Home » Posts tagged 'disease'
Tag Archives: disease
Hoffman et al (2016) questioned laypeople and medical students and residents on a 15-question questionnaire regarding different beliefs people have about racial differences. The point of the questionnaire was to ascertain how people are biased in regard to racial differences in pain and how the bias affects the treatment the individual of the certain racial group. Only two of the questions had anything to do with pain. In this article, I will answer the questions one by one.
1. On average, Blacks age more slowly than Whites.
This one is true (though they rate this question as false). I don’t know why, though, because there are differences between black and white skin and these differences affect the rate of aging between races.
Campiche et al (2019) found that there is a difference in aging regarding skin in different ethnies (the cohorts were French and Mauritanian). The average age was 46 for the French and 56 foe the Mauritanians, and the Mauritanians still looked younger! Campiche et al (2019) write:
The difference in age between our Caucasian and Black African cohorts (median age 46 years vs 56 years) could bring into question the comparisons of the two cohorts. Nevertheless, we mostly found that Caucasians displayed more severe signs of aging than Black Africans which is in line with the common understanding that the onset of aging in fair skin starts earlier than in darkly pigmented skin and that there were differences in the appearance of lip lines and facial pores.
This question is true, contrary to the claims of Hoffman et al (2016).
2. Black people’s nerve-endings are less sensitive than White people’s nerve-endings.
I can find no literature on this matter and the only articles point me to Hoffman et al (2016) and different articles on the matter. I accept the claim as false.
3. Black people’s blood coagulates more quickly–because of that, Blacks have a lower rate of hemophilia than Whites.
Blacks’ blood does clot faster than whites, and part of the cause is differences in the PAR4 gene family (Bray et al, 2013). The reason that blacks’ blood clots faster than whites’ is due to the effects of thrombin, an enzyme that activates the molecule responsible for blood clotting. Blacks do have a lower rate of hemophilia than whites, though, but not by much (13.2 cases/100,000 for whites compared to 11 for blacks) (Soucie, Evatt, and Jackson, 1998). The question is true, contra Hoffman et al (2016).
4. Whites, on average, have larger brains than Blacks.
They stated that this question is false, which is bizarre. I am aware of no literature that attests to the claim that whites do not have larger brains than blacks. Many analyses back the claim that whites have larger brains than blacks (though Nisbett disagrees and states that there are studies that show the contrary but does not leave a citation) (Rushton, 1997). (Though see Race and Brain Size: Blacks Have Bigger Brains for an alternate view.)
5. Whites are less susceptible to heart disease like hypertension than Blacks.
They say this claim is true. And it is. Hypertension (high blood pressure) is a physiological variable which means that social environment can greatly affect it (Williams, 1992). Higher rates of obesity drive this association as well. American blacks have a lower rate of CHD than whites (7.2 compared to 7.8) but this is reversed for women (7.0 compared to 4.6) (Leigh, Alvarez, and Rodriguez, 2016). The CDC, though, says that the rate of heart disease is the same between blacks and whites, at 23.8 percent though (slightly higher than the 23.5 percent average).
6. Blacks are less likely to contract spinal cord diseases like multiple sclerosis.
7. Whites have a better sense of hearing compared with Blacks.
They state that this claim is false. Pratt et al (2009) state that hearing loss is more likely to occur in white over black elderly patients.
8. Black people’s skin has more collagen (i.e., it’s thicker) than White people’s skin.
They state that this claim is false, and it is. That there is no difference in skin thickness between blacks and whites is irrelevant, though. Black skin is more compact, with greater intercellular cohesion (LaRuche and Cesarini, 1992; Rawlings, 2006).
9. Blacks, on average, have denser, stronger bones than Whites.
10. Blacks have a more sensitive sense of smell than Whites; they can differentiate odors and detect faint smells better than Whites.
This claim is false, according to Hofmann et al. And I can find nothing in the literature on the matter so I will accept their claim.
11. Whites have more efficient respiratory systems than Blacks.
They state that this claim is false. However, Schwartz et al (1988) state that “Controlling for sex, age, standing height, and body mass index, blacks had consistently lower levels of lung function for most measures.” This claim seems to be true.
12. Black couples are significantly more fertile than White couples.
They state this claim is false. Wellons et al (2008) state that “black women were more likely to have experienced infertility.” So the claim is in the opposite of what Hoffman et al question.
