The metabolic syndrome is the name of a cluster of risk factors that, when they appear together, dramatically raise your risk of heart disease, heart failure, stroke and diabetes, as well as other non-cardiovascular conditions. Like smoking, it’s one of the strongest predictors of heart disease. “Nearly one in three Americans have metabolic syndrome. Many people don’t recognize that they have the condition and underestimate the risks it presents,” says Chiadi E. Ndumele, M.D., M.H.S. , cardiologist at the Johns Hopkins Ciccarone Center for the Prevention of Heart Disease. “Understanding that you have metabolic syndrome in the first place can help motivate you to make the needed changes.”
Well, everyone, I am sensitive to psyllium so I experimented and it kind of worked! I made a half recipe using chia seed I ground in my Vitamix into 5 buns. They didn’t really rise but the flavor was quite good. Might add garlic and onion powder next time. I was able to slice the skinny bun and have a burger on it. Yum! Hadn’t had a burger on a bun for ages! Worth a try! I did weigh everything and was very precise so inaccurate quantities would not be an issue. Maria, any ideas on how to make this mixture rise some? I’m sure I’m not the only one with psyllium issues. Can’t have flax much either and I think if I have the chia too often that will give me tummy trouble also. One more question Maria. Is there a reason for no salt in the egg white protein bread? I don’t really like the flavor or texture but thought salt and seasonings would help. Thank you, Maria! You have made my meals so much more enjoyable! So grateful!
I waited awhile to try this, certain it would be blah but decided to give it a go. I did add a pinch of salt and I used Brummel and brown butter, made with yogurt, as it lowered the fat and calories. toasted and spread some sugar free strawberry preserves. really good! texture took a bit to get used to but so excited to be able to eat bread! not on keto but recently diagnosed as diabetic so bread is a nono bc of all the carbs.
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Metabolic syndrome (metabolic syndrome X, insulin resistance syndrome, dysmetabolic syndrome, hypertriglyceridaemic waist, obesity syndrome, Reaven syndrome) is the name for a group of risk factors that increase the risk for ischaemic heart disease (IHD), diabetes and stroke (Fig. 23.1). The metabolic syndrome is diagnosed when at least three of the IHD risk factors listed in Table 23.1 are present. Whether the syndrome, which affects possibly 25% of the US population, is a specific syndrome, and nothing more than the sum of its parts, is controversial.
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.
^ 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).
^ Klein MS, Buttchereit N, Miemczyk SP, Immervoll AK, Louis C, Wiedemann S, Junge W, Thaller G, Oefner PJ, Gronwald W (February 2012). "NMR metabolomic analysis of dairy cows reveals milk glycerophosphocholine to phosphocholine ratio as prognostic biomarker for risk of ketosis". Journal of Proteome Research. 11 (2): 1373–81. doi:10.1021/pr201017n. PMID 22098372.
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 , 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  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 . Once activated, PGC-1α interacts with the PPAR family of nuclear receptors  and the FOXO family of transcription factors  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 , SOD2 [76, 282, 289, 292–294], catalase , 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].
The low carbohydrate content of the ketogenic diet prevents blood sugar spikes and stabilizes insulin levels. Chronically high insulin levels and the disrupted incretin signaling (gut derived molecules) lead to insulin resistance over time (pre-diabetes). This means that our cells are not willing to take up vast amounts of glucose anymore and more and more insulin is needed for glucose uptake – a vicious cycle.
Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in patients treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components.
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.
There are two main types of diabetes. In Type I diabetes, the insulin producing cells in the pancreas are destroyed by an immune response resulting in insulin deficiency. In Type II diabetes insulin is still secreted, but the cells in the body no longer respond adequately and so glucose uptake is not triggered. Sometimes pregnancy can trigger a period of diabetes (gestational diabetes), which resolves after giving birth.
