Study: Lack of Deep Sleep Promotes Insulin Resistance

I habitually trawl the news and science journals, and often find studies that illuminate, confirm, or refute some salient point. I’ve decided to start noting these when I stumble across them, almost more for my own benefit than for yours.

But first, more about me:

When I was in high school, probably starting around 11th grade, I got a pretty severe case of computer addiction. This was really too bad, because it was 1973 or so, and the PC just literally didn’t exist, and wouldn’t yet for years.

So, I would stay up until 3:30am at night, reading books on programming and writing programs in notebooks. I even wrote a BASIC interpreter in APL in 1974, replete with user accounts and full system administration, and got about half of it entered and debugged before the local college’s sole APL terminal broke down, never to be repaired.

Since I still lived in the real world, I had to get up at 7:30am every day and go to school. My dad would have breakfast ready for me and I’d stumble down to the table, eat my sandwich, drink my orange juice, and drive off. Of course, this made staying awake during any class that wasn’t absolutely riveting pretty difficult, but as I say, I had the computer sickness bad.

And then, even as early as my sophomore year in college, I was known for incredible snoring; my roommates would literally pile shoes near their beds where they could hurl them at me to get me to change position, not that I’d remember this in the morning. This turned out to be sleep apnea, which remained undiagnosed for a good 15 years.

Finally, during much of my adult life, up until just the last year or two, I would stay up fairly late, lucky to get six hours of uninterrupted sleep, if that.

Well, (and this will surprise you, I know), it turns out that all this was bad.

A recent study showed that failing to get enough deep sleep, even for as little as just a few consecutive nights, caused insulin resistance equivalent to gaining 20 or 30 pounds, even in slim, healthy young adults, raising glucose levels 23%, on average.

From the Reuters article:

[Researchers Esra Tasali and Eve Van Cauter’s] team wanted to see if a disruption in deep sleep could increase the risk for type 2 diabetes.

[Their] team studied nine adults between the ages of 20 and 31, who spent two consecutive nights in a sleep lab where they slept undisturbed for 8.5 hours each night.

Then, for three nights, the researchers disrupted their sleep with noise just as brain wave activity indicated they were drifting off into deep sleep. The sounds were loud enough to disturb deep sleep, but subtle enough not to wake the study participants.

The effect was to reduce slow-wave deep sleep by about 90 percent without altering total sleep time.

At the end of each study, the researchers injected a sugar or glucose solution into each subject and measured their blood sugar and response to insulin, the hormone that regulates the glucose.

After three nights of disturbed sleep, eight of the nine volunteers had become less sensitive to insulin, without increasing the production of insulin…

Reduced sleep often results from obesity and age. While most young adults spend 80 to 100 minutes per night in slow-wave sleep, this decreases to just 20 minutes for adults over 60.

“Any condition that involves a decrease in deep sleep is linked to an increase in diabetes risk. That is the case for aging and sleep apnea. This study really demonstrates a causal link,” Van Cauter said.

News Accounts:

Article from Reuters on Yahoo News:
“Lack of deep sleep may raise diabetes risk”
December 31, 2007

Article from AP on Yahoo News
“Sleep disruptions may up diabetes risk”
January 1, 2008

Article in The Guardian
“Disturbed sleep brings risk of type 2 diabetes, says study”
January 1, 2008

Study Publication:

Abstract in the Proceedings of the National Academy of Sciences
“Slow-wave sleep and the risk of type 2 diabetes in humans”
January 2, 2008

Your Doctor’s Prescriptions: Not Private

I’ve often idly wondered whether or not drug or insurance companies could tell how many and what kind of prescriptions my doctor orders (not just for me, but for everyone), since that would be an obvious conflict-of-interest, allowing the drug companies to kickback some sort of carrot (e.g. solid gold bars), or the insurance companies to apply some sort of stick (e.g. kicking doctors out of their network) to doctors who were writing the most prescriptions for the newest, fanciest, most highly-profitable drugs.

And while I’m sure that kickbacks would be illegal, or at least, I hope they are, I just wondered if, in the current system, the companies could find out what prescriptions the doctors were actually writing…

And it turns out that not only are doctors’ prescription-writing habits public, but the companies that collect and sell such data just successfully sued to prevent Maine from enacting a law making the data private:

U.S. District Judge John Woodcock concluded that the law, which was scheduled to take effect Jan. 1, would prohibit “the transfer of truthful commercial information” and “violate the free speech guarantee of the First Amendment.”