13. Whites are less likely to have a stroke than Blacks.
They state that this claim is true, and it is. Minorities are more likely to have a stroke than whites. Brevata et al (2005) write that blacks are more likely to have severe strokes than whites. The claim is true.
14. Blacks are better at detecting movement than Whites.
This seems like a bizarre claim. They state that it is false and I will accept it as false since I can find no literature on the matter.
15. Blacks have stronger immune systems than Whites and are less likely to contract colds.
Europeans and Africans have different immune systems. The immune system of black Americans is stronger than whites’. Twenty-four hours after being infected with salmonella and listeria bacteria, researchers found that the white blood cells from black Americans responded quicker than that of the white blood cells from white Americans. The white blood cells from black Americans ridded the infection about three times quicker than the white blood cells from black Americans. They stated that this claim is false, but it appears to be true.
So, by my count, out of the 15 questions asked, 8 of them have a factual basis (with some in the opposite direction), compared to Hoffman et al’s (2016) assertion that only 4 of them are true. In any case, there are a lot of myths about racial differences out there, and some of these questions by Hoffman et al are myths. Though some of them do have a factual basis. I wonder what kind of literature they referred to when asking these questions, because the literature that I am aware of when it comes to some of these matters is different compared to what Hoffman et al (2016) claim. Racial/ethnic differences do, obviously, exist but there are many myths involved with them.
Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? Surely Roberts would agree that we use her socio-political concept of race when it comes to medicine, but not treat them like biological races. Roberts is an anti-realist about biological races, whereas Hardimon is not—he recognizes that there is a minimalist and social aspect to race which are separate concepts.
In his book Rethinking Race: The Case for Deflationary Realism, Hardimon (2017, Chapter 8) discusses race and medicine after discussing and defending his different race concepts. If race is real—whether socially, biologically, or both—then why should we ignore it when it comes to medical contexts? It seems to me that many people would be hurt by such a denial of reality, and that’s what most people want to prevent, and which is the main reason why they deny that races exist, so it seems counterintuitive to me.
Hardimon (2017: 161-162; emphasis his) writes:
If, as seems to be the case, the study of medically relevant genetic variants among races is a legitamate project, then exclusionism about biological race in medical research—the view that there is no place for a biological concept of race in medical research—is false. There is a place for a biological concept of race in the study of medically relevant genetic variants among races. Inclusionism about biological race in medical research is true.
So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). Sure, some critics would argue that we should be looking at the individual and not their racial or ethnic group. But consider this: Imagine that an individual has something wrong and standard tests do not find out what it is. The doctor then decides that the patient has X disease. They then treat X disease, and then find out that they have Y disease that a certain ethnic group is more likely to have. In this case, accepting the reality of biological races and its usefulness in medical research would have caught this disease earlier and the patient would have gotten the help they needed much, much sooner.
Black women are more likely to die from breast cancer, for example, and racism seems like it can explain a lot of it. They have less access to screening, treatment, care, they receive delays in diagnoses, along with lower-quality treatment than white women. But “implicit racial bias and institutional racism probably play an important role in the explanation of this difficult treatment” (Hardimon, 2017: 166). Furthermore, black women are more than twice as likely to acquire a type of breast cancer called “triple negative” breast cancer (Stark et al, 2010; Howlader et al, 2014; Kohler et al, 2015; DeSantis et al, 2019). Of course, this could be a relevant race-related genetic difference in disease.
We should, of course, use the concepts of socialrace when discussing the medical effects of racism (i.e., psychosocial stress) and the minimalist/populationist race concepts when discussing the medically relevant race-related genetic diseases. Being eliminativist about race doesn’t make sense—since if we deny that race exists at all and do not use the term at all anymore, there would be higher mortality for these “populations.” Thus, we should use both of Hardimon’s terms in regard to medicine and racial differences in health outcomes as both concepts can and will show us how and why diseases are more likely to appear in certain racial groups; we should not be eliminativists/exclusionists about race, we should be inclusionists.
Hardimon discusses how racism can manifest itself as health differences, and how this can have epigenetic effects. He writes (pg 155-156):
As philosopher Shannon Sullivan explains, another way in which racism may be shown to influence health is by causing epigenetic changes in the genotype. It is known that changes in gene expression can have durable and even transgenerational effects on health, passing from parents to their children and their children’s children. This suggests that the biological dimensions of racism can replicate themselves across more than one generation through epigenetic mechanisms. Epigenetics, the scientific study of such changes, explains how the process of transgenerational biological replication of ill health can occur without changes in the underlying DNA sequence.
