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[…] One of the things I’ve grown to love over the years is fried eggs with runny yolks. They’ve become a regular breakfast for me on the weekends. However, when I do regular low carb high fat meals, I like to have toast to dip into the egg yolks. Psyllium low carb bread seems to be all the rage right now, so I came up with this coconut flour psyllium husk bread that is perfect with my morning eggs. I’m not really sure who started the low carb psyllium bread trend, but one of the first breads I’ve found was Maria Emmerich’s Amazing Bread. […]
I want you to start drinking. A lot. Of water. (Sorry for the letdown.) In fact, I want you to drink only water. Never, ever, ever drink a calorie. Stick with water, and drink a lot of it. It’s good for you, and like an early salad, water can help keep hunger at bay. I’d also like you to avoid diet sodas, at least on a regular basis. Though they don’t have any calories, diet sodas cause folks who drink a lot of them to have a harder time losing weight. No one is sure why.
With the recent research findings, and the increasing availability of exogenous ketones, it is unsurprising that some authors have said (with a hint of skepticism) that they “could be the next magic bullet’ for athletes39. More research is required to understand the best use cases, doseage protocols, compounds etc, however it is clear that exogenous ketones are a new ‘tool’ in the athlete’s arsenal that can be used to provide an alternative, energetically favourable fuel source without needing dietary manipulation. 
On a keto diet, carbs provide only about 5 percent of daily calories, compared to anywhere between 40–60 percent on a “standard diet.” Reducing carbohydrate consumption this drastically means that the majority of empty calories from highly processed foods must be eliminated from your diet, including things like white bread and rolls, pasta, rice or other grains, sugar-sweetened beverages, desserts, etc. These are the same foods that tend to cause fluctuating blood sugar levels, cravings for more carbs and sugar, low energy and contribute to overeating in general.
We’ve been on the Keto journey since the end of February last year and this is my favourite bread recipe so far, I just made a loaf and it turned out great. I don’t have a food processor so I did use my blender and for ingredients I only used the almond flour, coconut flour, baking powder, butter, salt, 8 egg whites (all I had left in the fridge) and the only optional ingredient I added was stevia. The texture was still really nice without the extra ingredients which is a nice option and this tasted like a regular loaf of bread, I’ll definitely be making this again!!
The key sign of metabolic syndrome is central obesity, also known as visceral, male-pattern or apple-shaped adiposity. It is characterized by adipose tissue accumulation predominantly around the waist and trunk.[5] Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level, impaired fasting glucose, insulin resistance, or prediabetes. Associated conditions include hyperuricemia; fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease; polycystic ovarian syndrome in women and erectile dysfunction in men; and acanthosis nigricans.

This “lazy” keto bread recipe is anything but boring: Crumbling the butter directly into the dough creates moist and tender biscuits for all your sweet and savory recipes. Plus, this recipe takes 30 minutes from start to finish and keeps each biscuit macro-friendly at 3 net carbs. Stay more Bulletproof and use the sour cream and whey protein swaps suggested in the recipe, plus avoid eating flaxseed too often.


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I saw this recipe today and went out and bought the ingredients. I made it exactly like the instructions state. Mine actually did rise while it baked. But there is no yeast in this. Was it the baking powder and egg whites? It’s still fluffy and light. But all I taste is egg whites and coconut from. The coconut flour. I could definitely see how this will be an amazing bread… But I’m not sure what I did wrong. I used 12 egg whites just like the recipe called for. I also used the suggested items. Any idea on what I did wrong? I had to have messed up something…


Apart from administering insulin, the fastest way to lower your blood glucose is to engage in physical activity. Exercise results in an increased sensitivity to insulin. It causes your muscle cells to take up more glucose, leaving less of it to circulate in your bloodstream during and after the physical activity (which means a lower blood glucose when you test). Frequent, regular exercise is very important to good blood glucose control no matter what type of diabetes you have. Research has shown that it is vital in warding off long-term complications like neuropathy, retinopathy, and heart and kidney diseases. Don't forget to check with a doctor, though, before making any major changes to your exercise routine. And, if you have type 1 diabetes and your glucose is 250 mg/dl or higher, check for urine ketones. You should not exercise if ketones are present.
