Will This Kick Me Out Of Ketosis?
A common question people have when starting keto is “will this kick me out of ketosis?” I’m going to address as many items as I can think of and explain why it will or will not kick you out of keto. This is going to be as comprehensive as possible so either use ctrl + f to find what you’re looking for or buckle up and read on. How do humans enter ketosis in the first place? Things will become much more clear if we explain how humans enter ketosis. Mainly, liver glycogen is what determines if ketones will be produced. Specifically, glycogen in the liver signals malonyl-coa to be formed by carboxylating acetyl-coa. Acetyl-coa is used in many processes and it’s the main substrate used to be turned into ketones. The wiki on regulation of ketogenesis which applies to this scenario says “When the body has no free carbohydrates available, fat must be broken down into acetyl-CoA in order to get energy. Acetyl-CoA is not being recycled through the citric acid cycle because the citric acid cycle intermediates (mainly oxaloacetate) have been depleted to feed the gluconeogenesis pathway, and the resulting accumulation of acetyl-CoA activates ketogenesis.” Basically, when there is more acetyl-CoA than oxaloacetate, the acetyl-CoA becomes acetoacetate, a ketone body. In plain English, carbs provide oxaloacetate, so if it doesn’t have carbs, it likely isn’t going to kick you out of ketosis. I’ll state the exceptions later. Why do humans enter ketosis so readily? Humans enter ketosis faster than any animal on the planet. It usually takes 24-36 hours before we enter ketosis.This is because we have huge brains and tiny bodies. Our brains need ~400 calories/day, which for most people that equates to 20% of our total energy demands. To put this in perspective, most anim Continue reading >>
How long does it take for sugar cravings to go away on keto?
Most people that start a keto diet plan find that they have some intense cravings for sugar in the beginning, but will dissipate after a few weeks. Even the seasoned low carber will tell you that they have cravings every once in a while, sometimes burning inside them so deep they want to give up to temptation. That’s where sweeteners come in, where you can make or bake things you usually can’t eat. Of course, you will have to watch out because most things that say “carb free” actually still contain carbs. Make sure you take the net carbs of any impacting sweetener into consideration when tracking your macros. As a general rule of thumb, it’s always best to try to avoid sweeteners in the beginning. They’re well known to cause cravings and some may stall your progress with over-use. Stay strict and try to only occasionally consume sweet treats when you are on a low carb diet. Types of Sweeteners In general, there are a few classifications of sweeteners. There are natural sweeteners, sugar alcohols, and synthetic sweeteners (or artificial sweeteners). There are a few others that aren’t exactly classified in these categories (like glycerin based sweeteners) but they are quite uncommon and rarely used, so we’ll skip going over them. For a ketogenic diet, I personally suggest sticking with erythritol and stevia (or a blend) because they are both naturally occurring, don’t cause blood sugar or insulin spikes, and sweeten just perfectly. When used in combination, they seem to cancel out the aftertaste that each has, and work like a charm. When you purchase sweeteners, make sure to take a look at the ingredients on the packaging. You normally want the pure sweetener, rather than having fillers such as maltodextrin, dextrose, or polydextrose which can cause spik Continue reading >>
What is a glycemic index diet?
A glycemic index diet is an eating plan based on how foods affect your blood sugar level. The glycemic index is a system of assigning a number to carbohydrate-containing foods according to how much each food increases blood sugar. The glycemic index itself is not a diet plan but one of various tools — such as calorie counting or carbohydrate counting — for guiding food choices. The term "glycemic index diet" usually refers to a specific diet plan that uses the index as the primary or only guide for meal planning. Unlike some other plans, a glycemic index diet doesn't necessarily specify portion sizes or the optimal number of calories, carbohydrates, or fats for weight loss or weight maintenance. Many popular commercial diets, diet books and diet websites are based on the glycemic index, including the Zone Diet, Sugar Busters and the Slow-Carb Diet. Purpose The purpose of a glycemic index (GI) diet is to eat carbohydrate-containing foods that are less likely to cause large increases in blood sugar levels. The diet could be a means to lose weight and prevent chronic diseases related to obesity such as diabetes and cardiovascular disease. Why you might follow the GI diet You might choose to follow the GI diet because you: Want to lose weight or maintain a healthy weight Need help planning and eating healthier meals Need help maintaining blood sugar levels as part of a diabetes treatment plan Studies suggest that a GI diet can help achieve these goals. However, you might be able to achieve the same health benefits by eating a healthy diet, maintaining a healthy weight and getting enough exercise. Check with your doctor or health care provider before starting any weight-loss diet, especially if you have any health conditions, including diabetes. The glycemic index The GI Continue reading >>
What is glycerin used for?
