Sunday, July 15, 2012

The Nutrition Debate #59: What I Eat and Why: The Very Low Carb Ketogenic Diet (VLCKD)

I eat a Very Low Carbohydrate Ketogenic Diet (VLCKD) because I want to lose weight, and do it in a healthy way, and because I want it to be easy (of course) and not involve hunger. I also want to eat in a way that achieves good blood glucose control (I’ve been a Type 2 diabetic for 26 years), and I want to continue to maintain the incredible improvement in my blood lipids (cholesterol), and regain the blood pressure improvement I had when I was at my lowest weight.
I didn’t know it when I started to eat Very Low Carb, but I had a medical condition that has come to be known as the Metabolic Syndrome, with all five indications: central obesity, T2DM (or pre-diabetes), hypertension, elevated triglycerides and low HDL. When I kept to the VLCKD, all five of these indications were mediated by this diet.
I know I have sufficiently restricted my carbohydrate intake to be in ketosis by testing my blood glucose in a fasting state (before eating breakfast). Since I am a Type 2 diabetic with impaired glucose tolerance and insulin resistance, if I have glucose stores available for energy (in the form of glycogen in the liver or muscle cells), or amino acids stored in the liver (from  eating too much protein) from which the liver will make glucose (through a process called gluconeogenesis), my fasting blood sugars will be above ‘normal’ for me (average 126, range 114 to 137). When I return to dietary ketosis, my fasting blood glucose drops to the 80s and 90s (average 93). That’s me. Your Mileage May Differ. We are all different.
My pancreatic function and other aspects of my metabolism are broken and have been for many years. I, like many Type 2s and even pre-diabetics (diagnosed and undiagnosed!), cannot tolerate more than very small amounts of carbs (low GI or otherwise). I must accept that I will never be able to do so without “excursions” (dangerously elevated levels) of “sugar” (blood glucose) circulating in my system. Inevitably, that will lead either to diabetic complications (eye, nerve or kidney disease), or one of the Diseases of Civilization that are strongly associated with Type 2 diabetes, such as cardiovascular disease, hypertension, and various cancers . So, what do I need to eat to remain in a mild state of ketosis?
Breakfast and lunch are easy for me because, as Richard K. Bernstein, MD, recommends in his book The Diabetes Solution, I eat the same thing every day. Breakfast is two fried eggs, two strips of bacon and 12 oz of coffee with 2oz of half and half and two packets of Splenda. K:G ratio = 1.88:1. It would be better if I could forego the artificial sweetener.
For lunch, (when I remember to eat it – I’m really not hungry, so I’m not “reminded”), I eat a can of King Oscar brand Mediterranean style Brisling sardines in olive oil. I drink the oil in the can too (about 1 Tbs). Lunch K:G ratio = 2.93:1.        I sometimes wash it down with diet ice tea (again, with artificial sweetener). Of course, water would be a better choice.
For dinner, we eat a medium portion of protein (with skin and/or fat on) and a portion of vegetables with melted butter or olive oil. Sometimes, with salmon for example, we use a sauce made with crème fraiche. We like roasted meats, including chicken, spare ribs, lamb chops, short ribs or a petite filet (with the leftover slices for breakfast instead of bacon). We also like to rub our cuts of meat with herbs and olive oil before roasting. We sometimes roast the vegetables too, after tossing them in olive oil and sea salt. Cauliflower, Brussels sprouts and asparagus are especially good this way.
We avoid the sugary vegetables (carrots, peas, beets and corn) and of course all the starchy root vegetables. As a general rule we also try not to eat vegetable oils (high in n6s). Instead of store bought mayonnaise (made with soy bean or canola oil), we make our own using equal parts coconut oil, olive oil and MCT (medium chain triglyceride) oil , with a little flax seed oil to “up” the Omega 3s. Coconut oil is also a medium chain triglyceride that makes more ketones than long chain dietary fats. It is also metabolized directly and thus is easily “burned” and less likely to be stored as body fat.
This menu usually adds up to about 1,200 calories a day, which is at least 1,000 less than I probably use. That negative calorie balance adds up to at least 7,000 a week, which is 2 pounds, the amount I would like to lose each week. The balance of energy comes from my fat stores, as long as I am in dietary ketosis and my blood insulin level is low. That only occurs because my carbohydrate intake is very low, and protein moderate, allowing my dietary and body fat to break down for fuel. This diet is about 5% carb, 25% protein and 70% fat. The K:G ratio of most meals is >1.5. This is a VLCKD.                  
© Dan Brown 7/15/12

