I was reading through the comments on this recipe and noticed a number of posts by people who were disappointed because they had followed the recipe to the letter and the bread still didn’t turn out like yours. You did your best to help them sort out what the problem might be, but there were two issues that I didn’t see addressed that might make a difference: altitude and relative humidity. I live in Irvington, Alabama (near Mobile). I have been baking gluten-free for over twenty years and I realized long ago that nearly every recipe I used from Bette Hagman’s books had to be adjusted or they wouldn’t turn out. Then I remembered something from my earlier baking days using wheat flour. Most of the recipes I used noted that liquids and leavening have to be adjusted based on altitude and relative humidity to get recipes to rise properly and to avoid gumminess. That is, if you live at a much higher or lower altitude than Maria, or you live in a much wetter or drier climate, you will have to tweak the liquids and leavening to suit the area where you live. Start with about two tablespoons less water if you’re getting gummy results. Start with about one teaspoon less baking powder if your bread is rising too fast and forming a bubble. I imagine getting this recipe to work is like making any other kind of bread; after you’ve made it come out right a few times, you get a feel for what the dough should look/feel like in order to turn out.

I used the egg white powder with the recommended amount of water on the egg white can in addition to the 12 oz. of water called for in the recipe. The bread tastes good, but is fairly dense. I didn’t have many eggs and wanted to try the recipe, but I think next time I’ll use fresh egg whites. I’ll also have to figure out what to do with the leftover yolks.

More specific to mitochondrial function, treatment with BHB + ACA (1 mM each) has decreased O2•− production in isolated rat neuronal mitochondria following glutamate exposure [109]. This occurred in conjunction with decreased NADH levels, suggesting that ketones may additionally decrease mtROS production by enhancing electron transport along the mtETC after NADH oxidation and, in turn, decreasing mitochondrial Δp and associated O2•− production. The observed decrease in mitochondrial O2•− production occurred independently of glutathione [109], but in isolated and stunned hearts from guinea pigs, treatment with 5 mM ACA increased GSH and the NADPH/NADP+ ratio [110], suggesting that glutathione may be involved to some extent.
My blood sugar is in the pre-diabetic range. D-ribose raises my blood sugar quite a bit. Test and see what it does for you before committing to taking it. Start testing your blood sugar 1/2 hour after taking the D-ribose and every 1/2 hour for about 2 hours to fully test the effects. If you take it in a liquid on an empty stomach, it can get into your bloodstream pretty fast.
Some Inuit consume as much as 15–20% of their calories from carbohydrates, largely from the glycogen found in raw meats.[43][44][47][45][50] Furthermore, the blubber, organs, muscle and skin of the diving marine mammals that the Inuit eat have significant glycogen stores that are able to delay postmortem degradation, particularly in cold weather.[51][52][53][54][55][56]
To get into ketosis without supplementation, you have to keep your insulin levels low. Supplementing with exogenous ketones can help get you into ketosis [17]. However, you won’t have achieved the same beneficial physiological changes as you would have from a well-formulated ketogenic diet or fasting. This is why we at Nutrita don’t recommend exogenous ketones as a substitute for a well-formulated ketogenic diet.

You’ll recall, from the point I made above, that my brain requires about 400 to 500 kcal of glucose per day (100 to 120 gm).  You’ll also recall (from the video, above) that I can store about 100 to 120 gm of glucose in my liver.  While I can store much more in my muscles, (on the order of about 300 to 350 gm), because muscles lack the enzyme glucose-6-phosphatase, glucose stored in muscle as glycogen is unable to re-enter the bloodstream and is meant for the muscle and the muscle alone to use.  In other words, muscle glycogen is a stranded asset of glucose in the body to be used only by the muscle.
You should always be in touch with your doctor about your disease and any changes you make or problems that you notice. Having that line of open communication is key to gaining knowledge and insight into what can make your life and your health better. Try the things mentioned in this article, but if they don’t help, then talk to your physician about what else is available for you.

