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.)
I want you to start drinking. A lot. Of water. (Sorry for the letdown.) In fact, I want you to drink only water. Never, ever, ever drink a calorie. Stick with water, and drink a lot of it. It’s good for you, and like an early salad, water can help keep hunger at bay. I’d also like you to avoid diet sodas, at least on a regular basis. Though they don’t have any calories, diet sodas cause folks who drink a lot of them to have a harder time losing weight. No one is sure why.
Ketosis is the metabolic process of using fat as the primary source of energy instead of carbohydrates. This means your body is directly breaking down its fat stores as energy instead of slowly converting fat and muscle cells into glucose for energy. You enter ketosis when your body doesn’t have enough glucose (carbohydrates) available. The prime function of the ketogenic diet is to put the body in ketosis.
In general, a person with metabolic syndrome is twice as likely to develop IHD and five times as likely to develop diabetes as someone without it. The probability of developing metabolic syndrome is also closely linked to a lack of physical activity and the fact of being overweight/obese. Other causes include insulin resistance, ethnicity (often Asian), family history, older age and other factors (Box 23.1). Associated diseases and signs may be raised uric acid levels, hepatic steatosis, haemochromatosis and acanthosis nigricans. Metabolic syndrome may be associated with inflammatory periodontal disease.

Weighed my ingredients…used Jay Robb Psyllium ground down to half the amount exactly…used almond flour from nuts.com….used All Whites 100% Egg Whites. Bread fell about one minute after I took it out of the oven. Do you cool yours out of the pan or in it? Does that matter? Could that be the problem? Or could it be my vinegar? Have had it a few months…does it get old? Help!!! I promised my husband if he let me spend all this $ on ingredients I could give him a nice loaf of bread for sandwiches! So disappointed! But determined!
It’s well known that adherence to the prescribed diet is usually low and self-reported food intake is very unreliable. So there’s no way to guarantee that the participants strictly adhered to the diet. Because it requires a lot of discipline and planning to stay in ketosis for a long time without interruption, it won’t be possible to perform a long-term study that guarantees uninterrupted ketosis using old study methods. This may change soon with improved self-tracking devices.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Long-term compliance is low and can be a big issue with a ketogenic diet, but this is the case with any lifestyle change.  Even though the ketogenic diet is significantly superior in the induction of weight loss in otherwise healthy patients with obesity and the induced weight loss is rapid, intense, and sustained until at least 2 year, the understanding of the clinical impacts, safety, tolerability, efficacy, duration of treatment, and prognosis after discontinuation of the diet is challenging and requires further studies to understand the disease-specific mechanisms.
Once your yeast is proofed, add in the egg, egg whites, lightly cooled melted butter (you don't want to scramble the eggs or kill the yeast!) and vinegar. Mix with an electric mixer for a couple minutes until light and frothy. Add the flour mixture in two batches, alternating with the sour cream, and mixing until thoroughly incorporated. You want to mix thoroughly and quickly to activate the xanthan gum, though the dough will become thick as the flours absorb the moisture. 
So when i made this bread it didnt really stay the way i wanted it to be because when i took it out it looked like regular bread but after like 5-10 minutes it sunk down and mine turned blueish-purpleish….is that good?? I dont think i will be making this again….and i measured out all the ingredients too so i dont know what i did wrong…. PLEASE HELP!!!!!!!!!!!!!
In controlled studies on exercise-trained humans and animals, ketogenic diets have been shown to increase fat oxidation [8, 167] and expression or activity of carnitine palmitoyltransferase [167, 168] and β-HAD [168, 172], demonstrating that nutritional ketosis induces adaptation beyond exercise. Similarly, in a study comparing the independent and combined effects of exercise and a ketogenic diet on rats, the combination resulted in greater β-HAD and citrate synthase activities in skeletal muscle and higher maximal O2 consumption than either intervention alone, further indicating the potential for exercise to magnify adaptations induced by nutritional ketosis [156].