Monday, July 9, 2012

The Nutrition Debate #58: What is Dietary Ketosis?

Fasting ketosis occurs “after a few days of fasting,” “when liver glycogen stores are depleted” and “the body shifts from a glucose-based metabolism to a fat-based one,” as Lucas Tafur explains at his Ketogenic Nutrition website. It is a physiologic state that Dr. Richard Veech, the “go-to” expert on ketone bodies at The National Institutes of Health, calls “the normal state of man.” But ketosis can “either be triggered by fasting or by diet,” Tafur says. Therein lies the key.
Dietary ketosis is the adaptive response, or “acquired evolutionary mechanism, [that] shifts [the body] from a glucose-based metabolism to a fat-based one,” Tafur explains. This shift occurs when the carbohydrates are unavailable for fuel. (Carbs were scarce in ice age winters.) The enzymes that break down fat for energy are controlled by insulin which is very responsive to the presence of carbohydrate. Dietary ketosis is achieved by the sustained and sharply curtailed intake of carbohydrates. How sharply? It varies. Your mileage may vary (YMMV), so I’ll give you my experience.
But first, a little more science and a little math. (Sorry, but I think some of my readers will find this both a useful proof and perhaps even a useful tool). A part of everything we eat becomes fuel, primarily glucose, or equivalent. That’s good because glucose quickly converts to energy, and the body (the brain, in particular) needs a little glucose – about 30-35 grams a day, either directly as glucose or as constituted in a form (e.g. ketone bodies) that substitutes for it perfectly.
Fat (either body or ingested) is a triglyceride and is made up of 3 fatty acid molecules and 1 glycerol molecule. Note the stem ‘gly.’ Each triglyceride molecule that is broken down to free fatty acids to enter the blood stream for energy leaves a glycerol molecule to join with another to make glucose. About 10% of ingested or stored (body) fat becomes glucose.
Protein is dismantled (digested) into its component amino acids which circulate to the muscles. What is left over goes to the liver and cannot circulate again in amino acid form. However, when the body needs glucose, the liver makes it from stored amino acids through a process called gluconeogenesis (“glucose-new-creation”). About 54% of the protein we eat is glucogenic, i.e. can become glucose, especially if we eat too much at any one meal. It is stored and then reconstituted and circulated as glucose!
Carbohydrates – almost all of them from the simple sugars to complex starches – digest to glucose. Some starches will be digested slowly, but simple sugars and highly processed carbs in products sold in boxes and bags will break down fast to the monosaccharides glucose fructose or galactose. In the case of fructose, they will stop at your liver which protects your body from them. Your liver will convert excess fructose into fat by lipolysis. The glucose circulates in your blood to be taken up by the cells as fuel. Circulating glucose raises insulin levels taking you out of ketosis.
The mechanism then to achieve dietary ketosis is this: eat a very low carbohydrate, moderate protein and high fat diet. Expressed as a formula (here’s the math part):
 K/G ratio = (0.9*FAT+0.46*PRO)/ (0.1*FAT+0.54*PRO+1*CHO.),
where K = ketogenic molecules and G = glucose molecules.
The fat, protein and carbohydrates (CHO) are all entered in grams (weight). The desired ratio of numerator to denominator is >1.5. That is considered a “ketogenic ratio.” Put another way, the ratio of ketogenic molecules to glucose molecules should be at least 1.5 to 1, stated >1.5:1, in each meal, every day.
Because this dietary regimen is very high in fat and very low in carbs, you will not be hungry between meals. Trust me. You will not. It’s 5PM as I write this and I haven’t eaten since breakfast. I forgot, honestly. My stomach did not remind me it was time to snack or to eat lunch. You will not crave snacks. You won’t want them. You will be satisfied (satiated) by the high fat and moderate protein in each meal…, so long as you don’t eat carbohydrates.
Once you are in dietary ketosis, fatty acids are used as the major source of fuel. But, the “balanced diet” folks say, this could cause a problem for the brain because fatty acids do not cross the blood-brain barrier. Fortunately, the liver uses the fatty acids from the breakdown of triglycerides (both body fat and ingested fat) to synthesize ketone bodies which enter the brain and substitute for glucose. This adaptive process in the brain’s energy metabolism increases its energy reserves. Ketone bodies are actually a more efficient fuel for the brain than glucose. The body’s fat stores are depended on, and depletion of the body’s protein store in muscle is avoided. In other words, your body uses fat for fuel. Your lose weight but not muscle.
 In the next column I will describe what I eat on a Very Low Carbohydrate Ketogenic Diet (VLCKD). Stay tuned.
© Dan Brown 7/8/12

