No fat gain while eating well during the Holiday Season: Palatability isolines, the 14-percent advantage, and nature’s special spice

Like most animals, our Paleolithic ancestors had to regularly undergo short periods of low calorie intake. If they were successful at procuring food, those ancestors alternated between periods of mild famine and feast. As a result, nature allowed them to survive and leave offspring. The periods of feast likely involved higher-than-average consumption of animal foods, with the opposite probably being true in periods of mild famine.

Almost anyone who adopted a low carbohydrate diet for a while will tell you that they find foods previously perceived as bland, such as carrots or walnuts, to taste very sweet – meaning, to taste very good. This is a special case of a more general phenomenon. If a nutrient is important for your body, and your body is deficient in it, those foods that contain the nutrient will taste very good.

This rule of thumb applies primarily to foods that contributed to selection pressures in our evolutionary past. Mostly these were foods available in our Paleolithic evolutionary past, although some populations may have developed divergent partial adaptations to more modern foods due to recent yet acute selection pressure. Because of the complexity of the dietary nutrient absorption process, involving many genes, I suspect that the vast majority of adaptations to modern foods are partial adaptations.

Modern engineered foods are designed to bypass reward mechanisms that match nutrient content with deficiency levels. That is not the case with more natural foods, which tend to taste good only to the extent that the nutrients that they carry are needed by our bodies.

Consequently palatability is not fixed for a particular natural food; it does not depend only on the nutrient content of the food. It also depends on the body’s deficiency with respect to the nutrient that the food contains. Below is what you would get if you were to plot a surface that best fit a set of data points relating palatability of a specific food item, nutrient content of that food, and the level of nutrient deficiency, for a group of people. I generated the data through a simple simulation, with added error to make the simulation more realistic.

Based on this best-fitting surface you could then generate a contour graph, shown below. The curves are “contour lines”, a.k.a. isolines. Each isoline refers to palatability values that are constant for a set of nutrient content and nutrient deficiency combinations. Next to the isolines are the corresponding palatability values, which vary from about 10 to 100. As you can see, palatability generally goes up as one moves toward to right-top corner of the graph, which is the area where nutrient content and nutrient deficiency are both high.

What happens when the body is in short-term nutrient deficiency with respect to a nutrient? One thing that happens is an increase in enzymatic activity, often referred to by the more technical term “phosphorylation”. Enzymes are typically proteins that cause an acute and targeted increase in specific metabolic processes. Many diseases are associated with dysfunctional enzyme activity. Short-term nutrient deficiency causes enzymatic activity associated with absorption and retention of the nutrient to go up significantly. In other words, your body holds on to its reserves of the nutrient, and becomes much more responsive to dietary intake of the nutrient.

The result is predictable, but many people seem to be unaware of it; most are actually surprised by it. If the nutrient in question is a macro-nutrient, it will be allocated in such a way that less of it will go into our calorie stores – namely adipocytes (body fat). This applies even to dietary fat itself, as fat is needed throughout the body for functions other than energy storage. I have heard from many people who, by alternating between short-term fasting and feasting, lost body fat while maintaining the same calorie intake as in a previous period when they were steadily gaining body fat without any fasting. Invariably they were very surprised by what happened.

In a diet of mostly natural foods, with minimal intake of industrialized foods, short-term calorie deficiency is usually associated with short-term deficiency of various nutrients. Short-term calorie deficiency, when followed by significant calorie surplus (i.e., eating little and then a lot), is associated with a phenomenon I blogged about before here – the “14-percent advantage” of eating little and then a lot (, ). Underfeeding and then overfeeding leads to a reduction in the caloric value of the meals during overfeeding; a reduction of about 14 percent of the overfed amount.

So, how can you go through the Holiday Season giving others the impression that you eat as much as you want, and do not gain any body fat (maybe even lose some)? Eat very little, or fast, in those days where there will be a feast (Thanksgiving dinner); and then eat to satisfaction during the feast, staying away from industrialized foods as much as possible. Everything will taste extremely delicious, as nature’s “special spice” is hunger. And you may even lose body fat in the process!

