4th Thursday Update

April 28, 2016

It rained yesterday, but today there wasn't a cloud in the sky, and it was warm. Seemingly a nice day for a run at lunchtime at work. However, a mountain lion was sighted on the property this morning, and I'm easily intimidated by reports of nearby predators. So, I decided to head for the state park after work instead. Seemingly a more likely place to be attacked by a mountain lion, but then, nobody had warned me that any man-eating beasts had been spotted there today, so that was where I decided to get my running done.

I admit that I chose a route which kept me fairly distant from the central meadow where pack-hunting has been observed. The closest thing to predators I ran into were mountain-bikers who sometimes came diving out of side-trails at top speed, and scared the hell out of me. Also, there were a lot of wild turkeys. This must be mating season: the males were making dramatic displays of their tail-feathers. It's possible they were mooning me, but I prefer to think I wasn't the one they were trying to make an impression on.

 


Hydration and blood sugar

I see that someone recently was referred by Google to this site when they did a search on "can I take a laxative when having high blood sugar?". Not a question I had heard before, or had thought about either, so I decided to look into it. I didn't think laxative use had any bearing on blood sugar, but I thought I'd look into it to be sure. And I found out that laxatives can have an impact on blood sugar, although in a rather indirect way: laxative use becomes an issue if it results in dehydration.

You'd have to be using a pretty strong laxative to dehydrate yourself with it, or so it seems to me. Unless you're prepping yourself for a colonoscopy the next morning, using whatever ninja-level laxative treatment the gastroenterologist ordered, I wouldn't have thought dehydration would be a big concern. But apparently people do become dehydrated when using laxatives. And, of course, diabetic people have colonoscopies just like everybody else.

Anyway, the real issue worth discussing is not laxatives in particular, but dehydration in general -- which can happen to you whether you take laxatives or not. (Exercising in warm weather, without taking in enough extra water to correct for it, is a more common cause of the problem.) What effect does dehydration have on blood sugar?

The most obvious connection between dehydration and blood sugar is that, when you are dehydrated, your blood is less watery; the total fluid volume of your blood supply declines, but only because there is less water in it. There isn't any less sugar in it, just less water to dilute the sugar. So, your blood glucose test result (which is a measure of glucose concentration in the blood) inevitably goes up when you become dehydrated.

There are other effects of dehydration which make this problem even worse. When you are dehydrated, the brain secretes a hormone called vasopressin, mainly for its effect on the kidneys (it alters kidney functioning, so that more water is retained instead of excreted in the urine). But vasopressin has other effects; it is involved in other regulatory functions. It causes blood vessels to constrict, raising blood pressure (which would otherwise drop due to reduced blood volume). Another effect of vasopressin is to effect liver function: it promotes gluconeogenesis -- the process by which the liver converts other compounds into glucose and releases the glucose into the bloodstream. So, not only does dehydration concentrate the glucose in your blood, it results in the liver adding even more glucose to what's already in your blood. Also, there is apparently reason to think that, over the long haul, dehydration (if it occurs frequently) impairs insulin sensitivity, thus making blood glucose harder to keep under control. People who are often dehydrated face a heightened risk of becoming diabetic, apparently because of impaired insulin sensitivity.

The good news here is that dehydration is a pretty easy problem to fix: drink a lot of water, and then drink some more. It's only in cases of severe dehydration -- we're talking heat stroke here -- that drinking water won't fix the problem: when you're dehydrated badly enough, the stomach lining can no longer take in water: if you swallow it, it comes right back up. When things get that bad, you have to be taken to the emergency room and get rehydrated intravenously. Most of us never get that bad; drinking water is all we need to do.

I suppose I shouldn't end this without talking about what happens when you go too far in correcting for the problem, and take in too much water. This is a real problem, and a dangerous one, called hyponatremia. It is sometimes called "water intoxication", although that's kind of a stupid name for it. The word hyponatremia doesn't mean "too much water", it means "too little salt". Hyponatremia typically strikes endurance athletes during warm weather, who drink a great deal of water to avoid dehydration. Because of the loss of salt from the bloodstream during prolonged sweating, the addition of large amounts of the water to the bloodstream can cause the blood to have a much lower concentration of salt than the body's cells do. Osmotic pressure (the tendency of water to flow through cell membranes to equalize the concentration of a substance on both sides of the cell well) causes cells to absorb too much water and become swollen. This affects various body functions, but swelling of brain cells is particularly painful and dangerous. People can pretty easily die from hyponatremia. (That's why sports drinks have salts added to them -- it's a hedge against hyponatremia.) Anyway, drink water if you're dehydrated, but don't drink bottle after bottle of it and push yourself into hyponatremia. Moderation in all things!

