At Atomicdust, we have a slight obsession with the television series Lost. The fact that we have more than one image of John Locke hanging around our office should be proof enough, but just in case you’re not sold…

Matt, our resident Lost expert, not only hosts finale parties at the end of each season, but he comes up with invitations, decorations, and videos to accompany them.

That’s right, we said videos.

This isn’t your typical fan video from YouTube. This is not images of Kate and Jack (or Kate and Sawyer, or Sawyer and Juliet or…) set to ‘Endless Love.’ This video has a plot, ‘acting’, and parts of it were even filmed on location in Costa Rica.

Just in time for the big premiere tonight, Matt has released Part One of the Season 6 Finale Video on his blog Matt’s Lost His Mind!

Check it out (and make sure to look for Atomicdust-ers Mike and Matt in starring roles!):
Part One of the LOST Season 6 Finale Video

I got home from work today and I was feeling pretty lazy. I plopped down on the couch and grabbed the remote. I looked to my right and saw the rowing machine staring at me. I didn’t want to get on it, but I had felt that way yesterday and the day before too.

I half heartedly strapped my feet in and began to row.

I only expected to do 10 minutes but I kept pushing and cranked out a full twenty. I actually felt better.

I guess the trick is to just do it. exercise invigorates the mind and body, or so they say…I do actually feel a bit more energetic.

get out there and get on it.

A business trip and a late night pizza commercial derailed me for a bit last week. I got back on it and just crossed the 270 threshold to 269.

If you haven’t read the New York Times Magazine article about low carb dieting here’s a link…

My Ketostix are officially turning pink again.

here’s a recipe for low carb Italian beef.

5lbs beef roast
1/2 jar pepperchinni
5 cloves garlic
1 sm package fresh basil
2 tsp salt

put all of this in a crockpot or a saucepan over low heat and cook for at least three hours. shred with tongs or a fork. Your non low carb friends can eat it on a baguette or rye bread.

Homer Simpson would squeal with delight

Starting tomorrow, the folks at The Wine & Cheese Place will launch a major offensive in the war against vegetarianism. More specifically, they’ll announce the first artisan bacon to be featured in what they deem “the year of the BACON at TWCP.”

But this is just the beginning: TWCP has huge plans, as you may have gathered from the quote. Monthly (or more frequently, depending on demand – c’mon, biweekly!), the stores will feature a new and different artisan bacon in what’s basically a bacon-of-the-month club … except you don’t have to sign up for anything, do any research or pay shipping costs. All you have to do is arrive in time to buy some before it sells out.

According to TWCP, the fastest and surest way to get details is through its blog or Facebook page. As for the bacon to be announced Wednesday? It sounds like a very worthy debut; this will be its initial offering in St. Louis, and it’s gotten rave reviews elsewhere. Otherwise, I’m not telling – because I want to be first in line.

– Dennis Lowery

Via Sauce Magazine

I’ll be there…

Tired of the same old you? Tired of being out of shape and out of luck with the opposite sex? Tired of being overweight and under-attractive?

Yeah! Oh, hello. I’m White Goodman, Owner, Operator, and Founder of Globo Gym America Corp, and I’m here to tell you that you don’t have to be stuck with what ya got.

Here at Globo Gym, we understand that “Ugliness” and “Fatness” are genetic disorders, much like baldness or necrophilia, and it’s only your fault if you don’t hate yourself enough to do something about it.

And that’s where we come in.

Globo Gym employs a highly-trained, quasi-cultural staff of personal alterational specialists. And with our competitively-priced on-site cosmetic surgery, we can turn that Frankenstein you see in the mirror every morning into a Franken-fine!

Of course you’ll still be you in a legal sense, but think of it as a thinner, more attractive, better you than you could ever become without us. How do I know? Well, I’m not only the founder of Globo Gym. I’m also a client.

That’s me. Six years and 600 pounds ago… before I knew how much I hated myself. But that all changed once I founded Globo Gym. But don’t just take my word for it. Listen to these Globo-Gymers tell you how it is.

Someone asked me what my motivation was… I think this scene from Dodgeball pretty much sums it up, “it’s only your fault if you don’t hate yourself enough to do something about it.”

I’ve been on strict low carb since Sunday. I’ve shed 7 lbs and I’m currently at 271.8

last night I had 20 naked drummies from Hooters. delicious.

when I get home I’m going to row for 20 minutes.

I read an interesting article on the New York Times Magazine. I’ve copied it here in its entirety.

Give it a read, you may learn something new.

What if It’s All Been a Big Fat Lie.

by Gary Taubes
If the members of the American medical establishment were to have a collective find-yourself-standing-naked-in-Times-Square-type nightmare, this might be it. They spend 30 years ridiculing Robert Atkins, author of the phenomenally-best-selling ”Dr. Atkins’ Diet Revolution” and ”Dr. Atkins’ New Diet Revolution,” accusing the Manhattan doctor of quackery and fraud, only to discover that the unrepentant Atkins was right all along. Or maybe it’s this: they find that their very own dietary recommendations — eat less fat and more carbohydrates — are the cause of the rampaging epidemic of obesity in America. Or, just possibly this: they find out both of the above are true.

When Atkins first published his ”Diet Revolution” in 1972, Americans were just coming to terms with the proposition that fat — particularly the saturated fat of meat and dairy products — was the primary nutritional evil in the American diet. Atkins managed to sell millions of copies of a book promising that we would lose weight eating steak, eggs and butter to our heart’s desire, because it was the carbohydrates, the pasta, rice, bagels and sugar, that caused obesity and even heart disease. Fat, he said, was harmless.

