Kurt Harris MD

An Archevore is someone who eats based on essential principles, and also someone who hungers for essential principles. Take your pick.

Exploring these principles is one of my interests, but not the only one.

So you may find commentary here about other issues in medicine, health, other sciences, or just about anything.

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Tuesday
Feb082011

Therapy versus Life

What the heck?

I mean, when did this happen, really? When did our default self-concept make the turn from life to therapy?

I used to think this was a narcissistic "American" trait. Maybe we yanks spread it to the rest of the post-industrial world, but it seems to be everywhere now. And in the nutrition blogosphere I think it is the biggest dividing line - magical bullshit and neurotic yearning for immortality on one hand and the simple desire to live a good life without premature crippling diseases on the other.

We have people who want to eat healthy, and we have people who are living some perpetual existential crisis where they think you can cheat death and all disease if you just get all the numbers right. I confess these latter people drive me nuts.  A huge contingent who think there is a "secret" to health and longevity the way there must be a secret to wealth, early retirement, being happy and finding love. They want to believe none of these worthy things are as hard or elusive as thousands of years of history, if not our own lives, have taught us. 

These are the people who buy "The Secret" and books by Tim Ferriss. People who fantasize that life is all about "tricks" and "hacks". Perpetual youth and effortless happiness. Little study or real work required. Everyone can outsource everything and no real value need ever be produced.

Go through your blogroll of nutrition websites and books, and for each one, count how many special supplements are recommended. Then add the number of numerical recommendations for dietary parameters (wide ranges don't count) that are presented as if you might come to harm if you don't follow them. Then add the fraction of food items in our environment that are portrayed as being problematic, if not deadly. Then, add up the annual number of laboratory tests that are described as being critical to monitoring your health and square it. Then, add the total number of drugs that are suggested for otherwise healthy people who have never had a heart attack, cancer or a stroke, intended to treat these laboratory numbers as if they were diseases (they are not), and square that.

Then add them up S + DP + % F + Labs*Labs + Drugs*Drugs = TI

We can call this the "therapy index". I suggest that this therapy index will give you a good insight into the way the writer envisions health. A high TI means the writer thinks you are sick. That we are all sick. That anyone who has ever lived is born sick and needs therapy - their therapy - to be fixed. A catalogue of tricks and hacks and supplements and drugs and obsessive monitoring.

The writer has a weltanshaaung - a world view - that is Cartesian and mechanistic in proportion to the TI. Thinking about health like an engineer or keynesian economist instead of a biologist.

Now if the human diet in the 21st century were just fine, then a score of 0 on the TI might be achievable. PaNu certainly makes proscriptions, but the default stance is life, not therapy. You don't need fixing so much as to just stop injuring yourself.

A Cartesian view of the human organism is most opposed to the primary evolutionary assumption that should inform our thinking - the baseline assumption of a biologically informed view of humans. That there is a dietary metabolic milieu that we are adapted to, and the best chance we have of optimizing our health is to try and emulate it, not arbitrarily "improve" it.

The likelihood that we can "improve" upon this EM2 by doing something or adding something that was not a part of it already is similar to the probability that adding novel organic compounds to the gas tank or oil pan of my Porsche will "improve" its performance.

Not likely.

Living in ketosis 24/7 - even though this requires persistent avoidance of starches or peculiar amounts of coconut

Multivitamins - even though you eat real, whole foods

Antioxidants - even though there is not a shred of evidence for a benefit, and some evidence of harm

Prebiotics and Probiotic supplements - even though you already eat real, whole foods

Fish Oil, Krill Oil, or even copious fish - even though a minority of hominin evolution could have had an excess of marine n-3s and grass fed beef fat and butter is all you need if you avoid TemPOs

Iodine - even though humans evolved the capability to live with a huge range of iodine in the diet -  a nonsense book by Brownstein claims that 90% of the population is iodine deficient - actual science shows that iodine downregulates thyroid hormone synthesis and can flare Hashimoto's

Eating well beyond satiety - even though you are getting fat and feel like shit, you have been told by someone that this will "heal" your metabolism

Thyroid hormone - You feel fine and have normal thyroid labs but you take thyroid hormone from pigs every day to "improve" your LDL levels

Here is how it works in my world. When you come to me and tell me my car will last longer if I put some new compound in the gas tank, and the engineers in Stuttgart have never heard of it, and the manual tells me the car was not designed for it and doesn't need it, I say "prove it".  Don't theorize, actually prove it. The burden of proof is on you to prove your artificial maneuver that defies the design of the car will make it "better". I have no similar burden - you are the one claiming magic, not me.

PaNu is the precise opposite of this totally speculative therapeutic approach. The car comes into the shop. The owner tells us about how it ran fine until he bought some "magic elixir" and started adding it to the gas tank a few years ago. The first thing we do in my shop is stop adding it.

Here is the important part. Even if we stop adding the damaging substance, and we are still a bit broken, it does not follow that any magic elixir added to the tank will fix any damage. It might, but there is no more evidence for that than there was for adding some magic elixir to the car when it ran fine.

Of course, the car metaphor is apt but incomplete. The human body is not a machine, it is self-regulating biological system. So the fact that this is biology means there is even less reason to add unproven nonsense to our tanks.

My car cannot fix itself. The human body often can if we just stop ruining it.

So I would encourage you to ask yourself, what are you looking for? Do you think there is a "secret"? Are you fantasizing about immortality? Is everything a tweak or a hack or a trick? Do you think every problem in your life can be fixed by changing your diet?

