To promote a better understanding of what constitutes a well-formulated ketogenic diet, we have identified 10 key characteristics:
Sustains nutritional ketosis
Maintains or improves lean body mass and performance
Effective electrolyte, mineral and hydration management
Fat provides majority of dietary energy in all phases
Counting calories is not necessary for success
Totally or predominantly composed of ‘whole foods’
Short-term very low-calorie diets should be avoided until proven effective in long term studies
Contraindicated for chronic conditions unless a credible long-term maintenance phase has been demonstrated
On going expert medical supervision required for medication management of chronic conditions (e.g., type 2 diabetes, hypertension)
A well-formulated ketogenic diet does not necessarily adhere to traditional dietary guidelines
The emphasis is on whole foods.
Defining Characteristic #6: A WFKD is preferably composed of all or mostly whole, unprocessed foods.
Choose fresh unprocessed vegetables, meats, eggs, dairy, berry fruit, and minimally seasoned nuts and seeds when possible
Fresh frozen choices with no added sugar and minimal processing are also encouraged
Fermented foods with no added sugar are allowed (e.g., yogurt, sauerkraut, pickles, kimchi).
Specialty frozen low carbohydrate meals can be used as needed
Exceptions to whole foods (electrolyte replacement): Magnesium and Bouillon (sodium)
Purified protein sources, specialized fats, high potency vitamin formulations, and meal-replacement formulations should be used sparingly.
Defining Characteristic #7: Any ketogenic regimen under 1000 kcal/d (very-low calorie diets (VLCD)) does not qualify as a WFKD due to a lack of adequate macronutrients and calories for long-term sustainability.
To our knowledge there are no published studies of sizeable cohorts fed a VLCD for up to 6 months that did not demonstrate substantial weight regain within 12 months. While very restricted prepared formula or food-based diets can have dramatic short-term effects on body weight and disease reversal, these benefits have proven to be fleeting when viewed one to two years post intervention.
Defining Characteristic #8: If intended to treat, manage, or reverse a chronic condition, a WFKD needs to have a credible maintenance phase that can be followed for years and decades.
For people with underlying insulin resistance in particular, a well-formulated ketogenic diet eaten to satiety frequently allows one to achieve a natural transition into a sustainable maintenance pattern of eating.
A short-term ketogenic diet or VLCD followed by the re-introduction of carbohydrate in amounts that reverse nutritional ketosis is seldom successful at maintaining weight loss or metabolic health long-term.
Long-term severe voluntary calorie restriction resulting in constant hunger is NOT a credible, sustainable maintenance strategy.
High volume exercise, particularly in individuals with a history of diabetes or obesity, is rarely an effective weight maintenance strategy in the absence of some degree of on-going carbohydrate restriction.
Defining Characteristic #9: A therapeutic WFKD requires expert supervision and avoidance of unnecessary cycling in and out of nutritional ketosis.
If intended to improve diabetes or hypertension, inconsistent and intermittent restriction of carbohydrate intake alone or in combination with restriction of total calories in the context of on-going medication use adds unacceptable risk of medication side-effects.
While time restricted feeding or intermittent fasting for periods less than 24 hours may be tolerated within the definition of a WFKD, any fasting longer than 24 hours, even if infrequent, is not likely to confer long-term benefits for those with chronic medical conditions.
Defining Characteristic #10: A well-formulated ketogenic diet does not necessarily adhere to traditional dietary guidelines.
A well-formulated ketogenic diet has characteristics that cannot be consistent with traditional dietary guidelines.
A “ketogenic diet” that is very energy restricted but contains a substantial carbohydrate content (e.g., 50% or more of energy), moderate protein, and low fat is not a well-formulated ketogenic diet.
Always consult with a trained physician when beginning a well-formulated ketogenic diet, especially if you have any health conditions and/or you are taking any medications.
If all of these ten characteristics are not addressed correctly, it is likely not a well-formulated ketogenic diet.
Nutritional ketosis achieved by consuming a well-formulated ketogenic diet can be a safe and sustainable therapy for a variety of conditions, particularly those driven by underlying insulin resistance or inflammation. To have a lasting effect, however, in most cases the physiological blood ketone levels characteristic of nutritional ketosis need to be maintained, along with adequate intake of electrolytes and minerals. When used to reverse disease states requiring medication withdrawal, constant medical oversight during the early phases of the dietary intervention is needed.
With attention to these 10 defining characteristics, we have demonstrated that a safe and sustainable state of nutritional ketosis is within reach for a majority of motivated adults who choose to try it.
SOURCE: The Ten Defining Characteristics of a Well-Formulated Ketogenic Diet
Stephen Phinney, MD, PhD, Jeff Volek, PhD, RD on August 13, 2018. This post has been condensed from the original Virta Post.
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Today’s focus is on: Ten Defining Characteristics of a Well-Formulated Ketogenic Diet by Stephen Phinney, MD, PhD, Jeff Volek, PhD, RD
To promote a better understanding of what constitutes a well-formulated ketogenic diet, we have identified 10 key characteristics:
Sustains nutritional ketosis
Maintains or improves lean body mass and performance
Effective electrolyte, mineral and hydration management
Fat provides majority of dietary energy in all phases
Counting calories is not necessary for success
Totally or predominantly composed of ‘whole foods’
Short-term very low-calorie diets should be avoided until proven effective in long term studies
Contraindicated for chronic conditions unless a credible long-term maintenance phase has been demonstrated
On going expert medical supervision required for medication management of chronic conditions (e.g., type 2 diabetes, hypertension)
A well-formulated ketogenic diet does not necessarily adhere to traditional dietary guidelines
Note: This Post contains the first 5 characteristics. The remaining 5 will follow next week.