If such changes to the DNA sequences can be transmitted to the next generation in the developmental system, then that means that the social can—and does—has an effect on our biology and that it can be passed down through subsequent generations. It is simple to explain why this makes sense: for if the developing organism was not plastic, and genes could not change based on what occurs in the environment for the fetus or the organism itself, then how could organisms survive when the environment changes if the “genetic code” of the genome were fixed and not malleable? For example, Jasienska (2009) argues that:
… the low birth weight of contemporary African Americans not only results from the difference in present exposure to lifestyle factors known to affect fetal development but also from conditions experienced during the period of slavery. Slaves had poor nutritional status during all stages of life because of the inadequate dietary intake accompanied by high energetic costs of physical work and infectious diseases. The concept of ‘‘fetal programming’’ suggests that physiology and metabolism including growth and fat accumulation of the developing fetus, and, thus its birth weight, depend on intergenerational signal of environmental quality passed through generations of matrilinear ancestors.
If the environmental quality—i.e., current environmental quality—is “known” by the developing fetus through cues from the mother’s nutrition, stress etc, then a smaller body size may be adaptive in that certain environment and the organism may survive with fewer resources due to smaller body size. In any case, I will discuss this in the future but it was just an example of a possible epigenetic modification on current slaves. I, personally, have noticed that a lot of blacks are really skinny and have really low body fat—who knows, maybe this could be part of the reason why?
This is something that sociologist Maurizio Meloni (2018) calls “the postgenomic body”—the fact that biology is malleable through what occurs in our social lives. So not only is the human brain plastic, but so is the epigenome and microbiome, which is affected by diet and lifestyle—along with what we do and what occurs to us in our social lives. So our social lives, in effect, can become embodied in our epigenome and passed down to subsequent generations. Similar points are also argued by Ulijaszek, Mann, and Elton (2012). (Also see my article Nutrition, Development, Epigenetics, and Physical Plasticity.)So in effect, environments are inherited too, and so, therefore, the environments that we find ourselves in are, in effect, passed down through the generations. Meloni (2018) writes:
On the other hand, by re-embedding the individual within a wider lineage of ancestral experiences and reconfiguring it as a holobiontic assemblage, it may literally dissolve the subject of emancipation. Moreover, the power of biological heredity may be so expanded (as it includes potentially any single ancestral experience) to become stronger than in any previous genetic view. Finally, the several iterations of plasticity that emerge from this genealogy appear so deeply racialized and gendered that it is difficult to quickly turn them into an inherently emancipatory concept. Even as a concept, plasticity has an inertial weight and viscosity that is the task of the genealogist to excavate and bring into view.
Thus, current biological states can be “tagged” and therefore be epigenetically transmitted to future generations. Think about it in this way: if epigenetic tags can be transmitted to the next generation then it would be presumed that that environment—or a similar one—would be what newer generations would be born in. Thus, the plasticity of the organism would help it in life, especially the immediate plasticity of the organism in the womb. Likewise, Kuzawa and Sweet (2008) argue:
that environmentally responsive phenotypic plasticity, in combination with the better-studied acute and chronic effects of social-environmental exposures, provides a more parsimonious explanation than genetics for the persistence of CVD disparities between members of socially imposed racial categories.
Of course, if we look at race as both a biological and social category (i.e., Spencer, 2014), then this is not surprising that differences in disease acquisition can persist “between members of socially imposed racial categories.” Phenotypic plasticity is the big thing here, as noted by many authors who write about epigenetics. If the organism is plastic (if it can be malleable and change depending on external environmental cues), then disease states can—theoretically—be epigenetically passed to future generations. This is just like Jasienska’s (2009, 2013, Chapter 5) argument that the organism—in this case, the fetus—can respond to the environmental quality that it is developing in and, therefore, differences in anatomy and physiology can and do occur based on the plasticity of the organism.