It is a colourless,odourless, viscous liquid that is widely used in pharmaceutical formulations . Glycerolhas three hydroxyl groupsthat are responsible for its solubility in water and its hygroscopicnature. The glycerol backbone is central to all lipids known as triglycerides. Glycerolis sweet-tasting and of low toxicity. Approximately 950,000 tons per annum are produced in the USA and Europe; 350,000 tons of glycerol were produced per year in the United States alone from 20002004. Productionwill increase as the EU directive 2003/30/EC is implemented, which requires the replacement of 5.75% of petroleum fuels with bio fuel across all Member Statesby 2010, as glycerol is a byproduct in the production of biodiesel. It isprojected that by the year 2020, production will be six times more than demand. Triglycerides found in fats and oils are by definition esters of glycerol with long-chaincarboxylic acids; the hydrolysis (saponification) or transesterification of these triglycerides produces stoichiometric quantities of glycerol. In this scheme, glycerol is produced as a co-product in the production of long-chaincarboxylate salts used as soaps It is also a by product of the production of biodiesel via transesterification. This form of crude glycerin is often dark in appearance with a thick, syrup-like consistency. Triglycerides (1) are treated with an alcohol such as ethanol (2) with catalytic base to give ethyl esters of fatty acids (3)and glycerol (4): Glycerol from triglycerides is produced on a large scale, but the crude product is of variable quality, with a low selling price of as low as 1-8 U.S. cents perpoun Continue reading >>
Is xylitol safe for dogs?
I use Xylitol in my simple whitening toothpaste and by far the most asked question in the comments of that post is about the safety of xylitol usage. Though it is absolutely not safe (and can even be deadly) to dogs, there is some evidence that it has benefits in humans, especially for oral use. What is Xylitol? Xylitol is a polyalcohol or sugar alcohol found in many fruits and vegetables and extracted from corn or birch wood to make a sweetener that is similar in taste to sugar but with about 40% fewer calories. Even though Xylitol is extracted from natural sources, it goes through a process called sugar hydrogenation to become a shelf stable white powder for food and dental use. Though technically considered a low-digestible carbohydrate, it does not impact blood sugar levels the way sugar does (and this is one of the reasons it is so dangerous to dogs). It can have a laxative effect in humans (more on that below) but it generally considered safe for human use, though it is a FODMAP and can be problematic for some people. It is widely used in chewing gum, oral health products and as a sugar substitute for those with diabetes or blood sugar related problems. Xylitol is even recommended in the natural health community and is in many anti-candida recipes and diets. But, is Xylitol actually healthy or safe? Xylitol as a Sweetener? Xylitol is a somewhat controversial sweetener, but is often promoted as safe for human consumption as a healthier alternative to sugar. Certainly, I don’t think it is saying much for something to be a healthier alternative to sugar, especially with all the problems sugar can cause, and just because something is considered safe for consumption, doesn’t necessarily mean it is healthy. I have my concerns with the way Xylitol is processed and it Continue reading >>
Is dextrose bad for you?
Glucose is the sugar our body extracts from food and transports via our bloodstream to our cells as energy. While found in our bodies, it can also be produced artificially (Dextrose is a component in most processed and packaged products as a sweetener) and is also known as corn sugar or grape sugar. Dextrose can also be used medically, for example as treatment, for Hypoglycemia (low blood sugar). Due to availability and low production costs, Dextrose is used extensively for a range of applications but is Dextrose bad for you ? It’s a fairly common question and in the following article, we investigate the pros and cons of Dextrose, potential side effects, and impact on patients with Diabetes, Kidney Disease, and Heart Disease. Dextrose is a component in most natural starchy foods such as wheat, potatoes, and rice; it’s also obtained naturally from living organisms. Honey and fruits are other rich sources of Dextrose. The baking industry uses Dextrose as a sweetener and resembles a fine powder (similar to icing sugar) or syrup. Also employed in hospitals for intravenous injections Dextrose is mixed with sterile water, combined with sodium and sometimes combined with amino acids. The solution can then be administered intravenously to patients who are unable to consume sufficient nutrients. Dextrose is also found in tablet or oral gel form and is available from most over-the-counter pharmacies. Is Dextrose Bad for You? If you are allergic to Dextrose, then it is of course, wise to avoid foods that contain it. There are specific medical conditions that MAY Continue reading >>
Can poison ivy cause dermatitis?
