A Doctor with diabetes relates his health recovery with low carb nutrition.

In relation to the previous post regarding the video of Dr Tim Noakes, here is a short video of the Doctor mentioned by Dr. Noakes.

This video also communicates the points very well. Both videos were made by “karen skinny”, and I hope she keeps up the good work.

A comment I would make is that this does not at all have to be a high protein diet. In fact, some people do not get the full benefits of low carbohydrate nutrition if they embrace a high protein intake. A moderate protein consumption is usually best.

Also, note that he needed to pay close attention to his medications as he started the change in eating pattern. It would have been very dangerous if he had not reduced the diabetes medication and blood pressure medication as needed as his food intake changed.

Finally, I do not recommend the Dukan diet.

At 8:40 minutes, this video is also a good choice for helping you communicate with friends, family and your health care team about low carbohydrate nutrition.

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This video communicates well about metabolic syndrome and carbohydrates

Tim_Noakes_TEDxCapeTown_Ross_Hillier_lower_res

Tim_Noakes_TEDxCapeTown_Ross_Hillier_lower_res (Photo credit: TEDxCapeTown)

Professor Tim Noakes MD is very well known internationally as a runner and expert in sports medicine.  In this well done video, he describes how eating the recommended “prudent diet”, emphasising low fat and high grain intake, for 3 decades was accompanied by increasing weight and lack of sense of well-being, despite being an active athlete.

His health and sense of well-being have been turned around by adopting a low carbohydrate lifestyle. You can see in the video how happy he is with the results.

This is a good video to share with family, friends and your health care practitioners.

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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.

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

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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

Increased Intestinal Permeability Shown in Obesity

There are an uncountable number of things that may contribute to obesity.  We also don’t have a good understanding of the causes of metabolic syndrome and why some people develop it and others don’t.

In this study of a small number of women (20 in the lean group, 20 in the obese group), there was increased intestinal permeability in the obese women.

Note that this study shows correlation, not causation.  That is, this does not indicate whether:

  • obesity increases the chance of developing higher intestinal permeability
  • higher intestinal permeability increases the chance of becoming or remaining obese, or
  • these two things happen together from some common cause.

In addition, the study showed that those with higher intestinal permeability tended to be those with indicators of metabolic syndrome.  Again, this study reports correlation and does not provide insight on causation.

Their Conclusions:

We demonstrated that intestinal permeability parameters in obese women are positively correlated with anthropometric measurements and metabolic variables. Therapeutic interventions focused on intestine health and the modulation of intestinal permeability should be explored in the context of obesity.

Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors.

Teixeira TF, Souza NC, Chiarello PG, Franceschini SC, Bressan J, Ferreira CL, Peluzio MD.   Clin Nutr. 2012 Mar 21. [Epub ahead of print]

PMID: 22444236

NOTE:  I did not read the full article (it is not open access).

Carpe Your Blood Sugar

What if the urgent public health issue of the day is less obesity itself and more about the elevated blood sugar (glucose) levels that occur in the majority of those with higher amounts of body fat?

What if the true cut-off level for concern is less than the target values now used for screening tests, diagnosis and for management targets in diabetes?

What if the urgency comes from the combination of two factors:

  • the fact that at last estimate about half (46%) of the adult population in the US (for example, but other countries are headed in the same direction) have pre-diabetes or diabetes, and
  • these elevated glucose levels are now optional for the majority of people, because a different approach to management can be used (at least, for those who have access to regular medical care and the personal resources to manage a care plan involving self-monitoring of blood glucose).

What if having similarly elevated blood glucose levels (including below the threshold for diagnosis of diabetes) means that people who are classed as ‘normal’ body weight face many of the most worrisome health issues that we have incorrectly been blaming on the total body fat itself?

What if swings in blood glucose are itself a major driver of weight gain and those swings can be eliminated?

Metabolic Syndrome is a term used for a cluster of related medical problems or health indicators that have at their core a reduced ability for the body to handle glucose.  The root causes for this have not yet been understood, so we can’t say that we have a way to treat or correct the source cause of the metabolic syndrome itself.  But we can succeed in keeping the blood glucose in the normal range, and thus largely interfere with the means by which the metabolic syndrome causes damage.