Lastly, Jan Badke, author of Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics (Baedke, 2018), argues that, since the gene-centered view of biology has been upended (i.e., Jablonka and Lamb, 2005; Noble, 2006, 2011, 2012, 2017) for a postgenomic view (Richardson and Stevens, 2015). Genes are not closed off from the environment; all organisms, including humans, are open systems and so, there are relationships between the environment, developmental system, and the genome which affect the developing organism. Baedke and Delgado (2019) argue that the “colonial shadow … biologicizes as well as racializes social-cultural differences among human groups.” Since every race faces specific life challenges in its environment, therefore, each race shows a “unique social status that is closely linked to its biological status.” Thus, differing environments, such as access to different foods (i.e., the effects of obesifying foods) and discrimination can and are passed down epigenetically. Baedke and Delgado (2019: 9) argue that:
… both racial frameworks nutrition plays a crucial role. It is a key pathway over which sociocultural and environmental difference are embodied as racial difference. Thus, belonging to a particular race means having a particular biosocial status, since races include two poles – a social status (e.g., class, socio-economic status) and a biological status (disease susceptibility) – which are closely interlinked. Against this background, human populations in Mexico become an exemplar of types of bodies that are not only relocated to a destabilizing modernized world in which they suffer from socio-economic deprivation. What is more, they become paradigmatic primitive bodies that are unbalanced, biologically deprived, and sick. In short, in these recent epigenetic studies poor places and lifestyles determine poor bodies, and vice versa.
In sum, accepting the reality of race—both in a minimalist/populationist biological manner and social manner—can and will help us better understand disease acquisition and differing levels of certain diseases between races. Recognizing the minimalist/populationist concepts of race will allow us to discover genetic differences between races that contribute to variation in different diseases—since genes do not alone outright cause diseases (Kampourakis, 2017: 19). Being eliminativist/exclusionist about race does not make sense, and it would cause much more harm than good when it comes to racial disease acquisition and mortality rates.
Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the “oppression” is imagined, it can still have very real biological effects that could be passed onto the next generation—and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies; these effects also could have possibly manifested itself in regard to obesity in Latin America post-colonialism. Gravlee (2009) and Kaplan (2010) also argue that the social, too, manifests itself in biology.
(For further information on how the social can and does become biological see Meloni’s (2019) book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics, along with Meloni (2014)‘s paper How biology became social, and what it means for social theory. Reading Baedke’s and Meloni’s arguments on plasticity and epigenetics should be required before discussing these concepts.)
I’m watching Mystery Diagnosis right now, and I heard the narrator say that lupus is three times more common in African Americans than Caucasian Americans. (The woman was black.) So let’s look into it.
Lupus is a long-term autoimmune disease where the body’s immune system becomes hyperactive and attacks healthy tissue. It can damage any part of the body, skin cells, joints, organs. Many symptoms of lupus exist, like kidney inflammation, swelling, and damage to the blood, heart, joints, and lungs. No cure exists for lupus, though there are ways to minimize inflammation through diet and lifestyle.
Lupus is two to three times more likely to occur in women of color—blacks, Hispanics/Latinos, Native Americans, and others—compared to white Americans. Somers et al (2014) state that lupus affects 1 in 537 black women, “with black patients experiencing earlier age at diagnosis, >2-fold increases in SLE incidence and prevalence, and increased proportions of renal disease and progression to ESRD as compared to white patients.” However, Somers et al (2016) note that medical records may be poor or missing while the reliability of diagnosis is low for non-whites and non-blacks. They also note that race and ethny data in the US is based on self-ID for the parents and child on the birth certificate, but self-ID has almost a perfect relationship with geographic ancestry (i.e., race) (Tang et al, 2005).
Guillermo et al (2017: 7) write that:
Ethnicity is a biological and social construct, including not only genetic ancestry, but also cultural characteristics (language, religion, values, social behaviors, country of origin) yet it is an arbitrary definition . Race is oftentimes used interchangeable with ethnicity but it mainly refers to the biological features of groups of people. Given that there are differences in the clinical characteristics and prognosis among different populations, it is worth evaluating the impact of race/ethnicity in SLE. Genetic ancestry influences the risk for the incidence of SLE; for example, Amerindian ancestry is associated with an increased number of risk alleles for SLE , and also with an early age at onset , Amerindian and African ancestry are associated with a higher risk for kidney involvement [122,123] and European ancestry with a lower risk .
First, let’s look at ref , which is McKenzie and Crowcroft (1994), who Guillermo et al (2017) cite as saying that ethnicity is “an arbitrary definition.” They note that some researchers use Blumenbach’s terms (see Spencer, 2014). They claim that modern definitions class Asians as Caucasian or black … what? They state that modern definitions classify Asians as black because “all disadvantaged groups [are] “black populations,”
[since] the experience of racism is paramount.” This is ridiculous on so many levels.
