Peter Attia series on ketosis

Peter Attia MD has started a series of posts on ketosis.

This is important because he does a great job of producing highly informative, detailed, well-researched posts.

Part 1 is up, on The Eating Academy  http://eatingacademy.com/

Ketosis – Advantaged or misunderstood state? (Part I)

It was on Dr. Peter Attia’s blog that I first learned of the existence of a home blood ketone monitor, about last March, as I wrote about in a previous post.

Ketosis in a Nutshell – Part 6, A Hungry Man

weighing-scales

(When all else fails, read the instructions.)

A hungry man finds a haven – what was it?

He was a very hungry man.

That’s what worried him. That, and the weight gain.

“he had a pathological fear of hunger” *

“I was literally afraid of dieting. I was afraid of being hungry.”**

A bean pole in high school, when he graduated he “was 6 feet tall and weighed only 135 pounds”. But that didn’t last. “At college I became the biggest eater on campus.”

He went to medical school and then came a residency in cardiology. “I had the reputation of being the biggest chow-hound in the hospital.”  He gained weight over the years, but his mind failed to register this, as he still had a mental image of himself as slim.  Perhaps he also partly didn’t want to recognize it because he was so afraid of the hunger that is a routine part of low-calorie dieting.

It took seeing a photo of himself for Dr. Atkins to recognize the fact that he had become  “a fat man“, as he put it – in the typically kind way people have when they speak to themselves about their weight.  The year was 1963, and Dr. Atkins embarked on a quest.  Not willing to face the hunger of the usual calorie restricted approach, he “was looking for “The Hungry Man’s Diet.””. He hit the medical research to look for another way. Kids – this meant picking up and reading ink-on-paper “medical journals” that sat on shelves in the “library” of the hospital.

What was it that he found?

And why should we think about this now, 40 years later?

Why should we care what Dr. Atkins was reading or thinking in 1963, almost 50 years ago?  Why should it matter now what he put in his 1972 book?  After all, he published a number of books after that one. No-one should be held to what their medical ideas were 40 years ago – new information and experiences bring rapid changes in all areas of medicine.

Well, it’s not like things are going so good on the weight loss topic right now. I thought I’d have a read of his 1972 book. I have a paperback version of that book, published in 1973 by Bantam. What I read in that book grabbed my attention. For example, “The result of fifty years of prescribing a so-called “balanced diet” for patients who actually were suffering from a metabolic imbalance is a raging epidemic of over-weight.” (p.2).  If you look at a chart of changes in BMI over the past decades, you will see that 1972 is now considered to be “the good old days” when it comes to the battle of the bulge.

When all else fails, read the instructions.

The vast majority of people do very well with following a low carb, high fat eating plan that is well thought-out and explained – such as can be found in The Art and Science of Low Carbohydrate Living. For most people, there is no need to make it more complex. Some people follow the instructions closely, and yet don’t find that their weight reduces into the normal range. Different people need different solutions. Can we get some ideas by looking back to the original version of the most famous low carb plan.

What was at the core of Dr. Atkins’ “Revolution”?

(Terminology – will open in new window)

There is a common perception to think about the Atkins Diet in terms of the protein and the salads and the low carbs. What does his first book tell us about what he was thinking?

In his book “Dr. Atkins Diet Revolution”, published in 1972, he describes the research findings and line of thinking that led him towards his approach to obesity. I looked into some of the research he discusses and found it such a fascinating insight into the medical thinking of the time that I have included a discussion of that below. I think if you click on the links to the abstracts and papers you will enjoy the read.

In summary, researchers had found that hunger was suppressed after 1-2 days of total fasting, and that this reduction in hunger was correlated to an increase in blood levels of ketones. Other researchers found that this also happened on a very low carbohydrate diet – within 1-2 days hunger was “absent” (maybe a bit of an overstatement) and blood ketone levels had risen over that time period  Diet trials with patients eating to appetite of unlimited protein foods and fats, with very limited carbohydrates, showed weight loss with lack of hunger.

Dr. Atkins was ready to try this approach for himself. Dr. Walter Lyons Bloom had developed a 3-day food plan to test the low-carb theory. People ate eggs, bacon, meat and salad. Dr. Bloom reported that they developed the same lack of hunger as was noted when patients underwent total fasting. Dr. Atkins tried it and had the result he was after. He was loosing weight and not hungry. Now, what about the ketones? In the publications he had read, when ketones were tested they used blood ketone testing.  Dr. Atkins bought urine ketone test strips at a local pharmacy. He tested his urine and there was the purple color on the test strip showing that he was in ketosis.

Slowly he developed this 3-day sketch of a diet plan into a workable long-term plan that enabled a gradual return to a higher level of carbohydrate intake, according to individual tolerance.

** The above information and quotes are from chapter 3 of the 1972 book “Dr. Atkins’ Diet Revolution”, entitled “How I Arrived at This Diet Revolution”.

Let’s look at chapter 2, entitled “The Diet Revolution: It Will Change Your Life”.

“This is the diet revolution: the new chemical situation in which ketones are being thrown off – and so are those unwanted pounds, all without hunger.”

“I have arrived at the conclusion that ketosis is a state devoutly to be desired, because while you are in this happy state … your fat is being burned off with the maximum efficiency and minimum deprivation (since in ketosis your hunger disappears!).”

“Here’s how this diet is significantly different. During the first week on this diet, you cut your intake of carbohydrates down to what is biologically zero. This creates a unique chemical situation in the body, the one most favourable to the fastest possible burning of your body’s stored fat. Ketones are excreted, and hunger disappears.” (Here he was comparing his program to several diet programs of the day that reduced carbohydrates, but not to less than 60 grams per day, thus not creating significant ketosis in most people.)

“We must maintain this chemical situation if you’re to continue to lose without hunger.”

Let’s look at chapter 5, entitled “If You’re Always Fat, Chances are You’re “Allergic” to Carbohydrates”.

“It is not a true allergy as we doctors know it, but it is a sensitivity to carbohydrates in the diet, which results in an overproduction of insulin (hyperinsulinism).”

“For millions who suffer the endless physical and emotional miseries of being fat, it is a tragedy that so few authorities understand most overweight for what it is – a disordered carbohydrate metabolism, which affects some people and not others, that is quite apart from the amount of food, or calories, consumed.”

The rest of this chapter focuses on the many effects of a disordered carbohydrate metabolism, including high insulin, diabetes and aspects of what we now think of as metabolic syndrome.

You can read most of chapter 1 online. The first 6 pages of the 8 and a bit pages of chapter one are included in an Amazon preview. This preview is labeled as from 1981, but it is identical to the Bantam 1973 paperback version of the 1972 hard cover version that I have. Since this is on the Amazon site, this review might not still be there when you try the link. LINK

Carb Control for Health and Appetite, Ketosis for Hunger Control in Weight Loss?

As far as I can see from a careful reading of his book and from the papers he cites as influences, in 1972 Dr. Atkins saw his contribution as having been the development of a program that (1) targeted ketosis as a sustainable tool in weight loss, (2) made ketosis workable long term to last throughout the weight loss period and (3) offered a workable transition to a highly individualised flexible controlled carb lifestyle for long term health benefits. He refers to the fact that a number of popular books advocating low carb intake had been published by 1972, but none of them (according to his report, I don’t have copies of these books) presented ketosis as a unique aid to weight loss – by reducing appetite and allowing maximum fat burning – much less presenting a workable long-term way to achieve this. He stated that his goal was to find a way to lose weight without being tormented by hunger and he found it – ketosis.  He also understood the need to avoid the many harms from carbohydrate intolerance – by a lifelong practice of keeping carb intake within one’s personal tolerance limits.

In the 1972 book, Dr. Atkins advocated deliberately maintaining a state of nutritional ketosis until the last phase of the weight loss period. When the person is close to their goal weight, they were advised to slow the rate of weight loss by further increasing their carb intake – and thus the ketones in the urine would slowly fade away. He noted that for some people ketones don’t show in the urine, in which case they will have to rely on symptoms – are they hungry, having cravings, not feeling as well or no longer loosing weight/inches.

From that point on (once the weight was at goal), he emphasized that it was vital to maintain health and weight control by continuing to carefully control carb intake. He advised that it was fundamental to long term success to make the effort to adjust one’s carb intake – both amount and specific foods chosen – according to one’s individual tolerance. It was important to carefully monitor oneself over time for weight regain or signs of carb intolerance. This tolerance level might also change over time.

Regarding carbohydrate intake (amount and food sources) over the long term: “You’ll end up with a diet that’s as personal to you as a pair of contact lenses.” (p. 29)

During weight loss: “You will find which shade of purple correlates best with your own feeling, and this, for you, is the ideal.” (p. 130)

What about the role of protein intake when aiming for ketosis?

Unfortunately, there is no reference that I can find in the 1972 book to the potential role of moderate or high protein intake as something that might interfere with the development of ketosis. Dr. Atkins writes that protein can be metabolised to glucose, but he doesn’t mention trying a lower protein intake (1) as a means to achieve ketosis for those whose urine test strips don’t turn colour or (2) as a means to enable weight loss for those whose weight loss is slow or stalled.

In the 2002 edition of his book “Dr. Atkins New Diet Revolution”, there is brief mention of the fact that too much protein can interfere with weight loss, but there is no focus on that.  For example, in Chapter 15 “Engine Stalled? How to Get Past a Plateau”, among the many suggestions given, there is no discussion of considering or lowering protein intake.

Chapter 20 “Metabolic Resistance: Causes and Solutions” is described this way: “This chapter is about extreme difficulty in losing weight … “. Adjusting protein intake is not discussed directly as a strategy, except in terms of the Fat Fast, which is one of many topics in this chapter. If the Fat Fast is successful and the Induction program is not, then Dr. Atkins suggests trying to adapt the Fat Fast, such as “simply follow the concept of increasing the ratio of fat to protein”.

In Chapter 17 “Lifetime Maintenance”, there is a statement and answer section.  One is “4. Misconception: You can eat any food so long as you do not exceed 20 grams of carbs a day.” The answer “Reality: If you eat junk foods or other nutrient-deficient carbohydrate foods instead of vegetables and other nutrient dense foods, you will miss most of the benefits I write about …”. No mention of amount of protein foods.

Yet, in the same section is Misconception #9, to which part of the answer is “Moreover, excess protein converts to glucose and can keep fat from becoming the primary fuel.” Brief statements similar to this are in 3 – 4 other places in the book, but never elaborated on. It seems from all this that Dr. Atkins dealt with this problem in the office, but that it just somehow didn’t make it into the book in a very clear way or with a description of how to tackle it.

Still, the vast majority of people can benefit greatly from a low carb diet, in the manner that Dr. Atkins taught, without needing to deliberately limit their protein intake – as long as they are following his instruction to eat as much food as required to feel satisfied, but no more.

Is there any difference in how to get into ketosis?

There are some differences here that are interesting to think about.