The short and long-term health benefits of nutritional ketosis (NK) include a reduction in hunger and cravings, reduced inflammation and improved insulin sensitivity. These benefits of NK predictably lead to improved metabolic health and major weight loss.
A thorough understanding of the proper composition and management of a well-formulated ketogenic diet (WFKD) is essential in order to achieve and sustain the benefits of nutritional ketosis. In the short-term, appropriate fluid and electrolyte/mineral intakes that match the unique requirements associated with keto-adaptation are necessary for optimum well-being and can markedly reduce or prevent symptoms of the so-called ‘keto-flu’. Getting and keeping this formulation ‘right’ for the individual is necessary to optimize and sustain metabolic health, disease reversal (e.g., type 2 diabetes, metabolic syndrome, hypertension), and major weight loss.
It is also important to keep in mind that for individuals who start out taking medication for a major disease like type 2 diabetes and/or hypertension, a WFKD is a powerful medical therapy which necessitates day-by-day medication management by an expert physician and team to prevent dangerous drug side-effects. We strongly recommend getting medical supervision before making any dietary changes, especially if you are on medications for blood sugar or blood pressure. A physician can help you safely adjust your medications so that they don’t drive your blood sugar or blood pressure too low. Both hypoglycemic (low blood sugar) and hypotensive (low blood pressure) episodes can be very dangerous.
Here are 10 necessary basic components to optimize the benefits of nutritional ketosis and to avoid the common pitfalls.
Defining Characteristic #1: A WFKD must result in sustained nutritional ketosis.
Due to individual variations in carbohydrate tolerance, total daily carb intake can range from nearly 0 to 70 g/d.
Since beta-hydroxybutyrate (BOHB) functions as both a fuel and regulatory signal, we have defined nutritional ketosis as an average serum BOHB concentration in the range between 0.5 mM and 4.0 mM as measured by a finger stick glucometer with a ketone testing.
Despite its reduced carbohydrate content, food needs to be tastefully prepared with adequate variety so as to be palatable and sustainable.
Defining Characteristic #2: A WFKD has to provide adequate macronutrients to preserve lean body mass and function.
In this protein dose range, the addition of dietary carbohydrate is not necessary to maintain lean body mass.
The combination of both carbohydrate and protein intakes at the upper ends of an individual’s tolerance range typically drives ketones down out of the NK range, particularly for those with underlying insulin resistance. For this reason, the best practice of a WFKD typically requires holding protein in moderation and adding just enough dietary carbohydrate to allow dietary variety and provide valuable micro-nutrients and minerals from vegetables, nuts/seeds, and berry fruit.
Defining Characteristic #3: A WFKD contains enough electrolytes and intercellular minerals to maintain optimum circulatory, muscle, and nerve functions.
Adequate sodium and potassium are provided to support circulatory volume and avoid potassium depletion resulting in impaired muscle anabolism (building up process)or adrenal stress.
Accelerated renal sodium excretion associated with nutritional ketosis raises the typical adult daily sodium intake requirement to 4 – 5 g/d with exceptions for those taking medications for hypertension or congestive heart failure.
Magnesium depletion signs/symptoms such as muscle cramps, muscle fasciculations (flicker under the skin),and persistent hypokalemia (deficiency of potassium)are common in adults due to poor dietary intake combined with medication and/or alcohol effects on renal excretion.
Magnesium intake often needs to be increased by food choices or supplementation to normalize neuromuscular and cardiac functions as well as lean body mass preservation independent of dietary protein adequacy.
Defining Characteristic #4: In all phases of a WFKD, the majority of daily energy intake will come from dietary fat.
In all phases, the majority of fat needs to come from mono-unsaturated and saturated sources from the foods themselves or as added natural fats.
Adequate omega-6 essential fats are obtained from whole food vegetable and animal/vegetable protein sources. Omega-6 rich vegetable oil sources should be routinely avoided whenever possible.
As weight loss stabilizes and glycemic control typically improves over the first year of a well-formulated ketogenic diet, it may be possible to add a small amount of additional (unprocessed)carbohydrates back into the diet while still maintaining nutritional ketosis.
Protein remains relatively constant over this time, while fat intake may increase to meet caloric needs.
This graph, Daily caloric intake and expenditure, illustrates a typical physiological weight loss response to a well-formulated ketogenic diet eaten to satiety rather than when prescribed as a rigid caloric restriction. Note that in this scenario, dietary protein is moderate and unchanged, carbohydrate is held constant or only slightly increased in a narrow range, and one’s spontaneous intake of fat increases to sustain satiety as major weight loss transitions into weight maintenance.
In insulin resistant adults, carbs are initially limited to 30 grams per day, then liberalized slowly while maintaining ketosis.
Daily protein prescribed in a range between 1.2 and 2.0g/kg reference weight (approx. 15% daily expenditure). Fat is consumed to satiety.
Defining Characteristic #5: Counting or restricting calories is not necessary for lasting success.
While many “diets” restrict calories in order to get results, a well-formulated ketogenic diet allows the individual to eat fat to satiety and still lose weight and improve metabolic health.