In any case, Southern Europeans are more likely to have a higher risk of renal involvement, and antibody production but along with that a lower risk of discoid rash whereas Western Europeans while Ashkenazi Jews “seem to be protected from neurologic manifestations” (see Richman et al, 2009). Asians and Native Americans in Canada are less likely to have manifestations than Africans; a type of lupus known as cutaneous vasculitis is more common in Native Americans from Canada, while Asians from Canada had a lower rate of serotisis and arthritis compared to Caucasians, Native Americans and African descendants (Peschken et al, 2015). However, Peschken et al (2015) note that while ethnicity was not that strong a predictor of damage accrual, low income was.
Kidney involvement is a major factor in the development of lupus (Bagamant and Fu, 2009), while it is more frequent in “Hispanics”, African-descendants, and Asians. Further, “Hispanics” and blacks are more likely to have end-stage renal failure than whites (Ricardo et al, 2015). When it comes to lupus nephritis—inflammation of the kidneys caused by lupus—“Hispanics” also have a better response to mycophenolate mofetil, which is an immunosuppressive drug that prevents organ rejection (Appel et al, 2009). After the onset of the disease, the disease declines slowly in “Hispanics”, then Africans, and finally fastest in whites. There also seems to be an SES factor in the aetiology of the disease. Sule and Petri (2005) write that “Socioeconomic status can have a major impact on SLE disease manifestations and mortality, independent of ethnicity“, while saying that association with SES is all over the place, with there being no relationship with SES and lupus acquisition.
Vila et al (2003) studied “Hispanics” from Texas and Puerto Rico. They noted that those from Texas accrued more damage than those from Puerto Rico. This is not surprising. “Hispanics” are not a homogenous group (they are a socialrace with no minimalist correlate, they have differing admixture from all over; “Hispanics” can be of any race. Vila et al (2007: 362) note that:
This diversity appears to be areflection of the great variability that exists between these populations with regards to their genetic, environmental and sociodemographic backgrounds.
“Hispanics” from the southeast part of America are different ethnically than those from the southeast.
Blacks and “Hispanics” have a higher rate of mortality than whites, but these differences disappear once SES is accounted for (Ward, Pyun, and Studenski, 1995; Kasitanon, Magder, and Petri, 2006; Fernandez et al, 2007). There could be some genetic differences between races/ethnies that contribute to disease differences between them. But as Kampourakis (2017: 19) notes in his book Making Sense of Genes:
… genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin.
In sum, there is a wide range of differences between races and ethnies when it comes to lupus. Is the main cause environmental or genetic? Neither, as genes and environment interact to form disease (and any other) phenotypes. So if one at-risk minority group has a low SES, that may be a risk factor. The fact that there are ethnic differences in response to autoimmune drugs when it comes to certain forms of lupus is interesting. The wide range of ethnic differences in the acquisition of the disease is interesting, with Ashkenazi Jews seemingly protected from the disease. In any case, there are racial/ethnic differences in the acquisition of this disease and to better treat those with this disease—and any other—we need to be realists about race, whether it’s biological or social, since there are very real disease and mortality outcomes between them.
The debate on what type of diet in regard to macronutrient differences rages on. Should we eat high carb, low fat (HCLF)? Or low carb, high fat (LCHF) or something in between? The answer rests on, of course, the type of diets that our ancestors ate—both immediate and in the distant past. In the 1990s, a frozen human was discovered in the Otzal mountains, which gave him the name “Otzi man.” About 5,300 years ago, he was frozen in the mountains. The contents of his stomach have been analyzed in the 27 years since the discovery of Otzi, but an in-depth analysis was not possible until now.
A new paper was published recently, which analyzed the stomach contents of Otzi man (Maixner et al, 2018). There is one reason why it took so long to analyze the contents of his stomach: the authors state that, due to mummification, his stomach moved high up into his rib cage. The Iceman was “omnivorous, with a diet consisting both of wild animal and plant material” (Maixner et al, 2018: 2). They found that his stomach had a really high fat content, with “the presence of ibex and red deer” (pg 3). He also “consumed either fresh or dried wild meat“, while “a slow drying or smoking of the meat over the fire would explain the charcoal particles detected previously in the lower intestine content.“(pg 5).
