Hi Maria, I love your bread recipes but can’t get over the one thing, the gritty texture you get in one every couple bites due to the psyllium husk, I have tried different brands and all have it. I haven’t tried Jay Robs yet. But have you tried ground up chia seeds instead by any chance? I read somewhere to just add twice the amount of water. Thanks
All I can say is WOW! I am a week in on this Keto way of eating and came across this simple recipe. Gotta admit, I didn’t think I would like it…I LOVE IT! So easy to make…took me 20 minutes total! It was light, moist and delicious. I used one small loaf pan, doubled the ingredients and made the regular one and the cheese mix in. Can’t wait to share the rest with my co-workers…we are doing this together. Will be back to check for other recipes. Thank you!
Low blood sugars can be caused by not eating enough, or by trying to lower your sugar too quickly. A blood sugar under 60 is considered dangerous. It can lead to confusion or loss of consciousness, which can be deadly. It is important to have a snack with you at all times in case this happens to you. If it does happen, think about what you did or didn’t do that lead to the low number. If it happens often, start writing things down to help you track what the cause is so that you can avoid it.
People with type 1 diabetes do not produce enough insulin, so their bodies are unable to regulate ketones, which can lead to a dangerous environment. Always consult with your doctor if you have diabetes before changing your diet, and look out for warning signs of ketoacidosis including: excessive thirst, increased urination, nausea, vomiting, abdominal pain, shortness of breath, weakness, fatigue and confusion.

Cirrhosis of the liver refers to a disease in which normal liver cells are replaced by scar tissue caused by alcohol and viral hepatitis B and C. This disease leads to abnormalities in the liver's ability to handle toxins and blood flow, causing internal bleeding, kidney failure, mental confusion, coma, body fluid accumulation, and frequent infections.


If for any reason you get a fail…a spongy loaf , or one with a buble don’t throw it away. Cut off the top bubble and cut into squares or triangles then taost for great pita like chips…cube the bottom sprinkle on some spices and toast or rebake for croutons…I have had my successes and failures wih this loaf but the ingredients are too expensive to waste…another idea would be to toast the bottom after you slice the top off and then add butter, garlic and cheese for a good garlic bread.
I tried this bread and on my first shot, it came out amazing and I didn’t even have a scale to weigh the measurements properly! I just used measuring cups. I ground up my psyllium husk (for all you Canadians, I used ‘Source of Life’ brand from my local health food store, product of BC) to a fine powder using my mini-food processor. Today I’m trying it out again but to my dismay I had only 2 cups of almond flour left so I decided to experiment and add 1/2 cup of coconut flour to the almond flour. I probably should have tweaked the other ingredients but I wasn’t sure how so I used the same amount of everything else. I know normally you have to double the eggs but I’m using both almond and coconut so we’ll see. It’s in the oven now. . .
First of all, almond flour bread will never have EXACTLY the same texture as wheat bread because it lacks the gluten. It will be slightly softer. But. Baking with almond flour is never an exact science. If your almond flour is coarser, just add an extra couple of tbsp next time and the bread will be firmer. Or try reducing the amount of water so it dries out more. I would not recommend changing the amount of egg (unless you used extra large eggs). Hope this helps!
Interestingly, one study showed that weightlifters on a ketogenic diet lost lean body mass, but this did not lead to a decrease in performance [16]. This suggests that the measured reduction of lean body mass was not due to a loss in actual muscle tissue, but probably due to a loss of water and glycogen content in the muscles. Muscles can be made to look bigger or achieve ‘the pump’ by eating lots of carbs which fills them with water and glycogen.

Usually, there are no immediate physical symptoms. Medical problems associated with the metabolic syndrome develop over time. If you are unsure if you have metabolic syndrome, see your healthcare provider. He or she will be able to make the diagnosis by obtaining the necessary tests, including blood pressure, lipid profile (triglycerides and HDL), and blood glucose.
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.
There is one exception to exercising with diabetes. If your blood sugar is too high (such as over 240) and you are spilling ketones into your urine, then exercise is only going to increase your blood sugar. You can buy a dipstick urine test to check for ketones, but the best thing to do would be to talk to your doctor about what is safe for you to do.
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.
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 Maria! Just wanted to say I love this recipe and I found a way to make similar single servings quickly that look like english muffins! I just use a greased ramekin and combine 2 tbsp almond flour, 2 tsp psyllium husk (or 1 tsp powder), pinch of salt and baking powder. Then stir in 2 tbsp + 2 tsp egg whites, 2 tbsp water, 1 tsp olive oil and 1/8 tsp apple cider vinegar. Microwave for 1 min then flip out onto a plate and microwave for another 30 sec. Toast and top with whatever you’d like! 🙂