Or do you see life as complex and tragic but sweet and rewarding, and are happy just to stack the odds in your favor with diet and then get on about your other business?

You do have other business than obsessing about what you eat, don't you?

Monday
Feb072011

Thoughts on Ketosis - II

Reader Ketotic has drawn me into the forums demanding to know why we should not be in ketosis all the time

Most readers will wonder why anyone would think such a thing, but in a nod to the zero-carbers who have peopled my readership I'll address some of his concerns. Those who are bored with this or who are irritated that the post is not liberally sprinkled with references can skip this.

Ketotic says:

I think the key issue regarding ketosis and evaluating its pro/cons is the degree of ketosis. We cannot compare ketosis induced by a 4:1:1 KD to ketosis by IF/LCKD. I think we can achieve an optimal degree of ketosis by combining an IF with a VLCD, without necessarily restricting too many food choices. While the glycogen/anaerobic performance/glucocorticoid issue is debatable (I workout at high intensities 2-3/week while on a IF/KD scheme), I have yet to see formal evidence that ketosis is metabolically stressful. When the body enters the least metabolically favorable scenario (starvation) ketosis is developed. It doesn’t make sense that ketosis would be developed to be more stressful. I don’t think that starvation is stressful because of ketosis, either, considering BOHB is the most efficient fuel. Micronutrient deficiency is strongly related with this point, reducing glucose needs also reduces the minimal amount necessary for several micronutrients like thiamin and Vit C.

Based on metabolomics, there is evidence that reducing glycolysis is beneficial. In this scenario, sporadic carbohydrate intake might be hormetic. Relying constantly on glucose (and so on glycolysis) as your main fuel is not optimal. Assuming that ketosis acts via hormesis means that you think that ketosis is stressful. Again, I haven’t seen evidence of this. On the contrary, most evidence shows that dietary glucose produces an inflammatory/immune response.

Finally, ketonuria does not always correlates to ketonemia.

Here are his comments parsed with my responses in roman:

I think the key issue regarding ketosis and evaluating its pro/cons is the degree of ketosis. We cannot compare ketosis induced by a 4:1:1 KD to ketosis by IF/LCKD

KGH: No one I know is measuring serum ketones to define ketosis. I mean ketosis due to VLC or zero carb with ketones in the urine. I do not mean the mild degree that is measurable in the serum on high fat diets with merely relatively low carbs. I am sure you don't mean that either.

I think we can achieve an optimal degree of ketosis by combining an IF with a VLCD, without necessarily restricting too many food choices.

KGH: Why would it be optimal? It might be therapeutic sometimes but there is zero evidence it would be optimal - I think you are theorizing, but making this kind of constraint on your diet should require high confidence and good evidence, not just a more-or-less plausible theory.

While the glycogen/anaerobic performance/glucocorticoid issue is debatable

KGH: It is not too debatable, really. It is reasonably well established.

I have yet to see formal evidence that ketosis is metabolically stressful. When the body enters the least metabolically favorable scenario (starvation) ketosis is developed. It doesnt make sense that ketosis would be developed to be more stressful.

KGH: It is developed to spare our structural proteins and conserve precious glucose for the brain, whether it is "stressful" or not. It certainly involves extra metabolic work. The fact that this happens only when we deprive our bodies of dietary glucose suggests it is stressful. It happens to spare our glycogen - the body is detecting that the glucose reserves are threatened. And it either spares our own muscle or reduces our demand for extra dietary protein to turn into glucose.

I dont think that starvation is stressful because of ketosis, either, considering B-OHB is the most efficient fuel.

KGH: It is only efficient if you think the steps it took to get it don't count.

Micronutrient deficiency is strongly related with this point, reducing glucose needs also reduces the minimal amount necessary for several micronutrients like thiamin and Vit C.

KGH: It is not at all necessary to have ketosis to minimize respiration based on glucose. A merely high fat diet with adequate glucose will do it. And of course as glucose is turned into fatty acids as needed, there is plenty of beta oxidation of fat going on even on a "high carb" diet. Especially when fasting.

Based on metabolomics, there is evidence that reducing glycolisis is beneficial. In this scenario, sporadical carbohydrate intake might be hormetic. Relying constantly on glucose (and so on glycolisis) as your main fuel is not optimal.

KGH: Relying on glucose? Is that what you mean by glycolysis? Glucose is used aerobically for most of the energy extracted (when mitochondria are around) whenever it can be. "Glycolysis" is anaerobic and only happens by itself when speed is necessary - like weight lifting. Do you have an IV drip with glucose going at night? Otherwise when you fast on a diet that has, say, 20% of calories as starch, you are not in ketosis (the way it is typically defined) yet your metabolism is still mostly based on fatty acids. You don't have to be in ketosis to have most of your metabolism based on fatty acids. 

Assuming that ketosis acts via hormesis means that you think that ketosis is stressful.

KGH: I did not say it acts via hormesis. I allowed that the benefits may be hormetic in the way that exercise or fasting could be. Depriving your body of a required metabolite and forcing it to adapt to same is pretty much a stress by definition.

Again, I havent seen evidence of this. On the contrary, most evidence shows that dietary glucose produces an inflammatory/immune response.

KGH: No, hyperglycemia may, but dietary glucose does not cause "inflammation" if you are normal. Fructose can be inflammatory, but under normal metabolic circumstances I don't buy that starch is.

Finally, ketonuria does not always correlates to ketonemia.

KGH: Agreed but not my point. Once you are keto-adapted after a few weeks, if you have ketones in the urine it means you are in ketosis enough that you are making more than you burn.