I had the same problem. Everything blended beautifully, rose in oven, then fell. Toothpick came out clean after 45 min of baking. I let it cool and then cut into it this morning and it has raw spots throughout the loaf. I am so disappointed because I killed a dozen eggs to make it and really don’t want to do it again. I wonder if the oven needs to be warmer and the cooking time needs to be increased?
Glycogen influences AMPK activity by binding to a glycogen binding domain on the β regulatory subunit of AMPK [205, 206]. In human and rodent skeletal muscle, AMPK activity is lower when glycogen is bound to this domain [207, 208] and higher when muscle is depleted of glycogen [209–212]. In direct contrast to the effect of AMP and ADP, glycogen inhibits the phosphorylation of AMPK by upstream kinases such as LKB1 [213]. Although muscle glycogen concentration has recently been demonstrated to be similar in ultra-endurance athletes regardless of a ketogenic or high-carbohydrate diet [8], concentrations generally decrease in response to dietary carbohydrate restriction [156, 166, 173, 214–221]. Furthermore, the long-term adaptations to nutritional ketosis that may enable some athletes to replenish glycogen at a normal rate may not apply to less physically active individuals.

Research on cinnamon’s blood sugar-stabilizing powers is a little mixed, and it may not be a wonder spice. But if you’re adding it to an already healthy diet, it may have a subtle benefit. Some studies suggest that cinnamon lowers blood sugar by increasing insulin sensitivity, or making insulin more efficient at moving glucose into cells. Try sprinkling it onto oatmeal or into low-sugar smoothies. Bonus: It tastes delicious!
PGC-1α is also influenced by p38 MAPK, which is well known for being involved in development [301] and adaptation [302] in skeletal muscle. PGC-1α is activated by p38 MAPK [283, 303] through phosphorylation [304], which prevents repression [303] by blocking interaction with the p160 myb binding protein [304]. In addition, expression of PGC-1α is increased by p38 MAPK [305, 306], and the overlap in bioenergetic and antioxidant signaling is further indicated based on p38 MAPK activation by AMPK [307–309], oxidative stress [310–314], and β-adrenergic signaling [280, 315, 316].
Has anyone tried this using a substitute for the eggs/egg whites? My husband seems to be sensitive to eggs (not sure which part, to be honest) and we’ve been making most recipes using agar agar as a substitute (for either whites or whole eggs) but this only works if the egg is a binder. I’m guessing that they are a leavening agent in the bread (please correct me if I’m wrong!) and I don’t know if agar would work in this recipe. I do have VersaWhip 600 – anyone ever tried that in a bread recipe?
This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated.
All of the factors associated with metabolic syndrome are interrelated. Obesity and lack of exercise tend to lead to insulin resistance. Insulin resistance has a negative effect on lipid production, increasing VLDL (very low-density lipoprotein), LDL (low-density lipoprotein – the "bad" cholesterol), and triglyceride levels in the blood and decreasing HDL (high-density lipoprotein – the "good" cholesterol). This can lead to fatty plaque deposits in the arteries which, over time, can lead to cardiovascular disease and strokes. Insulin resistance also leads to increased insulin and glucose levels in the blood. Excess insulin increases sodium retention by the kidneys, which increases blood pressure and can lead to hypertension. Chronically elevated glucose levels in turn damage blood vessels and organs, such as the kidneys. 
In 2005, the American Heart Association (AHA) in conjunction with the NHLBI also released a scientific statement regarding metabolic syndrome that includes a set of criteria that defines the condition. In order to provide more consistency in both patient care and research, the International Diabetes Federation, NHLBI, AHA, World Heart Federation, and the International Association for the Study of Obesity published a joint statement in 2009 that describes a "harmonized" definition of metabolic syndrome. Waist circumference, with population and country-specific criteria, replaced obesity as a measure of body status.
