This is the seventh and final installment in a series of posts in which I am laying out the most salient points from my 2012 Real Food Summit talk, “Weston Price on Primitive Wisdom.” See these links for part 1, part 2, part 3, part 4, part 5, and part 6.
How are we to place Price’s work in its appropriate context? How are we to respect and embrace the wisdom of our ancestors, while using modern science and our personal experience to refine and enrich the pool of accumulated wisdom? I will explore these questions in this final post.
There are many legitimate uses of evidence, some of which are as simple as collecting observations about the world for the sake of curiosity and appreciation. When it comes to evidence that should inform our decisions about how to eat and live to be healthy, I broadly categorize this evidence into three levels that should inform our decisions in a concerted manner, although each level should do so in its own particular way:
- Evidence supporting a framework for interpreting how to act in the face of uncertainty
- Experimental evidence demonstrating general cause-and-effect relationships
- Personal experience and self-experimentation
A Framework for Interpreting Uncertainty
Scientific uncertainty is all around us, and likely will be forever. The randomized experiment provides the closest approximation to a definitive demonstration of a cause-and-effect principle that we can obtain, but one experiment is never definitive and, no matter how many similar experiments scientists perform, questions are always left unanswered. This leaves us with scientific uncertainty, and the need for some kind of paradigm to help us decide what to do in the face of it.
This framework should form our “common sense,” a set of things we tentatively take for granted, pending more definitive evidence.
We all constantly act in the face of uncertainty. When we do so without an evidence-based framework, we still have a framework. What we have, however, is a “common sense” that takes the status quo for granted. This approach may seem sensible to those who have no reason to question it, but it leaves us captive to the status quo, one where degenerative diseases rein supreme.
In part 6, I shared the following quote from Nutrition and Physical Degeneration:
There are two programs now available for meeting the dental caries problem. One is to know first in detail all the physical and chemical factors involved and then proceed. The other is to know how to prevent the disease as the primitives have shown and then proceed. The former is largely the practice of the moderns. The latter is the program suggested by these investigations.
The first approach, the one Price opposed and the one based on knowledge without wisdom, superficially appeared to be based on scientific certainty. In reality, however, it took the status quo as its framework for interpreting uncertainty. Refined flour and sugar were the norm, and society’s managers added nutrients back to the diet one by one as science demonstrated their importance. Price argued for a “common sense” that took for granted diets associated with health rather than those associated with disease. In other words, a “common sense” rooted in evidence rather than in the status quo.
I argued in part 1 that Price’s basic study design was to examine “nature’s closest thing to a randomized controlled trial (RCT)” repeated in series for many peoples with different genetics and living in wildly different parts of the world. Price provided strong evidence that the replacement of traditional diets with the “displacing foods of modern commerce” caused the physical degeneration that ensued, especially the massive increase in cavities and dental deformities.
Much of what we can glean from Price’s work, however, is more observational in nature. Once we begin breaking down the dietary patterns into their individual components or begin looking at dietary changes specific to one of the “racial stocks” Price studied rather than those that were replicable across most or all of the groups, we leave “Nature’s RCT” and enter the realm of simple observations where inferences of cause and effect are much less clear.
It would be foolish, however, to dismiss all these more specific observations as having no value. Inferring cause and effect is not the only reason we observe things. Careful observations are almost always good for at least one thing: establishing the way things are. Price’s observations of groups that were nearly or completely free of certain diseases establishes two critical facts:
- This level of freedom from disease is possible, which is why Price called these groups standards of excellence.
- All of the characteristics of the diets and lifestyles of these groups are at least consistent with freedom from disease.
These observations are remarkable because they show that such characteristics are consistent with freedom of disease on a population level, which means that they protected even the members of those populations who were most vulnerable to disease.
An evidence-based “common sense” should take diets and lifestyles consistent with population-wide freedom from disease for granted. This should not be the end of the story. The other levels of evidence discussed below should also be included, but this should be the common sense background.
The alternative would be to take for granted diets and lifestyles inconsistent with population-wide freedom from disease, such as the refined and industrialized diets that prevail in our own society, simply because they represent the status quo.
In order to build this framework, we should expand our data to include that of other investigators taking Price’s approach. This could include, for example, studies of the freedom from heart disease enjoyed by the Maasai and Kitavans. Many of these findings lack a clear demonstration that these groups suffer from heart disease when modernized, but at least they provide us with examples of diets and lifestyles consistent with freedom from heart disease.