And from the other direction, our company’s prescription drug provider, MedCo Health, has a clause in their terms of service making it totally OK for them to call your physician and “discuss” your care with him or her, trying to convince them to write a prescription for something cheaper and more generic. You can’t even opt out of this and forbid them from doing it.

Just something to keep in mind when your doctor wants to put you on yet another drug.
(Or for that matter, when he doesn’t want to — let the paranoia blossom like poppies!)

Read the Full Story from the Associated Press on Yahoo:
“Judge overturns Maine law on Rx data”
December 22, 2007

Part 9:  …Especially Fructose

(Back to Parts One, Two, Three, Four, Five, Six, Seven, or Eight)

One piece of advice that you wouldn’t imagine to be controversial, at least, is to minimize your intake of sugar. But even here, the mainstream voice can surprise: the American Diabetes Association still to this day says that for diabetics, “Sucrose-containing foods can be substituted for other carbohydrates in the meal plan or, if added to the meal plan, covered with insulin or other glucose-lowering medications.” And since the ADA wants everyone, even diabetics, to get at least 130g of carbohydrates (about 520 calories) every day, why, hell, go ahead and have a soda!

Why would they feed extra sugar to someone whose body has impaired blood sugar control? It seems ludicrous, and in fact, I think it’s terrible advice. But to understand, at least in part, how this situation arose, we have to talk about fructose and the glycemic index.

The glycemic index is a measure of the effect a food has on blood glucose levels. The scale is defined such that a solution of glucose itself (which, as you can imagine, raises blood glucose levels substantially) is assigned a value of 100. A food that only raises blood glucose levels half as much would have a value of 50, and so on. Dieters are often advised to avoid foods with a glycemic index higher than 55.

Here’s a short table listing the glycemic index of a few foods, just to illustrate the idea. Lower is better. You can take these values as ‘very approximate’, since I pulled them from a random web site.

glucose                100
baked potato            95
refined white flour     85
table sugar (sucrose)   70
banana (ripe)           60
banana (unripe)         45
carrot juice            40
carrot (raw)            30
fructose                20
asparagus               15
beef                     0

Americans eat a lot of sugar, and about 1/2 of it is fructose (a kind of sugar found in fruit), either as table sugar (sucrose, which is 50% fructose, 50% glucose), or as high-fructose corn syrup, (HFCS, or HFCS-55, which is 55% fructose, 45% glucose).

Hey, and fructose was in the table above, nestled snugly down there with the vegetables. It has almost no effect (at least in the short term) on blood glucose or insulin levels. This led, in the 1980’s, to its promotion as a ‘healthy’ sugar, and table sugar, being half fructose, looked pretty attractive (for a sugar), especially compared to baked potatoes and bread made from refined white flour. In The New England Journal of Medicine, diabetologist John Bantle wrote, “We see no reason for diabetics to be denied foods containing sucrose.”

Sounds great! But mark the sequel:

Unlike glucose (70% of which is taken up by the body’s cells before ever encountering the liver), fructose is not immediately usable by the body; it must be metabolized in the liver, which converts it to triglycerides (“fructose-induced lipogenesis”). Now, this is bad enough — high triglyceride levels are a far better predictor of cardiovascular disease than total cholesterol — but it gets worse:

…fructose apparently blocks both the metabolism of glucose in the liver and the synthesis of glucose into glycogen, the form in which the liver stores glucose locally for later use. As a result, the pancreas secretes more insulin to overcome this glucose traffic-jam at the liver, and this in turn induces the muscles to compensate by becoming more insulin resistant. The research on this fructose-induced insulin resistance was done on laboratory animals, but it confirmed what Reiser at the USDA had observed in humans and published in 1981: given sufficient time, high-fructose diets can induce high insulin levels, high blood sugar, and insulin resistance, even though in the short term fructose has little effect on either blood sugar or insulin and so a very low glycemic index. It has also been known since the 1960s that fructose elevates blood pressure more than an equivalent amount of glucose does, a phenomenon called fructose-induced hypertension.

