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The only reason to continue to give this bad advice is the lingering fear of natural fat. If you’re going to avoid fat you need to eat more carbohydrates in order to get satiated. But in recent years the old theory about fat being dangerous has been proven incorrect and is today on its way out. Low-fat products are simply unnecessary. So this reason doesn’t hold up either.
Maria – I have been looking at this recipe for years. I have bought everything needed over time, down to the kitchen scale but never baked it. For some reason baking bread made me nervous! Well tonight I bit the bullet and tried it out. It was so easy!! I followed your recipe to a T, measured everything…it came our perfectly! Thank you for all you do! The bread is delicious it’s been years since I’ve enjoyed a slice of bread with butter on it! (Kerry a Gold of course!)
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Hi Maria! I just tried this recipe and it is ABSOLUTELY A.M.A.Z.I.N.G.!! Thank you SOOO much for sharing the recipe! One question- In the recipe you have 2 links to order the Psyllium. I just realized it after I placed my order through the first link, which is from your amazon store- The Frontiers Psyllium. I’m hoping that one works for the bread as good as the Jay Robb Brand!
Fathead dough is a low carb/keto dough that is made out of cream cheese, mozzarella cheese, eggs and a flour substitute. It started out as a pizza crust recipe published by Tom Naughton while he was creating the movie Fat Head. The recipe became an internet viral sensation and has since been adapted and modified for recipes beyond pizza crust, such as breadsticks, bread rolls and bagels.
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Ketosis could benefit patients with PD, as ketones provide an alternative energy source to the brain and also have antiinflammatory effects. Several research groups have shown that the ketogenic diet can have manifold beneficial effects in animal models of PD: alleviating motor symptoms, reducing inflammation, decreasing neuronal loss 61 ,62. Also, an in vitro model of PD (neurons in culture treated with a drug called MPTP) was used to demonstrate that addition of 4 mM of BHB was protective against neurodegeneration52. An early study of the ketogenic diet in PD patients reported very promising results: patients improved their clinical PD ‘score,’ as classified by factors including tremor, balance and mood 63. Whilst there are promising results, further clinical studies are required to demonstrate if the ketogenic diet or exogenous ketones (either alone or in combination) are a tolerable and efficacious intervention for PD.
If you’re sensitive to coffee in the morning, swap it for matcha, which will still give you that caffeine fix in a milder dosage. Plus, matcha has a great flavor that works well with sweet and savory items, like nuts, fruit and seeds. This breakfast bowl by Gnom Gnom uses chia seeds, nut milk, and coconut to provide 10 grams of fat and keeps carbs low at 0.5 net grams. For a smoother texture, add avocado.
Parkinson’s disease (PD) is caused by death of neurons in a region of the brain called the ‘substantia nigra.’ As well as loss of neurons, those that survive accumulate misfolded proteins called “Lewy Bodies,” exhibit increased inflammation and impaired mitochondrial function. PD is most common in individuals over the age of 60 and is primarily characterised by poor control of movement (shaking, rigidity etc). Neuronal death leads to decreased levels of a neurotransmitter called dopamine, which is a key factor in the deterioration of motor function. Current treatments for PD centre on replacing dopamine using a drug called L-DOPA, which is a precursor to dopamine. This drug treats the symptoms of PD but not the underlying cause.
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]
Insulin (in-suh-lin): A hormone made by the cells in your pancreas. Insulin helps your body store the glucose (sugar) from your meals. If you have diabetes and your pancreas is unable to make enough of this hormone, you may be prescribed medicines to help your liver make more or make your muscles more sensitive to the available insulin. If these medicines are not enough, you may be prescribed insulin shots.
For the eggs, beat the 4 eggs in a medium sized bowl until whites and yolks are combined. Heat a medium skillet (I used the same skillet as the pancakes) over medium-low heat. Add the butter and then the beaten eggs. Let the eggs cook until the edges begin to set. push the eggs with a rubber spatula scraping the bottom of the pan. scrape occasionally to get large folds of soft scrambled eggs. When the eggs are just set and still a little runny, remove from the heat.
