The evolution of costly traits: A challenge to a strict paleo diet orientation

The fundamental principle of the paleo diet movement is that we should model our diet on the diet of our ancestors. In other words, for optimal health, our diet should be as close to the diet of our ancestors as possible. Following this principle generally makes sense, but there are a number of problems with trying to follow it too strictly.

Some of those problems will have to wait for other posts. Examples are: our limited knowledge about what our ancestors really ate (some say: lean meat; others say: fatty meat); the fact that evolution can happen fast under certain circumstances (a few thousand years, not millions of years, thus recent and divergent adaptations are a possibility); the fact that among our ancestors some, like Homo erectus, were big meat eaters, but others, like Australopithecus afarensis, were vegetarians … Just to name a few problems.

The focus of this post is on traits that evolved in spite of being survival handicaps. These counterintuitive traits are often called costly traits, or Zahavian traits (in animal signalling contexts), in honor of the evolutionary biologist Amotz Zahavi (Zahavi & Zahavi, 1997). The implication for dieting is that our ancestors might have evolved some eating habits that are bad for human survival, and moved away from others that are good for survival. And I am not only talking about survival among modern humans; I am talking about survival among our human ancestors too.

Here is the most interesting aspect of these types of traits. Our ancestors may have acquired them through genetic mutation and selection (as opposed to genetic drift, which may lead some traits to evolve by chance). That is, they emerged not in spite, but because of evolutionary pressures.

The simple reason is that evolution maximizes reproductive success, not survival. If that were not the case, mice species, as well as other species that specialize in fast reproduction within relatively short lifespans, would never have evolved.

In fact, excessive longevity is akin to quasi-cloning through asexual reproduction, from an evolutionary perspective. It is bad because species need genetic diversity to exist in a constantly changing environment, and genetic diversity is significantly increased by sexual reproduction; the more, the better. Without plenty of death to match that, overpopulation would ensue.

Death is one of evolution’s main allies.

Genes code for the expression of phenotypic traits, such as behavioral (e.g., aggressiveness) and morphological (e.g., opposing thumbs) traits. Costly traits are phenotypic traits that evolved in spite of imposing a fitness cost, often in the form of a survival handicap.

In non-human animals, the classic example of costly trait is the peacock’s train, used by males to signal good health to females. This trait is usually referred to, wrongly, as the male peacock’s tail. Both males and females have tails, but only the males have the large trains, which are actually tail appendages.

What about humans?

One example is the evolution of testosterone markers in human males. Testosterone markers (facial masculinity) have been hypothesized to be handicaps evolved in part by human males to signal to females that they are healthy, essentially because testosterone suppresses the immune system. This apparently bizarre idea is known as the immunocompetence-handicap hypothesis (Rhodes et al., 2003).

This idea will sound bizarre to some, because of the notion that testosterone helps build muscle mass (which it does, together with other hormones, such as insulin), and arguably muscle mass helped our ancestors hunt and fight off predators. Yet, consider the following questions: If muscularity was so useful for hunting and fighting, why are humans so weak compared with other animals of similar size? Why are not females as muscular as males? Why is it so hard to gain muscle mass, compared to fat mass?

Another example is the evolution of oral speech in humans. The evolution of oral speech is one of the most important landmarks in the evolution of the human species, having happened relatively recently in our evolutionary history. However, the new larynx design required for oral speech also significantly increased our ancestors’ chances of death by choking during ingestion of food and liquids, and of suffering from various aerodigestive tract diseases such as gastroesophageal reflux, among other survival-related problems.

Yet, oral speech evolved because it enhanced overall reproductive success, in part by enabling knowledge communication (Kock, 2009), and also due to sexual selection (Miller, 2000). As Miller put it in his book The Mating Mind, ancestral women could gauge a man’s overall health by his ability to speak intelligently, in addition to other traits, such as testosterone markers.

Most of the sexual selection pressure during human evolution was placed by females on males, not the other way around. Ancestral women were more selective than men about who they had sex with; so are modern women, Sex and the City notwithstanding.

Now let us look at the connection with strict paleo dieting.

