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Glucose. Usually a fasting glucose test is performed but, in some cases, a healthcare practitioner may also order a post prandial glucose (after a meal) or a GTT (glucose tolerance test – several glucose tests that are taken before and at timed intervals after a glucose challenge). The goal of glucose testing is to determine whether a person has diabetes or a decreased ability to process glucose (impaired glucose tolerance), which can eventually result in diabetes.
Additional research has raised the possibility that metabolic syndrome adversely affects neurocognitive performance. [70] In particular, metabolic syndrome has been blamed for accelerated cognitive aging. [71] Patients with mental illnesses also face increased cardiometabolic risk due at least in part to socioeconomic factors such as greater poverty and poorer access to medical care. [72, 73]
It is known that different dietary components exert some effects on gut microbiome composition, mainly in relation to obesity and inflammatory states. In general, a Mediterranean diet has a positive effect while a high-protein diet seems to have detrimental effects due to putrefaction phenomena (Lopez-Legarrea et al., 2014; Flint et al., 2015). Few data are available at this time about the effects of KD on gut microbiota. For example, a study by Crawford et al. (2009) investigated the regulation of myocardial ketone body metabolism by the gut microbiota and demonstrated that, during fasting, the presence of gut microbiota improved the supply of ketone bodies to the heart where KBs were oxidized. In the absence of a microbiota, low levels of KB was associated with a related increase in glucose utilization, but heart weight was still significantly reduced. The myocardial-mass reduction was completely reversed in germ-free mice feeded with a ketogenic diet. Regarding food control we can hypothesize that the particular metabolic state of ketosis could provide some benefit to weight and food control via synergic actions between butyrate production by gut bacteria and circulating high blood ketones (Sanz et al., 2015).
I’ve done the bread today, I used ultra fine almond flour and didn’t read the warning on the packet that the amounts you shall use are less than fo normal normal almond flour. So the bread came out really dense and a little wet. I did slice it on a food slicer in very thin slices and dried them in the oven which gave great cracker-like bread which is amazing with cheese.

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.
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This paleo keto bread recipe makes a delicious option for coconut lovers. For a low-fuss loaf, blend coconut flour with ingredients like eggs, coconut oil, and salt — then bake away for a sturdy bread with only 1.3 net carbs per serving. Make this recipe totally nut-free (and more Bulletproof) by swapping almond milk with full-fat canned coconut milk.
I read through aaaaallllll the comments for research before I made this bread, one thing I noticed when making your protein buns was – when I used 2 teaspoons of baking powder they deflated when exiting the oven. When I reduced the BP to 1.5 teaspoons, they turned out fine. I made two batches with 2 tsp of BP – they turned out like raisins, and 2 batches with 1.5 tsp of BP and they turned out fine. No one posting mentioned adjusting the baking powder – perhaps that would help in this recipe since deflating is a problem, maybe there is too much chemical loft for the non-gluten structure to handle?
Hi Sahil, this is the first time I have seen a video from am so used to the 800Watt that and I love the way you show us how to make the Keto bread in a mug. But can you pleas tell me how many Watt your Microwave is as my new one is 1200 Watt and I am so used to the old 800Watt Microwave that I noticed that everything is getting cooked much quicker and I don’t want to over cook the bread.

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.
No you are not the only one who is trying the recipe, trust me, these people commenting did try it and sent me photos of their breads. You can also watch the short video on how to make it. I have tried it many times. You are probably not reading the servings and nutritional information- I mean 1 tbsp, because these are individual breads, baked in ramekins. One cup of every ingredient won’t fit on a single ramekin.

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.