Poison ivy will fight back hard when it is touched. With all the technological and pharmaceutical advancements, there is really no great remedy either to prevent or treat poison-ivy-caused dermatitis and allergic reactions. However, avoid contacting with the plant can prevent the rash and this is recommended especially for a type 1 and type 2 diabetes patient.The sap oil secreted by poison ivy called uruhiol is the culprit which once contacted must be washed off immediately. Poison ivy is not contagious although the rashes look red and filled with blisters often are shunned by people. The rash can spread to anywhere on the body if the urushiol still remains. In mild cases, when contracted some sort of home remedy is used either self prescribed, told by friends and relatives or by online search. This may include: blow drying the blisters, applying the inside part of a banana pill to the rashes, applying Jewel Weed extract, applying toothpaste, or taking an oatmeal bath, etc. Benadryl cream, calamine lotion and hydro-cortisone cream are often recommended by pharmacists when none of the above work. In the severe cases, patients will visit a physician and doctors will prescribe oral prednisone. So why do diabetes patients have to be extra careful about poison ivy: Although there is no concrete evidence that poison ivy increases blood sugar, but the prednisone will cause temporary increase in blood sugar. Poison ivy causes temporary inflammation and skin lesions and the healing process may be somewhat delayed in diabetes patients. Diabetes patients are more prone to skin Continue reading >>
What is Diatrax 1.0?
I am writing to ask for your help in locating beta testers for Version 1.0 of Diatrax (TM), a web-based self-management system that enables diabetics to download readings from their glucose monitors and send them over the Internet to a secure web server, giving them and their personal caregivers 24x7 access to annotated data and trend charts. The system has been developed by my firm, healthCache.com .
Why do people take beta test?
Participating in the beta test may help individuals better manage their blood glucose levels.
What format is Diabetes Update?
I send out Diabetes Update e-mail in HTML format, which all Web browsers and most modern e-mail programs can display. HTML has live links to all the sites named in the text so that with a simple click of a mouse you can connect to the site you have just been reading about.
What is Diatrax program?
We have developed the Diatrax program to integrate with clinical information systems being put in place at healthcare facilities now, to serve as part of diabetes education centre programs. This way, people who use the program will be able to share annotated blood glucose and ketone results with their personal caregivers. Caregivers will be able to customize blood glucose target ranges, and receive automated alerts when individuals are outside their range or demonstrate other problems. We are in the planning stages of clinical trials at the moment, with the local university medical center. We also are interviewing for a US site for trials.
What is the normal range for diabetes?
When tested at standardized labs, as most are nowadays, 4-6% is the normal range. The American Diabetes Association has a goal for patients' levels to be below 7%, but doesn't encourage doctors to take action until the level goes above 8%.
What is the normal range for blood glucose?
When tested at standardized labs, as most are nowadays, 4-6% is the normal range.
Is glycerin a carbohydrate?
But apparently the reason that glycerin is not listed as a carbohydrate by these manufacturers is that glycerin does not effect blood glucose or insulin levels, they say. The dispute over glycerin is bad enough.
Why is low FFA good for you?
This is good because lower plasma FFA concentrations increase or enhance muscle breakdown. Additionally, having a more stable glycemic response and insulin response leads to less carbohydrate oxidation. Stable blood glucose levels reduce insulin spikes so muscle growth will continue and fat will not be stored!
Why is low glycemic index important?
Low Glycemic Index foods may confer an advantage when eaten before prolonged strenuous exercise by providing a slow-release source of glucose to the blood without the accompanying insulin surge.
How does low glycemic index affect performance?
Low Glycemic Index Foods may positively affect maximal performance following sustained exercise by maintaining a higher plasma glucose level (measured at the end of 2 hours of strenuous exercise) as compared to high glycemic foods.
