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Ketosis Metabolism

Can You Really Fix Your Metabolism With The Keto Diet?

Can You Really Fix Your Metabolism With The Keto Diet?

The new best-selling book “The Keto Reset Diet” says it can fix a sluggish metabolism and train your body to be a fat-burning machine. Experts are skeptical. It isn’t just you. Dieting is an endless pursuit for many Americans. Around 45 million Americans go on a diet each year. And the weight eventually comes back for 33 to 66 percent of people who’ve dieted. In the New York Times best-seller “The Keto Reset Diet: Reboot Your Metabolism in 21 Days and Burn Fat Forever,” author and keto diet enthusiast Mark Sisson writes that “yo-yo dieting is severely destructive to your metabolism.” He claims that following a low-carb, high-fat diet will help “turn you into a ‘fat-burning beast’ and stay this way for the rest of your life.” The book explains that the three-week keto reset diet does this by reprograming your genes into a state of “metabolic efficiency” — which he considers burning fat, rather than being “dependent upon regular high-carbohydrate meals to sustain your energy, mood, or cognitive focus.” Critics say the science doesn’t support these claims. Does yo-yo dieting really affect your metabolism? A person’s resting metabolic rate (RMR) is largely based on their weight, but factors like age and genetics also play a role. When someone significantly restricts calories to lose weight, their body can also enter starvation mode. Their metabolism slows down considerably to conserve energy. Extremely low-calorie diets make it easier to regain weight after a diet is over. If someone with a slowed metabolism hits their target weight and celebrates by eating the same amount of daily calories a person with a typical RMR and of their same weight and age would eat, they could gain weight rapidly. Case in point: contestants from the TV show Continue reading >>

Differential Metabolic Effects Of Saturated Versus Polyunsaturated Fats In Ketogenic Diets

Differential Metabolic Effects Of Saturated Versus Polyunsaturated Fats In Ketogenic Diets

Ketogenic diets (KDs) are used for treatment of refractory epilepsy and metabolic disorders. The classic saturated fatty acid-enriched (SAT) KD has a fat:carbohydrate plus protein ratio of 4:1, in which the predominant fats are saturated. We hypothesized that a polyunsaturated fat-enriched (POLY) KD would induce a similar degree of ketosis with less detrimental effects on carbohydrate and lipid metabolism. Twenty healthy adults were randomized to two different weight-maintaining KDs for 5 d. Diets were 70% fat, 15% carbohydrate, and 15% protein. The fat contents were 60 or 15% saturated, 15 or 60% polyunsaturated, and 25% monounsaturated for SAT and POLY, respectively. Changes in serum β-hydroxybutyrate, insulin sensitivity (SI), and lipid profiles were measured. Mean circulating β-hydroxybutyrate levels increased 8.4 mg/dl in the POLY group (P = 0.0004), compared with 3.1 mg/dl in the SAT group (P = 0.07). SI increased significantly in the POLY group (P = 0.02), whereas total and low-density lipoprotein cholesterol increased significantly in the SAT group (both P = 0.002). These data demonstrate that a short-term POLY KD induces a greater level of ketosis and improves SI, without adversely affecting total and low-density lipoprotein cholesterol, compared with a traditional SAT KD. Thus, a POLY KD may be superior to a classical SAT KD for chronic administration. It has been known for many years that serum PTH rises with age, and it has been suggested that this rise may contribute to bone loss in postmenopausal women. It has been variously attributed to declining renal function, declining calcium absorption efficiency, and declining serum 25-hydroxyvitamin D [25(OH)D] levels. We studied the effects of age, weight, renal function, radiocalcium absorption, serum ionized Continue reading >>