Paleo man may have consumed certain types of food to help with his testosterone handicap, increasing his reproductive success. As far as evolution is concerned, this is fine – the genes are selfish, and could not care less about the host (Burt & Trivers, 2006; Dawkins, 1990). The guy will mate, but will not live as long as he would like, past reproductive age. Given this possibility, does eating exactly like paleo man make sense for a 50 year old married male today? That is where too much of a focus on a paleo diet may be a problem.

Of course "paleo man" is really a metaphor. There was no "one" paleo man. There are at least three hominid species in the Paleolithic period that differed significantly from each other: Homo sapiens, Homo erectus, and Homo habilis. If you go back in time a little further, we encounter other hominid species, such Australopithecus afarensis and Australopithecus africanus, who were mostly, if not strictly, vegetarians.

Evolution is very useful as a unifying principle to help us understand what is healthy today and what is not. But it cannot completely replace empirical research on nutrition. Some of that research will undoubtedly uncover nutrition habits that increase longevity and improve health today, even though they were not practiced by our paleo ancestors.

We know that highly refined carbs (e.g., white bread with no fiber) and sugars (e.g., table sugar) are too recent an addition to the human diet for us to have evolved to use them optimally for nutrition. So their association with the metabolic syndrome makes sense, from an evolutionary perspective. But there are very gray areas where paleo nutrition speculations cannot tell us much, and what they tell us may be misleading.

References:

Burt, A. & Trivers, R. (2006). Genes in conflict: The biology of selfish genetic elements. Cambridge, MA: Harvard University Press.

Dawkins, R. (1990). The selfish gene. Oxford, UK: Oxford University Press.

Kock, N. (2009). The evolution of costly traits through selection and the importance of oral speech in e-collaboration. Electronic Markets, 19(4), 221-232.

Miller, G.F. (2000). The mating mind: How sexual choice shaped the evolution of human nature. New York, NY: Doubleday.

Rhodes, G., Chan, J., Zebrowitz, L.A., & Simmons, L.W. (2003). Does sexual dimorphism in human faces signal health? Proceedings of the Royal Society of London: Biology Letters, 270(S1), S93-S95.

Zahavi, A. & Zahavi, A. (1997). The Handicap Principle: A missing piece of Darwin’s puzzle. Oxford, England: Oxford University Press.

Ischemic heart disease among Greenland Inuit: Data from 1962 to 1964

The traditional Inuit diet is very high in animal protein and fat. It also includes plant matter. Typically it is made up primarily of the following: fish, walrus, seal, whale, berries, and fireweed (of which syrups and jellies can be made).

Kjærgaard and colleagues (see under References, at the end of this post) examined data from an Inuit population in Greenland from 1962 to 1964, prior to the heavy westernization of their diet that is seen today. They investigated 96.9% of the whole population in three areas, including Ammassalik in East Greenland (n = 1,851).

Of those, only 181 adults, or 9.7 percent, had anything that looked like an abnormality that could suggest ischemia. This included ventricular hypertrophy (an enlargement of the heart chambers), leading to an overestimation because benign ventricular hypertrophy is induced by continuous physical exertion. These 181 adults were then selected for further screening.

Benign ventricular hypertrophy is also known as athlete's heart, because it is common among athletes. A prevalence of ventricular hypertrophy at a relatively young age, and declining with age, would suggest benign hypertrophy. The opposite would suggest pathological hypertrophy, which is normally induced by chronic hypertension.

As you can see from the figure below, from Kjærgaard et al. (2009), the pattern observed among the Inuit was of benign hypertrophy, suggestive of strong physical exertion at a young age.

A pattern of benign hypertrophy induced by robust physical activity is also consistent with reports by Stefansson (1958) about the life of the Eskimos in Northern Alaska. It is reasonable to assume that these Eskimos had a diet and lifestyle similar to the Greenland Inuit.

Back to Kjærgaard et al.’s (2009) study. The 181 adults selected for further screening then had a 12-lead ECG performed (this is a widely used test to check for heart abnormalities). The results suggested that only two men, aged 62 and 63 years, had ischemic heart disease. All in all, this suggests a prevalence of ischemic heart disease of 0.11 percent, which is very low.