Practically speaking, because it takes several days to raise blood ketone levels by following the ketogenic diet it has been virtually impossible to study the effects of ketosis on brain injury in humans. It is also complicated by the difficulty in quantifying the extent of the damage without repeated imaging and there is a lack of reliable biomarkers for concussion. Furthermore, concussions can’t be ‘administered’ to humans experimentally, making it impossible to study in a controlled setting. Therefore much of the proof of concept research looking a ketosis for concussion has been done in animals. Nevertheless, the results are promising: rats who were given a ketogenic diet or ketone precursors before67 and after68 a controlled concussive injury have were found to have improved brain energy metabolism, and improved cognitive and motor function post injury. Also, giving exogenous ketones as an injection post-injury protected the brain against glutamate induced excitotoxicity69 and alleviated the decrease in brain ATP that occurs due to the depression of glucose metabolism70. Therefore, as scientists’ ability to quantify concussion in humans improves, ketosis could be an interesting intervention to attempt to reduce the harmful after-effects.  

Given the prevalence of this category of illness, and the insidious nature of the conditions, an intervention with minimal side effects (vs. drugs) such as ketosis could be used as a first line intervention before attempting treatment with medication in some cases. However, there is still some way to go before research can conclusively address this possibility, individuals considering the diet should do so with full medical supervision.

While I do not really miss bread I do occasionally like a grilled cheese. I think this will also work well as a hamburger bun this Summer. It is a bit salty even when using unsalted butter, so I might cut that back a bit. It made a great grilled cheese though. I made mine in a small rectangular pan then cut it in half and grilled it in my cast iron pan with cheddar. Wonderful!
The discovery of many appetite-related hormones provided molecular basis for appetite control, decreasing the relevance of the metabolites hypothesis (Karatsoreos et al., 2013). Recently, Sumithran et al. demonstrated that there is a long-term persistence of changes in some peripheral hormones involved in food control (Sumithran et al., 2011). In this study, they found a significant difference in mean levels of many food intake-related hormones 1 year after the cessation of weight loss via the hypocaloric diet. There was a long lasting decrease of anorexigenic compounds: leptin, PYY, cholecystokinin, insulin, and pancreatic peptide and an increase of the orexigenic molecule ghrelin. Moreover, they found that hunger remained elevated 1 year after diet cessation. In a successive study the same group investigated hunger-related hormones after 8 weeks of KD, demonstrating that during ketosis the increase of ghrelin (a strong stimulator of appetite) was suppressed (Sumithran et al., 2013). These results are consistent with those of Ratliff et al (Ratliff et al., 2009), who found no significant change in fasting plasma ghrelin after 12 weeks of VLCD.

Metabolic syndrome is increasing in prevalence, paralleling an increasing epidemic of obesity. In the United States, where almost two thirds of the population is overweight or obese, more than one fourth of the population meets diagnostic criteria for metabolic syndrome. [25] In the United States, data from a 1999-2000 survey showed that the age-adjusted prevalence of metabolic syndrome among adults aged 20 years or older had risen from 27% (data from 1988-1994) to 32%. [26]
Ketosis is a metabolic state in which the liver produces small organic molecules called ketone bodies at “sufficient” levels, which I’ll expand upon later.  First, let’s get the semantics correct. The first confusing thing about ketosis is that ketone bodies are not all – technically — ketones, whose structure is shown below. Technically, the term ketone denotes an organic molecule where a carbon atom, sandwiched between 2 other carbon atoms (denoted by R and R’), is double-bonded to an oxygen atom.
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.
Since then, it’s safe to say I dove down the rabbit hole. The more I learned, the more I grew tired of reading so much misinformation on the topic. While there are more thoughtful people and articles on the subject of ketosis these days (e.g., here’s a thoughtful video on ketosis and ketogenic diets from one of my most important ketosis mentors, Steve Phinney, a co-founder of Virta Health1Disclosure: I’m an investor in, and advisor to, Virta Health.), there are still pieces like the one Vox published this month, that doesn’t exactly do the topic justice.
Perturbations in bioenergetic homeostasis induce signal transduction that leads to upregulation of mitochondrial capacity and antioxidant defense. Three key enzymes involved in the sensing of these perturbations and the subsequent induction of signal transduction are AMP-activated protein kinase (AMPK) and silent mating type information regulation 2 homologues 1 and 3 (SIRT1 and SIRT3).