Atkins allowed his readers to eat ”truly luxurious foods without limit,” as he put it, ”lobster with butter sauce, steak with béarnaise sauce . . . bacon cheeseburgers,” but allowed no starches or refined carbohydrates, which means no sugars or anything made from flour. Atkins banned even fruit juices, and permitted only a modicum of vegetables, although the latter were negotiable as the diet progressed.

Atkins was by no means the first to get rich pushing a high-fat diet that restricted carbohydrates, but he popularized it to an extent that the American Medical Association considered it a potential threat to our health. The A.M.A. attacked Atkins’s diet as a ”bizarre regimen” that advocated ”an unlimited intake of saturated fats and cholesterol-rich foods,” and Atkins even had to defend his diet in Congressional hearings.

Thirty years later, America has become weirdly polarized on the subject of weight. On the one hand, we’ve been told with almost religious certainty by everyone from the surgeon general on down, and we have come to believe with almost religious certainty, that obesity is caused by the excessive consumption of fat, and that if we eat less fat we will lose weight and live longer. On the other, we have the ever-resilient message of Atkins and decades’ worth of best-selling diet books, including ”The Zone,” ”Sugar Busters” and ”Protein Power” to name a few. All push some variation of what scientists would call the alternative hypothesis: it’s not the fat that makes us fat, but the carbohydrates, and if we eat less carbohydrates we will lose weight and live longer.

The perversity of this alternative hypothesis is that it identifies the cause of obesity as precisely those refined carbohydrates at the base of the famous Food Guide Pyramid — the pasta, rice and bread — that we are told should be the staple of our healthy low-fat diet, and then on the sugar or corn syrup in the soft drinks, fruit juices and sports drinks that we have taken to consuming in quantity if for no other reason than that they are fat free and so appear intrinsically healthy. While the low-fat-is-good-health dogma represents reality as we have come to know it, and the government has spent hundreds of millions of dollars in research trying to prove its worth, the low-carbohydrate message has been relegated to the realm of unscientific fantasy.

Over the past five years, however, there has been a subtle shift in the scientific consensus. It used to be that even considering the possibility of the alternative hypothesis, let alone researching it, was tantamount to quackery by association. Now a small but growing minority of establishment researchers have come to take seriously what the low-carb-diet doctors have been saying all along. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health, may be the most visible proponent of testing this heretic hypothesis. Willett is the de facto spokesman of the longest-running, most comprehensive diet and health studies ever performed, which have already cost upward of $100 million and include data on nearly 300,000 individuals. Those data, says Willett, clearly contradict the low-fat-is-good-health message ”and the idea that all fat is bad for you; the exclusive focus on adverse effects of fat may have contributed to the obesity epidemic.”

These researchers point out that there are plenty of reasons to suggest that the low-fat-is-good-health hypothesis has now effectively failed the test of time. In particular, that we are in the midst of an obesity epidemic that started around the early 1980’s, and that this was coincident with the rise of the low-fat dogma. (Type 2 diabetes, the most common form of the disease, also rose significantly through this period.) They say that low-fat weight-loss diets have proved in clinical trials and real life to be dismal failures, and that on top of it all, the percentage of fat in the American diet has been decreasing for two decades. Our cholesterol levels have been declining, and we have been smoking less, and yet the incidence of heart disease has not declined as would be expected. ”That is very disconcerting,” Willett says. ”It suggests that something else bad is happening.”

The science behind the alternative hypothesis can be called Endocrinology 101, which is how it’s referred to by David Ludwig, a researcher at Harvard Medical School who runs the pediatric obesity clinic at Children’s Hospital Boston, and who prescribes his own version of a carbohydrate-restricted diet to his patients. Endocrinology 101 requires an understanding of how carbohydrates affect insulin and blood sugar and in turn fat metabolism and appetite. This is basic endocrinology, Ludwig says, which is the study of hormones, and it is still considered radical because the low-fat dietary wisdom emerged in the 1960’s from researchers almost exclusively concerned with the effect of fat on cholesterol and heart disease. At the time, Endocrinology 101 was still underdeveloped, and so it was ignored. Now that this science is becoming clear, it has to fight a quarter century of anti-fat prejudice.

The alternative hypothesis also comes with an implication that is worth considering for a moment, because it’s a whopper, and it may indeed be an obstacle to its acceptance. If the alternative hypothesis is right — still a big ”if” — then it strongly suggests that the ongoing epidemic of obesity in America and elsewhere is not, as we are constantly told, due simply to a collective lack of will power and a failure to exercise. Rather it occurred, as Atkins has been saying (along with Barry Sears, author of ”The Zone”), because the public health authorities told us unwittingly, but with the best of intentions, to eat precisely those foods that would make us fat, and we did. We ate more fat-free carbohydrates, which, in turn, made us hungrier and then heavier. Put simply, if the alternative hypothesis is right, then a low-fat diet is not by definition a healthy diet. In practice, such a diet cannot help being high in carbohydrates, and that can lead to obesity, and perhaps even heart disease. ”For a large percentage of the population, perhaps 30 to 40 percent, low-fat diets are counterproductive,” says Eleftheria Maratos-Flier, director of obesity research at Harvard’s prestigious Joslin Diabetes Center. ”They have the paradoxical effect of making people gain weight.”

