Bruce Ames’ Triage Theory of nutrient deficiency, selenium, vitamin k, chromium, neurogenesis, breastfeeding, insulin resistance as short-term stress adaptation, pediatric nonalcoholic fatty liver disease

• Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage (2006)
  • “Inadequate dietary intakes of vitamins and minerals are widespread, most likely due to excessive consumption of energy-rich, micronutrient-poor, refined food… Deficiencies in many micronutrients cause DNA damage… Some of these deficiencies also cause mitochondrial decay.. and are associated with late onset diseases such as cancer. I propose DNA damage and late onset disease are consequences of a triage allocation response to micronutrient scarcity… Natural selection favors short-term survival at the expense of long-term health. I hypothesize that short-term survival was achieved by allocating scarce micronutrients by triage, in part through an adjustment of the binding affinity of proteins for required micronutrients. If this hypothesis is correct, micronutrient deficiencies that trigger the triage response would accelerate cancer, aging, and neural decay but would leave critical metabolic functions, such as ATP production, intact.”
• Vitamin K, an example of triage theory: is micronutrient inadequacy linked to diseases of aging? (2009)
  • “For 16 known vitamin K–dependent (VKD) proteins, we evaluated the relative lethality of 11 known mouse knockout mutants to categorize essentiality. Results indicate that 5 VKD proteins that are required for coagulation had critical functions… Genetic loss of less critical VKD proteins, dietary vitamin K inadequacy, human polymorphisms or mutations, and vitamin K deficiency induced by chronic anticoagulant (warfarin/coumadin) therapy are all linked to age-associated conditions… There is increased spontaneous cancer in Tgfbi mouse knockouts, and knockdown of Tgfbi causes mitotic spindle abnormalities. A triage perspective reinforces recommendations of some experts that much of the population and warfarin/coumadin patients may not receive sufficient vitamin K for optimal function of VKD proteins that are important to maintain long-term health.”
• Adaptive dysfunction of selenoproteins from the perspective of the triage theory: why modest selenium deficiency may increase risk of diseases of aging (2011)
  • “Here, we review about half of the 25 known mammalian selenoproteins; all of those with mouse knockout or human mutant phenotypes that could be used as criteria for a classification of essential or nonessential… On modest selenium (Se) deficiency, nonessential selenoprotein activities and concentrations are preferentially lost… The same set of age-related diseases and conditions, including cancer, heart disease, and immune dysfunction, are prospectively associated with modest Se deficiency and also with genetic dysfunction of nonessential selenoproteins, suggesting that Se deficiency could be a causal factor, a possibility strengthened by mechanistic evidence. Modest Se deficiency is common in many parts of the world; optimal intake could prevent future disease.”
• Effects of diets high in simple sugars on urinary chromium losses. (1986)
  • “ Compared to the reference diets, consumption of the high sugar diets increased urinary Cr losses from 10% to 300% for 27 of 37 subjects. Urinary Cr excretion of males and females was similar, and there was no significant difference in Cr absorption… between sexes when adjusted for the increased caloric intake of males. These data demonstrate that consumption of diets high in simple sugars stimulates Cr losses; this coupled with marginal intake of dietary Cr may lead to marginal Cr deficiency, which is associated with impaired glucose and lipid metabolism.”
• Neurogenesis in the Striatum of the Adult Human Brain (2014)
  • “In most mammals, neurons are added throughout life in the hippocampus and olfactory bulb. One area where neuroblasts that give rise to adult-born neurons are generated is the lateral ventricle wall of the brain. We show, using histological and carbon-14 dating approaches, that in adult humans new neurons integrate in the striatum, which is adjacent to this neurogenic niche. The neuronal turnover in the striatum appears restricted to interneurons, and postnatally generated striatal neurons are preferentially depleted in patients with Huntington’s disease. Our findings demonstrate a unique pattern of neurogenesis in the adult human brain.”
• Effect of breastfeeding compared with formula feeding on infant body composition: a systematic review and meta-analysis (2012)
  • “Compared with breastfeeding, formula feeding is associated with altered body composition in infancy.”
• Link between insulin resistance and hypertension: What is the evidence from evolutionary biology? (2014)
  • “The coexistence of insulin resistance and hypertension results in a substantial increase in the risk of developing cardiovascular disease and type II diabetes. Underlying the mechanisms is complex and may involve a low grade chronic inflammation and oxidative stress. As humans evolve, the thrifty genotype for high cytokine responder (eradication of injury), mild insulin resistance (protection against starvation), or sodium preservation (maintenance of body fluid),which favored our ancestors, aiding them in the survival of critical conditions such as famine, infection, trauma and physical stressors, may be positively selected, which may be maladaptive to our current, modern lifestyle, resulting in insulin resistance, hypertension, type II diabetes and cardiovascular diseases.”
• The Western dietary pattern is prospectively associated with nonalcoholic fatty liver disease in adolescence (2013)
  • “A Western dietary pattern at 14 years in a general population sample was associated with an increased risk of NAFLD at 17 years, particularly in obese adolescents. In centrally obese adolescents with NAFLD, a healthy dietary pattern may be protective, whereas a Western dietary pattern may increase the risk.”
• Pediatric nonalcoholic fatty liver disease (2013)
  • “Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the pediatric population… Like adults, most children with NAFLD are obese, and comorbidities include insulin resistance, hypertension, and dyslipidemia… insulin resistance and increased oxidative stress may lead to progressive disease… Lifestyle modification, including slow and steady weight loss, improved dietary habits, and increased daily, aerobic physical activity, remains the first-line approach in treating pediatric fatty liver disease. Antioxidant pharmacologic therapy such as use of vitamin E has shown some benefit in patients with biopsy-proven steatohepatitis. Nutrition plays an essential role not only in the development of fatty liver disease but also potentially in the treatment and prevention of progression to more severe disease.”