The first week is far more strict than what is now considered to be the “Induction” eating plan. The only carb sources allowed other than the small amounts present in flesh food, eggs and small amounts in such things as bullion, gelatin and spices were:

  1. hard, aged cheese up to 4 ounces a day
  2. heavy cream up to 4 teaspoons per day
  3. juice of one lemon or lime per day
  4. “two small salads a day (each less than one cupful, loosely packed) made only of leafy greens, celery, or cucumbers and radishes. …  Or else a sour pickle in place of a salad.”

In the second week, 5 – 8 grams of carbs are added to the daily diet, but this was the “old” way of counting the carbs, before Dr Atkins switched to subtracting the fiber content from the carb total, so serving sizes of vegetables were much smaller than now. That is, the serving amount of a vegetable that was said to give 5 grams of carbohydrate would actually contain much less “usable” carbs (sugars or starch) than 5 grams, because some of what was counted as “carbs” was fiber. Depending on what a person was choosing to eat, many would still be under the 20 grams of carbs (total carbs minus fiber) considered Induction Level now.

Thus, there would be a tendency for people to move into ketosis both faster and deeper in the first week, compared to the instructions from 1992 on, when “Dr. Atkins’ New Diet Revolution” was first published – which moved to a two week Induction period with less strict carb reduction. They would move into “week two” at a higher level of ketones than now and likely progress further into ketosis while following the “week two” instructions. For many people, depending on individual food choices, they would not be up to the carb intake of what is now the “Induction” phase until they reached week 3 and added another 5 – 8 grams of total carbs (total = fiber included in the count).

In fact, although it was called “week 2″, Dr. Atkins did not want to see anyone progress from the first week’s eating instructions until they were clearly displaying the symptoms and changes that suggested they were well into a state of ketosis. As well, of course, he expected to see the urine ketone test strips turn purple. “Now it is time to evaluate whether or not you may progress to level two.”  His criteria for moving up a stage in carb intake included such things as lack of hunger, correction of evening/night eating, sense of having more energy and losing weight/inches.

The week one instructions also could be used as recovery strategy to get back on track if one had any symptoms that too many carbs had been consumed – such as hunger or cravings. Again, these instructions would promote a faster move into a deeper level of ketosis that the later “Induction Phase” instructions.

Interestingly, when you look at the “Induction Phase” instructions in the 2002 edition of “Dr. Atkins’ New Diet Revolution” the daily intake of vegetables is limited to “approximately three cups – loosely packed – of salad, or two cups of salad plus one cup of other vegetables (see list …)”. Some higher carb foods, such as limited amounts of sour cream, avocado and tomato are allowed, but Dr. Atkins denotes these as “Special Category” foods and notes that they might need to be avoided if progress is not good. I think many people think of Induction Phase as including a lot more vegetables than that.

In Sum

Dr. Atkins’ 1972 book is the first presentation of a sustainable dietary program that deliberately overtly includes nutritional ketosis in a central role. In Dr. Atkins’ original presentation of his concepts, there was a dual emphasis on ketosis as the key to hunger control and fat mobilization during weight loss; along with carb control to individual tolerance as a key to health, to abstinence from trigger foods and to weight maintenance over time. There was an emphasis on a rapid transition into ketosis. There was an emphasis on targeting the degree of ketosis according to whether it met the duel main criteria of suppressed appetite with a sense of well-being. There was a strong emphasis on sustaining such a symptom-targeted state of ketosis until the weight loss phase was almost completed.

The vast majority of people do well with the instructions in low carb or low carb high fat (LCHF) currently recommended by responsible authors and bloggers. Still, there are those whose health goals are not achieved by following such instructions.  It may be worth considering aspects of other versions a low carb high fat approach. This has been a look back at history to review the roots of the current low carb lifestyle.

I found my journey into this book fascinating. This discussion focused on the ketosis aspect of it, but if you have or can access a copy of this book and you have a strong interest in the topic of low carb nutrition, you might enjoy reading this book as much as I have.

- – - – - – - – - – - – -

I’m doing my best to understand Dr. Atkins’ practice and thinking based on his books.  Because of a realistic need to keep things somewhat simplified in a book, there is likely a lot of Dr. Atkins’ insights and accumulated wisdom that didn’t appear in any of his books. There are a number of clinicians who have direct experience with Dr. Atkins who could provide much better history and insight – for example, Jacqueline A. Eberstein R.N. and Eric Westman M.D. It is Dr. Atkins’ books, however, that created the public perception about his work. Much of what is now called “Atkins” is a mis-interpretation or mis-representation of what people read, or half-remembered that they read, or thought they heard from a friend about what the friend read – - in his books.

* written by Jacqueline A. Eberstein, R.N., in her “Chapter 20: Thirty Years of Clinical Practice with Dr. Robert Atkins: Knowledge Gained”, included in the book “The Art and Science of Low Carbohydrate Living” by Jeff S. Volek, Ph.D., R.D. and Stephen D. Phinney, M.D., Ph.D.

- – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - -

More on the research that Dr. Atkins credited with informing his thinking about hunger, diet and obesity:

One line of thinking was to mimic starvation.

(Note that this is similar to how the ketogenic diet for epilepsy was developed, where they were trying as closely as possible to mimic starvation without the person starving.)

Fortunately, Dr. Atkins would not have had to look very far to find his first clues. In the July 28, 1962 edition of The Journal of The American Medical Association (JAMA, one of the most prominent medical journals in the world) there was a paper by Dr. Garfield Duncan and others.

“Correction and Control of Intractable Obesity: Practical Application of Intermittent Periods of Fasting” JAMA  1962;181(4):309312   abstract

They reported on their results with periods of total fasting (“non-nutritious liquids” and vitamins) lasting 4 to 14 days (in hospital) with 50 patients, and subsequent follow-up management.  The weight loss results were very good, but what caught Dr. Atkins’ attention was the fact that these patients did not experience undue hunger after the first 1-2 days.

“Anorexia was the rule after the first day of fasting” … that was interesting! (anorexia means lack of appetite)

Furthermore, “and paralleled the degree of hyperketonemia”.  In other words, hunger went down as blood ketone levels rose. It took about a day for the blood ketones to rise much.

Even more, “A sense of well-being was associated with the fast.”

Dr. Duncan was a very prominent diabetes specialist, with a strong interest in weight loss.(I see there is a Garfield Duncan Building at Pennsylvania Hospital). I found this interesting report about the work of Dr. Duncan – note that this report has to be viewed with some caution, as it apparently quotes a Reader’s Digest article from 1968, rather than a medical paper.

The other thing that really strikes me about this is that here was Dr. Duncan, a noted diabetes specialist, completely unafraid of the ketosis induced by the fasting. It is very regrettable that this correct understanding of diet-induced ketosis did not become common knowledge in the medical community.

There was also this article published in 1963 in The Transactions of The American Clinical and Climatological Association, 1963; 74:121-129.  LINK to full text.

“Intermittent Fasts in the Correction and Control of Intractable Obesity”

This paper reports Dr. Duncan’s experiences with now 107 “obese diabetic and non-diabetic patients”.  It is fascinating to read the full article and I encourage you to do so.  One interesting tid bit is that “in three cases of previously resistant psoriasis this disorder subsided during the reduction program”. (We keep re-inventing the wheel.)

The patients would be hospitalized for the initial fasting period, then sent home on a limited calorie diet (that was not low in carbohydrates).  At home, they would fast for 1-2 days at intervals, generally one day per week (patient examples given). Exercise was not permitted on fasting days.  Some information on the longer term is given, but it is limited in detail. Forty percent of patients regained to previous weight or more, 43% maintained their weight and 17% were still loosing at last follow-up, which was at 1 – 32 months. (This is not nearly an adequate look at the medium and long term outcomes.)

His conclusions include “The anorexia during total abstinence from food is associated with, and is believed to be due to, the hyperketonemia provoked by the fast.”.

Keep scrolling down the paper to the discussion among a number of doctors at the end, including other illuminating comments by Dr. Duncan, such as “once patients have been subjected to a total fast, invariably they prefer it to low calorie diets” – commenting on the one day weekly fasting program. They also discuss initial water weight loss and water weight regain with return to eating.

(That people preferred one day a week fasting to the daily miseries of a chronic low calorie diet hardly constitutes much of an advertisement for intermittent fasting.  It is more a comment on the limited options these people felt they had. Also, we don’t know if it would have been as useful without the initial period of strong ketosis. As well, truly long term results are not given. Finally, some people might move towards dis-ordered eating and restrict/rebound eating patterns in response to intermittent fasting.)

Dr. Duncan followed these papers with a number of other publications on this topic, until he retired in 1969, including looking at hazards of fasting and the use of allopurinol for high uric acid levels induced by fasting.

Dr Atkins also credits an influence from the work of Kekwick and Pawan, who published a number of papers on obesity in the 1950s and up to 1969.  What he understood from their work was that ketones also appeared in the urine after 48 hours without carbohydrates in the diet – thus you could have ketosis without fasting -  and the ketones were again associated with loss of hunger. The loss of hunger was interpreted to be because the body was satisfying its hunger by burning body fat stores.

Thus, to some degree you could mimic the effects of fasting by strictly limiting carbohydrates.

Another line of thinking was that there can be a defect in how the body utilized carbs.

He also looked at the work of Dr. Alfred W. Pennington, who felt that the core issue was a defect in the ability of people who were obese to metabolize carbohydrates. Dr. Pennington was targeting reduction of carbohydrates and interpreting the resulting ketosis as evidence that removing the effect of the abnormal carbohydrate metabolism now freed the body to use fat as fuel. Ketosis as a hunger-suppressed state was not his goal, it was a sign that he was at his goal – sufficient reduction in the adverse effect of carbs. He was not concerned that protein intake would have any impact on ketosis.

J Clin Nutr. 1953 Jul-Aug;1(5):343-8.

Treatment of obesity with calorically unrestricted diets.

PENNINGTON AW.  PMID:13096572   LINK to full text. (takes a while to load)
I think most of what is discussed and speculated in this paper is not of current interest because the concepts are so dated and the discussion seems somewhat contradictory.  However, lots of times people find things that are useful in practice, even though they might not know how it works or their theories may be off the mark. Interestingly, Dr. Pennington emphasises that one of the important instructions for the diet is to eat sufficiently fatty meat. “The proper proportion is 3 parts of lean to one part of fat.”  If the meat is not fatty enough, then one is to buy extra fat (such as the fat from around the kidneys – apparently one could readily purchase that at the time) and cook it and have it with the meat. This work received attention because it was, at least in the short term, effective.
There were attempts to replicate this work by other researchers, including two in Europe, published in French and Swedish. There was also a report published in Canada.
“Experiences with the Pennington Diet in the Management of Obesity” by Wilfred Leith, published in The Canadian Medical Association Journal 1961 June 24; 84(25): 1411-1414.  LINK to full text.
They describe the Pennington diet as having the dual goals of (1) carbohydrates under 50 grams a day and (2) a strong focus on bulky foods. Having a lot of bulk in the meal was thought (and still is a topic) to be a major contributor to satiety. (I think this is actually a highly individual thing.)  However, I think this is their own spin on it, reflecting this team’s interest in bulk as a means to satiety. Dr. Pennington’s 1953 paper reveals no evidence of a focus on bulky foods (also his target was under 60 grams of carbs).