The Ketogenic Diet's Effect On Cortisol Metabolism

The Ketogenic Diet's Effect On Cortisol Metabolism

(Related post: Red Light, Green Light: responses to cortisol levels in keto vs. longevity research) One of the myths surrounding ketogenic diets comes from misunderstanding the role of cortisol — the "stress hormone". In a previous post, we addressed one of the arguments behind this myth: the idea that to activate gluconeogenesis (to make glucose out of protein), extra cortisol must be recruited. That is just factually incorrect, as we showed in the post. The other argument, which we address here, is more complex. Like the previous cortisol myth, it involves a faulty chain of reasoning. Here are the steps: Ketogenic diets may raise certain measures of cortisol. Chronically elevated cortisol is correlated with metabolic sydrome, and therefore higher cortisol measures may indicate the onset of metabolic syndrome. Therefore, ketogenic diets could cause metabolic syndrome. Metabolic syndrome is a terrible and prevalent problem today. It is that cluster of symptoms most strongly identified with diabetes — excess abdominal fat, high blood sugar, and a particular cholesterol profile — but also correlated with other life-threatening conditions such as heart disease and cancer. In this post, we're going to explain some of the specifics of cortisol metabolism. We'll show how this argument is vague, and how clarifying it leads to the opposite conclusion. The confusion may all stem from misunderstanding one important fact: different measures of cortisol are not equivalent. First, though, there is an important reason why the argument doesn't make sense. We already know that a ketogenic diet effectively treats metabolic syndrome. As we will describe below, it turns out that certain cortisol patterns are strongly linked to metabolic syndrome, and might even be a cause of metabol Continue reading >>

Metabolic Effects Of The Very-low-carbohydrate Diets: Misunderstood

Metabolic Effects Of The Very-low-carbohydrate Diets: Misunderstood "villains" Of Human Metabolism

Go to: The Ketone Bodies are an Important Fuel The hormonal changes associated with a low carbohydrate diet include a reduction in the circulating levels of insulin along with increased levels of glucagon. This activates phosphoenolpyruvate carboxykinase, fructose 1,6-biphosphatase, and glucose 6-phosphatase and also inhibits pyruvate kinase, 6-phosphofructo-1-kinase, and glucokinase. These changes indeed favor gluconeogenesis. However, the body limits glucose utilization to reduce the need for gluconeogenesis. In the liver in the well-fed state, acetyl CoA formed during the β-oxidation of fatty acids is oxidized to CO2 and H2O in the citric acid cycle. However, when the rate of mobilization of fatty acids from adipose tissue is accelerated, as, for example, during very low carbohydrate intake, the liver converts acetyl CoA into ketone bodies: Acetoacetate and 3-hydroxybutyrate. The liver cannot utilize ketone bodies because it lacks the mitochondrial enzyme succinyl CoA:3-ketoacid CoA transferase required for activation of acetoacetate to acetoacetyl CoA [3]. Therefore, ketone bodies flow from the liver to extra-hepatic tissues (e.g., brain) for use as a fuel; this spares glucose metabolism via a mechanism similar to the sparing of glucose by oxidation of fatty acids as an alternative fuel. Indeed, the use of ketone bodies replaces most of the glucose required by the brain. Not all amino acid carbon will yield glucose; on average, 1.6 g of amino acids is required to synthesize 1 g of glucose [4]. Thus, to keep the brain supplied with glucose at rate of 110 to 120 g/day, the breakdown of 160 to 200 g of protein (close to 1 kg of muscle tissue) would be required. This is clearly undesirable, and the body limits glucose utilization to reduce the need for gluconeogenesis Continue reading >>