Calorie counting is not essential; however, individuals must be mindful not to eat past satiety or purposefully consume fats in excess of energy needs in an effort to increase ketone values.
For many people who have spent a lifetime eating a fat-restricted diet, which promotes inflammation and inhibits satiety, experiencing the prompt sense of having eaten enough (i.e., satiety, not fullness) that occurs with nutritional ketosis can be a new experience.
Note: This Post contains the first 5 characteristics. The remaining 5 will follow next week.
SOURCE: The Ten Defining Characteristics of a Well-Formulated Ketogenic Diet
Stephen Phinney, MD, PhD, Jeff Volek, PhD, RD on August 13, 2018. This post has been condensed from the original Virta Post.
I invite you to Follow my Blog, Facebook or be added to my email distribution list. My focus is to maximize my physical performance and mental clarity, body composition, and most importantly overall health with a wholesome diet and exercise.
I will bring you compelling articles on Ketogenic and GAPS diets, the Super Slow High-Intensity Exercise Program and supplements.
To follow my Blog, please click the Follow button to receive an email when the next posting is available. Hint: You may have to click the Accept and Close button before follow is available.
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What follows is a condensed form of the Transcript of their presentation.
First, Drs. Phinney and Volek discuss the history of the Ketogenic diet.
Dr. Volek introduced the terms used in the diet. Understanding ketone concentration is fundamental. If you’re eating a normal mixed diet, your ketones are suppressed. So your concentration of ketones in your circulating blood is for most people under 0.2 millimolar.
When you restrict carbohydrates to under fifty grams a day, you normalize ketones into the range of nutritional ketosis, which is between 0.5 to 4. So that’s an entire order of magnitude higher than you would have on a normal mixed diet but an entire order of magnitude lower than what you see in ketoacidosis.
When we’re eating a well-formulated Ketogenic diet you’re normalizing ketones into this range. When you do that over a sustained period of time that is keto-adaptation. You double your rate of fat oxidation when you’re in ketosis.
Obese people following a well-formulated Ketogenic diet don’t need to count calories, they will naturally restrict fat intake.
There’s nothing more potent than a Ketogenic diet to lower triglycerides and it also consistently raises HDL cholesterol.
We consistently see decreases in the small LDL particles. There’s increasing evidence that they are the most atherogenic particles circulating. We see improvements in glucose and insulin and measures of insulin sensitivity as well as improvements in hormone sensitivity so we see improvements in greater decreases in leptin.
We’ve also measured saturated fat levels, we find that despite consuming two to four times as much saturated fat on a Ketogenic diet that levels in the blood actually go down or stay the same.
When you’re eating saturated fat on a Ketogenic diet you’re promptly oxidizing that incoming saturated fat and converting it to co2 and water it. Saturated fat is a preferred fuel when you’re in ketosis. This is very important because elevated levels of saturated fat in the circulation and in membranes is consistently associated with higher risk for heart disease, diabetes even some types of cancer. Half the inflammatory markers we measured in human trials were significantly decreased and the group fed a Ketogenic diet compared to a low-fat diet. We’re seeing this a potent inflammatory mechanism in some of patients with type 2 diabetes.
A Ketogenic diet essentially reverses all the signs and symptoms of metabolic syndrome. The more carbs you eat the more you have a higher likelihood of developing the insulin resistant phenotype and if that progresses, type-2 diabetes.The more you restrict carbohydrates especially down to levels that induce ketosis, the less likely to develop type 2 diabetes. It’s driven by carbs in the diet. Everybody has a slightly different carb tolerance and it changes over the lifespan but this relationship between carbs and manifestation of insulin resistant phenotype versus keto-adapted phenotype holds true.
Dr. Phinney will talk to you about some of the characteristics of a well-formulated Ketogenic diet.
This is best visual representation we’ve come up with to differentiate the Ketogenic diet from a the standard American diet, the Mediterranean diet and the Paleo diet.
To achieve nutritional ketosis you have to get under 10% of a 2000-calorie diet, or about 50 grams of carbs. If you take your protein intake too high that protein intake begins to suppress ketogenesis. Your intake should be 20% or less protein. The energy your body burns comes from the 80% of fat.
What Goes into a Well Formulated Ketogenic Diet? In terms of about a 2,000-calorie per day intake, the fat is eaten to satiety rather than counting calories. When you take the carbs down and get that insulin signalling down,natural instincts drive fat intake.If we restrict carbs, what can you have?
Eating a moderate proteinintake the protein-based carbs might be 5 to 10 grams per day. If you eat 3 to 5 servings of non-starchy vegetablesper day that is in the 10 to 15 to gram range. If you eat 1 to 2 ounces of nuts and seedsper day that’s 5 to 10 grams.
There is a wide range of luscious foods and still stay in the 30 to 50 gram range.. The vast majority of the calories here are coming from fat, but only till they are satisfied. Dr. Phinney put up a screen that displays a typical menu.
People experience improvement. People with type 2 diabetes, taking a 100 units of insulin a day, have been taken off insulin. We (doctors) can do that when we get the diet composition right for the metabolic needs of each person. The key here is keepingprotein moderate and carbohydraterestricted.
The best way todetermine your individual carbohydrate tolerance is you get a finger stickglucometer with a ketone testing and measure your ketones.
Then what should I be eating? 90 grams of protein and 30 grams of carbohydrate that would be 120 calories of carb and 360 calories of protein and then eat fat to satiety. Most people were under eating total calories. The difference between their expenditure and their intake was basically unseen dietary fat but the dietary fat was coming from internal fat reserves.