(The authors of the article estimated the prevalence of ischemic heart disease at 1.1 percent, because they used the n = 181, as opposed to the original n = 1,851, in their calculation. The latter is the correct baseline sample size, in my opinion. Still, the authors present the 1.1 percent number as quite low as well, which it is.)

Recent statistics (at the time of this post's writing) suggest a prevalence of ischemic heart disease in the US of 6.8 percent. That is, the prevalence in the US is 63 times higher than among the Inuit studied (using the 0.11 percent as the basis for comparison). And, it should be noted that there are many countries with a higher prevalence of ischemic heart disease than modern US.

It is possible that the low prevalence of ischemic heart disease among the Inuit was partly due to a higher mortality of those with the disease than in modern US, where medical intervention can prolong one's life in the presence of almost any disease. That is, perhaps many of those Inuit with ischemia would die quickly, and thus would not be captured by a study like this.

It is doubtful, however, that this would explain a difference as large as the one observed. Moreover, if many Inuit were dying due to ischemia, there would probably be plenty of evidence suggesting that. (I would imagine that the mysterious deaths associated with chest pain, and other related symptoms, would be a constant topic of conversation.) Reports from early explorers, however, suggest the opposite (e.g., Stefansson, 1958), and are consistent with the study described here.

In conclusion, this study suggests that the diet and lifestyle of the Greenland Inuit prior to the 1960’s (i.e., not their traditional diet and lifestyle, but approaching it) could be seen today as heart-healthy (at least for them), even though the Greenland Inuit ate a lot of animal protein and fat.

References:

Kjærgaard, M., Andersen, S., Holten, M., Mulvad, G., Kjærgaard, J.J. (2009). Low occurrence of ischemic heart disease among Inuit around 1963 suggested from ECG among 1851 East Greenland Inuit. Atherosclerosis, 203(2), 599-603.

Stefansson, V. (1958). Eskimo longevity in Northern Alaska. Science, 127(3288), 16-19.

Guest Commentary: US Health Care Reform from a UK Perspective

Louisa Baxter, MD, MSc, MRCP
Harkness Fellow
Jefferson School of Population Health

When I landed at Philadelphia Airport in September after my 6-hour flight from Heathrow in London, I had half expected to be grilled by US Customs about my involvement in death panels and then turned back and sent home in disgrace. After 7 years spent in clinical practice in the UK, the home of “socialized” medicine, I had jumped at the opportunity to come to Jefferson School of Population Health to do some research and watch the tremendous theatre that is the US health care reform debate unfold across the country.

It has been an incredible 3 months; I have met clinicians from (nearly) every state, patients, hospital and health plan executives, researchers and policy makers. I have read commentaries in the New York Times, watched CNN and CSPAN, listened to Glenn Beck and Senator “You lie!” Joe Wilson and marveled at the heterogeneity of opinions around health care and its reform. As with all countries, it is clear that in the US the health care system faces significant challenges; the growing number of un- or underinsured, rising prices, the medical arms race, unwarranted variation in care and the lack of evidence base for many interventions, to name just a few.

From afar, it is easy to mock the debates as simply a circus fuelled by the special interests of big business and I fear that this is what many countries watching the US at the present time may do. But as an outsider to your system who has been given privileged access to the discussion, what has impressed me is the remarkable depth of feeling around the debate. It is clear, that hidden beneath very complicated policy wonkish jargon and the arguments at town hall meetings, that this is a discussion about what values and priorities should be at the very heart of your health system. It is something to be proud of, that so many voices can come together (relatively peacefully) to enter into the dialogue.

I have also been impressed by the kindness and openness of so many people both in Philadelphia and across the whole US. From everyone in the School at Jefferson, who have helped me through the maze of paperwork necessary to come over here, shown me the best delis to buy lunch and opened their homes to me, to passersby who have shown me how to post mail, how to ride the SEPTA and patiently given me directions, I am often surprised by the care that people take that of me as a guest in your country. If the death panels didn’t need me, it would be an incentive to stay.