Scientists are still arguing about fat, despite a century of research, because the regulation of appetite and weight in the human body happens to be almost inconceivably complex, and the experimental tools we have to study it are still remarkably inadequate. This combination leaves researchers in an awkward position. To study the entire physiological system involves feeding real food to real human subjects for months or years on end, which is prohibitively expensive, ethically questionable (if you’re trying to measure the effects of foods that might cause heart disease) and virtually impossible to do in any kind of rigorously controlled scientific manner. But if researchers seek to study something less costly and more controllable, they end up studying experimental situations so oversimplified that their results may have nothing to do with reality. This then leads to a research literature so vast that it’s possible to find at least some published research to support virtually any theory. The result is a balkanized community — ‘’splintered, very opinionated and in many instances, intransigent,” says Kurt Isselbacher, a former chairman of the Food and Nutrition Board of the National Academy of Science — in which researchers seem easily convinced that their preconceived notions are correct and thoroughly uninterested in testing any other hypotheses but their own.

What’s more, the number of misconceptions propagated about the most basic research can be staggering. Researchers will be suitably scientific describing the limitations of their own experiments, and then will cite something as gospel truth because they read it in a magazine. The classic example is the statement heard repeatedly that 95 percent of all dieters never lose weight, and 95 percent of those who do will not keep it off. This will be correctly attributed to the University of Pennsylvania psychiatrist Albert Stunkard, but it will go unmentioned that this statement is based on 100 patients who passed through Stunkard’s obesity clinic during the Eisenhower administration.

With these caveats, one of the few reasonably reliable facts about the obesity epidemic is that it started around the early 1980’s. According to Katherine Flegal, an epidemiologist at the National Center for Health Statistics, the percentage of obese Americans stayed relatively constant through the 1960’s and 1970’s at 13 percent to 14 percent and then shot up by 8 percentage points in the 1980’s. By the end of that decade, nearly one in four Americans was obese. That steep rise, which is consistent through all segments of American society and which continued unabated through the 1990’s, is the singular feature of the epidemic. Any theory that tries to explain obesity in America has to account for that. Meanwhile, overweight children nearly tripled in number. And for the first time, physicians began diagnosing Type 2 diabetes in adolescents. Type 2 diabetes often accompanies obesity. It used to be called adult-onset diabetes and now, for the obvious reason, is not.

So how did this happen? The orthodox and ubiquitous explanation is that we live in what Kelly Brownell, a Yale psychologist, has called a ”toxic food environment” of cheap fatty food, large portions, pervasive food advertising and sedentary lives. By this theory, we are at the Pavlovian mercy of the food industry, which spends nearly $10 billion a year advertising unwholesome junk food and fast food. And because these foods, especially fast food, are so filled with fat, they are both irresistible and uniquely fattening. On top of this, so the theory goes, our modern society has successfully eliminated physical activity from our daily lives. We no longer exercise or walk up stairs, nor do our children bike to school or play outside, because they would prefer to play video games and watch television. And because some of us are obviously predisposed to gain weight while others are not, this explanation also has a genetic component — the thrifty gene. It suggests that storing extra calories as fat was an evolutionary advantage to our Paleolithic ancestors, who had to survive frequent famine. We then inherited these ”thrifty” genes, despite their liability in today’s toxic environment.

This theory makes perfect sense and plays to our puritanical prejudice that fat, fast food and television are innately damaging to our humanity. But there are two catches. First, to buy this logic is to accept that the copious negative reinforcement that accompanies obesity — both socially and physically — is easily overcome by the constant bombardment of food advertising and the lure of a supersize bargain meal. And second, as Flegal points out, little data exist to support any of this. Certainly none of it explains what changed so significantly to start the epidemic. Fast-food consumption, for example, continued to grow steadily through the 70’s and 80’s, but it did not take a sudden leap, as obesity did.

As far as exercise and physical activity go, there are no reliable data before the mid-80’s, according to William Dietz, who runs the division of nutrition and physical activity at the Centers for Disease Control; the 1990’s data show obesity rates continuing to climb, while exercise activity remained unchanged. This suggests the two have little in common. Dietz also acknowledged that a culture of physical exercise began in the United States in the 70’s — the ”leisure exercise mania,” as Robert Levy, director of the National Heart, Lung and Blood Institute, described it in 1981 — and has continued through the present day.

As for the thrifty gene, it provides the kind of evolutionary rationale for human behavior that scientists find comforting but that simply cannot be tested. In other words, if we were living through an anorexia epidemic, the experts would be discussing the equally untestable ‘’spendthrift gene” theory, touting evolutionary advantages of losing weight effortlessly. An overweight homo erectus, they’d say, would have been easy prey for predators.

It is also undeniable, note students of Endocrinology 101, that mankind never evolved to eat a diet high in starches or sugars. ”Grain products and concentrated sugars were essentially absent from human nutrition until the invention of agriculture,” Ludwig says, ”which was only 10,000 years ago.” This is discussed frequently in the anthropology texts but is mostly absent from the obesity literature, with the prominent exception of the low-carbohydrate-diet books.

What’s forgotten in the current controversy is that the low-fat dogma itself is only about 25 years old. Until the late 70’s, the accepted wisdom was that fat and protein protected against overeating by making you sated, and that carbohydrates made you fat. In ”The Physiology of Taste,” for instance, an 1825 discourse considered among the most famous books ever written about food, the French gastronome Jean Anthelme Brillat-Savarin says that he could easily identify the causes of obesity after 30 years of listening to one ‘’stout party” after another proclaiming the joys of bread, rice and (from a ”particularly stout party”) potatoes. Brillat-Savarin described the roots of obesity as a natural predisposition conjuncted with the ”floury and feculent substances which man makes the prime ingredients of his daily nourishment.” He added that the effects of this fecula — i.e., ”potatoes, grain or any kind of flour” — were seen sooner when sugar was added to the diet.