 


The bright side of dark chocolate

Researchers at the University of Warwick think they have found evidence that daily consumption of a small amount of dark chocolate (that is, 100 grams -- about 3.5 ounces) is good for your health -- specifically in terms of preventing diabetes.

Something in dark chocolate seems to have the effect of increasing insulin sensitivity, which is obviously of use in preventing or ameliorating diabetes. It also has a positive effect on other biomarkers, such as liver enzymes.

Apparently the chocolate should be combined with coffee or tea (these drinks contain polyphenol, which seems to activate the beneficial effects of the chocolate).

I'm not necessarily recommending chocolate at a diabetes remedy (most forms of it are loaded with sugar, so you'll need to be careful about that), but I thought it might cheer you up to think that any chocolate sins you might succumb to in the near future can perhaps be redefined as a kind of therapy. Some people think of chocolate as therapy anyway, but they usually think of it as psychotherapy rather than diabetes therapy. Now you can claim it's either one.

However: as with drinking water as therapy for dehydration: moderation in all things!

 


3rd Thursday Update

April 21, 2016

Lower blood glucose after dinner than before breakfast may seem odd, but dinner was low-carb and came after a long run, so it makes sense.

 


Texas sharpshooter science!

The "Texas Sharpshooter Fallacy" is a particular kind of breakdown of logical thinking, caused by the natural human tendency to be fascinated by coincidences and to interpret coincidences as meaningful patterns. The fallacy takes its name from an old story about a Texan (the story makes him a Texan to explain his boastfulness) who likes to think of himself as a sharpshooter even though he has no skill at marksmanship. He spends an afternoon firing random shots at the side of a barn. After he's out of bullets, he goes to the barn, finds one place on the wall where several bullet holes happen to be bunched closely together, and paints a target around them so that they all seem to fall within a distinct bullseye. Then he shows people the target as evidence of what a good shot he is.

It is always easy to declare, in retrospect, a meaningful connection between things which happen to coincide. It's also easy to find things that coincide. Random data tends to clump. Flip a coin fifty times and you should expect to get streaks of several heads in a row, or several tails in a row. This bunching up of results is not a violation of randomness, but a perfect example of what a truly random sequence looks like. Strange coincidences are not nearly as strange as we like to think, so we should be hesitant about asking what they "mean". Usually they mean nothing, and we can put them in perspective by paying more attention to whatever doesn't fit the pattern we've spotted. In other words, we should ask how many bullet-holes are in the side of that barn which don't have a target painted around them because they aren't close together.

For example, there is a famous series of coincidental similarities between President Lincoln and President Kennedy which people love to quote (each was assassinated by someone with 15 letters in his name!), and although the list seems amazing if you don't think too deeply about it, skeptics have pointed out that (1) the differences between Lincoln and Kennedy are far more numerous than their similarities, and (2) long lists of coincidental similarities can be compiled about any pair of historical figures, or any pair of movies, or any pair of books. We love coincidences, and we like to dwell on them. We love to focus on an apparent pattern, while ignoring anything which doesn't fit the pattern. Who cares that Lincoln had a beard and Kennedy didn't, for example? Clearly that means nothing, because it doesn't fit the pattern of similarities. Focusing on it would spoil the game. (But if both men had been bearded, we would have been happy to add that fact to the list of similarities between them.)

Of course, even if we ignore the skeptics, there still doesn't seem to be anything especially meaningful about Lincoln having a secretary named Kennedy and Kennedy having a secretary named Lincoln. If some strange supernatural force was involved in determining the names of these presidential secretaries, what exactly was it trying to achieve, and what should we make of the result? By the way, it turns out that Lincoln didn't actually have a secretary named Kennedy -- some anonymous person invented this detail to make the list of coincidences more uncanny. Spotting an apparent pattern can make people so excited that they not only begin to see evidence for that pattern everywhere they look, they often begin fabricating evidence, to "prove" that the pattern is real. (Pro tip: fake evidence is not needed when something is real.) Some of the other details on the list of Lincoln/Kennedy coincidences are also wrong, or questionable, or overstated.

