I was well aware of the dearth of mainstream knowledge of NK, and particularly the conflation of NK with diabetic ketoacidosis (DKA), a pathologic state that results from the complete or near absence of insulin, which is what prompted my writing and desire to share my journey. And I was once in the wanker category of folks who spoke with “authority” about ketosis, despite knowing somewhere between zero and nothing on the topic. I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 during my residency explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA. Not only that, the ketogenic diet could be seen as the antithesis of a “healthy” diet by conventional standards. I could see how this was a difficult proposition for many to acknowledge.
Based on the reciprocal activation described above, nutritional ketosis is likely to activate SIRT1 and SIRT3 indirectly through activation of AMPK. However, more direct activation of sirtuins by nutritional ketosis is possible. Since reduction of NAD+ to NADH occurs outside of mitochondria only during glycolysis, which is less active during nutritional ketosis, more cytosolic NAD+ remains oxidized, further facilitating activation of SIRT1 [247]. In addition to the decrease in glucose availability during nutritional ketosis, glycolysis may be further inhibited through activation of pyruvate dehydrogenase kinase and subsequent inhibition of pyruvate dehydrogenase (PDH), which occurs in response to dietary carbohydrate restriction [248–251] or infusion of BHB, ACA, or fatty acids [252]. Consistent with the relevance of these factors to nutritional ketosis, a ketogenic diet (% energy: 89 fat, <1 carbohydrate, and 10 protein) has decreased expression of PDH in mouse liver [36]. More importantly, there is direct evidence of nutritional ketosis promoting an increase in NAD+ concentration. Treatment with BHB + ACA (1 mM each) has increased NADH oxidation in rat neocortical mitochondria [109], and a ketogenic diet (Bio-Serv F3666) has increased NAD+ concentration in rat hippocampus [253]. There is also evidence of nutritional ketosis regulating sirtuin expression. A low-carbohydrate (20% of energy) diet combined with ketone esters (6% w/v) has increased SIRT1 protein content in brown adipose of mice [149], and a ketogenic diet (% energy: 90 fat, 0 carbohydrate, and 10 protein) has increased SIRT3 expression in mouse liver [37].
I have great respect for Harvard Medical School. I notice that they support their readers posting comments and I am most appreciative of the article and all the many thoughtful comments by the readers. The readers seem to have the most expertise here and I hope that the doctor who wrote the article will think long and hard about the comments by readers. After 35 years of clinical practice in mental health, I notice that all issues of emotion involve medical issues, nutrition, and the gut bacteria. I would say that these issues and all of the executive brain functions seem to improve with ketogenic principles. For those that apply it in a flexible and smart manner, it appears to improve every area of their lives. I strongly encourage the author of the article to take one class via The Institute for Functional Medicine. If he is open to more learning he can take more classes and get certified. I’m sure a fine doctor, he will be an even better doctor and personally healthier, if he gets more training. Are we all open to new learning(especially us healthcare providers)?
Magnesium seems to be of particular importance when it comes to keeping blood sugar balanced. Deficiencies in this mineral have been linked to an increased risk of diabetes, and one study found that people with the highest magnesium intake were 47 percent less likely to develop diabetes. Supplementing with magnesium has also been shown to lower blood sugar and improve insulin sensitivity. Making a point to consume plenty of magnesium-rich foods—leafy green veggies like spinach and Swiss chard, pumpkin seeds, almonds, black beans, dark chocolate, and avocado—is smart in general, as magnesium plays a role in over 300 biochemical reactions in the body. Nosh on some chromium-rich foods like broccoli, barley, and oats, while you’re at it. One study found that the combined effects of chromium and magnesium were more beneficial than either mineral alone.
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Metabolic syndrome is not merely a single disease but a collection of pathological conditions (i.e., abdominal obesity, insulin resistance, dyslipidemia, hyperglycemia, and hypertension) that increase the risk of developing diabetes and cardiovascular diseases. Low adiponectin levels directly correlate with the development of metabolic syndrome after adjusting for age, sex, and BMI [106,107]. In a study of Japanese adults, an increase in the number of metabolic syndrome components was associated with decreasing adiponectin levels [108]. Hypoadiponectinemia also appears to be a predictor for the future development of metabolic syndrome in obese individuals [109,110].
As you may recall, about 60% of the energy we expend, say 1,800 kcal/day for someone consuming 3,000 kcal/day in weight balance, is purely devoted to keeping us alive by generating enough ATP (“energy currency”) to do 2 things: allow ion gradients to function and allow muscular relaxation.  So, obviously, we can’t tolerate – literally even for one minute – insufficient ATP production.  In fact, one of the most potent toxins known to man (cyanide) exerts its effect on this process by inhibiting the electron transport chain which generates the bulk of the ATP our body produces.  Even the most transient interruption of this process is fatal.
Moreover, recent studies show that the Inuit have evolved a number of rare genetic adaptations that make them especially well suited to eat large amounts of omega-3 fat.[57][58][59] And earlier studies showed that the Inuit have a very high frequency—68% to 81% in certain arctic coastal populations—of an extremely rare autosomal recessive mutation of the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation[60][61]—which results in a rare metabolic disorder known as carnitine palmitoyltransferase 1A (CPT1A) deficiency and promotes hypoketotic hypoglycemia—low levels of ketones and low blood sugar.[62] The condition presents symptoms of a fatty acid and ketogenesis disorder.[62] However, it appears highly beneficial to the Inuit[60] as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis.[63][64] Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells.[64] In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (altered mental state due to improper liver function), enlarged liver and high infant mortality.[65] Inuit have been observed to have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown.[57][66][67][68] Ethnographic texts have documented the Inuit's customary habit of snacking frequently [69] and this may well be a direct consequence of their high prevalence of the CPT1A mutation[70] as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise.[57][70] The high frequency of the CPT1A mutation in the Inuit therefore suggests that it is an important adaptation to their low carbohydrate diet and their extreme environment.[57][60][70]
What are the ideal levels of blood sugar? A blood sugar or blood glucose chart identifies ideal levels throughout the day, especially before and after meals. The charts allow doctors to set targets and monitor diabetes treatment, and they help people with diabetes to self-assess. Learn more about guidelines, interpreting results, and monitoring levels here. Read now
Toasting it did no good as it had that “plastic” smell that Mizzsingbabe mentioned. I tried cutting a very thin piece, loading it with butter, garlic powder, salt and grilling in cast iron fry pan, then broiling it but still cannot get past the plastic/smell taste. So I wasted 3 cups of (not cheap) almond flour along with all the other ingredients.
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Hi Aamash, Sometimes egg whites from a carton are more difficult to beat to stiff peaks, though I do use those all the time myself. Usually it’s best to add some cream of tartar when beating especially if you are using the whites from a carton. This will help them come to stiff peaks. Having the egg whites at room temperature also helps, versus cold from the fridge.
This is brilliant. I made it today not in a mug but a cereal bowl. So it was bigger. I could only eat half. Rather filling. I layered it with cream cheese and a thin slice of smoked ham for mid afternoon snack. Slight bitter after taste which i think is from the baking powder. I am going to make it again with herbs like some others have suggested. Thanks HBK😚
I made this late last night and awoke this morning to a beautiful loaf of delicious bread. It even smelled like bread baking. I had to use a mix of blanched and unblanched almond flour due to running out of blanched. I used NOW psyllium powder which is finer in texture than Jay Robb but all I had on hand so I weighed it (like everything else) but didn’t run it through the blender. I also added a dropper full of stevia glycerite to add a subtle sweetness. I’ve made the bun version before and they were really good but the stevia addition seemed to round out the taste and enhance the flavor in a very satisfying way. It rose beautifully and fell slightly but evenly upon cooling overnight. This loaf is perfect! Tomato sandwich, here I come.