The Biggest Loser Fail And That Ketogenic Study Success

The Biggest Loser Fail And That Ketogenic Study Success

This week, splashed all over the New York Times, was an article about a paper written by Kevin Hall, a senior researcher at the National Institutes of Health. It was published in Obesity and titled “Persistent metabolic adaptation 6 years after ‘The Biggest Loser competition“. This generated a lot of hand-wringing about the futility of weight loss. NYT: After ‘The Biggest Loser,’ Their Bodies Fought to Regain Weight The study, along with another study presented by Kevin Hall seemed to generate more anxiety about the insulin hypothesis being dead. Of course, both these studies fit in perfectly with the hormonal view of obesity and reinforces once again the futility of following the Caloric Reduction as Primary approach. You could review my 50ish part series on Hormonal Obesity if you want a more in-depth view. So, let’s dive in an explain the findings of both of Dr. Hall’s excellent papers. His conclusions, well, let’s just say I don’t agree with them. The studies, though, were very well done. The Biggest Loser Let’s start with the first paper about the Biggest Loser. Essentially, what it did was follow 14 of the 16 Biggest Loser contestants. At the end of the show, they had all lost significant amounts of weight following a Eat Less, Move More approach. Contestants eat about 1000 – 1200 calories per day and exercise like mad people. What the study showed is that basal metabolism drops like a piano out of the Empire State building. It plummets. They are burning about 800 calories less per day than previously. The new paper shows that this metabolic rate does not recover even 6 years later. In other words, if you reduce your ‘Calories In’, your ‘Calories Out’ will automatically drop. This makes sense. If your body normally eats 2000 calories Continue reading >>

Metabolism And Ketosis

Metabolism And Ketosis

Dr. Eades, If the body tends to resort to gluconeogenesis for glucose during a short-term carbohydrate deficit, are those who inconsistently reduce carb intake only messing things up by not effecting full blown ketosis? If the body will still prefer glucose as main energy source unless forced otherwise for at least a few days, is it absolutely necessary to completely transform metabolism for minimal muscle loss? Also, if alcohol is broken down into ketones and acetaldehyde, technically couldn’t you continue to drink during your diet or would the resulting gluconeogenesis inhibition from alcohol lead to blood glucose problems on top of the ketotic metabolism? Would your liver ever just be overwhelmed by all that action? I’m still in high school so hypothetical, of course haha… Sorry, lots of questions but I’m always so curious. Thank you so much for taking the time to inform the public. You’re my hero! P.S. Random question…what’s the difference between beta and gamma hydroxybutyric acids? It’s crazy how simple orientation can be the difference between a ketone and date rape drug…biochem is so cool! P.P.S. You should definitely post the details of that inner mitochondrial membrane transport. I’m curious how much energy expenditure we’re talkin there.. Keep doin your thing! Your Fan, Trey No, I don’t think people are messing up if they don’t get into full-blown ketosis. For short term low-carb dieting, the body turns to glycogen. Gluconeogenesis kicks in fairly quickly, though, and uses dietary protein – assuming there is plenty – before turning to muscle tissue for glucose substrate. And you have the Cori cycle kicking in and all sorts of things to spare muscle, so I wouldn’t worry about it. And you can continue to drink while low-carbing. Continue reading >>

Mitochondria: The Ketogenic Diet—a Metabolism-based Therapy

Mitochondria: The Ketogenic Diet—a Metabolism-based Therapy

Abstract Mitochondria are the energy-producing organelles of the cell, generating ATP via oxidative phosphorylation mainly by using pyruvate derived from glycolytic processing of glucose. Ketone bodies generated by fatty acid oxidation can serve as alternative metabolites for aerobic energy production. The ketogenic diet, which is high in fat and low in carbohydrates, mimics the metabolic state of starvation, forcing the body to utilize fat as its primary source of energy. The ketogenic diet is used therapeutically for pharmacoresistant epilepsy and for “rare diseases” of glucose metabolism (glucose transporter type 1 and pyruvate dehydrogenase deficiency). As metabolic reprogramming from oxidative phosphorylation toward increased glycolysis is a hallmark of cancer cells; there is increasing evidence that the ketogenic diet may also be beneficial as an adjuvant cancer therapy by potentiating the antitumor effect of chemotherapy and radiation treatment. This article is part of a Directed Issue entitled: Energy Metabolism Disorders and Therapies. Continue reading >>