Health Care Reform: Implications of Pending Legislation

At yesterday’s monthly health policy forum, we had the pleasure of hearing Dr. Valerie Arkoosh discuss the health care reform battle currently underway in Congress. From her professional perch as President of the National Physicians Alliance in Washington, DC, Dr. Arkoosh has witnessed the wrangling up close. Her detailed yet straightforward side-by-side comparison of the House and Senate bills was illuminating and highlighted several key elements with the potential to affect academic medical institutions, either positively or adversely. Some of the issues she mentioned included: changes to Disproportionate Share payments for Hospitals (DSH), allowing for Medicaid reimbursement at Medicare levels for primary care, payment bundling, provision of resources for education and training of health care providers, and malpractice reform, to name just a few.

What do you think about the House Bill versus the Senate Bill? How can we help move the dialogue in Washington beyond a discussion of health insurance to a more comprehensive conversation about health care reform?

David Nash, MD, MBA
Dean, Jefferson School of Population Health

AMSA Quality Institute

In the past three days, nearly two dozen medical students and premeds descended on the Jefferson School of Population Health for the Second Annual AMSA Quality and Safety Institute. AMSA is the American Medical Student Association, an important national membership organization that seeks to create a group of future physician leaders for our country. Recognizing the growing importance of quality and safety in the curriculum, these students spent a weekend learning about the cultural barriers to quality, the tools to measure quality and the ins and outs of moving ahead with key campus projects at their home institutions. The faculty came from JSPH, Christiana Care, Drexel U College of Medicine, The NBME, New York Hospital Cornell Medical Center, and RWJ Medical School. The students participated in lectures, workshops, two dinner programs as they built their leadership portfolios. Quality and Safety are NOT ELECTIVES and these students will go forth to put this critical information into the standard med school curriculum. They are armed and dangerous!!---most current faculty know little about this entire field. It is time to recognize how important these issues are to training the doctor of tomorrow. WHAT is your school doing to tackle this challenge?? Should every medical school participate is such an Institute?? What more can AMSA do to institutionalize this approach to learning?? DAVID NASH DEAN JSPH

Okinawa: The island of pork

The original inhabitants of the Ryūkyū Islands, of which the island of Okinawa is the largest, are believed to have the highest life expectancy in the world.

One of the staples of their diet is sweet potatoes. The carbohydrate percentage of a sweet potato is about 20; that is, each 100 g of sweet potato mass has about 20 g of carbohydrates. Sweet potatoes have a medium-high glycemic index, and are often avoided by those with impaired insulin sensitivity, and certainly by diabetics.

The other main staple of their diet is pork, as you may have inferred from the title of this post. The quote below is from the first of the three links provided below the quote.

Pork appears so frequently in the Okinawan diet that to say "meat" is really to say "pork." [...] It is no exaggeration to say that the present-day Okinawan diet begins and ends with pork.

        http://www.wonder-okinawa.jp/026/e/pork.html

        http://www.okinawaindex.com/index/?tid=2&cid=250&id=2

        http://ci.nii.ac.jp/naid/110000220190/en

So, what is the secret of the Okinawans’ longevity? Maybe it is the diet. Maybe it is the lifestyle. Maybe it is the fact that their mothers and fathers are Okinawans (the heritability of longevity has been estimated to be about 33%, and to be higher among females than males). Here are some interesting points that are worth noting:

- Their diet is not only of meat, but includes plenty of it.

- Their diet is not particularly low in saturated fat, and maybe it is high in it.

- Their diet is not particularly low in dietary cholesterol, and maybe high in it, since they eat the pig whole, including the parts (e.g., organs) rich in dietary cholesterol.

- Their diet is not a no carb diet, not even a typical low carb diet, but it seems to be very low in refined carbs and sugars.

Muscle loss during short-term fasting

This is an issue that often comes up in online health discussions, and was the topic of a conversation I had the other day with a friend about some of the benefits of intermittent fasting.

Can the benefits of intermittent fasting be achieved without muscle loss? The answer is “yes”, to the best of my knowledge.

