Access Dr. Bernstein – diabetes control with low carb

Aside

Diabetes Solution

Diabetes Solution (Photo credit: Earthworm)

Every month the highly-respected Dr. Richard K Bernstein has a teleconference.

From the email I received:

“Ask Dr. Bernstein Webcast and Teleconference !!! – TONIGHT!  Wednesday, Oct 31, 2012 Special Topic Diabetes/cancer and CVID

Please Ask Dr. Bernstein Your Questions NOW! By emailing us at publisher@diabetesincontrol.com or by going to www.askdrbernstein.net
Join the Ask Dr. Bernstein Webcast and conference call on Monday Oct 31,2012 7PM CST, 8PM EST and 5PM West Coast Time. Dr. Bernstein will answer your questions

To attend, visit: http://cdset.c.topica.com/maapWXOacaxnobtVXqrbaeQyvr/
Or Primary dial in number: Phone number: (206) 402-0100 PIN Code: 900326#  “

(Note: for Canadian readers, this is definitely not the Dr. Bernstein of the diet clinic chain.)

Dr. Bernstein has endeavored over many decades to get out his message of blood glucose control to normal levels, and the essential role of low cab intake in that process.

The medical literature starts to shift

Eggs

Eggs (Photo credit: pietroizzo)

That creaking sound you hear is the slow reluctant shifting of the medical literature.

We are starting to see more medical papers and research that reflect the concepts of addressing carb intolerance by reducing carb intake – and thus increasing fat intake.

(1) It is not surprising that this is a well done study – note Jeff Volek as one of the authors:

Whole egg consumption improves lipoprotein profiles and insulin sensitivity to a greater extent than yolk-free egg substitute in individuals with metabolic syndrome.

Blesso CN, Andersen CJ, Barona J, Volek JS, Fernandez ML.

Metabolism. 2012 Sep 26. pii: S0026-0495(12)00318-6. doi: 10.1016/j.metabol.2012.08.014.  PMID: 23021013  LINK to abstract

Note that the study participants were not eating low carb – they were having 25-35% of their diet as carbohydrates – which is still a lot less than the carb intake in the “usual” diet.

The study results carry an extra meaning in that this supports the concept that there are many differences in metabolism between people who are eating a carb load that is under or over their personal tolerance limit. Thus, given that carb intolerance is so wide-spread in the general population, any research done on people eating “usual” amounts of carbs cannot be assumed to apply to people eating carb amounts that are within their carb load tolerance. This applies even more so for those eating very low carb or who are adapted to a state of nutritional ketosis.

Thanks for heads-up on this study to a tweet from @CavemanDoctor.

(2) Thankfully, full text is on-line for this extensive review article:

Sugar restriction: the evidence for a drug-free intervention to reduce cardiovascular disease risk.

Thornley S, Tayler R, Sikaris K.

Intern Med J. 2012 Oct;42 Suppl 5:46-58.  PMID: 23035683   LINK to full text

You can click for the PDF version, which is easier to read.

Telling People They Don’t Exist – still

Motivational Poster - Support

Motivational Poster – Support (Photo credit: Raymond Brettschneider)

Inconvenient people challenge our mind-set and push our comfort zone.

This is not about shaming. It is about something subtly different – which is discounting other people’s experiences when they don’t match your own – even to the point of shunning.

Re-posted – Originally posted May 20, 2012.

One of my pet peeves is when people are, in effect, told that they don’t exist.

An example?  I get a migraine and flu-like symptoms if I eat even a tiny amount of gluten.  I don’t have celiac disease, I have gluten sensitivity. This has a major impact on the day-to-day living of my life and is something I can never afford to forget, ignore or down-play any time I am around food. Yet, to the vast majority of my own medical colleagues I don’t exist. They recognize the existence of a person occupying the space my body is in. However, what they see there is a person who isn’t me as I know myself to be. They see some deluded or self-deluded not very competent person who holds a questionable and likely false belief that places them in the ranks of the crackpots who think they are harmed by wheat, in the absence of laboratory proof. The recent recognition of gluten sensitivity as a medical condition (see this post) has not received wide-spread attention and is likely to be slow to be incorporated into routine medical practice.

People who have gained substantial health benefits from following a low-carb lifestyle are often treated in the same way. Many people report how frustrated they have felt when their doctors, their friends or work colleagues, or family members have discounted their stories and/or, even worse, discounted them as individuals for the decisions they have made and the “obviously false” conclusions they have come to.

But consider, does it ever happen the other way?

A few months ago I had an experience that has stayed in the back of my mind since.  On one of the blogs about low carb nutrition, I was reading an older post and the looong list of 50 or more comments under it. There was a lot of back-and-forth commenting among the contributors and with the author.  There was a good spirit of comradery evident. Everybody who raised a question, interesting idea or dilemma was responded to  — that is, everyone except one soul. One person posted a comment asking for insight or helpful comment on her situation – asking, that is, for help.  This soul was ignored as if she had leprosy. Her comment fell into a black pit.  The others resumed their conversations as if she didn’t exist.

