Normally, the body breaks down carbohydrates, fat, and (sometimes) proteins to provide energy. When carbohydrate is consumed in the diet, some is used immediately to maintain blood glucose levels, and the rest is stored. The hormone that signals to cells to store carbohydrate is insulin. The liver stores carbohydrate as glycogen, this is broken down and released between meals to keep blood glucose levels constant. Muscles also store glycogen, when broken down this provides fuel for exercise. Most cells in the body can switch readily between using carbohydrates and fat as fuel. Fuel used depends on substrate availability, on the energy demands of the cell and other neural and hormonal signals.
Nutrition: What is it and why is it important? Nutrition is the supply of materials that organisms and cells require to live. Humans need seven major types of nutrients to function. A nutritionist studies nutrients, how the body uses them, and the relationship between a person’s diet and their health. Here, learn more about nutrients and what a nutritionist does. Read now
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).
Ketogenic diets have become popular in recent decades for their demonstrated positive effects on weight loss (Bueno et al., 2013), though the precise mechanism of action is not fully understood (Paoli, 2014). In fact there is contradictory data about KD in mice and rats. In fact, there are contradictory data about KD in mice and rats. For example whilst a huge amount of data confirm that KD in humans is effective in weight reduction, improving lipidemia and glucose tolerance (Bueno et al., 2013), it has been recently demonstrated that a long-term KD (22 weeks) caused dyslipidemia, a pro-inflammatory state, hepatic steatosis, glucose intolerance and a reduction in beta and alpha cell mass, all without weight loss in mice (Ellenbroek et al., 2014). Two considerations should be made: (1) the induction of ketosis and the response to ketosis in humans and mice are quite different and (2) mice and humans have different life spans, and results obtained in mice after several weeks on the diet can correspond to months on the diet in humans (Demetrius, 2005, 2006).
Herbal health remedies foundation that you can trust for ALS. When he went to herbal health remedies foundation for 3 weeks and they did a cleansing program to get toxins out of his body, when my brother went home he was on IV vitamins. Then he took out all the mercury filling out of his mouth. Took lots of vitamins etc… what I do know is they gave him 2 years and he lived almost 7 years. I think what made the most difference for him was the AMAZING care he had, he stayed at home with family and friends. “Food for the soul” is what I call it. I miss him so bad. Website:http://herbalhealthremediesfoundation.com Contact their email: firstname.lastname@example.org
The Mediterranean diet is palatable and easily sustained. In addition, recent studies have shown that when compared to a low fat diet, people on the Mediterranean diet have a greater decrease in body weight, and also had greater improvements in blood pressure, cholesterol levels, and other markers of heart disease -- all of which are important in evaluating and treating metabolic syndrome.
Research shows that Western diet habits are a factor in development of metabolic syndrome, with high consumption of food that is not biochemically suited to humans. Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance. The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance.
In a subsequent series of experiments, glucose metabolism in C. elegans was inhibited by knockdown of the insulin receptor, insulin-like growth factor 1 (IGF-1) receptor, and insulin receptor substrate 1 (IRS-1) . Consistent with the previous study , inhibition of glucose metabolism increased mitochondrial respiration concomitant with ROS-dependent increases in lifespan, stress resistance, and antioxidant enzyme activity. However, in this case, detection of ROS was mitochondria-specific, and repeated measures allowed for changes in antioxidant enzyme activities to be evaluated more closely in relation to the timing of changes in mtROS. Compared to controls, inhibition of glucose metabolism resulted in higher mitochondrial O2 consumption at 12 h, higher mtROS production at 24 h, and higher activities of SOD and catalase at 48 h, suggesting a dependence of antioxidant activity on mtROS and a dependence of mtROS on mitochondrial respiration. The most striking result is the lower mtROS at 120 h, indicating that the initial increase in mtROS and subsequent increase in antioxidant enzyme activity ultimately lowered net mtROS production to a level lower than controls, which is the proposed explanation for the more than twofold increase in lifespan. As with the previous study, this demonstration of mitohormesis is further supported by the changes in ROS production, antioxidant enzyme activity, and lifespan having been prevented with antioxidant treatment.
Insulin is the medication that will bring blood glucose down the fastest. Someone who uses mealtime insulin can take correction doses to lower blood glucose. This requires a thorough understanding of when to inject, how often to give correction doses, and how much insulin to use. You will need to work with your doctor or diabetes educator to learn how to do this.