Among the experts in obesity, there is a sea change over the past few years moving towards the realization that the amount of extra fat itself is not the major driver of the degree of health impact of the obesity.  Yes, there are physical impacts of simply being a larger size, such as stress on the joints.  At very high levels of body fat, there can be other serious effects of the physical size, such as strain on the heart and fluid accumulation in the legs.  Certainly we must keep in mind and be very aware that there are emotional impacts, which are related to such factors as weight-based discrimination and (unfairly) feeling personally inadequate for not loosing weight when surrounded by the attitude that it should be so easy.  There are also economic impacts, including discrimination in the work place.

But there is an “illness” aspect that the obesity experts refer to.  Some people who are overweight or obese are actually quite healthy in their metabolism. It is thought that these are not the ones who are headed (at least, not any more than usual) for heart attack, stroke, cancer or the other “illness” consequences that we have come to consider to be caused by high body fat itself. Having a high amount of body fat is not a sole determiner for whether someone is more at risk of these outcomes than someone of “normal” body weight.

Metabolic syndrome is thought to be the major part of the difference, as well as some other factors, such as inflammatory molecules coming from body fat stores, most particularly those in the abdomen.  Control of blood glucose levels, it could be argued, is the most readily attainable change that can be implemented at this time.

Blood sugar levels respond very quickly, in a matter of days, weeks or, at most, months when a well-designed and individually adjusted program is instituted that focuses on reducing the intake of glucose-producing foods, adjusted to create an eating plan that the individual finds acceptable as a long-term aspect of their medical care.

My new web site and blog has been set up as a place to consider these ideas, the relevant research, the experiences of clinicians, the input of people affected by high blood glucose and the implications for individuals and for public health.

www.carpeyourbloodsugar.com

Still in infant form, please visit “Carpe your blood sugar”.

Weight Health, Satiety and Carb Control – A Framework

I have added somewhat to my page previously called “About” and now called “Overview”.  Because this is meant to communicate the heart and soul of what the blog is about and why it exits, I post here the page content in full:

                        “over the past decade, everything has changed…. “

This is a blog dedicated to weight health and to the discussion of satiety as the guiding light and principal most likely to result in success for most individuals.

“Satiety”  (sa-TY-i-tee)  – as I will use it here, is the sense of having satisfied one’s appetite for food; one’s appetite has been satisfied by the food consumed.

“Weight Health” – refers to the fact that there is a lot more involved in a person’s health and well-being than simply how much body fat they may be carrying. The amount of body fat must not be such a dominant concern that other aspects of health and well-being are neglected, discounted or put in jeopardy.  A better term would be “body composition health” since it is now understood that many of the people who are slim or have a  body weight in the “normal” range are suffering harm from relatively small amounts of body fat, but tucked hidden within their bellies.

Why bother?

Because over the past decade everything has changed. Excitement and hope are the realistic, practical outcome.

We used to think we knew what we were doing when it came to weight (fat) loss.  If only people could be disciplined and follow the medical advice, all would be solved.  Just eat less and move more.  Go hungry, if need be. Even if you get very hungry, tough it out and above all “don’t break your diet”.  “Diet” always referred to a limit on the total calories consumed in a day. (The limit being a calorie number given or being a set limit on total food servings, which is just a less obvious way of setting a calorie limit.)

There is a growing chorus of voices suggesting/demanding a total re-thinking of the approach to weight control, from the basic concepts on up.

Why?

Calorie-restricted dieting has not saved us.  For the population as a whole, the message has not stopped a growing crisis of obesity.  For people who are individually prescribed such diets as part of their medical care, the long-term results are stunningly disappointing.  This reality is now just so obvious to everyone that it cannot be ignored or brushed aside any longer.  Yes, some people do well and we need to learn from them, but over-all we are getting further behind.

Calorie-restricted dieting may have unexpectedly and quietly caused long-term harm. There is a growing movement of rejection of calorie-restricted dieting for various reasons, suggesting that this practice might increase the risk of dis-ordered eating patterns, eating disorders, food addiction, depression, lowered metabolism, etc.  There is an urgent need for research to answer these concerns.

The past decade has brought us new information and understandings that profoundly change our options and demand a re-working of our concepts.

Such as:

Obesity itself is not a major cause of death or illness.  The amount of body fat is generally not the major factor in obesity-associated death and illness, other than at very high levels of body fat. Some people can be quite obese and not have much health impact (excluding effects related to physical size, such as stress on joints.)  The type of medical harms that we usually associate with obesity can show up also in those who are in the normal body weight category, but are “metabolically obese”.