The popular belief that high-fat diets cause obesity and several other diseases such as coronary heart disease, diabetes, and cancer has not been observed in recent epidemiological studies. Studies carried out in animals that were fed high-fat diets did not show a specific causal relationship between dietary fat and obesity. On the contrary, very-low-carbohydrate and high-fat diets such as the ketogenic diet have shown to beneficial to weight loss.

Hello, I’m sure you must roll your eyes at getting yet another post about glitches when making this bread. Unlike the first loaf I made I had four loaves turn out gummy. it still makes reasonable toast but I’d like to avoid this the next time I make the bread. I used your recommended almond flour, and I really ground the psyllium. However in narrowing things down there are two factors that may have contributed to the problem: 1) I mixed up two loaves at a time and I wonder if the dough was too heavy for my mixer and did not combine sufficiently. 2) I may have let a very small amount of yolk fall into the whites. Would either of these caused the gummy texture? Thanks for this amazing website. We purchased all your books and find them a wealth of information. Liz

The prevalence of metabolic syndrome increases with age, with about 40% of people older than 60 years meeting the criteria. [26] However, metabolic syndrome can no longer be considered a disease of only adult populations. Alarmingly, metabolic syndrome and diabetes mellitus are increasingly prevalent in the pediatric population, again in parallel with a rise in obesity. [50]
While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores,[72][73] studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat, relative to carbohydrates.[74] Some clinicians refer to this period of keto-adaptation as the "Schwatka imperative" after Frederick Schwatka, the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.[75]
To think of it another way, if you start with stored energy – glucose or fat, for example, which if burned in calorimeter will give off varying amounts of heat – and you’re willing to convert their carbon, hydrogen, and oxygen molecules into another form with less energy – water and carbon dioxide which, if burned, produce very little heat – it’s a fair trade!  The ETC is simply the vehicle that allows our body to make the switch.
But without carbs, sandwiches aren’t available either, and if there’s one thing followers of these diets miss the most, it’s got to be bread. Luckily, enterprising food-lovers following a keto diet have figured out a work-around. It’s called “90 Second Keto Bread” and it’s popping up all over the internet. Think of it like a mug cake version of a biscuit that happens to look a lot like an English muffin.
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^ Feinman, R. D; Pogozelski, W. K; Astrup, A; Bernstein, R. K; Fine, E. J; Westman, E. C; Accurso, A; Frassetto, L; Gower, B. A; McFarlane, S. I; Nielsen, J. V; Krarup, T; Saslow, L; Roth, K. S; Vernon, M. C; Volek, J. S; Wilshire, G. B; Dahlqvist, A; Sundberg, R; Childers, A; Morrison, K; Manninen, A. H; Dashti, H. M; Wood, R. J; Wortman, J; Worm, N (2015). "Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base". Nutrition. 31 (1): 1–13. doi:10.1016/j.nut.2014.06.011. PMID 25287761.
I made the bread yesterday but came out wet and gummy. I will try again but I would recommend anyone trying this bread for the first time to just make half the recipe until you get it right so you are not wasting expensive ingredients. This is what I am going to do. Also it was a good point about humidity. I live in a very humid area so I will have to try decreasing the water.

Moving more . Even if you’ve never exercised before, you can start now and markedly reduce your risks. Even moderate amounts of activity will make a difference with heart markers. Walking is a good starter plan for many people. “I tell my patients to get an activity tracker,” Ndumele says. “Aim for 5,000 steps a day and work up to at least 10,000 steps a day.” Talk to your doctor to get the go-ahead on the types of workouts you want to try.

