Fructose has recently been the focus of much interest as a possible contributor to the current epidemic of metabolic diseases. What is fructose, and why is it implicated in metabolic disease?

Fructose is a hexose with the same chemical formula, C₆H₁₂O₆, as glucose. These two sweet-tasting molecules differ structurally, however, as fructose has a keto-group on the second carbon while glucose presents an aldehyde group on the first carbon. Free fructose, together with free glucose, is present in small amounts in fruits and honey. The main part of today’s dietary fructose intake comes from sucrose, a disaccharide composed of one molecule of glucose linked to a molecule of fructose through an alpha 1-4 glycoside bond.

The link with metabolic disease is partly circumstantial. Fructose consumption has been low throughout most of human history, but started to increase after the crusades, when Europeans became acquainted with sucrose produced from sugar cane in Asia. It was at first a luxury product, but consumption rapidly increased in the 16th and 17th centuries when sugar became more widely available as a consequence of colonial trading. Its consumption was boosted, first by the introduction of new beverages – tea, coffee, and cocoa in the 17th to 18th centuries; and second with the production of chocolate bars, ice-creams, and sodas at the beginning of the 20th century. Total sugar consumption thus increased from less than 5 kg/person/year in the 1800s to about 40 kg at the turn of the 19th century, and about 70 kg/person/year in 2006. In short, a rapid and continuous increase in consumption has been observed from 1750 until the present day.

http://www.biomedcentral.com/1741-7007/10/42

Abstract

Objective: Most aggressive cancers demonstrate a positive positron emission tomographic (PET)

result using 18F-2-fluoro-2-deoxyglucose (FDG), reflecting a glycolytic phenotype. Inhibiting

insulin secretion provides a method, consistent with published mechanisms, for limiting cancer

growth.

Methods: Eligible patients with advanced incurable cancers had a positive PET result, an Eastern

Cooperative Oncology Group performance status of 0 to 2, normal organ function without diabetes

or recent weight loss, and a body mass index of at least 20 kg/m2

. Insulin inhibition, effected by

a supervised carbohydrate dietary restriction (5% of total kilocalories), was monitored for macronutrient intake, body weight, serum electrolytes, b-hydroxybutyrate, insulin, and insulin-like

growth factors-1 and -2. An FDG-PET scan was obtained at study entry and exit.

Results: Ten subjects completed 26 to 28 d of the study diet without associated unsafe adverse

effects. Mean caloric intake decreased 35  6% versus baseline, and weight decreased by

a median of 4% (range 0.0–6.1%). In nine patients with prior rapid disease progression, five

with stable disease or partial remission on PET scan after the diet exhibited a three-fold higher

dietary ketosis than those with continued progressive disease (n ¼ 4, P ¼ 0.018). Caloric intake

(P ¼ 0.65) and weight loss (P ¼ 0.45) did not differ in those with stable disease or partial

remission versus progressive disease. Ketosis was associated inversely with serum insulin

levels (P ¼ 0.03).

Conclusion: Preliminary data demonstrate that an insulin-inhibiting diet is safe and feasible in

selected patients with advanced cancer. The extent of ketosis, but not calorie deficit or weight loss,

correlated with stable disease or partial remission. Further study is needed to assess insulin

inhibition as complementary to standard cytotoxic and endocrine therapies.

Abstract

Accumulating evidences suggest that foods that were regularly consumed during the human primates and evolution, in particular during the Paleolithic era (2.6-0.01 x 10(6) years ago), may be optimal for the prevention and treatment of some chronic diseases. It has been postulated that fundamental changes in the diet and other lifestyle conditions that occurred after the Neolithic Revolution, and more recently with the beginning of the Industrial Revolution are too recent taking into account the evolutionary time scale for the human genome to have completely adjust. In contemporary Western populations at least 70% of daily energy intake is provided by foods that were rarely or never consumed by Paleolithic hunter-gatherers, including grains, dairy products as well as refined sugars and highly processed fats.

Accumulating evidences suggest that foods that were regularly consumed during the human primates and evolution, in particular during the Paleolithic era (2.6-0.01 x 10(6) years ago), may be optimal for the prevention and treatment of some chronic diseases. It has been postulated that fundamental changes in the diet and other lifestyle conditions that occurred after the Neolithic Revolution, and more recently with the beginning of the Industrial Revolution are too recent taking into account the evolutionary time scale for the human genome to have completely adjust. In contemporary Western populations at least 70% of daily energy intake is provided by foods that were rarely or never consumed by Paleolithic hunter-gatherers, including grains, dairy products as well as refined sugars and highly processed fats. Additionally, compared with Western diets, Paleolithic diets, based on recently published estimates of macronutrient and fatty acid intakes from an East African Paleolithic diet, contained more proteins and long-chain polyunsaturated fatty acids, and less linoleic acid. Observational studies of hunter-gatherers and other non-western populations lend support to the notion that aPaleolithic type diet may reduce the risk of cardiovascular disease, metabolic syndrome, type 2diabetes, cancer, acne vulgaris and myopia. Moreover, preliminary intervention studies using contemporary diet based on Paleolithic food groups (meat, fish, shellfish, fresh fruits and vegetables, roots, tubers, eggs, and nuts), revealed promising results including favorable changes in risk factors, such as weight, waist circumference, C-reactive protein, glycated haemoglobin (HbAlc), blood pressure, glucose tolerance, insulin secretion, insulin sensitivity and lipid profiles. Low calcium intake, which is often considered as a potential disadvantage of thePaleolithic diet model, should be weighed against the low content of phytates and the low content of sodium chloride, as well as the high amount of net base yielding vegetables and fruits. Increasing number of evidences supports the view that intake of high glycemic foods and insulinotropic dairy products is involved in the pathogenesis and progression of acne vulgaris in Western countries. In this context, diets that mimic the nutritional characteristics of diets found in hunter-gatherers and other non-western populations may have therapeutic value in treating acne vulgaris. Additionally, more studies is needed to determine the impact of gliadin, specific lectins and saponins on intestinal permeability and the pathogenesis of autoimmune diseases.