Ketosis is an adaptive state that beats the alternative of glycogen depletion or muscle wasting that it is designed to counter. This makes it "good". In the same way, muscle wasting to keep your brain supplied with glucose is "good". Good in the sense of beating the alternatives. That does not mean we should seek to live continuously in either state, though does it?

For a good discussion of mostly short term adverse effects of ketosis, based on a conversation I had with Peter a while ago, you can go here.

I will allow that there could be theoretical benefits to spending some time in ketosis. And there are therapeutic uses of ketogenic diets for people who are sick. But those who propose that a metabolic state that evolved as a response to a dietary deficiency is per se a desirable state to be in all the time have the burden of proof. This is the same burden of proof faced by those advocating anything that is outside the known evolutionary history of our species.

Synthetic resveratrol, megadoses of fish oil, 10,000 units a day of vitamin D year-round, statins, deriving the majority of your fuel needs from coconut oil, any supplement to a real food diet - for all of these things the advocates have the burden of proof.

So, once more for emphasis. Ketosis* can be useful therapeutic maneuver, but there is no evidence using current knowledge of metabolism or evolutionary reasoning that we should strive to be in this atypical state all the time.


* I define Ketosis in the usual paleosphere way. Eating a low enough digestible carbohydrate intake to induce serum levels of ketones much higher than those eating a carbohydrate replete diet. This will usually be a carbohydrate intake below the amount that would be necessary to run your brain on nothing but glucose, but still higher than the basal glucose requirement of the brain once keto-adapted, where the brain is running as much as half on ketones. We usually use ketones in the urine (ketonuria) as evidence of ketosis, but this is not 100% reliable, as the rate they are burned influences how many are spilled into the urine. The carbohydrate amount necessary to keep out of significant ketosis varies, but Kwasniewski uses 10% of kcal, and Lutz uses 70 g/day which is roughly the same if you are 2800 kcal/day but more if you eat less. Bernstein uses 30g/day for his diabetes diet, but this is meant to ensure micronutrient intake from non-starchy veggies and will not keep you out of ketosis.

Sunday
Feb062011

Thoughts on Ketosis - I

I'm getting questions about ketosis, as well as my evolving views on starches, to I'll describe my own experience with ketosis and starch intake.

Before my dietary transition, I always ate a fairly animal-fat heavy diet. I simply stopped eating sugar and flour in the fall of 2007, and I had never really eaten that much in the way of starchy vegetables. So when I read that "carbohydrates" were the likely cause of diseases of civilization, I pretty much axed them. I still ate onions, tomatoes, asparagus, green salads etc. It was an easy transition, with no "carb flu" or indeed any adverse effects to speak of. I had increased energy and slow weight loss without any hunger, which stopped at about 6-9 months. I did have substantial improvements in long-time IBS and atopic symptoms, as well as some unusual symptoms that may have represented a peripheral neuropathy. (Interestingly, these improvements came with wheat reduction, long before wheat was totally eliminated.)

My total carb consumption went from maybe 35 -40% (already moderate) down to maybe 40 or 50 g/day - about 7%. At that level I was usually mildly positive on urine ketone test strips. I started out with no evidence of any metabolic disorder and weighing 169 lbs at 5' 11''. I had been a consistent runner for about 10 years. Interestingly, and supporting Richard Nikoley's walking experience as well as Gary Taubes assessment of the inefficacy of exercise for weight loss - my peak fat and weight of 169 lbs corresponded exactly to the summer I was running about 25 miles a week. Both before and after that time I weighed less by about 5 lbs.

Early in my reading, after GCBC, I flirted with the idea that ketosis or very minimal carbohydrate intake might have been a consistent or even necessary feature of our evolutionary environment. It was easy to discard this idea pretty quickly, though, as most of the anthropological and ethological evidence argues against it. You would have to think that the exceptional periods of European occupation by hominins during glacial maxima were more important than the other parts of our dietary environmental experience. Or that the Inuit foodway was typical of hunter gatherers and not an exceptional late paleolithic niche.

So I still entertained (and still do now) the idea that ketosis could be a useful therapeutic maneuver, in cases of neurodegenerative diseases which seem to be marked by already acquired defects in glucose metabolism (Alzheimer Dementia, Parkinson's) and I've done quite a bit of reading on ketosis as a CR Mimetic (calorie restriction mimetic) for treatment of cancer or life extension. So far, though, nothing I've seen contradicts my assessment that for normal people deep ketosis is not something that needs to be sought, and I've seen no evidence that failure to maintain ketosis is a cause of diseases of civilization or that ketosis will lead to a preternaturally long lifespan (worms notwithstanding).

For over 2 years, I continued to eat at the border of ketosis because my weight was stable at 151 lbs and I felt fine that way. All the while long time readers will remember that (when this was still an "argument clinic") I was fighting defensive actions against assaults alternating between WAPF fanatics (not you, Chris!) upset about wheat, and the meat- and-water zero-carb hezbollah who could not understand why I could not see that glucose in the diet was a poison.

During the 2 years I was eating less than 10% CHO, and often much less, I ran an average of twice a week 5K and did McGuff style (actually just what I learned in high school football and swimming) weight training about twice a week. The running is always done just before the weight training. I would usually work out fasted, and the only adverse effect of the low carbohydrate intake - that I can identify in retrospect - was mild orthostatic hypotension for an hour or so after the workout. I would feel a bit lightheaded if I stood up quickly from a squatting position. I cannot be certain that it was not the fasting state, though, as now I usually work out in the evenings non-fasted.