Like chili, but with a fried egg on it. This recipe is also made with breakfast sausage patties instead of ground beef or turkey to give it a morning twist (and pack in the protein). Pair this recipe from I Breathe I'm Hungry with your usual favorite chili toppings, like sour cream or chives. (Hint: It's also a perfect recipe to break out for early morning football tailgates.)
Not quite sure if I’m doing it wrong but the mixture isn’t liquidy at all, it’s almost dry, it’s a bit difficult to mix and I had to add a tablespoon of water to even mix it. It didn’t come out fluffy looking like yours did, it’s rather dense (I guess from overmixing), but it doesn’t taste bad. I also added a pinch of oregano, cumin and garlic powder. I toasted it and had some hummus with it. 🙂 Any idea how to fix the batter or what I’m doing wrong?
Last point of background: Everything I’ve just presented is based on data from starving subjects.  If one restricts carbohydrate intake, typically to less than about 20-50 gm/day (dependent on timing and carbohydrate composition), and maintains modest but not high protein intake (because protein is gluconeogenic – i.e., protein in excess will be converted to glycogen by the liver), one can induce a state referred to as “nutritional ketosis” with similar physiology to what I’ve just presented without resorting to starvation.  Why you’d do this is something I will discuss later.
Like fiber and protein, fat buffers blood sugar spikes. In fact, unsaturated fats have been specifically linked to improved insulin resistance. Just be sure to avoid refined fats, including trans fats and processed vegetable oils, like corn, soybean, and safflower oils, which can be pro-inflammatory. Sources of quality fats to consider adding to your diet include: nuts, olive oil, ghee, coconut oil, avocado, and fatty fish like salmon.
In dairy cattle, ketosis is a common ailment that usually occurs during the first weeks after giving birth to a calf. Ketosis is in these cases sometimes referred to as acetonemia. A study from 2011 revealed that whether ketosis is developed or not depends on the lipids a cow uses to create butterfat. Animals prone to ketosis mobilize fatty acids from adipose tissue, while robust animals create fatty acids from blood phosphatidylcholine (lecithin). Healthy animals can be recognized by high levels of milk glycerophosphocholine and low levels of milk phosphocholine.[76] Point of care diagnostic tests are available and are reasonably useful.[77]

Ketones may also be important, or even necessary, for the bioenergetic signaling associated with mitohormesis. As will be discussed later, peroxisome proliferator-activated receptor α (PPARα) is a nuclear receptor that is responsible for many of the bioenergetic adaptations associated with nutritional ketosis and mitohormesis [120]. In mice, a ketogenic diet (% energy: 90 fat, 0 carbohydrate, and 10 protein) increased blood BHB concentration to 1-2 mM and upregulated expression of numerous PPARα targets in the liver [37]. However, in mice fed a nonketogenic low-carbohydrate diet (% energy: 75 fat, 15 carbohydrate, and 10 protein), which did not raise blood concentration of BHB, the increased expression of PPARα targets did not occur [37], implying that induction of PPARα signaling by a ketogenic diet is dependent on ketones. This response may be, at least in part, a result of the epigenetic effects of BHB. In addition to HDAC inhibition, BHB also influences gene expression through β-hydroxybutyrylation of histone lysine residues [121]. In the livers of mice subjected to prolonged fasting, this β-hydroxybutyrylation has been associated with upregulation of PPAR signaling, oxidative phosphorylation, fatty acid metabolism, the proteasome, and amino acid metabolism related to redox balance [121]. Upregulation of these pathways is largely influenced by β-hydroxybutyrylation of the histone residue H3K9 [121], which is also involved in the upregulation of antioxidant defense through BHB-induced HDAC inhibition [103]. This potential for BHB to influence expression of both mitochondrial and antioxidant genes through a common histone residue is further indication of the overlap between bioenergetics and antioxidant defense and suggests that if mitohormesis is indeed induced during nutritional ketosis, induction may be dependent on ketones and may therefore not occur during a low-carbohydrate diet that is not ketogenic.