The Mediterranean diet is palatable and easily sustained. In addition, recent studies have shown that when compared to a low fat diet, people on the Mediterranean diet have a greater decrease in body weight, and also had greater improvements in blood pressure, cholesterol levels, and other markers of heart disease -- all of which are important in evaluating and treating metabolic syndrome.

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With all of the nutrition information available today about improving blood sugar, it can be a bit daunting to know which information is correct and which is not. It is so important to look to what science-based evidence and research says about the subject. But even more, we need this science to be translated into easy to understand advice so that we can actually incorporate it into our lives and benefit from it. This is the most important factor.
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).
Oregano and Sage: One group of researchers tested a variety of herbs and spices for a specific antioxidant activity that help to prevent an increase in hemoglobin A1C, a protein maker in the blood that is affected by blood sugar levels. They found that two of the herbs with the highest antioxidant levels were oregano and sage (1)…can you say Italian food?

BHB, in addition to being an important energy substrate, is also a signaling molecule [100–102]. Although not induced through mtROS, BHB inhibits class I and II histone deacetylases (HDACs) in a dose-dependent manner, resulting in greater histone acetylation regardless of whether BHB is elevated through fasting, caloric restriction, or infusion [103]. This inhibition is associated with increased expression of forkhead box O (FOXO) 3a and metallothionein II and increased protein content of FOXO3a, SOD2, and catalase [103]. Consistent with these changes, the kidneys of mice with elevated blood BHB concentrations (∼1.2 mM) were protected from paraquat-induced (50 mg/kg) oxidative damage to proteins and lipids, which was indicated by lower levels of protein carbonyls, 4-HNE, and lipid peroxides [103]. Upregulation of antioxidant defense by BHB-induced HDAC inhibition also appears to be the mechanism through which exogenous BHB extends lifespan in C. elegans [95]. The dependence of this response on FOXO3a, NFE2L2, and several bioenergetic signaling proteins that influence the activities of these two transcription factors [95] is indicative of the overlap between bioenergetics and antioxidant defense that is characteristic of mitohormesis.
I made your bread yesterday. You are right–it IS the best tasting keto bread yet! And I’ve made dozens of recipes through the years! I enlarged it–made a recipe and a half, and used a 9×5 glass pan. I confess, I did make a mess of it at one point. I used carton egg whites, and they didn’t do as well as fresh egg whites do. I ended up with a lot of foam on top and liquid on the bottom. I tried adding the dough to it, but had trouble smoothing out the many lumps. Soooo, I used my hand mixer to mix the whole mess. I put it in the pan and decided to just throw it out, thinking it could never turn into a good loaf of bread. But I went ahead and put it in the oven, and it turned out great! The rise was higher than any other almond flour bread I’ve ever made. So it’s obviously a very “forgivable” recipe. Many thanks!!

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.  


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