The extreme alpine environment in which the Iceman lived and where he have been found (3,210 m above sea level) is particularly challenging for the human physiology and requires optimal nutrient supply to avoid rapid starvation and energy loss . Therefore, the Iceman seemed to have been fully aware that fat displays an excellent energy source. On the other hand, the intake of animal adipose tissue fat has a strong correlation with increased risk of coronary artery disease . A high saturated fats diet raises cholesterol levels in the blood, which in turn can lead to atherosclerosis. Importantly, computed tomography scans of the Iceman showed major calcifications in arteria and the aorta indicating an already advanced atherosclerotic disease state . Both his high-fat diet and his genetic predisposition for cardiovascular disease  could have significantly contributed to the development of the arterial calcifications. Finally, we could show that the Iceman either consumed fresh or dried meat. Drying meat by smoking or in the open air are simple but highly effective methods for meat preservation that would have allowed the Iceman to store meat long term on journeys or in periods of food scarcity. In summary, the Iceman’s last meal was a well-balanced mix of carbohydrates, proteins, and lipids, perfectly adjusted to the energetic requirements of his high-altitude trekking. (Maixner et al, 2018: 5)
They claim that “the intake of animal adipose tissue fat has a strong correlation with increased risk of coronary artery disease“, of course, citing a paper that the AHA is involved in (Sacks et al, 2017) which says that “Randomized clinical trials showed that polyunsaturated fat from vegetable oils replacing saturated fats from dairy and meat lowers CVD.” This is nonsense, because dietary fat guidelines have no evidence (Harcombe et al, 2016; Harcombe, Baker, and Davies, 2016; Harcombe, 2017). Saturated fat consumption is not even associated with all-cause mortality, type II diabetes, ischemic stroke, CVD (cardiovascular disease) and CHD (coronary heart disease) (de Sousa et al, 2015).
Thus, if anything, what contributed to Otzi man’s arterial calcification seems to be grains/carbohydrates (see DiNicolantonio et al, 2017), not animal fat. Fats, at 9 kcal per gram, were better for Otzi to consume, as he got more kcal for his buck; eating a similar portion in carbohydrates, for example, would have meant that Otzi would have had to spend more time eating (since carbs have less than half the energy that animal fat does). Since his stomach had ibex (a type of goat) and red deer, it’s safe to say that many of his meals consisted mainly of animal fat, protein with some cereals and plants thrown in (he was an omnivore).
We can then contrast the findings of Otzi’s diet with that of Neanderthals. It has been estimated that, during glacial winters, Neanderthals would have consumed around 74-85 percent of their diet from animal fat when there were no carbohydrates around, with the rest coming from protein (Ben-Dor, Gopher, and Barkai, 2016). Furthermore, based on contemporary data from polar peoples, it is estimated that Neanderthals required around 3,360 to 4,480 kcal per day to winter foraging and cold resistance (Steegmann, Cerny, and Holliday, 2002). The upper-limit for protein intake for Homo sapiens is 4.0 g/bw/day while for erectus it is 3.9 g/bw/day (Ben-Dor et al, 2011), and so this shows that Neanderthals consumed a theoretical upper-maximum of protein due to their large body size. So we can assume that Neanderthals consumed somewhere near 3800 kcal per day. The average Neanderthal is said to have consumed about 292 grams of protein per day, or 1,170 kcal (with a lower end of 985 kcal and an upper end of 1,170 at the high end) (Ben-Dor, Gopher, and Barkai, 2016: 370).
Then if we further assume that Neanderthals consumed no carbohydrates during glacial winters, that leaves protein as the main source of energy, since the large game the Neanderthals hunted were not around. Thus, Neanderthals would have consumed between 2,812 and 3,230 kcal from animal fat with the rest coming from protein. We can also put this into perspective. The average American man consumes about 100 grams of protein per day, while consuming 2,195 kcal per day (Ford and Dietz, 2013). For these reasons, and more, I argued that Neanderthals were significantly stronger than Homo sapiens, and this does have implications for racial differences in athletic ability.
In sum, the last meal of Otzi man is now known. Of course, this is a case of n = 1, so we should not draw too large a conclusion from this, but it is interesting. I don’t see why the composition of the diets of any of Otzi’s relatives would have been any different (or that the contents of his normal diet would have been any different). He ate a diet high in animal fat like Neanderthals, but unlike Neanderthals, they ate a more cereal-based diet which may have contributed to Otzi’s CVD and arterial calcification. We can learn a lot about ourselves and our ancestors through the analysis of their stomach contents (if possible) and teeth (if possible), and maybe even genomes (Berens, Cooper, and Lachance, 2017) because if we learn what they ate then we can maybe begin to shift dietary advice to a more ‘natural’ way and avoid diseases of civilization. But, we have not had time to adapt to the new obesogenic environments we have constructed for ourselves. It’s due to this that we have an obesity epidemic, and by studying the diets of our ancestors, we can then begin to remedy our obesity and other health problems.
