Thanks for starting a new recipe since the comments were getting out of hand on the sub rolls post 🙂 Can you say what size loaf pan you used for this. I have tried the recipe twice in a loaf pan of 2 very different sizes, and they turned out radically different. I think there is a sweet spot which you obviously found with yours. I’d like to find it for mine, too. Thanks for the great bread recipe. It’s one of the only recipes I know by heart because it is so elegantly simple.
Hi Maya, I’m new to your website and I’m anxious to try out this bread recipe. I’m helping my 27 year old son lose some weight. He’s on some pretty potent medication that has caused him to crave carbs thus putting on quite a bit of weight over the past few years. Since I’m his caregiver and also a Certified Nutritionist, I’m looking for some healthy alternatives to make his transition a bit easier and he loves bread.
Metabolic syndrome, also known as Insulin Resistance Syndrome (IRS) and Syndrome X, is a cluster of metabolic and anthropometric traits including glucose intolerance, upper body fat distribution (increased intra-abdominal fat mass), hypertension, dysfibrinolysis, and a dyslipidemia (characterized by high triglycerides, low high-density lipoprotein [HDL] cholesterol, and small dense low-density lipoprotein [LDL] particles).1 Metabolic syndrome constitutes a powerful risk factor complex to identify individuals at increased risk for future Type 2 diabetes and cardiovascular disease (CVD). Insulin resistance and abdominal obesity are two central components of the syndrome and are integrally involved in its pathogenesis. Insulin resistance is a metabolic abnormality in which peripheral tissues exhibit a subnormal biologic response to the glucose-lowering action of insulin. Insulin resistance not only antedates the development of diabetes but is also a major metabolic defect (together with impaired insulin secretion and elevated hepatic glucose production) that maintains hyperglycemia in patients with overt disease. The central role of abdominal adiposity underscores the importance of body fat distribution regarding the metabolic consequences of obesity. Individuals with metabolic syndrome are also more prone to develop other pathologic conditions including polycystic ovary syndrome, non-alcoholic steatohepatitis (NASH), cholesterol gallstones, sleep disorders, and some types of cancer. Thus, metabolic syndrome is responsible for a tremendous burden of human disease and social costs, and nutritional therapy is key to both its prevention and limiting its progression to Type 2 diabetes and CVD.
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Meanwhile, the KD induces a ketosis that is not a pathological but physiological condition occurring on a daily basis. Hans Krebs was the first to use the term “physiological ketosis” despite the common view of it as oxymoron (Krebs, 1966); this physiological condition, i.e., ketosis, can be reached through fasting or through a drastically reduced carbohydrate diet (below 20 g per day). In these conditions, glucose reserves become insufficient both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle and for the supply of glucose to the central nervous system (CNS) (Felig et al., 1969; Owen et al., 1969) (Figure (Figure1).1). It is well-known that the CNS cannot use FAs as an energy source because free FAs cannot cross the blood-brain barrier (BBB). This is why the brain normally uses only glucose. After 3–4 days without carbohydrate intake (KD or fasting) the CNS must find alternative energy sources as demonstrated by Cahill et al. (Owen et al., 1967, 1969; Felig et al., 1969; Cahill, 2006). These alternative energy sources are the ketones bodies (KBs): acetoacetate (AcAc), β-hydroxybutyric acid (BHB) and acetone and the process of their formation occurring principally in the mitochondrial matrix in the liver is called ketogenesis (Fukao et al., 2004). Usually the concentration of KB is very low (<0.3 mmol/L) compared to glucose (≅ 4 mmol) (Veech, 2004; Paoli et al., 2010). Since glucose and KB have a similar KM for glucose transport to the brain the KB begin to be utilized as an energy source by the CNS when they reach a concentration of about 4 mmol/L (Veech, 2004), which is close to the KM for the monocarboxylate transporter (Leino et al., 2001).
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Thanks for this inputs. 20 years ago I gain 17 pounds a year for 5 years. I was healthy but my dr told me start diet, any diet just come back in a month I want to see you start loosing… I started Atkins and lost 7 pound in a month. She was checking my progress every six months and checking my condition. I lost 64 pounds in 3 years. Now I started eating out of control. I am eating healthy but too much… I gain 40 pound back after 20 years. Now I will start again my Atkins to take off 30 pounds…
High blood sugar levels coupled with high blood ketones, on the other hand, will mean that you have a pathologically low level of insulin – something non-diabetics do not suffer from. This can lead to ketoacidosis – a potentially life-threatening condition. If this happens, you’ll need to inject more insulin; if you’re at all unsure of what to do, contact a medical professional. Coveting really high blood ketones for weight control is not worth the risk for type 1 diabetics.
^ Greenberg CR, Dilling LA, Thompson GR, Seargeant LE, Haworth JC, Phillips S, Chan A, Vallance HD, Waters PJ, Sinclair G, Lillquist Y, Wanders RJ, Olpin SE (April 2009). "The paradox of the carnitine palmitoyltransferase type Ia P479L variant in Canadian Aboriginal populations". Molecular Genetics and Metabolism. 96 (4): 201–7. doi:10.1016/j.ymgme.2008.12.018. PMID 19217814.
Low blood sugars can be caused by not eating enough, or by trying to lower your sugar too quickly. A blood sugar under 60 is considered dangerous. It can lead to confusion or loss of consciousness, which can be deadly. It is important to have a snack with you at all times in case this happens to you. If it does happen, think about what you did or didn’t do that lead to the low number. If it happens often, start writing things down to help you track what the cause is so that you can avoid it.
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Dr. Campos, it is unfortunate that you retain the medical community’s negative stance on the ketogenic diet, probably picked up in medical school when you studied ketoacidosis, in the midst of an obesity and type II diabetes epidemic that is growing every year, especially among populations who will never see the Harvard Health Letter. The medical community has failed in reversing this trend, especially among children, and the public is picking up the tab, in the form of higher health insurance premiums to treat chronic metabolic diseases which doctors cannot cure. The ketogenic diet does not bid its adherents to eat unhealthy processed meats, and the green leafy vegetables that it emphasizes are important in a number of nutritional deficiencies. People lose weight on the ketogenic diet, they lose their craving for sugar, they feel more satiety, they may become less depressed, their insulin receptors sensitivity is improved, and these are all the good outcomes you fail to mention. There is a growing body of research which demonstrates the neuroprotective effects of the ketogenic diet to slow cancer progression, as well as diseases like Parkinson’s and Alzheimer’s, for which there are no effective medical treatments. Please respect your patients by providing them with evidence-based medical outcomes, not opinions.
Divya, I’m happy to hear the flavor was great, but sorry to hear the bread was flat! I’ll try to help you troubleshoot…first I would check to make sure that your baking powder is fresh. Also, did you use the full cup of egg whites? Did you use a 9 by 5-inch loaf pan? Did you cook it at 350F and is your oven properly calibrated? Did you bake it for the amount of time the recipe calls for?