During this time, Jonsson authored a food blog, Gastroville.com (now closed), demonstrating great understanding and in-depth analysis of food, whilst also advising chefs and restaurateurs where to find the best ingredients. At the age of 44, he discovered a Paleolithic diet which did not aggravate his allergies, and was finally able to make the transition from food critic and blogger to restaurateur. It was the first time the self-taught chef had worked in a commercial kitchen and after just one year, it received a coveted Michelin star.
How friendly are they to dietary requirements? I have been before they turned to a no choice menu model, and I greatly enjoyed being able to pick my own four courses composed mostly of fish, as I don't eat red meat. I looked into going again and emailed them with some questions, twice and they never got back to me. Shame as I enjoyed it, though for that amount of money I would expect them to provide better service by giving me a response!
Mikael Jonsson Diet To Go
We have eaten at some of best restaurants in London and the highest praise we can give Hedone is that is that it is without a doubt the best. Our only regret was that we went for the tasting menu and not the Carte Blanche menu, but this will be remedied with a return visit. A note to C.Elder, below, we were asked both when we booked and when we sat down at the restaurant if we had any dietary requirements so they seem quite happy to accommodate diners requirements. I would suggest giving them a call.
To c.elder - Somewhat off topic - but if you are avoiding seeds because you have something like diverticular disease - you might want to set up an appointment with your family doctor to discuss your diet. There are new findings/recommendations that - among other things - pretty much debunk the old ideas about avoiding seeds and the like. We will be dining at Hedone for the first time later this month - and are really looking forward to it!
Earlier this year I was advised to move to a gluten free diet. Hedone was the first top-end restaurant I visited with this limitation. The meal I had was absolutely outstanding. Furthermore it is only as time has gone by that I have realised how different restaurants treat people with different limitations. At most (even top end) restaurants I will be directed to a course that I can eat or there may be a substitute, often I am very happy, sometimes the lack of effort is clear; at Hedone a complete new menu was created for me separate from my other three diners that I was sharing dinner with. Not just substitutes but clear well thought out courses. I had dinner at Hedone pre-gluten diet and thought it wonderful, now gluten restricted, somehow its better and clearly that is because as a complete package this restaurant is the best in London.
Aim. Models combining diabetes and atherosclerosis are important in evaluating the cardiovascular (CV) effects and safety of antidiabetes drugs in the development of treatments targeting CV complications. Our aim was to evaluate if crossing the heterozygous glucokinase knockout mouse (GK+/-) and hyperlipidemic mouse deficient in apolipoprotein E (ApoE-/-) will generate a disease model exhibiting a diabetic and macrovascular phenotype. Methods. The effects of defective glucokinase on the glucose metabolism and on the progression and regression of atherosclerosis on high-fat diets were studied in both genders of GK+/-ApoE-/- and ApoE-/- mice. Coronary vascular function of the female GK+/-ApoE-/- and ApoE-/- mice was also investigated. Results. GK+/-ApoE-/- mice show a stable hyperglycemia which was increased on Western diet. In oral glucose tolerance test, GK+/-ApoE-/- mice showed significant glucose intolerance and impaired glucose-stimulated insulin secretion. Plasma lipids were comparable with ApoE-/- mice; nevertheless the GK+/-ApoE-/- mice showed slightly increased atherosclerosis development. Conclusions. The GK+/-ApoE-/- mice showed a stable and reproducible hyperglycemia, accelerated atherosclerotic lesion progression, and no lesion regression after lipid lowering. This novel model provides a promising tool for drug discovery, enabling the evaluation of compound effects against both diabetic and cardiovascular endpoints simultaneously in one animal model.
Evidence for an association between the local food environment, diet and diet-related disease is mixed, particularly in the UK. One reason may be the use of more distal outcomes such as weight status and cardi...
