AHS18

The aim of this talk is to give a high-level overview of heart disease and other chronic condition root causes. It will also zero in on who is really at the greatest risk, and needs to take the most decisive actions to avoid heart attack or an early death. How do we identify and save these people? Luckily there is a science-based strategy to do so - but how much of it is ancestral in nature?

There exists a large body of evidence that those who participate in higher levels of physical activity have a reduced likelihood of developing a variety of cancers compared to those who engage in lower levels of physical activity. It will be proposed that although most of us are aware that physical exercise is important, we are less familiar with the underlying biological mechanisms and how best to use exercise/physical activity as medicine.

Allopathic conventional ophthalmology currently espouses the belief that age-related macular degeneration (AMD) is a disease primarily caused by aging and genetics, with ‘environmental factors’ coming in a distant third.  The authors’ recently published research proffered the hypothesis that it is the ‘displacing foods of modern commerce’ that are the primary and proximate cause of AMD.  The evidence in support of this hypothesis correlates elevated consumption of processed, nutrient-deficient and potentially toxic foods, with rising prevalence of AMD in multiple nations; whereas evidence for consumption of native, traditional, nutrient-dense diets in multiple nations, is correlated with rarity of AMD.  U.S. CDC food consumption data, correlating processed food laden diets with multiple diseases of Western civilization, including heart disease deaths, type 2 diabetes, stroke, cancer, obesity, and severe vision loss secondary to AMD, will be reviewed, thus challenging the belief system that AMD is primarily a disease of aging and genetics. 

Learning Objectives: 

•  At the conclusion of this activity, participants will have a fundamental appreciation of age-related macular degeneration (AMD) as the leading cause of severe vision loss and blindness in people over the age of 65.
• Participants will be able to recite some evidence that AMD was a rare disorder in the 19th century, rising to epidemic proportions in developed nations by the late 20th century, in correlation to rising processed food consumption. 

Participants will be able to discuss U.S. CDC evidence for elevated processed food consumption and higher incidence and prevalence of heart disease deaths, hypertension, type 2 diabetes, stroke, cancer, obesity, and severe vision loss and blindness, the majority of the latter being secondary to AMD.

The leading cause of vision fluctuations for many of us today has nothing to do with our “prescriptions.” It is almost exclusively an issue of poor tear quality. Any light that enters our eyes interacts first with our tear film, not our cornea or any other fixed ocular structure. An irregular or insufficient tear layer results in blurred, inconsistent vision. Unfortunately, there are more people experiencing these symptoms than ever before. Modern indoor environments have caused our blink rates to decrease and the rate of tear evaporation to increase. Medications have reduced our tear production. A lack of Omega-3 fatty acids in our modern western diets has changed tear chemistry, making the tears less stable. Fortunately, there are dietary guidelines and lifestyle modifications dry eye sufferers can implement to improve comfort and consistency of vision and ultimately increase quality of life.

What explains the modern pandemics of obesity, diabetes, cardiovascular disease, autoimmunity, asthma and cancer—and also depression, anxiety and addiction? Is contemporary life too stressful? While chronic, excessive exposure to stressors such as anti-nutrients, toxins, UV, or psychological stress can cause illness, so can insufficient physical challenge. Hormesis -- beneficial stress -- activates endogenous defense, repair and adaptive mechanisms, thereby improving health, fitness and resilience. The hardier lives of our ancestors were indeed protective against illness. I will examine the biological mechanisms behind four main types of hormesis: (1) structural remodeling of tissues and organs, such as bone, muscle and the eye, in response to activity; (2) immunity and detoxification by exposures that train endogenous defenses; (3) metabolic adaptation in response to diet, exercise, cold exposure and hypoxia; and (4) psychological resilience against depression, anxiety and addiction, by challenges that re-sensitize receptors We are suffering from a deficiency of hormesis!