Why did they do the study? “The treatment of the obese patient has followed a stereotyped pattern for the past 20 years. Prescribing a simple low caloric diet and sympathetic handling of the patient, the usual method, had not been a rewarding form of clinical treatment. Usually, the patient was disturbed by a continual gnawing sense of hunger.”  Saying it like it is – not always a striking feature in medical writing today.

Ketogenic diet for a body weight control system gone bust?

Body Snark Free Zone Sign

Body Snark Free Zone Sign (Photo credit: The Lingerie Addict)

Body Weight Control System Gone Bust?

If you can’t fix it, patch it …

Nutritional ketosis may work as a patch for you.

For decades there has been interest in the idea that a person’s body weight control system can start to mal-function. This has been thought to be part of the reason that it can be very difficult for people who have been obese to return to a normal body weight and maintain that over time.

This topic became prominent again last week with the publication of a paper that sheds a tiny bit of light on the matter.

To read about this study, see:

Obesity-programmed mice are rescued by early genetic intervention.”

“effectiveness of treatment to normalize body weight and adiposity declined progressively as the level of obesity at the time of Pomc induction increased. Thus, our study using a novel reversible monogenic obesity model reveals the critical importance of early intervention for the prevention of subsequent allostatic overload that auto-perpetuates obesity.”  LINK to FULL TEXT

The meaning of all this is just that it supports the notion that a person’s body weight control system can start to malfunction in a way that doesn’t just recover when the cause of the weight gain has been corrected.  It doesn’t prove this and doesn’t tell us how this might happen or what to do about it.

If you can’t (for now) fix it, find a work-around.

The goal in the long run is to have the best functioning of your body that is possible, within the context of what you find worthwhile. That includes the best functioning of your body weight control system – which is expressed in the functioning and balance of the appetite/satiety system.

There are countless things that can interfere with the proper functioning of these systems – leaving you fighting a tendency to gain weight or having great difficulty in losing weight without chronic hunger (or, on the other hand, being too thin or too easily loosing weight).  Some of these things can be changed and some can’t.  Hopefully , over time research and new understandings will keep shifting these interfering things from the “can’t do anything about it” group to the “this is what you can do about it” group.  Some things might theoretically be in the “you can change it” group, but those changes might be out of reach (currently) for the individual.  Some examples of that may be certain medications that are currently essential for that person or chronic poor sleep they are (currently) unable to find a way to remedy.

The core strategy, from the start and ongoing, is to do as much as you are (currently) able, or (currently) know how, to support the best functioning of your body weight control systems. All too often, though, that is not enough to allow a person to meet their body weight goals (without sustained hunger). Yes, the core strategy still is to keep trying to find ways to improve your health, including ways to improve the proper functioning of your body weight control systems. But if you are still struggling with your weight health or hunger, is there something more you can do while you are waiting for the perfect answer or personal perfection (not recommended)?

I think that nutritional ketosis is, for most people, a valuable option here. I have addressed this topic in more depth in my recent post:

To take this from concept to real life, consider the personal stories posted on

Free Abbott meter offer – glucose, ketone

Aside

Sadly only available to those in the US. If you are in the US, you might want to look into this offer from Abbott.

“In an effort to help you manage your blood sugar levels, your health insurance company is offering to  upgrade your blood glucose monitoring system, at absolutely no cost to you.1″

They have 3 test meters on offer, one of which is their meter that can test blood ketones and blood glucose – The Precision Xtra Blood Glucose and Ketone Monitoring System.

This is announced as a free meter UPGRADE, so check out the details.  LINK

Information on blood ketone testing – page on my blog My Keto Haven

Thanks to Jimmy Moore of Livin’ La Vida Low Carb for tweeting the tip.

Uric Acid and Hunger and Fat Storage?

Drinking soda

Drinking soda (Photo credit: Ernst Vikne)

High fructose promotes elevated uric acid in the blood.

And ..

High levels of uric acid in the blood may be a much greater cause of disease and death than we thought.

And …

Does uric acid promote hunger and fat storage when fructose intake is high?

And …

Is it possible that, in some people, chronic high glucose exposure (sugar and starch) awakens an enzyme that starts converting some of the glucose to fructose??? (very speculative for now)

Uric acid

Uric acid (Photo credit: Wikipedia)

There was a fascinating interview with Dr. Richard J Johnson on Jimmy Moore’s Livin’ La Vida Low Carb Show on October 24/12. (LINK to page and podcast)

It inspired me to look into the topics that were raised and put up a page so people can see some of the publications and research involved. By the way, I have to also say that I am not meaning to imply support for what Dr. Johnson proposes in that interview regarding an approach to weight loss – and I imagine what he said in the interview would be what is in his new weight loss book.

* * * This is an evolving story. See updates in addendums below. * * *

Uric Acid – Is There a New Story?

For decades there has been debate about whether high serum levels of uric acid plays a role as a culprit in cardiovascular disease and other (non-gout) chronic conditions or is just a bystander.  It has been known that uric acid levels tend to be higher in people who also have insulin resistance, obesity, high blood pressure, cardiovascular disease, diabetes, chronic renal disease, etc. Is the uric acid contributing to these conditions, or is it just a consequence of the body state that produced the disease or a marker of the damage or disruption associated with the disease?

With the questions not clearly answered, in practice it has been dealt with as a marker – in other words, it has not been clinical practice to try to reduce uric acid just for its own sake, other than in the context of gout or uric acid kidney stones.

This may be about to change. There has been a recent wave of research which suggests that high levels of uric acid may indeed be causing substantial damage to our health and happiness. Nothing is for sure on this front yet, but the implications of this line of research are profound. Why the rising interest lately?

Uric Acid Levels and Gout – “A second wave”

Thanks, fructose.

  • Higher levels of uric acid are becoming more common.
  • If elevated levels of uric acid are a cause or aggravating factor for many common conditions, perhaps this also needs attention in people who have uric acid levels that we now consider “high normal”.

The tendency for high uric acid levels is partly genetic, but diet also contributes to the problem. The historic dietary reasons for elevated uric acid are still there – or even more so – alcohol, seafood, meat, flesh food in general.  To this list is added a new aggravator that wasn’t a significant problem in the past – high intake of fructose.

A perspective on diet and gout.

Kedar E, Simkin PA.

Adv Chronic Kidney Dis. 2012 Nov;19(6):392-7. PMID: 23089274  Abstract

“The incidence of gout has also risen in recent years, to the point that we are now seeing what is regarded by some as a “second epidemic” of gout.” … “Fructose is a powerful driver of ATP catabolism that, in turn, leads to the production of uric acid.” … “this reopens the opportunity for dietary control of hyperuricemia”

Uric Acid – Is There a Really, Really New Story?

Have we found “The Thrifty Gene”?

Into this situation comes a provocative hypothesis explained in the paper below.  Humans are unusual among mammals regarding uric acid. Almost all mammals have an enzyme called “uricase” that can break down uric acid.  Humans, the great apes, and the lesser apes do not have this enzyme. In the human lineage, it was lost about 15 million years ago.  This means that humans have a higher blood level of uric acid than most mammals and the level is more easily influenced by diet.

In this paper, Dr. Richard J Johnson and others propose the hypothesis that the loss of the enzyme uricase may actually represent the “thrifty gene” that has been proposed as an explanation for man’s striking tendency to accumulate fat stores.

Uric acid: a danger signal from the RNA world that may have a role in the epidemic of obesity, metabolic syndrome, and cardiorenal disease: evolutionary considerations.

Johnson RJ, Lanaspa MA, Gaucher EA.

Semin Nephrol. 2011 Sep;31(5):394-9. PMID: 22000645 

LINK to full text. (and scroll down to see conflict of interest.)

“An increase in uric acid may have some protective effects on survival in the setting of severe energy depletion, such as may occur with starvation, or with tissue injury and ischemia. We hypothesize in early primates faced with intermittent starvation, the loss of uricase may have therefore provided a survival advantage. A rise in uric acid may have potentiated fructose effects to gain fat, and may have led to a greater activation of the immune system.” (emphasis mine)

(Note: the populations they are referring to are thought to have lived mostly on fruit and thus had a very high fructose intake – it takes a lot of fruit to give you, say, 2000 calories a day – likely not less than 200 grams per day of fructose postulating fructose as less than half of the carb intake.)

Conversion of Glucose to Fructose in the Liver – - What??

Now, that sounds really scary, but I can’t find anything on this. Dr. Johnson refers to it in the interview as a new concept that is very preliminary at this stage. He does not give a reference for it. It is interesting to speculate about, as it would be one explanation for how sometimes weight gain and appetite just suddenly seem to take off out of control.  Many people report that their experience with their weight gain has its ups and downs and generally tends to get harder over time, but suddenly it just seems to shift into high gear and becomes relentless.

This may just be startling speculation that will turn out to be nothing but a scary story.

Is There a Low Carb Connection?

It is well established that when people are transitioning into nutritional ketosis their serum uric acid levels go up – which is thought to be because the kidneys are so busy handling the ketones they are not used to having to deal with. Over the initial weeks, the body adapts more to being in ketosis. The kidneys adapt more and the muscles start participating in handling the ketones by taking up acetoacetate and from that producing beta-hydroxybutyrate, which is sent back into the blood stream.  Within 4-6 weeks, this process of adaptation results in the serum uric acid dropping down to a level at or below where it was before.

For more about this, read “The Art and Science of Low Carbohydrate Living” by Jeff Volek Ph D, RD, and Stephen Phinney MD, Ph D. (link in sidebar of this blog “the book to give your doctor”)

For most people, this is not noticed and is not an issue. For some people, it is possible that an attack of gout could be precipitated. An attack can occur as the uric acid level is falling, not only as it is rising. Most people who are at risk for gout attack will already know this (by having had an attack) by the time they are thinking about going on a very low carb diet. However, some people may not know they are at risk.

Many of the doctors who are very experienced with the use of low carb nutrition will take the precaution of making sure the person takes the medication allopurinol to help prevent a gout attack over the first 4-6 weeks. From the information above, one perhaps might need to be more suspicious for trouble with uric acid if the person has been consuming a lot of fructose. Perhaps it would even be worthwhile to take an initial step of stopping high fructose intake for several days or a week before switching to a low carb eating plan.

Addendum: Oct 30/12 For more on this subject, read the transcript or listen to the audio of a 50 minute discussion between Dr. Stephen Phinney and Dr. Richard Johnson, posted on Me and My Diabetes on May 11, 2011. Extensive discussion of uric acid and of keto-adaptation. LINK

Addendum: January 24/13 LINK to article on gout and uric acid in the context of dietary carbohydrates and low carb, written by Gary Taubes, posted on fourhourworkweek.com

Addendum: March 9/13 Further published reasearch by Dr. Richard Johnson:

“Uric acid stimulates fructokinase and accelerates fructose metabolism in the development of fatty liver.” PLoS One. 2012;7(10):e47948  LINK to PubMed abstract, includes link to full text.

