Excess abdominal fat leads to excess free fatty acids in the portal vein, increasing fat accumulation in the liver. Fat also accumulates in muscle cells. Insulin resistance develops, with hyperinsulinemia. Glucose metabolism is impaired, and dyslipidemias and hypertension develop. Serum uric acid levels are typically elevated (increasing risk of gout), and a prothrombotic state (with increased levels of fibrinogen and plasminogen activator inhibitor I) and an inflammatory state develop.
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Metabolic syndrome (metabolic syndrome X, insulin resistance syndrome, dysmetabolic syndrome, hypertriglyceridaemic waist, obesity syndrome, Reaven syndrome) is the name for a group of risk factors that increase the risk for ischaemic heart disease (IHD), diabetes and stroke (Fig. 23.1). The metabolic syndrome is diagnosed when at least three of the IHD risk factors listed in Table 23.1 are present. Whether the syndrome, which affects possibly 25% of the US population, is a specific syndrome, and nothing more than the sum of its parts, is controversial.
Too much fat at the waist . Although obesity in general raises your risk of metabolic syndrome, excess belly fat (being “apple-shaped”) is the riskiest kind of fat, defined as more than 40 inches around the waist for men, or more than 35 inches for women. Ask your doctor about different measurements for your ethnicity, Ndumele says. “Individuals of Asian descent are thought to have an increased risk at a lower threshold of belly fat, for example.”
Insulin resistance. Insulin is a hormone that helps your body use glucose -- a simple sugar made from the food you eat -- as energy. In people with insulin resistance, the insulin doesn't work as well, so your body keeps making more and more of it to cope with the rising level of glucose. Eventually, this can lead to diabetes. Insulin resistance is closely connected to having excess weight in the belly.
Despite continuous advances in the medical world, obesity continues to remain a major worldwide health hazard with adult mortality as high as 2.8 million per year. The majority of chronic diseases like diabetes, hypertension, and heart disease are largely related to obesity which is usually a product of unhealthy lifestyle and poor dietary habits. Appropriately tailored diet regimens for weight reduction can help manage the obesity epidemic to some extent. One diet regimen that has proven to be very effective for rapid weight loss is a very-low-carbohydrate and high-fat ketogenic diet.[1][2][3]
Maria, can you clarify the recipe as far as fluid ounces versus weighted ounces? For example, for the boiling water, 1.5 cups of water is 12 fluid ounces, but 1.5 cups of water does not weigh 12 weighted ounces. As I watch your video, you weigh the boiling water in a measuring cup, but once again I’m not sure if it’s supposed to be 12 fluid or weighted ounces. And is that true for the vinegar and egg whites as well… fluid ounces versus weighted ounces?
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.

As a matter of fact, in animal models intracerebroventricular injections of long-chain FA reduced hypothalamic expression of NPY. NPY is an important orexogenic neuropeptide that is a downstream target of leptin and insulin in the hypothalamus. In some forms of hyperphagic obesity, characterized by elevated plasma leptin and insulin levels, the lack of action of insulin on NPY expression could explain the pathological condition. Central administration of oleic acid, fatty-acid synthase, or CPT-1 inhibitors prevents the rise in hypothalamic NPY mRNA induced by fasting (Obici et al., 2003). But glucose level is also involved in KD's food control mechanisms. According to glucostatic theory (Mayer, 1955) data indicates that ketosis did not influence FA glucose but instead stimulated the elevation of post-prandial glucose (Sumithran and Proietto, 2013) in non-diabetic subjects, while in diabetics there was a reduction of fasting glucose (Westman et al., 2008). It is important to note that carbohydrate availability may increase cellular levels of long-chain FA-CoA through an increase of malonyl-CoA, which inhibits oxidation of FAs.
Attempt #4 or 5, I lost count 🙂 I measured everything by weight (ounces and grams as you listed) not by cups or tsps, etc. Put in oven at 375 since I don’t have convection and the previous attempts didn’t rise. This one rose beautifully! Nice beautiful color! Cooked 80 minutes. Let cool completely in my 8×4 metal loaf pan. Several hours later, I decided to take out of pan and cut a slice. It caved a little in on the sides, it looks similar to your 12 oz water picture, but it is wet. I’m not sure you’d call it gummy but definitely too much moisture again. And, I thought I finally had one! Back to the testing…I’ve gone thru 1/2 my Honeyville 5 lb bag and haven’t had one successful loaf yet 🙁
KBs can cross the BBB but not in a homogenous manner. For example, past experiments have demonstrated that BHB utilization is different in various brain areas (Hawkins and Biebuyck, 1979). Areas without BBB, hypothalamic regions and the lower cortical layers have a higher BHB metabolism compared to the lower one of the basal ganglia (Hawkins and Biebuyck, 1979). Also the metabolic meaning of the three KBs is different: while the main KB produced in the liver is AcAc, the primary circulating ketone is BHB. The third one, acetone, is produced by spontaneous decarboxylation of AcAc, and it is the cause of the classic “fruity breath.” Acetone does not have any metabolic functions, but it can be used as a clinical diagnostic marker. BHB acid is not, strictly speaking, a KB because the ketone moiety has been reduced to a hydroxyl group. Under normal conditions the production of free AcAc is negligible and this compound, transported via the blood stream, is easily metabolized by various tissues including skeletal muscles and the heart. In conditions of overproduction, AcAc accumulates above normal levels and a part is converted to the other two KBs. The presence of KBs in the blood and their elimination via urine causes ketonemia and ketonuria. Apart from being the fundamental energy supply for CNS, glucose is necessary for the replenishment of the quota of oxaloacetate, since this intermediate of the tricarboxylic acid cycle (TCA) is labile at body temperature and cannot be accumulated in the mitochondrial matrix. Hence it is necessary to refurnish the TCA with oxaloacetate via the anaplerotic cycle that derives it from glucose through ATP dependent carboxylation of pyruvic acid by pyruvate carboxylase (Jitrapakdee et al., 2006). This pathway is the only way to create oxaloacetate in mammals. Once produced by the liver, KBs are used by tissues as a source of energy (Fukao et al., 2004; Veech, 2004; McCue, 2010): initially BHB is converted back to AcAc that is subsequently transformed into Acetoacetyl-CoA that undergoes a reaction producing two molecules of Acetyl-CoA to be used in the Krebs cycle (Figure ​(Figure22).
Hunger and satiety are two important mechanisms involved in body weight regulation. Even though humans can regulate food intake by will, there are systems within the central nervous system (CNS) that regulate food intake and energy expenditure. This complex network, whose control center is spread over different brain areas, receives information from adipose tissue, the gastrointestinal tract (GIT), and from blood and peripheral sensory receptors. The actions of the brain's hunger/satiety centers are influenced by nutrients, hormones and other signaling molecules. Ketone bodies are the major source of energy in the periods of fasting and/or carbohydrate shortage and might play a role in food intake control.