The weight loss continues over several months and until people reach a new steady state. We don’t count calories. From day one and in maintenance our dietary instruction are: restrict carbs to 20-50 grams depending on tolerance and proteins to 90 grams and eat fats till satisfied.
First characteristic, sustained nutritional ketosis appears to have better clinical response than the intermittent ketosis in terms of degree of weight loss and improvement in insulin resistance.
Next, it needs to maintain lean body mass and function. A well-formulated Ketogenic diet, when not overeating protein maintains or increases lean body mass.
Next, electrolyte and mineral management, when someone enters the state of nutritional ketosis sodium excretion increases. When you combine a Ketogenic diet where the sodium restricted diet in somebody who doesn’t have obvious need for sodium restriction, (hypertension or congestive heart failure), you’ll cause a decrease circulating volume and that leads to a symptoms and side effects that are oftentimes called the keto flu.It is actually an inadequacy of an essential nutrient called sodium to meet physiological needs. The solution is to add sodium to your daily intake.
We have data from five published studies. The yellow, the purple one and the green one are all studies that used formula weight loss diets under a thousand calories per day for the roughly the first three to five months and then were followed up from anywhere to a year to two years.
In all of these cases by the end of the first year weight regain is beginning. The blue line shows a case for type 2 diabetes, where when people are eating fat to satiety from day one. The weight loss is slower but it’s more progressive and that at the end of year one we don’t see what rebound and weight regain.
Because a chronic condition such as type 2 diabetes isn’t going to be cured in one year, why use something, which is only going to provide transient benefit and then begin to lose control and gain that weight back. A well-formulated Ketogenic diet will have a lasting benefit.
People who are on medications for hypertension or type 2 diabetes have to have real-time medication management through the physician and pharmacist or nurse to avoid the side-effects of too much medication in the context of too little carbohydrate coming in and dramatically improving insulin sensitivity.
Lastly, a well-formulated Ketogenic diet does not necessarily here to traditional dietary guidelines.
In the next to last slide the first point is the need to provide adequate sodium. With the exception of hypertension or congestive heart failure or conditions where people have to restrict sodium our experience clinically is we need to provide them with 5 grams of sodium intake per day.(I understand that to be natural salt not processed salt.)
For different cultures the low point in terms of mortality for measured sodium excretion, the optimum intake is about 4 grams per day without people being in nutrition of ketosis? Add nutritional ketosis 5 is a modest number.
When somebody is in weight maintenance, the average person burning 2,000 calories a day needs to eat about 150 grams of fat per day. Whenyou’re in nutritional ketosis and you’vedoubled your rate of fat oxidation. Itappears that some of the first fats thatget into the pathway for oxidation arethe saturated fats and in spite of higher intake, they don’t build up in theblood and if anything are reduced.
Worrying about saturated fats is only associated when you’re combining them with a significant proportion of carbohydrates in your diet. Gettingadequate potassium and magnesium asminerals as those are important, thosecome from leafy greenvegetables and to some degree berryfruits or homemade bone broth.
In the last slide, ketones are fuel for the brain, heart function, and multiple organ systems and for gut function.
If you eat dietary fiber and your microbiome makes it into butyrate, an optimal fuel for the gut that’s easily replaced with beta-hydroxybutyrate, a by-product of a Ketogenic diet.
Beta-hydroxybutyrate is a beneficial regulatory hormone that regulates the body’s defence against oxidative stress and inflammation, which has an impact on longevity and lifespan impact on inflammatory diseases and cell signalling and mitochondrial function.
Source: Dr. Stephen Phinney and Dr. Jeff Volek on the Basic Science of Ketosis and Keto-Adaptation
Dr. Stephen Phinney and Dr. Jeff Volek co-authored several books, including The Art and Science of Low Carbohydrate Living and The Art and Science of Low Carbohydrate Performance.
I invite you to Follow my Blog, Facebook or be added to my email distribution list. My focus is to maximize my physical performance and mental clarity, body composition, and most importantly overall health with a wholesome diet and exercise.
I will bring you compelling articles on Ketogenic and GAPS diets, the Super Slow High-Intensity Exercise Program and supplements.
To follow my Blog, please click the Follow button to receive an email when the next posting is available. Hint: You may have to click the Accept and Close button before follow is available.
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I have wondered about the role of fiber. I found it hard to get enough in my diet. As I have learned from this article, as long as I am in nutritional ketosis I should not worry.
There are a few dietary recommendations that have been so ingrained in our minds that we accept them without question. The need for dietary fiber and the proposed benefits of a high fiber diet seem to be two of these.
Adults are generally encouraged to consume at least 25 to 30 grams of fiber per day. A well-formulated ketogenic diet (WFKD), while necessarily restricted in its carbohydrate content, can include several classes of foods that provide fiber (e.g., vegetables, seeds, nuts), but on average may only provide about half this amount.
However, the nutritional ketosis resulting from a WFKD causes the liver to produce beta-hydroxybutyrate (BOHB), and BOHB has the potential to replace some of the functions of dietary fiber. Many of the benefits of fiber are attributable to its fermentation by bacteria, which produce short-chain fatty acids (SCFAs) in the colon, especially one called butyrate. SCFA has metabolic properties that are very similar to those of BOHB. Therefore, a well-formulated ketogenic diet may provide many of the benefits of fiber, without a high carbohydrate intake.
