’t get to construct your own reality using cherry-picked studies that don’t mean what you think they mean (like Look AHEAD; Dr. Sharma states that we may never know if weight reduction can save lives in type II diabetics, however the three studies on low-carb diets cited above lend credence to the idea that we can).
Please see my previously linked Obesity Facts page for more. Once you’ve read that, get back to me. Until then, I’m putting the brakes on this discussion.
Of course, you’re putting the brakes on this discussion, you have substantial replies other than your one-liners. You need to censor people when you have no substantial response, that’s not intellectually honest.
All in all, JayMan is giving very dangerous ‘advice’, when the literature says otherwise in regards to lifestyle interventions and all-cause mortality. You can talk about genes for this or that all you want; you’re just appealing to genes. Light physical exercise shows that mortality risk can be decreased; that’s not too hard for most people.
I know JayMan talks about genes for this and that, yet he does not understand that obesogenic environments drive this epidemic (Lake and Townshend, 2006; Powell, Spears, and Rebori, 2011; Fisberg et al, 2016). He doesn’t seem to know about the food reward hypothesis of obesity either. Think about obesogenic environments and food reward and how our brains change when we eat sugar and then things will begin to become clearer.
JayMan is giving out deadly ‘advice’, again, without the correct credentials. Clearly, as seen in both of my responses to him, taking that ‘advice’ will lead to lower quality of life and lower life expectancy. But I’m sure my readers are smart enough to not listen to such ‘advice’.
(Note: Diet and exercise under Doctor’s supervision only)
On Twitter, JayMan linked to a video about a time traveling dietician who travels back to the 70s to give nutritional advice to a couple. He kept going back on what he said, re eggs and cholesterol, Paleo diet, etc. Then at the end of the video, the ‘time traveling dietician’ says “It turns out it’s genetic. It doesn’t matter whether you exercise or what you eat.”
I then asked JayMan if he was advising people to not diet or exercise—and if he was doing so—what credentials does he have to give such advice? “Appeal to authority!” So if some random guy gave me legal advice and I asked his credentials, is that an appeal to authority? Similarly, if someone is trying to give me medical advice, is asking where he got his medical license an appeal to authority? The thing is, people have specialties for a reason. I wouldn’t take diet and exercise advice from some anon blogger with no credentials, just like I wouldn’t take legal advice from a biologist. Anyway, I’ll review some studies on exercise, dieting, and sitting in regards to all-cause mortality.
Sitting and all-cause mortality
Listening to such advice—like not dieting or exercising—will lower your quality of life and life expectancy. The longer you sit, the more likely you are to have rolled shoulders among other postural imbalances. One of the biggest reasons that sitting is related to all-cause mortality (Chau et al, 2013; Biddle et al, 2016). So listening to this shitty advice to ‘not exercise’ will lead an individual to having a lower QoL and lower life expectancy.
Sitting is associated with all-cause mortality because if, say, one is sitting at a desk for 8 hours per day then goes home and sits for the rest of the day, circulation will not get not get to the lower extremities. Furthermore, even mild-to-moderate exercise attenuates the situation (Chau et al, 2013). Further, reducing sedentary behavior (and of course, watching less TV) can possibly raise life expectancy in the US (Katzmarzyk and Lee, 2012). They found that cutting daily sitting time to less than three hours can increase life expectancy by two years (and, of course, quality of life). There is a large body of research on sitting and all-cause mortality (Stamatakis et al, 2013). It’s also worth noting that too much sitting decreases life expectancy—even with exercise. So JayMan’s (unprofessional) advice will lead to someone having a shitty life quality and lower life expectancy.
Dieting, and all-cause mortality
This is a bit trickier. I know that dieting for weight loss doesn’t work (Aamodt, 2016; Fung, 2016)—that is, traditional dieting (high-carb diets). The traditional advice is to eat high-carb, low-fat and moderate protein—this is due to what occurred in the 70s—the demonization of fat and the championing of carbs. This, clearly, is wrong. This has led to the obesity epidemic and the cause is our evolutionary novel environments. The main reason is that we have constructed environments for ourselves that are novel, and thus we’ve not had enough time to adapt to what we eat/how we live our new lives in our modernized world.
Indeed, even hunter-gathers don’t have our disease rates that we have—having low to no cases of our diseases of civilization (see Taubes, 2007 for a review). Why is this? It’s because they are physically active and they do not eat the same processed carbohydrates that we in first-world societies do.
In regards to exercise and all-cause mortality, people who exercise more often have a lower chance of dying from all causes than more sedentary people (Oja et al, 2016; O’Donovan et al, 2017). So it’s becoming clear that JayMan is just talking out out his ass here. I’d love to hear any MD say to a patient “Don’t diet, don’t exercise. Don’t eat well. It doesn’t work.” Because that MD will be a shill for Big Food.
Further, when I say ‘diet’, I don’t mean eating below the BMR. Your ‘diet’ is what you eat, and by changing your diet, you’re changing to healthier habits and eating higher-quality foods. People like JayMan make it seem like you should eat whatever you want and not to exercise. Following this advice, however, will lead to deleterious consequences.
It DOES matter what you put into your body; it DOES matter if you exercise or not. If you do not, you will have a lower life expectancy than who does exercise and eats well.
On a side note, I know that dieting does not work for weight loss. Traditional dieting, that is. Dr. Jason Fung, world-renowned obesity, diabetes and intermittent fasting expert, has people lose and keep their weight off. He actually understands what causes obesity—insulin. Higher insulin levels are also tied to the obesity pathway through lack of glucagon receptors (Lee et al, 2014). Why is this important? First, we have to understand what insulin does in the body. Once you understand what insulin does in the body then you will see why JayMan is wrong.
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 this all together, insulin indirectly stimulates the accumulation of fat into the adipose tissue.
Does this physiologic process sound that you can ‘eat whatever you want’? Or does it tell you that you should lower your carb intake as to not induce blood glucose spikes which lead to an increase in insulin? Over time, these constant blood glucose/insulin spikes lead to insulin resistance which has the body produce more insulin due to the insulin resistance resulting in a vicious cycle.
So, it seems that in order to have a higher QoL and life expectancy, one must consume processed carbs very sparingly.
These behaviors of over consuming processed carbohydrates come down to the environments we have constructed for ourselves—obesogenic environments. An obesogenic environment “refers to an environment that helps, or contributes to,
obesity” (Powell, Spears, and Rebori, 2010).
Our current obesogenic environment also contributes to dementia and cognitive impairment. What makes environments ‘obesogenic’ “is the increased presence of food cues and the increased consumption of a diet which compromises our ability to resist those cues” (Martin and Davidson, 2015). So if our obesogenic environments change, then we should see a reduction in the number of overweight/obese people.
Diet is very important for Type II diabetics. For instance, TII diabetics can manage, and even reverse, their disease with a low-carb ketogenic diet (LCKD) lowering their hBA1c, having a better lipid profile, cardiac benefits, weight loss etc (Westman et al, 2008; Azar, Beydoun, and Albadri, 2016; Noakes and Windt, 2016; Saslow et al, 2017). I wonder if JayMan would tell TII diabetics not to diet or exercise…. That’d be a recipe for disaster. TII diabetics need to keep their insulin down and eating an LCKD will do that; taking JayMan’s ‘advice’ not to diet or exercise will quickly lead to more weight gain, an exacerbation of problems and, eventually, death due to complications from not correctly managing the disease. JayMan needs to learn the literature and understand these papers to truly understand why he is wrong.
Exercise and all-cause mortality
The relationship between vigorous exercise and all-cause mortality is well studied. Gebel et al (2015) conclude that “Independent of the total amount of physical activity, engaging in some vigorous activity was protective against all-cause mortality. This finding applied to both sexes, all age categories, people with different weight status, and people with or without cardiometabolic disease.” Reduced exercise capacity also causes higher all-cause mortality rates (McAuley et al, 2016).
Unfit thin people had two times higher mortality rate than normal weight fit people. Further, overweight and obese fit people had similar mortality rates when compared to normal weight fit people (Barry et al, 2013). Clearly, physical activity needs to be heightened if one wants to live a longer, higher quality life. This runs completely opposite of what JayMan is implying.
Exercise into old age is also related to higher cognition and lower mortality rate in when compared to individuals who do not exercise. Exercise also protects against cognitive degeneration in the elderly (Bherer, Erikson and Lie-Ambrose, 2013; Carvalho et al, 2014; Paillard, 2015). If you want to keep your cognition into old age and live longer, it seems like your best bet is to exercise at a young age in order to stave off cognitive degeneration.
Strength and mortality
Finally, one last thing I need to touch on is strength and mortality. Strength is, obviously, increased through exercise. Stronger men live longer—and are protected from more disease such as cancer—than weaker men, even when controlling for cardiorespiratory fitness and other confounds (Ruiz et al, 2008).
As I have covered in the past, differences in grip strength account for differences in mortality in men—which also has a racial component (Araujo et al, 2010; Volkalis, Halle, and Meisinger, 2015). The stronger you are, the less chance you have of acquiring cancer and other maladies. Does the advice of ‘don’t exercise’ sound good now? It doesn’t, and I don’t know why anyone would seriously imply that dieting and exercise doesn’t work.
Dieting (meaning eating a higher quality diet, not attempting to lose weight) and exercise do work to increase life expectancy. The advice of “don’t do anything, it’s genetic” makes no sense at all after one sees the amount of literature there is on eating mindfully and exercising. I know that exercise does not induce weight loss, but it does contribute to living longer and staving off disease.
People should stay in their lane and leave things to the professionals—the people who are actually working with individuals every day and know and understand what they are going through. The canard of ‘eat whatever, don’t exercise, it’s genetic’ is very dangerous, especially today when obesity rates are skyrocketing. JayMan needs to learn the literature and how and why exercise and eating right leads to a higher quality of life and life expectancy. Thankfully, people like JayMan who say not to diet or exercise have no pull in the real world.