In the case of the Lincoln/Kennedy coincidences, most people aren't trying to draw any specific conclusion about the meaning of the pattern; they just want to suggest that the pattern is too weird and unlikely not to mean something, even if we have no idea what the meaning is. There is nothing consequential about the way people interpret the Lincoln/Kennedy coincidences. Public policy isn't going to hinge on it. The Texas Sharpshooter approach, in which we isolate the coincidences and ignore the non-coincidences, is pretty harmless if the only result of it is people saying "Ooooooh, spooky!".

The Texas Sharpshooter approach is not so harmless when it is applied to medical research, however; it can easily lead us to make false conclusions about what causes (or cures) a given health problem. The issue is relevant to research in any scientific field, or course, but it applies with special force to medical research, because of certain real-world practicalities which make medical research different from other kinds of research:

The secretiveness of medical research is especially problematic, and especially likely to promote the Texas Sharpshooter Fallacy: if a clinical trial of an experimental drug is attempted six times, and gets negative results on five of those six attempts, only the successful one is published. Somehow it has become the norm in clinical publishing to release positive results but not negative ones, even though this is patently a case of painting a target around the hits while hiding the misses. It's hard to see why anyone thinks such a biased process counts as science at all, yet few scientists dare to protest -- perhaps because most of them have signed agreements with their funders not to reveal what the unpublished studies found.

The Texas Sharpshooter Fallacy is very likely what has nurtured the never-ending quest to replace the diabetes drug metformin (a medication which has been around so long that it's a cheap "generic" pharmaceutical) with something more profitable. Sorry, I shouldn't have said "more profitable", I should have said "safer and more effective". With enough failed studies going unpublished, and enough successful ones hyped, you can paint a bullseye around a new drug and eventually get the drug approved by the FDA. Countless new and expensive would-be replacements of metformin have been put on the market. But a recent review published in the Annals of Internal Medicine says metformin remains the best "first line" choice for drug therapy for Type 2 diabetes. The drugs seeking to replace it tend to have too many side effects and concerns about possible cardiac risks. I realize that not everyone tolerates metformin well, so there can be legitimate reasons for wanting to have alternatives to it, but the evidence seems to show that the drugs seeking to replace it are not safer and better, they're just more expensive and more profitable to the drug companies.

The Texas Sharpshooter Fallacy also tends to be a powerful weapon in the hands of influential scientists seeking to establish (and rule) a cult-like community of opinion within their field. "Soft" sciences, such as psychology and sociology, are notoriously prone to this kind of thing: ideas can hang on for decades in the face of disconfirming evidence, simply because academics fear it would be "career suicide" to contradict Sigmund Freud or Margaret Mead; they know that heretics are excluded and shamed. Something of this sort has apparently been going on for decades in the field of nutrition.

The cult in this case surrounds the influential (apparently far too influential) nutritionist Ancel Keys, creator and ruthless promoter of the idea that saturated fat in the diet is the cause of heart disease and probably also obesity and diabetes. He was up against rival scientists (such as John Yudkin) who argued that the real issue was dietary sugar, not dietary fat. Keys won the day with a combination of attacks on Yudkin and a grand exercise in Texas Sharpshooting known as the Seven Countries study, which compared heart disease rates in seven countries and found that the countries with the highest heart disease rates also had the highest consumption of saturated fat. Excluded from the studies were countries (such as France and Germany) which were already known to have low heart disease rates and diets high in saturated fat. Including such countries would have ruined the study, of course; by including only countries which happened to fit the pattern he was hoping to find, Keys was able to paint a bullseye around the particular set of bullet holes that served his purpose. (For more on this depressing history, see The Guardian.)

Recent decades have seen a relentless buildup of evidence showing that the saturated-fat hypothesis was wrong -- that sugar is the real dietary problem we need to solve. But nutritionists are still circling the wagons, still attacking anyone who questions the Ancel Keys orthodoxy as a dangerous crank. But here's the interesting thing about Ancel Keys these days: he's dead. That matters in science, although in theory it should not. As the physicist Max Planck pointed out: "A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it." Science is said to advance one funeral at a time. As Keys recedes into history, and more and more of the nutritionists who were trained never to question his views die off, it will become increasingly possible for us to confront the truth about what our societal sugar addiction has done to us.

