I spend a lot of time thinking about food and health and have a suspicion that we’ve missed a crucial over-arching principle: “food should be alive” – or at least recently so. During our evolution ‘food’ meant anything with nutritional value that we could get our paws on and that tasted okay without acutely poisoning us. Something that’s often overlooked as people argue over optimal foods for health, is that living hunter-gatherers and similar populations eat widely varying proportions of fat, protein, and carbohydrate1, but all show a near-absence of non-communicable diseases (NCDs), even with excess food availability2.
One thing that ‘ancestral’ diets did have in common was that they contained almost no milled grains (flours) or refined sugars. These foods are universally eaten now, so nutritional studies rarely test their presence vs. absence. However, the clues are there; low carbohydrate diets help with obesity and type-two diabetes3, but similar benefits against overweight and diabetes have been reported for higher carbohydrate diets but without flour and sugar4,5. The degree of processing appears to be what matters.
The question is, if flour and sugar are important agents of chronic disease, how can they do this if carbohydrate from root vegetables and fruit do not? After all, if you eat 70% of your calories as unprocessed carbohydrate, like a Kitavan2, this is surely going to produce considerable blood glucose and insulin responses. Perhaps the only place flour/sugar vs starchy vegetables are properly different is during digestion, when still inside the tube of the gut…
At this point, we should touch on some mechanics of obesity gleaned from animal models. Almost all mouse obesity models need mice to have gut bacteria, the mice won’t overeat with a sterile gut. When overeating begins, inflammatory markers are seen in the small bowel (not the colon – despite it having manifold more bacteria)6. This inflammation interferes with fullness-sensing nerves7, then similar inflammatory changes occur in the energy-regulatory areas of the brain, causing the mice to overeat.
If bacterial-driven inflammation in the small bowel is indeed a crucial step in altering the brain’s regulation of body weight, then the role of flour/sugar in overweight starts to look very interesting indeed8. Plant cells store carbohydrates at no more than 20-25% by weight (remember, life is ~80% water). Flours (milled grass seeds) and sugar are far more dense, a potentially more nutritious growth medium for microbes. Plant cells differ from flour/sugar in other ways too – they’re not keen on being dinner. They’ve survived hundreds of millions of years of evolutionary conflict with bacteria trying to get at their carbohydrate stores, and likely come armed for a molecular fight. The microbial ecosystem of a healthy small bowel presumably has niches occupied by interdependent species carrying out different tasks upon periodically-arriving food’s semi-digested cells. Getting the nutrients before host absorption likely involves much sequential cooperation between species, creating an ecosystem with a complexity that may rival that of a healthy river.
In contrast, a small bowel ecosystem regularly fed a Western diet of flour/sugar could be expected to be very different. Using the river analogy, easy excess nutrients favor species best able to capitalize, reducing ecosystem diversity like an algal bloom with fertilizer run-off. Pathogens may prosper, and work to breach host defences9. This is all happening right next to lymphatic tissue where the bulk of the body’s immune cells are to be found. Changes here might explain the pro-inflammatory nature of western diets, and the improvements in autoimmune conditions many report after eliminating flour and sugar. It should be emphasized that currently there has been relatively little study of small bowel microbes. The above reasoning is why one might expect study here to be highly informative.
We’ve long suspected that natural foods are better for health, but there are now clues that living foods might play a crucial part in a delicately evolved dance between host, microbe, and food that has played out for millions of years. This dance needs all three dancers to be up to speed on the steps. The sudden replacement of one element with a slurry of flour might trigger a cascade of microbial changes that lead to overweight or disease in the susceptible. The theoretical approaches we should adopt to correct this mismatch are already well known to be effective, and in some countries are already the basis of public health advice: “Unprocessed foods are better for health”. Usefully, a diet of only unprocessed foods may even produce remission of some chronic non-communicable diseases.
Read the full Evolutionary Mismatch series:
- Introduction: Evolutionary Mismatch and What To Do About It by David Sloan Wilson
- Functional Frivolity: The Evolution and Development of the Human Brain Through Play by Aaron Blaisdell
- A Mother’s Mismatch: Why Cancer Has Deep Evolutionary Roots by Amy M. Boddy
- It’s Time To See the Light (Another Example of Evolutionary Mismatch) by Dan Pardi
- Generating Testable Hypotheses of Evolutionary Mismatch by Sudhindra Rao
- (Mis-) Communication in Medicine: A Preventive Way for Doctors to Preserve Effective Communication in Technologically-Evolved Healthcare Environments by Brent C. Pottenger
- The Darwinian Causes of Mental Illness by Eirik Garnas
- Is Cancer a Disease of Civilization? by Athena Aktipis
- The Potential Evolutionary Mismatches of Germicidal Ambient Lighting by Marcel Harmon
- Do We Sleep Better Than Our Ancestors? How Natural Selection and Modern Life Have Shaped Human Sleep by Charles Nunn and David Samson
- The Future of the Ancestral Health Movement by Hamilton M. Stapell
- Humans: Smart Enough to Create Processed Foods, Daft Enough to Eat Them by Ian Spreadbury
- Strohle A, Hahn A, Sebastian A. Latitude, local ecology, and hunter gatherer dietary acid load: implications from evolutionary ecology. Am J Clin Nutr. 2010;92(4):940–945.
- Lindeberg S. Food and Western Disease: Health and Nutrition from an Evolutionary Perspective. Oxford: Wiley-Blackwell; 2010.
- Feinman R, R Sundberg et al. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition. Jan 2015. 31 (1), 1-13.
- Lindeberg S, Jonsson T, Granfeldt Y, et al. A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia. 2007;50(9):1795–1807.
- Gardner CD, Trepanowski JF, Del Gobbo LC, Hauser ME, Rigdon J, Ioannidis JPA, Desai M, King AC. Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin SecretionThe DIETFITS Randomized Clinical Trial. JAMA. 2018;319(7):667–679.
- Ding S, Chi MM, Scull BP, et al. High-fat diet: bacteria interactions promote intestinal inflammation which precedes and correlates with obesity and insulin resistance in mouse. PLoS One. 2010;5(8): e12191.
- de Lartigue, Barbier de la SC, Espero E, Lee J, Raybould HE. Diet-induced obesity leads to the development of leptin resistance in vagal afferent neurons. Am J Physiol Endocrinol Metab. 2011; 301(1):E187–E195.
- Spreadbury I. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012;5:175-89.
- S. Manfredo Vieira, M. Hiltensperger, V. Kumar, D. Zegarra-Ruiz, C. Dehner, N. Khan, F. R. C. Costa, E. Tiniakou, T. Greiling, W. Ruff, A. Barbieri, C. Kriegel, S. S. Mehta, J. R. Knight, D. Jain, A. L. Goodman, M. A. Kriegel. Translocation of a gut pathobiont drives autoimmunity in mice and humans. Science 09 Mar 2018 : 1156-1161.