Clearly, to live longer, eat right, don’t sit for too long (because even if you exercise, sitting too long will lower your life expectancy) and exercise into old age and your chance of acquiring a whole slew of deleterious diseases will be lessened.
Edit: (The correlation between aggression and testosterone isn’t .14 as Book et al (2001) state; the true correlation is .08 (Archer, Graham-Kevan and Davies, 2005) So it’s even lower than I thought. This is one of the many reasons why testosterone does not cause crime. It’s just feminist bullshit and fear mongering from people who do not understand the hormone and what it does in the body. The misconceptions come from Rushton’s r/K selection bullshit which has been summarily refuted.)
Recently, I’ve written at length on racial differences in testosterone and how the correlation between testosterone and physical aggression is .14. Pitifully low to account for the cause of crime and any overall differences in racial crime (that will be touched on at length in the future). Tonight I will show, yet again, why testosterone does not cause crime by looking at what times most crimes are committed by both adults and children under the age of 18. This will definitively put the ‘testosterone causes crime’ myth to bed for good.
Before I get into the time of day that most crimes are committed, I must talk about the production of testosterone in the body. There are no ‘genes for’ testosterone (although men who had three certain alleles had a 6.5 fold higher risk of having low testosterone; Ohlsson et al, 2011, I am unaware of there being a variation by race; over 10,000 Caucasian men were studied). There is, however, an indirect control of testosterone synthesis by DNA. DNA regulates the production of testosterone by coding for enzymes that convert cholesterol to testosterone (testosterone is a cholesterol-based hormone).
There are five simple steps to the production of testosterone: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone). That’s how testosterone is produced in the body. It is indirectly controlled by DNA.
Above is a graph from the Office of Juvenile Justice and Delinquency Prevention which shows the time of day that most crimes are committed. Notice how crime goes up as the time of day goes on and since kids are at school, they’re more likely to fight. This then peaks at 3 pm when kids are getting out of school.
Now look at rates of crime for adults. At its peak of 10 pm, it’s vastly lower than that of people under the age of 18, which is important to keep in mind. You can see how at 8 am that rates of crime are low for adults and high for kids, right when they would be entering school so there would be a lot of other kids around and the chance for violence goes up. Keep the times of 8 am (kids when they enter school), 12 pm (when most kids go on lunch) and 3 pm (when most kids get out of school) along with the hours of 12 pm to 8 pm for adults (when 74 percent of crimes are committed by adults).
- In general, the number of violent crimes committed by adults increases hourly from 6 a.m. through the afternoon and evening hours, peaks at 10 p.m., and then drops to a low point at 6 a.m. In contrast, violent crimes by juveniles peak in the afternoon between 3 p.m. and 4 p.m., the hour at the end of the school day.
- Nearly one-third (29%) of all violent crime committed by juvenile offenders occurs between 3 p.m. and 7 p.m. In comparison, 26% of all violent committed by adult offenders occurs between 8 p.m. and 12 p.m.
So since testosterone varies by day and levels are highest at 8 am and lowest at 8 pm (Brambilla et al, 2009; however testing men aged 45 years of age and older is fine before 2 pm due to a blunted circadian rhythm; Long, Nguyen, and Stevermer, 2015), then how could testosterone account for why men commit most of their crimes at night and why the crime that children commit spikes when they go to school, go to lunch and get out of school? The answer is that it doesn’t because testosterone does not cause crime. What testosterone does cause, however, are feelings of confidence and dominance, which does not—surprisingly—lead to increased aggression and assault on others (Booth et al, 2006).
What testosterone does cause, however, is social dominance and success, not physical aggression and maladjustment (Shcaal et al, 1996). The effects of environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Furthermore, aggressive behavior is first noticed in infancy and reaches its peak before school age (Tremblay et al, 2004; Cote et al, 2006). Though testosterone does seem to have an effect on aggression in preschool boys, however genetic and environmental causality has not been established (Sanchez-Martin et al, 2000).
Nevertheless, the meta-analyses I cited last week show that testosterone has an extremely low correlation of .14, so other factors must be at play. However, Sanchez-Martin et al (2000:778-779) also note that “Tremblay et al (1998) suggested that associations between testosterone titer and physical aggression are likely to be observed in contexts where such attack leads to social dominance. This may be true of the preschool boys in the present study. The data generated in the present study generally support Scerbo and Kolko (1994), who studied older children (7 to 14 years of age). They found a significant relationship between testosterone levels and aggression (as assessed by clinical staff).”
It’s interesting to note that in the case of Scerbo and Kolko (1994) that after controlling for age and size, testosterone correlated with aggression when rated by staff but not parents or teachers. ‘Staff’ refers to clinic staff at a facility where the children were assessed for hyperactivity disorders. Of course, the staff would rate higher levels of aggression compared to parents of teachers—people who are around the children every day—since they would want a higher chance for diagnosis for certain drugs to ‘cure’ the hyperactivity, but I digress. Testosterone does not induce aggression in children, but it does induce social dominance and confidence which does not lead to aggression (Rowe et al, 2004; Booth et al, 2006).
There was also little difference in testosterone between socially dominant prisoners and aggressive prisoners (Ehrenkraz, Bliss, and Sheard, 1974). Furthermore, the testosterone increase leading to pubertal development in boys is not associated with increased aggression (Tremblay et al, 1998; Booth et al, 2006: 171). Indeed, increased body size is a marker for physical aggression in children, and I doubt these children have high muscle mass so, I assume, they have high levels of body fat and thusly lower levels of testosterone than they would have if they were leaner. Yet another strike against the ‘testosterone causes crime/physical aggression’ hypothesis.
Indeed, this has some implications for the honor culture hypothesis of why low-income blacks have higher levels of testosterone than similarly aged blacks with some college (Mazur, 2016). The patterns for crime as shown by the OOJDP shows that crime rises as the day progresses from the morning until its peak at 3 pm for children and then sharply declines while for adults it peaks at 10 pm.
Testosterone does increase when a challenge is issued; when one man feels his reputation is threatened, the propensity for violence is increased, but this was most notably seen in Southern men (Cohen et al, 1996). So the same would be said for this ‘culture of honor’ found in low-income black neighborhoods, the so-called ‘code of the street’ as stated by Anderson (1994: 88): “Moreover, if a person is assaulted, it is important, not only in the eyes of his opponent but in the eyes of his “running buddies,” for him to avenge himself. Otherwise, he risks being “tried” (challenged) or “moved on” by any number of others. To maintain his honor, he must show he is not someone to be “messed with” or “dissed.””
This culture of honor is found all over the world, including Brazil where homicide can be explained by the need to maintain honor and can be understood by taking into account cultural factors; biological, psychological and socioeconomic factors do not explain murder in Northeast Brazil as well as honor and culture (de Souza et al, 2015). People in honor cultures also have a higher chance of self-harm (Osterman and Brown, 2011) as well as a higher chance of committing violence in school (Brown, Osterman, and Barnes, 2009).
Testosterone does not cause crime; it does not cause aggression. Increases in testosterone before, during and after events are a physiologic process to prime the body for competition. As cited above, dominant behavior does not necessarily lead to violence in most cases, which may be surprising for some. Indeed, honor and culture may explain a nice amount of the homicide and violence rate in the South. Since testosterone is highest at 8 am and lowest at 8 pm and the rates of crime committed by adults and children are vastly different than the diurnal variance in the day, then testosterone does not cause crime and its increase is not associated with crime, but social dominance and confidence which does not lead to crime.
Hopefully—if anyone still believes testosterone to be the boogeyman its made out to be—I’ve put those misconceptions to rest. Racial differences in testosterone cannot be the cause of racial differences in crime—because there is either no statistical difference in testosterone between the races or the difference is non-existent. Testosterone is clearly a beneficial hormone—as I have extensively documented. Misunderstandings of the hormone are abound—especially in the HBD sphere—only due to literally a few paragraphs in a book (Rushton, 1997) and one study that showed blacks have higher testosterone than whites which was the cause of their higher rates of prostate cancer (Ross et al, 1986). The study is hard to find so I had to buy access to it. I will cover this in the future, but I discovered that they assayed the subjects when it was convenient for them—between the hours of 10 am and 3 pm—which is unacceptable. You cannot gauge racial differences in testosterone from a small study (n=50) and a non-representative sample (college students). For these reasons, the study should be thrown in the trash—especially when formulating evolutionary hypotheses.
Testosterone is one of the most important hormones for vital functioning. By knowing how it is processed in the body and that there are no ‘genes for’ testosterone (‘low testosterone genes’ notwithstanding) along with how testosterone has a low relationship with physical aggression one should not be scared of having high levels, on the contrary, one should be scared of having low levels. I have once again proven my case that testosterone is not related to violence in showing the diurnal variation in testosterone levels in adults, as well as the time of day that crimes are committed by both adults and children. High testosterone means high confidence and high dominance—and those two traits have a lot to do with masculinity—which do not lead to violence.
I know why testosterone does not cause crime—because I have an understanding of the hormone, how its produced in the body and what its effects on the body are. The most important thing to note here, is that even if blacks had 15 percent higher testosterone than whites, it still wouldn’t explain higher rates of crime or disease such as prostate cancer. So those who try so hard to prove that blacks have higher levels of the hormone do so in vain, because even if they did it wouldn’t mean anything for any theories they may have. The myth of testosterone causing aggression and crime need to be put to bed for good.
In part I, I showed how Dale Russel’s contention that the troodon would have evolved into a bipedal ‘dinosauroid’ with human locomotion and a human-sized brain was pure fantasy. I ordered the book of his that Rushton cited in his book Race, Evolution, and Behavior and I finally received it last week. When I read the relevant parts, I yawned because it’s the same old stuff that I’ve covered here on this blog numerous times. Since literally the only relevant part in the book about the troodon is the final 7 pages, that’s what I will cover today—along with a few more lines of evidence that large brains lie outside reptilian design (Gould, 1989).