Sunday, July 1, 2012

The Nutrition Debate #57: What is Ketogenic Nutrition?

A few months ago a very well read fellow blogger, Beth Mazur, commented on a post of mine. She said she shared my view that as lay bloggers we play a valuable intermediary role as generalists, or “foxes,” in a world of specialists, “the hedgehogs.” She was referring to a recent essay by Harry Rutter in The Lancet (sorry, log-in required). Rutter was referring to a popular 1953 essay, “The Hedgehog and the Fox,” by British philosopher Isaiah Berlin. It’s a good read.

In a separate post on her own blog, Weight Maven, Beth introduced me to Lucas Tafur with a piece he wrote on the “Old Friends Hypothesis,” referring to gut flora. Gut flora is an emerging and interesting area of nutrition research. It seems even my favorite MD, Kurt Harris, is telling us “to look at other things” besides “NAD’s.” Harris was referring to Neolithic Agents of Disease, his construct and original prescription of dietary constituents to avoid: wheat, fructose and Omega 6 fatty acids. His lengthy comment on Paleo Hacks, here, which Beth brought to my attention, was pretty cryptic, though. Harris’s thinking is apparently “evolving,” but that is one of the aspects I like best about his approach to dietary science.

Lucas Tafur is also an interesting story. Before he created the Luca Tafur site, his blog was called Ketogenic Nutrition. It is inactive now but still “up.” It provided me with a nostalgic look back at what proved for me to be a very effective way to lose weight (170 pounds). Tafur, whose bio is on both websites, quotes one of the world’s leading experts on ketone bodies, Dr. Richard L. Veech of the National Institutes of Health: "Doctors are scared of ketosis. They're always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man.” Put into context, in the continuum of our day-to-day existence, we’re either in a fed or a fasting state. The fed state begins with eating and continues until the food has been digested and absorbed. The fasting state then begins and continues until we eat again. When fasting, the body is said to be in ketosis.

When we are in a fed state, we derive our energy largely from glucose. This is called a glycogenic state. When we are in a fasting state, the body derives its energy from our fat stores, both from the liver and from our adipose (fat) tissue, which breaks down by lipolysis. Who can doubt that it has been that way for thousands of generations? We were hunters and gatherers, not grazers. That is the way we were “designed.”  For just a few generations, we have gone astray, with disastrous consequences. Of course, what has happened in the last few generations is not an evolutionary adaption; it is but an aberration. It is also a completely reversible change once we come to see and accept what “we” (complicit with our agricultural/industrial enterprise and the associated “public health” and media establishments) have done to ourselves. We can return to a fed and then fasting Way of Eating in which ketosis is one of “the normal states of man.”