The only thing that made me change my carbohydrate intake was a dramatic increase in physical work requirement. In June of 2010, I had to work about 60 hours a week doing real work on some buildings I own. I mean, carpentry, painting, bricklaying, hanging gutters, climbing on ladders. What happened was I started to lose weight. With no increase in appetite. It wasn't that I had difficulty doing the labor, I was just dropping weight. I got down to about 145 lbs with a month of this type of work and decided to increase my carb intake to see if it would increase my appetite. I added a large bowl of generic rice krispies with half and half every morning and made sure I got at least 100g/day of starch (or minimal sugar, lactose etc.) and eat three times a day. That was all it took. I gained back all of the lost weight in about another month and have kept at 100 to 150 g/day of mostly starch since then. I've increased by workout intensity a bit in the past few months, but it's nowhere neat the total work I did for several months of the summer. Weight right now is 153 lbs.

Things to Note:

1) Weight is less than 1% different between VLC diet with 7% carbs and LC at 20% or more

2) Body temperature has been exactly the same at each carb intake level and the same as it was for me in medical records from over 20 years ago when I ate 50% carbs and had much more body fat. By "exactly the same" I mean the thyroid enthusiasts would claim I have a "low metabolism", yet my wife can't understand how I sit around in the winter with only a t-shirt on. 97.5 F orally. Normal labs. Normal ultrasound (I owned the machine)

3) My own n=1 experience doesn't prove anything but does bias me to believe in Stephan's set point idea and not in the idea that the more CHO you eat the more you will store fat. That idea makes no evolutionary sense, either.

3) My own experience argues against the idea that you will "ruin your metabolism, starve, die, get hypthyroid, etc. by eating VLC for years, but does argue that work tolerance and exercise tolerance will be much better if you eat substantially above the level required to just stay out of ketosis. I don't really feel any different with changed CHO intake, but I don't deny that many people are quite sensitive to changed CHO intake.

I've never advocated anyone eat VLC, only described that I often did. It is not necessary to eat VLC to stop the metabolic damage of the SAD. VLC might only be necessary if you have diabetes or need to lose a lot of weight. PaNu is not intrinsically a weight loss prescription. It is not therapy. It is just eating in a non-damaging way.

So in keeping with the mission of the blog, which is just to share what I know, I am letting you know my experience. I am not recommending any particular level of macronutrient intake for anyone. I am open to the idea that macronutrient ratios outside of wide parametric ranges might be important, but I think it is an unproven concept. You can see from recent posts I don't think the very concept makes much sense.

I don't routinely measure my CHO intake or anything else. Everyone will want to know, so I will say that my purely speculative idea is that as long as there are enough animal foods in the diet, a range of 15 to 60% carbohydrates (exact numbers not important) are probably all equally healthy as long as the NAD are avoided.

I intend to keep eating at least 20% starch, which is twice the Kwasniewski number, to give myself a buffer against ketosis and because I speculate that this is about the level at which your glycogen stores start to get optimized. I certainly feel that way. The post-workout orthostasis is completely gone*.

Oh, and Rice Krispies (of whatever brand) have have only a few grams of added sugar in a bowl. It's really just toasted white rice. A good sized bowl is maybe 40 g of starch, a few grams of sugar, plus whatever lactose if you add H/H or milk. For lunch and/or dinner add sweet potatoes, white potatoes and whatever green veggies and dessert fruit you eat and that should do it.

 

*Interestingly, the orthostasis was independent of my resting blood pressure. It's been steady at about 118/66 all along. Before I first went VLC it was about 125/75 or so.

Saturday
Feb052011

No Such thing as a macronutrient part II - Carbohydrates (revised)

Note: I've added significantly to this part of the 3 part essay, so to make sure you see it all, I've re-posted.

Now we can have some fun, as I think I can demonstrate to you that this is by far the least metabolically useful macronutrient category.

GLUCOSE and STARCH

Here is plain old glucose:

 

I like these stereo models – black is carbon, red is oxygen and white is hydrogen. First is the unstable open form and next is the six carbon ring.

Much of the confusion in the nutrition wars is engendered by the dual roles that molecules have – as both food components and as internal fuel molecules. Dean Ornish and Dr. Davis think the palmitic acid our bodies use for fuel while we sleep is poison if we eat it. Zero-Carbers like Charles Washington think the oldest fuel in our evolutionary history – glucose - used by organisms a billion years ago and without which the brains of modern mammals cannot survive for more than a few minutes – is an unnatural toxin if you eat it.

Both views ignore basic facts of medical physiology and defy evolutionary history.

Hypergylcemia is bad, but hyperglycemia is caused by pathologic loss of glucoregulatory control, not simply by eating a food that has glucose in it.

High serum free fatty acids (NEFA or non-esterified fatty acids) in the context of metabolic syndrome is a marker for metabolic syndrome and the NEFA in this context may even mediate some of the pathology. But that does not mean it is necessary to avoid foods with saturated fat in them due to their “lipotoxicity”.

Both of these ideas confuse the effects of molecules as internal metabolites with their suitability as food. Our cells do not “see” glucose in the form of glycemic index or load – they only see hyperglycemia in the pathologic state where insulin fails to control release of glucose from the liver or clear it from the blood.

Our cells do not “see” the long chain fatty acids that we eat, they are deconstructed at the gut, packaged into chylomicrons and then distributed for storage as triglycerides or for fuel use as NEFA or free fatty acids. Absent a pathologic state, free fatty acids will be in the blood based on the demand for them as fuel, and this will be controlled in concert with the availability of glucose (The Randle cycle) but independently of whether we just ate steak or butter. Our Paleolithic ancestors did not have to be careful to avoid too much starch or too much saturated fat at one sitting. To suggest so would require that normal humans eating real food are in grave danger without access to fitday’s calculator. Only focusing on test-tube science to the exclusion of common sense can lead to such ideas.

