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).
Although the majority of links between energy sensing and antioxidant defense are manifested further downstream, there is some direct influence at the level of AMPK and sirtuins. AMPK is activated by oxidative stress [259, 260], likely through ATP depletion and a subsequent increase in the AMP to ATP ratio, or facilitation of tyrosine phosphorylation, which occurs independently of AMP and ATP concentrations . SIRT3 contributes more directly to antioxidant defense by deacetylating and activating SOD2 [261–263]. The overlapping effect of SIRT3 on antioxidant defense and bioenergetics is further supported by SIRT3 knockout increasing lipid peroxidation in conjunction with decreased O2 consumption in mouse skeletal muscle and also by SIRT3 knockdown increasing H2O2 production and decreasing O2 consumption in myoblasts .
The gut-brain link is important not only for the hormones produced by the gut, but also for the long-term body weight regulation. Studies in mice indicate that the gut microbiome influences both sides of the energy balance by contributing to nutrient absorption and regulating host genes that affect adiposity [however there are conflicting reports (Parks et al., 2013; Schele et al., 2013)]. However, it remains uncertain just how important gut microbiota are for nutrient absorption in humans. A cohort study has demonstrated that the nutrient load is a key variable that can influence the gut/fecal bacterial content over short time frames. Furthermore, the observed associations between gut microbes and nutrient absorption indicates a possible role of the human gut microbiota in the regulation of the nutrient intake and utilization (Jumpertz et al., 2011).
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Bioenergetic and oxidative stressors may be largely responsible for inducing many of the beneficial adaptations to exercise, and for this reason, exercise research provides much of the basis for mitohormesis [4–6]. As previously discussed, an increase in fat oxidation appears to be a prerequisite for increasing mtROS and, in turn, inducing mitohormesis. Given that ketogenic diets prominently increase fat oxidation during submaximal exercise [8, 88, 214–216, 218, 219, 376–381], the combination of the two interventions may induce mitohormetic adaptations to a greater extent. Furthermore, much of the signaling that is relevant to mitohormesis, and likely induced by nutritional ketosis, is also induced by exercise, further suggesting the possibility of an additive or even synergistic effect. Demonstrating this, exercise or muscle contraction increases activity, activation, or expression of AMPK [209–211, 275, 284, 382–386], SIRT1 [384–389], SIRT3 [272, 390, 391], NFE2L2 [358, 360, 392], p38 MAPK [284, 305, 313–315, 393–395], PGC-1α [275–279, 284, 305, 314, 385–389, 396–400], NRF-1 , and TFAM [358, 388, 389]. Exercise also increases expression or activity of antioxidant enzymes [313, 358, 360, 396, 397, 401], uncoupling proteins , and bioenergetic proteins involved in oxidative phosphorylation [396, 397, 400] and the citric acid cycle , all of which appear to be at least partly mediated by ROS-induced activity of p38 MAPK [284, 310, 313, 314], PGC-1α [284, 310, 397, 401], TFAM [310, 314, 358, 397], NRF-1 [310, 358, 397], NRF-2 [358, 360], and NFE2L2 .
In addition to the seaweed and glycogen carbohydrates mentioned above, the Inuit can access many plant sources. The stomach contents of caribou contain a large quantity of partially digested lichens and plants, which the Inuit once considered a delicacy. They also harvested reindeer moss and other lichens directly. The extended daylight of the arctic summer led to a profusion of plant life, and they harvested plant parts including berries, roots and stems, as well as mushrooms. They preserved some gathered plant life to eat during winter, often by dipping it in seal fat.
There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.
Mediterranean diet: Traditional cuisine of countries bordering the Mediterranean Sea, shown to reduce the risk for heart disease, diabetes, some cancers and dementia. On the menu: Plenty of fruits, vegetables and beans, along with olive oil, nuts, whole grains, seafood; moderate amounts of low-fat yogurt, low-fat cheese and poultry; small amounts of red meat and sweets; and wine, in moderation, with meals.
NRF-1 and NRF-2 are transcription factors that increase expression of TFAM , which is required for full initiation of mtDNA transcription [343–345] and hence mitochondrial biogenesis. PGC-1α induces expression of NRF-1 and NRF-2 and facilitates TFAM expression by coactivating NRF-1 . Oxidative stress increases this signaling [346, 347] in conjunction with increased mitochondrial biogenesis . AMPK also contributes to mitochondrial biogenesis, but by inducing mitochondrial fission through phosphorylation of mitochondrial fission factor (MFF) , which is in addition to and independent of AMPK's role in activating PGC-1α.
In general, a person with metabolic syndrome is twice as likely to develop IHD and five times as likely to develop diabetes as someone without it. The probability of developing metabolic syndrome is also closely linked to a lack of physical activity and the fact of being overweight/obese. Other causes include insulin resistance, ethnicity (often Asian), family history, older age and other factors (Box 23.1). Associated diseases and signs may be raised uric acid levels, hepatic steatosis, haemochromatosis and acanthosis nigricans. Metabolic syndrome may be associated with inflammatory periodontal disease.
Nuclear factor erythroid-derived 2-like 2 (NFE2L2 or NRF2) is a transcription factor that has a prominent role in antioxidant signaling and also influences mitochondrial bioenergetics. The NFE2L2 abbreviation is used in this review to avoid confusion with nuclear respiratory factor 2, which despite being a different protein, has overlapping function with NFE2L2 and shares the same NRF2 abbreviation . Although the mechanisms of NFE2L2 signaling are not fully elucidated , oxidative stress has a clear role in interacting with cysteine residues of Kelch-like ECH-associated protein 1 (Keap1), which decreases proteasomal degradation of NFE2L2 and thereby allows entry of NFE2L2 into the nucleus to induce transcription [351–355]. Although the influence of PGC-1α on antioxidant enzyme expression is not dependent on NFE2L2 [76, 356], PGC-1α increases NFE2L2 expression , indicating that NFE2L2 activity is influenced by perturbations in both energy and redox homeostasis. NFE2L2 primarily increases expression of antioxidant enzymes, including SOD1 , SOD2 , catalase [358–361], GPx , NQO1 [354, 359–362], GCL [359–361], GST , GSR [359–361], and Prx1 , but also increases expression of proteins involved in mitochondrial biogenesis and bioenergetics including NRF-1, NRF-2, TFAM, cytochrome c oxidase, and citrate synthase .
When you are separating the eggs if you use the method of pouring the egg from one half of the shell to the other you have to be extremely careful because the sharp shell can easily break the yolk. There are tools that you can purchase that will cradle the yolk and let the white run into a separate bowl. Or, you can use your hands. You need to make sure that your hands are extremely clean and fresh from being washed. Break the egg into one hand and let the white slip between your slightly separate fingers. The yolk will settle into your hand and the white will slip off into the bowl.
Pancakes. They’re a breakfast classic. You see them on just about every breakfast menu you’ve ever looked at and for good reason. But sadly they are not low carb, even in the slightest. So what if I told you that you can have your pancakes on a low carb diet and eat them without feeling guilty? With these Keto Silver Dollar Pancakes you can do just that.
I just tried this recipe in my kitchen. OMG thank you so so much for this wonderful idea! The only thing I think I will try next time is to add just a dash or so of salt to the mug before microwaving (although it already tastes great!). I think it will be fun to experiment with adding some different seasonings or herbs to the batter before baking it, too, just for variety.
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?