Alyssa, one more thing. Both the bowl and the beaters need to be spotlessly clean. If there is one hint of oil anywhere the whites will not beat properly. Nicole is correct about not using a plastic bowl. Plastic will even absorb oil to say nothing of the microscopic amounts that get into the surface when it’s scratched. When baking it is always best to use a metal or glass bowl for all of your mixing.
Metabolic syndrome is defined as the presence of a cluster of risk factors that are associated with a significantly higher risk for cardiovascular disease in the general population. The definitions for metabolic syndrome from different expert groups are somewhat different but generally include measures of adiposity, dyslipidemia, hypertension, and abnormal fasting blood glucose levels. Insulin resistance is the dominant but not the only condition underlying the pathogenesis of metabolic syndrome. The different components of the metabolic syndrome are independent risk factors for the development and progression of chronic kidney disease (CKD); hence, patients with metabolic syndrome are significantly more likely to have CKD. Conversely, metabolic syndrome is highly prevalent in patients with ESRD, including among those undergoing maintenance dialysis.
In 1977 and 1978, Gerald B. Phillips developed the concept that risk factors for myocardial infarction concur to form a "constellation of abnormalities" (i.e., glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension) associated not only with heart disease, but also with aging, obesity and other clinical states. He suggested there must be an underlying linking factor, the identification of which could lead to the prevention of cardiovascular disease; he hypothesized that this factor was sex hormones.[66][67]

This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.
I could go on for days about how a good diet can keep your blood sugar in control. To receive the most efficient information, set up a meeting with a dietician to look at your specific needs and you recent sugar readings. They can provide you with recipes and tools which make it easier for you to know exactly what you are putting into your body. 40 states in the United States require insurance companies to cover a meeting with a dietician for those with diabetes. Check with your insurance to see if this benefit is available for you.
L-glutamine, an amino acid needed in large amounts by your body, has been shown to help build lean muscle by suppressing insulin levels and stabilizing blood sugar. One study found that supplementing with L-Glutamine for six weeks improved body composition in patients with type 2 diabetes. L-glutamine has also been shown to help heal a leaky gut, which is important for digestive health and immunity. In addition to supplements, you can find L-glutamine in foods such as bone broth, grass-fed beef, cottage cheese, spirulina, asparagus, broccoli rabe, salmon, and turkey.
Continue to adhere to medical advice for overall health . It’s important to work with your doctor to assess your overall risk of metabolic syndrome and related heart problems, says Ndumele. Get key markers (such as blood pressure, cholesterol, and blood sugar) checked as recommended by your doctor. If you’ve been prescribed medication for high blood pressure, high cholesterol or insulin resistance, be sure to take it as directed.
The metabolic syndrome can be induced by overfeeding with sugar or fructose, particularly concomitantly with high-fat diet.[36] The resulting oversupply of omega-6 fatty acids, particularly arachidonic acid (AA), is an important factor in the pathogenesis of metabolic syndrome.[medical citation needed] Arachidonic acid (with its precursor – linoleic acid) serve as a substrate to the production of inflammatory mediators known as eicosanoids, whereas the arachidonic acid-containing compound diacylglycerol (DAG) is a precursor to the endocannabinoid 2-arachidonoylglycerol (2-AG) while fatty acid amide hydrolase (FAAH) mediates the metabolism of anandamide into arachidonic acid.[37][35] Anandamide can also be produced from N-acylphosphatidylethanolamine via several pathways.[35] Anandamide and 2-AG can also be hydrolized into arachidonic acid, potentially leading to increased eicosanoid synthesis.[35]
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).
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]
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^ Jump up to: a b Cardona A, Pagani L, Antao T, Lawson DJ, Eichstaedt CA, Yngvadottir B, Shwe MT, Wee J, Romero IG, Raj S, Metspalu M, Villems R, Willerslev E, Tyler-Smith C, Malyarchuk BA, Derenko MV, Kivisild T (2014). "Genome-wide analysis of cold adaptation in indigenous Siberian populations". PLOS One. 9 (5): e98076. Bibcode:2014PLoSO...998076C. doi:10.1371/journal.pone.0098076. PMC 4029955. PMID 24847810.
But comprehensive transcriptional profiling of glucose-sensing neurons is challenging, as glucokinase (Gck) and other key proteins that transduce glucose signals are expressed at low levels. Glucose also exerts a hormonal-like action on neurons; electrophysiological recordings demonstrated, for example, that hypoglycemia activates growth hormone-releasing hormone (GHRH) neurons, suggesting a mechanistic link between low blood glucose levels and growth hormone release (Stanley et al., 2013).
^ Jump up to: a b Sinclair, H. M. (1953). "The Diet of Canadian Indians and Eskimos" (PDF). Proceedings of the Nutrition Society. 12 (1): 69–82. doi:10.1079/PNS19530016. ISSN 0029-6651. It is, however, worth noting that according to the customary convention (Woodyatt, 1921 ; Shaffer, 1921) this diet is not ketogenic since the ratio of ketogenic(FA) to ketolytic (G) aliments is 1.09. Indeed, the content of fat would have to exactly double (324 g daily) to make the diet ketogenic (FA/G>1–5).
143. Echtay K. S., Winkler E., Frischmuth K., Klingenberg M. Uncoupling proteins 2 and 3 are highly active H+ transporters and highly nucleotide sensitive when activated by coenzyme Q (ubiquinone) Proceedings of the National Academy of Sciences. 2001;98(4):1416–1421. doi: 10.1073/pnas.98.4.1416. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

