Saharan Hunter-Gatherers Unearthed

The media recently covered an archaeological discovery in Niger that caught my attention. In the middle of the Sahara desert, researchers found a hunter-gatherer burial site containing over 200 graves ranging from about 10,000 to 4,500 years old. During this period, the region was lush and productive.

There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.

Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.

Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.

Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.

Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:

Among the Tenerian graves was a heart-rending burial tableaux [SIC!!]: A young woman was lying on her side. Pollen under her body suggested that she was placed on a bed of flowers. Lying on their sides facing her were two young children, their fingers interlocked with hers, leaving a tangle of bones.

Haha, I couldn't let the spelling error slide, it should be 'tableau'. Hey, I'm half French, give me a break.

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Fit at 70

In my professional life, I study neurodegenerative disease, the mechanisms of aging, and what the two have in common. I was reading through a textbook on aging a few months ago, and I came across an interesting series of graphs.

The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.

We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.

Kitava: Wrapping it Up

There's a lot to be learned from the Kitava study. Kitavans eat a diet of root vegetables, coconut, fruit, vegetables and fish and have undetectable levels of cardiovascular disease (CVD), stroke and overweight. Despite light smoking. 69% of their calories come from carbohydrate, 21% from fat and 10% from protein. This is essentially a carbohydrate-heavy version of what our paleolithic ancestors ate. They also get lots of sunshine and have a moderately high activity level.

The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.

The Kitavan diet is low in fat, and most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.

Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This raises the possibility that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and withholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? White flour and sugar maybe?

Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.

The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from near-complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.

The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed seed oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.

Cardiovascular Risk Factors on Kitava, Part IV: Leptin

Leptin is a hormone that is a central player in the process of weight gain and chronic disease. Its existence had been predicted for decades, but it was not identified until 1994. Although less well known than insulin, its effects on nutrient disposal, metabolic rate and feeding behaviors place it on the same level of importance.

Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.

Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.

The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.

Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others. This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so it's possible that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.

The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.

This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.

So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.

This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?

There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at industrial food.