The gastrointestinal tract (GIT) plays a central role in the control of energy balance. Many molecules produced by the GIT exert hunger or satiety effects on the brain. Ghrelin is a peptide produced mainly by the stomach's oxyntic cells that stimulates ghrelin secretion in the hypophysis and has some neuroendocrine activities. However, its orexigenic properties are the most relevant to us and ghrelin is the only known peripheral orexigenic hormone (Date, 2012). Cholecystokinin (CCK) is a peptide produced mainly in the duodenum and jejunum that acts on the vagus nerve and directly on the hypothalamic nuclei. CCK is an anorexigenic factor and it reduces food intake, meal size and duration (Murphy et al., 2006). Three other related hormones are pancreatic polypeptide (PP), amylin, and peptide YY (PYY). PP is a peptide produced by the endocrine pancreas in relation to the caloric content of meals, and it reduces food intake both in rodents and humans. Amylin is a peptide co-secreted with insulin; its main effect on food control is a reduction of meal sizes and food intake (Murphy et al., 2006). Peptide YY (PYY) is produced in the gut and is similar to PP. PYY is stored in intestinal cells and released into the circulation as PYY3−36, a truncated form of PYY. The release of PYY3−36 is dependent on a meal's caloric and fat content (Veldhorst et al., 2008). The glucagon-like peptide 1 (GLP-1) is produced by the cleavage of pro-glucagon gene in the intestine. It acts as incretin at a pancreatic level, promoting insulin secretion and as neuro hormone on hypothalamic nuclei, inducing satiety (Valassi et al., 2008).
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Metabolic syndrome is a clustering of cardiovascular risk factors that leads to an increased risk for premature cardiovascular disease and increased susceptibility of developing type 2 diabetes mellitus. The syndrome represents a collection of multiple derangements that include elevated blood pressure, impaired glucose tolerance or insulin resistance, atherogenic dyslipidemia (i.e., high triglycerides, low high‐density lipoprotein [HDL] cholesterol, and small low‐density lipoprotein [LDL] particles), proinflammatory and prothrombotic properties, and obesity, with a particular contribution of abdominal obesity. There are two definitions for adults: World Health Organization, 1998 and the National Cholesterol Education Panel (NCEP), Third Adult Treatment Panel, 2001.
When your carb intake is that low, your body can't burn glucose (a.k.a the sugar from carbs) for energy like it normally would. So instead, it burns fat for energy, a process that then releases ketones as a byproduct, says Eric Klett, M.D. an endocrinologist and associate professor of medicine and nutrition at the University of North Carolina at Chapel Hill. (This process explains why people on the keto diet see such crazy weight-loss results.)
sdLDL. This is a measurement of the number of small dense low-density lipoprotein molecules a person has. LDL varies in size, and the smaller denser molecules, which tend to form when elevated triglycerides and VLDL are present in the blood, are thought to be more aggressive in causing atherosclerosis. This test is now commercially available, but is not performed by many laboratories and is not ordered frequently. Its ultimate clinical utility has yet to be determined. It may be evaluated in a LDL particle testing.
Some investigators feel that mitochondrial dysfunction and compromised brain glucose metabolism may play a role in the development of autism. As autism is sometimes accompanied by seizures such as those seen in epilepsy (which could be improved by the ketogenic diet), the diet has been trialled in a small number of case studies. These cases have shown that the ketogenic diet can lead to improvements in the childhood autism rating scale score 78 ,79, however dietary adherence may prove even more of a challenge with these children, decreasing the viability of the ketogenic diet as an intervention.   
314. Wadley G. D., Nicolas M. A., Hiam D. S., McConell G. K. Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training. American Journal of Physiology-Endocrinology and Metabolism. 2013;304(8):E853–E862. doi: 10.1152/ajpendo.00568.2012. [PubMed] [CrossRef] [Google Scholar]

Conversely, the term “ketone bodies” refers to 3 very specific molecules: acetone, acetoacetone (or acetoacetic acid), and beta-hydroxybutyrate (or beta-hydroxybutyric acid), shown below, of which only 2 are technically ketones.  (The reason beta-hydroxybutyrate, or B-OHB, is not technically a ketone is that the carbon double-bonded to the oxygen is bonded to an –OH group on one side, technically making B-OHB a carboxylic acid for anyone keeping score.)


the abnormal accumulation of ketones in the body as a result of excessive breakdown of fats caused by a deficiency or inadequate use of carbohydrates. Fatty acids are metabolized instead, and the end products, ketones, begin to accumulate. This condition is seen in starvation, occasionally in pregnancy if the intake of protein and carbohydrates is inadequate, and most frequently in diabetes mellitus. It is characterized by ketonuria, loss of potassium in the urine, and a fruity odor of acetone on the breath. Untreated, ketosis may progress to ketoacidosis, coma, and death. See also diabetes mellitus, ketoacidosis, starvation. ketotic, adj.

tips for making this bread with coconut flour and those getting purple results! i made half the recipe and made the following changes: 3/4 cups of water, 1 teaspoon baking powder, 1/2 teaspoon baking soda. my bread which previously came out purple and with very dense patches came up much fluffier and with more bread like ‘holes’ and also had the colour of normal brown bread! i baked it in a small loaf and the bread rose a lot but the top half was basically a tunnel. the rest of it is good ‘bread’ though! 🙂