This is what my mother taught me 40 years ago, backed up by the vague observation that Italians tended toward corpulence because they ate so much pasta. This observation was actually documented by Ancel Keys, a University of Minnesota physician who noted that fats ”have good staying power,” by which he meant they are slow to be digested and so lead to satiation, and that Italians were among the heaviest populations he had studied. According to Keys, the Neapolitans, for instance, ate only a little lean meat once or twice a week, but ate bread and pasta every day for lunch and dinner. ”There was no evidence of nutritional deficiency,” he wrote, ”but the working-class women were fat.”

By the 70’s, you could still find articles in the journals describing high rates of obesity in Africa and the Caribbean where diets contained almost exclusively carbohydrates. The common thinking, wrote a former director of the Nutrition Division of the United Nations, was that the ideal diet, one that prevented obesity, snacking and excessive sugar consumption, was a diet ”with plenty of eggs, beef, mutton, chicken, butter and well-cooked vegetables.” This was the identical prescription Brillat-Savarin put forth in 1825.

It was Ancel Keys, paradoxically, who introduced the low-fat-is-good-health dogma in the 50’s with his theory that dietary fat raises cholesterol levels and gives you heart disease. Over the next two decades, however, the scientific evidence supporting this theory remained stubbornly ambiguous. The case was eventually settled not by new science but by politics. It began in January 1977, when a Senate committee led by George McGovern published its ”Dietary Goals for the United States,” advising that Americans significantly curb their fat intake to abate an epidemic of ”killer diseases” supposedly sweeping the country. It peaked in late 1984, when the National Institutes of Health officially recommended that all Americans over the age of 2 eat less fat. By that time, fat had become ”this greasy killer” in the memorable words of the Center for Science in the Public Interest, and the model American breakfast of eggs and bacon was well on its way to becoming a bowl of Special K with low-fat milk, a glass of orange juice and toast, hold the butter — a dubious feast of refined carbohydrates.

In the intervening years, the N.I.H. spent several hundred million dollars trying to demonstrate a connection between eating fat and getting heart disease and, despite what we might think, it failed. Five major studies revealed no such link. A sixth, however, costing well over $100 million alone, concluded that reducing cholesterol by drug therapy could prevent heart disease. The N.I.H. administrators then made a leap of faith. Basil Rifkind, who oversaw the relevant trials for the N.I.H., described their logic this way: they had failed to demonstrate at great expense that eating less fat had any health benefits. But if a cholesterol-lowering drug could prevent heart attacks, then a low-fat, cholesterol-lowering diet should do the same. ”It’s an imperfect world,” Rifkind told me. ”The data that would be definitive is ungettable, so you do your best with what is available.”

Some of the best scientists disagreed with this low-fat logic, suggesting that good science was incompatible with such leaps of faith, but they were effectively ignored. Pete Ahrens, whose Rockefeller University laboratory had done the seminal research on cholesterol metabolism, testified to McGovern’s committee that everyone responds differently to low-fat diets. It was not a scientific matter who might benefit and who might be harmed, he said, but ”a betting matter.” Phil Handler, then president of the National Academy of Sciences, testified in Congress to the same effect in 1980. ”What right,” Handler asked, ”has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?”

Nonetheless, once the N.I.H. signed off on the low-fat doctrine, societal forces took over. The food industry quickly began producing thousands of reduced-fat food products to meet the new recommendations. Fat was removed from foods like cookies, chips and yogurt. The problem was, it had to be replaced with something as tasty and pleasurable to the palate, which meant some form of sugar, often high-fructose corn syrup. Meanwhile, an entire industry emerged to create fat substitutes, of which Procter & Gamble’s olestra was first. And because these reduced-fat meats, cheeses, snacks and cookies had to compete with a few hundred thousand other food products marketed in America, the industry dedicated considerable advertising effort to reinforcing the less-fat-is-good-health message. Helping the cause was what Walter Willett calls the ”huge forces” of dietitians, health organizations, consumer groups, health reporters and even cookbook writers, all well-intended missionaries of healthful eating.

Few experts now deny that the low-fat message is radically oversimplified. If nothing else, it effectively ignores the fact that unsaturated fats, like olive oil, are relatively good for you: they tend to elevate your good cholesterol, high-density lipoprotein (H.D.L.), and lower your bad cholesterol, low-density lipoprotein (L.D.L.), at least in comparison to the effect of carbohydrates. While higher L.D.L. raises your heart-disease risk, higher H.D.L. reduces it.

What this means is that even saturated fats — a k a, the bad fats — are not nearly as deleterious as you would think. True, they will elevate your bad cholesterol, but they will also elevate your good cholesterol. In other words, it’s a virtual wash. As Willett explained to me, you will gain little to no health benefit by giving up milk, butter and cheese and eating bagels instead.

But it gets even weirder than that. Foods considered more or less deadly under the low-fat dogma turn out to be comparatively benign if you actually look at their fat content. More than two-thirds of the fat in a porterhouse steak, for instance, will definitively improve your cholesterol profile (at least in comparison with the baked potato next to it); it’s true that the remainder will raise your L.D.L., the bad stuff, but it will also boost your H.D.L. The same is true for lard. If you work out the numbers, you come to the surreal conclusion that you can eat lard straight from the can and conceivably reduce your risk of heart disease.

The crucial example of how the low-fat recommendations were oversimplified is shown by the impact — potentially lethal, in fact — of low-fat diets on triglycerides, which are the component molecules of fat. By the late 60’s, researchers had shown that high triglyceride levels were at least as common in heart-disease patients as high L.D.L. cholesterol, and that eating a low-fat, high-carbohydrate diet would, for many people, raise their triglyceride levels, lower their H.D.L. levels and accentuate what Gerry Reaven, an endocrinologist at Stanford University, called Syndrome X. This is a cluster of conditions that can lead to heart disease and Type 2 diabetes.