High-sensitivity C-reactive protein has been developed and used as a marker to predict coronary vascular diseases in metabolic syndrome, and it was recently used as a predictor for nonalcoholic fatty liver disease (steatohepatitis) in correlation with serum markers that indicated lipid and glucose metabolism. Fatty liver disease and steatohepatitis can be considered as manifestations of metabolic syndrome, indicative of abnormal energy storage as fat in ectopic distribution. Reproductive disorders (such as polycystic ovary syndrome in women of reproductive age), and erectile dysfunction or decreased total testosterone (low testosterone-binding globulin) in men can be attributed to metabolic syndrome.
β-hydroxybutyrate and, in some cases, acetoacetate contribute to protection against oxidative stress by decreasing production of mitochondrial reactive oxygen species (mtROS), by increasing expression or protein content of antioxidant enzymes through histone deacetylase (HDAC) inhibition, and by directly scavenging the hydroxyl radical (•OH). Upregulation of antioxidant enzymes through HDAC inhibition includes manganese superoxide dismutase (SOD2), catalase, and metallothionein II and is likely mediated by the transcription factor forkhead box O 3a (FOXO3a).
Loaded with protein-packed ground beef, sharp cheddar, veggies, and everyone's favorite taco add-ons (salsa and sour cream, anyone?), this skillet from Peace, Love, and Low Carb is like eating nachos for breakfast — minus the chips. The best part: It can be meal prepped ahead of time for a week's worth of breakfasts. (Just leave the toppings off and add them after you've heated up a serving in the morning.) Who says tacos only belong on Tuesdays?
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 , 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 . In muscle, expression of many of the bioenergetic and antioxidant proteins previously discussed is dependent on PGC-1α . Upstream, activation of PGC-1α is dependent on AMPK  and SIRT1 [242, 269] and partly dependent on SIRT3 . Furthermore, activation of SIRT1 is dependent on AMPK , 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 , 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 . 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  and the activities of AMPK [259, 260], SIRT3 , p38 MAPK [311, 312], PGC-1α [76, 77, 260, 283], FOXO3a , and NFE2L2  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).
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).
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.
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  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.  It also increases risk of stroke, fatty liver disease, and cancer.  (See Prognosis.)
Metabolic syndrome is the commonly observed clustering of obesity, high blood pressure, abnormal blood lipids, and insulin resistance. Some healthy debate exists regarding its definition and existence, but it is clinically apparent that the components of metabolic syndrome occur together more often than expected by chance. Investigations into monogenic diseases that model features of the common metabolic syndrome have uncovered responsible genes. Genome-wide association studies of the components of the metabolic syndrome have been enormously successful. Research will continue to uncover how metabolic pathways interact to form the metabolic syndrome and its subsequent risk for atherosclerosis and diabetes.
Blood pressure goals are generally set lower than 130/80. Some blood pressure medications offer more benefits than simply lowering blood pressure. For example, a class of blood pressure drugs called ACE inhibitors has been found to also reduce the levels of insulin resistance and actually deter the development of type 2 diabetes. This is an important consideration when discussing the choice blood pressure drugs in the metabolic syndrome.
So I made my own coconut-flour from flaked coconut(according to a recipe I found on line). Psyllium Husk i managed to find only in whole husks form so I grind it up to a powder in a blender. I understand now it sounds like a recipe for disaster but I don’t have another choice (getting the ingredients from the internet will take about 2 weeks and until then it is all I have).
Under conditions of abundant glucose (and sufficient insulin sensitivity) the brain is primarily converting glucose to pyruvate (left side of figure). Pyruvate is then shuttled into the mitochondria and converted into acetyl CoA with the help of a very important enzyme called pyruvate dehydrogenase (PDH). I’m going to come back to this enzyme, in part II of this series, because this is where the story gets very interesting. Acetyl CoA (which is also a direct byproduct of fatty acid breakdown) is then combined with oxaloacetate and so begins the Krebs Cycle, which generates all the reducing agents to feed the ETC and generate massive amounts of ATP.
Note that urine measurements may not reflect blood concentrations. Urine concentrations are lower with greater hydration, and after adaptation to a ketogenic diet the amount lost in the urine may drop while the metabolism remains ketotic. Most urine strips only measure acetoacetate, while when ketosis is more severe the predominant ketone body is β-hydroxybutyrate. Unlike glucose, ketones are excreted into urine at any blood level. Ketoacidosis is a metabolic derangement that cannot occur in a healthy individual who can produce insulin, and should not be confused with physiologic ketosis.