Cinnamon supplements may modestly improve blood sugar in people with type 2 diabetes whose blood sugar is not well controlled with medication. In addition, one small study found that a branded cinnamon extract reduced fasting blood sugar by an average of about 10 mg/dL in prediabetic men and women with metabolic syndrome. Keep in mind, however, that only certain varieties of cinnamon have been shown to have this effect, and long-term safety studies have not been conducted.
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82. Schwarz J. M., Neese R. A., Turner S., Dare D., Hellerstein M. K. Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection. Journal of Clinical Investigation. 1995;96(6):2735–2743. doi: 10.1172/jci118342. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
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Despite continuous advances in the medical world, obesity continues to remain a major worldwide health hazard with adult mortality as high as 2.8 million per year. The majority of chronic diseases like diabetes, hypertension, and heart disease are largely related to obesity which is usually a product of unhealthy lifestyle and poor dietary habits. Appropriately tailored diet regimens for weight reduction can help manage the obesity epidemic to some extent. One diet regimen that has proven to be very effective for rapid weight loss is a very-low-carbohydrate and high-fat ketogenic diet.[1][2][3]

Emerging data suggest an important correlation between metabolic syndrome and risk of stroke. [58] Each of the components of metabolic syndrome has been associated with elevated stroke risk, and evidence demonstrates a relationship between the collective metabolic syndrome and risk of ischemic stroke. [59] Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators. [60]
You’ll recall, from the point I made above, that my brain requires about 400 to 500 kcal of glucose per day (100 to 120 gm).  You’ll also recall (from the video, above) that I can store about 100 to 120 gm of glucose in my liver.  While I can store much more in my muscles, (on the order of about 300 to 350 gm), because muscles lack the enzyme glucose-6-phosphatase, glucose stored in muscle as glycogen is unable to re-enter the bloodstream and is meant for the muscle and the muscle alone to use.  In other words, muscle glycogen is a stranded asset of glucose in the body to be used only by the muscle.
Keeping a log of your blood sugars is a great way to be knowledgeable about your body and how it is reacting to foods and events. To start, check before and after every meal, along with one in-between meal check. It is important that you keep a log of these blood sugars, along with all of the foods that you are eating, activities you are performing and any insulin or medications that you are taking. Do this for a week, and see if you can identify any patterns. Take this log to your doctor and talk to them about your findings.
Add yeast and maple syrup (to feed the yeast, see notes) to a large bowl. Heat up water to 105-110°F, and if you don't have a thermometer it should only feel lightly warm to touch. Pour water over yeast mixture, cover bowl with a kitchen towel and allow to rest for 7 minutes. The mixture should be bubbly, if it isn't start again (too cold water won't activate the yeast and too hot will kill it). 
After a period of time, your body becomes adapted to using ketones as fuel instead of glucose. Your muscles begin to learn to convert acetoacetate into a ketogenic substance called beta-hydroxybutyrate, or BHB. BHB then becomes the new preferred ketogenic source of energy, including to fuel all brain activity. What is not needed is expelled from the body as waste.

In the United States, children are becoming obese at triple the rate compared with the 1960s, making the study and treatment of this problem paramount. The epidemic of metabolic syndrome in children and adolescents is an international phenomenon, leading the International Diabetes Foundation to publish an updated consensus statement to guide diagnosis and further study of the condition. [51, 52]
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 [322] and SIRT1 [325]. In a variety of organisms, tissues, and cell types, FOXO3a increases mitochondrial biogenesis and expression of TFAM [329], 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) [322], thioredoxins [287, 323], Prx3 [287, 334], Prx5 [287], and metallothioneins I and II [322], 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 [324], 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 [339]. FOXO3a also induces expression of LKB1 [340] and NAMPT [341], indicating a feed-forward cycle of activation with AMPK and sirtuins. Like PGC-1α, FOXO3a transcriptional activity is inhibited by insulin through PKB [331].
