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The CrossFit stimulus—constantly varied high-intensity functional movement coupled with meat and vegetables, nuts and seeds, some fruit, little starch, and no sugar—prepares you for the demands of a healthy, functional, independent life and provides a hedge against chronic disease and incapacity. This stimulus is elegant in the mathematical sense of being marked by simplicity and efficacy. The proven elements of this broad, general, and inclusive fitness, in terms of both movement and nutrition, are what we term our CrossFit Essentials.

Dr. Malcolm Kendrick concludes his series on the response to injury hypothesis for cardiovascular disease (CVD) by observing that reducing risk relies on doing at least one of three things, and ideally all three: protecting the endothelium from damage, reducing blood coagulability, and improving the body’s healing processes. Kendrick highlights several specific ways to protect the endothelium, from quitting smoking to getting more sun to increasing potassium intake.

Read MoreWhat Causes Cardiovascular Disease? The Response to Injury Hypothesis, Part 4

“Blood-vessel disease was common (among the ancient Egyptians), contrary to assumptions that it arises from urban stress and a modern high-fat diet,” Dr. Michael Eades, MD, reads aloud to the audience at the CrossFit Health Conference on Aug. 1, 2018. After reading this quote in a book, Eades began to research the dietary factors that may have contributed to the high incidence of heart disease among the ancient Egyptians. In this presentation, Eades shares some of the outcomes of that research, taking his audience “on a journey through the anthropological literature and what that means in terms of ‘off the carbs.’”

Read MorePaleopathology and the Origins of the Paleo Diet

This 2017 review summarizes the potential of a ketogenic diet to enhance the effects of radiotherapy. Radiotherapy is constrained by the damage it causes to healthy cells. As a result, any simultaneous treatment that can either increase the damage radiotherapy does to cancer cells or protect healthy cells from damage may increase its effectiveness. Potential benefits of a ketogenic diet alongside radiotherapy include the reduction of cancer cells’ ability to repair DNA, the slowing of tumor growth and repopulation, and the protection of healthy cells against the harms of radiotherapy by shifting them from an anabolic/growth-centric state to a non-dividing state.

Read MoreFasting, fats, and physics: Combining ketogenic and radiation therapy against cancer

Dr. Malcolm Kendrick analyzes the hypothesis that atherosclerotic plaque develops when the rate of damage to the endothelium exceeds the body’s rate of healing. This means factors that can cause plaques to develop and grow accelerate endothelial damage, create larger and more difficult-to-clear thrombi, and/or impair healing. Kendrick provides examples of these factors — examples as diverse as sickle cell disease, taking immunosuppressants, and smoking — and claims this hypothesis for the cause of cardiovascular disease links risk factors that may not seem to have anything in common.

Read MoreWhat causes cardiovascular disease? The response to injury hypothesis, Part 3

This 2018 review summarizes links between metabolic syndrome, insulin resistance, and Alzheimer’s disease. Observational evidence increasingly shows diabetes, obesity, and other forms of metabolic disease are linked to increased risk of Alzheimer’s disease, and that patients with Alzheimer’s disease are more likely to be insulin-resistant than peers who do not have the disease. The reviewers find insufficient evidence to support a direct cause-and-effect relationship between metabolic disease and Alzheimer’s disease, but available evidence strongly suggests the former increases risk of the latter.

Read MoreInsulin Resistance in Alzheimer's Disease

Dr. Malcolm Kendrick revisits the response to injury hypothesis as an alternative to the cholesterol hypothesis for explaining the etiology of atherosclerosis. He evaluates three “facts” used to support the cholesterol hypothesis — 1. fatty streaks are early-stage plaques, 2. there is a high concentration of cholesterol in plaques, which must have been derived from LDL, and 3. the lipoprotein found in plaques is LDL — and finds they are all overly simplified or false.

Read MoreWhat causes cardiovascular disease? The response to injury hypothesis, Part 2

This 2015 review hypothesizes how insulin resistance develops in the brain and cerebral insulin resistance contributes to neurological and metabolic disease. The authors argue brain insulin resistance is both a consequence and cause of metabolic distress, and impaired brain insulin signaling can account for both the difficulty of reversing obesity and some of its neurological and metabolic comorbidities.

Read MoreImpaired insulin action in the human brain: causes and metabolic consequences

“What scientists do and what journalists do are similar in that we’re both supposed to be establishing reliable knowledge about the universe,” Gary Taubes told the audience at the annual CrossFit Health Conference on July 31, 2019. Taubes, an award-winning investigative journalist, has spent the last several decades turning a critical eye toward places where received wisdom in the fields of science and medicine has diverged from reliable knowledge. In this presentation, he evaluates what the experts say about why we get fat and explains why has become a critic of the consensus.