Because sucrose and high-fructose corn syrup (HFCS-55) are both effectively half glucose and half fructose, they offer the worst of both sugars. The fructose will stimulate the liver to produce triglycerides, while the glucose will stimulate insulin secretion. And the glucose-induced insulin response in turn will prompt the liver to secrete even more triglycerides than it would from the fructose alone, while the insulin will also elevate blood pressure apart from the effect of fructose…

The effect of fructose on the formation of advanced glycation end-products — AGEs, the haphazard glomming together of proteins in cells and tissues — is worrisome as well. Most of the research on AGE accumulation in humans has focused on the influence of glucose, because it is the dominant sugar in the blood. Glucose, however, is the least reactive of all sugars, the one least likely to attach itself without an enzyme to a nearby protein, which is the first step in the formation of AGEs. As it turns out, however, fructose is significantly more reactive in the bloodstream than glucose, and perhaps ten times more effective than glucose at inducing the cross-linking of proteins that leads to the cellular junk of advanced glycation end-products. Fructose also leads to the formation of AGEs and cross-linked proteins that seem more resistant to the body’s disposal mechanisms than those created by glucose. It also increases markedly the oxidation of LDL particles, which appears to be a necessary step in atherosclerosis.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 200-201

The above is especially alarming considering that our national per-capita consumption of sugars has increased from a stable historical mean of 110-120 pounds per year from the 1920’s (or even the 1950’s) up to almost 150 pounds per year (almost half a pound a day!), with virtually all of the increase due to high-fructose corn syrup (e.g. soda pop, Snapple, ice cream, candy, low-fat yogurt, salad dressings, you name it).

As for me, I’ve cut back my consumption of all kinds of sugars…especially on added fructose.

To be continued…

We Train (But Not In Vain)

My buddy Larry Helmerich lured me into going on some mass-transit adventures in Los Angeles recently. It’s fun, and we’ve enjoyed learning the ropes of the system.

Today, we tried getting from his house in Sylmar (maybe 25 miles NW of downtown Los Angeles) to Old Town Pasadena (maybe 15 miles north of Los Angeles). It’s about a 35-minute or 40-minute drive from Larry’s house. We made it in 70 minutes, on mass transit, for $8 per person, round-trip.

(I should mention that Larry took all of the pictures that don’t actually feature him as a subject)

Here we are at the Sylmar MetroLink Station. First there’s me, because it’s my blog:
Tom, at the Sylmar MetroLink Station

…and here’s Larry. He has basically always been this thin. And, yes, if you’re curious, he’s had to work at it all his life — he doesn’t just get it for free. At a recent reunion of his former Interactive Systems Software colleagues, they speculated that he had sold his soul to the Devil, but I know Larry, and he would have gotten a better deal than just just being thin and young — he’s one of those hagglers. Still thin, though, almost as if he’d been working out, pretty much daily, for the last nine months:
Larry, at the Sylmar MetroLink Station

The train arrived dead on time:
MetroLink train arriving at Sylmar station.

…and in practically no time, we were down at Union Station, in downtown Los Angeles:
Union Station, Los Angeles, Seen from Track 5

The transfer to the Gold Line was included in our MetroLink ticket, and before we knew it, we were up in Old Town Pasadena, at the Del Mar station (where my old friend John Blackburn and I once smoked cigars, not knowing that it wasn’t allowed — we figured it out when we saw a sign with a bunch of NO’s!, and I said, “Oh, a sign with that many NO!’s has got to include smoking cigars.” We high-tailed it out of there, only to run smack-dab into a night guard. It would have been ironic to have been ticketed for my twice-yearly cigar, but fortunately, he just bade us a cheery good evening.)

Here’s the Del Mar station. Each station is visually distinct, which is both pleasing, and helpful for wool-gathering passengers to notice their stop:
Del Mar Station, Gold Line, Pasadena, California

And really, what the heck is this thing for? Just to say, “Yep, this is Del Mar Station, where the crazy thing is?”:
Del Mar Station, Gold Line, Pasadena, California

I told Larry that I thought I’d seen a restaurant that John and I used to frequent, though I wasn’t really sure, because face-blind people are also bad at recognizing landmarks.