Snapshot: Two Pathways to Colonic Fuel and Health
Followers of a Western Diet depend upon fiber to produce butyrate. Butyrate is a preferred fuel to nourish the cells lining the large intestine (colon).
We now know that a ketogenic diet can induce the liver to produce anywhere between 75 to 150 grams of beta-hydroxybutyrate (BOHB) every day. Both butyrate and BOHB can be used by mitochondria as an efficient fuel, and both have anti-inflammatory and epigenetic effects.However, in this inflammation-modulating role, BOHB is more potent.
So, here’s our (Drs. Phinney and Volek) hypothesis: while high dietary fiber plus an optimum microbiome is critical to one’s health when eating a Western diet, this less important for the ketogenic diet. This is because adequate dietary carbohydrate restriction can induce the liver to produce many-fold more grams of BOHB than one could produce as butyrate via colonic fermentation. Thus, the keto-adapted individual might still be able to function without the need for as much fiber.
Strong biochemical evidence indicates that many of the benefits of fiber fermentation in the colon can be replaced by the normal physiological production of BOHB by the liver during a well-formulated ketogenic diet.
What is Fiber? Fiber is composed of various components of plants such as vegetables, grains, legumes, nuts, and fruits that are neither digested nor absorbed in the small intestine but are fermented by bacteria in the colon.
Fiber is often further separated into two categories:
Soluble (absorbs water, increases stool bulk, prone to fermentation)
Insoluble (promotes motility, less prone to fermentation)
Soluble fiber plays a supporting role in colon health, but only if one has an optimized microbiome that produces butyrate. Fiber primarily facilitates the production of SCFAs like butyrate, they are the real stars of the show.
Short-Chain Fatty Acids: Three SCFAs – acetate, propionate and butyrate – are produced in the intestinal lumen by bacterial fermentation of dietary fiber. Butyrate provides many of the health-promoting effects associated with colonic fermentation of fiber.
Butyrate acts as a histone deacetylase (HDAC) inhibitor. HDACs are enzymes that regulate specific genes and can help reduce unwanted cell growth and oxidative stress. BOHB is also an HDAC inhibitor. Both butyrate and BOHB bind to the same cell surface receptor in the colon, which means they can have similar tumor suppressing effects upon binding. This is likely one of the underlying mechanisms by which fiber intake is understood to contribute to a reduction in the incidence of colon cancer.
The Influence of Fiber on Components of Health: Some of the benefits that have been attributed to fiber including: improved gut health and motility, reduced risk of Cardiovascular disease (CVD), improved glycemia and insulin sensitivity, as well as help with weight control. Fiber contributes to these aspects through the action of butyrate.
While fiber is thought to increase gut motility and ease of bowel movements, (butyrate regulates fluid and mineral balance) the effect of minerals like magnesium and sodium, as well as hydration status, cannot be overstated. Stool water content significantly effects motility. This is especially true for those on a WFKD. Careful attention to magnesium, sodium and fluid intakes can improve constipation.
Cardiovascular Health. When we look more closely at the effect of fiber on coronary heart disease (CHD), we need to consider factors such as increased SCFA production and decreased caloric intake, as well as increased antioxidants, vitamins and minerals. These factors are known to influence inflammation, which is increasingly acknowledged to be a driver in the development of CHD. In fact, a sustainable diet that reduces inflammation may prove to be more beneficial for cardiovascular health than fiber.
Type 2 Diabetes and Weight Control. Most well-designed studies have not shown significant, sustained weight reduction that is attributable to fiber in individuals consuming high fiber real-foods.
Interestingly, individuals with Type 2 Diabetes (T2D) have fewer butyrate-producing bacteria in their gut, suggesting a potential protective role of butyrate in this disease. Based on current evidence, it is difficult to attribute a significant impact in improving T2D to fiber alone.
Gut Microbiome. It has been shown that diet can dramatically alter the content of the gut microbiota and the microbiome can affect your health in general.
The gut microbiota is also a potential factor in obesity and T2D as well as auto-immune diseases and other conditions. Therefore, as we continue to learn more about the role the microbiome plays in the modulation of health and disease, we will learn how the composition of the diet can influence these outcomes.
Dietary Fiber in the Context of a Ketogenic Diet. As we look at the proposed benefits of fiber, we can see that for those individuals who are on a WFKD, many of these positive effects are also achieved. We want to emphasize that butyrate appears to be the powerful actor behind fiber. Thus, in the context of a WFKD, the internal production of BOHB by the liver can reduce or eliminate the need for butyrate to achieve the desired health outcomes.
As a result, the need for a high dietary fiber intake may in fact be conditional and based upon the overall and consistent composition of the diet. If an individual is in nutritional ketosis, it may not be necessary to consume a high fiber diet (>25g per day) to achieve the health effects attributed to fiber.
Source: Stephen Phinney, MD, PhD Brooke Bailey, Ph.D Jeff Volek, PhD, RD on March 4, 2019
I invite you to Follow my Blog, Facebook or be added to my email distribution list. My focus is to maximize my physical performance and mental clarity, body composition, and most importantly overall health with a wholesome diet and exercise.
I will bring you compelling articles on Ketogenic and GAPS diets, the Super Slow High-Intensity Exercise Program and supplements.
To follow my Blog, please click the Follow button to receive an email when the next posting is available. Hint: You may have to click the Accept and Close button before follow is available.