Watch The Quality of Calories: Competing Paradigms of Obesity Pathogenesis, a Historical Perspective

Prof. Timothy Noakes explicates the most persuasive critiques of Ancel Keys’ claim that dietary fat causes coronary heart disease. First among these is one by two of Keys’ contemporaries, Jacob Yerushalmy and Herman Hilleboe, who warned, "No matter how plausible such an association may appear, it is not in itself proof of a cause-effect relationship. ... But quotation and repetition of the suggestive association soon creates the impression that the relationship is truly valid, and ultimately it acquires status as a supporting link in a chain of presumed proof." Noakes claims quotation and repetition became the hallmark of the method by which Keys convinced the world his hypothesis was the singular truth, thereby altering the trajectory of 70 years of medical practice and dietary guidelines and contributing to the global obesity epidemic.

Read MoreIt's the Insulin Resistance, Stupid: Part 7

Over the past 40 years, sugar intake (and thus fructose intake) has increased dramatically in Western diets, rising to 15-17% of total daily caloric consumption. This rise comes alongside increasing evidence linking fructose to diabetes, fatty liver disease, and cardiometabolic risk factors. This brief 2019 review summarizes the mechanisms by which fructose drives these metabolic diseases.

Read MoreDietary Fructose and the metabolic Syndrome

Type 2 diabetes is generally thought to be chronic and progressive, marked by an inevitable decline in beta cell function and increase in plasma glucose levels. Current pharmaceutical treatments are fundamentally unable to alter the course of the disease. Bariatric surgery has been shown to rapidly normalize glucose levels, even prior to weight loss. This study tested whether severe caloric restriction — similar to that seen alongside bariatric surgery — could lead to similar glycemic benefits. The study found that a very low-calorie diet rapidly improves liver insulin sensitivity and gradually improves pancreatic function in the process reversing Type 2 diabetes.

Read MoreReversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol

For the past 170 years, there have been two main competing ideas about what causes cardiovascular disease. One of them, the cholesterol or lipid hypothesis, has come to dominate. The alternative hypothesis has had different names over the years — e.g., the encrustation hypothesis, thrombogenic hypothesis, and response to injury hypothesis. In the first article in this four-part series, Dr. Malcolm Kendrick explains this alternative hypothesis, outlines its brief history, and proposes why it may have fallen out of favor.

Read MoreWhat causes cardiovascular disease? The response to injury hypothesis, Part 1

In the 1950s, Ancel Keys worked to make the diet-heart and lipid hypotheses famous, leading to the decades-long demonization of saturated fat and cholesterol that has continued to shape the Western diet ever since. Here, Prof. Tim Noakes levels several critiques at Keys’ influential research. Noakes compares Keys’ claims to the data and sources upon which they are based and determines Keys’ evidence is weak, associational, and epidemiological at best, and wilfully deceptive at worst. While the inadequacy of Keys’ evidence has been discussed before, Noakes adds to the conversation by arguing Keys’ major findings are derivative of earlier research by Drs. Haqvin Malmros and John Gofman — research Keys strategically sought to discredit, according to Noakes. Noakes also discusses the historical context in which Keys developed his theories in order to shed light on some possible motivations for Keys’ subterfuge.

Read MoreIt’s the insulin resistance, stupid: Part 6

This trial indicates metformin suppresses gains in strength and muscle mass associated with resistance training in elderly patients. Its results support previous research suggesting the drug suppresses the benefits of resistance training in multiple populations. In patients who do not require immediate improvements in glycemic control, metformin’s suppression of exercise-induced muscle strength and size gains could increase risk of disability and mortality. These risks may provide an argument for not prescribing metformin to elderly patients. In diabetic and prediabetic patients, it is worth considering non-pharmaceutical treatments that lead to improved glycemic control without reducing the benefits of exercise.

Read the article Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults

Research published in the 1950s led to the incorrect assumption that glucose is dependent upon insulin to get into cells, and that exogenous insulin reduces hyperglycemia by driving glucose into cells, particularly muscle cells. These ideas were disproved in the 1970s but became dogma nonetheless. Dr. Michael Eades summarizes the salient points from an article by Drs. Paul and J. Sonksen that sets the record straight. “This classic paper serves as an excellent primer on all aspects of glucose action, ketosis, lipolysis, and the many ways diabetes can manifest,” Eades explains.

Read MoreInsulin is not required for glucose uptake into cells

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