The scenario: We hunted, we ate and we were satisfied. Think of the lion lying around after consuming a kill. After a while he became hungry and hunted again while he continued to get his energy from fat stores. The body shifted from being a “sugar burner” to a “fat burner.” As Dr. Veech said: “the normal state of man.” The fed state is when the body uses carbs to make glucose for energy. The fasting state is when the body uses fat to make ketone bodies for energy. But, as Tafur then points out, ketosis can “either be triggered by fasting or by diet.” Therein lies the key for us today.

The rest of this column is excerpted from Lucas Tafur’s Ketogenic Nutrition  website, where he provides footnotes as well: “Fasting ketosis develops after a few days of fasting, when liver glycogen stores are depleted. The body, as an acquired evolutionary mechanism, shifts from a glucose-based metabolism to a fat-based one.” “Studies have shown that the adaptive response to fasting is regulated not by energy restrictions per se, but by carbohydrate restriction. This is because the rate limiting enzyme of ketogenesis…is controlled by insulin levels.”

“The body’s main energy store is adipose tissue. Fat is more calorie-dense, meaning that it yields more energy per gram than glucose. Fat is the body’s preferred fuel, ketones being a “super fuel” that can be used by some tissues that haven’t evolved to use free fatty acids (FFA) such as the brain. Ketone bodies help the body spare amino acids by reducing the need for glucose. This way muscle mass is maintained…. Without ketosis, body protein stores would be cannibalized…. “

“The body stores fat primarily as saturated fat because it is metabolically more efficient than glucose and produces less toxic residues when metabolized. Exogenous glucose is the first substrate to be used because it is toxic to the body. It produces metabolic disregulation caused by hyperglycemia, which triggers an inflammatory and autoimmune response. Ketosis represents the opposite scenario; it protects the body during a life threatening situation like starvation.” (end)

So, Tafur gives a fine description of fasting ketosis, but what is dietary ketosis? It is the subject of the next column.

© Dan Brown 7/1/12

Sunday, June 24, 2012

The Nutrition Debate #56: Metabolic Disregulation

Readers of Dr. Kurt Harris’s Archevore website may have noticed that at the end of the Archevore Diet tab there is a footnote, the last clause of which is “…or it may just be too late.” Since Dr. Harris is not currently blogging, this cryptic remark has me wondering: “just…too late” for what? Can he mean too late to restore “normal” carbohydrate metabolism? And, most importantly (naturally), I’d like to know if this alarming news applies to me. I wonder if Dr. Harris ever explained that comment in one of his posts. It is a hard subject to Google. What are the key words: “Just too late”?
Anyway, I have noticed that many bloggers in the ‘nutrisphere,’ including many of the most cutting-edge, scientific ones, have drifted away from low-carb to Paleo to Paleo with “safe carbs.” Most of these bloggers do not clearly differentiate between “healthy people” and people who have developed issues with metabolic regulation. Significantly, neither do the American Diabetes Association, the USDA’s Dietary Guidelines for Americans or the public health establishment in general. Just ask almost any traditionally-schooled “certified” dietician or Certified Diabetes Educator (CDE).