Metabolic syndrome (basically intolerance of carbohydrates, with insulin resistance and a gradual worsening of blood sugar control) and inflammation are the major “toxic factors” in both obesity and those who are normal weight but with deep belly fat. The increase in health problems that show up in studies on obese people are mostly from metabolic syndrome and inflammation – such as increased hypertension, diabetes, heart attack and stroke (among other impacts).  Diabetes then brings its own set of consequences such as kidney disease, eye disease, nerve damage and even further increase in risk for heart attack and stroke.  Researchers also feel that the inflammation and the carbohydrate intolerance increase the risk for cognitive dysfunction, dementia and cancer.  Most, but not all, people, who struggle with their weight have metabolic syndrome (or show evidence of being headed that way).  Most, but not all, people who have normal body weight do not (or not yet) have metabolic syndrome.

The signs of metabolic syndrome can be improved and often reliably and effectively treated by the use of an individually-adjusted carbohydrate-limiting food plan.  Also, and critically, most of the benefit of this treatment can be achieved with or without weight loss even close to “normal” range. “Carbohydrates” is the term used for any and all of the sugars and starches in foods.  There is carbohydrate intolerance, so lower the intake of total carbohydrates and change the foods eaten to lower the surge of glucose absorbed after a meal. For best benefit, also take other measures to improve carbohydrate tolerance, such as exercise.  When carefully applied and adjusted for the individual over time, experienced clinicians find that, almost universally, there is substantial improvement in blood pressure, blood fats and blood sugars and/or insulin levels (among other improvements).  (There is consistent clinical experience and some research showing this, more research would help.)

With effective relief from the burden of metabolic syndrome, with its accompanying elevated insulin levels, there is almost always a substantial reduction in excess body fat stores.  This is likely related mostly to reductions from previously elevated insulin levels.  When insulin levels are high, the body’s metabolic machinery favours turning the carbohydrate you eat into fat and storing it. High insulin levels also strongly resist the release of fat from stores to allow burning it off.

Relief from the damaging effects of metabolic syndrome/insulin resistance are much more important medically than whether there is substantial reduction in body weight. Studies into what is “the best” eating plan to achieve weight loss are off the mark on two counts (1) there will never be a best plan, it will depend on the individual metabolism and circumstances and goals and (2) it is vastly more important to find what are the best set of eating plans that, individually, allow the most protection from the harms associated with obesity, principally from metabolic syndrome and inflammation.

Control of body weight involves countless factors and very complex body systems, so no one intervention will ever be all that is needed.  Carbohydrate reduction/restriction is of major importance and benefit for those who have carbohydrate intolerance, but not all people who have high body fat have carbohydrate intolerance.  Unfortunately, low carb eating is not enough in itself to result in normal weight in all circumstances.  It is not magic.  Being on a low carb eating plan does not mean that you are living in a bubble, not affected by all the other factors that affect weight control such as high calories, poor sleep, food addictions, medications that promote weight gain, etc, etc.

If you have metabolic syndrome or a tendency to it, low carb eating can greatly improve your health and greatly improve your weight control while you work on finding the other things you need to do to further improve your weight control.

Nutritional ketosis is a powerful medical tool and can play an important role separate from any carbohydrate intolerance and separate from weight loss.

Low carb eating is actually four medical interventions confused together:

  • (1) as a means to protect the body from the various harmful effects of  carbohydrate intolerance/insulin resistance (metabolic syndrome), including lowering  blood insulin levels to allow a tipping of the balance from fat storage to fat release for burning and
  • (2) as a means to maintain abstinence for people who find that they have an addiction-like response to sweet or starchy foods or to fatty foods that are sweet or starchy (they can learn that they do not need to eat any sweet or starchy foods)
  • (3) as a means to improve the ability to maintain a stable blood sugar within the healthy range by dietary means with or without the help of medications (in the least dosages, thereby lessening medication adverse effects)
  • (4) as a means to be in the metabolic state known as “nutritional ketosis“.  Without going into the details here, nutritional ketosis is a normal physiological state that is part of your basic ancient metabolic flexibility.  In this state, you are burning fats and a fat-derived substance called “ketones” for almost all of your body needs.  In this state you need and burn a very small amount of glucose.  This small amount of glucose is critically needed, but your body can make it from protein and you don’t really need any from your food (if your body is working normally – this is not true in certain disease states and with certain medications, such as insulin and others that lower blood glucose).