But I was right, it was the wonderful Crown City Brewery (where they give you a special T-shirt after you’ve drunk 100 different beers):
Entrance, The China Factory Mall, Pasadena, California

Entrance, Crown City Brewery, The China Factory Mall, Pasadena, California

We feasted on beer and sundries, and returned to the outside world, passing both the Del Mar station:
Entrance, Del Mar Station, Gold Line, Pasadena, California
Tom Chappell in Pasadena, California

…and the Castle-Green compound:

Castle-Green, Pasadena, California
Castle-Green, Pasadena, California

We wandered around, stopping in a travel store, where I bought a Tilley LT6B Breathable Nylon Hat (Canadian, with a lifetime guarantee). I was pleased to find that not only did they have hats in my freakishly-large head size (7 3/4), but even had, in stock mind you, size 7 7/8 — presumably for encephalitis victims.

I don’t have pictures of me buying the hat, or of Larry making a purchase at the lovely Pasadena Apple Store, but I do have a picture of this rooftop reindeer ball:
Reindeer Ball, Decoration on top of building at Christmas, 2007, Pasadena, California

Then, because fewer MetroLink trains run on Sunday than on Saturday, it was time for us to head back to the lovely Del Mar station…
Del Mar Station, Gold Line, Pasadena, California
Sign, Del Mar Station, Gold Line, Pasadena, California

…and from there, back to Union Station…
Ceiling, Union Station, Los Angeles

Ceiling, Union Station, Los Angeles

…where we caught the return MetroLink.

Look at this first photo: that could be any shrunken old geezer. “Hey, you kids get off of that scaffolding!”:
Tom Chappell, on Train, Los Angeles, wearing a Tilley Hat

…but no! Apparently, I’m actually jolly!:
Tom Chappell, on Train, Los Angeles, wearing a Tilley Hat

Here’s my old friend, Industry Figure Larry Helmerich, also reasonably jolly:
Larry Helmerich, on Train, Los Angeles

Larry Helmerich, on Train, Los Angeles

Back safely in Sylmar, victorious, with our swag!
MetroLink train arriving at Sylmar station.

Part 8: Insulin, High Blood Sugar, and Dementia

(Back to Parts One, Two, Three, Four, Five, Six, or Seven)

By the 1990’s, researchers started reporting that heart disease and Alzheimer’s seemed to share risk factors: hypertension, atherosclerosis, and smoking were all associated with an increased risk of Alzheimer’s disease.

The connection with insulin and high blood sugar is concrete: “Type 2 diabetics have roughly twice as much risk of contracting Alzheimer’s disease as nondiabetics. Diabetics on insulin therapy…[have] a fourfold increase in risk. Hyperinsulinemia and metabolic syndrome are also associated with an increased risk of Alzheimer’s disease.”

In part, this is due to vascular damage, which is more common in diabetics — and vascular damage in the brain is a well-known cause of dementia.

But vascular dementia aside, there are two other lines of evidence linking high blood sugar and/or high insulin levels to Alzheimer’s disease proper:

  1. When blood sugar levels are high, the excess sugars are more likely to semi-randomly bind with proteins — the sugar molecules are sticky, in a chemical way, to protein molecules. In fact, they’re so sticky that a protein might end up folded over and attached in more than one place to a sugar molecule, or multiple proteins may glom together with one or more sugar molecules into a big untidy mess.

    These glycated (“sugar-frosted”) proteins can end up as twisted, gnarled Advanced Glycation End-products (“AGEs”), which can overwhelm and confound our bodies’ clean-up crews. Plus, they’re a source of oxidative stress, generating free radicals. Bad news all around.

    Now, organic chemicals depend on their shape as much as their chemical formula for their actions: Our bodies, for example, can only use so-called right-handed sugar; the chemically-identical, but physically mirror-imaged left-handed sugar is indigestible. As another example, Mad Cow disease is caused by a perfectly-normal protein being folded into an abnormal shape, which “infects” other proteins by encouraging them to take on this same dysfunctional and highly-stable shape. Not only are the proteins wrong, they like being wrong, and are good at persuading other proteins to join their evil gang.

    But I digress. The main point here is that your body’s workhorse chemicals can get an unwelcome sugar coating that is difficult to remove. In fact, one of the better tests for diabetes and insulin resistance is the A1c, which measures the percentage of your hemoglobin that has become sugar-frosted. Mine is 5.2%. We like it to be below 6.0%. Diabetics are happy to get it down to 7.0%. Unlike the fasting blood glucose test, which measures blood sugar levels due to what you’ve been doing in the last few hours, the A1c measures your average blood sugar level over the last two to three months. And the reason it can do that is because once your hemoglobin has been glycated, it tends to stay that way.