The current trend in nutrition blogs is “healthy eating,” a good thing, but insufficient for the rapidly growing percentage of the population who are becoming carbohydrate intolerant. This manifests itself in weight gain, of course, but also in associated lipoprotein and blood glucose disregulation, known collectively as Metabolic Syndrome. I wonder sometimes if the blogger/researcher/clinician does not him or herself suffer from metabolic disregulation. I do, and by changing what I eat I found a fix.  So I think this is worth blogging about at length.
The largest audience of “seekers” on diet-related matters, I’ve noticed, are those with a weight issue. They may be a little overweight, a lot overweight, obese or even morbidly obese, and they all want to lose weight effectively and permanently. I was and still am one of those. When I weighed 375 pounds I wanted to lose weight. When my doctor suggested Atkins, I had no idea I would eventually lose 170 pounds. Nor did I realize that I would dramatically improve my lipid health and my T2DM and my hypertension. Neither, however, did I imagine that I would later regain 70 of the pounds I had lost and ‘give back’ some of my health gains, except interestingly my lipid panel gains.
I know that weight loss is the primary area of readers’ interest because my blog, The Nutrition Debate, covers a wide subject area, but my most popular columns (which Blogger tracks for me) are about diets and weight-loss. The problem of losing weight and keeping it off is intractable. That is not to say that there is not also a very large audience of people out there generally who follow nutrition who have a keen interest in “healthy eating.” These include a large cohort who wishes to avoid the Diseases of Civilization and others like the Paleo/Ancestral Health movement, the slow food people, the CSA movement and the fitness community. All of these do not necessarily need, and are not looking for, a therapeutic diet, unlike those of us who already have damaged metabolisms.
 So, that is the distinction that I think has to be made. I enjoy reading about neurotransmitters and hormones and enzymes and the latest, “our old friends” the gut flora. However, for me personally, I am keenly interested in what it means “…to be just too late”. There is a failed mechanism in MY metabolism such that for me it is “just too late?” By whatever name -- insulin resistance, or impaired glucose tolerance, or carbohydrate intolerance, or leptin resistance, or some consequence of any and/or all of these conditions, I must be resigned to what one commenter said on another blog, that: “Some of us cannot tolerate more than small amounts of carbs, and probably will never be able to do so.”
If so, as this becomes clearer to me, or perhaps as I come to accept what is already pretty clear, that will mean that I need to adopt for the rest of my days the Way of Eating that I followed when I lost 170 pounds. That is what someone who has T1DM or is gluten and/or casein intolerant has to do. Except that these folks – and I know a few people who have one or both of these disorders – don’t have a choice. They will die (the Type 1s), or wish they would (figuratively speaking), if they do not follow a strictly prescribed way of eating all day every day for the rest of their lives. In that sense I’m lucky. I can cheat and think I got away with it…at least in the short term. But there’s the rub. It is an insidious disease. I have to “own up” to it: I have a disregulated metabolism.  It is “just too late” for me. There, I said it.
© Dan Brown 6/24/12