Usually, there are no immediate physical symptoms. Medical problems associated with the metabolic syndrome develop over time. If you are unsure if you have metabolic syndrome, see your healthcare provider. He or she will be able to make the diagnosis by obtaining the necessary tests, including blood pressure, lipid profile (triglycerides and HDL), and blood glucose.
What is the link between ketones and diabetes? Ketone is a chemical produced by the body when fats are broken down for energy. Ketone testing is important for people with diabetes, because high levels can lead to diabetic ketoacidosis (DKA), when acid levels become too high in the blood and the person loses consciousness. Find out when and why to do ketone testing. Read now
As described throughout the previous sections, there are many instances of codependencies and feed-forward loops in bioenergetic and antioxidant signal transduction, which supports the well-known potential for metabolic stimuli, such as diet or exercise, to have a profound physiological influence. Given the central role of mitochondria in oxidative phosphorylation and ROS production, the overlap between bioenergetic and antioxidant signaling is not surprising and is possibly an outcome of evolution favoring efficiency. PGC-1α is at the center of this overlapping and complex network of codependencies. The likely role of PGC-1α as a coactivator of FOXO3a indicates a possible dependence of FOXO3a transcriptional activity on PGC-1α [287], indicating FOXO3a as a central mediator as well. Furthermore, FOXO3a induces transcription of PGC-1α [287, 322, 367], and formation and antioxidant transcriptional activity of the PGC-1α-FOXO3a complex are partly dependent on interaction with SIRT1 [325]. In muscle, expression of many of the bioenergetic and antioxidant proteins previously discussed is dependent on PGC-1α [265]. Upstream, activation of PGC-1α is dependent on AMPK [242] and SIRT1 [242, 269] and partly dependent on SIRT3 [270]. Furthermore, activation of SIRT1 is dependent on AMPK [242], which may also be the case for SIRT3. AMPK and PGC-1α are therefore two key factors, with critical supporting roles of the sirtuins, in the signal transduction linking bioenergetics to antioxidant defense. Further supporting the relevance of this linkage to nutritional ketosis, expression of AMPK, SIRT1, FOXO3a, and NFE2L2 is required for extension of lifespan in C. elegans by exogenous BHB [95], and expression of AMPK, p38 MAPK, and NFE2L2 is required for the extension of lifespan, also in C. elegans, by mitohormesis induced through inhibition of glucose metabolism [73]. The induction of AMPK [259, 260], SIRT3 [263, 329], p38 MAPK [310–313], PGC-1α [76, 77, 260, 282, 283], FOXO3a [324, 331, 333], and NFE2L2 [358–360] activity by oxidative stress also makes this signaling highly relevant to mitohormesis [263, 282, 360], especially given that activation of these proteins has been shown to decrease mitochondrial or cellular ROS [76, 263, 282, 289, 323, 332, 334, 356, 359, 367]. Furthermore, mitochondrial biogenesis [346] and the activities of AMPK [259, 260], SIRT3 [329], p38 MAPK [311, 312], PGC-1α [76, 77, 260, 283], FOXO3a [324], and NFE2L2 [368] are increased by H2O2, more specifically associating this signaling with mitohormesis. Given that AMPK and sirtuins are upstream of the majority of this signaling and that AMPK and sirtuin activities are stimulated by both bioenergetic and oxidative stressors, these stressors are likely the primary signals through which nutritional ketosis may induce the mitochondrial and antioxidant adaptations characteristic of mitohormesis (Figure 2).
I have never commented on a recipe post ever. But i’ve tried so many mug breads and honestly Paola, this is the best hands down. It tasted lovely with a pleasing texture, more biscuit/scone like, which i am not complaining about. I used vanilla whey protein (which was sweetened) omitted the sweetener and used heavy cream in place of sour cream. Such a treat. Will be making again and again for sure.
In low carb and keto baking, we’re concerned with two things: 1) keeping carbs low, and 2) still achieving a baked good that has great flavor and texture (because if we can’t gag it down there’s just no point, right? Lol). Low carb bread recipes are usually gluten free and grain free (although we’ve seen a couple that use oat fiber), but then the challenge is to get creative to get the right combination of ingredients to yield something that rises properly and tastes good.
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