First off, all of Rushton’s contentions in the final pages of his book (Rushton, 1997) need to be rebutted. Rushton (1997: 294) writes that dinosaur brains were ‘progressing’ in size for 140 million years, but neither of Russel’s writings that I have (Russel 1983; 1989) have the statement in them.
In the book Up From Dragons: The Evolution of Human Intelligence neuroscientist, evolutionary psychologist John Skoyles and science writer Dorian Sagan—the son of Carl Sagan—speak briefly about reptilian intelligence and why they wouldn’t have reached our levels of intellect:
But cold-bloodedness is a dead-end for the great story of this book—the evolution of intelligence. Certainly reptiles could evolve huge sizes, as they did over vast sweeps of Earth as dinosaurs. But they never could have evolved our quick-witted and smart brains. Being tied to the sun restricts their behavior: Instead of being free and active, searching and understanding the world, they spend too much time avoiding getting too hot or too cold. (Skoyles and Sagan, 2002: 12)
Hopson (1977: 443) writes:
I would argue, as does Feduccia (44), that the mammalian/avian levels of activity claimed by Bakker for dinosaurs should be correlated with a great increase in motor and sensory control and this should be reflected in increased brain size. Such an increase is not indicated by most dinosaur endocasts.
Most importantly, if some dinosaurs DID have bird-sized brains, the above contention would still hold. Hopson concludes that, except for coelurosaurs “the range of behaviors that existed in dinosaurs, as inferred from trackways and skeletal morphology, may not have lain much outside the observed range in ectothermic crocodilians” (Hopson, 1977: 444).
Since the conjecture/’thought experiment’ of the troodon was rebutted last week, it’s pretty conclusive that large brains lie outside of reptilian design; they need to spend so much time avoiding getting too hot or cold—as well as hunt and eat—so exploring the world and learning was not possible for them—along with the fact that they didn’t have a primate morphology and thus didn’t have the ability to fully manipulate their environment as we do which would further select for larger brains. However, as Hopson (1977) notes, animals with higher metabolic rates had larger brains; coelurosaurs had high metabolic rates and the largest dinosaur brains (Russel, 1983; 1989)—but that doesn’t mean they would have eventually evolved human-like intelligence, bipedalism or brain size and to say otherwise is fantasy.
Furthermore, there is large variation in encephalization and encephalization is not universal in mammals (Shultz and Dunbar, 2010).
Here is the thing about brain size increases: it is a local level trend. A local level trend is a trend that occurs within one or a few related species. This is exactly what characterized brain evolution; there is large variation depending on what the environment calls for (Boddy et al, 2012; Montgomery et al, 2012; see also island gigantism; Bromham and Cardillo, 2007; Welch, 2009; and also see the deep sea rule; Mcclain, Boyer, and Rosenberg, 2006). So these local trends differ by species—even one population split by, say, 50 miles of water will speciate and become evolve a completely different phenotype due to the environment of time. That is evolution by natural selection; local change, not any inherent or intrinsic ‘progress’ (Gould, 1996).
The same local level trend occurs with parasites. Now think about parasites. The get selected for ‘complexity’ or a decrease in ‘complexity’ depending on what occurs in their host. Now, looking at it from this perspective, the body is the host’s environment while the earth is ours; so my example for an environmental change would be, as usual, the asteroid impact hitting the earth blocking out the sun and decreasing high-quality food all throughout the earth. Surely I don’t need to tell you what would occur…
Russel (1989) writes:
Examples of evolutionary changes that occured at ever-increasing speeds include the initial diversification of animals in the sea 650 and 550 million years ago, the attainment of tree stature in land plants between 410 and 360 million years ago, and the diversification of mammals between 200 million years ago and the present. Changes like this have resulted in increased organismal complexity, which, in combination with a general increase in number of species, has made the biosphere of the modern Earth so much richer than it was several hundred million years ago. It is reasonable to suppose that animals living in a complex environment might find it advantageous to possess complex nervous systems in order to have access to a greater variety of responses. Indeed, the largest proportion of brain weight in an animal has also increased at an ever-increasing rate across geological time. The brain has become evidently larger in animals as diverse as insects, mollusks, and backboned creatures. Relative brain size can be taken as an indication of biotic interactions.
He references time periods that correspond with decimations (mass extinctions). Decimations lead to diversification. Think back to the Cambrian Explosion. During the Cambrian Explosion, many more lifeforms existed than can be currently classified. Therefore, according to the decimation and diversification model, greater diversity of life existed in the past. When decimations (defined as a reduction in the anatomical forms of life from mass extinction) occur, the niches that become extinct quickly become filled.
The time periods that Russel references are when mass extinctions occurred. This is how diversification occurs. What allowed for this ‘organismal complexity’ and increase in the number of species (though body plans are limited due to the Burgess Decimation) is due to the decimations. Decimation and diversification proves that evolution is not progressive.
A ‘trend’ in biology is directional change in a group stat using the mean, median or mode. Any existence of a trend from the mean (‘progress’) tells us nothing about the underlying mechanisms behind it.
To wrap this all up, even if a trend in X were to be discovered, it still wouldn’t tell us a thing about the underlying mechanisms causing it, nor will it tell us about any increasing tendency.
The analogy of the drunkard’s walk (Gould, 1996) is why ‘progress’ doesn’t make sense. Further, niche construction matters as well. When organisms construct their own niches, change occurs based on those niche constructions. Milk-drinking 8kya in Europe and African farmers diverting water for their crops having mosquitoes come by and gaining a resistance to malaria are two examples of niche construction (Laland et al, 2009). That’s another barrier to progress!
In sum, Dale Russel says nothing I’ve not heard before in regards to ‘progressive’ evolution. He only describes ever-increasing ‘complexity’ which is due to decimations and further diversification by organisms to fill empty niches. Any type of ‘progress’ would have been stymied by mass extinctions.
Further, the fact that species can consciously—in a way—guide their own evolution through the manipulation of the environment once again shows how evolution doesn’t mean progress—it literally only means local change and any type of local change, no matter to what type of environment, will cause concurrent increases/decreases on whichever relevant traits that will give the organism the best chance for survival in that environment.
This is why evolution is not progressive; and even if scientists were to identify one thing, still, a causal mechanism won’t be able to be inferred. Ruseel (1989) describes right and left walls of complexity—nothing more. Dinosaurs didn’t have the body plans to have our brain size, bipedalism and intelligence, nor did they have the right type of blood, nor did they have the time to search and learn about the world due to being constrained to their cold-blooded system—being a slave to the sun, always attempting to avoid overheating or getting too cold (Skoyles and Sagan, 2002). The so-called ‘dinosauroid’ is an impossibility and implies a teleological lean to evolution—as if our morphology (or something similar from an unrelated organism) will always evolve if we replay the tape of life again (Gould, 1989; 1996). This is what Russel is pretty much arguing, and he is 100 percent wrong as noted above.
Bromham, L., & Cardillo, M. (2007). Primates follow the ‘island rule’: implications for interpreting Homo floresiensis. Biology Letters,3(4), 398-400. doi:10.1098/rsbl.2007.0113
Boddy, A. M., Mcgowen, M. R., Sherwood, C. C., Grossman, L. I., Goodman, M., & Wildman, D. E. (2012). Comparative analysis of encephalization in mammals reveals relaxed constraints on anthropoid primate and cetacean brain scaling. Journal of Evolutionary Biology,25(5), 981-994. doi:10.1111/j.1420-9101.2012.02491.x
Gould, S. J. (1989). Wonderful life: the Burgess Shale and the nature of history. New York: Norton.
Gould, S. J. (1996). Full House: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Hopson, J. A. (1977). Relative Brain Size and Behavior in Archosaurian Reptiles. Annual Review of Ecology and Systematics,8(1), 429-448. doi:10.1146/annurev.es.08.110177.002241
Laland, K. N., Odling-Smee, J., Feldman, M. W., & Kendal, J. (2009). Conceptual Barriers to Progress Within Evolutionary Biology. Foundations of Science, 14(3), 195–216. http://doi.org/10.1007/s10699-008-9153-8
Mcclain, C. R., Boyer, A. G., & Rosenberg, G. (2006). The island rule and the evolution of body size in the deep sea. Journal of Biogeography,33(9), 1578-1584. doi:10.1111/j.1365-2699.2006.01545.x
Montgomery, S. H., Capellini, I., Barton, R. A., & Mundy, N. I. (2010). Reconstructing the ups and downs of primate brain evolution: implications for adaptive hypotheses and Homo floresiensis. BMC Biology,8(1), 9. doi:10.1186/1741-7007-8-9
Russell, D. A. (1983). Exponential evolution: Implications for intelligent extraterrestrial life. Advances in Space Research,3(9), 95-103. doi:10.1016/0273-1177(83)90045-5
Russell, D. A. (1989). An Odyssey in Time: The Dinosaurs of North America. Minocqua, WI: Published by NorthWord Press in association with National Museum of Natural Sciences.
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Shultz, S., & Dunbar, R. (2010). Encephalization is not a universal macroevolutionary phenomenon in mammals but is associated with sociality. Proceedings of the National Academy of Sciences,107(50), 21582-21586. doi:10.1073/pnas.1005246107
Skoyles, J. R., & Sagan, D. (2002). Up From Dragons: The Evolution of Human Intelligence. New York: McGraw-Hill.
Welch, J. J. (2009). Testing the island rule: primates as a case study. Proceedings of the Royal Society B: Biological Sciences,276(1657), 675-682. doi:10.1098/rspb.2008.1180
By Scott Jameson
I’ve been active in the blogosphere for around 24 hours now and I’ve already gotten a negative response from someone who happens to be wrong. That’s a win in my book.