Her social crime for which she received shunning – she dared to report that she was having little progress with weight loss despite a persistent and apparently well-applied very low carb/ketogenic diet. The post was old and the comments section had been closed, so I couldn’t respond to her myself.  I don’t think there was any attempt here to shame – just that her existence was inconvenient.

It is easy to love the idea that going low-carb is a sure-fire ticket to weight loss heaven.  This idea makes people smile and feel confident and enthusiastic.

The up-side  — the enthusiasm helps the knowledge spread.

The down-side  — since there is and never will be a sure-fire ticket to weight loss heaven, some individuals can feel unrecognized and discounted. Also, people who are broadly knowledgable about weight control issues recognize this as a false concept and this contributes to lack of respect for the message that low-carb nutrition is a valuable medical intervention (thus limiting the spread of the knowledge).

Low-carb nutrition and nutritional ketosis are very powerful and broadly beneficial tools that can help with weight loss in many ways. There are people who need other tools in addition or instead. Also, the benefits of low-carb nutrition can be swamped or over-ridden by other factors  – for example, certain medications or high stress states.

Many people do spectacularly well when adopting low-carb nutrition as a means to weight loss. Many others do very well or at least do well.  Messaging that focuses on dramatic weight loss, though, can mean that people miss the knowledge of how low-carb nutrition may benefit their health even in the absence of substantial weight loss.  It can mean that people get discouraged and miss out on the many other potential benefits.

“The reasonable man adapts himself to the world.  The unreasonable man persists in trying to adapt the world to himself.  Therefore, all progress depends on the unreasonable man.”  – George Bernard Shaw

If you have benefited from low-carb nutrition, or someone you love has, you might owe a debt to someone somewhere in the past who was not able to achieve success with weight loss with the use of the knowledge and advice they then had access to. The knowledge and understanding of low-carb nutrition is only available to us today because of the determined efforts of one individual after another, acting in response to this lack of success.

If you have a story of fabulous, easy success to tell  – please share it, share it!  Be proud, strut, jump up and down.

I would like to encourage the practice of avoiding suggesting that because it was easy  – or even just that it was possible – for you, that this means it would be or should be the same for all others.

That “unreasonable person” whose response isn’t the same as others’ is a person we can all learn from.  Their situation may be just about to spur some new understanding that will benefit us all some day.

Addendum:  I realize that I might have left that sounding as if there was only one incident that concerned me. Unfortunately, I have more than once read posted comments that flat out stated that since that person had achieved a great outcome with controlled carb intake, that this meant all was solved for everyone else if they would only just get with the program – again meaning that anyone still visibly overweight could be judged on the spot as someone who just wasn’t trying hard enough. I guess being addicted to feeling superior is something that doesn’t show at the waist band.

Addendum Oct 30/12 – Part of what was on my mind leading up to this post was Jimmy Moore’s blog post April 30th about the criticism he received. Now, that is a bit different situation, because it involved much more than discounting. But, it is a perfect illustration of the point I make toward the bottom of this post about all progress being due to the “unreasonable man” and that the people who have the most difficult time are the people who can show us another part of the path forward. This turned out to be oh-so-true in Jimmy Moore’s case – as we have watched unfold over the past 6 months. This post (May 20th) was several weeks before Jimmy’s famous first post about his nutritional ketosis experience – which was posted June 14th. So, at the time this was originally posted, Jimmy had not announced his new successful strategy  – so it seemed that he was still in a situation where his body was “unreasonably” not responding to the best strategies he knew of at the time – strategies that worked fabulously for many other people.

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.

Glucose Control Wins – Test!

A kit used by a woman with gestational diabetes.

A kit used by a woman with gestational diabetes. (Photo credit: Wikipedia)

Another week, another information packed newsletter from Diabetes in Control. If you have any reason to be interested in blood sugar control (that is, if you are alive and plan to be for a while), I highly recommend you sign up for their newsletter. I can’t highlight on this blog all that they publish that is important, or I would be posting little else.

There are many items in this week’s newsletter worth your attention. LINK  – this week’s newsletter is #649, if you need to search for it.

One is a report of a study, this time done in Sweden, that looked at 5 year outcomes among patients with inadequately controlled diabetes whose HgA1c improved versus those for whom it didn’t improve or worsened. It is important to note that this is a correlation study – there would be some other factors in the mix as to why some people’s HgA1c improved and others didn’t. Trouble is, we can’t do a causation study, as you can’t with-hold treatment from people

“Patients who had suboptimal glycemic control and reduced their HbA1c value by slightly less than 1% were 50% less likely to die within 5 years than were patients whose HbA1c did not improve….”

“After adjusting for baseline risk factors and treatment changes during the study period, patients whose HbA1c decreased were half as likely to develop cardiovascular or coronary heart disease as were those whose levels increased. They were also 33% less likely to experience fatal cardiovascular disease and 41% less likely to die from any cause than were those in the poorly controlled group. All of these differences were statistically significant.”