And who knows? Once we are free to confront it, we might even be able to do something about it!

 


2nd Thursday Update

April 14, 2016

 


Why it's hard to make a perfect drug

Because so many different mechanisms and chemical signals are involved in regulating blood glucose, there are great many possible ways of interfering with the process. The reason there are so many different kinds of drugs for Type 2 diabetes is that the disease presents the pharmaceutical industry with a vast array of potential drug "targets". There are a great many naturally occurring compounds in human blood which tend to have the effect of driving blood sugar up or down, and there is always the possibility that a new drug can reduce excessive blood sugar by boosting the effect of a compound which tends to drive blood sugar down, or by inhibiting the effect of a compound which tends to drive blood sugar up.

The problem is always: what else does the drug do, besides reducing excessive blood sugar? It's pretty unlikely that the drug won't do anything except have the effect you want it to have. And the other effects it has might be difficult to discover, especially if they only become an issue in particular situations which you aren't studying.

The anti-nausea drug thalidomide was effective at controlling morning sickness in pregnant women, and it seemed to do the women no harm. The drug was approved in Europe (not in the USA), and it was after large numbers of pregnant women started taking it that the world found out what else thalidomide did: it caused severe limb deformities in the babies these women were carrying. This history is often cited by American drug regulators as a cautionary tale about the hazards of approving a drug without thoroughly investigating its effects.

However, even under the most cautious regulatory regime, it is impossible to know for certain that a new drug doesn't cause harmful effects under circumstances which weren't checked, or on a time-scale too long to be checked.

The real testing phase of a drug begins when it is approved and doctors prescribe it for large numbers of people -- and this testing phase continues for many years. Often a drug which has been widely used for a long time falls under suspicion because it seems as if the people taking the drug are having more heart attacks or cancer or liver problems than expected. Sometimes a popular drug is taken off the market because of problems discovered after approval. Diabetes drugs seem to be especially at risk for this sort of this thing.

Lately, concerns have been raised about the "gliptins" -- a family of diabetes drugs technically known as DPP-4 inhibitors.

DPP-4 inhibitors act to block the effect of a protein called DPP-4. The motive for doing that is that DPP-4 inactivates the "incretins" (such as GLP-1) which tend to reduce blood glucose by stimulating the release of insulin (the glucose-lowering hormone) and blocking the release of glucagon (the glucose-raising hormone). From the standpoint of controlling Type 2 diabetes, incretins are good, and anything which blocks the effect of incretins is bad. If DPP-4 inactivates incretins, then DPP-4 is bad, and a gliptin drug which inhibits DPP-4 is just what the doctor ordered.

Okay, so what else do the gliptin drugs do?

That hasn't been too clear. There have been indications that these drugs increase the risk of heart disease (many diabetes drugs seem to have that effect to one degree or another, which is a bit ironic, considering that heart disease is the number one "complication" of diabetes and all diabetes drugs should be preventing it). But now there are indications of problems in another area: do the gliptin drugs promote cancer?

Actually, although the newest findings on drugs and cancer are focused especially on gliptins, they have disquieting implications for many other drugs and supplements which we think of as beneficial.

It turns out that gliptins also act as "anti-oxidants" -- that is, they inhibit the oxidation of other compounds. Although anti-oxidants have been sold to the public as cancer-fighting chemicals which protect healthy cells from oxidative stress, and therefore protect them from becoming cancerous, there is another side to anti-oxidants: they also protect cancer cells from being knocked out by the immune system or by chemotherapy. Anti-oxidants may very well reduce the risk of cells becoming cancerous, but for any cancerous cells that are present, it appears that anti-oxidants allow them to thrive -- and spread.

Researchers are reporting in Science Translational Medicine that they studied two gliptins commonly prescribed for diabetes, plus another anti-oxidant (alpha-lipoic acid) which is often used in high doses to combat diabetic neuropathy. Although these anti-oxidant drugs were not found to cause cells to become cancerous, they were found to promote metastasis (spreading and colonization) of existing cancer cells.