Why is glycerine used in nutrition bars?
The use of glycerine in nutrition bars helps to control insulin spikes. Usually when consumers eat a large nutrition bar, they are NOT eating any other food at the same time. This gives the glycemic index of the bar an important impact on the glycemic response, which is crucial to insulin action.
How does insulin affect the body?
Insulin increases the use of glucose by most of the body's tissues. Insulin also promotes fa tty acid synthesis . If the amount of carbohydrates ingested exceeds the amount that can be utilized for immediate energy, the excess becomes used for fat synthesis.
Why is insulin important for muscle building?
When the quantity of glucose being transported into the liver exceeds what can be used and/or stored as liver glycogen, insulin promotes the conversion of this excess glucose into fatty acids with the ultimate result of increased fat deposition. Controlling insulin spikes is important to muscle building.
How does insulin affect muscle growth?
When the quantity of glucose being transported into the liver exceeds what can be used and/or stored as liver glycogen, insulin promotes the conversion of this excess glucose into fatty acids with the ultimate result of increased fat deposition. Controlling insulin spikes is important to muscle building. It is also vital for fat burning as well as for reducing body-fat storage.
Does alcohol cause insulin resistance?
As the alcohol-induced impairment was recapitulated by t-butanol (a non-metabolizable alcohol) and not antagonized by 4-methylpyrazole, the insulin resistance was likely mediated by alcohol and not one of its oxidative metabolites [117]. Furthermore, numerous studies have also demonstrated impaired whole-body IMGU in chronic alcohol-fed rats and mice [14,15,28,118,119,120,121]. Chronic alcohol-fed mice also show whole-body insulin resistance, as assessed using an insulin tolerance test [100]. To the contrary, another study indicated that alcohol-fed mice were actually more insulin sensitive and that alcohol feeding could partially ameliorate high-fat diet-induced impairment in insulin action [90].
What is the prevailing glucose concentration?
The prevailing blood glucose concentration is representative of discrete metabolic processes which regulate the rate of appearance (Ra) for glucose versusthose which consume and regulate glucose disappearance (Rd). Glucose Ra represents glucose influx into the circulation primarily from the liver via glycogenolysis and gluconeogenesis as well as nutrient absorption from the gastrointestinal tract, with the relative contribution of each source determined by the nutritional state of the host and the experimental circumstances. As few metabolic studies are performed in the fed condition, contribution of glucose from gastrointestinal tract absorption to whole-body glucose Ra is typically considered be nominal after an overnight (or longer) fast. Further, despite the possibility that alcohol may increase intestinal glucose absorption, any alcohol-induced change in whole-body glucose Ra is primarily considered a manifestation of glucose output by the liver [25,26].
Does alcohol affect insulin secretion?
The strong consensus from in vitroand ex vivomodels, although not entirely consistent, suggests that alcohol inhibits insulin secretion. Using the isolated perfused pancreas, alcohol did not alter basal insulin secretion but did impair glucose-stimulated insulin secretion (GSIS) in a dose-dependent manner [101]. Other studies reported that alcohol inhibits both early- and late-phase insulin secretion by the perfused rat pancreas [101,102]. Acute in vitrotreatment with alcohol or its metabolite, acetaldehyde, also dose-dependently reduces GSIS in isolated islets [103]. Moreover, a similar alcohol-induced reduction was observed when alcohol was administered in vivoand islet insulin secretion was assessed in vitro[104]. Likewise, incubation of INS-1 cells with 60 mM alcohol acutely reduced basal insulin secretion in a gamma-aminobutyric acid (GABA)-dependent manner [105]. In one of the most thorough in vitroexamination of the effect of alcohol on insulin secretion, alcohol had a dose-dependent inhibitory effect on basal and GSIS in INS-1 cells, dependent in part upon the duration of cell exposure to alcohol [106]. This inhibitory effect resulted from impaired muscarinic signaling and PKC activation, but was K-ATP channel-independent. Lastly, basal and GSIS are decreased in isolated islets from chronic alcohol-fed mice [100]. Thus, alcohol and its metabolites appear to have a consistent inhibitory effect on GSIS under in vitroconditions.
Does alcohol affect IMGU?