I refuse to believe our bodies could be that stupid.

Glucose is a necessary internal fuel source and metabolite and it is also a food and the building block of foods that have the longest evolutionary history of any food that mammals use. It is a fact that we do not require glucose in the diet, and that we can make it from amino acids if we don't eat it. However, rather than viewing this as evidence that glucose is not important, we should view this as evidence that glucose is so metabolically important that we have evolved way to make sure we always have it. Fatty acids as fuel came later, and required the evolution of eukaryotic cells, which have the the mitochondria that probably started out as symbionts (helpful parasites) but now are the cellular furnaces that are the only way we can burn fatty acids as fuel.

Humans make and secrete amylase, the enzyme that allows digestion of starch, both in the saliva and in the exocrine pancreas. Amylase copies show some variability, with some human groups having perhaps 50% more activity than others. However, all humans have at least three times more activity than chimpanzees. It would seem a stretch to claim that any group of humans has “lost” the ability to eat starch, as that is the sole purpose of amylase – to hydrolyse starch, which is a polymer of glucose molecules, into glucose, which our small bowel has no difficulty absorbing. If we are not broken, glucose or starch that is consumed is absorbed and rapidly cleared by the liver and muscle cells. It can then be burned as fuel (preferentially) stored for later as glycogen (the body’s version of starch – another glucose polymer) or in some cases turned into fat – known as de novo lipogenesis. All this partitioning is done based on metabolic needs in a normal person. Arguments that humans are not “supposed” to eat any starch are, in my opinion, inconsistent with ethology (study of human societies), established paleoanthropology and medical science.

Glucose and starch in the DIET are not poisons in a healthy human.

In a healthy person, it makes little difference metabolically how fast the glucose is delivered. I do not think there is any pathology caused by the “glycemic index” of foods based on their content of glucose or its polymers.

So the first two carbohydrates in our scheme are versions of the phylogenetically oldest fuels that mammals use, fuels which are an absolute requirement of our brains. There is no good evidence that it is unnatural for humans to have foods that contain them as some portion of their diet.

Glucose is also found in shorter molecules, and paired with other simple sugars, or monosaccharides, to make disaccharides and longer molecules called oligosaccharides. Some of these other simple sugars are only different from glucose metabolically in minor ways. Lactose is glucose paired with galactose. If you have lactase to cleave the lactose dimer (disaccharide), glucose is glucose and galactose is converted to glucose after absorption.

FRUCTOSE

One of the simple sugars glucose is often paired with is Fructose.

Fructose is special. I would argue that fructose is so special that even calling it a “carbohydrate” is misleading. Later on I’ll discuss cellulose, which like starch is a polymer of glucose, but which, as the main component of indigestible sawdust, could not be metabolically more different than starch. So we can have polymers made of the very same lego-like building blocks, but because they are attached to each other in a different way, it is really a completely different substance.

In the case of fructose, we have a monosaccharide that has the same chemical formula and a caloric content equivalent to glucose, but is treated quite differently by the body because it has a different 3- dimensional structure.

 

1)   Fructose is found in plants foods only, and especially in their fruit. Plants use fructose to attract animals like us to the fruit, so we will eat it and spread their digestion-resistant seeds about via our feces. The plant is not thinking of us when it does this. Fructose is fructose and is tolerated in reasonable amounts (whether you get it from table sugar, honey or high fructose corn syrup), but because fructose is tasty we have bred fruit and cultivated plants in order to increase its availability dramatically. Fructose has easily become an order of magnitude more abundant in our diets in the past few hundred years than it was at any time in the preceding several million years of human evolution. If fructose were as benign as saturated fat or starch, this would be no problem, but I am pretty sure it is not.

2) Like glucose, there is no dietary requirement for fructose, but unlike glucose, we do not require fructose for use as an internal fuel. There is no organ like the brain that has an absolute fructose requirement. In fact, our body has mechanisms that evolved specifically to keep most cells from being exposed to too much of it.

3)   Because fructose spends more time than glucose in the unstable and reactive open configuration, it can react with proteins in a chemical reaction known as the maillard reaction. This results in glycation – attachment of a sugar – to other molecules, especially proteins. As proteins can be important structurally or as enzymes, this can have pathologic consequences. These glycated compounds are known as advanced glycosylation end products – AGEs.

4)   Fructose absorption in the gut is most efficient when paired with equimolar (one-for-one equivalent) amounts of glucose.

5)   When there is fructose in excess of glucose, or even when there is a large amount of fructose with glucose, there is often malabsorption in the small bowel – this can lead to rapid fermentation by bacteria in the colon, or abnormal overgrowth of bacteria in the distal small bowel. I speculate that fructose malabsorption is actually a defense mechanism to keep the liver from being overwhelmed by this metabolic poison, and the fact that we have not evolved a mechanism to handle big-gulp doses of fructose to the small bowel indicates modern quantities are likely outside of our evolutionary experience – the EM2.

6)   When fructose is absorbed, it goes via the portal vein directly to the liver, and the liver attempts to clear it completely so it cannot get into the general circulation. This is good, as fructose seems to be about 10 times more likely to cause glycation than glucose. Even small amounts of it can wreak havoc.

7)   To keep fructose out of the general circulation, it must be immediately burned or stored as fat. Fructose is related to the spectrum of serious diseases known as NAFLD (non-alcoholic liver disease), including fatty liver and cirrhosis.