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This is the second of two Posts. In the first Post Thomas N. Seyfried Ph.D., in his down-to-earth no nonsense style,discusses his latest cancer research. https://www.youtube.com/watch?v=APwnkpD_BfI
For those who are suffering with or know someone who is suffering with cancer, my hope is that you watch the video and then present the video and the paper to your doctor.
Your knowledge may convince the doctor consider this approach that uses food and no radiation or chemotherapy.
NIH Paper: Nuclear Transfer Experiments disproved the gene theory of cancer, Dr. Seyfried’s scientific paper with the 243 supporting studies.
This Post highlights some of the important points of Dr. Seyfried’s research paper.
Emerging evidence indicates that cancer is primarily a metabolic disease involving disturbances in energy production through respiration and fermentation. The genomic instability observed in tumor cells and all other recognized hallmarks of cancer are considered downstream epiphenomena of the initial disturbance of cellular energy metabolism.
Cancer growth and progression can be managed following a whole body transition from fermentable metabolites, primarily glucose and glutamine, to respiratory metabolites, primarily ketone bodies.
Introduction: A major impediment in the effort to control cancer has been due in large part to the confusion surrounding the origin of the disease.
Provocative question: does cancer arise from somatic mutations? Most of those who conduct academic research on cancer would consider it a type of somatic genetic disease where damage to a cell’s nuclear DNA underlies the transformation of a normal cell into a potentially lethal cancer cell.
Inconsistencies with a nuclear gene origin of cancer. Inconsistencies regarding the somatic nuclear gene theory of cancer come from nuclear/cytoplasmic transfer experiments between tumorigenic and non-tumorigenic cells. Several investigators showed that tumorigenicity is suppressed when cytoplasm from non-tumorigenic cells, containing normal mitochondria, is combined with nuclei from tumor cells. Moreover, the in vivo tumorigenicity of multiple human and animal tumor types is suppressed when the nucleus from the tumor cell is introduced into the cytoplasm of a nontumorigenic cell. Tumors generally did not form despite the continued presence of the tumor-associated mutations.
The conclusion that cancer can be best defined as a type of mitochondrial disease. The nuclear transfer studies are summarized in Figure 1, highlighting the role of the mitochondria in suppressing tumorigenesis.
Fig. 1. Role of the nucleus and mitochondria in the origin of tumors.This image summarizes the experimental evidence supporting a dominant role of the mitochondria in the origin of tumorigenesis as described previously. Normal cells are depicted in green with mitochondrial and nuclear morphology indicative of normal respiration and nuclear gene expression, respectively. Tumor cells are depicted in red with abnormal mitochondrial and nuclear morphology indicative of abnormal respiration and genomic instability. (1) Normal cells beget normal cells. (2) Tumor cells beget tumor cells. (3) Delivery of a tumor cell nucleus into a normal cell cytoplasm begets normal cells despite the persistence of tumor-associated genomic abnormalities. (4) Delivery of a normal cell nucleus into a tumor cell cytoplasm begets tumor cells or dead cells but not normal cells. The results suggest that tumors do not arise from nuclear genomic defects alone and that normal mitochondria can suppress tumorigenesis.
Respiratory insufficiency as the origin of cancer and the ‘Warburg effect’… there is only one common cause into which all other causes of cancer merge, the irreversible injuring of respiration.
The key points of Warburg’s theory are:
(i) insufficient respiration initiates tumorigenesis and ultimately cancer,
(ii) energy through glycolysis gradually compensates for insufficient energy through respiration,
(iii) cancer cells continue to ferment lactate in the presence of oxygen and
(iv) respiratory insufficiency eventually becomes irreversible (54–58).
Mitochondrial structure is intimately connected to mitochondrial function. …
Fig. 2. Typical ultrastructure of a normal mitochondrion and a mitochondrion from a human glioblastoma. Normal mitochondria contain elaborate cristae, which are extensions of the inner membrane and contain the protein complexes of the electron transport chain necessary for producing ATP through OxPhos. The mitochondrion from the glioblastoma (m) is enlarged and shows a near total breakdown of cristae (cristolysis) and an electronlucent matrix. The absence of cristae in glioblastoma mitochondria indicates that OxPhos would be deficient. The arrow indicates an inner membrane fold.
Cristae contain the proteins of the respiratory complexes and play an essential structural role in facilitating energy production through OxPhos.
It is obvious that mitochondrial function or OxPhos sufficiency cannot be normal in tumor cells that contain few if any mitochondria. Glycolysis and lactate fermentation would need to be upregulated in these tumor cells in order to compensate for the absence of OxPhos.
Connecting the links from respiratory insufficiency to cancer origin. The path from normal cell physiology to malignant behavior, where all major cancer hallmarks are expressed, is depicted in Figure 3.Any unspecific condition that damages a cell’s respiratory capacity but is not severe enough to kill the cell can potentially initiate thepath to a malignant cancer. Reduced respiratory capacity could arisefrom damage to any mitochondrial protein, lipid or mtDNA. Someof the many unspecific conditions that can diminish a cell’s respiratorycapacity thus initiating carcinogenesis include inflammation,carcinogens, radiation (ionizing or ultraviolet), intermittent hypoxia,rare germline mutations, viral infections and age.
