Who cares about what humans have eaten in the past?

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After a big week in Australia and New Zealand talking about fat and cholesterol, things are settling down a bit.  As we all draw a collective breath, I have been reflecting on a few things.  One thing that struck me was the immediate objection of my position on the study of human food in the context of evolutionary biology.  Dr Lisa Te Morenga commented immediately on my blog site after my post laying out some logic and evidence for higher fat lower carb diets. Lisa and I have talked about my approach a bit recently.

Lisa is a Research Fellow in the Department of Human Nutrition at the University of Otago. Her research interests involve the effects of macronutrient composition on physiological endpoints associated with increased risk of preventable diseases.  So she is really following this with interest, and skepticism I imagine (we like skepticism, it just goes both ways).

She had some detailed comments about studies which was great. I raced off and found them, so thanks. She also said this “And on the topic of Paleo diets, it is worth remembering that our fabulously healthy paleo ancestors were lucky to make it to the ripe old age of 35, which is hardly a ringing endorsement of the paleo diet.”

Or did they?? Given we are all interested in actual evidence here, I was supplied a very good reference by Jamie Scott and thought I might share some of the conclusions with you here.  It was really interesting.

These guys (reference) went and did a massive amount of data collection and modelling looking at life expectancies in Sweden in the 1750s, modern US life expectancies, the life expectancy of several modern hunter gatherer tribes, and that of captive and wild chimpanzees.

First, I won’t pretend I understand all the mathematical modelling.  Second, no one actually recorded how long prehistoric hunter gatherers actually did live.  So this is speculation, but speculation with serious data and rationale. It’s interesting to think about how long our ancestors lived and what they probably died from.

I think that consideration of the environment(s) our ancestors were exposed to, and how these affected their biology, is what scientists in every area of biology do.  Why would nutritional science and the study of chronic disease be any different? Anyway, here is summary of the study’s main findings (their words not mine):

(from the paper)

  1. Post-reproductive longevity is a robust feature of hunter-gatherers and of the life cycle of Homo sapiens. Survivorship to grandparental age is achieved by over two-thirds of people who reach sexual maturity and can last an average of 20 years.
  2. Adult mortality appears to be characterized by two stages. Mortality rates remain stable and fairly low at around 1 percent per year from the age of maturity until around age 40. After age 40, the rate of mortality increase is exponential (Gompertz) with a mortality rate doubling time of about 6–9 years. The two decades without detectable senescence in early and mid-adult- hood appear to be an important component of human lifespan extension.
  3. The average modal age of adult death for hunter-gatherers is 72 with a range of 68–78 years. This range appears to be the closest functional equivalent of an “adaptive” human life span.
  4. Departures from this general pattern in published estimates of life expectancy in past populations (e.g., low child and high adult mortality) are most likely due to a combination of high levels of contact-related infectious disease, excessive violence or homicide, and methodological problems that lead to poor age estimates of older individuals and inappropriate use of model life tables for deriving demographic estimates.
  5. Illnesses account for 70 percent, violence and accidents for 20 percent, and degenerative diseases for 9 percent of all deaths in our sample. Illnesses largely include infectious and gastrointestinal disease, although less than half of all deaths in our sample are from contact-related disease.
  6. Comparisons among hunter-gatherers, acculturated hunter-gatherers, wild chimpanzees, and captive chimpanzees illustrate the interaction of improved conditions and species differences. Within species, improved conditions tend to decrease mortality rates at all ages, with a diminishing effect at older ages. Human and chimpanzee mortality diverge dramatically at older ages, revealing selection for a longer adult period in humans.

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Frequency distribution of ages at death f(x) for individuals over age 15 shows strong peaks for hunter- gatherers, forager-horticulturalists, acculturated hunter-gatherers, Sweden 1751–79, and the United States 2002 (both sexes). All curves except for Sweden and the United States are smoothed using Siler estimates. 

The seven decades hypotheses – also called the grandmother hypotheses

My second musing this week is the idea that grand parenting and multigenerational survival up to seven decades conferred a reproductive and therefore evolutionary advantage to be selected for in prehistoric humans.  It revolves around an extended cultural and skill development related to our big brain and long learning and skill acquisition period.

This is a very cool theory.  It proposes that the existence of grand parents of both sexes was a selective pressure on the gene pool.

It proposes that timing of life events is best understood as an “embodied capital” investment process. Embodied capital is organized somatic tissue, which functionally increases lifetime adult income and includes strength, skill, knowledge, and other abilities. Humans are specialists in brain-based capital. High levels of knowledge and skill are required to exploit the suite of high-quality, difficult-to-acquire resources humans consume. Those abilities require a large brain and a long time-commitment to development. This extended learning phase, during which productivity is low, is compensated for by higher productivity during adulthood. Since productivity increases with age, the time investment in skill acquisition and knowledge leads to selection for lowered mortality rates and greater longevity, because the returns on the investments in development occur at older ages. According to this model, the long human life span co-evolved with the lengthening of the juvenile period, increased brain capacities for information processing and storage, and intergenerational resource flows. It is a two-sex model, as it proposes that both men and women engage in learning-intensive food production tasks; these activities result in delayed productivity until older ages, selecting for life span extension in both sexes.