8)   Excess fructose, chiefly via the liver volunteering to “taking one for the team” causes a variety of negative effects that are linked to pathologic insulin resistance, metabolic syndrome, a general inflammatory state, and of course obesity.

9)   Finally, fructose has no immediate effect on insulin release, but is linked to pathologic hyperinsulinemia via it’s effects on the liver. This is the exact opposite of glucose, which requires insulin to partition it when eaten, but for which there is no good evidence to relate it to chronic pathologic hyperinsulinemia.

(Note: This does not mean eating glucose is harmless once you have metabolic syndrome. You also have to be careful of large boluses of fat once your gallbladder is diseased. This doesn’t mean eating fat caused your gallstones, though - quite the opposite in fact.)

So fructose is a “carbohydrate” that has the same chemical formula as glucose, but unlike glucose, is very highly reactive with other molecules, is obligately metabolized by the liver, is malabsorbed by the majority of the normal population, can lead to NAFLD including fatty liver and cirrhosis, and in my view, is thus partly accountable for the current epidemic of metabolic syndrome, obesity and all the related diseases of civilization, including coronary disease and epithelial tumors.

Why do we lump harmless starch and possibly toxic fructose together and say they are equivalent macronutrients? They seem to have very little in common metabolically. Who cares about the paper chemical formula?

How many human diet trials or animal trials have you seen that lump them together? How many that treat them as totally separate variables like they should?

INULIN

So we’ve seen how two “carbohydrates” that have the same numerical chemical formulae, glucose and fructose, have little else in common metabolically. I already hinted at how the way we attach glucose monomers to each other can result in either an easy-to-digest source of fuel (starch) or something you can build ships and houses out of (cellulose) that you cannot really absorb at all. (Some of your colonic bacteria may hydrolyse and consume limited amounts of less lignified cellulose and turn it in into fatty acids you can then absorb – perhaps more on that in future posts.)

So what happens if you take what is arguably a dose-dependent toxin like fructose and make a polymer out of it – long chain molecules made of almost nothing but fructose? (There is often a terminal glucose molecule attached to inulins and shorter fructose polymers called fructans.)

You get a fashionable “prebiotic”, a “soluble fiber” called INULIN.

Now there is no time for a long digression on the merits of pro- or pre-biotics. For now I’ll say that there are theoretical reasons to think small amounts of some types of fiber may be beneficial and are well within the realm of our evolutionary history, but the idea that fiber supplements or the large amounts that come with a vegetarian diet are necessary to optimum health is at best unproven. Massive amounts of fiber are not likely to be any more a requirement than massive amounts of starch or saturated fat. Good? Maybe. The more the better? Very implausible. We're not gorillas.

Inulin is considered a soluble fiber, because it cannot be hydrolysed and digested in our small bowel, but the bacteria in our colon can eat it – and the result is fermentation into short-chain fatty acids and lactate. Oh, and I almost forgot. Gas. Hydrogen and CO2 are produced. If you have Irritable bowel syndrome (IBS) and really want to suffer, just eat a whole onion or a bunch of Jerusalem artichokes. You might want to warn anyone you cohabit with, though.

RESISTANT STARCH -RS

Resistant starch is a digestible starch that survives to make it to the colon. When you eat cold leftover baked potatoes or cold pasta, some of the starch granules re-aggregate into a form that makes them less accessible to digestion, similar to their form before cooking. The starch that makes it to the colon is then eaten by colonic bacteria similar to the fate of inulin.

FODMAPS

FODMAPS are a group of carbohydrates that have in common that they are poorly absorbed in the small bowel, but can serve as a feedstock for our colonic bacteria. FODMAP stands for fermentable – oligo- di- and monosaccharides and polyols. And fermentation means that bacteria or fungi can anaerobically digest it in our colons.

What FODMAPs have in common is that they make it to the colon without being hydrolysed and absorbed in the small bowel the way our fuel-source starches and regular sugars are. They can all be considered “prebiotics”. However, unlike longer molecules like inulin that are also fermented in the colon, the FODMAPs tend to be rapidly fermented in the proximal parts of the colon, rather than slowly fermented more distally. This rapid proximal fermentation can even lead to increased growth of bacteria in the terminal ileum – the distal part of the small bowel that attaches to the proximal colon – then you have SIBO (small intestinal bacterial overgrowth).

So what are they?

Oligosaccharides (OS) are short polymers of simple sugars. Short polymers of glucose are just glucose oligosaccharides – they are hydrolysed and absorbed just like starch. To be a FODMAP, the OS must have a bond or bonds that we have no enzyme to hydrolyse (break apart). One example is Raffinose, which is Galactose (milk sugar) joined to the fructose sugar of sucrose by an alpha bond. Galactose – Fructose –Glucose. Alpha galactosidase (a-gal) is the enzyme used to break the alpha bond. Humans and hindgut fermenting mammals don’t make it, but bacteria do. The best illustration of the effects of eating a lot of raffinose remains the campfire scene in Blazing Saddles. Raffinose is one of the main OS found in beans. The A-gal enzyme is the active ingredient in “Beano”.

Fructans and fructo-oligosaccharides (FOS) are FODMAPs found in wheat and may account for much of the GI distress encountered with high-wheat diets, and conversely for much of the relief obtained by eliminating wheat.