The argument we’re having is, as best I can tell, why some populations out there just don’t have obesity as an observed phenotype amongst their members. TL;DR: Pumpkin Person and Robert Lindsay believe that genetics explain why there are no obese New Guineans. But it ain’t so.
The original context is an old Pumpkin Person post. Much of what he’s saying here doesn’t seem too off-base; for example he says that behavioral genetics may explain much of the differences in BMI between individuals within the same population. True. It is possible that some people are genetically inclined to eat more or unhealthier foods, rather than simply being genetically inclined to putting on weight regardless of what they do.
As an aside, genotypes that affect how you digest things also probably explain part of the BMI gap between skinny folks and fat folks within the first world. The APOA2 gene for example has a recessive allele that is associated with higher BMI in people who eat more saturated fats. The interactions between genes and environment which determine BMI are complicated and not yet fully understood, but I’m willing to bet that being genetically worse at processing certain nutrients is a part of the problem, and that being genetically inclined to stuff your face is a part of the problem as well. PP is probably right about that issue.
Where he and Lindsay get it wrong is using examples of people from Podunk, New Guinea as evidence for obesity “being genetic” (relative term). Obesity is a gene-environment interaction such that, without certain environmental inputs, you simply won’t get the phenotype. History tells us that that input is processed carbohydrates.
There was a time when people could have used Australian Aboriginals or Inuit or Pima Indians as examples of groups of people who just don’t have obese folks amongst their numbers, just as Lindsay did with a few populations. Homo sans lardicus. Then the White Devils showed up with their refined Einkorn wheat products and their firewater and so on. Now those populations have fat people in them.
There’s an ongoing debate as to whether some populations are more resistant to the fattening effects of processed carbs or not. My guess is, the answer’s yes (and you’d look at Europeans and East Asians to see the more carb-resistant people, in theory) but that topic would merit its own post. That being said, every population in the world will almost assuredly have obese people in it after you introduce processed carbs. All of the populations that were introduced to this diet, now have fat people in them.
Heritability of BMI is high within the first world because the relevant environmental input is pretty uniform: everybody has access to potatoes, everybody has access to broccoli. As PP points out, which you’re likely to eat and how much you’re likely to eat likely depends on your genetics. As I point out, how your body processes the nutrients also has a likely genetic component. But the environmental contribution to our within-population differences in BMI is low (~20%) because we all have access to roughly the same stuff.
Rural New Guineans, lacking a bunch of processed carbs, could hardly get fat if they tried their best to. That’s a big between-population, nonheritable cause for a phenotypic difference; this means that environment probably explains most of the BMI gap between them and us. If I wanted evidence to refute Lindsay’s assertion that New Guineans are skinnier thanks to genetics, I’d find a population of urbanized New Guineans somewhere with higher average BMI. Such a group would have New Guinean genetics but a “developed” environment vaguely similar to ours; if they were fatter than their rural ken, then Lindsay’s hypothesis that New Guineans are just genetically obesity-free would be falsified.
Do racial differences in penis size exist? The average person may say yes, due to viewing porn and hearing ‘stories’ from their friends, ie anecdotal accounts. But is this true? JP Rushton was at the helm of this resurrected idea, stating that an inverse relationship existed between penis size and brain size. He cites a WHO study on condom size showing that African countries get the biggest condoms, yet I cannot find the paper discussing it. PP wrote an article, Non-black men are so jealous of black penis size, citing the same study Rushton (1997) cited in his book Race, Evolution, and Behavior. I will discuss PP’s musings on racial differences in penis size.
A pet peeve of mine is that a lot of non-black men in the HBD blogosphere believe everything that professor J. Philippe Rushton said about ethnic differences in IQ and brain size, but when it comes to black men having the largest penis size, they suddenly turn into HBD deniers, ranting and raving about how the research is wrong. Well, I’m sorry but HBD is not here to serve your racist supremacy, HBD is here to celebrate ALL RACES, NOT YOURS ONLY!!!! If the data shows that black men have the largest penis size, then shut up and get over it. What kind of man gets jealous over another man’s penis size anyway? A sick, twisted, perverted sinful one. Healthy well adjusted normal guys don’t even know how large their penis is, and couldn’t care less, because they have other things going for them like a girlfriend, a career, and sports, and their mind’s not in the gutter. The only legitimate reason to care is for science, so here are the FACTS:
Exactly, the only reason to care is for science. And the science shows no differences. What data shows differences in penis size? Something you can directly access right now without relying on a secondhand source to prove your claim?
According to data from the World Health Organization Global Programme on AIDS Specification and Guidelines for Condom Procurement (1991, p 33, Table 5), assuming a normal distribution, I estimate the average white American man has a penis length of 162 mm (SD = 19) , and the average African American man has a penis length of 170 mm (SD = 19). (since 5% of black men are longer that 200 mm, and 2% of white men are, while 27% of white men have penises shorter than 151 mm, while 15% of black men do).
No hyperlink to the study? Why do you rely on a secondhand account? Why didn’t you show the table?
Just found some information on the WHO study he cited. The information from which the WHO data is derived is derived from American blacks and Caucasians, not any subjects from Europe or Africa. He also asked 150 people on a Toronto shopping mall what their penis size was (back to garbage self-reports), and finally, who is this French army surgeon he brings up? So many questions.
Also, PP, asking the questions and questioning his data and what he wrote isn’t “disagreeing on him on this and agreeing with him on everything else”, as you of all people know how critical o am of Lyn and Rushton. Yet you seem to eat up everything they write, thinking they can never be wrong. Why is that?
Rushton (1997) writes on pg 169 of Race, Evolution, and Behavior:
Data provided by the Kinsey Institute have confirmed the black-white difference in penis size (Table 8.2, and items 70-72 of Table 8.4). Alfred Kinsey and his colleagues instructed their respondents on how to measure their penis along the top surface, from belly to tip. The respondents were given cards to fill out and return in preaddressed stamped envelopes. Nobile (1982) published the first averages of these data finding the length and circumferences of the penis for the white samples was smaller than for the black sample. (Flaccid length = 3.86 inches [9.80 cm] vs. 4.34 inches [11.02 cm]; erect length = 6.15 inches [15.62 cm] vs. 6.44 inches [16.36 cm]; erect circumference = 4.83 inches [12.27 cm] vs. 4.96 inches [12.60 cm] respectively.)
Self-reports? Please. Self-reports are notoriously embellished. Moreover, the amount of black Americans in the Kinsey study was in double digits.
I can never find certain papers online, so that really hinders any further discussion on this.
If anyone can find any of these papers, leave a comment.
Harvey, P. H., & May, R. M. (1989). Out for the sperm count. Nature, 337, 508-9.
Short, R. V. (1979). Sexual selection and its component parts, somatic and genital selection, as illustrated by man and the great apes. In J. S. Rosenblatt, R. A. Hinde, C. Beer, & M-C Busnel (Eds.), Advances in the Study of Behavior, Vol. 9. New York: Academic
When it comes to scrotal circumference, I don’t have exact figures, but Rushton cites scholars showing that Africans exceed Europeans: Short, 1979; Ajmani, Jain & Saxena, 1985.
I found Ajmani et al (1985), they state that in 320 healthy Nigerians, average penile length was 3.21 inches, while scrotal circumference was 8.37 inches. PP says he didn’t have exact figures, but they were in Rushton’s references (which I see he didn’t check). Rushton doesn’t cite data on European scrotal circumference so how is that saying that ‘Africans exceed Europeans’ when only Nigerians were examined? Remember: studies are only applicable to the demographic tested. Extrapolating that data on to the whole of Africa makes no sense. Moreover, any data on Europeans is only for that specific ethny tested. Unless the whole of the European continent is averaged out, you cannot say that these differences exist.
This doesn’t even touch on Lynn’s “data” on penis size:
Lynn attempts to justify his belief that there are differences between races in penis length on the basis that European and Asian males have lower levels of testosterone than Africans and that the “reduction of testosterone had the effect of reducing penis length, for which evidence is given by Widodsky and Greene (1940).” Widodsky and Greene (1940) is actually a study of the effects of sex hormones on the penises of rats. This is hardly convincing evidence that there are racial differences in testosterone levels or that a reduction in penis length ever occurred in human history.
Lynn’s claims about differences in penis length between races build on earlier claims by Rushton and Bogaert (1987). The Rushton and Boagert paper is striking for its use of non-scholarly sources (Weizmann, Wiener, Wiesenthal, & Ziegler, 1991). These include a book of semi-pornographic “tall tales” by an anonymous nineteenth century French surgeon that makes wildly inconsistent claims about genital sizes in people of different races. Lynn also refers to this book without mentioning any problems with this as a source of information. Another odd data source cited by Rushton and Bogaert is an article authored by a certain “P. Nobile” published in Forum: International Journal of Human Relations. This publication is better known to the public as “The Penthouse Forum”, a popular men’s magazine. [This is pretty well known and embarrassing that Rushton did that.]
The data sources that Lynn uses in his recent paper are hardly much better. One of them is a book by Donald Templer (another self-professed race realist) called Is Size Important? Templer is not a urologist but a psychologist so why he would claim to be an authority on this subject is unclear. Lynn’s other source is the world penis size website. These are both self-published sources that have not been independently verified. A blogger named Ethnic Muse has carefully examined this site’s references and found that a number of articles listed on the site either do not exist under the name given or do not discuss penis size at all. There are also numerous discrepancies between the values provided by the website and the actual values given by the references. Therefore, the information on this website cannot be trusted and no conclusions should be drawn from it.
Pretty embarrassing for race-realism, to be honest. Looks like the data from “P. Nobile” is from a Penthouse webforum that he ‘published’ his ‘results’ in, instead of a scholarly journal. Rushton did state ‘forum’ (not stating it was the ‘Penthouse forum’, though), but why should we take this as proof of anything?
