Update: November 22, 2017 — This has been an ongoing blog post draft that I’m moving to a page so I can continue to add to it and make updates. Enjoy!

My research around this diet choice has not ended, and what I’m realizing is the dietician I saw is basing her recommendations on “accepted” science that is 50 years old. I briefly mentioned the notion of fats & cholesterol being bad for you in a previous post, and how it’s not accurate.

Currently, the overarching dietary recommendations being made are meant for an entire population and do not take into account the individuality that exists between humans. Conventional health care is almost entirely focused on suppressing symptoms, versus identifying the underlying cause of a problem. Additionally, making sweeping changes in our health care system when new evidence appears takes time — sometimes DECADES. Being an informed consumer and your own health advocate is the sad reality of our system. (Primary care doctors spend — on average — 8 minutes in an appointment with their patient. Hardly enough time to do … well… anything.)

Here’s the information I’ve been collecting:

Easier to understand items:

Straight Science

  • Cholesterol (is not bad for you)
    • Djoussé, L , ‘Dietary cholesterol and coronary artery disease: a systematic review.’ , 11 ( 6 ): Curr Atheroscler Rep2009 ; 418 – 22
      Abstract: Coronary heart disease (CHD) remains one of the leading causes of death in the United States and other industrialized nations. A better understanding of modifiable risk factors for CHD is critical in order to effectively prevent this disease. Dietary factors known to influence the risk of CHD include saturated fats, trans-fats, and polyunsaturated fatty acids. Although higher plasma levels of low-density lipoprotein cholesterol are associated with an increased risk of coronary disease and lipid-lowering therapy has been shown to reduce the risk of cardiovascular disease, the relation between dietary cholesterol and the risk of CHD is not clearly understood. This article reviews the current evidence on the association between dietary cholesterol and the risk of CHD.
    • The Emerging Risk Factors Collaboration , ‘Lipid-Related Markers and Cardiovascular Disease Prediction’ , 307 ( 23 ): JAMA2012 ; 2499 – 2506
      Context: The value of assessing various emerging lipid-related markers for prediction of first cardiovascular events is debated.
    • Sniderman, A , Lawler, P , ‘The causal exposure model of vascular disease’ , 122: Clinical Science2012 ; 396 – 373
      Abstract: Primary prevention of cardiovascular disease is governed at present by the risk factor model for cardiovascular events, a model which is widely accepted by physicians and professional associations, but which has important limitations: most critically, that effective treatment to reduce arterial damage is often delayed until the age at which cardiovascular events become common. This delay means that many of the early victims of vascular disease will not be identified in time. This delay also allows atherosclerosis to develop and progress unchecked within the arterial tree with the result that the absolute effectiveness of preventive therapy is limited by the time it is eventually initiated. The causal exposure model of vascular disease is an alternative to the risk factor model for cardiovascular events. Whereas the risk factor model aims to identify and treat those at markedly increased risk of vascular events within the next decade, the causal exposure model of vascular disease aims to prevent events by treating the causes of the disease when they are identified. In the risk factor model, age is an independent non-modifiable risk  factor and the predictive power of age far outweighs that of the other risk factors. In the causal exposure model, age is the duration of time the arterial wall is  exposed to the causes of atherosclerosis: apoB (apolipoprotein B) lipoproteins, hypertension, diabetes and smoking. Preventing the development of advanced atherosclerotic lesions by treating the causes of vascular disease is the simplest, surest and most effective way to prevent clinical events.
    • Zeisel, S , ‘Choline: an essential nutrient for public health.’ , 67 ( 11 ): Nutrition Reviews2009 ; 615 – 623
      Abstract: Choline was officially recognized as an essential nutrient by the Institute of Medicine (IOM) in 1998. There is significant variation in the dietary requirement for choline that can be explained by common genetic polymorphisms. Because of its wide-ranging roles in human metabolism, from cell structure to neurotransmitter synthesis, choline-deficiency is now thought to have an impact on diseases such as liver disease, atherosclerosis, and, possibly, neurological disorders. Choline is found in a wide variety of foods. Eggs and meats are rich sources of choline in the North American diet, providing up to 430 milligrams per 100 grams. Mean choline intakes for older children, men, women, and pregnant women are far below the adequate intake level established by the IOM. Given the importance of choline in a wide range of critical functions in the human body, coupled with less-than-optimal intakes among the population, dietary guidance should be developed to encourage the intake of choline-rich foods.
  • Sugar (is the devil)
  • Ketogenic-Specific Information
    • Allen, Bryan G.; Bhatia, Sundershan K., ‘Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism’ , ( 2 ):Redox Biology2014 ; 963 – 970
      Abstract: Cancer cells, relative to normal cells, demonstrate significant alterations in metabolism that are proposed to result in increased steady-state levels of mitochondrial-derived reactive oxygen species (ROS) such as O2 and H2O2. It has also been proposed that cancer cells increase glucose and hydroperoxide metabolism to compensate for increased levels of ROS. Given this theoretical construct, it is reasonable to propose that forcing cancer cells to use mitochondrial oxidative metabolism by feeding ketogenic diets that are high in fats and low in glucose and other carbohydrates, would selectively cause metabolic oxidative stress in cancer versus normal cells. Increased metabolic oxidative stress in cancer cells would in turn be predicted to selectively sensitize cancer cells to conventional radiation and chemotherapies. This review summarizes the evidence supporting the hypothesis that ketogenic diets may be safely used as an adjuvant therapy to conventional radiation and chemotherapies and discusses the proposed mechanisms by which ketogenic diets may enhance cancer cell therapeutic responses.
    • Meidenbauer, J; Mukherjee, P; Seyfried, T , ‘The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer’ , 12 ( 12 ): Nutrition & Metabolism2015
      Background: Metabolic therapy using ketogenic diets (KD) is emerging as an alternative or complementary approach to the current standard of care for brain cancer management. This therapeutic strategy targets the aerobic fermentation of glucose (Warburg effect), which is the common metabolic malady of most cancers including brain tumors. The KD targets tumor energy metabolism by lowering blood glucose and elevating blood ketones (β-hydroxybutyrate). Brain tumor cells, unlike normal brain cells, cannot use ketone bodies effectively for energy when glucose becomes limiting. Although plasma levels of glucose and ketone bodies have been used separately to predict the therapeutic success of metabolic therapy, daily glucose levels can fluctuate widely in brain cancer patients. This can create difficulty in linking changes in blood glucose and ketones to efficacy of metabolic therapy.
      Results: The GKIC was used to compute the GKI for data published on blood glucose and ketone levels in humans and mice with brain tumors. The results showed a clear relationship between the GKI and therapeutic efficacy using ketogenic diets and calorie restriction.

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