Test ketones in the late morning or afternoon. Blood and urine ketones are usually lowest right after waking up. Try testing later on, preferably a few hours after eating. Even if you’re only in ketosis for a portion of the day, you’re still getting some benefits, as discussed in this talk by Dr. Steve Phinney: Achieving and maintaining nutritional ketosis.
I was so excited about making this bread. I recently cut all grains out of my life and I’m also in the process of going gluten free because i have a lot of digestive issues. I followed the recipe precisely. Checked the temp before taking it out of oven. It looked amazing nice and golden brown. I cut into it and i couldn’t wait for that first bite. I was so disappointed it has an odd flavor I just couldnt stomach and it was very salty to me. I tried a few tiny bites with different condiments and couldn’t eat it. After reading some comments, I see it is supposed to be unsalted butter. I used salted, but why did it seem to have a bitter sour taste to it?
Glucose-sensitive neurons have been identified in a number of CNS regions including the metabolic control centers of the hypothalamus. Medeiros et. al. have used patch-clamp electrophysiology to examine whether neurons in a specific specialized region known as the subfornical organ (SFO), an area where the blood-brain barrier is not present, are also glucose sensitive or not. These experiments demonstrated that SFO neurons are glucose-responsive and that SFO is an important sensor and integrative center of circulating signals of energy status (Medeiros et al., 2012).
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I am not a baker so I studied all the comments carefully, ordered the blanched almond flour but not the Robb psyllium powder, used instead a generic (Equate) brand; didn’t weigh anything and don’t have a convection oven. Baked for 60 minutes. This bread fell a little but after complete cooling (2 hours), I sliced this bread down the middle and found it pretty near perfect in consistency. The taste of it is heaven. Small bit of gumminess, so will reduce by 1 oz H2O next time. Thank you for sharing this amazing recipe.

I don’t think I have ever posted anything on any other blog before in my life, but this time it’s just plain necessary. 🙂 Basically, I just wanted to let you know that you are a GENIUS, this is by far the best grain free bread I have ever tasted!! I made it with almond flour and egg whites only, and even my boyfriend (who’s the type of guy who generally dislikes anything remotely healthy) had to admit that it’s pretty good — and that it doesn’t remind him of scrambled eggs. 🙂 So thank you, thank you, thank you!
If you need to lose weight, find an eating plan you can stick with. “Whatever results in lasting weight loss for you is the best approach for you,” Wright says. “If you make over-restrictive changes you can't maintain, as soon as you tire of that diet, you will fall back to what you did previously, gain weight, and raise your risk of type 2 diabetes.”
Several additional rodent studies have shown ketogenic diets to increase protein content of UCPs. However, since mitochondrial function was not measured in these studies, it is not known if uncoupling was affected by these changes in UCP content. In obese mice fed a ketogenic diet (0.4% of energy as carbohydrate), expression of UCP1 and UCP2 increased in adipose and the liver, respectively [148]. Similarly, expression of UCP1 has increased in brown adipose of mice fed a low-carbohydrate diet (18.5% of energy) supplemented with ketone esters (6% w/v) [149]. The increase in hepatic UCP2 expression during a ketogenic diet has been demonstrated by other studies as well [37, 150, 151]. Ketogenic diets also induce expression of UCP3 in skeletal muscle. In rats fed a ketogenic diet (% energy: 78.1 fat, 0 carbohydrate, and 21.9 protein) for 8 weeks, UCP3 expression increased in the soleus but not the extensor digitorum longus, which is consistent with the soleus containing mostly oxidative, type I muscle fibers [152]. In humans, glycogen depleting exercise followed by two days of a low-carbohydrate diet (0.7 g/kg body mass) increased UCP3 expression in the vastus lateralis [153].
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In recent times there has been an exponential increase in the rates of obesity and diabetes. Popular opinion has blamed (in turn) overconsumption of fat, overconsumption of carbs and sugar and overconsumption of calories. Whilst the overall calorie balance is a crucial factor that cannot be overlooked, it is also the case that different macronutrients in the diet (especially carbs and fat) have different effects on the body when consumed.  