The sadder one is multiple ‘references’ of Lynn’s that either don’t exist or don’t discuss penis size. Why trust these ‘sources’, when they aren’t controlled scientific studies?
Veale et al (2014) write:
It is not possible from the present meta-analysis to draw any conclusions about any diﬀerences in penile size across diﬀerent races. Lynn  suggest that penis length and girth are greatest in Negroids (sub-Saharan Africans), intermediate in Caucasoids (Europeans, South Asians and North African), and smallest in Mongoloids (East Asians), but this is based upon studies that did not meet our present inclusion and
The greatest proportion of the participants in the present meta-analysis were Caucasoids. There was only one study of 320 men in Negroids and two studies of 445 men in Mongoloids. There are no indications of diﬀerences in
racial variability in our present study, e.g. the study from Nigeria was not a positive outlier. The question of racial variability can only be resolved by the measurements with large enough population being made by practitioners following the same method with other variables that may inﬂuence penis size (such as height) being kept constant. Future studies should also ensure they accurately report the race of their participants and conduct inter-rater reliability.
This meta-analysis was only done on Caucasians, but from the previous study on 320 Nigerians cited from Rushton (Ajmani et al, 1985) and 445 Mongoloids, no racial differences were found. When an actual study gets carried out on this, I doubt that there would be any differences between races.
Orakwe and Ebuh (2007) again test Nigerians (5.2 inches), then compare them with Italians (4.92 inches), Greeks (4.79 inches), Koreans (3.78), British (5.11 inches), and American Caucasians (4.9 inches). The only statistical difference was between Nigerians and Koreans. They conclude:
There is the possibility of racial differences in penile sizes, but there is no convincing scientific background to support the ascription of bigger penile dimensions to people of the Black race.
I wouldn’t say there is a ‘possibility’ that it’s true, based on a population of Nigerians. We can say that ethnic differences may exist between Koreans and Nigerians, but to extrapolate that to all five races and say that racial differences exist and that it fits neatly into Rushton’s outdated 3-way racial model is incorrect. It wasn’t a representative sample of Nigerians (and I obviously don’t have access to the methods of the other papers, I will update this in the future when I find more data), and the bigger sample of the two samples that I cited showed a smaller size.
Do racial differences in penis size exist? We can’t really come to a conclusion based on the data we currently have. Using “””data””” from the Penthouse webforum and a self-reported survey online is embarrassing and the data shouldn’t be used in the discussion of whether these differences exist. The only reliable data on Africans, as far as I know, is on Nigerians; the study with the higher n showed a smaller length. The data so far, shows that no difference exist exists (Veale et al, 2014: 983).
Stephen Jay Gould was one of the biggest opponents of hereditarianism, one of Rushton and Jensens’s biggest opponents. He is the author of The Mismeasure of Man, which is still given to college students to read as a “definitive refutation of The Bell Curve” and an all out attack on factor analysis, IQ testing and the whole hereditarian position at large. A passage from the very end of his book Full House perfectly explains his thought process on this matter:
“The most impressive contrast between natural evolution and cultural evolution lies embedded in the major fact of our history. We have no evidence that the modal form of human bodies or brains has changed at all in the past 100,000 years—a standard phenomenon of stasis for successful and widespread species, and not (as popularly misconceived) an odd exception to an expectation of continuous and progressive change. The Cro-Magnon people who painted the caves of the Lascaux and Altamira some fifteen thousand years ago are us—and one look at the incredible richness and beauty of this work convinces us, in the most immediate and visceral way, that Picasso held no edge in mental sophistication over these ancestors with identical brains. And yet, fifteen thousand years ago no human social grouping had produced anything that would conform with our standard definition of civilization. No society had yet invented agriculture; none had built permanent cities. Everything that we have accomplished in the unmeasurable geological moment of the last ten thousand years—from the origin of agriculture to the Sears building in Chicago, the entire panoply of human civilization for better or for worse—has been built upon the capacities of an unaltered brain. Clearly, cultural change can vastly outstrip the maximal rate of natural Darwinian evolution.” (Gould, 1996: 220)
He wrote Full House as a sequel of sorts to his book Wonderful Life: The Burgess Shale and the Nature of History (currently on the way to my home which I will read in a few days of getting it), where he argues that progress is not the driver to evolution and that complexity does not rule as bacteria rule the planet. He argues that we are not in the “Age of Mammals”, but the “Age of Bacteria”. But how could you argue that there was no change in humanity from our most recent ancestors to today?
Eldredge and Gould pioneered the theory of punctuated equilibria in 1972. The theory states that species lie in a state of stasis (that is, a period of inactivity or equilibrium) and there is little morphological change before there is a rapid burst of change, which perfectly explains why there are few transitional fossils to be found. Punctuated equilibria is the missing piece to Darwin’s theory of evolution. But what does it have to do wth the evolution of Man?
As you can see, Eldredge and Gould’s theory states that all species spend an extremely long time in stasis, and for any phenotypic change to be noticed in the fossil record, the rapid burst in change had to occur.
Quoting Gould on culture and evolution (1996, page 219-20):
But human cultural change is an entirely distinct process operating under radically different principals that do allow for the strong possibility of a driven trend for what we may legitamately call “progress” (at least in a technological sense, whether or not the changes ultimately do us any good in a practical or moral way). In this sense, I deeply regret that common usage refers to the history of our artifacts and social orginizations as “cultural evolution.” Using the same term—evolution—for both natural and cultural history obfuscates far more than it enlightens. Of course, some aspects of the two phenomena must be similar, for all processes of genealogicallt constrained historical change must share some features in common. But the differences far outweigh the similarities in this case. Unfortunately, when we speak of “cultural evolution,” we unwittingly imply that this process shares essential similarity with the phenomenon most widely described by the same name—natural, or Darwinian, change. The common designation of “evolution” then leads to one of the most frequent and portentious errors in our analysis of human life and history—the overly reductionist assumption that the Darwinian natural paradigm will fully encompass our social and technological history as well. I do wish that the term “cultural evolution” would drop from use. Why not speak of something more neutral and descriptive—“cultural change,” for example?
From the two passages I cited above, to his work on punctuated equilibria, I can definitely see how and why he would believe that there has been no relevant human evolution in the past 50,000 years. These two quotes, one from Stephen Jay Gould and the other from evolutionist Ernst Mayr show the “conventional wisdom” about human evolution:
There’a been no biological changes in humans in 40,000 or 50,000 years. Everything we call culture we’ve built with the same body and brain
—Stephen Jay Gould
Something must have happened to weaken the selective pressure drastically. We cannot escape the conclusion that man’s evolution towards manness suddenly came to a halt.
These quotes are from page 1 of The Ten Thousand Year explosion. Many great thinkers have suggested that human evolution has halted ever since the emergence of behavioral modernity, however, this couldn’t be further from the truth. I fully understand why such great evolutionists like Gould and Mayr believe that human evolution has halted and their arguments make complete sense based on the data (punctuated equilibria for one). But to any knowledgeable race-realist, they know that these claims are bunk and that human evolution has most definitely accelerated within the last 10,000 years (due to agriculture, the advent of farming) that made it possible for a bigger population and, along with it, a higher chance for high IQ alleles and other positive traits to spread throughout the population as it increased fitness in the environment.
HOWEVER, agriculture was good and bad for us. The good increased our population size that made it possible for high IQ alleles to spread throughout the population. The bad was along with an increase in population size, living in one spot with large groups of people upped the chances for disease acquisition, that of which are not found in hunter-gatherer populations (because they’re constantly moving, not staying in one place). According to John Hawks, our brain size has decreased, going from 1500 cc on average to 1350 cc on average, and the cause is, and this is hard to believe with the advent of agriculture (and thus, supposedly better nutrition) worse nutrition due to the advent of agriculture. Another reason I can posit is that due to more group behavior and social cohesion, we could work together with others and that, over time, would shrink our brains since we wouldn’t have to “do all the thinking”, a type of “self-domestication”, if you will.
The denial of any human change over the past 50,000 years is clearly ridiculous, however it is grounded in solid science. But with the advent of The Ten Thousand Year Explosion by Cochran and Harpending, they blasted all of the misconceptions away about no genetic change in humanity over the past 50,000 years. But, to the dismay of those who believe in “progressive evolution”, the same agriculture that was responsible for this boom—this explosion—over the past ten thousand years is also the cause of our decreasing brain size and stature. I’ve documented the change of erectus or habilis into floresiensis, this is proof enough that evolution can “work backward” (whatever that means) and have an organism become “less complex” (going back to left and right walls of complexity, which I just wrote on last night). Floresiensis is the perfect example that an organism can become less complex than a predecessor and the cause, in this context, is due to less energy on the island which led to a decrease in caloric consumption and along with it a decrease in brain size since that was what was best for that environment (due to less caloric energy being available).
While Gould makes a compelling argument in arguing against the explosion of Man in the past 50,000 years, modern data tells us otherwise. This explosion was due, in part, to agriculture which led to more social cohesion (both of those variables are also leading to a decrease in brain size). With the understanding of Eldredge and Gould’s punctuated equilibria theory, you can then see how and why Gould denied the genetic change in anatomically modern humans over the last 50,000 years. He, however, is wrong here.
I fully agree with Gould that cultural change can outstrip Darwinian evolution—he is right there. But, to make the leap and then say that there is no basis for genetic change in AMH (anatomically modern humans) is clearly wrong. I know that Gould was driven by his politics, partly, to deny any change in human nature and genetics in the past 50,000 years. Though, I don’t care about that. I care about looking at one’s perspective through a scientific lens. While Gould is wrong on his views of hereditarianism, he is 100 percent correct on “progressive” evolution and that there is no so-called “drive to complexity”. It’s his views on human evolution as a whole that are wrong. We know that faster evolution gives rise to more racial differences, and, obviously, more “differences” can either be “good” or “bad” depending on the environmental context. In my tirades over the past 6 weeks on the non-progressiveness and non-linearity of evolution, I’ve shown that these differences can either go to the “left wall” or “right wall” of complexity.