The sirtuin isoforms SIRT1 [232, 233] and SIRT3 [234–236] are nicotinamide adenine dinucleotide- (NAD+) dependent deacetylases associated with longevity. Many reactions are regulated by the redox state of NAD+ and its phosphorylated form, NADP+. Among these reactions, a prominent role of reduced NADP+ (i.e., NADPH) is to support reductive biosynthesis and antioxidant defense, requiring the NADP+/NADPH ratio to be kept low [237]. In contrast, the NAD+/NADH ratio is kept high to support energy metabolism [237], thereby linking sirtuin function to bioenergetic status [238]. Although sirtuins are inhibited by high concentrations of NADH, their activity is influenced more by absolute NAD+ concentration than the NAD+/NADH ratio [238].
Where does nutrition info come from? Nutrition facts are provided as a courtesy, sourced from the USDA Food Database. You can find individual ingredient carb counts we use in the Low Carb & Keto Food List. Carb count excludes sugar alcohols. Net carb count excludes both fiber and sugar alcohols, because these do not affect blood sugar in most people. We try to be accurate, but feel free to make your own calculations.
A ketogenic diet could be an interesting alternative to treat certain conditions, and may accelerate weight loss. But it is hard to follow and it can be heavy on red meat and other fatty, processed, and salty foods that are notoriously unhealthy. We also do not know much about its long-term effects, probably because it’s so hard to stick with that people can’t eat this way for a long time. It is also important to remember that “yo-yo diets” that lead to rapid weight loss fluctuation are associated with increased mortality. Instead of engaging in the next popular diet that would last only a few weeks to months (for most people that includes a ketogenic diet), try to embrace change that is sustainable over the long term. A balanced, unprocessed diet, rich in very colorful fruits and vegetables, lean meats, fish, whole grains, nuts, seeds, olive oil, and lots of water seems to have the best evidence for a long, healthier, vibrant life.

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].

Hey Maria, I am baking my third loaf of your amazing bread. I’ve been having trouble with it rising and keeping risen, but it is still delicious. This time it has risen to new heights and I’m hoping it stay high. I don’t usually make comments because I almost always make changes to recipes. I added onion powder, garlic powder and caraway seeds. It bothers me when people give recipes poor ratings after they have changed them. Anyway, the reason for my comment is to thank you and tell you how brilliant, amazing and stupendous you are. Using psyllium is genius. I have been making various low carb breads for years, some that I invented, others not. Anyway, nothing I have made has ever come close to the taste or texture of yours. Thank you, thank you, thank you.
Additional indications of exogenous BHB upregulating antioxidant defense have been observed, although without consideration of HDAC inhibition. In rats, injection of BHB has increased activities of SOD and catalase and prevented the increase in lipid peroxidation and decreases in SOD, catalase, and GSH induced by paraquat injection, all of which were observed in kidney homogenate [104]. Furthermore, BHB also prevented the paraquat-induced decrease in nuclear NFE2L2, indicating involvement of antioxidant signaling [104]. Similarly, BHB treatment has increased FOXO3a, SOD2, and catalase content in cardiomyocytes [105], indicating that BHB may also influence antioxidant defense in the heart. In this study, BHB also prevented the decrease of FOXO3a, SOD2, and catalase content that resulted from H2O2 treatment [105]. Despite the amount of research that has been done on the antiseizure mechanisms of ketogenic diets, the influence of BHB on HDAC inhibition and related antioxidant defense appears to have not yet been investigated in brain tissue. However, BHB appears to inhibit HDAC2 in microvascular and neuronal brain cells [106], and BHB-induced HDAC inhibition is thought to have a role in the antiseizure effects of ketogenic diets [107].
Brittany, Thank you so much for leaving a comment! Without being there in the kitchen with you, it’s difficult to say what the issue was; however, I can definitely help you troubleshoot…did you cook it for the full amount of time the recipe calls for, and did you cover the top with foil for the last 15 minutes? If so, there might be an issue with your oven’s calibration (you can get an inexpensive oven thermometer to check this). Another tip is to let your eggs come to room temperature first. Another factor is the altitude at which you’re baking; if you’re at high altitude, you might need to slightly adjust the oven temperature and bake time. The other thing to remember is that there will usually be a little bit of fall to most keto breads (in fact, every keto bread we’ve ever made) because keto flours lack gluten and are naturally quite dense; however, you can see in the photos, we still got a good rise on this loaf. I hope these tips help!
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