The Man Who Touched His Own Heart
Page 37
6. According to Taussig’s hypothesis, because lizards, snakes, turtles, mammals, and birds all descend from a common ancestor with a heart with two atria and one ventricle, they should all share similar atrial deformities. This has not been tested in any formal way, but mammals and birds can both be born with holes in the wall (septum) between the atria. At least some lizards can too.
7. Functionally divided ventricles and associated coronary arteries also arose, independently, in another active group of vertebrates, the varanid lizards, which include komodo dragons. So next time you are tempted to tease a komodo, remember that it can run for a while because it has a four-chambered heart. Coronary arteries also appear to have arisen in some fish capable of prolonged activity, such as mackerels and tunas. At the opposite extreme, some slow-moving bottom-feeders like carp have no coronary circulation at all and go weeks or even months without any oxygen in their hearts.
8. This idea, often referred to as “ontogeny recapitulates phylogeny,” was long thought to be a generality in evolution, so much so that developmental stages were used to infer our ancestry. Generally speaking, our developmental stages do not rehash our evolution. However, in the specific case of our hearts, it seems as though the heart has become more complex in part by adding steps to development.
9. M. L. Kirby, T. F. Gale, and D. E. Stewart, “Neural Crest Cells Contribute to Aorticopulmonary Septation,” Science 220 (1983): 1059–61. Here one interesting exception is that some scientists, including Margaret Kirby, have begun to use chickens as models of congenital deformities of ancient parts of the hearts shared by birds and mammals, such as those related to the pulmonary artery.
10. In this special case, development repeats evolution’s trajectory. During development, the coronary arteries begin to grow only once the heart is big enough for some cells to start to become anoxic. Anoxia is a signal that the coronary arteries are necessary in each fetal bird or mammal. In humans, the coronary arteries are fully developed about three to six weeks into gestation.
16. Sugarcoating Heart Disease
1. For example, see L. Munson and R. J. Montali, “Pathology and Diseases of Great Apes at the National Zoological Park Zoo,” Zoo Biology 9 (1990): 99–105.
2. R. Margreiter, “Chimpanzee Heart Was Not Rejected by Human Recipient,” Texas Heart Institute Journal 33 (2006): 412.
3. For example, see L. J. Lowenstine, “A Primer of Primate Pathology: Lesions and Nonlesions,” Toxicologic Pathology 31 (2003): 92–102.
4. Which closed in 2012 (http://carta.anthropogeny.org/museum/collections/pfa).
5. Fortunately, both Yerkes and the foundation kept excellent records of just what had been squirreled away, when, and in what context.
6. I once cleaned out a freezer at the University of Connecticut and found, at the very back, a bag marked S. Cunningham—Costa Rican air, do not open. I, of course, opened it; it smelled just like Costa Rica.
7. At Yerkes, the average cholesterol level among 106 male chimps—across their lifetimes—was 211.1 mg/dl, which is regarded as borderline high in humans. Similar levels were observed at two other centers. On average, cholesterol levels are higher in chimps than in humans (even Western couch potatoes), but the biggest difference between humans and chimps in terms of cholesterol is timing. Cholesterol is high in infant chimpanzees and stays high, whereas cholesterol is low in young humans but increases over the years.
8. In this treatment, a horse is given white blood cells from a human. The horse then develops antibodies to the white blood cells. The horse serum, with those antibodies, is then injected into the patient. In theory, the antibodies in the horse’s serum are supposed to placate the patient’s immune system—which in aplastic anemia is overactive. In practice, no one knows why (or even really if) this treatment works.
9. H. Higashi et al., “Antigen of ‘Serum Sickness’ Type of Heterophile Antibodies in Human Sera: Identification as Gangliosides with N-Glycolylneuraminic Acid,” Biochemical and Biophysical Research Communications 79 (1977): 388–95.
10. See interview in J. Cohen, Almost Chimpanzee: Searching for What Makes Us Human (New York: Henry Holt and Company, 2010).
11. A. Varki et al., Essentials of Glycobiology, 2nd edition (New York: Cold Spring Harbor Laboratory Press, 2009).
12. E. Muchmore et al., “Developmental Regulation of Sialic Acid Modifications in Rat and Human Colon,” FASEB Journal 1 (1987): 229–35.
13. H. H. Chou et al., “A Mutation in Human CMP-Sialic Acid Hydroxylase Occurred After the Homo-Pan Divergence,” Proceedings of the National Academy of Sciences 95 (1998): 11751–56.
14. E. A. Muchmore, S. Diaz, and A. Varki, “A Structural Difference Between the Cell Surfaces of Humans and the Great Apes,” American Journal of Physical Anthropology 107 (1998): 187–98.