Fructose is a monosaccharide FODMAP functionally. By this, I mean that if you absorb it all in your small bowel, it is not a FODMAP. But if you get a big dose of free fructose  - fructose in excess of glucose in the same meal - or if you get a very large bolus even with the same amount of glucose - two coca-colas in a row, a binge on glazed donuts, a bunch of Christmas cookies at the office party – it is likely that some of the fructose, or even a lot of it, will escape digestion and absorption in the small bowel and make it to the colon.

Examples of polyol FODMAPs include xylitol and sorbitol. These are sugar alcohols. Sugar alcohols are not broken down in the small bowel, so they do not cause significant blood glucose elevation when eaten. They do get fermented in the colon, though, and it is possible to exacerbate irritable bowel syndrome or get osmotic diarrhea by, say, compulsively chewing sugarless gum or eating “diabetic” chocolates.

Inulin, polyols and FOS are all very common additives found in the junk marketed as “sugar-free”, “low carb”, or “diabetic”. Many are not aware of how much digestive upset they can cause. Another good reason to stick with real food and not eat anything that comes in a box, whether it says “low fat” or “low carb” or “sugar free”.

CELLULOSE

Rounding out the spectrum from most-to-least digestible, we can add Cellulose. Cellulose joined with lignin is wood. Even though it’s made of the same glucose as in starch, by having more chemically resistant bonds between the individual sugars you can build ships and houses and furniture out of it. Cellulose in plants without much lignin (iceberg lettuce) can be partially digested, but is best considered “indigestible fiber” with no caloric value and no health benefit, unless you believe the “scrubbing your colonic mucosa with a wire brush is good” theory.

So let’s summarize our paradigmatic carbohydrates in a "nutritionist" taxonomy:

Glucose and Starch - the oldest animal fuel

Fructose -a special carbohydrate that we have evolved to tolerate but that is toxic in industrial quantities

Soluble Fiber/RS - Inulin and other carbohydrates slowly digested in the colon. Overlaps with FODMAPs.

FODMAPs - carbohydrates indigestible in the small bowel that are rapidly fermented in the colon. May be problematic in excess.

Insoluble Fiber - Cellulose or other fibers that are not fermented significantly. The bran of grains or wood dust added to "heart healthy" breads are good examples.

Can we now apply these ideas to a taxonomy of carbohydrate sources -  a taxonomy of plants as foods?

Using some evolutionary reasoning, as well as some common sense, I would like to suggest a heirarchy of plant food desirability. I take it as axiomatic that whatever might be gained by eating plants, some key ideas should guide us.

1) A human can do with relatively little plant food, but cannot live at all without animals and the essential fatty acids and fat soluble vitamins they provide. With modern knowledge and care plants can provide essential amino acids when combined, but almost any animal can be eaten with monotony and provide all essential amino acids.

2) Most micronutrients necessary on an animal-based diet can be obtained by eating high quality animal sources, including offal. After all, the animal already ate the plants for you and either was replete in the diet or synthesized what was needed.

3) "Favor Food That is Defenseless when Dead". With rare exceptions, eating animals offers few trade-offs in terms of exposure to antinutrients or poisons in order to obtain fuel or nutrients.

4) Regardless of persistent claims regarding the uniqueness of particular plants and their abilities to provide x special compound that some observational or rodent study suggests protects against y, the idea that humans evolved to require any particular plant is implausible. The heterogeneity of the human diet in regard to plants, and the ability to live on very few animal species is an argument against the essentiality of particular plants. It is not a good argument for the necessity of consumption of a large variety of plants to obtain critical magical compounds from each one.

5) The frequently observed and logical behavior of modern hunter-gatherers, horticulturalists, primitive agriculturalists and wild animals suggests that if a plant is favored or sought, it ought to be the one that supplies the most energy density - fuel. The ONE thing that plants can do for us that animals can't is to relieve us of the burden of diverting amino acids from their critical structural uses to their inefficient conversion into mere fuel.

6) Plants consumed should therefore provide as much fuel as possible with exposure to as few antinutrients as possible. They should be close to the kinds of plants we evolved eating - as free of GMO modifications and artificial industrial processing as reasonably achievable.

So the top of the plant heirarchy will be:

Starchy Plant Organs - tubers and root vegetables. Sweet potatoes, cassava, root vegetables, white potatoes, etc.

Then, in descending order:

Green Vegetables - The "Atkins type" vegetables - leafy greens, etc.

Non-gluten Grains - white rice, corn - acceptable starch sources when not made a staple food

Legumes

Fruits

Gluten Grains

I think these kind of food categories, as well as the the more "nutritionist" categories preceding them, would be far more meaningful variables in a food frequency questionnaire or dietary trial than categories like "percentage of carbohydrate" where fructose and potato starch are lumped together, or "servings of fruits and vegetables" as if green beans and watermelon were remotely the same in dietary value.

Postscript:

I'm not going to list the constituents of every category here or argue about the exact order. I have suggested many times that the most benefit can be obtained by eliminating the last category of gluten grains. Gluten grains are so much worse than legumes that legume elimination may not even be that important. Let the lack of detail emphasize the non-essentiality of any plant category. You very likely don't need anything on this list beyond green vegetables, so you shouldn't be making a shopping list from it.

The point of these categories is to emphasize that my plant heirarchy is the opposite of the usual low-carb idea - the "it's OK, there are no net carbs in it" one.

I think eating 15-20% of calories as starch is healthier than being VLC (very low carbohydrate) on only green veggies and meat. Starchy Plant Organs give you the most useful plant vitamins and minerals, spare your body the work of making your own glucose via gluconeogenesis, keep you out of ketosis, and keep your glycogen stores topped off, all while avoiding the antinutrients in grains. If you are fairly active, you might notice a big difference between 20% starch and 5%.

