The best thing is to sip clear liquids at first (Gatorade light isn’t a bad choice), then I like to move on to bouillon.

A diet of whole foods would be high in magnesium and potassium. But a diet high in refined carbs, especially sugars, is not only low in magnesium but the resulting high BG levels which will cause a loss of what little magnesium is in the food. In addition, if a grain allergy has resulted in long term polyuria and urinary urgency such as I suffered with for many years then one can become chronically magnesium deficient. I realize now that for all these years I was leaking magnesium like crazy every time I urinated. The problem is that unless one figures it out like I did it is unlikely that any health care professional will clue in.

One of the strongest indications I had of the existence of a serious magnesium deficiency was heart palpitations so strong at times that they literally shook my whole body. My grandmother also suffered from such palpitations which suggests that I may have a genetic requirement for more than normal amounts of magnesium. One of the first things I remember as an infant was hearing my heart pounding in my sleep.

Now after several months on high doses of magnesium I am free for the first time of any palpitations so much so that I can’t even feel my heart beating when I place my hand over it on my chest. In addition, a chronic problem of dry flaking skin and spotty inflammation on my face that I have had since I was a teenager has also cleared up so remarkably so that people have started to comment on how young I look.

Before I started taking high doses of magnesium I took large doses of potassium with no effect whatsoever on my BP.

Interesting history. Thanks for passing it along.

From what I have read on magnesium if cellular magnesium levels are low and one is also deficient in potassium the magnesium balance must become positive before potassium will have any significant effect on BP. In terms of magnesium and its effect on hypertension when it is a factor it seems to take fairly large doses of supplemental magnesium to have an effect (about 800 mg/day). A lot of research intended to determine magnesium’s effect on hypertension failed because the dose was too low and/or forms of magnesium such as magnesium oxide were used.

There was also at least one study where magnesium was given to one group of subjects and an anti-hypertensive medication was given to another to see if they would lower BP. Both groups had normal BP at the start of the study. As would be expected the medication lowered BP but the magnesium supplement did not. The researchers then concluded that magnesium has no effect on BP. But they forgot to stipulate ‘in subjects with normal BP”.

I can’t imagine how someone could get plenty of dietary potassium and not get plenty of magnesium. It could happen, of course, with supplementation. But a whole-food diet high in potassium should be pretty high in magnesium as well.

So I’m eating dinner with some friends last night, and we begin to get into an argument over red meat. Of the three other people there, one says he has scaled it down because he has heard it causes cancer if eaten too much. The other two say that is true and that red meat causes cancer. I begin to argue with the other two that humans have been eating meat, including cows, for a long time, and people didn’t get colon cancer like they do today, hundreds of years ago. They argue with me that it only increases your risk, and that genetics plays into it, as well. They think that because one graduated having studied oncology pharmacology (or some variation of those terms) and the other biology, that gives them a better understanding of these studies (which I personally doubt they have read) and thus the ability to say red meat is bad. We came to a dead end when I refused to agree with them. Now, I haven’t seen the study or studies they claim are recent and in fairly respectable journals, but knowing you and your wife’s work, and your blog here, I felt justified in blindly disregarding their claims. I cannot tell you what a frustrating experience it was, however, especially having no information to directly argue their points. I can only imagine what you two have gone through in arguing yours. Have you recently read or addressed any of these studies that have come out? I can’t point to any specific ones (though I could try to call their bluff and tell them to point me to the correct ones) and have you had any opinions on them if so? I was just so mad; I need to get back at them! Haha. Thanks!