As the number of closely related dependent kin eligible to receive investment decreases after age 65, the fitness benefits of longer life decrease and there is less evolutionary incentive to pay increasing maintenance and repair costs to remain alive and functional beyond this period.

Chronic degenerative diseases rare

Most modern humans will die from a chronic disease or its complications.  We all have to die sometime from something, but the problem with chronic disease is the disability and reduced quality of life before death. We now live longer than ever before in human history, but the quality of life may be impaired.  What we seek to do in public health is think about how we can maximize both quality and quantity of life (or get the best trade off). There are also economic considerations – if we have people dying slowly form chronic diseases, that costs a lot of money in care and management.

So how do our ancestors compare with us, in terms of cause of death?

Most died from illness or accident; only about 1/10 from degenerative diseases. Remember that the leading cause of death worldwide is now chromic disease and the bulk of people in the developed world can expect to die form a chronic disease. We also know that chronic disease will likely result in more than a decade of health-related disability before death. So people did die young. Many died at birth and in the first few years of life.  The overall chance of death at anytime up to the age of 40 was higher and most likely due to illness, accident, or warfare. After that, there is quite an increase in mortality, with the modal age of death around 72 years.

Degenerative deaths were relatively few, confined largely to problems early in infancy and late-age cerebrovascular problems, as well as attributions of “old age” in the absence of obvious symptoms or pathology. Heart attacks and strokes appear rare and do not account for these old-age deaths (see Eaton, Konner, and Shostak 1988), which tend to occur when sleeping. It has often been remarked that few risk factors for cardiovascular disease exist among active members of small-scale societies (Eaton et al. 1994), although compromised lung or kidney functioning can interact with cardiac fibrosis or moderate arterial stenosis to cause cardiac arrest. Obesity was rare, hypertension was low, cholesterol and triglyceride levels were low, and maximal oxygen uptake was high. Overall, degenerative disease accounted for 6–24 percent (average 9 percent) of deaths, with the highest representation among Northern Territory Aborigines. Neoplasms and heart disease each accounted for 9 of the 42 deaths due to degenerative illness. It should be pointed out, however, that chronic illnesses as causes of death are the most difficult to identify, since more proximate causes are likely to be mentioned. To our knowledge there have been no focused studies or mention of Alzheimer’s, Parkinson’s, or other forms of dementia. 

Does carb burning age you?


Grant was out for his weekly hill ride with his old mate Stephen. Stephen was now in his nineties and Grant just about to turn 90. The day was sunny and warm. At halfway, they stopped and had a coffee and talked about their grandchildren, each showing off a bit to the other. On the last high hill Grant took off and lead out a sprint. It was all good until just as they hit the top, Grant felt a sudden pain in his chest and dropped dead. Stephen, after a lifetime of never quite winning the hill sprints, seeing him falter took his chance and rode past him – at the exact moment he finally won a sprint, he too felt a sudden pain and dropped dead.

Neither man even had the chance to pull over and unclip from their carbon racing bikes. They lay turtle up, each having won the final sprint to the line.

As Mark Sisson puts it, “they lived long and dropped dead”. Good quantity and great quality.

Anyway, that’s my little fantasy and thought experiment about how I should die along with my long time mate Stephen Farrell, who strangely thrashes me at everything except hill climbs.

Two things are inevitable in life, death and taxes.

I’m here to talk about the first one. I am assuming we want both quantity and quality of life. How do you get the most “bang for your buck” so to speak? The first clue might be in the caloric restriction data – eat less live longer. Sounds feasible, and some data support this idea. The unappealing thing, to me at least, is that eating is fun, enjoyable, and perhaps in the end the trade off isn’t worth it because you are alive but had to go hungry the whole time so life was just way less fun. But there are new data and new hypotheses about how glucose metabolism may be the driver, not caloric restriction.

How glucose metabolism fits in

I want to spend the main part of this blog summarizing (at least as well I can summarize a complex neurophysiology paper) how glucose metabolism controls the aging process, mainly through the brain. I’m talking about a paper just published in Trends in Endocrinlogy and Metabolism called “Metabolic mystery: aging, obesity, diabetes, and the ventromedial hypothalamus” available here. First, its hardly light bedtime reading, unless you quickly want to fall asleep. Second, there is so much complex genetics, animal study material, and hormonal and neuronal mechanistic stuff it takes a very long time to get through it. So I’ll spare you all the challenge and get straight to the major hypotheses and practical implications.

They start by revisiting the well known phenomenon that caloric restriction can increase lifespan, in at least some animals. Possibly humans and primates, although the jury is still out on that, and the only decent primate study wasn’t a decent study after all because of the high sugar diets for both caloric restriction and ad lib feeding groups.