Some quotes, much more in the full text:

- Recently we have found that glucose can be converted to fructose inside cells via the polyol pathway, an accessory route consisting of two enzymes, aldose reductase which converts glucose to sorbitol and sorbitol dehydrogenase that metabolizes it to fructose

- The novel finding in this study relate to the discovery for a causal role for uric acid in fructose-induced fat accumulation in the liver.

- These studies could potentially explain why subjects with hyperinsulinemia show an enhanced metabolic response to fructose

“SYNERGISTIC EFFECT OF URICASE BLOCKADE PLUS PHYSIOLOGIC AMOUNTS OF FRUCTOSE-GLUCOSE ON GLOMERULAR HYPERTENSION AND OXIDATIVE STRESS IN RATS.” Am J Physiol Renal Physiol. 2013 Jan 9. LINK to PubMed

- quote: “These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose.” That means research on fructose in rats is invalid when considering human health and disease.

“Elevated serum uric acid levels are associated with non-alcoholic fatty liver disease independently of metabolic syndrome features in the United States: Liver ultrasound data from the National Health and Nutrition Examination Survey.” Metabolism. 2013 Mar;62(3):392-9. LINK to abstract on PubMed

- quote: “Elevated uric acid level is independently associated with ultrasound-diagnosed NAFLD in a nationally representative sample of United States nondiabetic adults. Increasing uric acid is associated with increasing severity of NAFLD on ultrasonography. These findings warrant further studies on the role of uric acid in NAFLD.”

Some of the Current Research and Opinion:

“Does uric acid qualify as an independent risk factor for cardiovascular mortality?”

- – Clin Sci (Lond). 2012 Oct 9.  PMID: 23043434  LINK to abstract

“Hyperuricemia and metabolic syndrome in children with overweight and obesity.”

“The prevalence of hyperuricemia was 53%.”

- – Endocrinol Nutr. 2012 Oct 19. English, Spanish. PMID: 23089370 LINK to abstract

“Uric acid induces Hepatic Steatosis by Generation of Mitochondrial Oxidative Stress: Potential Role in Fructose-Dependent and-Independent Fatty Liver.”

- – J Biol Chem. 2012 Oct 3 PMID:23035112  LINK to full text

“Serum uric acid as an independent predictor of mortality in high-risk patients with obstructive coronary artery disease: A prospective observational cohort study from the ET-CHD registry, 1997-2003.”

- – J Cardiol. 2012 Oct 19. PMID: 23088935  LINK to abstract

“Elevated serum uric acid predicts angiographic impaired reperfusion and 1-year mortality in ST-segment elevation myocardial infarction patients undergoing percutaneous coronary intervention.”

- – J Investig Med. 2011 Aug;59(6):931-7. PMID: 21415772  LINK to abstract

How Do You Lower Uric Acid Levels in the Blood?

The topic of uric acid levels has mostly been thought of in terms of gout. Yes, over time there has been interest in uric acid levels in relation to cardiovascular disease and other topics, but this has not reached day-to-day clinical practice yet.

Therefore, when research is done looking at how you bring down “high” uric acid levels, they are generally looking at levels above the normal range, rather than paying a lot of attention to people who have higher or lower values within the normal range. This has been changing as researchers have begun to explore other health impacts of uric acid.

Up to now, the consensus has been that you can have only a small impact on your uric acid levels by changes in diet – in the range of 1 mg/dl.  In gout, you want to keep the uric acid level below 6 mg/dl.  Since people with gout can start out with uric acid levels much above this, generally even a determined effort at dietary change is not going to get the person out of having gout attacks or gouty arthritis – medication is still going to be needed.  The topic of making diet changes in order to lower serum uric acid levels receives some attention, but not a strong focus.

But what if:

  • uric acid was about many common medical problems
  • that can affect a very high percent of the population
  • for which we don’t now have the prevention and treatment tools we desperately need
  • at levels in the blood that we have thought of as “normal”
  • and diet choices could make a meaningful impact?

What if lowering uric acid by 1 mg/dl turns out to be a very meaningful amount when it comes to cardiovascular disease risk?  What if we can find ways to lower the uric acid by more than this?  It hasn’t been considered a hot topic of research – maybe it just needs more research attention.

The diet advice that is currently given generally focuses on gout. In this case there are two issues mixed together. One issue is lowering serum uric acid. The other issue is avoiding things that can trigger a gout attack – which may relate to abrupt changes in uric acid levels, not just to the level itself.

According to Mayo Clinic, the things to consider in terms of diet for gout are:

  • avoid foods that are particularly high in purines – this includes anchovies, sardines, herring, mackerel and organ meats  - such as liver, kidney, sweetbreads and brains
  • all meat, poultry, seafood and fish contain purines and should be limited to 4-6 ounces per day. Among these foods, red meat, fatty fish and shellfish are particularly associated with gout attacks.
  • they report that “saturated fat lowers the body’s ability to eliminate uric acid”. (Note: they don’t give the reference for this – if it is high blood levels of fat that do this, then this does not mean that dietary saturated fat is to blame.)
  • alcohol intake is well known as a trigger for gout attacks. Beer is especially notorious for this. Alcohol interferes with the ability of the body to eliminate uric acid – although they suggest that, if not in the midst of a gout attack, for most people 1-2 moderate servings of a wine per day may not be as issue (in terms of gout attacks).
  • fructose increases the risk of gout attacks – fructose is in sucrose and fruit, but most people who are having high exposure to fructose are getting it in drinks sweetened with HFCS – high fructose corn syrup.
  • they report that studies have shown low-fat dairy products can lower the risk of gout
  • drink plenty of fluids. There is limited research suggesting that coffee intake of 4-6 cups per day may lower the risk of gout in men.

Besides these factors, researchers in Japan have published preliminary work suggesting that a high alkaline diet, and thus less acidic urine, supports uric acid excretion compared to a high acid diet. (Note: There is a similar principle used in the treatment of people who get uric acid kidney stones, but the purpose is different. For uric acid kidney stones, a pillar of the prevention strategy is to alkalinize the urine. This is generally done with citrate or bicarbonate. The purpose is to shift the uric acid to sodium urate. The sodium urate is vastly more soluble than uric acid is and so this avoids the uric acid precipitating out and forming stones. Most people with uric acid stones do not have elevated serum uric acid.)

There is also very limited research suggesting that rutin and quercetin may help with uric acid excretion, but the research seems to have been only done on rats so far — and the results may very well not apply to humans.

There has long been discussion of whether intake of cherries or cherry extract may help protect against gout attacks. There has been a small amount of research, but nothing clear has emerged. It may be that researchers will take more interest in this now that interest in uric acid is heating up. See report below of intake of cherries and lowering of serum uric acid level.

(1) Less Acidic Urine

Effect of urine pH changed by dietary intervention on uric acid clearance mechanism of pH-dependent excretion of urinary uric acid.

Kanbara A, Miura Y, Hyogo H, Chayama K, Seyama I.

Nutr J. 2012 Jun 7;11:39.  PMID: 2267616   LINK to full text.

In this study, the people on the alkaline-producing diet (read the paper, it may not be what you think) achieved a urine pH of 6.5 to 7.0 and had greater excretion of uric acid (despite lower dietary intake) than the group on the acid-forming diet, who dropped to a urine pH between 6.0 and 5.5 (more acidic). (Note: neither diet was high in fructose.)

(2) Rutin and Quercetin

Rutin attenuates metabolic changes, nonalcoholic steatohepatitis, and cardiovascular remodeling in high-carbohydrate, high-fat diet-fed rats.

Panchal SK, Poudyal H, Arumugam TV, Brown L.

J Nutr. 2011 Jun;141(6):1062-9.  PMID: 21508207  LINK to full text.

Quercetin ameliorates cardiovascular, hepatic, and metabolic changes in diet-induced metabolic syndrome in rats.

Panchal SK, Poudyal H, Brown L.

J Nutr. 2012 Jun;142(6):1026-32.  PMID: 22535755  LINK to abstract.

Allopurinol, quercetin and rutin ameliorate renal NLRP3 inflammasome activation and lipid accumulation in fructose-fed rats.

Hu QH, Zhang X, Pan Y, Li YC, Kong LD.

Biochem Pharmacol. 2012 Jul 1;84(1):113-25. PMID: 22426011 LINK (abstract)

A Contrary Report:

Effects of genistein, apigenin, quercetin, rutin and astilbin on serum uric acid levels and xanthine oxidase activities in normal and hyperuricemic mice.

Huang J, Wang S, Zhu M, Chen J, Zhu X.

Food Chem Toxicol. 2011 Sep;49(9):1943-7. PMID: 21600261 LINK (abstract)

(3) Cherries and Cherry Extract

Consumption of cherries lowers plasma urate in healthy women.

Jacob RA, Spinozzi GM, Simon VA, Kelley DS, Prior RL, Hess-Pierce B, Kader AA.

J Nutr. 2003 Jun;133(6):1826-9.  PMID: 12771324  LINK to full text

- – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – - – -

Other Resources:

(1) LINK to the abstract of study Dr. Johnson mentions in the interview regarding fructose and weight loss – which he mentions was done in Mexico. Note that this is a small and very brief study and the results don’t actually seem to fit his argument.

The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial.

Madero M, Arriaga JC, Jalal D, Rivard C, McFann K, Pérez-Méndez O, Vázquez A, Ruiz A, Lanaspa MA, Jimenez CR, Johnson RJ, Lozada LG.

Metabolism. 2011 Nov;60(11):1551-9. PMID: 21621801

(2) Genetic disorders resulting in hyper- or hypouricemia.

Sebesta I.

Adv Chronic Kidney Dis. 2012 Nov;19(6):398-403. PMID: 23089275  Abstract

Ketosis in a Nutshell – Part 5, A Hunger Haven

English: life saving ring hanging on wall ‪Nor...

Being in nutritional ketosis reduces hunger.

Just that.

It is worth taking a full pause and letting that sink in if you are not already well familiar with this.

You don’t have to be overweight for nutritional ketosis to have this effect:

- you don’t have to be trying or wanting to lose weight

- you don’t have to have metabolic syndrome

- you don’t have to have blood sugar problems

- you don’t have to have insulin problems

- you don’t have to have any problems with carbohydrates.

You don’t have to be a person who would otherwise be interested in a low carbohydrate diet in order to have this response to being in nutritional ketosis.

As mentioned in Part 2, this is simply a normal usual aspect of how your body functions when adapted to being in a sustained state of nutritional ketosis – that is, when “keto-adapted”. (list of terminology is at the bottom of Part 1 of this series)

In any situation where persistent hunger is interfering with achieving health goals, consideration can be given to a careful trial of nutritional ketosis. This would also likely be true in many or most situations where the urge to eat was felt or interpreted as “cravings” rather than as “hunger”.

