I’m discouraged to see that nowhere in the article nor in the comments is there a mention of a diet’s best fit to genetics. Consider if someone is an APOE E2 carrier and/or has certain polymorphisms of the APO5 gene. These are quite rare in Okinawa but much more prevalent in the USA (12% of the population). According to a number of well-designed studies, these genetic characteristics point to a higher fat, lower carbohydrate diet as beneficial and even a “moderate” carb diet as problematic.
Hi Maria, glad you like the bread! Good question about the olive oil – on the one hand using the same amount as butter would mean you stick with the same wet/dry ratio, on the other had olive oil doesn’t firm up at room temperature, but butter and coconut oil do. Therefore, I’d try using a bit less olive oil than butter, maybe 40g instead of 60g. You could also get hold of refined coconut oil, which does not have the coconut taste, for example this one.
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4.) Fill the dough into a loaf tin lined with baking paper. If you don’t use a silicone loaf pan line ALL SIDES with parchment paper so the bread will release easily. Smooth the top, but don’t press down too much – keep as much air in the dough as possible. Bake at 180 Celsius / 350 Fahrenheit for about 45 minutes or until a knife inserted comes out clean!


Saturated fat: A type of fat found in abundance in butter, whole milk, ice cream, full-fat cheese, fatty meats, poultry skin, and palm and coconut oils. Saturated fat raises levels of heart-threatening LDL cholesterol in your bloodstream. It can also interfere with your body’s ability to absorb blood sugar easily. Limiting saturated fat can help control your risk for heart disease.
Although convincing, the bulk of evidence in relation to the inhibitory effects of ketosis on appetite is still anecdotal. Preliminary scientific reports seem to support this phenomenon, and the evidence shows that KD is more effective, at least in the short/medium-term, on fat loss (Paoli, 2014). It was demonstrated that diet-induced weight loss leads to changes in energy expenditure and in appetite-regulating hormones that facilitate weight regain and the return to initial energy homeostasis (Sumithran et al., 2011). This response to alteration of energy balance nullifies the success of many dietary approaches. It is well-known that the long-term success of a nutritional approach is defined by the amount of weight regain and is the main problem regarding the so-called weight cycling or “yo-yo” effect (Jeffery, 1996). A recent study by our group has demonstrated that a brief ketogenic period, if followed by a longer period of correct Mediterranean diet could avoid this yo-yo effect (Paoli et al., 2013). During the ketogenic period subjects reported less hunger, confirming previous studies (Nickols-Richardson et al., 2005; Johnston et al., 2006; Johnstone et al., 2008) on hunger-suppression effect of ketogenic diet. Despite these clinical findings, the mechanisms of action of ketosis on appetite reduction are still not completely understood. Clinical results are suggestive of both direct and indirect (via modifications of hunger-related hormones concentration) actions of KBs on appetite (Sumithran et al., 2013).
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Another mechanism that could be involved in food-regulation during KD is the gamma aminobutyric acid (GABA) and glutamate regulation. Wu et al. demonstrated that GABAergic signaling from the NPY/AgRP neurons to the parabrachial nucleus (located in the dorsolateral part of the pons) is involved in many regulatory sensory stimuli including taste and gastric distension, regulate feeding behavior. GABA signaling seems to prevent animals from anorexia when AgRP neurons were destroyed (Wu et al., 2009). These findings are yet another contradictory aspect of KDs and food behavior; ketosis should increase the availability of glutamate (via diminution of transamination of glutamate to aspartate) and therefore increase GABA and glutamine levels; moreover, in ketosis, the brain imports a huge amount of acetate and converts it through glia into glutamine (an important precursor of GABA) (Yudkoff et al., 2008). The result of these mechanisms, together with the increased mitochondrial metabolism and flux through the TCA cycle, is an increased synthesis of glutamine and a “buffering” of glutamate. These results are not consistent with the well-documented anorexigenic effect of KDs, and therefore the GABA hypothesis cannot be taken into account despite the mild euphoria often reported during a KD that is probably due to the action of BHB (Brown, 2007) and can help to reduce appetite.
In the United States, children are becoming obese at triple the rate compared with the 1960s, making the study and treatment of this problem paramount. The epidemic of metabolic syndrome in children and adolescents is an international phenomenon, leading the International Diabetes Foundation to publish an updated consensus statement to guide diagnosis and further study of the condition. [51, 52]
This recipe is like having last night's cake for breakfast — except it's fiber-filled chia seed pudding instead. This dessert-like breakfast from Healthy Sweet Eats is hardly a disappointing substitute, though. Fresh cherries add sweetness, while whole almonds add crunch (and more fiber). Plus, it's made with strongly brewed coffee to give you an extra jolt of caffeine with your usual cup of java.