Fig. 3. Mitochondrial respiratory dysfunction as the origin of cancer. Cancer can arise from any number of non-specific events that damage the respiratory capacity of cells over time. The path to carcinogenesis will occur only in those cells capable of enhancing energy production through fermentation (substrate level phosphorylation, SLP). Despite the shift from respiration to SLP the ΔG′ of ATP hydrolysis remains fairly constant at approximately −56 kJ indicating that the energy from SLP compensates for the reduced energy from OxPhos. The mitochondrial stress response or retrograde signaling will initiate oncogene upregulation and tumor suppressor gene inactivation that are necessary to maintain viability of incipient cancer cells when respiration becomes unable to maintain energy homeostasis. Genomic instability will arise as a secondary consequence of protracted mitochondrial stress from disturbances in the intracellular and extracellular microenvironment. Metastasis arises from respiratory damage in cells of myeloid/macrophage origin. The degree of malignancy is linked directly to the energy transition from OxPhos to SLP. This scenario links all major cancer hallmarks to an extrachromosomal respiratory dysfunction. The T signifies an arbitrary threshold when the shift from OxPhos to SLP might become irreversible.
Can tumor somatic mutations arise as a downstream epiphenomenon of abnormal energy metabolism? Evidence indicates that a persistent retrograde response or mitochondrial stress response leads to abnormalities in DNA repair mechanisms and to the upregulation of fermentation pathways. Oncogene upregulation becomes essential for increased glucose and glutamine metabolism following respiratory impairment.
The metabolic waste products of fermentation can destabilize the morphogenetic field of the tumor microenvironment thus contributing to inflammation, angiogenesis and progression. Normal mitochondrial function is necessary for maintaining intracellular calcium homeostasis, which is required for chromosomal integrity and the fidelity of cell division. Aneuploidy can arise during cell division from abnormalities in calcium homeostasis. In this general picture, the abnormal genomic landscape seen in tumor cells is considered a downstream epiphenomenon of dysfunctional respiration and protracted oncogene-driven fermentation. In other words, the somatic mutations arise as effects rather than as causes of tumorigenesis. The nuclear transfer experiments support this view (Figure 1).
Exploiting mitochondrial dysfunction for the metabolic management of cancer.If cancer is primarily a disease of energy metabolism, then rationalstrategies for cancer management should be found in those therapiesthat specifically target tumor cell energy metabolism. These therapeuticstrategies should be applicable to the majority of cancers regardlessof tissue origin, as nearly all cancers suffer from a commonmalady, i.e. insufficient respiration with compensatory fermentation.
As glucose is the major fuel for tumor energy metabolism through lactate fermentation, the restriction of glucose becomes a prime target for management. It is well known that ketones can replace glucose as an energy metabolite and can protect the brain from severe hypoglycaemia. Hence, the shift in energy metabolism associated with a low carbohydrate, high-fat Ketogenic diet administered in restricted amounts (KD-R) can protect normal cells from glycolytic inhibition and the brain from hypoglycemia.
The metabolic shift from glucose metabolism to ketone body metabolism creates an anti-angiogenic, anti-inflammatory and proapoptotic environment within the tumor mass. The general concept of a survival advantage of tumor cells over normal cells occurs when fermentable fuels are abundant, but not when they are limited. Figure 5 illustrates the changes in whole body levels of blood glucose and ketone bodies (β-hydroxybutyrate) that will metabolically stress tumor cells while enhancing the metabolic efficiency of normal cells.
Implications for novel therapeutics. Once the whole body enters the metabolic zone described in Figure 5,relatively low doses of a variety of drugs can be used to further targetenergy metabolism in any surviving tumor cells. It is interestingthat the therapeutic success of imatinib (Gleevec) and trastuzumab(Herceptin) in managing BCR-ABL leukemia cells and ErbB2-positive breast cancers, respectively, is dependent on their ability to target signalling pathways linked to glucose metabolism.
Fig. 5. Relationship of circulating levels of glucose and ketones (β-hydroxybutyrate) to tumor management. The glucose and ketone values are within normal physiological ranges under fasting conditions in humans and will produce anti-angiogenic, anti-inflammatory and pro-apoptotic effects. We refer to this state as the zone of metabolic management. Metabolic stress will be greater in tumor cells than in normal cells when the whole body enters the metabolic zone. The values for blood glucose in mg/dl can be estimated by multiplying the mM values by 18. The glucose and ketone levels predicted for tumor management in human cancer patients are 3.1–3.8 mM (55–65 mg/dl) and 2.5–7.0 mM, respectively. These ketone levels are well below the levels associated with ketoacidosis (blood ketone values greater than 15 mmol). Elevated ketones will protect the brain from hypoglycemia.
Poff et al. also recently showed a synergistic interaction between the KD and hyperbaric oxygen therapy (HBO2T) (Figure 6). A dependency on glucose and an inability to use ketones for energy makes tumor cells selectively vulnerable to this therapy.
Besides drugs that target glucose, drugs that target glutamine can also be effective in killing systemic metastatic cancer cells.
The novelty of the metabolic approach to cancer managementinvolves the implementation of a synergistic combination of nutritionalketosis, cancer metabolic drugs and HBO2T. … This therapeutic strategy produces a shift in metabolic physiology that will not only kill tumor cells but also enhance the general health and metabolic efficiency of normal cells, and consequently the whole body. We view this therapeutic approach as a type of ‘mitochondrial enhancement therapy’.