How do whites and blacks differ by muscle fiber and what does it mean for certain health outcomes? This is something I’ve touched on in the past, albeit briefly, and decided to go in depth on it today. The characteristics of skeletal muscle fibers dictate whether one has a higher or lower chance of being affected by cardiometabolic disease/cancer. Those with more type I fibers have less of a chance of acquiring diabetes while those with type II fibers have a higher chance of acquiring debilitating diseases. This has direct implications for health disparities between the two races.
Muscle fiber typing by race
Racial differences in muscle fiber typing explain differences in strength and mortality. I have, without a shadow of a doubt, proven this. So since blacks have higher rates of type II fibers while whites have higher rates of type I fibers (41 percent type I for white Americans, 33 percent type I for black Americans, Ama et al, 1985) while West Africans have 75 percent fast twitch and East Africans have 25 percent fast twitch (Hobchachka, 1988). Further, East and West Africans differ in typing composition, 75 percent fast for WAs and 25 percent fast for EAs, which has to do with what type of environment they evolved in (Hochhachka, 1998). What Hochhachka (1998) also shows is that high latitude populations (Quechua, Aymara, Sherpa, Tibetan and Kenyan) “show numerous similarities in physiological hypoxia defence mechanisms.” Clearly, slow-twitch fibers co-evolved here.
Clearly, slow-twitch fibers co-evolved with hypoxia. Since hypoxia is the deficiency in the amount of oxygen that reaches the tissues, populations in higher elevations will evolve hypoxia defense mechanisms, and with it, the ability to use the oxygen they do get more efficiently. This plays a critical role in the fiber typing of these populations. Since they can use oxygen more efficiently, they then can become more efficient runners. Of course, these populations have evolved to be great distance runners and their morphology followed suit.
Caesar and Henry (2015) also show that whites have more type I fibers than blacks who have more type II fibers. When coupled with physical inactivity, this causes higher rates of cancer and cardiometabolic disease. Indeed, blacks have higher rates of cancer and mortality than whites (American Cancer Society, 2016), both of which are due, in part, to muscle fiber typing. This could explain a lot of the variation in disease acquisition in America between blacks and whites. Physiologic differences between the races clearly need to be better studied. But we first must acknowledge physical differences between the races.
Disease and muscle fiber typing
Now that we know the distribution of fiber types by race, we need to see what type of evidence there is that differing muscle fiber typing causes differences in disease acquisition.
Those with fast twitch fibers are more likely to acquire type II diabetes and COPD (Hagiwara, 2013); cardiometabolic disease and cancer (Caesar and Henry, 2015); a higher risk of cardiovascular events (Andersen et al, 2015, Hernelahti et al, 2006); high blood pressure, high heart rate, and unfavorable left ventricle geometry leading to higher heart disease rates and obesity (Karjalainen et al, 2006) etc. Knowing what we know about muscle fiber typing and its role in disease, it makes sense that we should take this knowledge and acknowledge physical racial differences. However, once that is done then we would need to acknowledge more uncomfortable truths, such as the black-white IQ gap.
One hypothesis for why fast twitch fibers are correlated with higher disease acquisition is as follows: fast twitch fibers fire faster, so due to mechanical stress from rapid and forceful contraction, this leads the fibers to be more susceptible to damage and thus the individual will have higher rates of disease. Once this simple physiologic fact is acknowledged by the general public, better measures can be taken for disease prevention.
Due to differences in fiber typing, both whites and blacks must do differing types of cardio to stay healthy. Due to whites’ abundance of slow twitch fibers, aerobic training is best (not too intense). However, on the other hand, due to blacks’ abundance of fast twitch fibers, they should do more anaerobic type exercises to attempt to mitigate the diseases that they are more susceptible due to their fiber typing.
Black men with more type II fibers and less type I fibers are more likely to be obese than ‘Caucasian‘ men are to be obese (Tanner et al, 2001). More amazingly, Tanner et al showed that there was a positive correlation (.72) between weight loss and percentage of type I fibers in obese patients. This has important implications for African-American obesity rates, as they are the most obese ethny in America (Ogden et al, 2016) and have higher rates of metabolic syndrome (a lot of the variation in obesity does come down food insecurity, however). Leaner subjects had higher proportions of type I fibers compared to type II. Blacks have a lower amount of type I fibers compared to whites without adiposity even being taken into account. Not surprisingly, when the amount of type I fibers was compared by ethnicity, there was a “significant interaction” with ethnicity and obesity status when type I fibers were compared (Tanner et al, 2001). Since we know that blacks have a lower amount of type I fibers, they are more likely to be obese.