Going from a standard-American diet to a well-formulated low-carb or ketogenic diet is a health upgrade. However, it usually comes with unpleasant but temporary symptoms of carbohydrate withdrawal, also known as the keto flu. This is easily addressed by using Nutrita to properly follow a ketogenic diet or simply by familiarizing yourself with basic electrolyte management.


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How, exactly, does our body take pyruvate (from glucose) or acetyl CoA (from fat) and generate so much ATP?  The answer lies in the beauty of the Krebs Cycle, which feeds into a process called the electron transport chain (or ETC), I alluded to above.  Since the adage ‘you can’t get something for nothing’ is as true in biochemistry as it appears to be in life, to get all that ATP (i.e., stored energy in the form of the phosphate bond), we need to give up something.  What the ETC does give up, as its name suggests, is electrons.  Through a series of redox reactions the ETC trades the stored energy held by electrons going from higher to lower energy states in exchange for the chemical energy stored in the bonds of the third phosphate group on an ATP molecule.
Metabolic syndrome is not merely a single disease but a collection of pathological conditions (i.e., abdominal obesity, insulin resistance, dyslipidemia, hyperglycemia, and hypertension) that increase the risk of developing diabetes and cardiovascular diseases. Low adiponectin levels directly correlate with the development of metabolic syndrome after adjusting for age, sex, and BMI [106,107]. In a study of Japanese adults, an increase in the number of metabolic syndrome components was associated with decreasing adiponectin levels [108]. Hypoadiponectinemia also appears to be a predictor for the future development of metabolic syndrome in obese individuals [109,110].
Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in patients treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components.[27]
Made this bread this morning Will use a little less water next time as along the bottom of the loaf about ½ an inch deep was a bit doughy & it did sink in the middle was also a darker colour than the one in the picture but is so yummy Have sliced it into peices & put 2 slices into bags in the freezer for when I have toast for breakfast Going to make another loaf tomorrow as my husband thought it was great So pleased to have finally found a bread recipe I can enjoy Thank u so much Really enjoy browsing on here
Sorry, I realized I should have clarified which kind of freshly milled flours. Specifically, wheat, rye and spelt. I have been using freshly milled flour for over a year now and my family loves it. I have recently bought 3 of your books and I am learning all kinds of wonderful new things, but I am having a hard time letting go of freshly milled flour completely. Your thoughts on the subject would be much appreciated!
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Version two was almond flour only. Right away I could tell the recipe would need some modifications. Almond flour doesn’t soak up nearly as much liquid as coconut flour, resulting in a very soupy batter. I added two more tablespoons of almond flour, which was double the amount of coconut flour, and it still wasn’t nearly as thick. After its short stint in the microwave, this bread turned out very moist, soft, and rather flimsy, but was pleasantly bland enough to go with any filling I wanted.
Insulin (in-suh-lin): A hormone made by the cells in your pancreas. Insulin helps your body store the glucose (sugar) from your meals. If you have diabetes and your pancreas is unable to make enough of this hormone, you may be prescribed medicines to help your liver make more or make your muscles more sensitive to the available insulin. If these medicines are not enough, you may be prescribed insulin shots.
So, if I’m deprived of a dietary source of glucose, I depend solely on my liver to release glycogen (a process known as hepatic glucose output, or HGO).  How long can HGO supply my brain with sufficient glucose? It depends on a few things that impact both the “source” and the “sink” of glucose.  Other competing sinks for glucose (e.g., activity level, thermogenic needs) and sources (e.g., glycerol and gluconeogenic amino acid availability) can make a difference for a while. But, in a state of starvation we’ve only got about one to three days before we’re in trouble.  If our brain doesn’t get a hold of something else, besides glucose, we will die quite unceremoniously.
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Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose.[1][2] It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides[3]). Ketones can also be consumed in exogenous ketone foods and supplements.
I just want to say that I love your blog and am in love with your brownie recipe!! It’s a godsend and I was just as excited with this recipe as a result. Unfortunately, my bread fell short for some reason..No matter how long I toast it, it’s spongy and moist in the center…I’ve done everything as directed but substituted the butter for coconut oil. I measured it exactly too. Could that be why the bread is awfully wet in the middle or is there another reason? I tasted quite a bit of the psyllium husk as well which was okay..I’m thinking of making it with flax seed next time.
Metabolic syndrome is a multiplex risk factor that arises from insulin resistance accompanying abnormal adipose deposition and function. [4] It is a risk factor for coronary heart disease, as well as diabetes, fatty liver, and several cancers. The clinical manifestations of this syndrome may include hypertension, hyperglycemia, hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C), and abdominal obesity. (See Prognosis, Workup, Treatment, and Medication.)