Even if you are not interested in bulking up or becoming a bodybuilder, you probably want to keep the muscle tissue you have. As a norm, muscle takes a long time, and effort, to build. It is generally easier to lose muscle than it is to gain it. Fat, on the other hand, can be gained very easily.

Body fat percentage is positively correlated with measures of inflammation markers and the occurrence of various health problems. Since muscle tissue makes up lean body mass, which excludes fat, it is by definition negatively correlated with inflammation markers and health problems.

As muscle mass increases, so does health; as long as the increase in muscle mass is “natural” – i.e., not caused by things like steroids, for instance.

In short-term fasts (e.g., up to 24 h) one can indeed lose some muscle as the body produces glucose using muscle tissue through a process known as gluconeogenesis. In this sense, muscle is the body’s main reserve of glucose. Adipocytes are the body’s main reserves of fat.

Muscle loss is not pronounced in short-term fasts though. It occurs after the body’s glycogen reserves, particularly those in the liver, are significantly depleted. This often happens 8 to 12 hours into the fast, depending on how depleted the glycogen reserves are when one starts fasting.

When the body is running short on glycogen, it becomes increasingly reliant on fat as a source of energy, sparing muscle tissue. That is, it burns fat, often in the form of ketone bodies, which are byproducts of fat metabolism. This state is known as ketosis. There is evidence that ketosis is a more efficient state from a metabolic perspective (Taubes, 2007, provides a good summary), which may be why many people feel an increase in energy when they fast.

The brain also runs on fat (through ketone byproducts) while in ketosis, although it still needs some glucose to function properly. That is primarily where muscle tissue comes into the picture, to provide the glucose that the brain needs to function. While glucose can also be made from fat, more specifically a lipid component called glycerol, this usually happens only during very prolonged fasting and starvation.

You do not have to consume carbohydrates at all to make up for the glycogen depletion, after you break the fast. Dietary protein will do the job, as it is used in gluconeogenesis as well.

Dietary protein also leads to an insulin response, which is comparable to that elicited by glucose. The difference is that protein also leads to other hormonal responses that have a counterbalancing effect to insulin, by allowing for the body's use of fat as a source of energy. Insulin, by itself, promotes fat deposition and prevents fat release at the same time.

When practicing intermittent fasting, one can increase protein synthesis by doing resistance exercise (weight training, HIT), which tips the scale toward muscle growth, and away from muscle catabolism.

This may actually lead to significant muscle gain in the long term. Fasting itself promotes the secretion of hormones (e.g., growth hormone) that have anabolic effects.

The following sites focus on muscle gain through intermittent fasting; the bloggers are living proof that it works.

  http://bradpilon.com/

  http://leangains.com/

Muscle catabolism happens all the time, even in the absence of fasting. As with many tissues in the body (e.g., bones), muscle is continuously synthesized and degraded. Muscle tissue grows when that balance is tipped toward synthesis, and is lost otherwise.

Muscle will atrophy (i.e., be degraded) if not used, even if you are not fasting. In fact, you can eat a lot of protein and carbohydrates and still lose muscle. Just note what happens when an arm or a leg is immobilized in a cast for a long period of time.

Short-term fasting is healthy, probably because it happened frequently enough among our hominid ancestors to lead to selective pressures for metabolic and physiological solutions. Consequently, our body is designed to function well while fasting, and triggering those mechanisms correctly may promote overall health.

The relationship between fasting and health likely follows a nonlinear pattern, possibly an inverted U-curve pattern. It brings about benefits up until a point, after which some negative effects ensue.

Long-term fasting may cause severe heart problems, and eventually death, as the heart muscle is used by the body to produce glucose. Here the brain has precedence over the heart, so to speak.

Voluntary, and in some cases forced, short-term fasting was likely very common among our Stone Age ancestors; and consumption of large amounts of high glycemic index carbohydrates very uncommon (Boaz & Almquist, 2001).

References:

Boaz, N.T., & Almquist, A.J. (2001). Biological anthropology: A synthetic approach to human evolution. Upper Saddle River, NJ: Prentice Hall.

Taubes, G. (2007). Good calories, bad calories: Challenging the conventional wisdom on diet, weight control, and disease. New York, NY: Alfred A. Knopf.