It won’t be appropriate in all situations and it will not suit all people.

“Reduces” hunger  – not “eliminates” hunger

  • nutritional ketosis is part of our normal physiology, so we can adapt to different food availability situations. It would not be very pro-survival if it made people totally disinterested in finding or eating food. Your body doesn’t want you to be so disinterested in food that you become malnourished, start to waist away or starve.
  • in nutritional ketosis, if you ignore or over-ride your body’s signals to eat or to consume fluid you can go into an unhealthy state of higher ketones and dehydration that can be associated with loss of appetite (and vomiting, nausea and sleepiness) – but this does not happen under normal circumstances where a person is not fasting or skipping meals. It has been noted to happen sometimes during the initial transition to ketosis in the treatment of epilepsy – but this transition has traditionally been done with an initial period of fasting. Under “normal circumstances” you are responding to your body’s signals for food and water – not refusing available food when you are hungry (no surprise if this turns out to be not a good idea).

We don’t know a lot about this so far:

  • people vary in how easily they go into ketosis (how much they need to restrict carbs and whether they need to consciously restrict protein)
  • people vary in the level of blood ketones they have on similar food intake
  • people vary in how they feel at different levels of blood ketones, even when there has been a period of adaptation
  • people vary in how much they have a lessening of hunger when keto-adapted, although there tends to be more appetite suppression at higher ketone levels
  • people vary in how much their bodies use their own body stores of fat for fuel

As we understand it for now, the lessening of hunger and the use of body fat stores go hand in hand.  If body fat stores are being mobilised from the fat deposits, and being burned for energy, there will be less hunger signals saying “eat more”.  If, for some reasons (or many reasons) the fat stores are not being mobilised, the body will signal for more food intake.

Contrary to rumour, there is nothing about being in ketosis that guarantees weight loss.  You can be well-established in a state of keto-adaptation and not lose weight while eating to satiety.  You are still in a state of burning primarily fat for fuel, but it is fat from the food you eat, rather than from your body.  Having ketones in your blood or urine does not indicate where the fats are coming from that you are burning.

I don’t think there has been any research on this, but it seems pretty clear from people’s experiences that you can be in at least a mild state of ketosis and gain body fat stores.  I really don’t see a reason why not.

Using Nutritional Ketosis as a Tool in Weight Control

  1. Context is everything – best health requires an individualized holistic approach.
  2. What does it look like when this is going well?
  3. What is going on when things are not going well?
  4. Concerns? – There are always concerns.

(1) Using Nutritional Ketosis within a Satiety-Oriented Approach to Weight Health

(I digress  – I can’t brush this close to my bug-bear topic without touching it – if this is not of interest to you, please skip ahead ’till you see #### .)

There are two types of harm associated with high amounts of body fat stores:

  • what we usually think of – the harms from high body fat itself, from visceral fat, from associated conditions both as causes and consequences of obesity/visceral fat, from emotional impacts, from prejudice and discrimination, and so on.
  • the harms caused by what people do in their efforts to avoid weight gain and reduce body fat stores

I think this second type of harm has been underestimated as a major driver of the current obesity epidemic – and I mean this separately from the topic of diet composition in terms of carbs, fat, etc. I am particularly concerned about the potential for harm when the public has the impression that the medical community and policy bodies view putting up with sustained hunger as benign, as effective and as an advisable strategy for weight control.

I consider that calorie-restricted dieting, which intrinsically includes the instruction to not eat when hungry if the calorie limit has been reached, should generally be reserved for situations where a satiety-focused approach is, for some reason, inappropriate or not effective or not effective enough.

What does a “Satiety-Focused Approachmean? (see also Overview)

  • General health, individual circumstance, over-all quality of life and individual goals take precedence over total body fat when considering body composition targets, as is true in all situations where there is consideration of body fat stores.
  • If reduction or stabilization of body fat stores is desirable and this is not occurring, interventions are chosen that don’t require restriction of food intake in the face of sustained hunger (no imposition of a calorie cap). 
  • The interventions are designed to facilitate achieving satisfactory satiety with no excess hunger (i.e. hunger other than in the pre-meal period) while undergoing weight loss. 
  • Failure to meet the chosen goal (whether weight stabilization, reduction of body fat stores, more food “peace”, etc.) over time is a valuable feedback from the body that more needs to be done to reduce appetite drive and facilitate satiety. 
  • Any attempt to impose a calorie cap will ruin this essential feedback and risks sabotaging progress towards a successful long-term strategy (which will actually be composed of a combination of strategies).

The most ideal outcome is to have the appetite/satiety control system performing its proper function of maintaining a healthy body weight and, if the body weight is too low or too high, nudging the body towards reaching that person’s best body weight.

Things that favour improved functioning of the appetite/satiety control system are intrinsically things that favour health in general and the over-all best functioning of the body. There are countless things that can disrupt appetite/satiety control.

Just to give a few examples, for some people, simply resolving one of the disrupters below might be enough allow recovery of appetite/satiety balance:

  • getting enough sleep
  • dealing with stress
  • re-establishing regular eating patterns, including breakfast (avoiding restrict/rebound patterns)
  • becoming able to safely reduce, change or stop certain medications that may be interfering
  • avoiding high-sugar liquids.

One of the most important and effective things that can be done to favour proper functioning of the appetite/satiety control system is to consider whether the person is under any form of harm or strain from the amount and/or type of carbohydrates in their diet.  At the present time, in Canada and in all the “developed” nations of the world, the biggest cause of ill-health in the area of nutrition or metabolism is carbohydrate intake in amount/type that is beyond the individual’s current ability to handle without adverse impact (what I think of as “glucose load strain“) – causing metabolic ill-health and its consequences. I think this is having more ill-health impact than obesity itself.

An individually tailored change in type of carbohydrate, with or without a reduction in total amount of carbohydrate, will help many (not all) people who struggle with their weight or who are normal weight but have excess visceral fat. This strategy can help the appetite/satiety function by:

  • lessening swings in insulin and demand for insulin, thus lessening exposure to high blood levels of insulin
  • lessening swings in blood glucose
  • making control of blood glucose much easier in diabetes or pre-diabetes
  • thus helping to preserve health (which helps preserve future ability to control weight) and reducing requirements for medications – with their potential for side effects
  • avoidance of trigger foods in those with sugar craving/addiction or food craving/addiction that involve sweet taste, starchy foods and/or foods that mix sweetness, sugars or starches with fats.

It’s not all about the carbs. However, your carb intake is something that you have control over, whereas you might not be able to do as much as you would like about your sleep, your stress, the medications you require, your level of chronic pain, and so on.  Still, long term results are best served by the broadest possible effort to maintain your health. (Remembering that carbs are not just about weight and, in fact, the impact of carbs on metabolism is much more important.)

With a satiety-focused approach, improving weight control rests on improving general health, including burdens on body function and regulation. Doing the most possible to promote appetite/satiety function equals doing the most possible to promote health and un-burden the person and the body.

This will not always be enough. There may be disruptors that, at the present time at least, cannot be resolved.  There may be essential medications that can’t be safely stopped, there may be unresolvable sleep problems, there may be long-term consequences on body regulation that have been brought about by high body weight or by losing substantial amounts of weight, and so on.

If it can’t be “fixed”, find a “patch” or “work-around”.  ####

When a person’s appetite/satiety control system needs a little extra help, from my point of view the first choice “work-around” to give consideration to is taking advantage of the appetite-suppressing effects of nutritional ketosis. (Recognizing that there are other weight control or “obesity management” interventions that derive all or a major part of their effectiveness through their impact on appetite/satiety balance including obesity management medications and surgeries.)

A very high exercise level could be considered to function as a “work-around” in those individuals for whom it results in reaching a balance point of calorie expenditure versus appetite.

Calorie restriction remains an option in considered situations and for some people this can be very useful and become their favoured, successful and long-term intervention. It should certainly be tried before obesity management surgery and should be at least considered and offered before obesity management medications.

(2) What Does it Look Like When Things are Going Well?

I refer you back to two of the stories I link to on the previous Part 4, near the bottom of the page.

  • Jimmy Moore’s story is the best that I have seen in terms of demonstrating the difference between his experiences with a very low carb eating pattern and his experiences with nutritional ketosis. Not everyone will feel the difference between the two as profoundly as he has and certainly most people will not have such a dramatic weight loss. (links below)
  • Tommy mentions in one of his blog posts that he was starting to have a little weight regain after holding stable for years. He took advantage of blood ketone testing.  He tightened his diet, succeeded in increasing his blood ketone levels and this helped with his weight.

(3) What is Going on When Someone Who has Plenty of Fat Stores is Keto-adapted and Not Losing Weight?

We don’t know. The short answer is that they are not having enough suppression of appetite to allow their food intake to drop down enough to allow weight loss.

I know that’s not much of an answer, but it is the state of the art at the moment.

As I see it, there would be at least these four things to consider:

(1) The body may be defending the fat stores that are present because of some signalling that is giving the message that the body fat stores are getting low or for some other reason need to be defended:

  • this might be considered “appropriate” – for example, a woman of 5′ 2″ who is finding that her weight loss is stalled at 120 lb. when she wants to get to 115 lb. I sympathise, but her body “has a mind of its own”
  • or “inappropriate” – for example, someone who’s weight loss stalls when they are still 50 pounds above the “normal” weight category – perhaps the body is getting erroneous signals that fat stores are low or for some other reason need to be defended

(2) There may be something (or many things) interfering with mobilising fat from the fat stores. In this situation, the person can still be in ketosis as long as they satisfy their hunger by mostly eating fats, and keep their carb and protein intake low enough.  This can still be very valuable in helping prevent weight regain, helping prevent cravings and “unintended” eating, and other potential benefits.

(3) The level of ketosis may not be enough for that person to have enough appetite suppressing effect in order to allow food intake to fall enough to achieve weight loss.

  • there may be something interfering with the ability to burn enough fats (whatever the source of the fat) to meet the majority of body energy needs – whether due to a disease, toxic influence, medication or a rare genetic metabolic problem.
  • the intake of carbohydrates and/or protein may be too high to allow ketosis for that person at that time.
  • the internal supply of carbs may be too much – continued next paragraph.
  • if the internal supply of carbs can be too much, I wonder if the internal supply of protein can occasionally briefly be too much – such as when tissue is being broken down after an injury or after very intensive exercise or when there is bed rest, particularly in someone who has developed and maintained large muscle mass through regular exercise. I haven’t heard anyone comment on this and this is just speculation on my part.
  • if the person is not very active and has a relatively slow metabolism (generally people’s metabolism slow a bit with the passing decades and people who have lost weight can have a slowed metabolic rate long term) they really may not need to eat very much. They still need their protein for their body lean mass. Once they have that protein and a bit of carbs in their veges and possibly a few nuts or cream or cheese, they may not actually be burning a very high amount of fat to counter-balance that.