What is the link between ketones and diabetes? Ketone is a chemical produced by the body when fats are broken down for energy. Ketone testing is important for people with diabetes, because high levels can lead to diabetic ketoacidosis (DKA), when acid levels become too high in the blood and the person loses consciousness. Find out when and why to do ketone testing. Read now


In addition to increased mitochondrial demand and mtROS production, there are several other commonalities in the mechanisms through which exercise and nutritional ketosis induce adaptive signaling. Exercise-induced activation of AMPK is greater when the exercise is performed in a glycogen depleted state [209–211, 382, 383], and exercise-induced activation of p38 MAPK [315] and PGC-1α [277–279] occurs at least partly through β-adrenergic signaling. Although changes in NAD+ and NADH are difficult to measure and are complicated by conflicting results, exercise is also likely to increase sirtuin activation by increasing the NAD+ to NADH ratio [402].
I just made this bread and it is beautiful! I cannot believe how well it rose-finally a nice rounded full loaf of bread! BUT…the bottom sticks and in order to get it out, I really have to abuse it, which causes some deflation and a not-as-pretty-as-it-should-be loaf. Ended up with a hole on the bottom that got stuck in the pan. I am using a coated aluminum pan with generous amount of coconut oil. Any tips? I put this loaf back in the oven on a cookie sheet to firm up the crust areas that are damaged. Thanks!
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We can say that no species, including humans, could have survived for millions of years without the ability to withstand brief periods of hunger or starvation (Amen-Ra, 2006). These periods of fasting are themselves ketogenic (McCue, 2010) during which the concentrations of insulin and glucose decrease while that of glucagon increases in the attempt to maintain normal blood glucose levels. When the body passes from a condition of food abundance to one of deprivation (or else via VLCKD simulated deprivation), there is, with a slight delay, an increase in the concentration of free FAs as well as KB in the blood. Thus, from this point of view KD could be compared to caloric restriction for fasting. These manipulations of nutrients, both in quantity and quality, seem to not only act on blood glucose/KB level but also to promote changes in metabolic pathways and cellular signaling. How this kind of metabolic condition (ketosis) can affect satiety and hunger mechanisms is still a matter of debate.
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.
^ Jump up to: a b c Clemente FJ, Cardona A, Inchley CE, Peter BM, Jacobs G, Pagani L, Lawson DJ, Antão T, Vicente M, Mitt M, DeGiorgio M, Faltyskova Z, Xue Y, Ayub Q, Szpak M, Mägi R, Eriksson A, Manica A, Raghavan M, Rasmussen M, Rasmussen S, Willerslev E, Vidal-Puig A, Tyler-Smith C, Villems R, Nielsen R, Metspalu M, Malyarchuk B, Derenko M, Kivisild T (October 2014). "A Selective Sweep on a Deleterious Mutation in CPT1A in Arctic Populations". American Journal of Human Genetics. 95 (5): 584–589. doi:10.1016/j.ajhg.2014.09.016. PMC 4225582. PMID 25449608.
Drug treatment may be necessary to address other aspects of metabolic syndrome. Hypertension should be treated. Statins may be prescribed to treat unhealthy lipid levels. Some healthcare practitioners also recommend aspirin to decrease the risk of inappropriate blood clots. Some may prescribe medications to increase insulin sensitivity (although there is not widespread agreement on this).
Follow the adage, “Eat breakfast like a king, lunch like a prince, and dinner like a beggar.” While a small bedtime snack of about 100 to 150 calories is OK, be sure supper is at least four hours before retiring for the day. “Eating more at the end of the day may escalate the risk of obesity and diabetes,” explains Wright, author of The Prediabetes Diet Plan. “Evidence suggests you may need to secrete more insulin to regulate your blood sugar compared to eating earlier in the day.”
People suffering from diabetes and taking insulin or oral hypoglycemic agents suffer severe hypoglycemia if the medications are not appropriately adjusted before initiating this diet. The ketogenic diet is contraindicated in patients with pancreatitis, liver failure, disorders of fat metabolism, primary carnitine deficiency, carnitine palmitoyltransferase deficiency, carnitine translocase deficiency, porphyrias, or pyruvate kinase deficiency. People on a ketogenic diet rarely can have a false positive breath alcohol test. Due to ketonemia, acetone in the body can sometimes be reduced to isopropanol by hepatic alcohol dehydrogenase which can give a false positive alcohol breath test result. 
This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.
First I tried using coconut flour only. The batter was very thick and pasty and the resulting bread was very firm and dry, like a really dry biscuit. It did, however, keep its shape well and toasted up evenly golden-brown in a skillet with oil. I thought about trying again with more liquid, but that wouldn’t solve its fatal flaw: the strong, overwhelming coconut flavor. Even chicken and sun-dried tomato pesto could barely cover it up.
Version two was almond flour only. Right away I could tell the recipe would need some modifications. Almond flour doesn’t soak up nearly as much liquid as coconut flour, resulting in a very soupy batter. I added two more tablespoons of almond flour, which was double the amount of coconut flour, and it still wasn’t nearly as thick. After its short stint in the microwave, this bread turned out very moist, soft, and rather flimsy, but was pleasantly bland enough to go with any filling I wanted.