Thank you for the recipe. I was going to give up gluten free bread making but your recipe made my day! I used ghee instead of butter as I was too lazy to melt butter. It rose prettily in the oven. Such a nice loaf of bread. Definitely not eggy and it even has the fluffiness of bread. I would like to double the recipe and make it in a 1 lb loaf pan. Do you think that’s feasible? Many thanks,
Also that’s absolutely wrong information about microwaves. Breast milk is not microwaved because of the uneven heating which can cause ‘hot spots’ which will lead to your baby’s mouth being burned. It does nothing to the nutrition of the milk itself or the proteins. There is a lot of fear mongering about microwaves and most people don’t understand the basic principle of how it works. It’s like people who blindly say there are ‘chemicals’ in food not realizing that everything is a chemical compound, even drinking water. So don’t worry 🙂
Further indicating that ketones influence mtROS production through alteration of electron transport, treatment of rat hippocampal slices with BHB + ACA (1 mM each) prevented the increase in mtROS and mitigated the decrease in ATP production that otherwise result from inhibition of mtETC complex I with rotenone . In mitochondria isolated from the brains of mice injected with BHB, although inhibition of complex I with rotenone and 1-methyl-4-phenylpyridinium increased rather than decreased mtROS production, the BHB treatment prevented the decrease in O2 consumption caused by inhibition of complex I, and this occurred independently of uncoupling . Consistent with the results from hippocampal brain slices, the BHB treatment also mitigated the decrease in ATP production caused by complex I inhibition . These effects were prevented by inhibition of complex II with 3-nitropropionic acid or malonate, indicating that BHB primarily influences mitochondrial respiration at complex II , which is consistent with ketolysis increasing formation of succinate and FADH2. However, in mutated cells prone to complex I disassembly and an associated severe decrease in complex I activity, treatment with BHB + ACA (5 mM each) increased both the assembly and activity of complex I , indicating that ketones somehow promote repair of complex I damage and may therefore influence mitochondrial respiration at more than one site.
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].
Maria I have ALL your books, except your 30 day cleanse, and I have attempted the 7 day weight loss and healing plan, and dairy free I might add, but was so hungry and dizzy on it! My husband pointed out the the “lunch” area, item, says Side. Well I’ve read it 3 times – the front of the book and such, it doesn’t say add food to the “SIDE”…it says use this plan. Also you maybe have said elsewhere, but the math is wrong on the second page for total calories….lastly the intermittent fasting – I thought I read previously in the Metabolism book that you shouldn’t fast more than 3 days at a time, but this book doesn’t mention that. Have you updated your thoughts?
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.
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.
We’ve longed been told that calorie restriction, increasing exercise and reducing dietary fat intake are the keys to weight loss. But, if you’ve ever attempted to control your weight by subsisting on fewer calories — especially from mostly bland “diet foods”— you’re already probably aware that this typically produces minimal results and is extremely hard to stick with long-term or consistently.
AMP competes with ATP for binding to the γ regulatory subunit of AMPK [177, 178] and by doing so, greatly increases AMPK activity, but only in the presence of an upstream kinase such as liver kinase B1 (LKB1) . This binding of AMP to the γ subunit appears to promote AMPK activity through at least two mechanisms: facilitated phosphorylation of the α subunit [180–183] and inhibition of dephosphorylation by protein phosphatases 2Cα and 2Ac [179, 181, 183, 184]. ADP also binds to the γ subunit of AMPK to inhibit dephosphorylation [183, 185, 186] and possibly facilitate phosphorylation . This is important to the energy sensing sensitivity of AMPK based on the much higher physiological concentration of ADP compared to AMP . Data on changes in AMP and ADP levels in response to a ketogenic diet are lacking. However, the decreased availability of carbohydrate and increased mitochondrial uncoupling (previously described) during nutritional ketosis suggest a decline in ATP production, at least until compensatory adaptations occur. A decline in ATP implies a relative increase in AMP and ADP, which would facilitate AMPK phosphorylation and activation. In addition, ketogenic diets are commonly reported to have a satiating effect , which may further increase the AMP and ADP to ATP ratios through spontaneous caloric restriction.
It is important that you check your blood sugar levels on a regular basis. It is the one way that you are able to check and see if what you are doing is working, or if any changes are needed to be made in your lifestyle. Don’t think of checking your sugar as some type of pass or fail test. It’s just like any other numerical value that you get, such as your weight. You may not like what you see, but you can always do your best to improve it.
