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].

Metabolic syndrome, also known as Insulin Resistance Syndrome (IRS) and Syndrome X, is a cluster of metabolic and anthropometric traits including glucose intolerance, upper body fat distribution (increased intra-abdominal fat mass), hypertension, dysfibrinolysis, and a dyslipidemia (characterized by high triglycerides, low high-density lipoprotein [HDL] cholesterol, and small dense low-density lipoprotein [LDL] particles).1 Metabolic syndrome constitutes a powerful risk factor complex to identify individuals at increased risk for future Type 2 diabetes and cardiovascular disease (CVD). Insulin resistance and abdominal obesity are two central components of the syndrome and are integrally involved in its pathogenesis. Insulin resistance is a metabolic abnormality in which peripheral tissues exhibit a subnormal biologic response to the glucose-lowering action of insulin. Insulin resistance not only antedates the development of diabetes but is also a major metabolic defect (together with impaired insulin secretion and elevated hepatic glucose production) that maintains hyperglycemia in patients with overt disease. The central role of abdominal adiposity underscores the importance of body fat distribution regarding the metabolic consequences of obesity. Individuals with metabolic syndrome are also more prone to develop other pathologic conditions including polycystic ovary syndrome, non-alcoholic steatohepatitis (NASH), cholesterol gallstones, sleep disorders, and some types of cancer. Thus, metabolic syndrome is responsible for a tremendous burden of human disease and social costs, and nutritional therapy is key to both its prevention and limiting its progression to Type 2 diabetes and CVD.
Maria, can you clarify the recipe as far as fluid ounces versus weighted ounces? For example, for the boiling water, 1.5 cups of water is 12 fluid ounces, but 1.5 cups of water does not weigh 12 weighted ounces. As I watch your video, you weigh the boiling water in a measuring cup, but once again I’m not sure if it’s supposed to be 12 fluid or weighted ounces. And is that true for the vinegar and egg whites as well… fluid ounces versus weighted ounces?
All of the factors associated with metabolic syndrome are interrelated. Obesity and lack of exercise tend to lead to insulin resistance. Insulin resistance has a negative effect on lipid production, increasing VLDL (very low-density lipoprotein), LDL (low-density lipoprotein – the "bad" cholesterol), and triglyceride levels in the blood and decreasing HDL (high-density lipoprotein – the "good" cholesterol). This can lead to fatty plaque deposits in the arteries which, over time, can lead to cardiovascular disease and strokes. Insulin resistance also leads to increased insulin and glucose levels in the blood. Excess insulin increases sodium retention by the kidneys, which increases blood pressure and can lead to hypertension. Chronically elevated glucose levels in turn damage blood vessels and organs, such as the kidneys. 
Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO2 in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions.[9] Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, defined as acidosis if blood pH falls below 7.35.
We’ve been on the Keto journey since the end of February last year and this is my favourite bread recipe so far, I just made a loaf and it turned out great. I don’t have a food processor so I did use my blender and for ingredients I only used the almond flour, coconut flour, baking powder, butter, salt, 8 egg whites (all I had left in the fridge) and the only optional ingredient I added was stevia. The texture was still really nice without the extra ingredients which is a nice option and this tasted like a regular loaf of bread, I’ll definitely be making this again!!
Patterns can be great because they help you figure out what is causing undesirable blood sugar values. A good way to track of it is to keep a journal of all of the food you eat, activities you do and your blood sugar levels for 1 week. During this week, check your sugar before and after you eat, as well as in between meals. Also document any insulin that you give yourself.
I finally made this recipe. (I have made many of your others and use them often.) It did fall slighty but I was still able to slice it after it cooled. It was also purple, which is just fine with me. I toasted in the oven this morning and it was nice and crisp. I can’t tell you have happy I was to dip it in my fried egg this morning. Thanks, Maria, for all you do!
Like fiber, protein tempers insulin secretion, leading to a more gradual rise in blood sugar after a meal. It also fills you up better than any other nutrient. Eating a protein-rich breakfast may be particularly important, as it helps set the tone for the rest of the day. The amount of protein you need in your diet depends on a number of factors, but general protein recommendations for healthy adults are 0.8 to 1.0 gram per kilogram of body weight (55 to 68 grams per day for someone who’s 150 pounds). Good animal sources include wild-caught fish, grass-fed beef, and pasture-raised chicken and eggs. If you’re vegetarian or vegan, load up on these eight plant-based protein sources.