To deny the speed of evolution ever since modern behavior, and even the agricultural revolution is wrong. Too much evidence has piled up for that position. I do, after reading a lot of Gould’s work recently, understand how and where he came from with that argument, all though he was clearly wrong. Culture is learned—not biologically inherited. The cultural norms we know well are learned behaviors.
Finally, and what it seems Gould didn’t realize, is that there is gene-culture coevolution. Learned social information is central to our adaptations as humans. New cultural tendencies may force a novel and new evolutionary selection pressure that may incur new phenotypic changes. In this sense, genes and culture simultaneously evolve side-by-side with each other. Again, stressing that there is no “unilateral direction” in which these changes go, they just occur based on new environmental pressures. Thusly, to say that there is any “progress” or any inherent “drive” in evolution makes no sense. Due to which cultures we “inherit” that will drive which changes occur in that population but not another, they’d be different (as we know all genetically isolated humans are), but none would be “better” than another since they have incurred new traits to better survive in that environment; each different culture will further gain a different phenotype due to the differing culture which puts a differing selective pressure on that population.
The notion of no change in humans over the last 50,000 years is wrong. It has been driven by the rise in agriculture (giving us both positive and negative traits) along with each culture that each population adopted due to the differing selection pressures and environments over the course of their evolution genetically isolated from every other human culture. These differing cultural tendencies also gave rise to slightly faster evolution and different and novel environments in comparison to other populations. With these variables working in harmony with each other, these then accelerated human evolution (for better or worse). That same advent of behavioral modernity 50,000 years ago gave rise to the Out of Africa event. Humans then spread across the planet. In time, after being differing “founding populations” for the current races/ethnies today, differing cultures were adopted due to the differing evolutionary pressures. This is the main reason why genetically isolated human populations show such stark differences between them: Because evolution has sped up since the advent of behavioral modernity, agriculture and the adoption of culture by humans that have all contributed to making Man so different compared to the rest of the Animal Kingdom.
I came across this garbage from the DailyStormer the other day, Racial Realities of Southern Europe that has, of course, huge misconceptions on the genetic history of Southern Europe. This “Sven” guy–like most Nordicists–cherry-picks to prove his idiotic and untrue points, like most Nordicists. I won’t be going through the garbage video on the site (since it’s too boring and his fake voice irritates me) but I’ll go through the comments section.
Italy once contained Rome, but Rome lost its racial purity when it made citizens of all races, only later to be rescued by the invasion of new and vigorous barbarian stocks.
Stupid. No basis in reality–only has a basis in Nordicist fantasies.
The crazies in the comments ramble on and on about “blonde-haired Jesus”, the founding Romans having blonde hair, Spartans and Macedonians had blonde hair (wut?), Iberians were blonde (as if they don’t have a sizeable population that is blonde today). All idiotic garbage that no serious person who has ever read any serious genetic studies takes seriously.
“His Name is YHVH” says:
And I’m not going to debate this. I’ve read meticulous translations of Homer, and Arthur Kemp, and the viking invasion of Greece after the volcanic eruption.
Who in the hell cites March of the Titans seriously for genetics or anything else for that matter? He has such a warped view of history, muh Nordics was Egyptians, muh Nordics was Native Indians, muh Solutrean Hypothesis, muh blonde-haired, blue-eyed Greeks and Romans. Idiocy with no basis in reality. It’s funny. Nordicists get on Afrocentrists for attempting to steal European history, yet Nordicists DO THE SAME THING. Nordicists and Afrocentrists are two sides of the same coin. Yet neither of them realize that. Come on guys, #its2016 don’t cite trash like MotT and expect to get taken seriously by anyone who knows what they’re talking about.
So, you want to be superior to the niggers and the mestizzos and the chinamen but then you don’t want to be inferior to anything above you, thus acknowledging superior and inferior exist on the one hand when it suits you conveniently and then arguing against it when it does not. Now which is it?
This “Sven” guy thinks that the Nordic race originate in North Africa. But what do genetic studies tell us? I’ll quote Razib here:
read this paper: http://arxiv.org/pdf/1502.02783.pdf i have blogged extensively on this, i’m not going to repeat myself at length. #becauseIts2016 and the data is out there.
One may say “The Nordic traits are recessive so it’s impossible for us to have been a result of mongrelization”.
one may say that if you are retarded. i can name two “nordic traits,” lactase persistence and skin color, which are not recessive. the former is mostly dominant (h ~ 1) while the latter exhibits midparent parent values closer to light than dark (h > 0.5). others, like eye and hair color are more recessive (h < 0.5). but one can not say that an individual is mostly recessive or dominant, as that is not even wrong.
if you are a “racerealist” you should know these basic facts of human population genetics in 2016. otherwise you are a racemythist.
(of course, anyone who has seen my son would laugh at the idea that “nordic traits” are recessive like ~20% of northern europeans he is a het. on KITLG locus with one loss of function allele)
(oh, and also, nordic traits are recent anyway, so ancestry is less important than you think: http://www.nature.com/nature/journal/v528/n7583/abs/nature16152.html)
Nordicists et al, it’s #2016, please get up to speed on the latest studies and data. If you won’t get up to speed on the matter, don’t even call yourself a ‘race-realist’, you’d be better off calling yourself a ‘race-mythist’ as Razib says.
No, I believe Aryan originated in central asia, and migrated to Europe.
“Wesley Lysander” says:
Combined data from two large mtDNA studies provides an estimate of non-Caucasoid maternal ancestry in Italians. The first study sampled 411 Italians from all over the country and found five South Asian M and East Asian D sequences (1.2%) and eight sub-Saharan African L sequences (1.9%). The second study sampled 465 Sicilians and detected ten M sequences (2.2%) and three L sequences (0.65%). This makes a total of 3% non-white maternal admixture (1.3% Asian and 1.7% African), which is very low and typical for European populations, since Pliss et al. 2005, e.g., observed 1.8% Asian admixture in Poles and 1.2% African admixture in Germans. (Plaza et al. 2003; Romano et al. 2003)
Similar data from the Y-chromosome reveals Italians’ even lower non-Caucasoid paternal admixture. Both studies obtained samples from all over the mainland and islands. No Asian DNA was detected anywhere, but a single sub-Saharan African E(xE3b) sequence was found in the first study’s sample of 416 (0.2%), and six were observed in the second study’s sample of 746 (0.8%). The total is therefore a minuscule 0.6%, which decreases to 0.4% if only Southern Italians are considered and 0% if only Sicilians are considered.Again, these are normal levels of admixture for European populations (e.g. Austrians were found to have 0.8% E(xE3b) by Brion et al. 2004). (Semino et al. 2004; Cruciani et al. 2004)
An analysis of 10 autosomal allele frequencies in Southern Europeans (including Italians, Sicilians and Sardinians) and various Middle Eastern/North African populations revealed a “line of sharp genetic change [that] runs from Gibraltar to Lebanon,” which has divided the Mediterranean into distinct northern and southern clusters since at least the Neolithic period. The authors conclude that “gene flow [across the sea] was more the exception than the rule,” attributing this result to “a joint product of initial geographic isolation and successive cultural divergence, leading to the origin of cultural barriers to population admixture.” (Simoni et al. 1999)
More Nordicist idiocy with no basis in reality.
Science proves Mediterranean people are exposed to sun radiation more often, and that’s it. Scandinavian people get their pale features from being exposed to colder climates more often. Any pan-Nordic theory that all other Europeans are icky tainted negroes has long been debunked.
So you need science to tell you that Meds are exposed to more sun from being closer to the equator? ….I see.
Right at the beginning of the chapter he explains that the only true Mediterraneans left are the Welsh and the Irish.
This guy is such an idiot. I guess the Germans are negro because they have 1.2 percent negro admixture. “Through DNA research”. He doesn’t keep up on the latest studies. Dumb prole. Moreover, Mediterranean peoples stretch from Southern Europe to North Africa to the Middle East; they are all Mediterranean people. Though, people who don’t keep up on the latest studies and only retarded dogma think otherwise.
“Eric Stryker” says:
Another weird thing is that Stoddard himself looks almost textbook Mediterranean.
Then “Sven” says:
What he looks like bears no relevance to his work at all.
I see you are now reduced to ad hominem equivalent in your quest to discredit his work.
This is GOLD coming from someone like him. I wouldn’t doubt that this guy is one of those people to throw away a source because it comes from a leftist magazine or throw something away and disregard it because a Jew wrote it. Such hypocrisy.
“Sven” then says:
I can’t stop laughing! This is coming from the prole moron who says all of these lies SEEKING TO BEND THE TRUTH TO TRY AND MAKE IT SUIT HIMSELF. People’s idiocy and lack of introspection into their views never ceases to amaze me.
Soooooo why should any other sources be thrown away for where they come from? People say “H-he’s a Jew don’t listen!!!” But that has “no relevance to his work at all.”
“Eric Stryker” says:
Truest thing said in that thread. Biblical Nordic Spartans? Who the hell believes this garbage?
Just like a Jew you try to smear White racial researchers like Stoddard and claim Josephus as one of yours.
Hey, let’s go of some old book and not modern-day genetic studies! You’re a Jew because you disagreed with me.
This Sven moron thinks that Nords originated in North Africa!! My sides!!!
Anyone reading this, to see the true origin of the Nords, read this.
Nordics were not in pre-historic Germania in large numbers when Rome was being built, they were mainly in the Levant, North Africa and southern Europe.
I am convinced that this guy is retarded. Nordics came from North Africa, the Levant and Southern Europe? CITATION NEEDED. I already showed that Nordic traits are recent, so how the hell could they originate in MENA countries and South Europe?