The athlete’s gut is a double-edged sword; while regular training appears to provide a number of potentially beneficial changes to the gut microbiota (and overall health), gastrointestinal (GI) distress and issues with fuelling (both during and around training) are also some of the commonest problems associated with athletic performance. Traditional recommendations for athletes include a diet enriched with refined carbohydrates and prolonged periods training at a high percentage of VO2Max. However, both of these can be associated with negative effects on both the gut and overall performance. Additionally, a number of different foods and macronutrient balances can cause GI distress in athletes both during and outside of training. The ancestral athlete wishing to perform in a modern sport also tends to under-eat due to reduced energy density in their food, with a number of downstream negative effects. The underlying physiology, and strategies to optimise health and performance, will be presented.

Inuit peoples are among the many cultures with a traditional diet of predominantly animal sourced foods and negligible carbohydrate. One might expect, then, that they would have been in ketosis most of the time. Some historical evidence suggests otherwise, leading to intense debate. Because the Inuit have been treated as an archetype and historical precedent for nutritional ketosis, stakes in this outcome appear high. If even the Inuit were not in ketosis, it seems that adopting a long-term, ketogenic lifestyle may be misguided, perhaps even dangerous. In this talk, I will present existing literature reporting ketosis measurements in Inuit populations, and explain why they are difficult to interpret. I will delve into research on the CPT1A Arctic variant, its effects on fat metabolism, and its potential selective advantages. Finally I will discuss the relevance of these observations in the broader context of ketosis and historical human diets.

What makes us think that ketogenic diets will pay off in treatment of prevention of cancer? Our evolutionary past was more variable and less regular than today and ketone bodies were surely a food of our ancestors. The Warburg effect, simply understood as reliance of cancers on glycolysis (non-aerobic) even in the presence of oxygen, may be more dynamic process for coping with changing environment and we want to know where ketone bodies fit in. In this, we want to understand how caloric restriction, the only firmly established treatment or prevention of cancer, bears on de facto or explicit inclusion of carbohydrate restriction. Perhaps most elusive, we want to understand the effect of reactive oxygen species.

Anthropologists have long reported that human craniofacial volumes have been diminishing since the advent of agriculture in the Middle East some 10-12,000 kya. Pre-industrial skeletal specimens reveal that H. sapiens had spent nearly their entire 250+ kya existence with wide palates, nasal cavities and faces. Soft tissues, such as brains and tongues, do not often get preserved within the fossil record, but anthropologists can nonetheless accurately infer brain and tongue volumes from the osseous structures that had been lifelong occupied by each of them. Given that functioning/resting tongues should help develop and occupy the palatal vault in a similar manner as do growing brains develop/occupy the cranial vault, it can also be accurately inferred that AMH’s had lived with well-postured and properly functioning tongues for the hundreds of thousands of years that had preceded the Industrial Revolution, which also implies optimal respiratory competence (i.e., habitual nose-breathing during wakefulness and sleep).

Red meat has been unfairly vilified as unhealthy, bad for the environment, and unethical to eat. We in the ancestral health community know that red meat is great nutritionally, but some still don't understand the incredible benefits well-managed cattle can have on the land. Diana will discuss recent research showing that cattle can help sequester carbon and will critique the moral defense of vegetarianism, proving that eliminating them from our food system could cause more harm than good. She will also show a clip from her upcoming film project, "Kale vs. Cow: The Case for Better Meat".

The quinolone drugs are touted as being the first synthetic or "man-made" antibiotics. This presentation demonstrates how our research indicates that the mechanism of action observed in quinolone drugs such as ciprofloxacin has been present and utilized by plants as an adaptation against infections. Furthermore, drugs and plants within the quinolone family should be used with discretion in order to avoid deleterious side effects and to prevent the spread of antibiotic resistant bacteria.

Julian Jaynes' "The Origin of Consciousness in the Breakdown of the Bicameral Mind" posits a provocative but well-supported thesis: inhabitants of early agricultural civilizations were not conscious as we are today. They literally heard the voices of their gods, who commanded them to sow and reap and build monuments in the most rigid, authoritarian, hierarchical societies ever to exist - “palace economies.” What if this were true? In this presentation, I unite several well-substantiated but orphaned theories and inconvenient facts from archaeology, botany, history, medicine, and psychology - including work by and about Julian Jaynes, Gobekli Tepe, Wadley and Martin, clinical schizophrenia, Richard Dawkins, and Jonathan Sauer - into a startling yet coherent narrative that explains how we literally lost our minds to wheat-based agriculture, and only regained consciousness after thousands of years.