The first step—the mantra of dLife from the very beginning—is test, don’t guess! To master your blood sugar, you must first know where it is. And if you only check first thing in the morning, you’re cheating at solitaire. If you want to truly master your blood sugar, you should fearlessly seek out your very worst, highest numbers. That means checking after meals. Don’t let that high number flashing on your meter get you down. Rejoice that you’ve found it. It’s just a problem to be fixed—and as you roll out the rest of these tips, those high numbers, like the walls of Jericho, are going to come a-tumblin’ down.
The advice above is therefore not only illogical, but also works poorly. It completely lacks scientific support according to a Swedish expert investigation. On the contrary, in recent years similar carbohydrate-rich dietary advice has been shown to increase the risk of getting diabetes and appears to potentially worsen blood sugar levels long-term in people who already have type 2 diabetes. The advice does not improve their health in other important ways either.
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Scheme of orexigenic and anorexigenic effects of ketosis. The picture is highly schematic. For more details please see the text. AMPK, AMP-activated protein kinase; CCK, cholecystokinin; GABA, gamma-aminobutyric acid; BHB, β-hydroxybutyric acid; FFA, free fatty acids; ROS, reactive oxygen species; NPY, neuropeptide Y; AgRP, agouti gene-related protein.
The exact cause of metabolic syndrome is not known. Many features of the metabolic syndrome are associated with "insulin resistance." Insulin resistance means that the body does not use insulin efficiently to lower glucose and triglyceride levels. Insulin resistance is a combination of genetic and lifestyle factors. Lifestyle factors include diet, activity and perhaps interrupted sleep patterns (such as sleep apnea).
Why is the keto diet good for you? A keto diet is one that prioritizes fats and proteins over carbohydrates. It can help reduce body weight, acne, and the risk of cancer. Find out about the mechanisms through which it achieves these benefits and the research that supports it. This MNT Knowledge Center article also discusses the risks of the diet. Read now

Lowering your overall intake of carbohydrates is also important for balanced blood sugar, but you don’t need to cut them completely (they're still a crucial source of fuel for your body). Simply swap out refined carbohydrates like bread, white pasta, and candy for fiber-rich, whole-food sources such as whole grains, sweet potatoes, and fruit, which contain a number of vitamins, minerals, and antioxidants essential for health.
Following a low calorie diet: The exact mechanism whereby caloric restriction can slow or prevent cancer is unknown. It may be linked to: decreased blood glucose (less fuel for cancer cells), raised ketones (antiinflammatory, decreased oxidative stress, decreased ability to use glucose) . Animal models have shown that caloric restriction is closely related to tumour incidence and progression94.
Another product of elevated levels of free FA is polyunsaturated FA (PUFA). The potential ability of PUFA to block seizure activity in the brain is speculated to be associated with KD. Some mechanisms are thought to be a direct inhibition of voltage-gated sodium and calcium channels, modulation of a lipid-sensitive potassium channel, the activity of the sodium pump to limit neuronal excitability, or the induction of expression and activity of proteins in the mitochondria, thereby inducing a neuroprotective effect by partially inhibiting the production of reactive oxygen species (ROS) (Bough and Rho, 2007; Paoli et al., 2014).
The key with diabetes is always consistency. A steady intake of the right amount of carbohydrates helps in keeping things under better control and prevents blood sugar spikes. Although many people believe that low-carb is best, that is not true during pregnancy. You need the carbohydrates for the growth of the fetus and to keep your energy level up. Talk to your doctor and nutritionist about what is best for you.
Carbohydrates need to be consistent. You don’t want to eat all of your daily carb count in one meal. That will cause your blood sugar to spike, and then drop during the other meals. Giving your body a steady amount of carbohydrates will provide a stable amount of energy. It will also help your body make enough insulin to keep your blood sugar at a healthy number.
Before we begin, a disclaimer in order: If you want to actually understand this topic, you must invest the time and mental energy to do so.  You really have to get into the details.  Obviously, I love the details and probably read 5 or 6 scientific papers every week on this topic (and others).  I don’t expect the casual reader to want to do this, and I view it as my role to synthesize this information and present it to you. But this is not a bumper-sticker issue.  I know it’s trendy to make blanket statements – ketosis is “unnatural,” for example, or ketosis is “superior” – but such statements mean nothing if you don’t understand the biochemistry and evolution of our species.  So, let’s agree to let the unsubstantiated statements and bumper stickers reside in the world of political debates and opinion-based discussions.  For this reason, I’ve deliberately broken this post down and only included this content (i.e., background) for Part I.
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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As you could probably figure out I love my cast iron skillets, but my second favorite piece of cookware is definitely the Instant Pot, followed by my smoker/grill combo but I’m getting off track.  Anyway, if you’ve never made hard boiled eggs in the Instant Pot, no offense… but you’re doing it wrong. This post from SkinnyTaste covers all the details to make perfect hard-boiled (or soft-boiled) eggs every time that are the absolute easiest to peel.  