“Sven” then says:
I guess you must think Nordics were sitting in the ice, freezing their asses off doing nothing and leaving no trace until they suddenly discovered civilisation in Europe in the first millennium.
This is one of the only things he said that’s true in this thread. That’s pretty much how it went down. What’s funny is that your ideological brethre–the Afrocentrists– call whites “cave beasts”. Who were these “cave beasts”? Nords! They were “living in caves” before Rome cultured and civilized them. Both the Romans and Greeks had pretty unkind words for the barbarians to the North.
Then “Sven” cites all of his garbage “Radio Stormer” podcasts as proof. Where are the genetic studies from Pubmed and PLOS Genetics? The fact that this guy had to link to his garbage and untrue radio show speaks volumes.
“Sven” then says that Copts and Berbers were Nordic. Ha! These Nordicists, man. They’ll say anything to grab others’ history, just like their cousins the Afrocentrists.
“His Name Is YHVH” comes back and says:
Correction, my uneducated friend, Nordics DID build Rome. They also built the pyramids, or didn’t you know, didn’t you see the blond hair mummies?
Why don’t you go read March of the Titans and learn about it?
“Go read MotT bro!! It’s the truth of European history and the white race!!” No serious person takes that book seriously. Hey didn’t you see the blonde hair mummies!!?? It’s not like the racial phenotypes we code aren’t recent or anything!!
I LOVE how these morons link to backwater websites and not Pubmed or PLOS Genetics for their information. Shows what they read!!!
The Bible itself tells you Jesus ancestors were White, fair, ruddy and blue eyed. It also tells you that the Spartans were descended from Judah in the book of Maccabees and Flavius Josephus Histories.
“Believe the Bible about genetics.” I wonder if these people read what Biblical scholars say on interpretations of the Bible. You know they don’t so, like their cousins the Afrocentrists and “black Israelites”, they take Bible verses and warp them to suit their needs. Isn’t it funny how these groups all hate each other but they’re cut from the same ideological cloth?
People like this guy just push anything that affirms their ideology. It’s not based in science–it’s based in fantasy. To see the true origin of the Nordics, see here, here, and here. Most of what Nordicists say–just like their ideological cousins the Afrocentrists–is not based in reality but based in fantasies.
This article from the Unz Review, What Race Were the Greek and Romans? harps on and on about the same things that “Sven” does. However, the author gets summarily dismantled in the comments.
PumpkinPerson seems to be making his blog “more politically correct“. So he seems to be removing his posts that he may deem “insensitive” to certain people. You run a (mostly) HBD blog. People who go to a HBD blog must know that they may come across certain truths that they may find uncomfortable–and even ‘offensive’. This seems like it’ll be my last reply to PP on this matter as he has removed the thread we were conversing about this matter in. Now that PP is becoming more ‘PC’, is he going to disavow his views on “progressive” evolution, “superiority and inferiority” when speaking about organisms and human races and “the concept of ‘more evolved'”?
RR: You’ve stated numerous times that evolution is progressive. Which is why I assume you’re equating “progress” with “more evolved”. Do you believe that more evolved implies progress or that progress implies more evolved?
PP: I PERSONALLY believe more evolved life is on average, superior to less evolved life, but there is nothing intrinsically progressive about being more evolved, and there’s no reasons for opponents of progress to avoid the term. In some cases, the more evolved form is clearly inferior such as when a dog evolved into a cancer.
That’s the point. The ‘more evolved’ organism is more often than not ‘inferior’ compared to its predecessor. This shows that there is no ‘progress’ to evolution. And the “more evolved” form became “inferior” to its predecessor due to changes in environment. If those environmental pressures were different, a whole slew of phenotypic changes would have occurred to have the “less evolved, inferior” organism be “superior” to its predecessor. This line of reasoning shows how idiotic of a concept “progress” in evolution is.
RR: Moreover, ancestral state reconstructions of absolute brain mass, body mass and EQ revealed patterns of increase and decrease in EQ within anthropoid primates and cetaceans.
PP: But the OVERALL pattern has been one of increase. The average brain size of ALL living mammals has TRIPPLED in 65 million years.
I just showed that there are increases AND decreases in the fossil record. No one denies that there has been an upward trend in brain size. However, as I’ve said to you previously, our brains have been shrinking for 20ky, with there being evidence that it’s been decreasing for 20ky. Sure, the trend over the past few million years shows an increase, but the trends for the past 30k years or so show a decrease and this is due to agriculture.
RR: Just showed this is wrong. (On morphology being an indicator of speciation)
PP: No you just cited a paper that agrees with your definition of species. That’s not an argument.
I cited this paper by Ernst May, What is a Species, and What is Not? where he says:
I analyze a number of widespread misconceptions concerning species. The species category, defined by a concept, denotes the rank of a species taxon in the Linnaean hierarchy. Biological species are reproducing isolated from each other, which protects the integrity of their genotypes. Degree of morphological difference is not an appropriate species definition. Unequal rates of evolution of different characters and lack of information on the mating potential of isolated populations are the major difficulties in the demarcation of species taxa.
Just because you believe that speciation is based on morphology doesn’t make it true, PP.
RR: Sure they are CORRELATED, but it doesn’t imply a cause. A relationship is not a cause. I just showed you a paper that shows you’re wrong but whatever.
PP: But a correlation is enough to show that evolution is progressive. Evolution correlates with progress = evolution is progressive.
RR: How would this be gauged? Would you say to look at the LCA and gauge morphological changes?
PP: That’s one way.
Well, now the onus on you is to provide evidence for your claim that there was no–or ‘hardly’–any morphological changes in equatorial populations. You have to prove that they stayed similar to the LCA. Good luck!
PP: No I’m arguing that FEWER changes occurred in Africa because there were fewer splits in the African branch (at least as conceptualized by Cavalli-Sforza)”
This is MEANINGLESS. This is a HUGE intuitive misconception on how people read phylogenies. Just because Africans didn’t ‘split’ based on phylogenies DOESN’T MEAN that they had little to no morphological changes. The racial phenotypes we code are recent, so this throws a wrench into your intuitive misconceptions on phylogenies.
RR: Prove it!
PP: The proof is that those humans who scientists believe have preserved the phenotype of the earliest modern humans (i.e. Andaman islanders, Papua New Guineans) all look very Negroid, as do those forensic reconstructions of ancient skulls you reject.
This isn’t proof. Just because scientists (like who?) ‘believe’ that Andaman Islanders and Papuans (no, no and no!!) “preserved the phenotypes of ancient humans” doesn’t mean that they are in any way, shape, or form SIMILAR to the original populations who migrated out of Africa 70kya!!!
Ancient skull reconstructions are meaningless. You cannot infer what type of lips an ancient human had. There are numerous problems with facial reconstructions, most specifically for this conversation, you cannot gauge certain things JUST from a skull:
The finished product only approximates actual appearance because the cranium does not reflect soft-tissue details (eye, hair, and skin color; facial hair; the shape of the lips; or how much fat tissue covers the bone). Yet a facial reconstruction can put a name on an unidentified body in a modern forensic case—or, in an archaeological investigation, a face on history.
It can ‘put a face to history’, however this reconstruction of, for instance, Mitochondrial Eve DOES NOT show what she actually looked like, specifically her lips, as seen above.
RR: I fully understand what you’re saying. Except I’ve shown how it’s wrong! You can’t say one branch means morphological change AND EVEN THEN, morphological change does not equal speciation as shown in the Mayr paper.
PP: You can say that if one branch has lots of splits, it implies environmental changes and pressures (since generally speaking, that’s what causes splits) and environmental changes generally cause morphological changes, which is one definition of species.
But this definition of species is wrong as I’ve just shown. Ernst Mayr shows, in the paper of his linked above, that morphology is not enough to denote speciation.
RR:Do you know better than people who do this for a living? There are multiple papers on misconceptions of cladograms and the like. I get its original nd I respect that. You’re a smart mother fucker pp. But that doesn’t mean you’re right here.
PP: I understand why you think I’m reading the trees wrong. I used to think the exact same way as you, and the sources you cite. Laymen shouldn’t make the simplistic assumption that higher branches = more evolved and that’s why scientists try to dispel that notion. Because the tree is just there to show relatedness, and evolution can happen or not happen at any point in the tree, no matter how many splits or non-splits occur.
Now you’re getting it!
PP: However once we understand all that, we have to ask ourselves, even though IN THEORY, any branch on the tree can evolve in any direction, and there’s nothing about the tree that implies a hierarchy, IN REALITY, is there a correlation between tree position and brain size and other measures of “progress”? I’ve provided evidence that there is. You can either ignore the evidence because it doesn’t fit the theory that branch placement is irrelevant, or you can realize that evolution is a little more nuanced than some simplistic introductory Berkeley paper implied.
Now you’re not. First off, the Berkely paper is not ‘simplistic’, nor is one of the papers that the Berkely papers cites, Understanding Evolutionary Trees by Gregory (2008). He shows the most common misconceptions one has on reading phylogenies. And most–if not all–of your misconceptions on phylogenies are brought up in the paper with great detail into the misconceptions as well as how to correct the misconceptions that one has while reading phylogenies. I’ve said to you, time and time again, that brain size is PREDICATED on the amount of kcal that one consumes. If were to eat 1000 kcal a day for, say, 2000 years, what would happen to our brain size as well as our body size? Would they stay the same, grow bigger or get smaller? Adequate kcal–as well as adequate nutrients–are the driver of brain size. Without those two variables, brain size wouldn’t have been increasing. Moreover, as I’ve documented two weeks ago, H. floresiensis showed a decrease in brain size as well as body size, having evolved from either H. erectus or H. habilis. This directly shows that brain size is dependent on the surrounding environment as well as the quality and quantity of the food that the organism consumes. Branch placement IS irrelevant. You can rotate the branches all around and that would throw your theory out the window. This is what you don’t understand.