In Tanner et al’s sample, both lean blacks and whites had a similar amount of type I fibers, whereas the lean blacks possessed more type I fibers than the obese black sample. Just like there was a “significant interaction” between ethnicity, obesity, and type I fibers, the same was found for type IIb fibers (which, as I’ve covered, black Americans have more of these fibers). There was, again, no difference between lean black and whites in terms of type I fibers. However, there was a difference in type IIb fibers when obese blacks and lean blacks were compared, with obese blacks having more IIb fibers. Obese whites also had more type IIb fibers than lean whites. Put simply (and I know people here don’t want to hear this), it is easier for people with type I fibers to lose weight than those with type II fibers. This data is some of the best out there showing the relationship between muscle fiber typing and obesity—and it also has great explanatory power for black American obesity rates.
Muscle fiber differences between blacks and whites explain disease acquisition rates, mortality rates (Araujo et al, 2010), and differences in elite sporting competition between the races. I’ve proven that whites are stronger than blacks based on the available scientific data/strength competitions (click here for an in-depth discussion). One of the most surprising things that muscle fibers dictate is weight loss/obesity acquisition. Clearly, we need to acknowledge these differences and have differing physical activity protocols for each racial group based on their muscle fiber typing. However, I can’t help but think about the correlation between strength and mortality now. This obesity/fiber type study puts it into a whole new perspective. Those with type I fibers are more likely to be physically stronger, which is a cardioprotectant, which then protects against all-cause mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015). So the fact that black Americans have a lower life expectancy as well as lower physical strength and more tpe II fibers than type I fibers shows why blacks are more obese, why blacks are not represented in strength competitions, and why blacks have higher rates of disease than other populations.The study by Tanner et al (2001) shows that there obese people are more likely to have type II fibers, no matter the race. Since we know that blacks have more type II fibers on average, this explains a part of the variance in the black American obesity rates and further disease acquisition/mortality.
The study by Tanner et al (2001) shows that there obese people are more likely to have type II fibers, no matter the race. Since we know that blacks have more type II fibers on average, this explains a part of the variance in the black American obesity rates and further disease acquisition/mortality.
Differences in muscle fiber typing do not explain all of the variance in disease acquisition/strength differences, however, understanding what the differing fiber typings do, metabolically speaking, along with how they affect disease acquisition will only lead to higher qualities of life for everyone involved.
Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508
Andersen K, Lind L, Ingelsson E, Amlov J, Byberg L, Miachelsson K, Sundstrom J. Skeletal muscle morphology and risk of cardiovascular disease in elderly men. Eur J Prev Cardiol 2013.
Ama PFM, Simoneau JA, Boulay MR, Serresse Q Thériault G, Bouchard C. Skeletal muscle characteristics in sedentary Black and Caucasian males. J Appl Physiol 1986: 6l:1758-1761.
American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.
Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7
Hagiwara N. Muscle fibre types: their role in health, disease and as therapeutic targets. OA Biology 2013 Nov 01;1(1):2.
Hernelahti, M., Tikkanen, H. O., Karjalainen, J., & Kujala, U. M. (2005). Muscle Fiber-Type Distribution as a Predictor of Blood Pressure: A 19-Year Follow-Up Study. Hypertension,45(5), 1019-1023. doi:10.1161/01.hyp.0000165023.09921.34
Hochachka, P.W. (1998) Mechanism and evolution of hypoxia-tolerance in humans. J. Exp. Biol. 201, 1243–1254
Karjalainen, J., Tikkanen, H., Hernelahti, M., & Kujala, U. M. (2006). Muscle fiber-type distribution predicts weight gain and unfavorable left ventricular geometry: a 19 year follow-up study. BMC Cardiovascular Disorders,6(1). doi:10.1186/1471-2261-6-2
Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.
Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439
Tanner, C. J., Barakat, H. A., Dohm, G. L., Pories, W. J., Macdonald, K. G., Cunningham, P. R., . . . Houmard, J. A. (2001). Muscle fiber type is associated with obesity and weight loss. American Journal of Physiology – Endocrinology And Metabolism,282(6). doi:10.1152/ajpendo.00416.2001
Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013