Hi Tammy, I still have to try the muffin tin method to ive you a better response. Why don’t you make the recipe using exact ingredients for one bread multiplied x 9-10 and divide between 12 muffin tin slots? I think this will work better. This way we are not changing the amount of eggs. If you use less eggs, the bread will be more dry, since it is gluten-free.
Maria and Craig: I made this recipe (into kaiser roll shapes) on Sunday night for the first time. I just ate my first sandwich (pork roast and mayo, yummy) on it and almost wept with happiness. It is SO good. The texture is PERFECT. It was easy and quick to make. And I can actually see my way to a GF lifestyle…sandwiches have been my bugaboo all along. Thank you, thank you for all your hard work and wonderful recipes!
Fortunately, since peaking in 2001-2002, the overall prevalence of metabolic syndrome in the United States has fallen, primarily due to decreases in the prevalences of hypertriglyceridemia and hypertension—and in spite of increases in the prevalences of hyperglycemia and obesity/waist circumference. [27]  Data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) showed that the age-adjusted prevalence of metabolic syndrome had fallen to approximately 24% in men and 22% in women. [28]
How many calories should I eat a day? A calorie is an amount of energy that a particular food provides. Consuming more calories than needed will result in weight gain, consuming too few will result in weight loss. How many calories a person should eat each day depends on a variety of factors, such as age, size, sex, activity levels, and general health. Read now
SIRT1 is present in the cytosol and nucleus [239], while SIRT3 is primarily located in mitochondria where it regulates bioenergetics and ROS production [239–241]. The sirtuins, particularly SIRT1, appear to participate in a feed-forward cycle of reciprocal activation with AMPK. In skeletal muscle, AMPK indirectly activates SIRT1 by increasing NAD+ through increased mitochondrial β-oxidation [242] and increased expression of nicotinamide phosphoribosyltransferase (NAMPT) [243], which is the rate-limiting enzyme in NAD+ synthesis [244]. Completing the cycle, SIRT1 and SIRT3 can deacetylate and activate LKB1, thereby promoting further activation of AMPK. LKB1 is known to be activated by SIRT1 in adipose and liver [245] and by SIRT3 in cardiac muscle [246].
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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188. Tomas E., Tsao T. S., Saha A. K., et al. Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation. Proceedings of the National Academy of Sciences. 2002;99(25):16309–16313. doi: 10.1073/pnas.222657499. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
I went to buy Xanthan gum at a store in my little town and it was like $17! I wasn’t paying that much, so I made it without but I will be ordering some online. I followed your directions exactly (minus Xanthan) and used Swerve for the sweetener. I couldn’t wait for it to cool so I had a piece right after it came out of the oven, it was delicious! I find it a tad sweet for bread, but that’s ok I’ll just cut back on the sweetener if I want to eat it for a sandwich..all sweeteners are a little different. It had a beautiful crust on it and was a tiny bit crumbly, almost reminds me more of muffin texture, I’m thinking maybe the Xanthan will give it more of a chewy bread texture?
Overweight individuals with metabolic syndrome, insulin resistance, and type 2 diabetes are likely to see improvements in the clinical markers of disease risk with a well-formulated very-low-carbohydrate diet. Glucose control improves due to less glucose introduction and improved insulin sensitivity. In addition to reducing weight, especially truncal obesity and insulin resistance, low-carb diets also may help improve blood pressure, blood glucose regulation, triglycerides, and HDL cholesterol levels. However, LDL cholesterol may increase on this diet.
When the kidneys filter blood, metabolic substrates such as glucose and ketones are re-absorbed to prevent energy wastage. If blood levels of a metabolite exceed the capacity of the kidney to reabsorb them, then a ‘spillover’ effect occurs and the metabolite (i.e. glucose or ketones) appear in the urine. However, urine is not a very reliable measure. Firstly, whilst following a ketogenic diet, adaptation occurs over time that means more ketones are reabsorbed in comparison to the early phase of the diet9. Furthermore, at higher levels of ketones, the appearance in the urine does not correlate to levels in the blood10. Similarly, after consumption of exogenous ketones, urine ketone levels were not in proportion to the levels in the blood11 this may be because of the rapid onset of ketosis in comparison to when ketosis is achieved with fasting or diet. Therefore urine test strips are useful as a guide but have several disadvantages to their use to accurately quantify levels of ketosis. 
Eat more fruits and vegetables. According to the 2015-2020 Dietary Guidelines, a person on a 2,000-calorie-per-day diet should eat 2.5 cups of vegetables and 2 cups of fruit a day. This amount will vary depending on how many calories you need. Be sure to choose a variety of fruits and vegetables. Different fruits and vegetables have different amounts and types of nutrients.
I have AS and am on a no starch diet to control the pain, which works very well for me. So I’m wondering if you have any idea how much starch is in the PH before I order it only to have the iodine test turn it black for starch, which would mean I can’t use and I’d have to throw it out? I can mix up my own baking powder without corn starch and all of the other ingredients are safe for me to eat, so my only concern is the PH. It looks so delicious and I’ve yet to find a truly tasty starch free bread recipe.

