Tuesday, October 9, 2012

The Ancestral Diet : an excellent model

"What causes fatness?"

Is this some kind of a joke? What kind of moron would ask such a question? Of course, the answer is in overeating and sedentary lifestyles, isn't it? If all fat people simply ate less and moved more, then they would be slim, wouldn't they? Isn't it also true that in order to lose weight, we must impose caloric restriction or increase caloric expenditure constantly (or better yet, do both concurrently)?

Lets do a little quiz here to test your obesity smarts. True or False?

  1. All fat people are bad at math and cannot count calories.
  2. All fat people are weak and lack the willpower to resist food. 
  3. All fat people eat more and move less than all lean people.

If you have answered True to any of the above, I don't need to know. The case I am trying to make is that the causes and hence, the treatment of obesity are greatly misunderstood today. Understanding how we got so fat requires a paradigm shift because conventional wisdom didn't solve anything, and certainly does not look like it is about to provide answers anytime soon. 

In my opinion, Gary Taubes in his book Why we get fat and what to do about it, has struck the nail on the head (1). He states that conventional wisdom as it stands today, has failed miserably to explain the cause of obesity. Citing a "crowded room" example, Mr Taubes points out that saying "overeating causes obesity" is analogous to saying that too many people entered a room therefore it is crowded. It merely states the obvious and offers no meaningful explanation as to what caused so many people to enter the room, making it crowded. Indeed, why do we overeat? According to Mr Taubes, the common wisdom of fatness got it wrong way around, that it is because we are obese that we overeat.

You see, obesity is not just a state of being really fat, and overeating is not just a behavioral aberration. Obesity is characterized by a complex host of metabolic abnormalities and inflammation. These factors mess up satiety signals driving us to overeat and at the same time, they cause abnormal production and accumulation of fats. Therefore, we become obese because we eat the type of food which causes obesogenic conditions in the first place, which then cause us to overeat. 

Now, if the real mischief indeed originated from the type of food consumed, the next question which begs to be asked would naturally be what types of food?

In my attempt to find some answers, I'd like to take us a step back, and first look at the health promoting efficacy of ancestral/traditional diets. A recent paper published in “Diabetes, Metabolic Syndrome, Obesity” comparing western diets with ancestral diets drew the conclusion that ancestral diets consistently produced lean bodies, high level of satiety, and excellent health markers (2).

At this point, I would like to point out that most studies which examine obesity and its dietary causes have done so by isolating a small part of one picture and then analyze that isolated part against the backdrop of existing information. This is akin to running around in the same circle - there is usually a high degree of conformity with the conventions of the day and hardly leaves room for maneuvers in terms of shedding new light on the issue.

Indeed, by researching only the dietary habits of western populations in the hope of singling out one "culprit", most studies have ignored a realm of possibilities which lay outside the western diet. For e.g., studies of western populations have missed the important fact that even the western individuals classified as "healthy" possess dramatically higher levels of leptin (hunger signaling hormone), elevated fasting insulin levels (hormone involved with carbohydrate metabolization and glucose uptake), as well as higher blood glucose, than those on ancestral diets.

In contrast, this report offers a different approach. Comparisons of ancestral diets with the western diet allow us to : (i) get to the source of a good diet which is proven to produce remarkable health, vs one which causes ill health; (ii) distill the relevant dietary differences between the two; (iii) build a coherent theory based on those facts.

Now, let me provide some background on the physiology of food-related inflammation and what it means to be leptin resistant, as they relate to obesity.

Diet-induced inflammation, leptin resistance.

It is well established that obesity is characterized by chronic inflammation and many syndromes of metabolic abnormalities. Severity of these conditions are linked directly to the levels of microbes in our gastrointestinal tract (GI). Bacterial lipopolysaccharide (LPS), a substance that forms the outer membrane of a certain bacteria, causes our immunity to react strongly at high levels. At lower levels, it creates a chronic state of inflammation in our bodies.

Additionally, pathogen-associated molecular patterns (PAMP), which is essentially our innate immune systems's defense response to the shedding of pathogens harbored in our bodies, also plays an inflammatory role. Both LPS and PAMP have been implicated in many modern diseases, including liver toxicity, non alcoholic fatty liver disease and obesity. The gateway to such inflammatory substances is thought to be via our GI tract. Administration of antibiotics to reduce gut microbes in experimental rodents successfully reduced circulating LPS, improved inflammatory markers and glucose tolerance, and caused a reduction in body weight and fat tissue.

Moreover, information on satiety is transmitted via the vagal nerve that innervates our upper GI to the central nervous system, based on the physical and chemical actions of food in our guts. Leptin resistance begins to occur when leptin's ability to regulate the vagal nerve's sensitivity to satiety signals is blunted, while simultaneously increasing appetite-stimulating hormones. At a later stage, leptin resistance progresses to the central nervous system directly, as sensitivity of the hypothalamus diminishes.