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Increases in cholesterol levels need discussion too. We do see temporary increases in cholesterol levels often as individuals transition onto a ketogenic diet. However, when you examine lipid particle size (a more important way to look at the cardiovascular risks), the risk pattern doesn’t seem to increase with a ketogenic diet. Harvard Health has written about lipid particle size here before: http://www.health.harvard.edu/womens-health/should-you-seek-advanced-cholesterol-testing-


Metabolic syndrome is a burgeoning global problem. Approximately one fourth of the adult European population is estimated to have metabolic syndrome, with a similar prevalence in Latin America. [25] It is also considered an emerging epidemic in developing East Asian countries, including China, Japan, and Korea. The prevalence of metabolic syndrome in East Asia may range from 8-13% in men and from 2-18% in women, depending on the population and definitions used. [29, 30, 31]
If you're healthy and eating a balanced diet, your body controls how much fat it burns, and you don't normally make or use ketones. But when you cut way back on your calories or carbs, your body will switch to ketosis for energy. It can also happen after exercising for a long time and during pregnancy. For people with uncontrolled diabetes, ketosis is a sign of not using enough insulin.
The goal of metabolic syndrome treatment is to reduce the risk of heart disease and diabetes by controlling the associated problematic health conditions (high blood pressure, high cholesterol, diabetes, insulin resistance). “A study in which 53 percent of people had metabolic syndrome at the start found that over three years, intensive lifestyle changes—mainly diet and exercise—resulted in the lowest risk of developing diabetes and the lowest risk of developing metabolic syndrome in those who didn’t have it,” Ndumele says. Recommended changes include:

Ketone bodies synthesized in the body can be easily utilized for energy production by heart, muscle tissue, and the kidneys. Ketone bodies also can cross the blood-brain barrier to provide an alternative source of energy to the brain. RBCs and the liver do not utilize ketones due to lack of mitochondria and enzyme diaphorase respectively. Ketone body production depends on several factors such as resting basal metabolic rate (BMR), body mass index (BMI), and body fat percentage. Ketone bodies produce more adenosine triphosphate in comparison to glucose, sometimes aptly called a "super fuel." One hundred grams of acetoacetate generates 9400 grams of ATP, and 100 g of beta-hydroxybutyrate yields 10,500 grams of ATP; whereas, 100 grams of glucose produces only 8,700 grams of ATP. This allows the body to maintain efficient fuel production even during a caloric deficit. Ketone bodies also decrease free radical damage and enhance antioxidant capacity.
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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.


If you are overweight, losing weight can help reduce your risk of types 2 diabetes. Eating smaller portions can help you cut calories and still feel satisfied. Wright recommends thinking of your hunger on a scale of 1 (not hungry) to 10 (starved) to help with portions. “People are more mindful about their food choices if they eat when their hunger is a 5 or 6,” she says. “That way, you are not desperate and starving.”

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This poses a real evolutionary dilemma.  We need an enormous amount of energy just to not die, but the single most important organ in our body (also quite energy hungry in its own right) can’t access the most abundant source of energy in our body (i.e., fat) and is, instead, almost solely dependent on the one macronutrient we can’t store beyond a trivial amount (i.e., glucose). Obviously our species wouldn’t be here today if this were the end of the story. But, to understand how we survived requires one more trip down biochemistry memory lane.  In the figure below (also included and described in the video) I gloss over a pretty important detail.
Abundant data suggest that patients meeting these diagnostic criteria have a greater risk of significant clinical consequences, the 2 most prominent of which are the development of diabetes mellitus [6] and of coronary heart disease. Pooled data from 37 studies involving more than 170,000 patients have shown that metabolic syndrome doubles the risk of coronary artery disease. [7] It also increases risk of stroke, fatty liver disease, and cancer. [8] (See Prognosis.)
The metabolic theory states that the root cause of cancer is a defect in mitochondrial energy production or ‘an irreversible injuring in respiration’91. Once the cells ability to produce energy is compromised, this is hypothesised to lead to the subsequent accumulation of changes that make the cell cancerous92. A key change is decreased mitochondrial glucose metabolism in cancer cells. Cancer cells ferment glucose to lactate (which happens outside of the mitochondria) at a much higher rate than normal cells93, in a change called ‘The Warburg Effect.’ This implicates damage to the mitochondria and failure in energy production as a central process of cancer progression. 

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Nutritional ketosis may initiate bioenergetic and mitohormetic signaling through an increase in catecholamines or adiponectin, a decrease in insulin or glycogen, or an increase in β-oxidation that leads to an increase in mitochondrial reactive oxygen species (mtROS) or NAD+. This leads to further signaling involving AMP-activated protein kinase (AMPK), silent mating type information regulation 2 homologue 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), forkhead box O 3a (FOXO3a), and nuclear factor erythroid-derived 2-like 2 (NFE2L2), ultimately leading to transcription of genes related to oxidative capacity, mitochondrial uncoupling, and antioxidant defense. These adaptations collectively contribute to resistance against oxidative stress. Other proteins involved include liver kinase B1 (LKB1), which activates AMPK; nicotinamide phosphoribosyltransferase (NAMPT), which facilitates SIRT1 activation through NAD+ synthesis; and nuclear respiratory factors 1 and 2 (NRF-1 and NRF-2) and mitochondrial transcription factor A (TFAM), which promote mitochondrial biogenesis.
In order to simulate a bread-like texture without using gluten, grain free and gluten free bread recipes often use a variety of different flours and binders. We’ve tried so many keto bread recipes that taste way too eggy or too much like almonds or coconut. The trick is to find a combination of ingredients that yields good flavor, as well as bready texture and a loaf that rises nicely.
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