Maria, I made your bread using NOW psyllium, it tastes more like a loaf of real bread than anything I’ve tried. It’s lots better than the pricey Low Carb Bread Company loaves that I have been buying on Netrition. I had previously tried a similar recipe that had coconut flour, and even though I added quite a bit of onion powder, the coconut flavor was still distinguishable, and I’m not a fan.
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.
Russel Wilder first used the ketogenic diet to treat epilepsy in 1921. He also coined the term "ketogenic diet." For almost a decade, the ketogenic diet enjoyed a place in the medical world as a therapeutic diet for pediatric epilepsy and was widely used until its popularity ceased with the introduction of antiepileptic agents. The resurgence of the ketogenic diet as a rapid weight loss formula is a relatively new concept the has shown to be quite effective, at least in the short run.
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Concussion (a mild form of TBI), is defined as a short term impairment of brain function caused by impact. Symptoms include dizziness, confusion and headache. When the brain suffers a concussive impact this triggers an acute cascade of cellular events that can eventually cause chronic problems. Firstly, immediately after impact there are changes to the concentrations of ions and neurotransmitters in and outside of the neurones. For example, the cells release potassium and glutamate (excitatory neurotransmitter); this can cause neuronal damage instantly64. The disruption to the equilibrium of substances within the brain must be corrected, which requires the action of the ATP dependant ion pumps in the cell membranes. In order to produce enough ATP the brain has a transient period of high glucose metabolism (within 30 minutes of impact), which is followed by a period of glucose metabolic depression that can last anywhere from 5 days to several months, depending on severity65. In this time the brain is starved of energy when it is unable to metabolise glucose, which can cause long term damage. Severe or repeated impacts can lead to development of conditions such as chronic traumatic encephalopathy (CTE).
The FOXO family of transcription factors is highly conserved and promotes longevity and resistance to cellular stress. Although there are a variety of FOXO isoforms with varying tissue distribution [318–320], FOXO3a has been the most thoroughly studied in relation to energy sensing, mitochondrial function, and antioxidant defense. Similar to PGC-1α, FOXO3a is activated through phosphorylation by AMPK [321–323] and deacetylation by SIRT1 [324, 325] and SIRT3 [326–329], and its transcriptional activity is at least partly dependent on AMPK  and SIRT1 . In a variety of organisms, tissues, and cell types, FOXO3a increases mitochondrial biogenesis and expression of TFAM , but is more known for increasing expression of antioxidant and repair proteins, including SOD2 [287, 330, 331], catalase [287, 330, 332, 333], glutathione S-transferase (GST) , thioredoxins [287, 323], Prx3 [287, 334], Prx5 , and metallothioneins I and II , as well as UCP2 [287, 322] and the DNA repair enzyme growth arrest and DNA damage-inducible 45 (GADD45) [322, 324, 335, 336]. FOXO3a is also activated by oxidative stress [324, 331, 333], possibly in a SIRT1-dependent manner , and likely mediated through c-Jun N-terminal protein kinase (JNK), which allows FOXOs to translocate to the nucleus by promoting dissociation of 14-3-3 [337, 338]. Furthermore, FOXO3a and SIRT3 interact in mitochondria to induce mitochondrial gene expression in an AMPK-dependent manner . FOXO3a also induces expression of LKB1  and NAMPT , indicating a feed-forward cycle of activation with AMPK and sirtuins. Like PGC-1α, FOXO3a transcriptional activity is inhibited by insulin through PKB .
Hi Kerstin, Sorry you had issues whipping the whites. It can sometimes be more difficult with the kind from a carton. The cream of tartar helps, but sometimes isn’t enough. Did you wait for the whites to be at room temp before beginning? This can help with whipping. Unfortunately the bread won’t turn out very well without getting the whites to stiff peaks. I hope it works for you next time, and if the cartons don’t work for you, you can try with the whites from whole eggs. You can use the yolks to make hollandaise sauce or creme brulee like this.