It might seem as if this is only an issue for a small number of people, but it turns out that it's not unusual for cancer patients also to be diabetic. After all, type 2 diabetes is common in the age brackets with the highest cancer risk, and being diabetic increases the cancer risk further. And although we might be tempted to say: "no problem, just make a rule that gliptins and other anti-oxidants shouldn't be given to cancer patients" -- it's not that simple. The trouble with that approach is that a lot of cancer patients don't yet know that they are cancer patients. The disease begins with microscopic tumors which might remain undetectable for years -- and might also be eliminated by the immune system before they can do any harm. If gliptins and other anti-oxidants have the effect of protecting those microscopic tumors from the immune system, and encouraging their spread, then for all practical purposes, the fact that these drugs don't "cause" cancer is the sort of quibble that only a lawyer could see as important. If these drugs result in more people dying of cancer than otherwise would, I see that as bit of a problem.

Anyway, this case illustrates the very difficult balance of risks that must be worked out when a drug is approved and used. If the drug "works" in the sense that it has the specific biochemical effect we wanted it to have, that alone is not good enough. What else does it do? If the drug solves one narrowly-defined health problem at the cost of creating more serious health problems later, it's not a good solution.

I don't know what will come of this new cancer research. Perhaps nothing more than a restriction on prescribing gliptins for diabetes patients who also have cancer. But it sounds as if we're due for a re-examination of the supposedly wonderful impact of anti-oxidants in general.

 


Surgery as a drug

The results are coming in: bariatric surgery (that is, weight-loss surgery, such as gastric bypass) is more effective than diabetes drugs in controlling blood glucose, in patients who are five years past the operation.

Apparently neither the surgery nor the drugs were compared with exercise, to see how well they do in comparison with that.

 


1st Thursday Update

April 7, 2016

 


Salt plus sugar is worse than salt alone!

Most of us are aware, in a vague sort of way, that hypertension (high blood pressure) is connected with sodium intake from salty foods. We're aware that a lot of doctors and medical associations think the human diet has become far too sodium-rich, and that hypertension has become a widespread problem as a result. We're aware that we're being asked to adopt a much less salty diet for this reason. We're also aware that we don't want to do anything of the kind. Nature designed us to crave salt, because in a state of nature it's hard to get enough of it. In the supermarket, however, it's easy to get more than enough of it -- and we do.

Most of the sodium in our diet doesn't come from the salt-shaker, or even from the foods we usually think of as salty. Most of it comes from processed foods (such as bread and soup), which can have extraordinary amounts of salt added to them without our being conscious of it. I have in front of me a very small can (5.5 ounces) of V8 Spicy Hot Vegetable Juice. It contains 450 milligrams of sodium -- which is 20% of the maximum safe daily intake of sodium as defined by the Food and Drug Administration. (They recommend keeping one's daily intake under 2300 mg, but the average American takes in 3400.)

The trouble is, it's easy to get used to a high level of saltiness in food, and after that point any food containing less than the amount of salt we expect seems unacceptably bland. Makers of processed foods have got into a kind of arms race in regard to saltiness -- they dare not fall behind the competition in delivering a major sodium payload to the consumer. Anyone who tries to cut down on daily sodium intake is going to have a hard time finding low-sodium foods (and is pretty sure to complain about the dullness of what he does find).

Diabetes patients, having already been asked to cut carbs, tend to be less than enthusiastic about cutting sodium as well. We know, of course, that hypertension is one of the health problems commonly associated with Type 2 diabetes, and that it contributes greatly to the elevated cardiac risk that diabetes patients face in general. We know that diabetes patients have more reason than anybody else to be vigilant about keeping blood pressure under control. And yet, it's hard not to take a defiant attitude on the sodium issue. One is tempted to protest: "I'm already sacrificing French fries and garlic bread and bananas, but that's not enough for you, is it? No, you won't be satisfied until you take away my chicken-broth, too! Is there anything else you want me to do without? Oxygen, maybe?".

It is especially galling to be asked to cut sodium intake when it's known that "salt responders" (people whose blood pressure is driven upwards by dietary sodium) are a minority within the population, so we're all being asked to cut sodium without knowing if we're one of the people for whom it will make a difference. One is tempted (by which I mean I am tempted) to ignore the whole issue, on the grounds that there's a good chance it's not irrelevant anyway.