Ketogenic Diets And Physical Performance

Ketogenic Diets And Physical Performance

Abstract Impaired physical performance is a common but not obligate result of a low carbohydrate diet. Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis. Introduction In the opinion of most physicians and nutrition scientists, carbohydrate must constitute a major component of one's daily energy intake if optimum physical performance is to be maintained [1]. This consensus view is based upon a long list of published studies performed over the last century that links muscle glycogen stores to high intensity exercise. It has also been reinforced by the clinical experience of many physicians, whose patients following low carbohydrate formula or food diets frequently complain of lightheadedness, weakness, and ease of fatigue. During the time that this consensus view of the necessity of carbohydrate for vigorous exercise was forming, the last pure hunting cultures among the peoples of North America finally lost out in competition with expanding European cultural influences. Between 1850 and 1930, the routine consumption of carbohydrates spread north from the U.S. Plains States through central Canada, where the indigenous peoples had heretofore made at most seasonal use of this nutrient class. However the last of these groups to practice their traditional diet, the Inuit people of the Canadian and Alaskan Arctic regions, were luckily observed by modern scientists before their traditional dietary practices were substantially altered. The reports of these early scientists imply that the Inuit people were physically unhampered despite consuming a diet that was essentially free of ide Continue reading >>

Ketosis

Ketosis

There is a lot of confusion about the term ketosis among medical professionals as well as laypeople. It is important to understand when and why nutritional ketosis occurs, and why it should not be confused with the metabolic disorder we call ketoacidosis. Ketosis is a metabolic state where the liver produces small organic molecules called ketone bodies. Most cells in the body can use ketone bodies as a source of energy. When there is a limited supply of external energy sources, such as during prolonged fasting or carbohydrate restriction, ketone bodies can provide energy for most organs. In this situation, ketosis can be regarded as a reasonable, adaptive physiologic response that is essential for life, enabling us to survive periods of famine. Nutritional ketosis should not be confused with ketoacidosis, a metabolic condition where the blood becomes acidic as a result of the accumulation of ketone bodies. Ketoacidosis can have serious consequences and may need urgent medical treatment. The most common forms are diabetic ketoacidosis and alcoholic ketoacidosis. What Is Ketosis? The human body can be regarded as a biologic machine. Machines need energy to operate. Some use gasoline, others use electricity, and some use other power resources. Glucose is the primary fuel for most cells and organs in the body. To obtain energy, cells must take up glucose from the blood. Once glucose enters the cells, a series of metabolic reactions break it down into carbon dioxide and water, releasing energy in the process. The body has an ability to store excess glucose in the form of glycogen. In this way, energy can be stored for later use. Glycogen consists of long chains of glucose molecules and is primarily found in the liver and skeletal muscle. Liver glycogen stores are used to mai Continue reading >>

How To Fix Your Broken Metabolism By Doing The Exact Opposite

How To Fix Your Broken Metabolism By Doing The Exact Opposite

We saw last week with the Biggest Loser study that basal metabolism plummets when you lose weight with calorie reduction. As contestants lose weight, they burn a lot less energy – up to 800 calories per day less than before. Some of that is expected, since there is less body tissue to maintain, but nevertheless, these contestants burn far less than expected even taking this into account. Even 6 years later, their basal metabolic rate (BMR) remains depressed, as do the contestants themselves. The story got a lot of coverage, but one thing was consistently missing. How to fix it.That’s what I’ll show you today, and it’s the opposite of what most people expect. So, let’s think about this problem in the context of the 2 compartment model of obesity that we have used before. There are two compartments for body energy. We take calories in as food. This gets stored in the short term as glycogen, or long term as body fat. Glycogen is easily converted to energy (calories out), but body fat, not so much. So we can consider the analogous situation where short term energy is stored in a refrigerator and long term in the basement freezer. Insulin’s role is to direct food into the basement freezer. When there is excess food that can’t be kept in the fridge, insulin directs it to the freezer. This is body fat and manufactured in the liver by the process of de novo lipogenesis. What causes insulin levels to be elevated depends partly on the foods we eat, but also by insulin resistance. Fructose, for example, plays a key role in elevating insulin resistance which will, in turn raise insulin levels. Insulin resistance leads to high insulin levels, which leads to higher resistance in a vicious cycle. That is, it can be self sustaining. So during weight loss, if we don’t ad Continue reading >>