Major findings of this review

  1. The energy mediating centre in the brain (the ventromedial hypothalamus) has specific glucose and FFA (free fatty acid) sensors.
  2. These sensors directly affect hepatic (liver) and peripheral (muscle and organ) glucose metabolism in opposite ways.
  3. High glucose in the blood drives a decrease in liver glucose production and an increase in glucose metabolism in other tissues. It’s vice versa for lower glucose and increased FFAs in the blood.
  4. Increased oxidation of glucose in peripheral tissues requires less oxygen to metabolise but results in more oxidative stress (i.e. damage) to the tissues. This damage is directly implicated in aging. Increased availability of insulin and insulin-like growth factor 1 (IGF-1) are also implicated in this process.
  5. Glucose on its own may not be enough. Increased mortality of Type 2 diabetics who are aggressively treated with exogenous insulin is evidence for this.
  6. Take home message – there is direct evidence that high dietary glucose load (read CARBOHYDRATE) Continue reading “Does carb burning age you?”

Be the best you can be


(pic: the entrance to AUT Millenium where I work)

I’ve wanted to start a blog for quite some time now. The trick is to get the technical skills together well enough to actually know how to run one and do it regularly. Well, I’m just about there.

What will I blog about?

I am really interested in the science of how we can be the best we can be. This crosses disciplines such as biology, medicine, pubic health, and productivity management. The cornerstones are nutrition, exercise, sleep, neuroscience, psychology and well-being. I’ll be covering these topics under the broad heading of the Science of Human Potential (the name of this blog).

I’ve been interested in human health and performance for my whole career. I started in psychology then into sport and exercise psychology, then into public health especially physical activity then obesity.

There have been some twists and turns along the way which might help to give a view of why I do what I do and where it can go.

About me

Sport and exercise has always been a massive part of my life. From an early age I played rugby union, learned to sail and race, and eventually ended up in the high school rowing squad. Rowing at my high school had no room for anything but high performance. So I was introduced to this at age 13. From there we won national championships most years. The combination of the sheer physicality of the sport and the team work and individual excellence required both mentally and physically really defined my teenage years and who I could become as an adult.

Being fit and involved in some sort of high performance activity has been part of my life since then.

I finished bachelors, Honors, and doctoral degrees in psychology at the University of Auckland by 1994. At the same time I had got into triathlon as a sport. I ended up racing semi-professionally. That’s code for “was never quite fast enough to earn a decent living, so had to supplement prize money income by working“. In the end I raced professionally in several world championships in long course triathlon, ironman and duathlon. That was great fun, and the skills and work ethic I have learned from triathlon are important to me.

The extra benefits from the high performance sport world, especially triathlo,n include:

  • I met my wife Louise because of triathlon. She ended up also as a professional triathlete, a better athlete than me. We’ve been married since 1995 and have three boys – Sam, Jackson and Daniel. Louise also started Vitality Works, a workplace health company acquired by Sanitarium in 2012. Vitality Works has allowed both of us to benefit from a huge amount of professional and personal development in health and well-being.
  • I figured out early that a high performance life is just as much work as a low performance life, so you may as well take the high performance life. It just requires a bit more work up front, but frankly you avoid work later and you get more choices.
  • I have the skills to stay fit and enjoy maximizing my biology for my own personal peak performance.
  • I still get to compete at a reasonable level in triathlon and running. This is cool because the age group triathlon and running groups are really fun, and you get to hang out with people of a similar performance, health, and happiness mindset.

My academic career began with part-time teaching in the Psychology Department at The University of Auckland during my PhD tenure. I moved to Australia (Central Queensland University in Rockhampton) and worked in the School of Psychology there for nearly 10 years. Most of our spare time then was dedicated to triathlon training and racing with Louise. I wasn’t going fast or far in the academic world at that point. Enter Kerry Mummery.

Kerry Mummery is now the Dean of Physical Education at the University of Alberta. He really mentored and started me on the journey to becoming a decent academic. We worked on several physical activity and health projects together. The most notable was 10,000 Steps. This started as a whole community project and morphed into a nationwide program which is still running successfully today.

This was the entrance into public health proper for me. I started at AUT in 2003 after the birth of Jackson our second son. Back in Auckland and into a new country with plenty to do. That’s when things really took off. I had the good fortune to have several great staff members and PhD students under my guidance. Almost all of these are still with me.

The highlights in the last decade are:

  • Working with dozens of talented doctoral and masters thesis students
  • Being highly successful in obtaining research grants and funding. This is the life of an academic and you live and die by this success. We are up over $20 million in funding.
  • A solid and respectable publication record. Ditto above. Important for gauging success. But by itself is unlikely to put much of a dent in the universe.
  • Being involved in Vitality Works. This has put a dent in the universe and allowed me to develop more formally into peak performance, well being and neuroscience.
  • Being the youngest full professor around for a while. That wore off as I aged!
  • Moving our work beyond physical activity into obesity, well-being, productivity, and nutrition/weight loss. Most recently the work we are starting in metabolic efficiency and weight is likely to put the biggest dent in the world.
  • Starting the Centre for Physical Activity and Nutrition and eventually morphing that into the Human Potential Centre at the new Millennium Campus.

So that’s where I’m at. Where I want to go now, and with this blog, is to explore the science behind what helps us “be the best we can be.” It’s an emerging and multidisciplinary science. Let’s go!