    When this process happens to brain proteins, the results aren’t pretty:

  2. Investigators studying AGEs have proposed that Alzheimer’s starts with glycation — the haphazard binding of reactive blood sugars to…brain proteins. Because the sugars stick randomly to the fine filaments of the proteins, this in turn causes the proteins to stick to themselves and to other proteins. This impairs their function and, at least occasionally, leaves them impervious to the usual disposal mechanisms, causing them to accumulate in the spaces between neurons. There they cross-link with other nearby proteins, and eventually become advanced glycation end-products. All of this would then be exacerbated by the fact that the glycation process itself generates more and more toxic reactive oxygen species (free radicals), which in turn causes even more damage to the neurons. In theory, this is what causes the amyloid plaques and leads to the degeneration of neurons, the cell loss, and the dementia of Alzheimer’s. The theory is controversial, but the identification of AGEs in the plaques and tangles of Alzheimer’s is not.

    …from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 206

  3. And what about high insulin levels? Sure, they’re implicated as well. Imagine, for a moment, that you’re a pancreas. Your host eats a sugary meal, extremely delicious, but blood glucose levels are rising, and must be suppressed. Quick, a shot of insulin! Perfect, the glucose levels go down (or don’t, depending on how insulin-resistant the host is).

    But consider: we need some mechanism to bring insulin levels back down to normal after the pancreas stops spewing it out into the bloodstream. And it turns out that there’s an enzyme, IDE (insulin degrading enzyme) that really likes to tear down insulin.

    Seems like a good system, but IDE has a second job, a side job, that it agreed to do in its spare time if there wasn’t much super-important insulin to tear down. Wanna guess? Yes, that’s right: tearing down the amyloid plaques that clutter the brains of Alheimer’s patients:

  4. The more insulin available in the brain, by this scenario, the less IDE is available to clean up amyloid, which then accumulates excessively and clumps into plaques. In animal experiments, the less IDE available, the greater the concentration of amyloid in the brain. Mice that lack the gene to produce IDE develop versions of both Alzheimer’s disease and Type 2 diabetes…

    In 2003, [Suzanne Craft, a neuropsychiatrist at the University of Washington], reported that when insulin was infused into the veins of elderly volunteers, the amount of amyloid in their cerebral spinal fluid increased proportionately. This implied that the level of amyloid protein in their brain had increased as well. The older the patient, the greater the increase in amyloid protein. As Craft sees it, if insulin levels are chronically elevated (hyperinsulinemia), then brain neurons will be excessively stimulated to produce amyloid proteins, and IDE will be preoccupied with removing the insulin, so that less will be available to clean up the amyloid…

    This isn’t to say that eating carbohydrate foods to excess is a [proven] cause of Alzheimer’s, only that mechanisms have now been identified to make the hypothesis plausible.

    …from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 208

Continued in Part Nine

Part 7: Safety Second — Deficiency

(Back to Parts One, Two, Three, Four, Five, or Six)

Will a low-carb diet lead to diseases of deficiency? It shouldn’t, because we don’t actually restrict the bulk of fruits and vegetables. Only refined sugar, flour, bread, potatoes, rice, beer, and those foods composed chiefly of these need be restricted.

This leaves a rather large remainder for our nutrition: this week, for example, I’ve had an apple, asparagus, broccoli, carrots, garlic, mushrooms, onions, tomatoes, yellow squash, and zucchini in mass quantities, in addition to copious amounts of delicious meat and cheese.

But what if we did eat only meat? Again, the experiment has already been done, and a long time ago:

In the early 1920s, a Harvard anthropologist-turned-Arctic-explorer named Vilhjalmur Stefansson publicized the idea of a carbohydrate-restricted diet based on fatty meat.

What follows is quite a long quote, but stick with it: I, at least, found it absolutely fascinating.

[Stefansson] was concerned with the overall healthfulness of the diet, rather than its potential for weight loss. [He] had spent a decade eating nothing but meat among the Inuit of northern Canada and Alaska. The Inuit, he insisted, as well as the visiting explorers and traders who lived on this diet, were among the healthiest if not the most vigorous populations imaginable.