The Ketogenic Diet And Weight Loss Plateaus

The Ketogenic Diet And Weight Loss Plateaus

I keep hearing people talk about their weight loss plateaus, and how they can get around them. Some go the extreme route of doing liquid fasting, others will ignore it and keep on keeping on. I wanted to put together a short list of common things that may be wreaking havok on the average ketogenic dieter, and go over some solutions that might help out. Keep in mind, this does not cover everything and it also covers a wide range of topics. As you read this, please read to the end. Don’t form ideas about your own body and apply the things that I am saying with no thought behind it. This is strictly for people that are hitting weight loss plateau’s and need some help. If you have only lost 1 or 2 pounds in a week, that is still weight loss and does not require action against it. Hidden Carbohydrates People on ketogenic diets eat more carbohydrates than they think. They’re hidden in vegetables, nuts, and certain meat products. Yes, that peanut butter you’re chomping on could be causing a problem! Especially if it’s store bought – that stuff is loaded with extra sugar. Some vegetables like Brussels sprouts, broccoli, and squash are common culprits that find their way into our lives on a frequent basis. You might think that they’re low carb, but in large consumption, those carbs really do add up. You can look at the list of the best low carb vegetables we’ve put together, so that you can be more aware of the vegetables you eat. Meat is the center of most of our lives, and there’s sugar everywhere you look. Some bacon is honey smoked, adding unnecessary carbs to an already delicious product. Why the madness? Look for bacon with no sugar added. When you start to look into Italian sausages, chorizo, and canned meats, there’s more carbs than most think. Some b Continue reading >>

A Ketogenic Diet Extends Longevity And Healthspan In Adult Mice

A Ketogenic Diet Extends Longevity And Healthspan In Adult Mice

Summary Calorie restriction, without malnutrition, has been shown to increase lifespan and is associated with a shift away from glycolysis toward beta-oxidation. The objective of this study was to mimic this metabolic shift using low-carbohydrate diets and to determine the influence of these diets on longevity and healthspan in mice. C57BL/6 mice were assigned to a ketogenic, low-carbohydrate, or control diet at 12 months of age and were either allowed to live their natural lifespan or tested for physiological function after 1 or 14 months of dietary intervention. The ketogenic diet (KD) significantly increased median lifespan and survival compared to controls. In aged mice, only those consuming a KD displayed preservation of physiological function. The KD increased protein acetylation levels and regulated mTORC1 signaling in a tissue-dependent manner. This study demonstrates that a KD extends longevity and healthspan in mice. To access this article, please choose from the options below Now available: purchase access to all research journal HTML articles for 6 or 36 hours. Click here to explore this opportunity. Purchase Access to this Article If you are a current subscriber with Society Membership or an Account Number, claim your access now. Continue reading >>

Metabolic Damage And Keto Adaptation – Why And How.

Metabolic Damage And Keto Adaptation – Why And How.

I have been getting questions about how to keto adapt, and how long does keto adaption take etc. and does keeping calories up while keto dieting, does this reduce metabolic damage or adaptation even if your carbs are very low? So what this question is kind of centering on is the concept about metabolic damage and adaptation. My take is that your body becomes very efficient at burning calories when you drive your calories lower and lower and do more and more steady state cardio. I’m not talking about 1 or 2 – 45 min cardio sessions a week, I’m talking more about one or two hours of cardio per day. So this is a high amount of cardio and very low calories. Essentially what you’re doing is you’re just kind of metabolically shocking your system and your body responds by becoming a lot more efficient. Now these mechanisms of efficiency are starting to get studied in the scientific world but that’s basically kind of what we are talking about. Right now there isn’t much evidence, but they do believe something is there. The basis of these adaptations is definitely present. So how this does relate specifically to a ketogenic diet, and you know because your carbs are really low, can you still keep your calories high so you don’t get these metabolic adaptations. And the answer is yes. So what about ketosis? Let’s Get Scientific for a Moment This is a really important key to remember, ketosis is not weight loss, instead ketosis is actually a metabolic state when fat is being burned as your primary fuel source and then ketones are being produced. Ketones are by products of fat metabolism. Fat is getting oxidized at a very high rate, which results in ketone production and then you can measure ketones in either your urine (not recommended as I discuss here in my TOP K Continue reading >>

What Is Ketosis?