Skeletal muscle represents the largest body depot responsible for IMGU [130,131]. Therefore, an acute alcohol-induced decrease in IMGU by skeletal muscle per se has been inferred from experiments where whole-body insulin-stimulated glucose uptake is decreased during the glucose clamp (after correction for any residual endogenous HGP) [28,117,120]. Direct evidence for the suppression of muscle IMGU by acute alcohol was also reported in humans using the A-V difference method [52]. In further support, an alcohol-induced decrease in insulin-stimulated glucose disposal by skeletal muscle has been consistently detected in rats using radiolabeled 2-DG [12,14,117,118]. Interpretation of these seemingly consistent findings is complicated by a report showing that the magnitude of alcohol-induced insulin resistance is strain-dependent, with a more severe peripheral resistance observed in Sprague-Dawley rats compared to Long-Evans rats [14]. In contradistinction, as described above, the alcohol-induced hepatic insulin resistance is more prominent in Long-Evans vs. Sprague-Dawley rats. It has been suggested this strain difference may be related to differences in the generation of reactive oxygen species [28].
Does alcohol increase glucose tolerance?
Oral consumption of a moderate dose of alcohol at various times preceding an OGTT in humans has also been reported to improve glucose tolerance, which in this case may have resulted from an increase in pancreatic insulin secretion [26,93]. Similarly, chronic alcohol-fed mice have been reported to have improved glucose tolerance [94]. Some of this apparent discrepancy between these studies and the ones discussed in previous sections may be explained by a biphasic dose response (inverted U-shaped curve) to alcohol [95]. In this study an intravenous (IV) GTT was performed on rats maintained on different percentages of alcohol in drinking water. The data herein show that both relatively low (1%–2%) and high (7%) amounts of alcohol do not alter glucose disappearance, but that moderate doses of alcohol (3%) increase glucose tolerance and reduce the AUC for glucose. Large population-based studies have also reported that moderate alcohol intake over many years (>10 years) improves glucose tolerance and reduces the glucose-induced insulin secretion [96], implying increased insulin sensitivity.
Does alcohol affect glucose homeostasis?
Glucose homeostasis is critical for normal functioning of the central nervous system and cells which have an obligatory requirement for this metabolic substrate. Acute and chronic alterations in the prevailing glucose concentration (i.e., hypoglycemia and hyperglycemia) can adversely impact cellular and organ function. This review focuses on the etiology of ethanol (i.e., alcohol)-induced changes in glycemic control and insulin action at the molecular, cellular and tissue level, integrating the response of key glucoregulatory tissues including skeletal and cardiac muscle, adipose tissue and liver. As the underlying mechanisms of alcohol-induced changes are oftentimes dependent on the exposure time and intoxication level, these variables will be identified and accounted for when relevant. We will narrow our discussion to the effects of insulin on carbohydrate metabolism, but certainly acknowledge the potent metabolic effects this hormone has on both lipid and protein metabolism as well as the effect of alcohol on the secretion of other hormones [1]. Also, the literature pertaining to the ability of alcohol to alter insulin signaling pertaining to metabolic processes other than carbohydrate metabolism (e.g., hepatocyte growth and survival) will not be reviewed due to its extensive nature and readers are referred to other work on this topic [2]. Lastly, there is an equally extensive collection of literature on the effects of alcohol in individuals with type I and type II (±obesity) diabetes and it is not possible to include a systematic review of this topic. Throughout, where possible, we have highlighted limitations of various approaches which may complicate data interpretation and provide suggestions for future research opportunities in this area.
Does alcohol increase GSIS?
In contrast to its effect on insulin secretion in vitroand ex vivo, alcohol administered in vivohas been shown to enhance GSIS; in some instances this potentiated secretion is sufficient to increase the rate of glucose clearance from circulation (e.g., improve glucose tolerance) [26,107], but in others glucose tolerance remains impaired [99,111]. This priming effect develops within several hours [108] and occurs at relatively low alcohol concentrations (10 mM) [85]. Moreover, the ability of alcohol to enhance insulin secretion in humans was maintained in response to repetitive glucose challenges given over a 2 h period [93]. Such a priming effect, however, has not been observed in rats either after acute alcohol administration [98] or chronic alcohol feeding [57], but alcohol did inhibit the stimulatory action of the insulin secretagogue tolbutamide [98].