While exercise is a great way to bring down your blood glucose immediately, remember that physical activity should be a part of your lifestyle, not just a tool for producing one good test result. Getting your recommended periodic A1C tests will help you and your doctor determine if your blood glucose control is on target. And when you use your meter to test at home and at work, be sure to look for patterns in the results. This can help you and your diabetes care team tell whether you need to adjust your diet, medications, or both. The most important thing you can do to manage diabetes well is to control your blood glucose, and exercise is a key step toward reaching that goal.
Thank you Mira for your quick reply. I didn’t make it that same day but I just made a batch now and they are excellent! I really enjoyed them. I made the recipe times 10 for 12 large muffin slots in the muffin tin. I’m thinking of shaping a larger round of batter on a parchment lined pan next time and after baking, carefully cutting in half to make 2 rounds to make a pizza crust. Thank you so much!!!
The gut-brain link is important not only for the hormones produced by the gut, but also for the long-term body weight regulation. Studies in mice indicate that the gut microbiome influences both sides of the energy balance by contributing to nutrient absorption and regulating host genes that affect adiposity [however there are conflicting reports (Parks et al., 2013; Schele et al., 2013)]. However, it remains uncertain just how important gut microbiota are for nutrient absorption in humans. A cohort study has demonstrated that the nutrient load is a key variable that can influence the gut/fecal bacterial content over short time frames. Furthermore, the observed associations between gut microbes and nutrient absorption indicates a possible role of the human gut microbiota in the regulation of the nutrient intake and utilization (Jumpertz et al., 2011).
While several national and international organizations use certain criteria to define metabolic syndrome, others, including the American Diabetes Association (ADA), question the value of the specific diagnosis of metabolic syndrome. They point out that the criteria, taken together, are no more useful at predicting the risk of cardiovascular disease or diabetes than the individual criteria considered separately. The science needs to be clearer, suggests the ADA, before metabolic syndrome be considered a definable syndrome.
As with other sources of oxidative stress, mtROS can damage enzymes and cell membranes and subsequently facilitate the pathogenesis of chronic disease . Oxidative damage to mitochondrial DNA (mtDNA) is of particular concern because of its proximity to the electron transport chain (mtETC). Furthermore, compared to nuclear DNA, mtDNA is more prone to oxidative damage and is not repaired as effectively [42–45], although this has been debated based on more recent evidence [46–50]. Unrepaired mtDNA damage leads to mitochondrial dysfunction, which is implicated in the pathogenesis of a variety of chronic diseases  and associated with shorter lifespan . Therefore, while moderate levels of mtROS have important roles in signaling and health, protection against excessive levels is also important.
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Drinking water helps your kidneys flush out excess blood sugar through your urine. One study found that people who drank more water had a lower risk of developing hyperglycemia (high blood sugar). Can’t seem to drink enough? If water is just too plain for your taste buds, add slices of citrus, or sip on a flavored seltzer or herbal tea throughout the day to hit your hydration quota.
The findings of a stable (Chearskul et al., 2008) or slightly increased response (Sumithran et al., 2013) of post-prandial FFA after KD can be viewed in the nutrient-static context. Elevated circulating FFA may actually reduce food intake and glucose production through actions on specific hypothalamic neurons (Obici et al., 2003). It has been suggested that this effect could be mediated by the increase of cellular concentration of long-chain FAs-CoA in the arcuate nuclei of the hypothalamus (Obici et al., 2003).
Increased reliance on mitochondrial respiration will increase the flow of electrons through the mtETC and, in turn, increase the potential for mtROS formation. Although oxidative stress is traditionally viewed as harmful, a modest increase in ROS is now established as a signaling stimulus that induces hormetic adaptation . In regard to mitohormesis and mtROS, such adaptation is largely centered around antioxidant defense [4–6], making mitohormesis an attractive target for the prevention and treatment of chronic disease.