What Is Ketosis?

"Ketosis" is a word you'll probably see when you're looking for information on diabetes or weight loss. Is it a good thing or a bad thing? That depends. Ketosis is a normal metabolic process, something your body does to keep working. When it doesn't have enough carbohydrates from food for your cells to burn for energy, it burns fat instead. As part of this process, it makes ketones. If you're healthy and eating a balanced diet, your body controls how much fat it burns, and you don't normally make or use ketones. But when you cut way back on your calories or carbs, your body will switch to ketosis for energy. It can also happen after exercising for a long time and during pregnancy. For people with uncontrolled diabetes, ketosis is a sign of not using enough insulin. Ketosis can become dangerous when ketones build up. High levels lead to dehydration and change the chemical balance of your blood. Ketosis is a popular weight loss strategy. Low-carb eating plans include the first part of the Atkins diet and the Paleo diet, which stress proteins for fueling your body. In addition to helping you burn fat, ketosis can make you feel less hungry. It also helps you maintain muscle. For healthy people who don't have diabetes and aren't pregnant, ketosis usually kicks in after 3 or 4 days of eating less than 50 grams of carbohydrates per day. That's about 3 slices of bread, a cup of low-fat fruit yogurt, or two small bananas. You can start ketosis by fasting, too. Doctors may put children who have epilepsy on a ketogenic diet, a special high-fat, very low-carb and protein plan, because it might help prevent seizures. Adults with epilepsy sometimes eat modified Atkins diets. Some research suggests that ketogenic diets might help lower your risk of heart disease. Other studies show sp Continue reading >>

Ppar Alpha: The Protein That Revs Up Metabolism And Ketosis

Ppar Alpha: The Protein That Revs Up Metabolism And Ketosis

PPAR alpha is a very important protein for metabolizing fat and for weight loss. If you want to interpret your genes, you can put them into SelfDecode. I’ve spoken about PPAR gamma. This post is about its related kin PPAR alpha, which has somewhat different effects. PPAR-alpha is a protein (transcription factor) that increases fat breakdown in the liver and elsewhere. Good metabolism is important for energy production. PPAR-alpha alters the expression of a large number of genes. PPAR-alpha is activated under conditions of calorie restriction and is necessary for the process of ketogenesis, a key adaptive response to prolonged fasting. PPAR-alpha is mainly found in the liver and brown fat, followed by the heart and kidney. Lower PPAR-alpha expression levels are found in the small and large intestine, muscle and adrenal gland. Activation of PPAR-alpha promotes uptake, utilization, and breakdown of fatty acids by increasing genes involved in fatty acid transport, binding, activation, and oxidation. Besides increasing fat utilization, it increases glucose production and bile synthesis/secretion (R). PPAR-alpha is critical for normal responses to fasting. Without PPARa, there is major metabolic disturbances including low levels of ketone bodies, hypoglycemia, and fatty liver. PPAR alpha helps with the detoxification of drugs and toxins (R). PPAR alpha is protective against heart disease by inhibiting macrophage inflammation and increasing cholesterol efflux (via LXR and ABCA1) (R). PPAR-a can help increase IGF-1, which will help you build muscle. Mice without PPAR-alpha have 40% less IGF-1 (R). PPAR alpha increases UCP-3 (R), which is important for fat loss. This and other mechanisms make PPAR alpha important for fat loss. Males are more prone to Th17 dominance, while fema Continue reading >>

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