Sunday, June 17, 2012

The Nutrition Debate #55: The Beleaguered Gary Taubes

I’ve just reread Gary Taubes’s “The Soft Science of Dietary Fat,” first published March 31, 2001 in Science and available in PDF format on any search engine. I recommend it to anyone interested in taking a fresh look at this subject through a clear prism. It is a brilliant exposition on a subject that has been distorted beyond recognition for more than 50 years.
I was motivated to read it again in search for a way to understand why and how so many intelligent people who should be informed about such things (including a friend who has been a Type I diabetic for over 60 years) “believe absolutely” that saturated fat and dietary cholesterol are “bad” for our health and should be avoided.  I’m not trying to change what she believes. She’s certainly an expert in her disease (T1DM) and a survivor of it. I just want to understand why.
Gary Taubes doesn’t need me to defend him. He “studied applied physics at Harvard and aerospace engineering at Stanford (MS, 1978,”) and then got “a master’s degree in journalism at Columbia University in 1981.” “He has won the Science in Society Award of the National Association of Science Writers three times,” according to his website. After “The Soft Science of Dietary Fat,” he became famous (and controversial) with his July 7, 2002 New York Times Sunday Magazine cover story, “What If It’s All Been a Big Fat Lie?” A polar-opposite rebuttal from The Center for Science in the Public Interest, a powerful vegan lobby group in Washington, DC, was published in their November 2002 newsletter.
Taubes went on in 2007, after 5 years of research and writing, to publish “Good Calories – Bad Calories” (“The Diet Delusion” in the UK, 2008), a seminal text for “the initiated.” In an “Afterwords” in the paperback edition, Taubes admits he had less impact on the medical establishment, particularly clinicians, than he would have liked. A more approachable text, “Why We Get Fat: And What to Do About It,” came out in 2010. Since then, he has been back on the cover of The New York Times Magazine with “Is Sugar Toxic” (April 13, 2011). Clearly Taubes’s books and articles all deal with controversy in medicine and nutrition.
Many physicians and researchers openly attribute Taubes for inspiring them in their career direction. He certainly has inspired me. He may even be the inspiration for the title of this blog, The Nutrition Debate. The debate needs to be continually renewed. We need to be constantly reminded at all levels, from simple nutrition “groupies” like me, who bundle ideas of others to put it out there for the world to consider. If the light level behind the mirror of conventional thinking is raised, perhaps the world will update their thinking with the “alternate hypothesis” that Taubes describes in “Good Calories – Bad Calories.” Perhaps, the silver back of the mirror will dissolve and become transparent. Following is an excerpt from Taubes’s 8,000 word essay in the 2001 Science magazine article “The Soft Science of Dietary Fat.”
“The original simple story in the 1950s was that high cholesterol levels increase heart disease risk. The seminal Framingham Heart Study, for instance, which revealed the association between cholesterol and heart disease, originally measured only total serum cholesterol. But cholesterol shuttles through the blood in an array of packages. Low-density lipoprotein particles (LDL, the “bad” cholesterol) deliver fat and cholesterol from the liver to tissues that need it, including the arterial cells, where it can lead to atherosclerotic plaques. High-density lipoproteins (HDLs, the “good” cholesterol) return cholesterol to the liver. The higher the HDL, the lower the heart disease risk. Then there are triglycerides, which contain fatty acids, and very low density lipoproteins (VLDLs), which transport triglycerides.
“All of these particles have some effect on heart disease risk, while the fats, carbohydrates, and proteins in the diet have varying effects on all these particles. The 1950s story was that saturated fats increase total cholesterol, polyunsaturated fats decrease it, and monounsaturated fats are neutral. By the late 1970s – when researchers accepted the benefits of HDL – they realized that monounsaturated fats are not neutral. Rather, they raise HDL, at least compared to carbohydrates, and lower LDL. This makes them an ideal nutrient as far as cholesterol goes. Furthermore, saturated fats cannot be quite so evil because, while they elevate LDL, which is bad, they also elevate HDL, which is good. And some saturated fats – stearic acid, in particular, the fat in chocolate – are at worst neutral. Stearic acid raises HDL levels but does little or nothing to LDL. And then, there are trans fatty acids, which raise LDL, just like saturated fat, but also lower HDL. Today, none of this is controversial, although it has yet to be reflected in any Food Guide Pyramid.”
Taubes is taking a few hits today in the Paleo world because of one of his ten “certain conclusions” from “Good Calories – Bad Calories:” that “insulin is the principal regulator of fat metabolism.” Maybe “a bridge too far,” but nobody in the Paleo World would dispute his first conclusion: “Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.” But, take note Loren Cordain and Robb Wolf, et. al.: Taubes was touting stearic acid while you guys were still in short pants (figuratively speaking, of course).                                               
© Dan Brown 6/3/12