Abstract

The purpose of this paper is to highlight the endocrine signaling of Western diet, a fundamental environmental factor involved in the pathogenesis of epidemic acne. Western nutrition is characterized by high calorie uptake, high glycemic load, high fat and meat intake, as well as increased consumption of insulin- and IGF-1-level elevating dairy proteins. Metabolic signals of Western diet are sensed by the nutrient-sensitive kinase, mammalian target of rapamycin complex 1 (mTORC1), which integrates signals of cellular energy, growth factors (insulin, IGF-1) and protein-derived signals, predominantly leucine, provided in high amounts by milk proteins and meat. mTORC1 activates SREBP, the master transcription factor of lipogenesis. Leucine stimulates mTORC1-SREBP signaling and leucine is directly converted by sebocytes into fatty acids and sterols for sebaceous lipid synthesis. Over-activated mTORC1 increases androgen hormone secretion and most likely amplifies androgen-driven mTORC1 signaling of sebaceous follicles. Testosterone directly activates mTORC1. Future research should investigate the effects of isotretinoin on sebocyte mTORC1 activity. It is conceivable that isotretinoin may downregulate mTORC1 in sebocytes by upregulation of nuclear levels of FoxO1. The role of Western diet in acne can only be fully appreciated when all stimulatory inputs for maximal mTORC1 activation, i.e., glucose, insulin, IGF-1 and leucine, are adequately considered. Epidemic acne has to be recognized as an mTORC1-driven disease of civilization like obesity, type 2 diabetes, cancer and neurodegenerative diseases. These new insights into Western diet-mediated mTORC1-hyperactivity provide a rational basis for dietary intervention in acne by attenuating mTORC1 signaling by reducing (1) total energy intake, (2) hyperglycemic carbohydrates, (3) insulinotropic dairy proteins and (4) leucine-rich meat and dairy proteins. The necessary dietary changes are opposed to the evolution of industrialized food and fast food distribution of Westernized countries. An attenuation of mTORC1 signaling is only possible by increasing the consumption of vegetables and fruit, the major components of vegan orPaleolithic diets. The dermatologist bears a tremendous responsibility for his young acne patients who should be advised to modify their dietary habits in order to reduce activating stimuli of mTORC1, not only to improve acne but to prevent the harmful and expensive march to other mTORC1-related chronic diseases later in life.

Abstract

OBJECTIVE:

The aim of this study was to determine the effectiveness of long-term consumption of nuts, seeds and vegetable oil (NSO) on weight, glucose, and lipid levels.

Complete article can be found here.

Effect of the Ketogenic Mediterranean Diet with Phytoextracts and low carbohydrates/high protein meals on weight, cardiovascular risk factors, body composition

Abstract

BACKGROUND:

There has been increased interest in recent years in very low carbohydrate ketogenic diets (VLCKD) that, even though they are much discussed and often opposed, have undoubtedly been shown to be effective, at least in the short to medium term, as a tool to tackle obesity, hyperlipidemia and some cardiovascular risk factors. For this reason the ketogenic diet represents an interesting option but unfortunately suffers from a low compliance. The aim of this pilot study is to ascertain the safety and effects of a modified ketogenic diet that utilizes ingredients which are low in carbohydrates but are formulated to simulate its aspect and taste and also contain phytoextracts to add beneficial effects of important vegetable components.

Abstract can be accessed here.

Despite the increasing use of very low carbohydrate ketogenic diets (VLCKD) in weight control and management of the metabolic syndrome there is a paucity of research about effects of VLCKD on sport performance.Ketogenic diets may be useful in sports that include weight class divisions and the aim of our study was to investigate the influence of VLCKD on explosive strength performance.

Background
Tumor patients exhibit an increased peripheral demand of fatty acids and protein. Contrarily, tumors utilize glucose as their main source of energy supply. Thus, a diet supplying the cancer patient with sufficient fat and protein for his demands while restricting the carbohydrates (CHO) tumors thrive on, could be a helpful strategy in improving the patients’ situation. A ketogenic diet (KD) fulfills these requirements. Therefore, we performed a pilot study to investigate the feasibility of a KD and its influence on the quality of life of patients with advanced metastatic tumors.

Complete article can be found here.