It took Reaven a decade to convince his peers that Syndrome X was a legitimate health concern, in part because to accept its reality is to accept that low-fat diets will increase the risk of heart disease in a third of the population. ”Sometimes we wish it would go away because nobody knows how to deal with it,” said Robert Silverman, an N.I.H. researcher, at a 1987 N.I.H. conference. ”High protein levels can be bad for the kidneys. High fat is bad for your heart. Now Reaven is saying not to eat high carbohydrates. We have to eat something.”

Surely, everyone involved in drafting the various dietary guidelines wanted Americans simply to eat less junk food, however you define it, and eat more the way they do in Berkeley, Calif. But we didn’t go along. Instead we ate more starches and refined carbohydrates, because calorie for calorie, these are the cheapest nutrients for the food industry to produce, and they can be sold at the highest profit. It’s also what we like to eat. Rare is the person under the age of 50 who doesn’t prefer a cookie or heavily sweetened yogurt to a head of broccoli.

”All reformers would do well to be conscious of the law of unintended consequences,” says Alan Stone, who was staff director for McGovern’s Senate committee. Stone told me he had an inkling about how the food industry would respond to the new dietary goals back when the hearings were first held. An economist pulled him aside, he said, and gave him a lesson on market disincentives to healthy eating: ”He said if you create a new market with a brand-new manufactured food, give it a brand-new fancy name, put a big advertising budget behind it, you can have a market all to yourself and force your competitors to catch up. You can’t do that with fruits and vegetables. It’s harder to differentiate an apple from an apple.”

Nutrition researchers also played a role by trying to feed science into the idea that carbohydrates are the ideal nutrient. It had been known, for almost a century, and considered mostly irrelevant to the etiology of obesity, that fat has nine calories per gram compared with four for carbohydrates and protein. Now it became the fail-safe position of the low-fat recommendations: reduce the densest source of calories in the diet and you will lose weight. Then in 1982, J.P. Flatt, a University of Massachusetts biochemist, published his research demonstrating that, in any normal diet, it is extremely rare for the human body to convert carbohydrates into body fat. This was then misinterpreted by the media and quite a few scientists to mean that eating carbohydrates, even to excess, could not make you fat — which is not the case, Flatt says. But the misinterpretation developed a vigorous life of its own because it resonated with the notion that fat makes you fat and carbohydrates are harmless.

As a result, the major trends in American diets since the late 70’s, according to the U.S.D.A. agricultural economist Judith Putnam, have been a decrease in the percentage of fat calories and a ”greatly increased consumption of carbohydrates.” To be precise, annual grain consumption has increased almost 60 pounds per person, and caloric sweeteners (primarily high-fructose corn syrup) by 30 pounds. At the same time, we suddenly began consuming more total calories: now up to 400 more each day since the government started recommending low-fat diets.

If these trends are correct, then the obesity epidemic can certainly be explained by Americans’ eating more calories than ever — excess calories, after all, are what causes us to gain weight — and, specifically, more carbohydrates. The question is why?

The answer provided by Endocrinology 101 is that we are simply hungrier than we were in the 70’s, and the reason is physiological more than psychological. In this case, the salient factor — ignored in the pursuit of fat and its effect on cholesterol — is how carbohydrates affect blood sugar and insulin. In fact, these were obvious culprits all along, which is why Atkins and the low-carb-diet doctors pounced on them early.

The primary role of insulin is to regulate blood-sugar levels. After you eat carbohydrates, they will be broken down into their component sugar molecules and transported into the bloodstream. Your pancreas then secretes insulin, which shunts the blood sugar into muscles and the liver as fuel for the next few hours. This is why carbohydrates have a significant impact on insulin and fat does not. And because juvenile diabetes is caused by a lack of insulin, physicians believed since the 20’s that the only evil with insulin is not having enough.

But insulin also regulates fat metabolism. We cannot store body fat without it. Think of insulin as a switch. When it’s on, in the few hours after eating, you burn carbohydrates for energy and store excess calories as fat. When it’s off, after the insulin has been depleted, you burn fat as fuel. So when insulin levels are low, you will burn your own fat, but not when they’re high.

This is where it gets unavoidably complicated. The fatter you are, the more insulin your pancreas will pump out per meal, and the more likely you’ll develop what’s called ”insulin resistance,” which is the underlying cause of Syndrome X. In effect, your cells become insensitive to the action of insulin, and so you need ever greater amounts to keep your blood sugar in check. So as you gain weight, insulin makes it easier to store fat and harder to lose it. But the insulin resistance in turn may make it harder to store fat — your weight is being kept in check, as it should be. But now the insulin resistance might prompt your pancreas to produce even more insulin, potentially starting a vicious cycle. Which comes first — the obesity, the elevated insulin, known as hyperinsulinemia, or the insulin resistance — is a chicken-and-egg problem that hasn’t been resolved. One endocrinologist described this to me as ”the Nobel-prize winning question.”

Insulin also profoundly affects hunger, although to what end is another point of controversy. On the one hand, insulin can indirectly cause hunger by lowering your blood sugar, but how low does blood sugar have to drop before hunger kicks in? That’s unresolved. Meanwhile, insulin works in the brain to suppress hunger. The theory, as explained to me by Michael Schwartz, an endocrinologist at the University of Washington, is that insulin’s ability to inhibit appetite would normally counteract its propensity to generate body fat. In other words, as you gained weight, your body would generate more insulin after every meal, and that in turn would suppress your appetite; you’d eat less and lose the weight.