Sunday, June 10, 2012

The Nutrition Debate #54: Loren Cordain, Robb Wolf and Kurt Harris

What do these three guys have in common? If you said Paleolithic nutrition, you would only get an argument from Kurt Harris. Although he started out with a huge bow to Gary Taubes, and then called his blog PaNu for Paleolithic Nutrition, he subsequently changed the name to Archevore. His thinking continues to evolve, and he no longer uses the word Paleo. His website says his thinking “is not derived from a single science or field of inquiry, but draws first on medical sciences like biochemistry and endocrinology, and only then looks back with history and paleoanthropology.” I like that.
Other differences between Harris and the other two is that Harris is an MD and has not (yet) written a book. Cordain has a PhD in exercise physiology, and Wolf has a BS in Biochemistry, a popular podcast on Paleolithic nutrition and exercise, and is a power lifting champ and weightlifting coach. He worked with Cordain in his biochemistry lab and describes Cordain as his mentor. Cordain’s book, “The Paleo Diet” (2002) was a best seller and has now come out in a revised edition (2011), which I have just read. I have also just read Wolf’s book, “The Paleo Solution,” published in 2010.
Both books preach essentially the basic Paleo prescription: no grains, no dairy, no added sugars, no legumes and very little salt. Eat only lean meat, non-starchy fruits and vegetables (for vitamins, phytochemicals and fiber) and mostly monounsaturated and some polyunsaturated fats.  Both diets cut you some slack in different ways. Cordain gives you a day or two “off diet” a week, to induce you to try it. Wolf says “just try it for a month” to see and feel the difference. Cordain allows a little honey; Wolf says, barring autoimmune problems, “it’s tough to build much of a case against grass-fed butter.” Both authors advocate lots of exercise.
Cordain’s “The Paleo Diet” is a useful introduction to the paleo way of eating, as are many online sources. It is designed for someone who doesn’t want to get “into the weeds” of the science, and asks the reader to trust in the author’s academic research credentials and lab staff. He assumes you won’t eat much organ meat, so he substitutes plant protein for the nutrients you would otherwise miss. He advises that you only eat “lean meat” and fats mostly from monounsaturated and polyunsaturated sources, the latter for the essential fatty acids (EFAs), n6 and n3, in the right balance. In the revised edition he says he has “softened his stance on the saturated fat issue,” allowing that stearic acid is “healthful,” unlike palmitic acid “which dominates the fat of feedlot cattle.”
Wolf’s book, “The Paleo Solution,” starts off with a primer in Paleo biochemistry for the non-geek. He works hard, and mostly succeeds, at making it “accessible.” His book also has a lot more energy and is more fun to read. It seems to be geared to a younger demographic. Interestingly, Cordain’s book makes many references to the bogey man of a decade ago (“fad low-carb diets”), while Wolf’s target is vegans. Personally, being a (Type 2 diabetic) low-carber myself, and acutely aware of the vegan menace in public health policymaking in Washington, I side with Wolf. It is interesting that both authors seem to need an antagonist.
Cordain’s book has an index but no footnotes and the bibliography adds only gravitas (and pages) – it isn’t divided by chapter – so there is no easy way to dig deeper into any of the claims made. It does include brief menu and recipe sections. Wolf’s book has no index or footnotes either, but the bibliography is divided by chapter. His menus incorporate some recipes. Both books are commercial in that their primary purpose appears to be pecuniary, although much of Wolf’s material is available online, gratis.
My favorite of these three, though, is Dr. Harris. His approach is so sublime. He says at his website, for example, “An Archevore is someone who eats based on essential principles, and also someone who hungers for essential principles. Take your pick.” And, “After hearing Gary Taubes on the radio, I had an epiphany and ever since I've been exploring the field of nutrition through the lenses of medicine and evolutionary biology.” And, “I have had a lifelong interest in science and medicine as culture, and believe all claims to scientific authority should be subject to thoughtful skepticism.” How can you not like this guy? His intellectual curiosity is the driver; the scientific method his “mechanism”; his vision pure. Unfortunately, in recent months he hasn’t posted on his blog, but his website Archevore is still ‘up.’ Take a look at it.
© Dan Brown 5/27/12