The internal supply of carbs being too high is what is happening in the first couple of days when transitioning into ketosis, as the liver’s supply of glycogen is depleted.  The liver produces glucose from glycogen, certain of the amino acids (components of protein), as well as a bit from fat molecules. The glucose is sent into the blood stream to prevent the blood glucose level from falling below normal range. The liver does this mostly under the direction of glucagon and the stress hormones — that is really a rough account, I can’t say I’m really up on the details.

If the blood glucose level is falling and the liver is not keeping up with need, a sudden surge in hormones can bring a surge in glucose output.  This most often happens with exercise and during the night, especially in the early morning and pre-dawn hours. When a sudden surge in hormones is triggered, this is not a finely calibrated response.  The resulting glucose output is generally more than what is needed. In someone with diabetes or glucose intolerance, this may show as a rise in blood glucose above normal, and insulin secretion will go up if their body has the ability to do so. In someone with normal insulin function, the rise in glucose will not be above the normal range, because insulin will go up to handle the glucose. Any rise in insulin inhibits ketone production.

Besides sudden surges of stress hormones, many people have raised stress hormone levels at various times of the day and night.  Many people have chronic elevations of stress hormones, particularly as they get older, and particularly at night.

I wonder if this has a bit of a role to play in why it is so famously difficult for post-menopausal women to lose weight.  This is a very large topic and this suggestion is not meant to over-simplify the picture, but, as a general group, post-menopausal women are famous for having poor quality sleep – and even more so if they have hot flashes or night sweats.  Some women in this situation may be producing enough glucose at night to trigger enough insulin to suppress ketone production.  This would not be detected by blood glucose testing if insulin function was normal.

Also, insulin resistance of the liver is common.  In this situation, the liver may produce substantially more glucose than is needed to maintain the needed blood glucose level.

(4) due to insulin resistance, when starting the diet insulin levels may be quite high and may take a while to come down to lower levels. Besides this, if the person has been habitually having a large amount of quickly-absorbed carbs at their meals, there body is adapted to this pattern. When they first adopt a low carbohydrate eating plan, this may take a few days to settle down, and in that time the person will be hungrier  and hungrier more often.

And … there is always the unexpected unknown.  As mentioned in Part 4, Jenny Ruhl has had some difficulties with very low carb diets, despite being unusually well informed and experienced.  We do know that Jenny has an unusual metabolism in that (1) she has an uncommon form of diabetes and (2) she had a very unusual (though very pleasing) profound response to Co-enzyme Q10).  The thing is, unusual metabolisms happen, and you might not know about it until later life.

Addendum Oct 18/12 – I knew I was forgetting some things in this list:

  • nutritional ketosis is just one influence on your appetite/satiety system.  If you have enough pro-appetite forces in your life, the effect of these may be stronger than the appetite-lessening effect of the keto-adaptation. The Rest of Reality always applies.
  • when you start into nutritional ketosis, you may be still in a restrict/rebound cycle.  The restrict/rebound cycle can take place within a day (low food first part of day, over-eating in later day), within a week (skimping food in week and rebound on weekend) or over months (“dieting”, then rebound after the diet) or over any other time period.  If you have just spent time deliberately eating less than your body is telling you to, even though you might then switch to a healthier approach that would be successful long-term, you still might have to go through the rebound phase set in motion by your previous restriction. This doesn’t mean you have to re-gain the weight, but you might re-gain some (e.g. rebuild muscle) or stall for a while until your body figures it has repaired and recovered from the forced weight loss.  To help this process, be kind to yourself in other ways, to promote recovery from the previous dieting stress – especially, don’t heap on more stress.
  • if you have lost weight recently, you may be in a ‘stall” or “plateau” that you just have to wait out. Stalls happen to every-one.
  • sights, smells, thoughts -  your appetite/satiety system is integrated with your entire functioning.  Seeing and smelling food already sets the digestive system in motion.  You may need to be careful how much you are exposed to foods that are of a type you are not intending to eat.  Thoughts matter – find other things to enjoy and be cautious about negative self-talk.  If you are exposed to food that is in keeping with your intended eating plans and you feel hunger – eat it (or, if that’s illegal, find food you own and eat that).

(4) Concerns About Nutritional Ketosis for Weight Control?

There are always concerns …..I have mentioned some of these near the bottom of Part 1 and in Part 2 and I’ll get back to this topic in a later post. (likely 3 more in this series)

……………………………………………………..

The field is starting to move quickly. As I have been preparing this, an important post has appeared on Dr. Richard D. Feinman’s blog (the biochemist, listed in my blogroll). The post is by Dr. Eugene Fine and he explains a research paper just published. The purpose of the research was to examine insulin lowering as a strategy in cancer treatment.  I expect research interest in this topic to expand rapidly.  Now it is in its very earliest stage and there are only baby steps towards a good working knowledge.

The point of interest in Dr. Fine’s post that relates to the topic of this post is the graph of insulin levels versus blood beta-hydroxybutyrate levels (the type of ketone measured when using blood ketone testing – also noted as beta-OHbutyrate) and how variable the ketone (beta-hydroxybutyrate) levels were between the participants when on a ketogenic diet even when strict care was taken to use diet compositions as identical as possible. Also, they clearly noted appetite suppression.

“(We tried to over-feed the patients in order to maintain weight and calorie intake, but it didn’t work: very low CHO diets do indeed cause spontaneous calorie restriction and weight loss, even when you try to prevent that.)”

To hear more about Dr. Eugene Fine’s work, look for Jimmy Moore’s upcoming podcast with him on Monday, October 22, 2012

To hear more about ketogenic diets and cancer, look for Jimmy Moore’s Ask the Low Carb Experts podcast tomorrow, Oct 18/12 with Dr. Colin Champ.

Related articles

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Some Research:

Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum.

Johnstone AM, Horgan GW, Murison SD, Bremner DM, Lobley GE.

Am J Clin Nutr. 2008 Jan;87(1):44-55.   PMID: 18175736   FULL TEXT

“In conclusion, the low-carbohydrate component of the high-protein regimen affects subjective motivation to eat, and volunteers feel less hungry and consume less energy, at least in the short term. Whether LC (ketogenic) diets are a suitable tool for weight loss will remain an important issue for some time, as more complex interactions between phenotype and diet composition are identified (23). This regimen appears to reduce calorie intake without increased hunger, and, therefore, it promotes compliance.”

………………………………………………..

The effects of a low-carbohydrate ketogenic diet and a low-fat diet on mood, hunger, and other self-reported symptoms.

McClernon FJ, Yancy WS Jr, Eberstein JA, Atkins RC, Westman EC.

Obesity (Silver Spring). 2007 Jan;15(1):182-7.  PMID: 17228046   FULL TEXT

“Hunger was significantly lessened in the LCKD group for as long as 3 months.”

“Furthermore, the present findings represent a replication and extension of previous studies demonstrating significant appetite suppression during an LCKD.”

Ketosis in a Nutshell – Part 4, Happy Campers More

shrimp (boiled), lemon juice, fresh cream, may...

shrimp (boiled), lemon juice, fresh cream, mayonnaise, salt, chervil (Photo credit: Wikipedia)

Nutritional Ketosis and Weight Loss

The other significant intentional use of nutritional ketosis has been for weight loss and weight control.

To be clear, nutritional ketosis is just one tool that can be used to assist with weight control. It is not suitable for everyone. Even for the people who do find it useful, the benefits will not be limitless. Many factors are involved in weight control, such as sleep and stress - it does not all come down to diet.

OK, Now for the Stories of Happy Campers -

Uhm, wait….

Yes, I do have some stories for you – two in particular make for very interesting reading. The most fascinating is the personal story of Dr. Atkins himself.  I will get into these stories, but first it is important to discuss some areas of confusion.

It is not such a simple matter to find stories for the topic of weight loss as it was for the previous topic of epilepsy control. Why? In the situation of ketogenic diets for epilepsy control, nutritional ketosis has been the agreed-upon target from the beginning (although this is changing with some of the less strict dietary regimes of the past decade).  The people were following strict diets that would clearly induce ketosis and these were consistently maintained over time (in those who had success with their seizures). They were all under the guidance of professional expert teams and meaningful research data was collected and published. When considering nutritional ketosis in the context of weight loss, the situation is much less clear.

Isn’t following a low carb diet about the same as being in ketosis?

Don’t we know all about this from the wide use of low carb diets over the past decades?

When people follow a very low carbohydrate eating plan, such as what is commonly thought of as “the Atkins Diet”, most of them will be in nutritional ketosis. (I put “the Atkins Diet” in parentheses as often people are following some concept of their own of what the Atkins Diet is, rather than truly following Dr. Atkins’ actual recommendations.) Some people will not be in ketosis – for various reasons their metabolisms are resistant to going into ketosis and/or they may be consuming an amount of protein that is too much for them.  Some people may be testing to monitor over time whether they are in ketosis or not.  Some are not.  As people start to eat more carbohydrates or more protein, individual people will move out of being in ketosis at different amounts of carbohydrate or protein intake.

Therefore, everyone who is in dietary ketosis is eating a low carbohydrate diet (unless they are taking a ketone-producing medical product or eating high amounts of medium chain triglycerides). However, not everyone eating a very low carbohydrate diet is in dietary ketosis.  It is now very clear that you can be carefully following a very low carbohydrate diet – for example, staying below 20 grams of carbohydrates a day – and yet not be in nutritional ketosis to any meaningful degree.

Unfortunately, the two things seem to have gotten somewhat mixed up together in many people’s minds.  I think somehow being in ketosis – turning the urine test strip purple – has come to be commonly viewed as just the far end of the low carb spectrum. In reality, being in ketosis is a metabolic state of its own with effects and implications that go beyond just leveling out the blood sugar levels, or lessening swings in insulin or other benefits of lessening the strain on the body from carb intake above an individual’s tolerance level..

What’s the big deal? Why does this matter?

  • being keto-adapted can help weight loss and weight control
  • the changes that happen with ketosis, if not understood, can interfere with weight control by causing confusion and discouragement

How can being keto-adapted help with weight control beyond a low carb lifestyle?

(1) Being in sustained ketosis provides some degree of lessening of appetite (more below).  This knowledge has faded from awareness or not been appreciated for the invaluable tool that it is.

(2) Some people might have a benefit to their brain function that results from their keto-adaptation. (See previous post in this series.) We don’t know enough about this yet, but many people report improvements in mental energy, focus and mood – these effects could be expected to improve a person’s ability to control their weight.  Scientifically, these effects are quite plausible and I hope the current interest in research on ketosis and brain function will expand quickly.  This is just speculation, but it is even plausible that being in ketosis may favour improved function of the appetite/satiety control centres of the brain if these centres might be (hypothetically) metabolically compromised in their function??  This topic is particularly interesting in view of the current concept of “Type 3 diabetes” (see the second post in this series).

(3) There may be other aspects of being keto-adapted that might be helpful in weight control – for example, some people feel that their muscles function better when in ketosis and then find it easier to be active. Some athletes are now using keto-adaptation as a high performance strategy. See HERE and HERE and HERE.