But there is a problem. Our bodies are not designed to associate eating very little, or not at all, with pleasure. Yet another thing that we can blame squarely on evolution! Success takes practice and determination, aided by the expectation of delayed gratification.

Refined carbohydrate-rich foods, palatability, glycemic load, and the Paleo movement

A great deal of discussion has been going on recently revolving around the so-called “carbohydrate hypothesis of obesity”. I will use the acronym CHO to refer to this hypothesis. This acronym is often used to refer to carbohydrates in nutrition research; I hope this will not cause confusion.

The CHO could be summarized as this: a person consumes foods with “easily digestible” carbohydrates, those carbohydrates raise insulin levels abnormally, the abnormally high insulin levels drive too much fat into body fat cells and keep it there, this causes hunger as not enough fat is released from fat cells for use as energy, this hunger drives the consumption of more foods with “easily digestible” carbohydrates, and so on.

It is posited as a feedback-loop process that causes serious problems over a period of years. The term “easily digestible” is within quotes for emphasis. If it is taken to mean “refined”, which is still a bit vague, there is a good amount of epidemiological evidence in support of the CHO. If it is taken to mean simply “easily digestible”, as in potatoes and rice (which is technically a refined food, but a rather benign one), there is a lot of evidence against it. Even from an unbiased (hopefully) look at county-level data in the China Study.

Another hypothesis that has been around for a long time and that has been revived recently, which we could call the “palatability hypothesis”, is a competing hypothesis. It is an interesting and intriguing hypothesis, at least at first glance. There seems to be some truth to this hypothesis. The idea here is that we have not evolved mechanisms to deal with highly palatable foods, and thus end up overeating them.  Therefore we should go in the opposite direction, and place emphasis on foods that are not very palatable to reach our optimal weight. You might think that to test this hypothesis it would be enough to find out if this diet works: “Eat something … if it tastes good, spit it out!”

But it is not so simple. To test this palatability hypothesis one could try to measure the palatability of foods, and see if it is correlated with consumption. The problem is that the formulations I have seen of the palatability hypothesis treat the palatability construct as static, when in fact it is dynamic – very dynamic. The perception of the reward associated with a specific food changes depending on a number of factors.

For example, we cannot assign a palatability score to a food without considering the particular state in which the individual who eats the food is. That state is defined by a number of factors, including physiological and psychological ones, which vary a lot across individuals and even across different points in time for the same individual. For someone who is hungry after a 20 h fast, for instance, the perceived reward associated with a food will go up significantly compared to the same person in the fed state.

Regarding the CHO, it seems very clear that refined carbohydrate-rich foods in general, particularly the highly modified ones, disrupt normal biological mechanisms that regulate hunger. Perceived food reward, or palatability, is a function of hunger. Abnormal glucose and insulin responses appear to be at the core of this phenomenon. There are undoubtedly many other factors at play as well. But, as you can see, there is a major overlap between the CHO and the palatability hypothesis. Refined carbohydrate-rich foods generally have higher palatability than natural foods in general. Humans are good engineers.

One meme that seems to be forming recently on the Internetz is that the CHO is incompatible with data from healthy isolated groups that consume a lot of carbohydrates, which are sometimes presented as alternative models of life in the Paleolithic. But in fact among influential proponents of the CHO are the intellectual founders of the Paleolithic dieting movement. Including folks who studied native diets high in carbohydrates, and found their users to be very healthy (e.g., the Kitavans). One thing that these intellectual founders did though was to clearly frame the CHO in terms of refined carbohydrate-rich foods.

Natural carbohydrate-rich foods are clearly distinguished from refined ones based on one key attribute; not the only one, but a very important one nonetheless. That attribute is their glycemic load (GL). I am using the term “natural” here as roughly synonymous with “unrefined” or “whole”. Although they are often confused, the GL is not the same as the glycemic index (GI). The GI is a measure of the effect of carbohydrate intake on blood sugar levels. Glucose is the reference; it has a GI of 100.

