I would like to know what led you to the conclusion to recommend eating in the morning and fasting in the evening instead of the other way around. You do not link any studies here that show TRF in the morning is better than TRF in the evening. You do state “Nighttime eating is well associated with a higher risk of obesity, as well as diabetes.” but I would hazard a guess that alot people that snack into the evening have many other factors at play that could effect their risk of obesity and diabetes and are possibly not fasting at all. I have been doing TRF from 12-8pm every day for almost a year and have seen vast improvements in my health, not least of which is a loss of 70 lbs, so it seems odd to read items 3 and 4 on your 4 ways to use this information for better health. If you have evidence that supports the idea that TRF in the evening is bad then I would like to see it and perhaps change my dieting habbits.
If you’re looking to get a jump start on your health and fitness goals this year, you may be thinking about trying the ketogenic diet. Maybe you’ve heard the phrase before — it’s a huge diet buzzword — but aren’t sure what it means. Here’s a primer: The ketogenic diet is an eating plan that drives your body into ketosis, a state where the body uses fat as a primary fuel source (instead of carbohydrates), says Stacey Mattinson, RDN, who is based in Austin, Texas.
Initial human studies that compared fasting every other day to eating less every day showed that both worked about equally for weight loss, though people struggled with the fasting days. So I had written off IF as no better or worse than simply eating less, only far more uncomfortable. My advice was to just stick with the sensible, plant-based, Mediterranean-style diet.
People use a ketogenic diet most often to lose weight, but it can help manage certain medical conditions, like epilepsy, too. It also may help people with heart disease, certain brain diseases, and even acne, but there needs to be more research in those areas. Talk with your doctor first to find out if it’s safe for you to try a ketogenic diet, especially if you have type 1 diabetes.
The least intrusive weight loss methods, and those most often recommended, are adjustments to eating patterns and increased physical activity, generally in the form of exercise. The World Health Organization recommended that people combine a reduction of processed foods high in saturated fats, sugar and salt and caloric content of the diet with an increase in physical activity.
There’s also some evidence that it might help with type 2 diabetes. “An emerging body of research is finding that a keto plan may have some real benefits thanks to its ability to improve the body’s ability to use insulin and also help control appetite, which can result in easier weight loss,” says Karen Ansel, R.D.N., co-author of Healthy in a Hurry.
Another difference between older and newer studies is that the type of patients treated with the ketogenic diet has changed over time. When first developed and used, the ketogenic diet was not a treatment of last resort; in contrast, the children in modern studies have already tried and failed a number of anticonvulsant drugs, so may be assumed to have more difficult-to-treat epilepsy. Early and modern studies also differ because the treatment protocol has changed. In older protocols, the diet was initiated with a prolonged fast, designed to lose 5–10% body weight, and heavily restricted the calorie intake. Concerns over child health and growth led to a relaxation of the diet's restrictions. Fluid restriction was once a feature of the diet, but this led to increased risk of constipation and kidney stones, and is no longer considered beneficial.
Although many hypotheses have been put forward to explain how the ketogenic diet works, it remains a mystery. Disproven hypotheses include systemic acidosis (high levels of acid in the blood), electrolyte changes and hypoglycaemia (low blood glucose). Although many biochemical changes are known to occur in the brain of a patient on the ketogenic diet, it is not known which of these has an anticonvulsant effect. The lack of understanding in this area is similar to the situation with many anticonvulsant drugs.
The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. The classic therapeutic ketogenic diet was developed for treatment of paediatric epilepsy in the 1920s and was widely used into the next decade, but its popularity waned with the introduction of effective anticonvulsant medications. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains, and sugar, while increasing the consumption of foods high in fat such as nuts, cream, and butter. Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.
The ketogenic diet is not a benign, holistic, or natural treatment for epilepsy; as with any serious medical therapy, complications may result. These are generally less severe and less frequent than with anticonvulsant medication or surgery. Common but easily treatable short-term side effects include constipation, low-grade acidosis, and hypoglycaemia if an initial fast is undertaken. Raised levels of lipids in the blood affect up to 60% of children and cholesterol levels may increase by around 30%. This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and if persistent, by lowering the ketogenic ratio. Supplements are necessary to counter the dietary deficiency of many micronutrients.
In so far as insulin promotes de novo lipogenesis and suppresses lipolysis in adipocytes it DOES help keep the fat inside. But in Hyperinsulinemia / Insulin Resistance with Impaired Glucose Tolerance lipolysis may not be sufficiently reduced and fatty acids and glycerin can be spilled at the same time that Triglycerides are being formed & stored. In the liver the glycerin gets converted to glucose producing hyperglycemia.
The ketogenic diet is a medical nutrition therapy that involves participants from various disciplines. Team members include a registered paediatric dietitian who coordinates the diet programme; a paediatric neurologist who is experienced in offering the ketogenic diet; and a registered nurse who is familiar with childhood epilepsy. Additional help may come from a medical social worker who works with the family and a pharmacist who can advise on the carbohydrate content of medicines. Lastly, the parents and other caregivers must be educated in many aspects of the diet for it to be safely implemented.
Gastrointestinal disorders are another common cause of unexplained weight loss – in fact they are the most common non-cancerous cause of idiopathic weight loss. Possible gastrointestinal etiologies of unexplained weight loss include: celiac disease, peptic ulcer disease, inflammatory bowel disease (crohn's disease and ulcerative colitis), pancreatitis, gastritis, diarrhea and many other GI conditions.
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In addition to improving your health, maintaining a weight loss is likely to improve your life in other ways. For example, a study of participants in the National Weight Control RegistryExternal* found that those who had maintained a significant weight loss reported improvements in not only their physical health, but also their energy levels, physical mobility, general mood, and self-confidence.
The nerve impulse is characterised by a great influx of sodium ions through channels in the neuron's cell membrane followed by an efflux of potassium ions through other channels. The neuron is unable to fire again for a short time (known as the refractory period), which is mediated by another potassium channel. The flow through these ion channels is governed by a "gate" which is opened by either a voltage change or a chemical messenger known as a ligand (such as a neurotransmitter). These channels are another target for anticonvulsant drugs.