So this makes PaNu very highly aligned with Kwasniewski on both ketosis and potatoes.

Ketosis is useful for weight loss, but it is not likely to be optimal to live in ketosis most of the time if you don't have to.

Saturday
Feb052011

FODMAPs

FODMAPS are a group of carbohydrates that have in common that they are poorly absorbed (malabsorbed) in the small bowel, but can serve as a feedstock for our colonic bacteria. FODMAP stands for fermentable – oligo- di- and monosaccharides and polyols. And fermentation means that bacteria or fungi can anaerobically digest the substance in our colons.

Fermentation of undigested leftovers happens normally in the colon, and although there is a gradient of bacterial colonization in the more proximal (closer to the mouth) gut, significant fermentation in the small bowel is abnormal and is referred to as SIBO – small intestinal bacterial overgrowth. FODMAPs, especially free fructose, may contribute to SIBO. SIBO may be what turns H.Pylori in the stomach from a harmless commensal into an ulcer-causing pathogen. Excess fructose may be the real “cause” of peptic ulcer disease.

Now, technically, most non-cellulose carbohydrates can be fermented in the colon. What FODMAPs have in common is that they make it to the colon without being hydrolysed and absorbed in the small bowel, like our fuel-source starches and regular sugars. They can all thus be considered “prebiotics”. However, unlike longer molecules like inulin that are also fermented in the colon, the FODMAPs tend to be rapidly fermented in the proximal parts of the colon, rather than slowly fermented more distally. It is this rapid proximal fermentation that can lead to increased growth of bacteria in the terminal ileum – the distal part of the small bowel that attaches to the proximal colon – then you have SIBO.

So what are they exactly? Oligosaccharides (OS) are short polymers (chains) of simple sugars. Short polymers of glucose are just glucose oligosaccharides – they are hydrolysed and absorbed just like starch. To be a FODMAP, the OS must have a bond or bonds that we have no enzyme to hydrolyse (break apart). Examples include raffinose, which is galactose (milk sugar) joined to the fructose sugar of the disaccharide sucrose by an alpha bond. Galactose – Fructose –Glucose. Alpha galactosidase (a-gal) is the enzyme used to break the alpha bond. Humans and hindgut fermenting mammals don’t make it, but bacteria do. The best illustration of the effects of eating a lot of raffinose remains the campfire scene in Blazing Saddles. Raffinose is one of the main OS found in beans. A-gal is also the active ingredient in “Beano”.

Fructans and fructo-oligosaccharides (FOS) are FODMAPs found in wheat and may account for much of the GI distress encountered on high-wheat diets, as well as for much of the relief obtained by eliminating wheat.

Fructose is a monosaccharide FODMAP functionally. By this I mean, if you absorb it all in your small bowel, it is not a FODMAP. But if you get a big dose of free fructose  - fructose in excess of glucose in the same meal - or if you get a very large bolus even with the same amount of glucose - two coca-colas in a row, a binge on glazed donuts, a bunch of Christmas cookies at the office party – it is likely that some of the fructose, or even a lot of it, will escape digestion and absorption in the small bowel and make it to the colon. There it will serve as food for bacteria, similar to the way the raffinose would, and with similar effects. As I’ve suggested, I view this as part of an evolutionary adaptation – part of a defense against fructose poisoning. The first line of defense is this limitation on our ability to absorb too much of it at once, sending the excess to the colonic compost pile for the bacteria to eat. The second line of defense is the liver, where the fructose we do absorb is sequestered by combustion or conversion into fat to keep it out of the circulation. (I sometimes wonder how many of those who think concerns about excess fructose reflect “alarmism” are aware of these simple facts about fructose metabolism.)

Examples of polyol FODMAPs include xylitol and sorbitol. These are sugar alcohols. Xylitol is used in “sugarless” gum as it is not fermentable by mouth bacteria and so does not encourage dental caries. Sugar alcohols are not broken down in the small bowel, so they do not cause significant blood glucose elevation when eaten. They do get fermented in the colon, though, and it is possible to exacerbate irritable bowel syndrome or get osmotic diarrhea from, say, compulsively chewing sugarless gum or eating “diabetic” chocolates. Polyols are also very abundant in apples, pears and peaches naturally.

Inulin, polyols and FOS are all very common additives found in the junk marketed as “sugar-free”, “low carb”, or “diabetic”. Many are not aware of how much intestinal upset they can cause. Another reason to stick with real food and not eat anything that comes in a box, whether it says “low fat” or “low carb” or “sugar free”.

How else to avoid excess FODMAPs ? Minimize excess fructose, onions, jerusalem artichokes, wheat, tomatoes, apples, peaches, pears. And minimize fruits with fructose substantially in excess of glucose (watermelon, apple).

Dr. Peter Gibson is the originator of the FODMAP concept. You can plug his name into pubmed and find quite a lot, but here are two links to good papers by him for further reading. Dr. Gibson has done research showing symptomatic relief in irritable bowel syndrome sufferers with FODMAP restriction and also speculates that they could play a role in development of the very serious inflammatory bowel diseases - such as Crohn's disease.

As many of the FODMAPs are soluble fiber "prebiotics", and there seem to be a lot of people advising you to eat more of these on purpose or even supplement with them as a "health" measure, Dr. Gibson's ideas might be something to consider. Even it you don't mind the additional gas they might give you.

 

FODMAP and crohns

http://www.ncbi.nlm.nih.gov/pubmed/15948806

FODMAP and functional bowel

http://www.ncbi.nlm.nih.gov/pubmed/20136989