Single-celled organisms are forced to multitask. With the evolution of multicellularity came many advantages, mostly the advantages of tissue specialization, but also, sex. There is a dark side to multicellularity, however: cancer. In fact, tumor formation is nearly universal in multicellular organisms.

Even so, the propensity to develop cancer varies widely among species: in rodents, cancer is nearly ubiquitous by the old age of two years. In contrast, elephants, over a life span of several decades, almost never develop cancer. (This is “Peto’s Paradox,” and the reason will be explained in this lecture.) Humans fall in between these extremes.

Why would cancer remain in the gene pool at all? There is evidence that the very traits that confer greater fertility to individual humans, and hence, reproductive success, also increase the risk of cancer.

On the level of the biosphere, cancer emerges along with reproductive advantages. Within the individual, cancer is an analogous evolutionary process. Cancer growth and spread takes place in an ecological system, the body, with its various metabolic niches that encourage variation in cancer cell phenotypes. (Recall from evolutionary biology that phenotype, not genotype, is the unit of natural selection.)

Cancer cells, as do any living entity, must deal with the realities of their immediate environment. The spatial arrangement of cancer cells, the “neighborhood,” and even the blocks within that neighborhood are not equal in terms of benefit to the cancer cell. Different neighborhoods give rise to different phenotypes: those cancer cells near a blood vessel enjoy greater access to oxygen, nutrients, and a pleasant, alkaline pH, whereas those farther away from the vascular supply are relatively deprived of these things. In fact, the position of a tumor cell on the pH, oxygen, and nutrient gradients within a single tumor mass determines its resistance to certain treatments, and also its propensity to metastasize, or spread.

With application of treatment, individual cancer cells susceptible to that treatment are destroyed. However, this leaves those cancer cells resistant to treatment to repopulate the tumor. With the the treatment-susceptible cells now gone, the treatment-resistant cells now have unencumbered access to all the supplies needed for unencumbered growth. They are enjoying the new lack of competition, called in evolutionary biology “competitive release.” They therefore grow quickly and repopulate the tumor.

The conventional treatment paradigm we oncologists work under advises using the “maximum tolerated dose,” MTD, applied at specific, non-varying frequencies. This is an attempt to kill as many tumor cells as possible while avoiding (sometimes just barely) killing the patient.

This model predictably engenders emergence of treatment-resistance in tumors, and such treatment has now been shown not to prolong survival, but to accelerate death in patients with “incurable” cancers. This is competitive release in action. In a bad way.

This lecture will explore recent research that has successfully challenged that approach, a new treatment paradigm called “adaptive therapy,” and based on the principles of evolution and ecology. Precedents include ecological theory that has devised successful approaches to pest management in agriculture, which mandates avoiding “competitive release” of resistant organisms. That is, total destruction of the pest is avoided in favor of “control,” a new equilibrium allowing lower—and tolerable—levels of the pest to survive.

In cancer treatment, the adaptive therapy approach uses small doses of several different drugs, applied singly or in combination, with long treatment breaks, and at intervals varying according to the patient’s response rather than calendar time. This is what differentiates adaptive therapy from “metronomic” chemotherapy.

The adaptive approach eschews “maximal tolerated dose” and maximum tumor cell kill in favor of reducing and maintaining some tumor burden indefinitely, but at a level where the patient is asymptomatic. In other words, instead of aiming for cure (not possible for the most common metastatic cancers of late adulthood), the goal is to keep the patient alive and feeling well. The population of treatment sensitive cells is put to work as competitive inhibitors of treatment-resistant cells.

Integrated into this approach are dietary maneuvers, such as carbohydrate restriction, exercise, hyperbaric oxygen therapy, etc. These may require specific timing in tumor evolution and treatment for optimal benefit.