108. Haces M. L., Hernandez-Fonseca K., Medina-Campos O. N., Montiel T., Pedraza-Chaverri J., Massieu L. Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions. Experimental Neurology. 2008;211(1):85–96. doi: 10.1016/j.expneurol.2007.12.029. [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.
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.  

Consistent with the mechanisms described above, changes in AMPK in response to a ketogenic or low-carbohydrate diet have been reported in several studies. In rodents, a ketogenic diet (Bio-Serv F3666) has increased AMPK activity in skeletal muscle [150] and AMPK phosphorylation in the liver [230], and a low-carbohydrate diet (18.5% of energy) supplemented with ketone esters (6% w/v) increased AMPK content in brown adipose [149]. In humans, a nonketogenic low-carbohydrate diet (% energy: 50 fat, 30 carbohydrate, and 20 protein) has increased AMPK phosphorylation in skeletal muscle [231].
In particular, eat a healthy diet that includes fruits, vegetables, and whole grains. Exercise is also important when it comes to preventing this condition. Regular physical activity will reduce your blood pressure, blood sugar, and cholesterol levels. The key is to try to maintain a healthy weight. Talk to your doctor before beginning an exercise program or radically changing your diet.
Inducing ketosis requires severely limiting your carbohydrate consumption, this way you cut off supply of glucose to your cells. In addition to severely restricting carbs, you also need to limit your protein consumption, since protein can be converted into glucose in small amounts. This is the exact reason that most low-carb diets (such as Atkins or the Paleo diet) do not result in ketosis, because they allow a high intake of protein that keeps supplying the body with enough energy that it doesn’t need to burn fat.
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Similarly, several studies have demonstrated that up to half or more of patients undergoing PD have metabolic syndrome, and at least one study has demonstrated a significant increase in the prevalence with initiation of PD therapy. The only study that made a head-to-head comparison concluded that metabolic syndrome was significantly more prevalent in patients undergoing PD compared with in-center HD. These observations have raised concerns that PD therapy itself may contribute to the development of metabolic syndrome. However, the prevalence of metabolic syndrome in patients undergoing in-center HD in the only study with head-to-head comparison was substantially lower than in other studies. Moreover, there are two challenges with the diagnosis of metabolic syndrome in patients undergoing PD. First, the intraperitoneal instillation of dialysate with PD results in an increase in waist circumference, an important component for the diagnosis of metabolic syndrome. Second, there is continuous systemic absorption of glucose from intraperitoneal dialysate, and hence, patients undergoing PD are never in a postabsorptive state. This results in overestimation of fasting glucose and lipid parameters. Finally, the results from studies examining the association of metabolic syndrome with cardiovascular events or all-cause mortality have been inconsistent. This is not surprising because the individual components of metabolic syndrome themselves do not portend a higher risk for death or cardiovascular events in patients with ESRD, including among those undergoing PD.
In essence, it is a diet that causes the body to release ketones into the bloodstream. Most cells prefer to use blood sugar, which comes from carbohydrates, as the body’s main source of energy. In the absence of circulating blood sugar from food, we start breaking down stored fat into molecules called ketone bodies (the process is called ketosis). Once you reach ketosis, most cells will use ketone bodies to generate energy until we start eating carbohydrates again. The shift, from using circulating glucose to breaking down stored fat as a source of energy, usually happens over two to four days of eating fewer than 20 to 50 grams of carbohydrates per day. Keep in mind that this is a highly individualized process, and some people need a more restricted diet to start producing enough ketones.
While the lipid abnormalities seen with metabolic syndrome (low HDL, high LDL, and high triglycerides) respond nicely to weight loss and exercise, drug therapy is often required. Treatment should be aimed primarily at reducing LDL levels according to specific recommendations. Once reduced LDL targets are reached, efforts at reducing triglyceride levels and raising HDL levels should be made. Successful drug treatment usually requires treatment with a statin, a fibrate drug, or a combination of a statin with either niacin or a fibrate.