It has been hypothesized that dietary cereal grain protein could cause leptin resistance by preventing leptin from binding to the leptin receptor [3]. Briefly, the hypothesis rests on the following propositions: (I) The global pattern of varying prevalence of diseases of affluence, such as obesity, cardiovascular disease and diabetes, suggests that some environmental factor specific to agrarian societies could initiate these diseases; (II) A diet based on cereal grain could be such an environmental factor; (III) Leptin resistance is also associated with diseases of affluence and could be a sign of insufficient adaptation to a diet based on cereal grain; (IV) Cereal grain proteins have sufficient properties (i.e. they are unique, are present in human food, are heat-stable, are resistant to gastro-intestinal breakdown, enter the human circulation, and bind to cell surfaces and receptors) to cause leptin resistance by inhibiting binding of leptin to the leptin receptor. The hypothesis is supported by a recent study on human genetic adaptation by Segurel et al., which showed positive selection of protective variants of the leptin receptor with regard to type 2 diabetes from the Neolithic period onward [4]. This indicates the onset of evolutionary pressure on the leptin receptor when significant amounts of cereal grain were adopted as food. Support also comes from animal studies, which show that dietary components can induce leptin resistance in rats in relatively short periods of time at normal body weight and leptin levels [5]. Dall et al. demonstrated that cereal grain protein in the form of digested wheat gliadin caused a 20% increase in weight gain when injected into non-obese diabetic (NOD) mice in a pre-diabetic state [6], possibly indicating the induction of leptin resistance. Dall et al. also demonstrated that digested wheat gliadin caused a dose-dependent increase in insulin secretion when incubated with rat insulinoma cells and rat islets, which was possibly caused by inhibition of current through ATP-sensitive K+ (KATP) channels [6]. These findings could be indirect evidence that digested wheat gliadin actually inhibits leptin binding, since leptin was previously reported to cause the opposite effect in insulinoma cells [7]. Further support comes from human clinical studies, in which El-Shebini et al. found that indices of leptin resistance are improved by replacing bread with vegetables in otherwise similar hypocaloric diets and with similar weight loss [8]. Another study by Ryberg et al. on the effects of a diet without cereal grains also showed significant effects on leptin [9]. Our previous dietary intervention study comparing effects of diets with and without cereal grains showed a strong correlation between relative change in leptin and cereal grain intake [10].
In this study, we tested the last proposition of the above hypothesis, which is that cereal grain proteins inhibit leptin binding. Cereal grain proteins have already been reported to bind to a receptor by Lammers et al., who found that cereal grain peptides derived from enzymatic digestion of wheat gliadin with the gut enzymes pepsin and trypsin under physiological conditions bind to the chemokine receptor CXCR3 expressed in mouse and human intestinal epithelia and laminae propriae, leading to zonulin release and increased intestinal permeability [11]. Kamikubo et al. reported that wheat germ agglutinin binds to the leptin receptor in vitro and inhibits binding of leptin to the leptin receptor [12]. Wheat germ agglutinin is found in common wheat flour but not in human blood [13]. We chose to examine cereal grain protein from wheat, which is the main source of vegetable protein in human food. The main protein component of wheat is gluten, which is the cohesive and elastic mass that remains after starch has been removed from cereal grain flour by rinsing with water. More specifically, wheat gluten is a composite of several kinds of proteins, such as gliadins (molecular weight 30 kDa) and glutenins (molecular weight 30-90 kDa). Gluten intake has increased greatly over the last hundred years and has accelerated during the last few decades [14,15]. This increase is largely due to breeding of gluten-rich cereal grain varieties and most recently by the use of extra gluten in baking and food processing to make dough easier to work and bread fluffier [15]. Soares et al. found that a gluten-free diet reduces leptin, adiposity, inflammation and insulin resistance in mice despite a similar energy intake [16]. Chirdo et al. reported the presence of non-degraded wheat gliadin in human serum (at a mean level of 41 ng/mL) [17], as previously also reported for other dietary proteins by Husby et al. [18,19].
GPR120 (Ffar4) has been postulated to represent an important receptor mediating the improved metabolic profile seen upon ingestion of a diet enriched in polyunsaturated fatty acids (PUFAs). GPR120 is highly expressed in the digestive system, adipose tissue, lung and macrophages and also present in the endocrine pancreas. A new Gpr120 deficient mouse model on pure C57bl/6N background was developed to investigate the importance of the receptor for long-term feeding with a diet enriched with fish oil. Male Gpr120 deficient mice were fed two different high fat diets (HFDs) for 18 weeks. The diets contained lipids that were mainly saturated (SAT) or mainly n-3 polyunsaturated fatty acids (PUFA). Body composition, as well as glucose, lipid and energy metabolism, was studied. As expected, wild type mice fed the PUFA HFD gained less body weight and had lower body fat mass, hepatic lipid levels, plasma cholesterol and insulin levels and better glucose tolerance as compared to those fed the SAT HFD. Gpr120 deficient mice showed a similar improvement on the PUFA HFD as was observed for wild type mice. If anything, the Gpr120 deficient mice responded better to the PUFA HFD as compared to wild type mice with respect to liver fat content, plasma glucose levels and islet morphology. Gpr120 deficient animals were found to have similar energy, glucose and lipid metabolism when fed HFD PUFA compared to wild type mice. Therefore, GPR120 appears to be dispensable for the improved metabolic profile associated with intake of a diet enriched in n-3 PUFA fatty acids. 2ff7e9595c
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