The success of the “adaptive therapy” approach is predicted by mathematical models of cancer treatment employing “game theory.” The success of adaptive therapy over MTD has been corroborated in early clinical trials in patients with advanced metastatic prostate cancer and small cell lung cancer. However, the adaptive model is not for use in pediatric cancer, of which 85% are curable even in advanced stages, or in cancers of adulthood shown to be curable with conventional approaches.

Goals:
Participants will be able to:

• Discuss the evolutionary reasons behind Peto’s paradox: why some multicellular organisms rarely develop cancer, and why humans are prone to cancer.

• Discuss the limitations of the “maximum tolerated dose” paradigm when used in treatment of most advanced, incurable metastatic cancers of adults, and contrast it with the “adaptive therapy” model.

Why on earth do paleo and ketogenic diets consistently appear dead last on the annual U.S. News & World Report "top 100 list of best diets"? Why, after innumerable studies dispelling the myths of low-fat, grain-based diets and the farce of mainstream dietary guidelines has near-zero progress been made toward overhauling this antiquated system? Why are responsible physicians like Dr. Timothy Noakes, Dr. Gary Fetteke and others harassed, investigated and dragged through the mud over benign (and accurate) remarks? And what will it take for us to transcend the Matrix and achieve ancestral health in an increasingly health-hostile modern world? This talk boldly looks at real evidence of what lies behind all the confusion and how we can actually take charge of this dystopic reality. The solutions are there, but are you prepared to take the red pill or the blue pill?

Polycystic kidney disease (PKD) is a monogenic disease affecting nearly 1:400 individuals, characterized by the accumulation of large, fluid-filled cysts that slowly replace healthy tissue until organ failure. These cystic cells also exhibit altered cellular metabolism favoring primarily glucose. The slow-onset of PKD implies environmental factors as causative agents for cyst growth with diet appearing to strongly effect PKD outcome as PKD patients suffer more frequently from metabolic disease and nephrolithiasis. By using an evolutionary perspective, we identified potential dietary causes of cyst growth and interventions for the treatment of PKD. Previously our lab found that caloric restriction effectively reduced disease progression in a rodent model of PKD and recently, we found that both a ketogenic diet and time restricted feeding reduce disease severity. Additionally, we discovered an evolutionarily conserved mechanism for the normal clearance of kidney microcrystals which appears to be aberrantly activated in PKD leading to cyst growth.

Evolutionary mismatch occurs when the current environment contains features that are different from the statistically-recurrent features present throughout a species’ evolutionary history. When this happens, adaptations selected to operate well in the context of those ancestral features may fail in the novel environment. Mismatches are occurring in the wild (as well as in captive environments) often due to human-induced rapid environmental change—frequently causing organisms to be caught in what are called “evolutionary traps,” and researchers are starting to recognize and actually employ these traps to control certain species Ancestral health, as a field of Darwinian medicine, can benefit from adopting a species-spanning, abstract understanding of mismatch such that mismatch effects—which can be thought of as “environmental mutations”—can provide the conceptual breakthrough that is needed to make serious progress at combating chronic disease, similar to how understanding microbes provided the conceptual breakthrough that made the germ theory possible.

Past attempts to estimate the plant: animal ratio of the Paleolithic Diet (e.g., Eaton and Konner, 1985; Cordain et al., 2000; Marlowe, 2005; Kuipers et al., 2010) were based mainly on recent hunter-gatherers’ data. I show that the available ethnographic data is misleading in that it is historically inaccurate and even if it were, significant technological and ecological changes since the Paleolithic prevents the application of this data to the prediction of Paleolithic diets.Archaeology is also a poor source of quantitative prediction of the plant: animal ratio of the Paleolithic diet since plants residues are only rarely preserved.This state of affairs leaves the human physiological record, such as anatomy, metabolism, and genes, as the primary source where an evolutionary record of past plant: animal ratio in the diet is preserved. This record is reviewed, and a clear picture of the plant: animal ratio to which we evolved emerges.