Are there more than these four types of basic elements of the effects of carb control or low carb eating on health?  There is a lot of discussion on this topic, but its too early for conclusions.

By understanding the needs of each unique person in regards to what aspects of carbohydrate control are most important for them, a fully individualised eating plan can be worked out that allows the greatest flexibility and freedom, with the least amount of restriction that achieves their goals and is consistent with their circumstances and informed choices.

Nutritional ketosis is a medical intervention which helps control appetite – independent of whether the person is insulin resistance or not.

Because nutritional ketosis is a tool in itself, it can be targeted more specifically as a goal if the benefits are considered worthwhile in any given person’s situation.  This may involve avoiding high intake of protein, use of MCT oil (a coconut oil derivative that readily converts to ketones in the liver), use of metformin to reduce abnormally excessive production of glucose by the liver, and other strategies. (MCT oil is stripped of all other nutrients and could only be used sparingly and thoughtfully as a medical intervention.)

Research and clinical experience over decades have improved the understanding of fully individualised carb-controlled eating as a long-term, essentially permanent lifestyle option, so the medical benefits are available in a sustained way (essentially acting like a long-term medication).

Food addiction-like responses, food triggering and brain sensitization have received increasing attention and come to be understood as key factors in weight control.  For people who have addiction responses to foods containing sugars and/or starches, the understanding that full abstinence is an option (there is no health requirement for intake of carbohydrates and they can be avoided except for those consumed daily in salads and non-starchy vegetables) can change their lives.

There is also improved understanding of dis-ordered eating patterns and the eating disorders.

This blog is my contribution towards putting into words the facts, concepts and options at play.

This blog is full of hope and enthusiasm that current new understandings and information, along with the networked communication of informed and determined people, can bring the needed tools into the grasp of many (possibly even most) people even with what we know and can share right now.

Let none be left behind - if you have a particularly difficult time achieving weight loss to your best healthy weight, then we all have something to learn from your journey.  I have had a personal life lesson in never, never, never, never, never, never, never, never, never give up and I encourage you (though some days you may need to pause from the striving) to put one try ahead of another. Given the massive research effort and the opportunity the internet gives us to put our heads together, hope is actually a very realistic attitude.

CONTEXT

My viewpoint is that all the researchers, clinicians, academics, policy makers and commentators are motivated from a true and honest heart.  Each one is striving for the goal of the best health and best fulfillment of life for individuals and for society as a whole.  Because there will not ever be one right best answer for weight health, and because not one of us knows yet the full collection of interventions/treatments that will bring access to weight health to all people, there are many different opinions.  Passionate discussion and rebuttal is the result.  But, “we fight because we care”.  Individuals who just want to collect their pay and go home would not waste time and energy on vigorous debate.  The more the crisis grows, the more testy the interactions can get.  We are all striving for the same goal.

This blog is written mostly from the point of view of the usefulness af low-carbohydrate nutrition  – as ONE OF the useful interventions to consider. There are countless factors that act together in determining an individual’s body weight at any particular time.  The vast majority of people who struggle with their weight will need to make use of a number of different interventions/treatments/lifestyle changes in their lives to achieve and maintain their desired healthy body composition.  Low-carb eating is not the sole intervention needed, nor is it important for all.

I’m not advocating for low-carb eating for all, I am advocating for the best health and fulfilling life for all, by whatever means prove to be best.  The proper stance of any physician, researcher, etc., is “let the truth win out”.  I write about low-carb nutrition because I think it is critically important that this option be more widely known and better understood.  There is a tremendous amount of confusion and mis-information about low-carb nutrition. This is hindering people from achieving what could be life-changing benefits.  What I am advocating, also, is that each person be aware that carbohydrate intolerance could be a factor in their health and that they receive knowledgable help, now and over the stages of their lives, in evaluating this impact and what it means for their health and for their food choices.

What I would like to see is carbohydrate awareness and carbohydrate literacy.

Each person’s body weight and composition is their own business. I would like to make a contribution towards improving the degree to which it is also their own free choice.

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