…The ability to thrive on such a vegetable- and fruit-free diet was also noted by the lawyer and abolitionist Richard Henry Dana, Jr., in his 1840 memoirs of life on a sailing ship, Two Years Before the Mast. For sixteen months, Dana wrote, “we lived upon almost nothing but fresh beef; fried beefsteaks, three times a day…[in] perfect health, and without ailings and failings.”

…None of Stefansson’s findings would have been controversial had not the conventional wisdom been — as it still is — that a varied diet is essential for good health.

…This philosophy, however, was based almost exclusively on studies of deficiency diseases, all of which were induced by diets high in refined carbohydrates and low in meat, fish, eggs, and diary products. When the Scottish naval surgeon James Lind demonstrated in 1753 that scurvy could be prevented and cured by the consumption of citrus juice, for example, he did so with British sailors who had been eating the typical naval fare “of water gruel sweetened with sugar in the morning, fresh mutton broth, light puddings, boiled biscuit with sugar, barley and raisins, rice and currants.” Pellagra was associated almost exclusively with corn-rich diets, and beriberi with the eating of white rice rather than brown.

…What nutritionists of the 1920s and 1930s didn’t then know is that animal foods contain all of the essential amino acids (the basic structural building blocks of proteins), and they do so in the ratios that maximize their utility to humans. They also contain twelve of the thirteen essential vitamins in large quantities.

…The thirteenth vitamin, vitamin C, ascorbic acid, has long been the point of contention. It is contained in animal foods in such small quantities that nutritionists have considered it insufficient and the question is whether this quantity is indeed sufficient for good health.

…the dangers of an all-meat diet were considered sufficiently likely that even Francis Benedict, as Stefansson told it, claimed that it was “easier to believe” that Stefansson and all the various members of his expeditions “were lying, than to concede that [they] had remained in good health for several years on an exclusive meat regimen.”

In the winter of 1928, Stefansson and Karsten Anderson, a thirty-eight-year-old Danish explorer, became the subjects in a yearlong experiment that was intended to settle the meat-diet controversy. The experiment was planned and supervised by a committee of a dozen respected nutritionists, anthropologists, and physicians. Eugene Du Bois and ten of his colleagues from Cornell and the Russell Sage Institute of Pathology would oversee the day-to-day details of the experiment.

For three weeks, Stefansson and Anderson were fed a typical mixed diet of fruits, cereals, vegetables, and meat while being subjected to a battery of tests and examinations. Then they began living exclusively on meat, at which point they moved into Bellevue Hospital in New York and were put under twenty-four-hour observation. Stefansson remained at Bellevue for three weeks, Anderson for thirteen weeks. After they were released, they continued to eat only meat for the remainder of one year. If they cheated on the diet, according to Du Bois, the experimenters would know it from regular examinations of Stefansson’s and Anderson’s urine. “In every individual specimen of urine which was tested during the intervals when they were living at home,” Du Bois wrote, “acetone [ketone] bodies were present in amounts so constant that fluctuations in the carbohydrate intake were practically ruled out.”

The experimental diet included many types of meat… Stefansson and Anderson each consumed an average of almost two pounds of meat per day, or 2,600 calories: 79 percent from fat, 19 percent protein, and roughly 2 percent from carbohydrates (a maximum of 50 calories a day), which came from glycogen contained in the muscle meat…

“The only dramatic part of the study was the surprisingly undramatic nature of the findings,” wrote Du Bois, when he later summarized the results. “Both men were in good physical condition at the end of the observation,” he reported in 1930, in one of the nine article he and his colleagues published on the study. “there was no subjective or objective evidence of any loss of physical or mental vigor.” Stefansson lost six pounds over the course of the year, and Anderson three, even though “the men led somewhat sedentary lives.” Anderson’s blood pressure dropped from 140/80 to 120/80; Stefansson’s remained low (105/70) throughout. The researchers detected no evidence of kidney damage or diminished function, and “vitamin deficiencies did not appear.” Nor did mineral deficiencies, although the diet contained only a quarter of the calcium usually found in mixed diets, and the acidic nature of a meat-rich diet was supposed to increase calcium excretion and so deplete the body of calcium. Among the minor health issues reported by Du Bois and his colleagues was the observation that Stefansson began the experiment with mild gingivitis (inflammation of the gums), but this “cleared up entirely, after the meat diet was taken.”