Metabolic syndrome promotes coronary heart disease through several mechanisms. It increases the thrombogenicity of circulating blood, in part by raising plasminogen activator type 1 and adipokine levels, and it causes endothelial dysfunction. [14] Metabolic syndrome may also increase cardiovascular risks by increasing arterial stiffness. [15] Additional mechanisms include oxidative stress, [16] which has been associated with numerous components of metabolic syndrome. [17]

Garlic: Potent, but effective. Garlic is known as one of the oldest medicines in the world…and with good reason. An animal study that administered high doses of raw garlic to rats for 4 weeks found that it had a profound effect of reducing blood glucose levels, as well as cholesterol and triglycerides compared to rats who did not receive raw garlic (2). They also tested rats with boiled garlic, and saw no changes in blood glucose, so the benefit comes from raw garlic.
Nice and firm. Baked it on the recommended temp, added 6 or 7 minutes. Pressed the middle and it was great. I let it cool. What was nice about it was obviously it’s low carb bread…hurray for that, but it cut well. Got 18 slices easily about 1/2 inch thick without breakage. Most importantly, it wasn’t greasy, or almond tasting overload, just delicious.
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While the lipid abnormalities seen with metabolic syndrome (low HDL, high LDL, and high triglycerides) respond nicely to weight loss and exercise, drug therapy is often required. Treatment should be aimed primarily at reducing LDL levels according to specific recommendations. Once reduced LDL targets are reached, efforts at reducing triglyceride levels and raising HDL levels should be made. Successful drug treatment usually requires treatment with a statin, a fibrate drug, or a combination of a statin with either niacin or a fibrate.

Yolks are great. Make a healthified custard, or a custard ice cream (Maria has recipies for both). I’m a diabetic and I got that way eating “real” food, not manufatured food. I baked. All from scratch, all homemade. But that meant traditional sugar and wheat flour. I had developed a number of reduced carb recipies on my own, but Maria’s recipies go all the way with better success than I would have guessed possible. (I still yearn for a good, two-day rise wheat and yeast bread — But I know allow myself this only once a quarter. It is not good for you.) I’m excited to try this. So far my favorite has been her psyllium powder/egg/boiling water version pizza crust. A homemade pizza made with this tastes as good as any pizza.
Well good luck Tiffany, I hope it works for you. I totally understand and feel your pain :). I have been trying to do the Protein Bread FOREVER! And nothing, I mean nothing, buying Jay Rob brand, buying a new stand mixer, everything I could think of and nothing ever worked and still doesn’t. I can make the buns and they are acceptable, but I would so love to make the loaf. Anyway, I’m wondering, since I live in Florida, does the atmophere, weather have anything to do with it? It is very humid here. Maybe that’s something that needs to be addressed??
This was my first time baking anything EVER and it turned out perfectly! I do find that the bread does taste a tad “eggy” but it’s soft and a perfect replacement for sandwich bread. I can finally have grilled cheese sandwiches again!! Next time around, I’ll double the recipe because the bread was smaller than expected. Thanks for this amazing recipe!

The effects of a ketogenic diet on cholesterol and triglycerides is complex. It is dependant on the exact composition of the diet, the genetic and physical characteristics of the individuals studied and other hormonal and environmental factors. Therefore, blood lipid changes whilst on the ketogenic diet can vary between individuals. This means that it is advisable to track your personal levels by having a blood test before starting the ketogenic diet and to follow this with regular testing to monitor any changes.  
Hi, I’ve made this recipe twice and LOVE the taste. However, both times the bread would rise so high in the oven, but as soon as I take it out to cool it deflated and middle sink down. What could’ve gone wrong? Over mixing? I did switch coconut flour to all almond flour instead. Could that be a problem? Please help as I’m anxious to make another batch. Thank you.

Although mitohormesis has not been studied comprehensively in higher-level organisms, its occurrence is supported by compelling evidence in lower-level organisms. For example, inhibition of glycolysis in C. elegans increased fat oxidation (based on nematode triglyceride content) and mitochondrial O2 consumption, which was followed by increases in ROS production at day 2 and catalase activity at day 6 [72]. The increase in catalase activity occurred in conjunction with increases in lifespan and resistance to the mitochondrial stressors sodium azide and paraquat. However, antioxidant treatment (N-acetylcysteine) decreased the elevation of ROS at day 2 and eliminated the resistance to sodium azide and paraquat treatments, indicating a requirement of ROS as a stimulus [72].


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