The GL provides a better way of predicting total blood sugar response, in terms of “area under the curve”, based on both the type and quantity of carbohydrate in a specific food. Area under the curve is ultimately what really matters; a pointed but brief spike may not have much of a metabolic effect. Insulin response is highly correlated with blood sugar response in terms of area under the curve. The GL is calculated through the following formula:

GL = (GI x the amount of available carbohydrate in grams) / 100

The GL of a food is also dynamic, but its range of variation is small enough in normoglycemic individuals so that it can be treated as a relatively static number. (Still, the reference are normoglycemic individuals.) One of the main differences between refined and natural carbohydrate-rich foods is the much higher GL of industrial carbohydrate-rich foods, and this is not affected by slight variations in GL and GI depending on an individual’s state. The table below illustrates this difference.

Looking back at the environment of our evolutionary adaptation (EEA), which was not static either, this situation becomes analogous to that of vitamin D deficiency today. A few minutes of sun exposure stimulate the production of 10,000 IU of vitamin D, whereas food fortification in the standard American diet normally provides less than 500 IU. The difference is large. So is the difference in GL of natural and refined carbohydrate-rich foods.

And what are the immediate consequences of that difference in GL values? They are abnormally elevated blood sugar and insulin levels after meals containing refined carbohydrate-rich foods. (Incidentally, the GL  happens to be relatively low for the rice preparations consumed by Asian populations who seem to do well on rice-based diets.)  Abnormal levels of other hormones, in a chronic fashion, come later, after many years consuming those foods. These hormones include adiponectin, leptin, and tumor necrosis factor. The authors of the article from which the table above was taken note that:

Within the past 20 y, substantial evidence has accumulated showing that long term consumption of high glycemic load carbohydrates can adversely affect metabolism and health. Specifically, chronic hyperglycemia and hyperinsulinemia induced by high glycemic load carbohydrates may elicit a number of hormonal and physiologic changes that promote insulin resistance. Chronic hyperinsulinemia represents the primary metabolic defect in the metabolic syndrome.

Who are the authors of this article? They are Loren Cordain, S. Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, Bruce A. Watkins, James H O’Keefe, and Janette Brand-Miller. The paper is titled “Origins and evolution of the Western diet: Health implications for the 21st century”. A full-text PDF is available here. For most of these authors, this article is their most widely cited publication so far, and it is piling up citations as I write. This means that not only members of the general public have been reading it, but that professional researchers have been reading it as well, and citing it in their own research publications.

In summary, the CHO and the palatability hypothesis overlap, and the overlap is not trivial. But the palatability hypothesis is more difficult to test. As Karl Popper noted, a good hypothesis is a testable hypothesis. Eating natural foods will make an enormous difference for the better in your health if you are coming from the standard American diet, and you can justify this statement based on the CHO, the palatability hypothesis, or even a few others – e.g., a nutrient density hypothesis, which would be closer to Weston Price's views. Even if you eat only plant-based natural foods, which I cannot fully recommend based on data I’ve reviewed on this blog, you will be better off.

The low modern potassium-to-sodium ratio: Big problem or much ado about nothing?

It has been argued that the diets of our Paleolithic ancestors had on average a much higher potassium-to-sodium ratio than modern diets (see, e.g., Cordain, 2002).

This much lower modern ratio is believed by some to be the cause of a number of health problems, including: high blood pressure, stroke, heart disease, memory decline, osteoporosis, asthma, ulcers, stomach cancer, kidney stones, and cataracts.

But, is this really the case?

The potassium-to-sodium ratio in ancient and modern times

According to some estimates, our Paleolithic ancestors’ daily consumption was on average about 11,000 mg of potassium and about 700 mg of sodium (salt). That yields a potassium-to-sodium ratio of about 16. Today’s ratio in industrialized countries is estimated to be around 0.6.

Just for the sake of illustration, let us compare a healthy Paleolithic diet food, walnuts, with a modern industrialized food that many believe to be quite healthy, whole-wheat bread. The table below (click on it to enlarge) compares these two foods in terms of protein, carbohydrate, fat, vitamin, and mineral content.