The interesting question here, at least to me, is why sodium would ever have anything to do with blood pressure -- and why it would cause hypertension for some people and not others.

The explanation turns out to be related to "osmotic pressure" -- the difficult-to-grasp phenomenon which causes the concentration of anything dissolved in fluid to equalize itself on either side of a permeable membrane. When the sodium concentration in the bloodstream goes up, the cells try to dilute it by releasing extra water into the bloodstream. This increases the total fluid volume of the bloodstream -- and therefore increases blood pressure.

This shouldn't be a problem, because the kidneys should get rid of the excess sodium in the bloodstream anyway, by leaking it into the urine. Sometimes, however, the kidneys don't do this, or at least don't do enough of it. This problem is called sodium retention. Because excess sodium isn't leaving the body fast enough, it builds up in the blood, the cells transfer water to the bloodstream to dilute the sodium, and blood pressure rises.

Apparently the "salt responders", the people whose blood pressure rises because of excess sodium intake, have a problem with sodium retention. But why would some people have a problem with sodium retention, if a lot of other people don't?

A bit of light appears to have been shed on this question by research that was reported by the American Physiological Society: sodium retention apparently results not merely from a high-sodium diet, but from a diet which is high in both sodium and fructose.

Sugar added to processed foods these days is usually in the form of High-Fructose Corn Syrup, a synthetic sugar which is particularly abundant in soft drinks. The researchers subjected rats to a high-fructose diet, and then introduced a high sodium diet on top of it. The result was a rapid onset of hypertension, in rats given both fructose and sodium (glucose was found not to have this effect).

It is always tricky to draw conclusions about human health based on rat physiology, but the evidence so far suggests that people whose blood pressure rises in response to high sodium intake might not have that problem if their intake of fructose were lower.

People with diabetes probably don't need a new reason to shun processed foods containing HFCS, but they've got one anyway! Avoid sweetened drinks, and the other products that processed-food companies like to sneak it into, and you might be able to eat your favorite salty foods without having your blood pressure get out of control!

Of course, it's worthless just to say that. Experimental confirmation is always needed. If you can control your blood pressure without going on a low-sodium diet (by avoiding HFCS, or by any other means), go with that. If it doesn't work, ask your doctor what else can be done.

 


Good News, Bad News

The good news: the University of California at Irvine finds that diabetes patents who control blood sugar, blood pressure, and LDL-cholesterol levels within guidelines reduce their risk of cardiovascular disease by 62%.

The bad news is that only 7% of us are actually doing that.

 


Join the club!

If misery truly loves company, diabetes patients have much to celebrate: diabetes rates worldwide have quadrupled since 1980. There are now about 450 million diabetes patients on the planet.

This isn't just an artifact of population growth. Diabetes prevalence has increased much faster than the population has.

Judging by the map, diabetes prevalence is highest in those countries that most Americans would rather not visit, and lowest in those countries that most Americans are considering emigrating to, in the event that an obnoxious rich guy who is famous for being famous becomes president.

 


1st Thursday Update

April 7, 2016

 


Salt plus sugar is worse than salt alone!

Most of us are aware, in a vague sort of way, that hypertension (high blood pressure) is connected with sodium intake from salty foods. We're aware that a lot of doctors and medical associations think the human diet has become far too sodium-rich, and that hypertension has become a widespread problem as a result. We're aware that we're being asked to adopt a much less salty diet for this reason. We're also aware that we don't want to do anything of the kind. Nature designed us to crave salt, because in a state of nature it's hard to get enough of it. In the supermarket, however, it's easy to get more than enough of it -- and we do.

Most of the sodium in our diet doesn't come from the salt-shaker, or even from the foods we usually think of as salty. Most of it comes from processed foods (such as bread and soup), which can have extraordinary amounts of salt added to them without our being conscious of it. I have in front of me a very small can (5.5 ounces) of V8 Spicy Hot Vegetable Juice. It contains 450 milligrams of sodium -- which is 20% of the maximum safe daily intake of sodium as defined by the Food and Drug Administration. (They recommend keeping one's daily intake under 2300 mg, but the average American takes in 3400.)