When you eat out at a nice place, what comes first? Oh, right. The so-perky-you-want-to-strangle-her girl named Brittany whose pleasure it is to serve you today. But I was talking about the meal itself. Most non-fast-food meals start out with a good salad. What could be healthier? Salads are generally low in both calories and carbohydrates. That means they are good for controlling blood sugar and controlling waistline expansion. An added bonus: if you get filled up with salad, you’ll be less hungry when it comes to the rest of the meal—so you’ll eat less of the stuff that’s “bad” for your blood sugar log. Eating less of that other stuff will help you with Tip Number 4.
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Glucose is stored in your liver and released as needed for energy. However, after carb intake has been extremely low for one to two days, these glucose stores become depleted. Your liver can make some glucose from amino acids in the protein you eat via a process known as gluconeogenesis, but not nearly enough to meet the needs of your brain, which requires a constant fuel supply.

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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Ultimately, cancer is highly complex, whereas some tumors may be highly responsive to carbohydrate restriction, others may become adapted to utilise fats or ketones. Cancer, and the treatments currently in use cause unpleasant systemic effects such as muscle wasting and compromise of the immune system, therefore any interventions should be undertaken under the guidance of a doctor. There are limited treatment options available for some types of cancer, many drugs have toxic side effects and many types of cancer have a poor prognosis. In these cases, considering metabolism as an adjunct to conventional treatments is interesting, and offers the potential of another avenue of attack on cancer.  
It is important to note that these herbs and spices are intended to support blood sugar maintenance and are not meant to replace diabetes/hyperglycemic medications. Research does show benefits to incorporating these herbs and spices, so enjoy incorporating them daily into your favorite recipes for a boost of flavor and blood sugar-lowering benefit.
NRF-1 and NRF-2 are transcription factors that increase expression of TFAM [342], 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 [288]. Oxidative stress increases this signaling [346, 347] in conjunction with increased mitochondrial biogenesis [346]. AMPK also contributes to mitochondrial biogenesis, but by inducing mitochondrial fission through phosphorylation of mitochondrial fission factor (MFF) [348], which is in addition to and independent of AMPK's role in activating PGC-1α.
The coordinated effects of AMPK, SIRT1, and SIRT3 are primarily mediated through PGC-1α, which is activated through phosphorylation by AMPK [242, 265] and deacetylation by SIRT1 [77, 242, 266–269]. SIRT3 also increases PGC-1α activity [270], possibly through cAMP response element binding protein (CREB) [271, 272], but the exact mechanism has not been elucidated. In addition to phosphorylating PGC-1α, activated AMPK also increases PGC-1α expression [260, 273–276]. Activation of β2-adrenergic receptors [277–280] and the adiponectin AdipoR1 receptor [281] also increase PGC-1α expression, independently of AMPK activation [278, 281]. PGC-1α activity is increased by oxidative stress [76, 77, 282–284], possibly through activation of AMPK [259, 260] or p38 mitogen-activated