How can ketosis cause confusion during weight loss?

If you are transitioning into ketosis and you are not well informed about what that means or how that can be expected to affect your body and your energy metabolism, you could be very confused or even distressed by changes you experience.  Without proper information, you might not even know you are going into ketosis.  You might not even understand that the way you are eating has made ketosis a possibility.

The same is true in reverse if you are in ketosis (intentionally, knowingly or not) and you unknowingly move into a slight degree of ketosis (where you are not really running substantially on ketones) or fully out of ketosis.

(1) rapid weight changes not related to changes in fat stores

When transitioning into ketosis, there is a rapid drop in body stores of glycogen, which causes a rapid drop in body weight from the weight of the glycogen and the water that had been associated with the glycogen. There is also a increase in sodium excretion, with some drop in body water from that, as well.  None of this weight is actually loss of body fat stores.  This can lead to false expectations of continued rapid weight loss.

Over time, the body adapts to the state of ketosis and there is some re-balancing in the body.  In terms of any regain of that body water, I don’t think there is much definitive to say at this point and it is bound to be highly variable between individuals.  However, to the extent that there were a slow regain of some of that water over the first 2-3 months, this would show up on the scales and falsely appear to be lack of progress in reduction of body fat.  The more dramatic the initial drop in body weight as water, the more chance that some return of that body water could, soon thereafter, give an impression of lack of progress in fat loss.

It can be very easy to move out of the ketotic state. One substantial serving of carbs can mean that the next day your body weight shoots up just as rapidly as it initially fell.  Only a very little bit of this would be actually fat – almost all of it would be water and glycogen.  This causes people great unhappiness and confusion and can precipitate a dark mood that then brings even further “off-plan” eating.

(2) changes in energy and sense of well-being

When you are transitioning into nutritional ketosis, you can feel quite “low” and tired for a few days or even a week or two as your body adapts to the new fuel mix.  Some people even call this “the Atkins flu”.  It will pass and there are ways to lessen these effects (such as increasing sodium intake – see Resources below).  The real problem comes if this is happening to you and you don’t understand why.  Once the transition period is well underway, people often feel better than they have in some time.  Imagine how confusing it is if these changes come and go unpredictably and with the real cause unknown and thus uncontrollable.  If the person moves out of ketosis for a few days, they may suddenly feel a real change in their sense of well-being.  If they then shift back into ketosis, it will take some days or a week or two again for them to get back to a keto-adapted state.

Without knowing the real cause for there mysterious changes in how they feel, they may incorrectly blame the problem on something else and start making other changes in their diet or lifestyle or health practices that can then lead to other confusions.  None of this bodes well for finding their best personal happy healthy stable eating pattern

(3) changes in appetite and cravings for starches and sweets

  • loss of the appetite-suppressing effect of being in ketosis
  • suddenly the brain is not getting the ketones it is adapted to, so it quickly starts using much more glucose than the liver has been used to supplying, potentially drawing down the blood sugar level.  When the brain gets hungry, it sends out signals to supply it with its emergency fuel – glucose.
  • when coming out of ketosis, for a few days the body is not fully adapted to glucose intake again and the blood sugar will go higher than it normally would, risking an exaggerated eventual insulin response which would compound the problem by causing an unusually sharp drop in blood sugar.  Remember that starch is pure glucose, so it isn’t just sugar that causes a flood of glucose into the body. The rapid drop in blood sugar would bring more hunger and a craving for carbs to bring the blood sugar back up. Repeat. Repeat again. By the time this roller-coaster settles down, several days have passed and the person has regained glycogen (and therefore a number of pounds) and can be very discouraged and also not understand what just happened to them.

Imagine a person who had become adapted to being in a sustained state of ketosis who then shifted their diet so slightly that they did not notice or did not think it was a significant.change. Imagine that person thinking that they were still following the diet, but they were no longer in ketosis.  They would not understand why suddenly they were both more hungry and having craving for carbohydrate foods.  They would just feel that “the diet stopped working” or “I don’t have the will power to stick to the diet”. A bit of extra hunger or craving, if due to being close to moving out of ketosis, can bring “a little nibble”, which would then be sure to bring a bit more hunger or craving.  As the ketone level then fell further, a few “nibbles” more would again cause more hunger, not relief of hunger. This hunger leading to more hunger is often the path that leads a person fully out of ketosis – and into a sharp spike and drop in blood sugar, as well, depending on the foods and amounts chosen.

There are many happy stories of sustained weight loss while eating low carb.

But very few that include (adequate) details about the topic of ketosis – although this can be expected to change dramatically over the next months.

Over the decades and until very recently, relatively few of the people who have reported their experience with low carbohydrate diets have included in those reports enough (or any) detail on their experiences with ketosis itself in order to be able to understand the impacts of nutritional ketosis on their experiences – both good and bad.

Thus, the stories of those people who actually experienced a sustained period of nutritional ketosis are, for the most part, not clearly separable from the stories of people who undertook low or very low carbohydrate diets without a period of being adapted to nutritional ketosis.  Generally, the stories of people who had problems with weight loss on low carb diets – or who found staying on the diet too difficult – do not contain information on whether they had attained keto-adaptation and what was going on with their ketosis situation during the time when they were having difficulties.

Stories of experiences with nutritional ketosis can be suspected within stories of people who have followed low carbohydrate eating plans.

When you hear or read stories of people’s experiences – good or bad – with following a low carbohydrate eating plan, keep in mind how their encounters with ketosis may have been a factor in their experiences with low carb.

Stories That are Clearly About Nutritional Ketosis for Weight Loss

(1) Patient Number 1 – The original Happy Camper using nutritional ketosis as an aid in his own weight loss – Dr. Robert C. Atkins.  Unfortunately, this post is getting too long already, so I will have to leave as this teaser – from how I read it, Dr. Atkins’ original focus was just as strongly on the vital role of nutritional ketosis as it was on the problems of carbohydrate intolerance.

(2) The story that is creating Major Buzz is Jimmy Moore’s recent experience, which he has been documenting in detail since the spring.  It should be pointed out that each person’s needs and medical situation is different, so his story is not intended to imply that his approach is for everyone or is the most healthful way for you to proceed.

I include it here because it highlights the difference between a very low carb diet and a targeted ketogenic diet.

I expect that few people would have an outcome as dramatic as Jimmy’s.  He obviously is able to go into a strong level of ketosis and feel very well while doing so.  People are very different in how readily they go into ketosis and how they respond to it. As I’ve said before, ketosis is not right for everyone. Jimmy’s response is in keeping with his earlier experiences of dramatic weight loss when he first went on a very low carb eating plan in 2004.  His results then were similarly “not typical mileage” – with a much more dramatic weight loss than many people achieve with the same diet changes.

(3) Jenny Ruhl’s recent experience - You have to scroll down to the comments section below her post to see where she reports that she did test positive for urine ketones throughout the trial 2 weeks, after the first couple of days. I include it here for some balance.  Also, it reflects some other people’s experiences that I have read about in the past months where the person has done blood testing for ketones and not had substantial weight loss when eating to satiety.  Note – in Jenny’s trial she did lose weight, but she remained hungry as she kept to a calorie cap.

What you eat is only part of the whole picture when it comes to what is determining your body weight (unless being in semi-starvation or putting up with chronic hunger, neither of which are tenable long-term).

Jenny is an extremely happy camper when it comes to a “to the meter” individually targeted lowering of carbohydrate intake as an essential aspect of controlling diabetes and glucose intolerance (see her other web site, facebook and books).

(4) Tommy Runesson in Sweden - very impressive weight loss, now stable at healthy weight.  Recently doing blood ketone testing and reporting this in detail on his blog.  Great blog for seeing the very tastey-looking food he photographs daily.

(5) More stories with testing of blood ketone levels are bound to be appearing in increasing numbers over the next months.  We really know only tidbits of info so far about this whole topic.

Places I would suggest to keep an eye out for more stories over the next months:

To be continued … this post has gotten too long.

Next: more on the topic of appetite reduction in nutritional ketosis and a look back almost 5 decades ago to the insights that started it all for Dr. Atkins.

Resources – Link to my page Resources – Low Carb and Ketosis

Related articles

Ketosis in a Nutshell – Part 3, Happy Campers Galore

the best part of whipped cream

the best part of whipped cream (Photo credit: thepinkpeppercorn)

Many people find that they are pleased (joyful even) to have the option of making use of nutritional ketosis to help them improve their health.

(terminology list at bottom of Part 1)

The numbers of those people are growing steadily as barriers to use of ketogenic diets fall:

  • in the neurological community, the diets have gone from being perceived as too onerous to use in all but rare cases – - to – - progressively becoming more practical and more palatable
  • in the weight loss community, use of nutritional ketosis has gone from often being perceived as an overly strict diet that a person will often “blow” and not use long term - – to – - being much better understood and developed into an eating style that many have adopted over many years with sustained health benefits
  • in both communities, people have gone from a situation with lack of support at the community and peer level – - to – - LOTS of peer support is now available online and in other forms
  • the day-to-day experience of the foods and the meals is much enhanced by the many recipe sources and “foodie” sites online
  • people are able to share their positive experiences with nutritional ketosis and network this information online
  • people are able to share their negative experiences with nutritional ketosis online and get trouble-shooting support
  • continued experience and research has shown that, while there is potential for side effects and there are certain cautions to keep in mind, with proper instruction in a nutritionally sound eating pattern and a reasonable degree of medical support, over-all nutritional ketosis can be used safely over time (with more intensive supervision needed for the stricter versions of the diet, for younger children, for people with more medical problems and medications – particularly during the transition phase)
  • particularly, one of the most important barriers has been concern over the safety of the very high fat intake that is an absolute requirement for long term use of nutritional ketosis.  Reams and reams and web page after web page have been written on this topic and I am not going to attempt a review of it here.  Research done on people following a ketogenic or very low carbohydrate diet in a clinical or research setting (and thus having received some instruction, support and lab monitoring) have not born out these concerns – although monitoring is important to spot the relatively small number of people who do not do well on such a diet.  Also, considerable doubt has been thrown on the concept that there exists any scientific evidence of harm from a high fat diet – at least in the absence of high glucose or a moderate or high carbohydrate intake (other than in those with specific genetic susceptibility).  The research has not separated out the impact of high fat from the impacts of glucose loads.

The availability of home blood ketone test meters and better understanding of their use is likely to substantially speed up the expansion in the use of nutritional ketosis (ketogenic diets) as it will likely help people achieve benefits more reliably and with less confusion and effort.

The Nutritional Ketosis “Nation” Comes from Two Founding Peoples:

(1) Ketosis for control of epilepsy in children

(2) Ketosis for weight loss

Nutritional Ketosis (ketogenic diet) for Epilepsy Control

  • for wonderful stories and pictures of people who have had dramatic recovery of their health from using a ketogenic diet for epilepsy control see HERE. This is a page of personal stories on the website of The Charlie Foundation.  Most of the stories are of kids, but some are reports by adults of their recovery with the diet when they were children.
  • more happy stories on the website of the U.K. organization Mathew’s Friends.  On their home page, click on About Us and then on Our Stories.