Sunday, May 20, 2012

The Nutrition Debate #53: On the Digestion and Absorption of Food

Food digestion physiology varies between individuals and with the composition and size of a meal. There are other factors, but a primer on what is most common and universal will be useful to understanding the various processes and their effect on our biological systems. This digest (note the pun) should provide some enlightenment.
Digestion, the hormonal process, has three phases. The cephalic phase begins when receptors in the head are stimulated by an emotional state (thought of food), sight, smell, taste and chewing. The cerebral cortex, the medulla oblongata and the hypothalamus are all involved. The vegus nerve is the messenger, triggering various enzymatic and hormonal activities. The gastric phase starts with distension, acidity, and the presence of amino acids and peptides in the stomach. The intestinal phase is initiated by distension, acidity, and osmolarity of digestive products in the intestine (we’ll explain).
Digestion, the mechanical and chemical process, begins with chewing. Chewing breaks food down to smaller units that are in turn broken down by enzymes to the smallest units to permit them to be absorbed, mostly in the small intestine, into the blood. Saliva containing mucus and the enzyme amylase is secreted from three pairs of salivary glands located in the mouth cavity. Mucus moistens the food and amylase partially digests polysaccharides (starches) into a disaccharide called maltose. About 30% of starch is broken down in the mouth (optimum pH: 6.8 or weakly acidic).
In addition, papillae on the surface of the tongue secrete the enzyme lingual lipase which begins the process of breaking down some fats from triglycerides into diglycerides. Long chain triglycerides cannot be absorbed unless completely broken down to monoglycerides, so the process starts here and continues in the stomach. As much as 30% of fat is broken down within 1 to 20 minutes of ingestion by lingual lipase alone, according to Wikipedia.
Food then passes through the pharynx and descends the esophagus to the stomach, a sac that stores and mixes and processes the food into a milky solution called chyme. Glands lining the stomach secrete hydrochloric acid, which is necessary for protein digestion by the enzyme pepsin. The stomach’s high acidity (optimum pH 1.8) inhibits the breakdown of carbohydrates within it, but it does produce a small amount of the enzyme lipase to continue the digestion of fats. So far, although the breakdown of food particles by enzymatic and mechanical action is continuing apace, virtually no absorption of nutrients into the bloodstream has occurred. The exceptions are water, some simple sugars, and other small molecules like alcohol that are absorbed in the stomach, passing through the membrane of the stomach and entering the circulatory system directly.
The final stages of digestion and most of the nutrient absorption occur in the next portion of the tract: the small intestine. The small intestine is divided into three segments – duodenum, jejunum and ileum. The duodenum in turn is connected to the hepato-pancreatic duct which connects to the liver and the gall bladder (to store and supply bile) and to the pancreas. These organs and glands provide digestive enzymes and an alkaline fluid (pH 8.5) to neutralize the acid being emptied from the stomach.
In the duodenum, dipeptides from protein in the stomach are broken down to amino acids by enzymes from the pancreas. The enzymes break down the disaccharides maltose, lactose and sucrose into the monosaccharides glucose, fructose and galactose.  The major portion of fat digestion, the breakdown of diglycerides by lipase into free fatty acids and glycerol, also happens here.
Absorption of nutrients occurs mostly in the jejunum and ileum. Amino acids (from protein) and the monosaccharides (glucose, fructose and galactose, all from carbohydrates) are water soluble nutrients and enter the blood directly through the villi and microvilli in the endothelial layer of the small intestine wall. The surface area of these many small structures (imagine a shag carpet) increases the absorption interface by 600 times, roughly equivalent to the surface of a tennis court. However, the products of fat digestion, fatty acids and glycerol, are not water soluble and therefore enter the circulation through the lymph system by a process called passive diffusion in which no energy is required.
Passive or simple diffusion requires no energy input from the body because it is driven by concentration. Fats, water and some minerals simply cross the membrane barrier because the concentration of the substance (fat, water, etc.) is lower on the other side. It is an equalization process. The small intestine is full of nutrients and the blood is not, so they cross over. This equalization process is also called osmosis, ergo ‘osmolarity of digestive products’ referred to above. 
Fructose is transported across the membrane barrier by a process called ‘facilitated diffusion,’ which means it may need a little help depending on the concentration gradient. Glucose and galactose, the other monosaccharides, as well as amino acids, also require energy for active transport, which occurs against a concentration gradient. See The Nutrition Debate #52, “The Thermic Effect of Foods,” for the energy requirements of protein digestion as compared to carbohydrates, especially of processed foods.
Finally, gastric emptying, which is the rate that food leaves the stomach to enter the small intestine, is tightly controlled. Liquids are emptied much more quickly than solids, and carbohydrates are emptied first, followed by protein, fat and fiber. Gastric emptying has attracted medical interest as “rapid gastric emptying is related to obesity and delayed gastric emptying syndrome is associated with Type 2 diabetes, aging and gastroesophageal (acid) reflux or GERD.” But that’s another subject. Next week: Paleo book reviews. 
© Dan Brown 5/20/12