Another product of elevated levels of free FA is polyunsaturated FA (PUFA). The potential ability of PUFA to block seizure activity in the brain is speculated to be associated with KD. Some mechanisms are thought to be a direct inhibition of voltage-gated sodium and calcium channels, modulation of a lipid-sensitive potassium channel, the activity of the sodium pump to limit neuronal excitability, or the induction of expression and activity of proteins in the mitochondria, thereby inducing a neuroprotective effect by partially inhibiting the production of reactive oxygen species (ROS) (Bough and Rho, 2007; Paoli et al., 2014).
Eating some protein, fiber, and healthy fat with all of your meals can help stabilize blood sugar and manage your appetite, especially when your meal also contains carbohydrate-dense foods like high-sugar fruits (mangos, grapes, cherries) or starchy vegetables (potatoes). Each of these nutrients helps balance blood sugar on its own, but they’re even better together. We love a good kale salad topped with avocado and grass-fed steak.
Hi Cindy, nut flour breads do not rise as much as wheat breads. Also, I used a small bread tin in the post – if you use a regular size bread pan your bread will end up flatter. What you can try next time is to try to keep the dough nice and fluffy, trying to keep as much air inside as possible (for example, not press it into the pan as much as you can). You could also try to whisk the egg whites until they’re stiff and fold them under last, which will make your dough lighter (=more air). I hope this helps
Urine test for diabetes: What you need to know Urine tests for diabetes check for protein, ketones, and glucose. They are frequently used for diagnosing and monitoring diabetes, and to assess people who are experiencing symptoms, such as fatigue or nausea. Depending on the results, recommendations may be given about medication or lifestyle changes that could help. Read now
According to most experts on the ketogenic diet, technically nutritional ketosis is defined by serum ketone levels (the amount of ketones in the blood) that fall between 0.5 to 3.0 mM. (3) Some believe that 1.5 – 3 mmol/L is “optimal ketosis,” which might contribute to the most weight loss. Every person is a bit different in terms of what exact macronutrient ratio will keep them in this range, while also allowing them to feel their best in terms of energy levels and other symptoms. You can experiment with different carb amounts while testing to see how this affects your ketone levels, aiming to remain in nutritional ketosis (0.5 to 3.0 mM), as long as you feel well doing so. Try to test at the same time each day for consistency and avoid testing right after exercise.
I tried this with the Psyllium husk powder I had (Konsyl) and it was too gummy. It looks like the Jay Robb is out of stock everywhere. If you had success with this bread using a different brand, would you share with me what brand worked? I could taste in the crust that this will be wonderful once I get the right psyllium. Thanks, everyone! I’m excited to nail this.
Hi Christy, It might be a little more difficult, but in theory possible. You’d need to stir the dry ingredients, then use a hand mixer instead of food processor to mix them with the butter. Then, after beating the egg whites separately, you’d need to mix in part of them, trying not to break them down, then fold in the rest once it’s easier to fold.
Dr. Sam has really made me so much believe in him by getting me cured with his herbal treatment. i really appreciate you Dr.Sam for bringing back happiness to my life again. thanks you so much,friends join me to thank him for what he has actually done for me i pray to you all for a good life and good health, and most especially to you Dr. Sam THANKS.
^ 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.
Hi Maria, glad you like the bread! Good question about the olive oil – on the one hand using the same amount as butter would mean you stick with the same wet/dry ratio, on the other had olive oil doesn’t firm up at room temperature, but butter and coconut oil do. Therefore, I’d try using a bit less olive oil than butter, maybe 40g instead of 60g. You could also get hold of refined coconut oil, which does not have the coconut taste, for example this one.
One hypothesised contributor to neuronal death is insufficient energy production, secondary to impaired mitochondrial function. However, it is unclear if this is in fact a cause or effect of PD. Whatever the case may be, patients with PD have been shown to have impaired mitochondrial energy production in the brain59 and lower brain glucose utilisation60. Another factor may be neuro-inflammation, which is also common in PD, and is thought to lead to further accumulation of Lewy Bodies and neuronal death.
Jennifer, The yeast has no carbs. The coconut sugar does have carbs, but the yeast feeds on it and through the process of fermentation uses the sugar for energy and releases carbon dioxide gas as a result. The yeast is for flavor, aroma, and in our opinion does help with a little bit of rise. Additionally, we don’t like to consider any foods “bad”, “off-limits”, or not keto. Instead, we opt to mainly eat nourishing real foods that fit into our daily macro intake. We hope this helps! Best of luck on your keto journey.