15. At the time, our differences were so little understood that the director of Yerkes, Thomas Insel, remarked in an interview in 1998 with the journal Science, “You could write everything we knew about the genetic differences (between humans and chimps) in a one-sentence article.” See A. Gibbons, “Which of Our Genes Make Us Human?” Science 281 (1998): 1432–34.
16. I focus here on how eating mammal meat (and mammal sialic acid) affects inflammation and heart disease, but this is not the only effect. Some deadly strains of E. coli bacteria produce toxins when they infect human bodies; it is the toxins that make these bacteria dangerous. One of the toxins these bacteria produce (known as subtilase cytotoxin, or SubAB) binds to the standard mammalian sialic acid. As a result, individuals who eat mammal meat are at risk from these toxins, but those who do not are not. See J. Cohen, “Eat, Drink, and Be Wary: A Sugar’s Sour Side,” Science 31 (2008): 659–61, and P. Tangvoranuntakul et al., “Human Uptake and Incorporation of an Immunogenic Nonhuman Dietary Sialic Acid,” Proceedings of the National Academy of Sciences 100 (2003): 12045–50.
17. D. H. Nguyen et al., “Loss of Siglec Expression on T Lymphocytes During Human Evolution,” Proceedings of the National Academy of Sciences 103 (2006): 7765–70; P. C. Soto et al., “Relative OverReactivity of Human Versus Chimpanzee Lymphocytes: Implications for the Human Diseases Associated with Immune Activation,” Journal of Immunology 184 (2010): 4185–95. A set of proteins called siglecs, which Ajit Varki discovered, bind to sialic acids. With the change in human sialic acids, these proteins have become less common in our bodies, which is relevant because the role of these compounds appears to be to put the brakes on the immune system, calming its response and encouraging it to offer peace rather than wage war.
18. Humans host several kinds of mites, including scabies mites (which are a problem) and Demodex mites (which my lab studies and which tend not to be a problem). These small creatures appear to be found on all adult humans, but we are constantly being colonized by different strains. Humans lack a third type of mites found on most other apes: fur mites. All other apes are covered with them. They are one of the groups of parasites we seem to have lost when we shed our fur.
19. If the heart disease seen in chimps is due to a virus (which it seems it might be), by losing sialic acid, we may have escaped the sort of heart disease chimps face.
20. These, like all measures of life expectancy, are averages.
21. It has been argued, quite plausibly, that the decrease in life expectancy associated with agriculture is better described as being associated with a major social transition. Transitions, it is suggested, predictably decrease life expectancy, as all hell breaks loose during the shift from one way of life to another.
22. For more on the shifting ecology of teeth, see C. J. Adler et al., “Sequencing Ancient Calcified Dental Plaque Shows Changes in Oral Microbiota with Dietary Shifts of the Neolithic and Industrial Revolutions,” Nature Genetics 45 (2013): 450–55.
17. Escaping the Laws of Nature
1. The idea apparently derives from the book of Exodus in which God gave Moses “two tables of testimony, tables of stone, written with the finger of God.” Those words were to be
“kept in the heart of man.”
2. J. Lehrer, “A Physicist Solves the City,” New York Times, December 19, 2010.
3. This required the physicist (or at least his students and assistants) to do something new: they had to comb census databases and other sources to understand the features of different blocks, neighborhoods, cities, and countries. They gathered data on density, walking speed, purchases, and nearly anything else they could find. If they did not consider clown density, for example, that is just because they couldn’t find any way to compile the data.
4. L. M. A. Bettencourt et al., “Urban Scaling and Its Deviations: Revealing the Structure of Wealth, Innovation and Crime Across Cities,” PLoS One 5 (2011): 1–9.
5. John Whitfield, In the Beat of a Heart: Life, Energy, and the Unity of Nature (Washington, DC: Joseph Henry Press, 2005).
6. Importantly, heart rate increases more slowly than body size because larger animals need progressively less active hearts, so the line relating the two variables is a curve unless one of the axes is logarithmic.
7. You might think, Well, why doesn’t the body just make bigger arteries and veins and produce more blood rather than altering its heart rate as a function of size? Here is where one of West’s great insights comes in. Because the number of capillaries is set by the size of an organism and their width is invariant, the total cross section of the vascular system is determined by body size. The body actually has no ability, evolutionarily, to change artery and vein size. The only way to pump more or less blood is by changing the heart rate.