What is an ancestral diet?

Data from ten populations of modern day hunter-gatherers, gathered throughout the late 1920s to 2006, consistently showed that those eating ancestral diets possessed lean bodies and virtually no metabolic abnormalities nor cardiovascular diseases. 

Of the ten populations, the Tarahumaras, Mexican Pimas and Arizona Pimas, whose diets included graduating degrees of western foods such as beans, maize/wheat/flour tortillas, processed meats, white bread, cereals, juices etc, saw corresponding increments in obesity, hypertension and diabetes.

Interestingly, ancestral diets that yielded good health outcomes spanned a very wide and different range of macronutrient compositions, dietary fiber, and nutrient density and glycemic index. For e.g., the Kitavans who subsisted on starchy root vegetables, leaves, fruit, with little fish, meat or fat, had a diet high in carbohydrates up to 70%. Conversely, the Masai's diet of cow's milk, blood and unprocessed meat, contained up to 66% saturated fats with cholesterol levels matching those of the U.S. Another important feature to note was the abundance of food available to these populations. There were neither food shortages nor caloric restrictions.

Yet, it did not seem to matter if some diets were high in carbohydrate while others ate mostly fats or protein ; or if one population consumed more calories than another; or if some diets contained little fiber; or even if they consumed foods that were high on the glycemic index. In spite of all these vastly different variables and the abundance of food, they all shared the same undifferentiated outcome - impeccable health markers with no incidences of obesity, hypertension, metabolic syndrome, and heart diseases.

What do genes and physical activity have to do with it?

Apparently, not as much as some of us would like to believe. From research, it appears that Kitavan islanders maintained their metabolic advantage only for as long as they ate their ancestral diets. Those islanders who transitioned into the western diet invariably became overweight.

Furthermore, historical data showed other hunter gatherers populations to develop signs of metabolic diseases once western foods were introduced, even though their physical activity remained high.

Carbohydrate density : the fundamental distinction.

It is quite clear that a western diet causes obesity while an ancestral diet does not. The most fundamental factor that distinguishes the western diet from an ancestral one is the "carbohydrate density" of the foods found commonly in the western diet.

"Carbohydrate density" is independent of the proportion of carbohydrate vs other macronutrients within the diet. It is evidenced that some ancestral diets contained a very high proportion of carbohydrates. However, sources of carbohydrates in these ancestral diet were in the form of tubers, fruits, leaves, stems etc. These cellular carbohydrates are stored within cell walls, and are able to retain most of its integrity throughout cooking and undergoes a longer digestive process. 

In contrast, acellular carbohydrates in the form of flour, sugar and processed foods, do not have the same "walled in" effect and hence, exert a very high concentration of  carbohydrate on our systems when consumed. The carbohydrate density of this new western diet burdens and confounds our GI in a way that ancestral diets do not, instigating the growth of new, harmful microbes in our guts that create toxic waste materials, and causes inflammation on top of leptin abnormalities. 

It should be noted that "carbohydrate density" is entirely different from "glycemic index" which measures the speed in which our blood glucose levels responds to dietary intake of carbohydrates. In fact, some ancestral foods consumed were high on the glycemic index, with no negative metabolic outcomes observed as long as they were cellular.

Although grains are cellular, they are considered a "carbohydrate dense" food. Due to their nature, storage of carbohydrates in grains was created for quick enzymic action to facilitate germination. Elevated levels of insulin and insulin resistance have been associated with obesity and diabetes. Since insulin is primarily mobilized by carbohydrate intake, dietary intake of carbohydrate dense foods might cause insulin irregularities.

Aren't whole grains healthy?

This is a difficult area to navigate where I honestly have no expert authority on. I can only report what I have read. As discussed above, grains are very dense in carbohydrates. There are some literature regarding allergenic and inflammatory properties found in grains (the most common being "gluten", the other being "lectin"). Personally, I exclude grains (even whole grains) from my own diet because I find that I have an adverse reaction to them. However, there are others I know who thrive well on whole grains, so all bets are off on this one. Suffice to say, my sentiments on refined grains and flour are not as flexible because I have absolutely nothing positive to say about them. The same can be said of sugar.

Here is what I have read. First, a study by The Pennsylvania State Universtiy in 2010, had shown only very modest improvements to heart diseases when refined grains were replaced with whole grains (3). This raises the questionability of the benefits of whole grains in this respect.

Second, as mentioned above, grains are "carbohydrate dense" foods, whereas carbohydrate sources of the ancestral diet were exclusively from consumption of vegetables including roots, leaves, bulbs, as well as fruits. In fact, when grains were introduced, signs of overweight or obesity and diabetes appeared.