Short version

Although remarkably effective for many patients, the ketogenic diet for epilepsy control fell into obscurity as more and more medications, as well as surgical options, came into use.  It was remembered the way it was in the early decades of use  - suitable for a very small number of people, requiring a specialised team and hospitalization to undertake, being very challenging and unpleasant, and presenting medical side-effects and potential nutritional compromise, such as growth restriction.  Time has brought much progress, though.  Now, not only is the “classic” version of the diet much easier and more pleasant than it was in the 1920′s and 1930′s when it was first in use, but also there are less stringent versions of the diet as an option.  In the past two decades, it is the pleased parents of the recovered kids who have pushed the medical community to play catch-up in recognizing this critical medical intervention.  Clinical use continues to rapidly expand around the world and researchers are expanding the horizons of the potential uses of ketogenic diets in medical care.

Longer version

It was in the 1920′s that the “classic” form of the ketogenic diet was developed and first used for epilepsy. They knew that sometimes people with epilepsy would improve during periods of fasting or starvation.  Trouble is, they didn’t know what it was about starvation that caused this improvement – or if it was due to a combination of factors.  They knew that the level of ketones went up during starvation and they knew that there also tended to be dehydration.  Also, in starvation there were not the nutrients to allow for growth.

The diet plans were being developed to try to help with children who were in very serious and difficult medical circumstances.  These children had severe epilepsy that was not responding to other medical treatments.  For this reason, the most effective diet plan possible was the goal. The “classic” ketogenic diet involved all three of these factors combined together.*

  • The diets were designed for the highest promotion of ketone levels in the blood – meaning the least protein compatible with health, tiny amounts of carbohydrates, and the rest as fat – all measured exactly.  They were trying to mimic starvation as closely as possible.
  • There was a limit placed on fluid intake – both the total amount per day and the amount at one time.
  • In addition, the diets were designed with precision to give the children substantially fewer calories per day than the standard calculations said they needed – in fact, only 75% of their calculated needs. The plan was that a child would not lose or gain a pound (despite the fact that normally children grow).  The children were weighed often (e.g. monthly). If the child lost or gained any weight, the food allotment would be adjusted up or down to correct for this.

These diets were dramatically beneficial for many of the children.  Still, some did not benefit and some had partial improvement.  The most remarkable finding was that some children, if they had excellent seizure control, could return to a full normal diet after a couple of years without the seizures coming back.. They were effectively cured of their epilepsy.  Given that the stakes were so high, the degree of response was frustratingly unpredictable.   It could also be erratic – sometimes a child who had been doing well would have a brief recurrence of seizures for no identifiable reason. Sometimes the seizures returned and no adjustment in diet could be found that resulted in regaining seizure control.  The seriousness of the situation, the great hope for improving the lives of these children, the unpredictable and sometimes erratic nature of the response and the lack of helpful insights from research or lab tests all combined together to make it difficult to stray from the “tried and true” version of the diet plans.  The diet plans required intensive highly expert supervision and were extraordinarily stringent, difficult and nutritionally tenuous.

It isn’t hard to understand why the use of the ketogenic diet for epilepsy control fell into obscurity as more and more prescription medications for seizure control were developed - along with more surgical options.  It languished for decades.  Where it did remain in use, by a dedicated team at John Hopkins, the passing decades brought substantial improvements in the practical application of the diet. A big reason for the diet becoming easier and more pleasant to use was the fact that tables of the detailed nutrient content of all common foods became available, which was not the case in the 1920′s.  This, along with home use of highly accurate food scales, enabled the design of diets composed of a greater variety of normal household foods.  Still, the implications of these developments went un-noticed by the greater medical community.

It was the parents who changed all that.  The hospital team kept the knowledge alive and developed it to a more usable form.  It was the parents who insisted (INSISTED) on spreading the word about the life-altering potential of the ketogenic diet.  Why the enthusiasm for a dietary treatment that still, despite the improvements, was still difficult and a serious medical intervention?  Many children continue to suffer from severe epilepsy despite being tried on any number of medications, medications in combination and despite the availability of improvements in surgical options.

In the early 1990s, the desperation of the situation these children and families faced led to a resurgence of interest in the ketogenic diet.  With The Charlie Foundation and Mathew’s Friends anchoring the voices from the parents’ and patients’ side, the medical community has scrambled to keep up as demand for and use of the ketogenic diet has rapidly expanded, now world-wide. (It only sounds like hyperbole because it is such a good story.)

Recently, doctors were very surprised to serendipitously find that a much less strict version of a ketogenic diet (rather than the “classic Ketogenic Diet”) could be very effective for some people for epilepsy control.  This finding led to the development of a specific dietary program called the “Modified Atkins Diet”.  It is very much like the classic Atkins Diet, but with some tweaking to make it more steady in its effects.

Another more liberal version of the diet was developed in 2002 based on the Glycemic Index. This is a diet that keeps total carbohydrates low (not as low as the above two versions), but also focuses on the quality of the carbohydrate foods chosen. It incorporates carbohydrate foods that are slow to digest – meaning that the glucose from the food is absorbed from the digestive tract slowly.  Refined sugars and high GI starches are avoided.

Other diet variations are the MCT Ketogenic Diet, which incorporates MCT oil, and the Modified Ketogenic Diet.

There is one confusing aspect to the terminology about the diets.  The use of ketogenic diets for epilepsy has evolved, until recently, as its own little insular world.  There were no other deliberate medical uses of ketosis in the early decades.  Neurologists got used to using the term “Ketogenic Diet” to describe the very specific highly regularized diet program they were using (including fluid restriction, 75% calories with normal weight children, three meals of identical nutrient balance, etc).  Why not?  No one else was using the term.  Now this causes some confusion as, of course, this is just one possible version of “a” ketogenic diet (a sustainable eating pattern that causes the development of ketosis).  It is helpful to refer to this as the “classic Ketogenic Diet” or “Classic Ketogenic Diet”.  Unfortunately, those in the epilepsy diet community are so used to using these terms (and so often are speaking to each other and implicitly know what each other means) that often the term “classic” is left off.  This can cause some confusion. Also there seems to have been some lack of understanding as it seems that at least some in the neurological community did not understand that the Atkins Diet was intentionally designed to promote the development of ketosis in the early stages – to take advantage of the known appetite suppressing effects of ketosis (ref – Atkins 1973 book, see next installment of this series).

The more acceptable the diets become, the more reason researchers have to delve into the science of what is going on in the body in response to the diets and what other medical conditions might benefit from the use of ketogenic diets.  We still don’t know exactly how these diets cause their beneficial effects.  It is clear that not everybody needs the same combination of diet mechanisms to achieve similar levels of benefit – that is, some people need stricter, more ketotic diets and others do as well with less strict diets. (For more details on the research, see some of the medical papers listed (with links) at the bottom of Part 2 of this series.)

To reflect the new understandings, a term now being used is “Metabolic Therapy”, which incorporates the idea that there are a number of ways to manipulate metabolism that may be harnessed for treatment of neurological conditions.

To see videos of a one day conference in Toronto, March 2010, about dietary treatment of epilepsy, including the various diet options and the treatment of adolescents and adults, please visit my web page HERE

Nutritional Ketosis for Weight Control   ….. to be continued next installment

* some of the core Ketogenic Diet principles detailed in the 1996 book “The Epilepsy Diet Treatment: An Introduction to The Ketogenic Diet, 2nd edition” by John M. Freeman, M.D., Millicent T. Kelly, R.D., L.D. and Jennifer B. Freeman of the John Hopkins Pediatric Epilepsy Center.

Other Resources:

The Charlie Foundation – an American organization that has played a central role in the resurgence over the past 2 decades in the use of the ketogenic diet for epilepsy control.  The web site offers extensive information. www.charliefoundation.org

“The Charlie Foundation was established in 1994 in order to raise awareness about the ketogenic diet as a treatment for childhood epilepsy. The modern success of the diet has led to new demands on the medical community. In order to meet these demands, the Charlie Foundation has expanded its priorities to include educational programs for dietitians and neurologists as well as support for clinicians and researchers working to perfect its administration and discover its mechanisms.”

Mathew’s Friends  – an organization in the U.K. that similarly plays a central role in providing information and supporting access to treatment.  Extensive information is available on their website.  http://www.matthewsfriends.org/

Books oriented to the dietary control of epilepsy:

The Keto Cookbook: Innovative Delicious Meals for Staying on the Ketogenic Diet

Ketogenic Diets: Treatments for Epilepsy and Other Disorders

Dietary Treatment of Epilepsy: Practical Implementation of Ketogenic Therapy

Fighting Back with Fat: A Parent’s Guide to Battling Epilepsy Through the Ketogenic Diet and Modified Atkins Diet

Ketone Testing Meters Compared

Jimmy Moore has an important post, on his Livin’ La Vida Low Carb blog, in which he compares the two available brands of blood ketone testing meters.

LINK

Included is some direct head-to-head testing done with the two meters.  It is also interesting to read the comments below the post for other people’s experiences.

Hopefully, if there is enough interest, a better unit with more affordable test strips will be developed – soon!

Jenny Ruhl reports her ketosis experiences

Jenny Ruhl has just posted another update – at the mid-point of her planned 2 week journey back into nutritional ketosis.  Jenny is very experienced in sustained ketosis, having spent 5 years maintaining nutritional ketosis in the recent past, plus years at a low carbohydrate intake above the point of significant ketosis  This unusual degree of personal experience, plus her extensive communication with others following low carb lifestyles and her broad knowledge of the research and the science, makes her reports especially valuable and insightful.

Her report is particularly important because she is one of those who don’t thrive when in ketosis, particularly over an extended period.  Individual differences in metabolism are very real.

Her post.

More on her history with nutritional ketosis, part of her discussions with Jimmy Moore on his Ask the Low Carb Experts podcast from September 20, 2012.  web page

Addendum Oct 15, 2012

Jenny posted about the outcome of her 2 week trial.  I commented on her trial and provide the link to her post in this excerpt taken from Part 4 of my Ketosis series -

Jenny Ruhl’s recent experience – You have to scroll down to the comments section below her post to see where she reports that she did test positive for urine ketones throughout the trial 2 weeks, after the first couple of days. I include it here for some balance.  Also, it reflects some other people’s experiences that I have read about in the past months where the person has done blood testing for ketones and not had substantial weight loss when eating to satiety.  Note – in Jenny’s trial she did lose weight, but she remained hungry as she kept to a calorie cap.

What you eat is only part of the whole picture when it comes to what is determining your body weight (unless being in semi-starvation or putting up with chronic hunger, neither of which are tenable long-term).

Jenny is an extremely happy camper when it comes to a “to the meter” individually targeted lowering of carbohydrate intake as an essential aspect of controlling diabetes and glucose intolerance (see her other web site, facebook and books).