“We must make an effort to identify patients who don’t respond to diabetes medications earlier.”

Test, test and target. Even small improvements can mean big benefits. Do you know where your post-meal glucose values go? Blood glucose test kits are not expensive. Don’t wait for your fasting blood sugar to go up before you take action.

English: Illustration of the changes in blood ...

English: Illustration of the changes in blood glucose over time following a high and low GI carbohydrate. Designed and made Public Domain by Scott Dickinson (user: Studio34), Sydney, Australia. (Photo credit: Wikipedia)

Compare these results to the results from studies targeting how closely diabetic subjects followed the researcher’s versions of good lifestyle habits. What works is “the facts, ma’am” – test you glucose, set post-meal targets and keep tweaking and trying. The winning strategy is to find out what really works for you by watching your personal responses.

Consider the dismal outcome recently reported for the Look AHEAD trial, which went for 11 years and cost $220 million, which focused on achieving weight loss and found NO benefit in terms of reduction of heart attacks or strokes in people with diabetes.

Washington Post article on the results - LINK

Analysis of the results that is more informative – from Tom Naughton LINK

Extensive resources can be found on the web sites listed in the sidebar under “Blood Sugar Health”.

See also my post Restoring normal blood glucose levels associated with less progression to type 2 diabetes

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

Anaphylaxis to meat – Oh, dear.

English: The tick Amblyomma americanum (Lone S...

English: The tick Amblyomma americanum (Lone Star tick) (Photo credit: Wikipedia)

Have a look at this paper.  It describes in detail a newly recognized medical problem.  The bite of the lone star tick can make a person allergic to all mammalian meat.  The reaction these people display is an anaphylactic reaction, the type of allergy reaction that can be profound and can be deadly.  What can be particularly confusing is that the reaction can be 3-6 hours after eating.  Anaphylactic reactions usually occur very rapidly after exposure to the trigger foods, so the diagnosis can be missed. These reactions tend to develop in severity over time.  A person might have some reaction episodes where the symptoms are partial or mild, and therefore are missed or mis-diagnosed, before later having reaction episodes that are severe and possibly rapidly fatal.

The full text of the paper is posted free online. Go to the abstract and click on PDF.

The authors list the key points as (quote):

1. A newly recognized syndrome of meat-induced delayed anaphylaxis has been identified and may explain some cases that were previously labeled idiopathic.

2 Individuals bitten by lone star ticks may develop IgE antibodies to galactose- α-1,3-galactose (alpha-gal) and later develop a reaction when exposed to alpha-gal present on mammalian meat.

3 Since the reaction typically occurs 3-6 hours after exposure, it usually presents as a patient waking up in the middle of the night, with hives and anaphylaxis, after having ingested meat for dinner.

4. Current guidance is to counsel patients to avoid all mammalian meat (beef, pork, lamb and venison).

Map of the range of the Lone Star Tick (Amblyo...

Map of the range of the Lone Star Tick (Amblyomma americanum). Red indicates where the species is normally found; Blue indicates other locations where the species has been reported. (Photo credit: Wikipedia)

Since this syndrome has only just been recognised, it will be awhile before we know how common it is.  If you suspect you might have had episodes of allergic reaction to meat, stop eating meat until you can discuss this with a doctor. Print out the article and take it with you. If you suspect you might now be in the midst of an allergic reaction to meat, seek urgent medical care now.

Thanks to tweet from @whole9life for heads up on this.

Another Low Carb and Happy Story

Bicycle Lane

Bicycle Lane (Photo credit: snofla)

I am enjoying Meghann Douglas’s blog Meghann’s Meltdown. It took me a while to get it about the title – she has lost over 100 pounds.

She incorporates a lot of activity, such as swimming and biking, into her day.

From one of her recent posts:

http://www.meghannsmeltdown.com/blog/2012/9/19/data-the-key-to-taking-control.html

“I resisted keeping data logs for a long time.  ……  As the importance of the carbohydrate/insulin imbalances became clearer to me, the more important it became to accurately measure and track those carbohydrates.  “Close enough” is not enough.  It’s work to monitor closely enough to stay under 50 grams of carbohydrates per day.  The difference in how I feel makes it worth the while.  The reduction in pain is worth it.  Thank goodness for online programmes and their phenomenal databases.  Calculating & balancing my own ration is vastly improved from all those livestock rations I used to balance!!!!

There’s another important side of this.  You need to keep that food log in order to be sure you’re actually eating ENOUGH.  This is a totally oddball concept to work your head around.  I have literally spent my life counting calories and fighting my own hunger (real or imagined) and the cravings.  Your biggest nemesis is that magic number you’ve chosen to never exceed.

Balancing our own low-carb food plan has almost completely eliminated ALL cravings.  Even further than this, you can forget to eat because you just don’t feel hungry.  You can look at things you couldn’t walk past before and honestly not even want them.”

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

…………………………………………………………………………………………………

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.”