There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.
thanks for your reply, maria! i can’t figure out why mine tastes so vinegar-y while no one else has had this problem. could it be the type of vinegar i’m using? It’s trader joe’s organic ACV. could i just reduce the amount of vinegar? or, in your baking experience, do you think i could i use lemon juice as the acid in place of the vinegar (or a mix of the two)? i think i could stand a lemon taste better than a vinegar taste…
You can find a mixed bag of studies in rodents; sometimes the ketogenic diet is amazing sometimes it’s terrible. The main reason why is because there are many kinds of ketogenic diets; what fats were used? how processed is the food and what was the method of processing? were these genetically manipulated mice or wild type? were they fed ad lib (to their hearts content), forced fed (hypercaloric) or had their calories restricted?
Other mechanisms that have been suggested include: changes in ATP production making neurons more resilient in the face of metabolic demands, altered brain pH affecting neuronal activity, direct inhibitory effects of ketone bodies or fatty acids on ion channels, alterations in amino acid metabolism, and changes in synthesis of the inhibitory neurotransmitter GABA. (10)
Another lipid marker of interest is blood triglyceride levels. Blood triglycerides are frequently elevated in the metabolic syndrome, and are a risk factor for cardiovascular disease111. A common misconception is that consuming high levels of fat leads to persistently high levels of blood triglycerides. However, there is data that suggests that a high fat diet does not affect blood triglyceride levels, and may even lower them21 ,112, especially following a period of adaptation113.
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.)
The reason a starving person can live for 40-60 days is precisely because we can turn fat into ketones and convert ketones into substrate for the Krebs Cycle in the mitochondria of our neurons. In fact, the more fat you have on your body, the longer you can survive. As an example of this, you may want to read this remarkable case report of a 382 day medically supervised fast (with only water and electrolytes)! If we had to rely on glucose, we’d die in a few days. If we could only rely on protein, we’d live a few more days but become completely debilitated with muscle wasting.
While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores, studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat, relative to carbohydrates. Some clinicians refer to this period of keto-adaptation as the "Schwatka imperative" after Frederick Schwatka, the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.
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I just tried this recipe in my kitchen. OMG thank you so so much for this wonderful idea! The only thing I think I will try next time is to add just a dash or so of salt to the mug before microwaving (although it already tastes great!). I think it will be fun to experiment with adding some different seasonings or herbs to the batter before baking it, too, just for variety.
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There is also exciting early research suggesting that ketosis may be beneficial for many other conditions, such as reducing the frequency and severity of migraine headaches, reversing PCOS, perhaps enhancing conventional brain cancer therapies, possibly slowing down the progression of Alzheimer’s disease, along with potentially helping people live longer, healthier lives.
Insulin resistance. Insulin is a hormone that helps your body use glucose -- a simple sugar made from the food you eat -- as energy. In people with insulin resistance, the insulin doesn't work as well, so your body keeps making more and more of it to cope with the rising level of glucose. Eventually, this can lead to diabetes. Insulin resistance is closely connected to having excess weight in the belly.
Although the hunger-reducing effect of KD is well-documented, its main mechanisms of action are still elusive. The global picture is complicated by the contradictory role of ketosis on anorexigenic and orexigenic signals (summarized in Figure Figure4).4). Ketones (mainly BHB) can act both orexigenically or anorexigenically. In the orexigenic mechanism, it increases the circulating level of adiponectin, increasing brain GABA and AMPK phosphorylation and decreasing brain ROS production. The anorexigenic mechanism triggers a main normal glucose meal response, increasing circulating post-meal FFA (thus reducing cerebral NPY), maintaining CCK meal response and decreasing circulating ghrelin. It can be postulated that the net balance of the contrasting stimuli results in a general reduction of perceived hunger and food intake. More studies are needed to explore the mechanism of potential beneficial effects of KD on food control.
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.
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.
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Make this keto bread pizza base crispy and thin, or roll it into a thicker, fluffier crust — no matter how you prepare it, this recipe cuts out all dairy, grains, and gluten for a total of 6 net carbs. Coconut flour and psyllium creates a firm texture, while apple cider vinegar lends a tangy flavor. To stay more Bulletproof, avoid eating garlic and psyllium husk too often.