Fig. 6. The KD and HBO2T (hyperbaric oxygen therapy) are synergistic in reducing systemic metastatic cancer in the syngeneic VM mouse model.
Advanced metastatic cancers can become manageable when their access to fermentable fuels becomes restricted. The metabolic shift associated with the KD-R involves ‘keto-adaptation’. However, the adaptation to this new metabolic state can be challenging for some people. The administration of ketone esters could conceivably enable patients to circumvent the dietary restriction generally required for sustained nutritional ketosis.
Definitions:
Angiogenic, formation of new blood vessels;
Apoptotic, programmed cell death;
Carcinogenesis, origin of cancer;
Cytoplasm, the material of a cell exclusive of that of the nucleus;
Epiphenomena, symptoms;
Extrachromosomal, outside the chromosome;
Fermentation, production of energy from a fuel;
Genome, hereditary factors;
Glioblastoma, A malignant tumor usually occurring in the cerebrum of adults;
Glycolysis, conversion of glucose resulting in energy;
Hypoglycaemia, Abnormally low levels of sugar (glucose) in the blood.
Respiration, the oxidative process occurring within living cells by which the chemical energy of organic molecules is converted into energy involving the consumption of oxygen and the production of carbon dioxide and water as byproducts;
Tumorigenic, cause tumours relating to the development of tumours;
I hope that these two Posts help you along the way to conquering cancer.
I invite you to Follow my Blog, Facebook or be added to my email distribution list. My focus is to maximize my physical performance and mental clarity, body composition, and most importantly overall health with a wholesome diet and exercise.
I will bring you compelling articles on Ketogenic and GAPS diets, the Super Slow High-Intensity Exercise Program and supplements.
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I would like to dedicate this Post to friends who lost their battle with cancer. This is for you Anne and Holly.
In this first PostThomas N. Seyfried Ph.D., in his down-to-earth no nonsense style,discusses his latest cancer research. Learn more about Dr. Seyfried in his Blog https://tomseyfried.com/blog/
Source: A Novel Therapeutic Strategy For Metabolic Management of Cancer
Thomas N. Seyfried received his Ph.D. in Genetics and Biochemistry from the University of Illinois, Urbana, in 1976. He did his undergraduate work at the University of New England, where he recently received the distinguished Alumni Achievement Award. He also holds a Master’s degree in Genetics from Illinois State University. Thomas Seyfried served with distinction in the United States Army’s First Cavalry Division during the Vietnam War and received numerous medals and commendations. He was a Postdoctoral Fellow in the Department of Neurology at the Yale University School of Medicine and then served on the faculty as an Assistant Professor in Neurology.
In his presentation, “A Novel Therapeutic Strategy For The Metabolic Management Of Cancer”, he discusses his latest research in treating and preventing cancer. In addition to his research on the ketogenic diet, he adds a new component, which adds drugs and procedures that create both chronic and intermittent acute stress on tumor cell energy metabolism, while protecting and enhancing the energy metabolism of normal cells. He calls this the “press- pulse” therapeutic strategy for cancer management is an approach, which includes the calorie restricted ketogenic diets used together with drugs and procedures.
A shift from respiration to fermentation is a common metabolic hallmark of cancer cells. As a result, glucose and glutamine become the prime fuels for driving the dysregulated growth of tumors. Press disturbances produce chronic stress, while pulse disturbances produce acute stress on populations. It was only when both disturbances coincide that population reduction occurred.
This general concept can be applied to the management of cancer by creating chronic metabolic stresses on tumor cell energy metabolism (press disturbance) that are coupled to a series of acute metabolic stressors that restrict glucose and glutamine availability while also stimulating cancer-specific oxidative stress (pulse disturbances), elevation of non- fermentable ketone bodies protect normal cells from energy stress while further enhancing energy stress in tumor cells that lack the metabolic exibility to use ketones as an efficient energy source.
Mitochondrial abnormalities and genetic mutations make tumor cells vulnerable metabolic stress. Optimization of dosing, timing, and scheduling of the press-pulse therapeutic strategy will facilitate the eradication of tumor cells with minimal patient toxicity. This therapeutic strategy can be used as a framework for the design of clinical trials for the non-toxic management of most cancers.
This video Post is the first of 2 parts. The second is Dr. Seyfried’s scientific paper with the 243 supporting studies.
For those who are suffering with or know someone who is suffering with cancer, my hope is that you watch the video and then present the video and the paper to the attending doctor.
Your knowledge may help the doctor consider this approach that uses food and no radiation or chemotherapy. To help you there are Definitions and Abbreviationsat the end of this post.
Part Two is in the next Post: Nuclear Transfer Experiments disproved the gene theory of cancer
I invite you to Follow my Blog, Facebook or be added to my email distribution list. My focus is to maximize my physical performance and mental clarity, body composition, and most importantly overall health with a wholesome diet and exercise.
I will bring you compelling articles on Ketogenic and GAPS diets, the Super Slow High-Intensity Exercise Program and supplements.
To follow my Blog, please click the Follow button to receive an email when the next posting is available. Hint: You may have to click the Accept and Close button before follow is available.
I thrive on feedback. Please let me know you are interested in the content by clicking Like, Commenting or sending me a message or email about the Post.
If you wish to contact me by Email, please email lpolstra@bell.net using this form.
This is best visual representation we’ve come up with to differentiate the Ketogenic diet from a the standard American diet, the Mediterranean diet and the Paleo diet.
2HealthyHabits 