Schwartz, however, can imagine a simple mechanism that would throw this ”homeostatic” system off balance: if your brain were to lose its sensitivity to insulin, just as your fat and muscles do when they are flooded with it. Now the higher insulin production that comes with getting fatter would no longer compensate by suppressing your appetite, because your brain would no longer register the rise in insulin. The end result would be a physiologic state in which obesity is almost preordained, and one in which the carbohydrate-insulin connection could play a major role. Schwartz says he believes this could indeed be happening, but research hasn’t progressed far enough to prove it. ”It is just a hypothesis,” he says. ”It still needs to be sorted out.”

David Ludwig, the Harvard endocrinologist, says that it’s the direct effect of insulin on blood sugar that does the trick. He notes that when diabetics get too much insulin, their blood sugar drops and they get ravenously hungry. They gain weight because they eat more, and the insulin promotes fat deposition. The same happens with lab animals. This, he says, is effectively what happens when we eat carbohydrates — in particular sugar and starches like potatoes and rice, or anything made from flour, like a slice of white bread. These are known in the jargon as high-glycemic-index carbohydrates, which means they are absorbed quickly into the blood. As a result, they cause a spike of blood sugar and a surge of insulin within minutes. The resulting rush of insulin stores the blood sugar away and a few hours later, your blood sugar is lower than it was before you ate. As Ludwig explains, your body effectively thinks it has run out of fuel, but the insulin is still high enough to prevent you from burning your own fat. The result is hunger and a craving for more carbohydrates. It’s another vicious circle, and another situation ripe for obesity.

The glycemic-index concept and the idea that starches can be absorbed into the blood even faster than sugar emerged in the late 70’s, but again had no influence on public health recommendations, because of the attendant controversies. To wit: if you bought the glycemic-index concept, then you had to accept that the starches we were supposed to be eating 6 to 11 times a day were, once swallowed, physiologically indistinguishable from sugars. This made them seem considerably less than wholesome. Rather than accept this possibility, the policy makers simply allowed sugar and corn syrup to elude the vilification that befell dietary fat. After all, they are fat-free.

Sugar and corn syrup from soft drinks, juices and the copious teas and sports drinks now supply more than 10 percent of our total calories; the 80’s saw the introduction of Big Gulps and 32-ounce cups of Coca-Cola, blasted through with sugar, but 100 percent fat free. When it comes to insulin and blood sugar, these soft drinks and fruit juices — what the scientists call ”wet carbohydrates” — might indeed be worst of all. (Diet soda accounts for less than a quarter of the soda market.)

The gist of the glycemic-index idea is that the longer it takes the carbohydrates to be digested, the lesser the impact on blood sugar and insulin and the healthier the food. Those foods with the highest rating on the glycemic index are some simple sugars, starches and anything made from flour. Green vegetables, beans and whole grains cause a much slower rise in blood sugar because they have fiber, a nondigestible carbohydrate, which slows down digestion and lowers the glycemic index. Protein and fat serve the same purpose, which implies that eating fat can be beneficial, a notion that is still unacceptable. And the glycemic-index concept implies that a primary cause of Syndrome X, heart disease, Type 2 diabetes and obesity is the long-term damage caused by the repeated surges of insulin that come from eating starches and refined carbohydrates. This suggests a kind of unified field theory for these chronic diseases, but not one that coexists easily with the low-fat doctrine.

At Ludwig’s pediatric obesity clinic, he has been prescribing low-glycemic-index diets to children and adolescents for five years now. He does not recommend the Atkins diet because he says he believes such a very low carbohydrate approach is unnecessarily restrictive; instead, he tells his patients to effectively replace refined carbohydrates and starches with vegetables, legumes and fruit. This makes a low-glycemic-index diet consistent with dietary common sense, albeit in a higher-fat kind of way. His clinic now has a nine-month waiting list. Only recently has Ludwig managed to convince the N.I.H. that such diets are worthy of study. His first three grant proposals were summarily rejected, which may explain why much of the relevant research has been done in Canada and in Australia. In April, however, Ludwig received $1.2 million from the N.I.H. to test his low-glycemic-index diet against a traditional low-fat-low-calorie regime. That might help resolve some of the controversy over the role of insulin in obesity, although the redoubtable Robert Atkins might get there first.

The 71-year-old Atkins, a graduate of Cornell medical school, says he first tried a very low carbohydrate diet in 1963 after reading about one in the Journal of the American Medical Association. He lost weight effortlessly, had his epiphany and turned a fledgling Manhattan cardiology practice into a thriving obesity clinic. He then alienated the entire medical community by telling his readers to eat as much fat and protein as they wanted, as long as they ate little to no carbohydrates. They would lose weight, he said, because they would keep their insulin down; they wouldn’t be hungry; and they would have less resistance to burning their own fat. Atkins also noted that starches and sugar were harmful in any event because they raised triglyceride levels and that this was a greater risk factor for heart disease than cholesterol.

Atkins’s diet is both the ultimate manifestation of the alternative hypothesis as well as the battleground on which the fat-versus-carbohydrates controversy is likely to be fought scientifically over the next few years. After insisting Atkins was a quack for three decades, obesity experts are now finding it difficult to ignore the copious anecdotal evidence that his diet does just what he has claimed. Take Albert Stunkard, for instance. Stunkard has been trying to treat obesity for half a century, but he told me he had his epiphany about Atkins and maybe about obesity as well just recently when he discovered that the chief of radiology in his hospital had lost 60 pounds on Atkins’s diet. ”Well, apparently all the young guys in the hospital are doing it,” he said. ”So we decided to do a study.” When I asked Stunkard if he or any of his colleagues considered testing Atkins’s diet 30 years ago, he said they hadn’t because they thought Atkins was ”a jerk” who was just out to make money: this ”turned people off, and so nobody took him seriously enough to do what we’re finally doing.”