Walnuts have a potassium-to-sodium ratio of about 205. The whole-wheat bread’s ratio is about 0.5; much lower, and close to the overall ratio estimated for industrialized countries mentioned above.

At the same time, walnuts provide a better nutritional value than whole-wheat bread, including a good amount of omega-3 fatty acids (2.5 g; of α-linolenic acid, or ALA). However, walnuts have a fairly high omega-6 fat content.

Also, many diabetics experience elevated blood glucose levels in response to whole-wheat bread, in spite of its glycemic index being supposedly lower than that of white bread. Walnuts do not seem to cause this type of problem, even though several people are allergic to walnuts (and other tree nuts).

Health effects of the potassium-to-sodium ratio

So, the potassium-to-sodium ratio appears to have been much higher among our Paleolithic ancestors than today. It is important to stress that, even though this is a possibility, we do not know this for sure. Animals go to great lengths to find salt licks, and then consume plenty of sodium in them. Our ancestors could have done that too. Also, we know that sodium deficiency can be deadly to both animals and humans.

As for the many negative health effects of a low potassium-to-sodium ratio in modern humans, we have reasons to be somewhat skeptical. One has to wonder if the studies that are out there do not conflate the effects of this ratio with those of other factors, such as smoking, heavy alcohol consumption, or consumption of industrialized high carb foods (e.g., cereals, pasta, refined sugars).

Another possible confounding factor is potassium deficiency, not the potassium-to-sodium ratio. Potassium deficiency, like other deficiencies of essential minerals, including sodium deficiency, is associated with serious health problems.

If potassium is deficient in one’s diet, it is also likely that the potassium-to-sodium ratio will be low, unless the diet is also equally deficient in sodium.

Let us take a look at a study by Ikeda et al. (1986), which included data from 49 regions in Japan, a country known for high consumption of sodium.

This study found a significant association between the potassium-to-sodium ratio and overall mortality and heart disease, but only among men, and not among women.

One wonders, based on this, whether another uncontrolled factor, or factors, might have biased the results. Examples are smoking and heavy alcohol consumption, which could have been higher among men than women. Another is chronic stress, which could also have been higher among men than women.

The researchers report that they found no association between the potassium-to-sodium ratio and mortality due to diabetes, liver disease, or tuberculosis. This ameliorates the problem somewhat, but does not rule out the biasing effect of other factors.

It would have been better if the researchers had controlled for the combined effect of covariates (such as smoking, alcohol consumption etc.) in their analysis; which they did not.

Moreover, the study found no association between the potassium-to-sodium ratio and blood pressure. This is a red flag, because many of the diseases said to be caused by a low potassium-to-sodium ratio are assumed to be mediated by or at least associated with high blood pressure.

Regarding the possible confounding effect of industrialized high carb foods consumption, it seems that many of these foods have a low potassium-to-sodium ratio, as the example of whole-wheat bread above shows. Thus, some of the health problems assigned to the low potassium-to-sodium ratio may have actually been caused by heavy consumption of industrialized high carb foods.

It is also possible that the problem is with the combination of a low potassium-to-sodium ratio and industrialized high carb foods consumption.

At the time the study was conducted, Japan was somewhat westernized, which is why industrialized high carb foods consumption might have been a factor. The US strongly influenced the Japanese after World War II, as it helped rebuild Japan’s economy.

In conclusion, the jury is still out there regarding whether the low modern potassium-to-sodium ratio is a big problem or much ado about nothing.

References:

Cordain, L. (2002). The Paleo Diet: Lose weight and get healthy by eating the food you were designed to eat. New York, NY: Wiley.

Ikeda, M., Kasahara, M., Koizumi, A., and Watanabe, T. (1986). Correlation of cerebrovascular disease standardized mortality ratios with dietary sodium and the sodium/potassium ratio among the Japanese population. Preventive Medicine, 15(1), 46-59.