Obesity has traditionally been thought of as a state of caloric imbalance, where the intake of calories exceeds the expenditure or ‘burning’ of calories. However, a more nuanced appreciation for the complex biochemistry and physiology of cellular energy generation suggests that obesity is a state of hormonal imbalance causing increased shunting of food energy into adipose tissue for storage, resulting in decreased satiety and ultimately leading to increased caloric intake. Adding to this hypothesis, we propose that obesity is also a state of nutrient and energy deficit, leading to decreased fatty acid mobilisation and oxidation, the result of which may be a natural disinclination towards physical activity. Added sugars (sucrose, a.k.a. table sugar and high-fructose corn syrup) may provide energy (4 kcal/g) but at current intakes they do not facilitate—and may even hinder—the production of energy. Not only do added sugars displace nutritionally superior foods in the diet, but they may also deplete nutrients from other foods that have been consumed, as well as from body stores, in order to enable their proper oxidation and liberate their calories as energy. Additionally, the consumption of added sugars damages the mitochondria and hence impairs energy generation. Moreover, overconsuming added sugars may result in a kind of ‘internal starvation’ (via leptin and insulin resistance) leading to further hunger signals in the body. Added sugars promote nutrient and energy deficit and through this novel pathway promote obesity.

Significant epidemiological and clinical evidence has emerged that suggests Alzheimer’s disease (AD) can be added to the list of chronic illnesses that are primarily caused by modern diets and lifestyles at odds with human physiology. High intakes of refined carbohydrates insufficient physical activity, suboptimal sleep quantity and quality, and other factors that may contribute to insulin resistance combine to create a perfect storm of glycation and oxidative stress in the brain. Specific neurons lose the ability to metabolise and harness energy from glucose, ultimately resulting in neuronal degeneration and death. Simultaneously, chronic peripheral hyperinsulinaemia prevents ketogenesis, thus depriving struggling neurons of a highly efficient alternative fuel substrate. The intimate association between type 2 diabetes and AD suggests that they have common underlying causes, namely insulin resistance and perturbed glucose metabolism. Preclinical evidence of AD is detectable decades before over symptoms appear, indicating that AD progresses over time, with observable signs manifesting only after the brain’s compensatory mechanisms have failed and widespread neuronal atrophy begins to interfere with cognition and performance of daily life tasks. That dietary and environmental triggers play pivotal roles in causing AD suggests that nutrition and lifestyle based interventions may hold the key to ameliorating or preventing this debilitating condition for which conventional pharmaceutical treatments are largely ineffective. Results from small scale clinical studies indicate that dietary and lifestyle strategies may be effective for reversing dementia and cognitive impairment. Increased research efforts should be dedicated towards this promising avenue in the future.

No abstract available.

Purpose of review This review provides a rationale for implementing carbohydrate restriction as a dietary therapy to improve biomarkers of cardiovascular health and suggests that this will require a paradigm shift away from what is currently promulgated as a ‘heart-healthy’ diet. Recent findings Type 2 diabetes mellitus (T2DM), metabolic syndrome, and related co-morbidities are major risk factors for cardiovascular disease (CVD). Ideally, then, a diet intended to support cardiovascular health should be one that improves or reverses these underlying risk factors. Carbohydrate restriction is effective for this purpose as well as for favorably impacting atherogenic dyslipidemia. Recent consensus reports from select national organizations have endorsed low-carbohydrate diets for improving glycemia and cardiovascular risk. Reluctance among public health organizations and some clinicians to more widely promote this therapeutic nutritional approach is driven primarily by the increase in serum low-density lipoprotein cholesterol (LDL-C) observed in a proportion of individuals who adopt a low-carbohydrate diet. Here we explore the rationale for using carbohydrate restriction to improve cardiovascular health by way of favorably impacting T2DM and insulin resistance, and why this salutary effect outweighs the potential adverse effects of an increase in serum LDL-C. Summary Carbohydrate restriction is a logical foundation for a dietary intervention intended to reduce CVD risk, particularly among individuals with T2DM or metabolic syndrome.