Evaluation of biological and clinical potential of paleolithic diet
Authors: Kowalski LM, Bujko J.
Mounting evidence suggests that foods that were regularly consumed during the Paleolithic era (more than 10,000 years ago) may prevent some chronic Western diseases.
It has been postulated that recent changes in our diet have been too rapid for the human genome to have completely adjusted.
In contemporary Western populations roughly 70% of the food intake comes from foods that were rarely consumed by Paleolithic hunter-gatherers – grains, dairy products, refined sugars and fats.
Observational studies of hunter-gatherers and other non-western populations lend support to the notion that a Paleolithic type diet may reduce the risk of cardiovascular disease, metabolic syndrome, type 2 diabetes, cancer, acne vulgaris and myopia.
Moreover, preliminary intervention studies using a contemporary diet based on Paleolithic food groups (meat, fish, shellfish, fresh fruits and vegetables, roots, tubers, eggs, and nuts), revealed promising results including favourable changes in risk factors, such as weight, waist circumference, C-reactive protein, glycated haemoglobin (HbAlc), blood pressure, glucose tolerance, insulin secretion, insulin sensitivity and lipid profiles.
Low calcium intake, which is often considered as a potential disadvantage of the Paleolithic diet model, should be weighed against the low content of phytates and the low content of sodium chloride, as well as the high amount of net base yielding vegetables and fruits.
Increasing evidence supports the view that intake of high glycemic foods and insulinotropic dairy products is involved in the pathogenesis and progression of acne vulgaris in Western countries.
In this context, diets that mimic the nutritional characteristics of diets found in hunter-gatherers and other non-western populations may have therapeutic value in treating acne vulgaris.
Additionally, more studies are needed to determine the impact of gliadin, specific lectins and saponins on intestinal permeability and the pathogenesis of autoimmune diseases.
Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity
Gastrointestinal Diseases Research Unit, Queen’s University, Kingston, Ontario, Canada
Diabetes Metab Syndr Obes. 2012; 5: 175–189.
Published online Jul 6, 2012. doi: 10.2147/DMSO.S33473
A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of non-Westernized populations, and the apparent efficacy of the modern “Paleolithic” diet on satiety and metabolism.
A novel hypothesis of obesity is suggested by consideration of diet-related inflammation and evolutionary medicine.
The obese homeostatically guard their elevated weight. In rodent models of high-fat diet-induced obesity, leptin resistance is seen initially at vagal afferents, blunting the actions of satiety mediators, then centrally, with gastrointestinal bacterial-triggered SOCS3 signaling implicated.
In humans, dietary fat and fructose elevate systemic lipopolysaccharide, while dietary glucose also strongly activates SOCS3 signaling. Crucially however, in humans, low-carbohydrate diets spontaneously decrease weight in a way that low-fat diets do not.
Furthermore, nutrition transition patterns and the health of those still eating diverse ancestral diets with abundant food suggest that neither glycemic index, altered fat, nor carbohydrate intake can be intrinsic causes of obesity, and that human energy homeostasis functions well without Westernized foods containing flours, sugar, and refined fats.
Due to being made up of cells, virtually all “ancestral foods” have markedly lower carbohydrate densities than flour- and sugar-containing foods, a property quite independent of glycemic index. Thus the “forgotten organ” of the gastrointestinal microbiota is a prime candidate to be influenced by evolutionarily unprecedented postprandial luminal carbohydrate concentrations.
The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a “double hit” by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena.
A dietary pattern with carbohydrates exclusively from cellular low-density sources may remove the root cause of a range of our most prevalent diseases. The potential savings in health-care costs should be borne in mind, and the hypothesis tested.
The increased storage life and convenience of some of our oldest agricultural products may come with a hitherto unrecognized metabolic cost. The foods eaten by hunter-gatherers, non-cereal horticulturalists, and those following a modern Paleolithic or “primal” diet are sharply delineated from modern foods by their lower carbohydrate densities.
Consumption of exclusively low-density carbohydrates is suggested to produce a less inflammatory GI microbiota, and may explain the apparent absence of overweight and metabolic disease in two of these groups, and the promising early data from the third.
This hypothesis may also explain:
(1) Why obesity incidence scales with refined food intake, but has such confusing correlatory patterns with macronutrients.
(2) Why calorie-controlled diets of Westernized foods require a perpetual fight with homeostatic correction mechanisms.
(3) The link between periodontal disease and systemic atherosclerotic disease and obesity.
(4) Why the benefits of a diet of fruit and vegetables have not been replicated by supplements of the constituent antioxidants, vitamins, minerals, and fiber alongside a Western diet.