Many questions about the role of such an important intermediate of lipid metabolism remains unanswered, e.g., the role of BHB in food control. For example, whether or not BHB could act as a satiety signal in the brain, considering its role in energy supply to CNS. We have to consider that the effects of KBs on hunger reduction can only be seen after many days following fasting or KD initiation (Paoli et al., 2010); this is consistent with the abovementioned threshold of brain utilization of KB as an energy source, i.e., 4 mmol/L (Veech, 2004), which is close to the Km for the monocarboxylate transporter (Leino et al., 2001). During the first days of fasting or KD there is a rise of BHB and adiponectin concentrations (Halberg et al., 2005). One of the putative causes of hunger in starved humans may be due—together with other causes—to adiponectin. When adiponectin binds to its receptor AdipoR1, AMP-activated protein kinase (AMPK) is phosphorylated in the ARC of the hypothalamus (Valassi et al., 2008). The increase of AMPK activity in the hypothalamus may increase food intake and hepatic glucose output in mice while the decrease seems to reduce food intake (Zhang et al., 2009). KDs can also act similarly to a caloric restriction on AMPK (Newman and Verdin, 2014). Interestingly, AMPK seems to have opposing actions on the liver, muscle tissues and the brain: in liver and muscle AMPK activation increases FA oxidation by decreasing malonyl-CoA concentrations (Malonyl-CoA is the first intermediate in the lipogenic pathway and is also an inhibitor of carnitine palmitoyltransferase-1 (CPT-1). CPT-1 activity can be limiting for FA oxidation), through the inactivation of the acetyl-CoA carboxylase 1 (ACC1). AMPK can also increase the activity of malonyl-CoA decarboxylase (MCD), which enhances the decrease of malonyl-CoA levels.
This is now my go to for lo-carb bread recipe. It is SO EASY! I made it last weekend, Instead of Xanthan gum I used konjac root powder, it worked just fine, my baking time was more like 50 minutes and I did cover the top loosely with foil for the first 15 minutes so the top wouldn’t brown so quickly (maybe why my cooking time was so long?) I also added a pinch of Bakers yeast (brewers yeast is NOT gluten free) just for flavor and stevia 3/4 T. This bread makes really good grilled cheese or avocado toast! Very yummy! Thanks for this recipe!
Cheryl, We use beef gelatin in this recipe to act as a binder and add a bit more chewiness to help simulate regular bread. (If you’re interested, we talk more about using beef gelatin in keto baking in this post: https://theketoqueens.com/crispy-low-carb-indian-flatbread-recipe/.) We haven’t experimented with this recipe to omit the beef gelatin, but you might be able to get a similar result using a bit more psyllium husk powder, flaxseed meal, ground chia seeds, xanthan gum, or guar gum. If you decide to play around with the recipe, please let us know how it goes!