Professional papers in evolutionary biology continue to host expressions in agreement with the pre-evolutionary metaphor of the scala naturae (the great chain of being), when contrasting ‘lower’ to ‘higher’ representatives of a given branch of the tree of life. How pervasive is the persistence of progressionist, pre-evolutionary language in contemporary papers?
We document here the prevalence of this unexpected linguistic survival in papers published between 2005 and 2010 by 16 top scientific journals, including generalist magazines and specialist journals in evolutionary biology. Out of a total of 67,413 papers, the unexpectedly high figure of 1,287 (1.91%) returned positive hits from our search for scala naturae language.
A quantitative appreciation of the survival of progressionist language in scientific papers is the first step towards its eradication. This will obtain by improving skills in tree thinking as well as by more careful editorial policy.
Wow! 1.91 percent, 1,287 papers returned positive hits for ‘great chain of being’ language. These terms need to be removed from evolutionary biology as they don’t allow the appreciation of the randomness in the evolutionary processes.
Evolution is a random process. It’s an unconscious, non-linear event as I have documented extensively over the past month.
I’ll end with a quote from Ernst May’s book What Evolution Is:
Another widespread erroneous view of natural selection must also be refuted: Selection is not teleological (goal-directed). Indeed, how could an elimination process be teleological? Selection does not have a long-term goal. It is a process repeated anew in every generation. The frequency of extinction of evolutionary lineages, as well as frequent changes in direction, is inconsistent with the mistaken claim that evolution is a teleological process. Also, there is no known genetic mechanism that could produce goal-directed evolutionary processes. Orthogenesis and other proposed teleological processes have been thoroughly refuted (see Chapter 4).
To say it in other words, evolution is not deterministic. The evolutionary process consists of a large number of interactions. Different genotypes within a single population may respond differently to the same change of the environment. These changes, in turn, are unpredictable, particularly when caused by the arrival at a locality of a new predator or competitor. Survival during a mass extinction may strongly be affected by chance. (Mayr, 1964: 121)
In my first article on this matter, I showed how Richard Lynn claims the average IQ in Italy is around “89-92” for Sicily and the South and around 103 for the North. I showed how he was wrong and what data he overlooked to fit his hypothesis. Lynn’s 2011 article IQs in Italy are higher in the north: A reply to Felice and Giugliano was a reply to Myth and reality: A response to Lynn on the determinants of Italy’s North–South imbalances. Felice and Giugliano brought up Lynn’s four main theses: a) the South’s “economic backwardness” in terms of economics ‘throughout history’; b) the evidence provided by Lynn wasn’t enough to ‘prove’ a cause of lower IQ for S. Italians; c) the evidence provided by Lynn wasn’t enough to show that S. Italians score lower than N. Italians; and d) the supposed ‘high rates of MENA admixture’ in S. Italians. I blew up all of these claims in the beginning of the year, more specifically I blew up up the claims about MENA admixture back in January. I’ll be going through Lynn’s 2010b article correcting any discrepancies. It’s worth noting that he still pushes the so-called ‘MENA admixture’ as being a substantial CAUSAL factor when there is NO evidence for this big of a ‘gap’ between the North and the South. The Lynn quotes will be from his 2010 paper linked above. I had also thought that ‘migrants’ from MENA countries could have contributed to the gap between the North and South, but since this isn’t the case for France then it shouldn’t be so for Italy. However, since Italy is a hub for these people when they first illegally enter Europe, they may stay and get counted as citizens and the children of these immigrants grow up and get accounted in the data. This is plausible, since a lot of ‘migrants’ may stay where they first get which is Southern Europe, mainly Sicily and Southern Italy.
We now present new data showing that IQs are higher in the north of Italy than in the south. In the previous study, data were presented for 12 Italian regions from the PISA (Program for International Student Assessment) 2006 study of the reading comprehension, mathematics and science performance of 15 year olds, regarded as measures of intelligence. We are now able to give similar data on the reading comprehension, mathematics and science performance of 15 year olds in 20 Italian regions obtained in the 2009 PISA study (OECD, 2010). These are given in Table 1. This shows, reading from left to right, the latitude of the Italian regions, the mean PISA scores for 12 regions for 2006 given in Lynn (2010a), the mean scores of 15 year olds on reading comprehension, mathematics and science understanding for the 20 Italian regions obtained in the 2009 PISA study, and the averages of the three 2009 PISA scores given because it provides a convenient summary of the scores on the three tests.
I already went through this in my previous article, but for clarity, I’ll go through this again.
Cornoldi, Giofrè, and Martini (2013) showed how there are problems inferring Italian IQ from the very PISA data that Lynn cites. There was a relevant decrease between the North and South. If the PISA test showed genetic proclivities between the North and South, why was there a relevant decrease in the three-year period? Because it is not an intelligence test, but a test of educational achievement. D’Amico et al (2011) conclude:
Our examination of intelligence test score differences between the north and south of Italy led to results that are very different from those reached by Lynn (2010a). Our results demonstrate that by using intelligence tests to assess differences in ability rather than using achievement scores as a proxy for intelligence, children from the south of Italy did not earn lower scores than those from the north of Italy. Rather, they were even higher in Raven’s CPM. However, we see no advantage in claiming that children in the south are “more intelligent” than children in the north, because these groups are different on a number of variables (e.g., environmental factors, educational influences, composition of the samples) that influence differences in test scores.
Either no difference or Southern Italians scored higher. When using purer measures of intelligence (Raven’s Progressive Matrices) so-called “differences” in “intelligence” disappear.
It will be noted that the regional differences in both language and math ability increase with age. For example, in language ability the regional differences in the youngest children (P2) range between 1.6 and −3.8, a difference of 5.4, while the differences in the oldest children (2S) range between 3.6 and −4.4, a difference of 8.0. Similarly, in math ability the regional differences in the youngest children (P2) range between 0.8 and −1.0, a difference of 1.8, while the differences in the oldest children (2S) range between 4.3 and −5.4, a difference of 9.7. These age differences would be predicted from the thesis that the regional differences have a genetic basis, because the heritability of intelligence increases during childhood (Plomin, DeFries, & McClearn, 1980, p. 334).
On other measures of achievement, such as the INVALSI examinations, Southern Italians do not score lower, and in some cases may even score higher (Robinson, Saggino, and Tommasi (2011). Moreover, the N/S differences in ‘cognitive ability’ don’t exist at age 7, the IQ/income relationship didn’t exist in the past, and the MENA admixture in Southern Italians is minute (Daniel and Malanima, 2011). The so-called MENA admixture that Nordicists and Lynn like to say is the subject of my next point.
Further data for the proportion of North African ancestry in the Italian regions are available in the frequency of the haplogroup E1b1b allele. This is a marker for North African ancestry, where it reaches frequencies above 50% and peaks at around 82% in Tunisia (Zalloua et al., 2008). The frequencies of the haplogroup xR1 and the E1b1b alleles are taken from Capelli et al. (2006), Capelli et al. (2007), Di Giacomo et al. (2003), Balaresque et al. (2010), Scozzari et al. (2001), and Semino et al. (2000). These data are given in columns 11 and 12 of Table 1 and the correlations between these and the other variables are given in Table 2.
As said and cited above, the so-called admixture from MENA populations in Southern Italians accounts for an extremely small fraction of the overall Southern Italian genome. The cause for lower achievement (“IQ” according to Lynn) in Southern Italians rests on this very pertinent point. And it’s wrong. Furthermore, and this is for Sicilians, the contribution of their genome by the Greeks is 37 percent, with the North African contribution being 6 percent. Daniel and Malanima (2011) ask ” Can the Greek heritage to the Western culture really be associated to a lower IQ?” The answer is, clearly, no. Moreover, a Central Italian province has the highest amount of MENA admixture, yet they have higher scores than Southern Italy. What does that tell you?
Richard Lynn’s Italian IQ data is garbage. Purer measures of intelligence such as Raven’s Colored Progressive Matrices show a decrease in the “intelligence gap” and in some cases, Southern Italians score higher than Northern Italians. When using measures of “IQ” from PISA data, these so-called differences disappear. Lynn’s data he cites in his 2010a paper don’t control for socio-cultural differences and school quality. There is numerous data that suggests the school quality in Southern Italy is worse than that of the North; this difference in school quality then affects educational achievement. Since PISA is a test of educational achievement and not intelligence (D’Amico et al, 2011), what accounts for these differences in achievement in the various studies may (and in my opinion, does) account for the differences in educational achievement between Northern and Southern Italians. The measurements in various studies may be influenced by the larger between-schools variability that is present in the South (Cornoldi et al, 2010; Daniel and Malanima 2011).
Finally, some people may point to the GDP differences between North and South Italy as proof of genetic/intelligence differences between them. However, the Mafia accounts for around a 20 percent drop in GDP in Southern Italy. To say that any differences in GDP can be accounted for without first controlling for things like this is dishonest. The presence of Mafia in areas shows lower growth and a sharper increase in murders. Each time homicides rise, GDP falls between 16-20 percent (Pinolli 2012). The presence of the Mafia had a devastating effect on the economies in that area between the 70s and 00s.
In sum, PISA is garbage to infer intelligence from as they are tests of achievement and not intelligence. Other tests of achievement show a decrease in the gap and/or Southern Italians scoring higher. Moreover, no substantial genetic differences exist between the North and the South, falsifying Lynn’s thesis for the causality of the differences between the North and the South. The oft-cited GDP difference between Northern and Southern Italy can be accounted for by the presence of the Mafia. Whenever the murder rate rises (due to Mafia activity), the GDP decreases. None of these factors have been taken into account and they explain the difference between the North and the South. It is environmental in nature–not genetic. Lynn’s Italian IQ data is garbage and should not be cited. It’s just a Nordicist fantasy that Southern Italians score lower than Nothern Italians.