Like many variables in diet, health, and disease, it behooves us to look beyond the bumper sticker explanation. I want to highlight a couple of posts I wrote, to attempt to provide a little more nuance and understanding to the subject: “Ketosis — advantaged or misunderstood state?” Parts I and II. Part I follows below. I’m hoping to write more on the topic in the not-too-distant future since there’s been a number of intriguing papers published recently (certainly since 2012). But I also wanted to bring these back into focus in light of the information I’m seeing more of on the interwebz. (You can also visit the Ketosis section of the site to view more articles on the subject.)
Ketogenic and low-carbohydrate diets greatly increase reliance on fat oxidation [78–89], which would logically be expected to increase mitochondrial respiration and mtROS production and, in turn, induce mitohormesis. Furthermore, mtROS produced through RET appears to have particular relevance to hormetic adaptation, including increased lifespan [90]. Nutritional ketosis is likely to increase RET by altering the FADH2 to NADH ratio. As the primary source of acetyl CoA shifts from glycolysis to β-oxidation and ketolysis, this ratio increases, more than doubling for β-oxidation of longer-chain fatty acids. Electrons from FADH2 reduce the CoQ pool through complex II and ETF-QO, thereby increasing RET [91, 92]. This induction of RET by alteration of substrate availability can also be influenced by configuration of mtETC complexes into supercomplexes [90]. The greater potential for mtROS production through RET is consistent with evidence of mitochondria producing more H2O2 during oxidation of palmitoyl carnitine versus pyruvate [93, 94]. Furthermore, succinate is generated during ketolysis by succinyl-CoA:3-oxoacid CoA-transferase (SCOT), which also promotes RET by reducing the CoQ pool through complex II. Demonstrating the likely role of RET in mitohormesis, particularly within the context of nutritional ketosis, extension of lifespan in C. elegans through BHB treatment is dependent on both complex I function and expression of bioenergetic and antioxidant proteins [95].

To encourage ketone production, the amount of insulin in your bloodstream must be low. The lower your insulin, the higher your ketone production. And when you have a well-controlled, sufficiently large amount of ketones in your blood, it’s basically proof that your insulin is very low – and therefore, that you’re enjoying the maximum effect of your low-carbohydrate diet. That’s what’s called optimal ketosis.

224. Noakes M., Foster P. R., Keogh J. B., James A. P., Mamo J. C., Clifton P. M. Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutrition & Metabolism. 2006;3:p. 7. doi: 10.1186/1743-7075-3-7. [PMC free article] [PubMed] [CrossRef] [Google Scholar]


Most people who have metabolic syndrome have insulin resistance. The body makes insulin to move glucose (sugar) into cells for use as energy. Obesity, commonly found in people with metabolic syndrome, makes it more difficult for cells in the body to respond to insulin. If the body can’t make enough insulin to override the resistance, the blood sugar level increases, causing type 2 diabetes. Metabolic syndrome may be a start of the development of type 2 diabetes.
Ketosis occurs either as a result of increased fat oxidation, whilst fasting or following a strict ketosis diet plan (ENDOGENOUS ketosis), or after consuming a ketone supplement (EXOGENOUS ketosis). When in a state of ketosis the body can use ketones to provide a fuel for cellular respiration instead of its usual substrates: carbohydrate, fat or protein. 
Whilst the diet is broadly acknowledged to be safe strategy where medications have failed, side effects such as kidney stones, hyperlipidemia and can occur47. Furthermore, maintaining dietary adherence in young school age children can be very challenging for caregivers. Exogenous ketones may be an alternative or a adjunct to the ketogenic diet in epilepsy. Early work suggests that exogenous ketones could have antiseizure effects. Injection of the ketones acetoacetate and acetone have been found to have anticonvulsant properties in animal models48, and an acetoacetate diester was found to protect against seizures in rats exposed to high levels of oxygen49. Further studies are required to understand specifically how ketone bodies affect seizure control, however for children who experience daily seizures a combination of the ketogenic diet and exogenous ketones could be helpful to manage their condition.    
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Although the first formal definition of metabolic syndrome entered medical textbooks not so long ago (1998), it is as widespread as pimples and the common cold . According to the American Heart Association, 47 million Americans have it. That's almost a staggering one out of every six people. The syndrome runs in families and is more common among African-Americans, Hispanics, Asians, and Native Americans. The risks of developing metabolic syndrome increases as you age.
Jennifer, The yeast has no carbs. The coconut sugar does have carbs, but the yeast feeds on it and through the process of fermentation uses the sugar for energy and releases carbon dioxide gas as a result. The yeast is for flavor, aroma, and in our opinion does help with a little bit of rise. Additionally, we don’t like to consider any foods “bad”, “off-limits”, or not keto. Instead, we opt to mainly eat nourishing real foods that fit into our daily macro intake. We hope this helps! Best of luck on your keto journey.

Embarrassing admission: I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA.  I am so embarrassed by my complete stupidity and utter failure to pick up a single scientific article to fact check this dogma I was spewing to this poor patient. If you’re reading this, sir, please forgive me. You deserved a smarter doctor.
Our keto bread recipe has a beautiful golden crust. It has great structure with a lovely rise and perfect bread-like crumb. It slices well for sandwiches or toasting, but you don’t have to toast or grill it to make it taste good. Sliced with a smear of salted butter is keto perfection. And it actually tastes like bread, not eggs or almonds or coconut. Additionally, this bread will keep well wrapped in the fridge for up to a week!
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