Further investigations of the genetics and mortality structures of these groups would be valuable to more clearly elucidate the causes of their freedom from heart disease. Ethnographic studies that shed further light on the details of diets and lifestyles traditional to such groups are also of great value.
While archeological investigations are of some value, their utility is much more limited than investigations of living people: sample size is generally poor; samples may be incomplete, such as isolated teeth or bones rather than complete skeletons with all parts intact; only a handful of health metrics are recorded in a skeleton; characterizing pre-historic diets is extremely difficult, and doing so with accuracy comparable to that achieved with living populations is probably impossible.
Finally, some have argued that there is an “osteological paradox” where improvements in health with increased longevity can allow diseases to more prominently record in the skeleton, giving a false appearance of decreased health. Nevertheless, as long as these limitations are acknowledged, archeological evidence can make a supplemental contribution to the framework.
Overall, I believe our “common sense” about diet and lifestyle should be to presume that the range of characteristics consistent with population-wide freedom from disease range from harmless to protective and vital until and unless clearly demonstrated otherwise, and to view deviations from this range of characteristics as suspect until and unless clearly exonerated from any role in disease.
Experimental Evidence Demonstrating Cause-and-Effect Relationships
As I argued in part 1, Price provided strong evidence that the transition from diets based on traditional, nutrient-dense foods to diets based on the “displacing foods of modern commerce” caused the physical degeneration that ensued.
While this finding is incredibly powerful in itself, it leaves much to be answered. Were some traditional diets superior to others? Were certain factors protective rather than others? Were some neutral, or some harmful? How do they work together in the proper balance? What is the full range of diseases attributable to diet?
For diseases that are less clearly attributable entirely to the nutritional transition, such as heart disease, what are the roles of sleep, stress, social structure, infection and other variables? How do all these factors interact with features unique to our own society? Do our modern lives place special demands on us?
We can broaden, deepen, and strengthen our understanding of Price’s work with experimental science, through which we can begin to provide answers to some of these questions. Valuable experimental evidence ranges from experimental animal and cell models that deepen our understanding of physiology to randomized, controlled, clinical trials in humans that provide clear evidence for effects on human health.
Personal Experience and Self-Experimentation
Each individual is unique and dynamic. As a result, one person’s nutritional needs may differ from another’s, and her needs at one time in her life may differ from her needs at another time in her life. Even after all the foregoing evidence is taken into account, then, a person must take into account her own experience.
Individual-level evidence can be broken down into two types: anecdotal and experimental. This division is similar to the division between evidence for consistency with good health and causation we saw between the first two levels.
If my body appears to respond well to a particular way of eating, for example, this doesn’t prove that this way of eating caused the positive response, but it shows that this way of eating is consistent with the positive response.
Alternatively, one can perform a randomized “n=1” experiment on oneself, which I’ve provided instructions for here. Such a randomized experiment provides clear evidence of a cause-and-effect relationship for the individual performing it. This approach, in its medically supervised manifestation, has its own body of scientific literature and is recognized by prestigious statisticians including those at the Centre for Evidence-Based Medicine at Oxford (see here).
Performing randomized self-experiments, of course, is resource-intensive, and whether it is a wise approach to pursue depends on how critical it is that someone find the most effective approach for himself.
Fitting It All Together
As an example of how all this might fit together, traditional diets of populations free of heart disease were rich in fat-soluble vitamins, while not necessarily high in fat, contained animal fats or tropical oils rather than vegetable oils.
As I’ve reviewed in Good Fats, Bad Fats, clinical trial evidence is inconclusive but more supportive of traditional oils than of modern vegetable oils.
Our knowledge of biochemistry and physiology, taken from many levels of experimental science, suggests that the micronutrient content of the oil and the overall diet is critical. As an example, vitamin K2 is found in animal fats and activates proteins that protect against soft tissue calcification. An individual might use this knowledge to verify that his diet is consistent with (or causing, if he chooses to randomize) freedom from coronary calcification, or, in due time, adequate activation of vitamin K-dependent proteins.
The work of Price and others following his approach thus lays our foundation of common sense, while experimental science broadens and deepens our understanding of how to achieve health, and our personal experience and self-experimentation fine-tunes our approach to an individual level best suited to each person. In this way, we seek knowledge not to replace the wisdom accumulated by our ancestors, but to build upon, expand, refine, and enrich this pool of accumulated wisdom.
Read more about the author, Chris Masterjohn, PhD, here.