Maria, I made this bread today – weighed my ingredients carefully and followed instructions. My only adaptation was adding a little liquid Stevia, cinnamon, and raisins right before putting into the bread pan. It raised nicely but fell a little while cooling and is pretty heavy, although tastes great. Any help on what I did wrong? (I’m not sure my water was boiling enough – it was just starting to bubble, not full rolling boil, when I added it. Would that make the difference?)


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^ Klein MS, Buttchereit N, Miemczyk SP, Immervoll AK, Louis C, Wiedemann S, Junge W, Thaller G, Oefner PJ, Gronwald W (February 2012). "NMR metabolomic analysis of dairy cows reveals milk glycerophosphocholine to phosphocholine ratio as prognostic biomarker for risk of ketosis". Journal of Proteome Research. 11 (2): 1373–81. doi:10.1021/pr201017n. PMID 22098372.
I made this after watching your video – which made all the difference since I realized I could use a electric mixer. I also measured carefully by weighing the egg whites……and it came out PERFECTLY. I’ve been hungry for a piece of toast with my egg in the morning, smothered in your ccnut oil/mac nut spread and cinnamon. Well, I didn’t wait until morning. Couldn’t resist two pieces toasted with my afternoon tea just now. Thanks so much, Maria.

It has recently been proposed that the ARC is required for the coordination of homeostatic circadian systems including temperature and activity. Authors tested this hypothesis by injecting saporin toxin conjugated to leptin into the ARC of rats. Wiater et al. showed that the leptin-sensitive network is required for entrainment of activity by photic cues and entrainment of temperature by food but is not required for entrainment of activity by food or temperature by photic cues (Wiater et al., 2013).
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).
Hi Amber, Yes, the baking powder and egg whites do help it rise a bit, just not as much as regular bread. It’s hard to say what went wrong, if anything. Everyone’s palate is a little different, so it’s possible you just didn’t like it, or maybe something didn’t go as it should have. It could be that the batter and whites weren’t folded together quite enough?
Sigh…..Made it with high hopes and boy did it smell good! I used all your brands and weighed it all, but I wound up with a loaf that did sink, which I don’t care if it sinks, but it was still gelatinous and wet on the inside. I hate wasting so much almond flour, but I will try again. What would you recommend I change? Decrease the water? It puffed up so beautifully and my husband told me it’s a good crust, lol. I cubed up the whole loaf and I’m trying to make it in to croutons now but I’m unsure those wet little cubes will ever dry out. This is my first flop. I have LOVED all your other recipes so far! Thank you!

The best part about this bread is that it makes it so much easier to eat a low carb diet. Yes, there are some savage beasts (joking) that don’t miss bread at all and are happy to just eat bacon seven times a day, but if you’re anything like me, bread was a staple of your diet growing up and you still have a look of yearning in your eyes when they drop that bread basket in the middle of the table at family dinner. I feel your pain. This low carb bread recipe is your shoulder to cry on.
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