8. An interesting aside here is the question of why mammals and birds need to stay warm in the first place. One camp suggests it allows them to be more active and get to the food, mates, and whatever else first. Another, though, suggests that warm-bloodedness evolved as a way to kill off fungal and other pathogens that cannot deal with body heat. Interestingly, the body temperature of the majority of mammals is just high enough to kill most fungi but not high enough to prove fatal to the mammals’ own cells.
9. Recently, this model has been fine-tuned. The wear and tear on our cells comes largely from the production of free radicals of oxygen. Those free radicals bang around in the cells and damage things, but they are produced during metabolism and so are inescapable. But just how bad their effect is seems to be mediated in part by the behavior of mitochondria. In some cells and animals, mitochondria spend most of their time producing heat rather than energy. When they do so, they generate fewer free radicals. As a consequence, they might also generate less wear and tear, and so it might be the case that animals whose mitochondria spend more time producing heat and less time producing energy live a little longer than would be predicted based on their heart rates, though this remains to be seen.
10. H. J. Levine, “Rest Heart Rate and Life Expectancy,” Journal of the American College of Cardiology 30 (1997): 1104–6.
11. Biologists used to think the same until, in 1970, the bear biologist Lynn Rogers began to study hibernating bears with questions of heart rate in mind. Rogers does dangerous things with bears. He follows his favorite ones through the forest, walking behind them as though on a walk with his favorite dog. They are used to him, mostly. Lynn spent more time with bears than anyone, aside from other bears. Who better to study how they hibernate. How do you study hibernating bears? Rogers crawled into a bear cave with an anal heart-rate monitor and probed several bears without event. He even put his head up to the hairy, stinking body of one hibernating bear. She did not stir; he could barely hear her heart. A few bears lifted their heads. One growled. But mostly they stayed still, inert. Then, on March 27, 1970, Rogers fell on a six-year-old female bear. Hibernating animals slept, it was thought at the time, so deeply as to seem harmless, but the baby alongside this six-year-old woke up. Still, the mother did not stir. Rogers couldn’t resist poking her. Could she be woken? He poked her some more, and suddenly her heart went from quiet to racing, 175 beats per minute—faster than had been recorded even from very active bears. The mother bear was not happy. That is when Lynn discovered two more things: that bears wake rapidly from their winter slumber and that, for a short distance, he could outrun a pair of sleepy but angry bears.
12. S. Telles et al., “An Evaluation of the Ability to Voluntarily Reduce the Heart Rate After a Month of Yoga Practice,” Integrative Physiological and Behavioral Science 39 (2004): 119–25.
13. Interestingly, the influence of yoga on heart rate, although it seems pronounced, has been little studied. This paper appears to be the last one published on the topic, and it came out in 2004.
14. Evolutionarily, this is an accurate impression. They belong in the family of the squirrels, Sciuridae.
15. Yes, miniature elephants actually did exist.
16. B. W. Johansson, “The Hibernator Heart—Nature’s Model of Resistance to Ventricular Fibrillation,” Arctic Medical Research 50 (1991): 58–62.
17. I. Oransky, “Wilfred Gordon Bigelow,” Lancet 365 (2005): 1616. In the paper that resulted from the talk, Bigelow was forced to note, “Since this article was written, Drs. Charles Bailey of Philadelphia and F. J. Lewis of Minneapolis have reported the successful use of this technic of cooling upon 2 patients.” Bigelow’s insight had, within just months, resulted in a successful heart surgery.
18. W. G. Bigelow and J. E. McBirnie, “Further Experiences with Hypothermia for Intracardiac Surgery in Monkeys,” Annals of Surgery 37 (1965): 361–65.
19. G. W. Miller, King of Hearts: The True Story of the Maverick Who Pioneered Open Heart Surgery (New York: Times Books, 2000).
20. Caffeine is similar enough to adenosine to bind its receptor and, thus, block the hibernation molecules from having their effect. In drinking coffee, you are convincing your body to ignore the signs that night or the long winter has arrived.
Postscript: The Future Science of the Heart
1. Failure is perhaps too strong a word because every medical failure spawns some innovation. The effort to transplant hearts, for example, pushed heart surgery forward, perhaps faster than it might have gone otherwise.
2. A. Abbott, “Doubts Over Heart Stem-Cell Therapy,” Nature 509 (2014): 15–16.
3. J. B. Andersen et al., “Physiology: Postprandial Cardiac Hypertrophy in Pythons,” Nature 434 (2005): 37–38; S. M. Secor and J. Diamond, “A Vertebrate Model of Extreme Physiological Regulation,” Nature 395 (1995): 659–62.
4. C. A. Riquelme et al., “Fatty Acids Identified in the Burmese Python Promote Beneficial Cardiac Growth,” Science 334 (2011): 528–31.
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