The trouble is, it's easy to get used to a high level of saltiness in food, and after that point any food containing less than the amount of salt we expect seems unacceptably bland. Makers of processed foods have got into a kind of arms race in regard to saltiness -- they dare not fall behind the competition in delivering a major sodium payload to the consumer. Anyone who tries to cut down on daily sodium intake is going to have a hard time finding low-sodium foods (and is pretty sure to complain about the dullness of what he does find).

Diabetes patients, having already been asked to cut carbs, tend to be less than enthusiastic about cutting sodium as well. We know, of course, that hypertension is one of the health problems commonly associated with Type 2 diabetes, and that it contributes greatly to the elevated cardiac risk that diabetes patients face in general. We know that diabetes patients have more reason than anybody else to be vigilant about keeping blood pressure under control. And yet, it's hard not to take a defiant attitude on the sodium issue. One is tempted to protest: "I'm already sacrificing French fries and garlic bread and bananas, but that's not enough for you, is it? No, you won't be satisfied until you take away my chicken-broth, too! Is there anything else you want me to do without? Oxygen, maybe?".

It is especially galling to be asked to cut sodium intake when it's known that "salt responders" (people whose blood pressure is driven upwards by dietary sodium) are a minority within the population, so we're all being asked to cut sodium without knowing if we're one of the people for whom it will make a difference. One is tempted (by which I mean I am tempted) to ignore the whole issue, on the grounds that there's a good chance it's not irrelevant anyway.

The interesting question here, at least to me, is why sodium would ever have anything to do with blood pressure -- and why it would cause hypertension for some people and not others.

The explanation turns out to be related to "osmotic pressure" -- the difficult-to-grasp phenomenon which causes the concentration of anything dissolved in fluid to equalize itself on either side of a permeable membrane. When the sodium concentration in the bloodstream goes up, the cells try to dilute it by releasing extra water into the bloodstream. This increases the total fluid volume of the bloodstream -- and therefore increases blood pressure.

This shouldn't be a problem, because the kidneys should get rid of the excess sodium in the bloodstream anyway, by leaking it into the urine. Sometimes, however, the kidneys don't do this, or at least don't do enough of it. This problem is called sodium retention. Because excess sodium isn't leaving the body fast enough, it builds up in the blood, the cells transfer water to the bloodstream to dilute the sodium, and blood pressure rises.

Apparently the "salt responders", the people whose blood pressure rises because of excess sodium intake, have a problem with sodium retention. But why would some people have a problem with sodium retention, if a lot of other people don't?

A bit of light appears to have been shed on this question by research that was reported by the American Physiological Society: sodium retention apparently results not merely from a high-sodium diet, but from a diet which is high in both sodium and fructose.

Sugar added to processed foods these days is usually in the form of High-Fructose Corn Syrup, a synthetic sugar which is particularly abundant in soft drinks. The researchers subjected rats to a high-fructose diet, and then introduced a high sodium diet on top of it. The result was a rapid onset of hypertension, in rats given both fructose and sodium (glucose was found not to have this effect).

It is always tricky to draw conclusions about human health based on rat physiology, but the evidence so far suggests that people whose blood pressure rises in response to high sodium intake might not have that problem if their intake of fructose were lower.

People with diabetes probably don't need a new reason to shun processed foods containing HFCS, but they've got one anyway! Avoid sweetened drinks, and the other products that processed-food companies like to sneak it into, and you might be able to eat your favorite salty foods without having your blood pressure get out of control!

Of course, it's worthless just to say that. Experimental confirmation is always needed. If you can control your blood pressure without going on a low-sodium diet (by avoiding HFCS, or by any other means), go with that. If it doesn't work, ask your doctor what else can be done.

 


Good News, Bad News

The good news: the University of California at Irvine finds that diabetes patents who control blood sugar, blood pressure, and LDL-cholesterol levels within guidelines reduce their risk of cardiovascular disease by 62%.

The bad news is that only 7% of us are actually doing that.

 


Join the club!

If misery truly loves company, diabetes patients have much to celebrate: diabetes rates worldwide have quadrupled since 1980. There are now about 450 million diabetes patients on the planet.

This isn't just an artifact of population growth. Diabetes prevalence has increased much faster than the population has.

Judging by the map, diabetes prevalence is highest in those countries that most Americans would rather not visit, and lowest in those countries that most Americans are considering emigrating to, in the event that an obnoxious rich guy who is famous for being famous becomes president.

 



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