…Nutritionists would establish by the late 1930s that B vitamins are depleted from the body by the ocnsumption of carbohydrates. “There is an increased need for these virtamins when more carbohyrdrate in the diet is consumed,” as Theodore Van Itallie of Columbia University testified t the McGovern’s Select Committee in 1973. A similar argument can now be made for vitamin C. Type 2 diabetics have roughly 30 percent lower levels of vitamin C in their circulation than do nondiabetics. Metabolic syndrome is also associated with “significantly” reduced levels of circulating vitamin C, which suggests that vitamin-C deficiency might be another disorder of civilization. One explanation for these observations — described in 1997 by the nutritionists Julie Will and Tim Byers, of the Centers for Disease Control and the University of Colorado respectively, as both “biologically plausible and empirically evident’ — is that high blood sugar and/or high levels of insulin work to increase the body’s requirements for vitamin C.

The vitamin-C molecule is similar in configuration to glucose and other sugars in the body. It is shuttled from the bloodstream into the cells by the same insulin-dependent transport system used by glucose. Glucose and vitamin C compete in the cellular-update process, like strangers trying to flag down the same taxicab simultaneously. Because glucose is greatly favored in the contest, the uptake of vitamin C by cells is “globally inhibited” when blood-sugar levels are elevated. In effect, glucose regulates how much vitamin C is taken up by the cells…if we increase blood-sugar levels, the cellular uptake of vitamin C will drop accordingly. Glucose also impairs the reabsorption of vitamin C by the kidney, and so, the higher the blood sugar, the more vitamin C will be lost in the urine. Infusing insulin into experimental subjects has been shown to cause a “marked fall” in vitamin-C levels in the circulation.

In other words, there is significant reason to believe that the key factor determining the level of vitamin C in our cells and tissues in not how much or little we happen to be consuming in our diet, but whether the starches and refined carbohydrates in our diet serve to flush vitamin C out of our system, while simultaneously inhibiting the use of what vitamin C we do have.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 320-326

Continued in Part Eight

Bike Ride: Re-entry (Now With More Words!)

After a nine-week hiatus, Ron and I hit the road again, reprising the ‘easy 50 miles‘ near Ron’s house.

We were supposed to get started by 10:00am, but when I went out to get my bike, it was honked, with a flat rear tire, the same tire that had gone flat on each of the last two rides, despite new tubes. It was pretty clear that this was a Sad Tire, and that the bike would need a quick tire-ectomy. And considering that the front tire was not any younger, a double bypass would probably be in order.

I gave Ron a call to let him know the situation, and took off for the Land of Ron. He called back to say that he’d found a bike shop that opened at 10:00am, hoorah! We were in by 10:10, out by 10:50, and were leaving Ron’s house on our bikes by 11:20am.

Oh, I forgot to mention the best part! So, when we were in the bike shop, choosing tires, the bike shop guy looked at me and said, “You’re not over 220 pounds — I’m going to give you the thinner tires, 23mm.”

That’s right! You can tell I’m not over 220, just by looking at me, because I’m only 214!

The ride was delightful — cool weather, clean air, and I didn’t have any of that late-in-the-ride tiredness that I often have. I usually crumple into a little ball near the end of the rides, but this time I turned in a pretty consistent performance. Ron was having a little more trouble keeping up, but he had been on enforced leave from bicycles for weeks, while I was galavanting around in fires — it’s not really fair.

Ron was amazing — he got his heart rate up to 177 beats per minute on Lynn Road. That’s the average maximum heart rate of 43-year-olds! I myself got up to 162 bpm on Wendy Rd. (“a 58-year-old”), which is about 10 bpm faster than I’ve seen this year. Getting there.

We celebrated near the end of the ride by sharing 1/3 of a bag of Skittles (I know — the debauchery), and sailed back into Ron’s place a little after 4:00pm. A beautiful ride, if a little cool. Would have been better if I had remembered to check my tires on Saturday.

Ride:
 total ascent:   1,574 feet
     distance:    51.2 miles

Tom:
  saddle time:    3:52     (not counting breaks)
average speed:    13.2 mph (not counting breaks)

Ron:
  saddle time:    4:08     (not counting breaks)
average speed:    12.2 mph (not counting breaks)

Man, I just felt great today — wait, what do you mean, I was slower than last time?