protein kinase (MAPK) [283, 284], or inhibition of glycogen synthase kinase 3β, which inhibits PGC-1α through phosphorylation [77, 283]. In contrast, insulin decreases PGC-1α activity through phosphorylation by PKB [285]. Once activated, PGC-1α interacts with the PPAR family of nuclear receptors [286] and the FOXO family of transcription factors [287] to influence expression of a variety of bioenergetic and antioxidant proteins. PGC-1α most notably increases transcription of proteins involved in mitochondrial biogenesis and respiration [76, 242, 265, 267, 269, 274, 279, 282, 285, 288–293] but also increases transcription of antioxidant proteins including SOD1 [76], SOD2 [76, 282, 289, 292–294], catalase [282], GPx [76, 294], thioredoxins [282, 283, 292], TRXR [282, 292], Prx3 [282, 292], and Prx5 [282, 292], as well as the mitochondrial uncoupling proteins UCP2 [76, 265, 282, 288, 294], UCP3 [76, 265, 294], and ANT [76, 295].
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In rats fed a ketogenic diet (Bio-Serv F3666) for 22 days, mitochondrial density (determined by electron microscopy) in the hippocampus increased in conjunction with increased transcription of 39 of the 42 mitochondrial proteins analyzed [162]. Similarly, mitochondrial content (mtDNA copy number) increased in skeletal muscle of mice fed a ketogenic diet (Research Diets D05052004; % energy: 89.5 fat, 0.1 carbohydrate, and 10.4 protein) for 10 months [163]. Higher mtDNA copy number was also observed in skeletal muscle of rats fed a high-fat, low-carbohydrate diet (% energy: 60 fat, 20 carbohydrate, and 20 protein) for 4 weeks in conjunction with daily injections of heparin (0.5 U/g) to increase circulation of fatty acids [87]. In humans, after just 3 days of a low-carbohydrate, high-fat diet (% energy: 50 fat, 34 carbohydrate, and 16 protein), fat oxidation significantly increased and 49% of the variance was explained by mtDNA content [79]. Despite this, the content of mtDNA did not change significantly, but this was expected given the brief duration of the diet.
Since then, it’s safe to say I dove down the rabbit hole. The more I learned, the more I grew tired of reading so much misinformation on the topic. While there are more thoughtful people and articles on the subject of ketosis these days (e.g., here’s a thoughtful video on ketosis and ketogenic diets from one of my most important ketosis mentors, Steve Phinney, a co-founder of Virta Health1Disclosure: I’m an investor in, and advisor to, Virta Health.), there are still pieces like the one Vox published this month, that doesn’t exactly do the topic justice.
You’ll need to use the dreaded E-word: exercise. But don’t freak out on me. I’m not saying you should go out and buy a treadmill or a gym membership. Rather, look for every excuse to exercise your body. Just use it whenever you can during the normal course of the day. Take the stairs instead of the elevator. Park farther from the door. Go fly a kite…on a calm day. At night, circumnavigate the couch during TV commercials.
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.
A combination of baking soda, lemon juice, and baking powder eliminates the need for yeast in this bubbly keto bread recipe. With tons of Italian seasonings, olive oil, and flaky salt sprinkled on top, you’ll want to include this loaf with every meal. Each generous slice is 3 net carbs — and to stay more Bulletproof, simply avoid eating garlic and xanthan gum too often.
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