(5) Why low-carbohydrate diets produce ad libitum weight loss, but low-fat diets do not.
(6) The relative resistance of European people to obesity and diabetes from Westernized diets.
We should not settle for the meager improvements attainable from the consensus dietary advice when it is already clear that so much more might be achieved. Our sights should be set high, to see how close we can move levels of industrialized metabolic health toward those enjoyed by non-Westernized populations. While many will resist making dietary changes of such magnitude, official advice must nonetheless point in the correct direction, allowing individuals to make informed decisions.
The social and financial burden of the epidemic of obesity and metabolic syndrome threatens the long-term viability of our health-care systems and perniciously undermines the other benefits of modern civilization, including redirection of scarce financial resources. If this dietary pattern is confirmed to work, practical policy solutions must be sought. Some grain cultivars may be found to produce less inflammation, sprouting techniques may be found to be of benefit, or grain production may be replaced with root-vegetable cultivation where practical.
Over time, the interplay between market forces, attainable agricultural yields, and the practicalities of food-distribution networks may allow shifting demand from a newly informed populace to reshape global agribusiness.A dietary pattern with carbohydrates exclusively from cellular low-density sources may remove the root cause of a range of our most prevalent diseases. The potential savings in health-care costs should be borne in mind, and the hypothesis tested.
Agrarian diet and diseases of affluence – do evolutionary novel dietary lectins cause leptin resistance?
Jönsson T1, Olsson S, Ahrén B, Bøg-Hansen TC, Dole A, Lindeberg S.
Department of Clinical Sciences, Lund University, Lund, Sweden
The global pattern of varying prevalence of diseases of affluence, such as obesity, cardiovascular disease and diabetes, suggests that some environmental factor specific to agrarian societies could initiate these diseases.
PRESENTATION OF THE HYPOTHESIS:
We propose that a cereal-based diet could be such an environmental factor. Through previous studies in archaeology and molecular evolution we conclude that humans and the human leptin system are not specifically adapted to a cereal-based diet, and that leptin resistance associated with diseases of affluence could be a sign of insufficient adaptation to such a diet.
We further propose lectins as a cereal constituent with sufficient properties to cause leptin resistance, either through effects on metabolism central to the proper functions of the leptin system, and/or directly through binding to human leptin or human leptin receptor, thereby affecting the function.
TESTING THE HYPOTHESIS:
Dietary interventions should compare effects of agrarian and non-agrarian diets on incidence of diseases of affluence, related risk factors and leptin resistance. A non-significant (p = 0.10) increase of cardiovascular mortality was noted in patients advised to eat more whole-grain cereals.
Our lab conducted a study on 24 domestic pigs in which a cereal-free hunter-gatherer diet promoted significantly higher insulin sensitivity, lower diastolic blood pressure and lower C-reactive protein as compared to a cereal-based swine feed.
Testing should also evaluate the effects of grass lectins on the leptin system in vivo by diet interventions, and in vitro in various leptin and leptin receptor models.
Our group currently conducts such studies.
IMPLICATIONS OF THE HYPOTHESIS:
If an agrarian diet initiates diseases of affluence it should be possible to identify the responsible constituents and modify or remove them so as to make an agrarian diet healthier.
Origins and evolution of the Western diet: health implications for the 21st century
Loren Cordain, S Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, Bruce A Watkins, James H O’Keefe, and Janette Brand-Miller
The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition?
Department of Anthropology and Radiology, Emory University, Atlanta.
Awareness of the ancestral human diet might advance traditional nutrition science. The human genome has hardly changed since the emergence of behaviourally-modern humans in East Africa 100-50 x 10(3) years ago; genetically, man remains adapted for the foods consumed then. The best available estimates suggest that those ancestors obtained about 35% of their dietary energy from fats, 35% from carbohydrates and 30% from protein. Saturated fats contributed approximately 7.5% total energy and harmful trans-fatty acids contributed negligible amounts. Polyunsaturated fat intake was high, with n-6:n-3 approaching 2:1 (v. 10:1 today). Cholesterol consumption was substantial, perhaps 480 mg/d. Carbohydrate came from uncultivated fruits and vegetables, approximately 50% energy intake as compared with the present level of 16% energy intake for Americans. High fruit and vegetable intake and minimal grain and dairy consumption made ancestral diets base-yielding, unlike today’s acid-producing pattern. Honey comprised 2-3% energy intake as compared with the 15% added sugars contribute currently. Fibre consumption was high, perhaps 100 g/d, but phytate content was minimal. Vitamin, mineral and (probably) phytochemical intake was typically 1.5 to eight times that of today except for that of Na, generally