In fact, when the American Medical Association released its scathing critique of Atkins’s diet in March 1973, it acknowledged that the diet probably worked, but expressed little interest in why. Through the 60’s, this had been a subject of considerable research, with the conclusion that Atkins-like diets were low-calorie diets in disguise; that when you cut out pasta, bread and potatoes, you’ll have a hard time eating enough meat, vegetables and cheese to replace the calories.

That, however, raised the question of why such a low-calorie regimen would also suppress hunger, which Atkins insisted was the signature characteristic of the diet. One possibility was Endocrinology 101: that fat and protein make you sated and, lacking carbohydrates and the ensuing swings of blood sugar and insulin, you stay sated. The other possibility arose from the fact that Atkins’s diet is ”ketogenic.” This means that insulin falls so low that you enter a state called ketosis, which is what happens during fasting and starvation. Your muscles and tissues burn body fat for energy, as does your brain in the form of fat molecules produced by the liver called ketones. Atkins saw ketosis as the obvious way to kick-start weight loss. He also liked to say that ketosis was so energizing that it was better than sex, which set him up for some ridicule. An inevitable criticism of Atkins’s diet has been that ketosis is dangerous and to be avoided at all costs.

When I interviewed ketosis experts, however, they universally sided with Atkins, and suggested that maybe the medical community and the media confuse ketosis with ketoacidosis, a variant of ketosis that occurs in untreated diabetics and can be fatal. ”Doctors are scared of ketosis,” says Richard Veech, an N.I.H. researcher who studied medicine at Harvard and then got his doctorate at Oxford University with the Nobel Laureate Hans Krebs. ”They’re always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man. It’s not normal to have McDonald’s and a delicatessen around every corner. It’s normal to starve.”

Simply put, ketosis is evolution’s answer to the thrifty gene. We may have evolved to efficiently store fat for times of famine, says Veech, but we also evolved ketosis to efficiently live off that fat when necessary. Rather than being poison, which is how the press often refers to ketones, they make the body run more efficiently and provide a backup fuel source for the brain. Veech calls ketones ”magic” and has shown that both the heart and brain run 25 percent more efficiently on ketones than on blood sugar.

The bottom line is that for the better part of 30 years Atkins insisted his diet worked and was safe, Americans apparently tried it by the tens of millions, while nutritionists, physicians, public- health authorities and anyone concerned with heart disease insisted it could kill them, and expressed little or no desire to find out who was right. During that period, only two groups of U.S. researchers tested the diet, or at least published their results. In the early 70’s, J.P. Flatt and Harvard’s George Blackburn pioneered the ”protein-sparing modified fast” to treat postsurgical patients, and they tested it on obese volunteers. Blackburn, who later became president of the American Society of Clinical Nutrition, describes his regime as ”an Atkins diet without excess fat” and says he had to give it a fancy name or nobody would take him seriously. The diet was ”lean meat, fish and fowl” supplemented by vitamins and minerals. ”People loved it,” Blackburn recalls. ”Great weight loss. We couldn’t run them off with a baseball bat.” Blackburn successfully treated hundreds of obese patients over the next decade and published a series of papers that were ignored. When obese New Englanders turned to appetite-control drugs in the mid-80’s, he says, he let it drop. He then applied to the N.I.H. for a grant to do a clinical trial of popular diets but was rejected.

The second trial, published in September 1980, was done at the George Washington University Medical Center. Two dozen obese volunteers agreed to follow Atkins’s diet for eight weeks and lost an average of 17 pounds each, with no apparent ill effects, although their L.D.L. cholesterol did go up. The researchers, led by John LaRosa, now president of the State University of New York Downstate Medical Center in Brooklyn, concluded that the 17-pound weight loss in eight weeks would likely have happened with any diet under ”the novelty of trying something under experimental conditions” and never pursued it further.

Now researchers have finally decided that Atkins’s diet and other low-carb diets have to be tested, and are doing so against traditional low-calorie-low-fat diets as recommended by the American Heart Association. To explain their motivation, they inevitably tell one of two stories: some, like Stunkard, told me that someone they knew — a patient, a friend, a fellow physician — lost considerable weight on Atkins’s diet and, despite all their preconceptions to the contrary, kept it off. Others say they were frustrated with their inability to help their obese patients, looked into the low-carb diets and decided that Endocrinology 101 was compelling. ”As a trained physician, I was trained to mock anything like the Atkins diet,” says Linda Stern, an internist at the Philadelphia Veterans Administration Hospital, ”but I put myself on the diet. I did great. And I thought maybe this is something I can offer my patients.”

None of these studies have been financed by the N.I.H., and none have yet been published. But the results have been reported at conferences — by researchers at Schneider Children’s Hospital on Long Island, Duke University and the University of Cincinnati, and by Stern’s group at the Philadelphia V.A. Hospital. And then there’s the study Stunkard had mentioned, led by Gary Foster at the University of Pennsylvania, Sam Klein, director of the Center for Human Nutrition at Washington University in St. Louis, and Jim Hill, who runs the University of Colorado Center for Human Nutrition in Denver. The results of all five of these studies are remarkably consistent. Subjects on some form of the Atkins diet — whether overweight adolescents on the diet for 12 weeks as at Schneider, or obese adults averaging 295 pounds on the diet for six months, as at the Philadelphia V.A. — lost twice the weight as the subjects on the low-fat, low-calorie diets.

In all five studies, cholesterol levels improved similarly with both diets, but triglyceride levels were considerably lower with the Atkins diet. Though researchers are hesitant to agree with this, it does suggest that heart-disease risk could actually be reduced when fat is added back into the diet and starches and refined carbohydrates are removed. ”I think when this stuff gets to be recognized,” Stunkard says, ”it’s going to really shake up a lot of thinking about obesity and metabolism.”