Many athletes would not consider following a ketogenic diets due to the limited evidence of a performance enhancing effect, the risk of side effects having a negative impact on performance and the difficulty in maintaining the lifestyle changes required to stay in ketosis. Exogenous ketones offer a method to deliver some of the benefits of ketone metabolism without requiring athletes to follow a strict ketogenic diet. Taking exogenous ketones creates a metabolic state that would not normally occur naturally: the state of having full carbohydrate stores as well as elevated ketones.

I was recently diagnosed with diabetes which I had had uncontrolled for an estimated seven years. I have done a lot of research and while there is a lot of diabetes information available, little was helpful for whatever reasons – too simplistic in nature, didn’t answer hard hitting questions, or didn’t apply forward thinking scenarios. This article is one of the best I have read because it is both clear and concise and givens you all of your essential important information in a single place – something everyone needs. Even after all of my research, I still learned a couple new things reading this article. Excellent reference.
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Thanks for replying. I guess I’ll just try it on both convection and regular and see which works out best! 🙂 I had made the sub roll in a regular oven with good results yet it didn’t turn out as well when baked on convection. That’s why I was wondering about the temperature and whether that was the culprit. Guess there’s only one way to find out. This experimenting can get expensive!
I made this yesterday and had 3 pieces. Had another 2 for breakfast today and after a few minutes I started feeling nauseated. The nausea got worse and worse, and I ended up projectile vomiting in the bathroom. I looked it up and it’s a symptom of psyllium husk overdose. I read that the max dosage per day is around 2tsp. I had around 10 times the daily dosage in my breakfast alone… I love all of Maria’s recipes but this is just a warning to watch out with the husk powder in this recipe! I did not grind mine to decrease the density of it. I am semi comatose in bed now while my husband takes care of our kids. 😁😁😁
Perturbations in bioenergetic homeostasis induce signal transduction that leads to upregulation of mitochondrial capacity and antioxidant defense. Three key enzymes involved in the sensing of these perturbations and the subsequent induction of signal transduction are AMP-activated protein kinase (AMPK) and silent mating type information regulation 2 homologues 1 and 3 (SIRT1 and SIRT3).
I just made it using all the the optional ingredients but I didn’t have a food processor so I whipped/mixed everything by hand. One thing I noticed is that the top of the bread cracked unevenly. Could I have over fluffed the egg whites? Maybe creating an artificial cut in the middle could solve that next time? It rose very well and nearly doubled in size, though the size is still a bit small for my liking. I will most likely use 1.5x the amount next time. It smells great and I’m about to chow down on this!
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]
sdLDL. This is a measurement of the number of small dense low-density lipoprotein molecules a person has. LDL varies in size, and the smaller denser molecules, which tend to form when elevated triglycerides and VLDL are present in the blood, are thought to be more aggressive in causing atherosclerosis. This test is now commercially available, but is not performed by many laboratories and is not ordered frequently. Its ultimate clinical utility has yet to be determined. It may be evaluated in a LDL particle testing.
Ketone esters (BHB-BD) could help to accelerate glycogen resynthesis32. After exercise that depletes muscle glycogen, the muscle uses carbohydrate from the diet to replenish these stores. An experiment was carried out where athletes undertook depletive exercise and then were given a ketone drink (or carbohydrate placebo) as well as glucose intravenously to maintain a high blood level (10mM). In this experiment, when the recovery drink contained ketone ester, more glucose was infused in order to maintain blood glucose at 10 mM, and muscle glycogen levels were 50% higher. However, the evidence is not conclusive: another study. 31 found that adding ketone ester to a protein and carbohydrate recovery drink did not enhance the normal rate of glycogen re-synthesis.  
Using a blend of almond and coconut flours, this sturdy keto bread will even hold up to freezing. Take 10 minutes to blend flours with baking powder, salt, butter, and egg whites, then bake for an easy loaf that won’t turn your kitchen upside down. Stay more Bulletproof and use grass-fed butter in this recipe — each slice will still run you just 1 net carb.
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