Just ask them to direct you to the studies they believe show that red meat causes cancer. If they are able to muster up any studies, I’m certain that they will be epidemiologic (observational) studies, which are meaningless in terms of proving causation. Epidemiologic studies can be used only the develop hypotheses, not to demonstrate causality. And they can be fudged in oh so many ways as to make them totally unreliable for anything other than for people who don’t do real science to get their names on published papers. In order to prove that red meat causes cancer, researchers would have to gather a group of subjects, randomize them into a red meat group and a non-red meat group, feed them their respective diets for a number of years, then see who gets cancer and who doesn’t. No such studies have been done, nor are such studies likely to ever be done. In the absence of such studies, there can be no proof that red meat causes cancer irrespective of how many worthless epidemiologic studies show that it does. For what they’re worth, here are a couple of epidemiologic studies that show that meat should be part of a healthy diet. (You can get free full text of these studies by clicking on pdf in the upper right.) And these come from one of the Nature family of journals. Since Nature is probably the world’s most prestigious scientific journal, it will be hard to discount them by saying that these studies are from second class journals.

Exactly. But I think the system exists mainly to handle exogenous glucose loads as opposed to endogenous glucose loads generated through gluconeogenesis. The fact that no one seems to be talking about this process suggests that not much consideration has been given to it. But I think it deserves more attention.

Think about what happens when teenager with a robust BG management system consumes a typical lunch consisting of several hundred grams of carbs from a large order of fries drowned in ketchup, a giant burger, 2 or 3 16 ounce (or larger) soft drinks and a giant sundae for dessert. You talked about this in an earlier post where people in line for food keep filling up their large cups with Coke or whatever. A meal like this would dump about 40 teaspoons of sugar into the digestive system of which a good part of it may be quickly absorbed glucose in the form of liquid sugar.

A potent first phase insulin response would blunt the initial glucose surge and keep BG under 140 mg/dl. Within 3 hours (maybe less) BG would back to the baseline of 85 mg/dl. As I understand the process the first and then the second phase insulin responses drove the glucose into the cells. Assuming the teenager was sitting around socializing with his friends he would not be burning more than maybe 6-7 grams of glucose per hour (1.5 teaspoons). So where did the rest of the 140 grams of sugar go? We know that the fructose went to the liver for processing. But if half the load was unbound glucose from HFCS this still leaves 60 grams of glucose. After insulin drove the glucose into the cells it had to have been converted to glycogen. But there has to be a limit on the rate at which glucose can be converted to glycogen. If the cells can’t convert glucose fast enough then one of the options available would be to start blocking (i.e. resisting) the entry glucose.

There is also a limit as to how much glycogen can be stored. You think it is around 200-300 grams. You could be right. But has anyone actually researched this? Based on the principles of carbohydrate loading it seems likely that glycogen reserves would be maximal with a high carb intake and minimal when the carb load is low. If so, then this suggests that glycogen reserves and glucoseglycogen conversion exists to manage exogenous glucose loads. If so, what happens when the rate of glucose intake exceeds the functional limits of the first phase insulin response and glucoseglycogen conversion. Not good things I am willing to bet.

I think the system was designed (by the forces of natural selection) to handle endogenous glucose loads, not exogenous. But our modern diet has forced it to try to handle an enormous endogenous glucose load, which is why we have a problem. The very best way to control blood sugars and other parameters of metabolic health is to leave them to the liver to manage. It’s only when we ingest a large load of carbs that the override mechanisms come into play and ultimately fail is if abused enough.

I read your material every day and share the highlights with my wife. Low-carb and no-grain works great for both of us.

In her work my wife encounters a wide range of research in the sciences. We thought you might be interested to know (if you don’t already) that Ross L. Cagan at Mount Sinai has developed Drosophila as a whole animal model system for studing type II diabetes. It turns out the flies develop all kinds of diabetic syndromes as well as aspects of fatty liver, kidney and heart disease when fed a high sucrose diet, but not on high fat or high protein.

fyi.

Thanks. Sounds interesting. I didn’t know the Drosophila model had been developed.

Rash seems to be subsiding after several weeks, it is not troubling me even after yesterdays utter burner of a workout in honor of our dojo holiday party.

@Leslie – I think if it were staph I’d be toast, I seem to be susceptible. Thanks!

-K

http://www.whale.to/v/sandler10.html

Maybe you’ve read it or are aware of the author.

I’ve never read it nor have I heard of the author. It’s pretty old. It does make the correct case for restricting sugar.