Third, grain restricted diets have been evidenced to significantly improve metabolic markers and reduce weight. According to the report, these trials are small and few but results have been consistent and unanimous. All ad libitum (i.e. no voluntary caloric restrictions) studies of the modern day "Paleolithic diet", which mirrors the ancestral diet, appeared to be superior to the "Mediterranean diet" in reducing weight and waist circumference, better blood sugar regulation, and increased satiety per caloric intake prompting a voluntary decrease in caloric consumption. 

However, the benefits of the Paleo diet was independent of this spontaneous decrease in food intake and increased weight loss. When energy intake was controlled to be equal across the board, the Paleo diet still produced better markers including lower blood pressure and improved lipid profiles. Both diets similarly emphasize unrefined, whole foods but the fundamental difference lies in "grain restriction" of the Paleo diet.

Fourth, Leptin levels were also found to have fallen by 31% after 12 weeks, in another ad libitum study on the Paleo Diet, which had a linear relationship with decreased consumption of cereal grains. It has been hypothesized that cereal grain causes leptin resistance.

Doesn't dietary fat make us fat?

Without a doubt, dietary fat has some part to play in the obesity epidemic and metabolic disorders. In numerous rodent experiments on obesity, fat intake was elevated specifically to induce that condition. In addition, differing fatty acids have been successfully shown to create inflammatory processes in the body.

Even so, fat in itself is arguably not the primary cause of obesity. In fact, I think dietary fat (including saturated ones) is so important to the human body that, in many cases, insufficient intake is the real issue. But this is a much more complicated subject and warrants a separate discussion (one which I plan to undertake in another blog post). The only exceptions I take are trans fat and poor quality oils, which I can say in no uncertain terms, will not only make us fat but will, in fact, kill us.

According to this paper, the accusation that dietary fat as the primary causative factor of obesity is unfounded. If indeed dietary fat causes obesity, then wouldn’t a diet that is lower in fat eradicate the problem? But surprisingly, in ad libitum studies comparing low fat diets with low carbohydrate one, it is the low carbohydrate ones that emerged ahead with greater weight loss as well as greater improvements to metabolic markers. Low fat diets work as effectively as low carbohydrate diets only when caloric intake was controlled in both diets. The significance here is "satiety". Low carbohydrate diets led to a spontaneous and voluntary reduction in caloric intake whereas the low fat diet did not promote satiety, and hence would work only equally effective if there caloric intake was restricted.

Moreover, as discussed above, ancestral diets that were very high in meat and/or fat intake did not yield any metabolic disorders nor obesity among its consumers. This is inline with the observation that simply a high consumption of dietary fats from unprocessed sources, on its own does not have obesogenic effects on the human body.

However, fat (refined ones) has been implicated to cause a "double whammy" when consumed together with acellular flours, sugars, carbohydrate dense and processed foods, as is the case of the western diet. When ingested in this manner, fat enriches the inflammatory microbes already in place in our guts, and also increases PAMPs and absorption of bacterial LPS, stimulating even more inflammation.

Conclusion

The ancestral diet is one which promotes efficient human energy homeostasis. Historical data shows that those who maintain ancestral diets without the influence of western foods retain leanness of the body and excellent metabolic health markers, even when matched against "healthy individuals" in western populations. 

Since the ancestral diet is strongly distinct from the western diet with regard to "carbohydrate density", acellular refined foods and grains remain implicated as the main causes of inflammation, metabolic irregularities and obesity. The western diet which commonly features a combination of high carbohydrates and refined fats, creates an inflammatory microbiota in the gut and absorption of pathogenic materials, leading to leptin resistance and obesity. 

In addition, consumption of fructose appears to induce de novo lipogenesis (fat generation in the liver), liver toxicity and contributes to non alcoholic fatty liver disease. On the other hand, glucose appears to increase activity in fat tissue. Fructose and glucose are both components of sugar which is also very prevalent in the western diet.

Finally, insulin’s ability to regulate fat accumulation in fat tissue i.e. lipogenisis, from a carbohydrate rich meal that is typical of a western diet, has also been inextricably tied to the obesity epidemic today.

Discouraging as it sounds, maintaining an ancestral-like way of eating is actually within the reach for most folks. I am not suggesting that we all become Flintstones, and acknowledge that it is impossible to eliminate ALL offensive foods. But, I believe that we will reap health benefits even if we can do as much as minimize our exposure to problematic foods and at the same time, including as much as possible of the good stuff to our diets. Improvements will commensurate with the effort one puts in. In other words, it is not all or nothing. And ending on a note of encouragement : studies have shown that just after 7 weeks, the ill effects of the western diet was reversed markedly by consuming an ancestral diet !

References:
  1. Taubes Gary. (2011). Why we get fat and what to do about it. New York: Anchor Books.
  2. Spreadbury Ian. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota and may be the primary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012 Jul; 5:175-189
  3. Harris KA, Kris-Etherton PM. Effects of whole grains on coronary heart disease risk. Curr Atherosclerosis Rep. 2010 Nov; 12(6):368-376.





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