All of this could be settled sooner rather than later, and with it, perhaps, we might have some long-awaited answers as to why we grow fat and whether it is indeed preordained by societal forces or by our choice of foods. For the first time, the N.I.H. is now actually financing comparative studies of popular diets. Foster, Klein and Hill, for instance, have now received more than $2.5 million from N.I.H. to do a five-year trial of the Atkins diet with 360 obese individuals. At Harvard, Willett, Blackburn and Penelope Greene have money, albeit from Atkins’s nonprofit foundation, to do a comparative trial as well.

Should these clinical trials also find for Atkins and his high-fat, low-carbohydrate diet, then the public-health authorities may indeed have a problem on their hands. Once they took their leap of faith and settled on the low-fat dietary dogma 25 years ago, they left little room for contradictory evidence or a change of opinion, should such a change be necessary to keep up with the science. In this light Sam Klein’s experience is noteworthy. Klein is president-elect of the North American Association for the Study of Obesity, which suggests that he is a highly respected member of his community. And yet, he described his recent experience discussing the Atkins diet at medical conferences as a learning experience. ”I have been impressed,” he said, ”with the anger of academicians in the audience. Their response is ‘How dare you even present data on the Atkins diet!’ ”

This hostility stems primarily from their anxiety that Americans, given a glimmer of hope about their weight, will rush off en masse to try a diet that simply seems intuitively dangerous and on which there is still no long-term data on whether it works and whether it is safe. It’s a justifiable fear. In the course of my research, I have spent my mornings at my local diner, staring down at a plate of scrambled eggs and sausage, convinced that somehow, some way, they must be working to clog my arteries and do me in.

After 20 years steeped in a low-fat paradigm, I find it hard to see the nutritional world any other way. I have learned that low-fat diets fail in clinical trials and in real life, and they certainly have failed in my life. I have read the papers suggesting that 20 years of low-fat recommendations have not managed to lower the incidence of heart disease in this country, and may have led instead to the steep increase in obesity and Type 2 diabetes. I have interviewed researchers whose computer models have calculated that cutting back on the saturated fats in my diet to the levels recommended by the American Heart Association would not add more than a few months to my life, if that. I have even lost considerable weight with relative ease by giving up carbohydrates on my test diet, and yet I can look down at my eggs and sausage and still imagine the imminent onset of heart disease and obesity, the latter assuredly to be caused by some bizarre rebound phenomena the likes of which science has not yet begun to describe. The fact that Atkins himself has had heart trouble recently does not ease my anxiety, despite his assurance that it is not diet-related.

This is the state of mind I imagine that mainstream nutritionists, researchers and physicians must inevitably take to the fat-versus-carbohydrate controversy. They may come around, but the evidence will have to be exceptionally compelling. Although this kind of conversion may be happening at the moment to John Farquhar, who is a professor of health research and policy at Stanford University and has worked in this field for more than 40 years. When I interviewed Farquhar in April, he explained why low-fat diets might lead to weight gain and low-carbohydrate diets might lead to weight loss, but he made me promise not to say he believed they did. He attributed the cause of the obesity epidemic to the ”force-feeding of a nation.” Three weeks later, after reading an article on Endocrinology 101 by David Ludwig in the Journal of the American Medical Association, he sent me an e-mail message asking the not-entirely-rhetorical question, ”Can we get the low-fat proponents to apologize?”

Photos: Spaghetti in olive oil: Which one is the culprit? (Lendon Flanagan); From pyramid to pear: The Agriculture Department’s recommendations may be partly responsible for America’s increasing obesity rates. Milk made whole: Is the full-fat kind healthier than skim? (Jennifer Durham/Getty Images)

As part of my New Years resolution to get below 200 lbs I bought myself a new rowing machine.

I’ve been really lazy lately and weighed in at 280 over the holidays. I am officially recommitted to weightless and will keep you all posted with my progress.

I rowed for 20 minutes this morning and felt like I was going to die. It’s going to be a slow start but I’m sure as my lung capacity gets back to normal I’ll be able to do a full hour.

I also started low carb yesterday. Another session on the rower and I should have all of my stored glycogen depleted.

Concept2 Model D Indoor Rowing Machine
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Whether you already row or are considering rowing as a way to keep in shape, cross train for another sport, or compete on the water, the Concept2 Model D indoor rowing machine is a terrific choice. Rowing offers several benefits over other exercises: it exercises your entire body, including the arms, legs, chest, back, and abs; its low-impact rhythm is easy on the knees and ankles; it burns a ton of calories because it uses so many muscle groups; and it relieves stress. The Model D adds to these benefits by offering such features as a quiet flywheel that’s designed to minimize noise while providing the smooth feel of rowing on the water, along with a spiral damper that lets rowers choose the feel of a sleek, fast boat or a slow, heavy boat.

The Model D offers a different rowing experience than the rowing you did as a kid. The difference lies in the sliding seat, which compresses and extends your legs with every stroke, in addition to the more obvious work being done by the back and arms. This promotes both strength and flexibility throughout the wide range of leg and arm motion, while challenging the back in the middle of the stroke and the abs at the end. In addition, customers say that the rhythmic nature of rowing helps clear the head and ease the stress of the day.

The Model D comes with a PM3 performance monitor that accurately tracks your distance, speed, pace, calories, and watts, with five display options for rowers–all data, force curve, rowing with a pace boat, bar chart, and large print. The monitor also provides easy menu-driven operation, letting you access a powerful list of features, including preset and favorite workouts, trials against a previous performance or pace boat, FISH games, animated rowers that teach techniques, and multiple language options. If motivation is what you need, you’ll find it in Concept2’s online challenges, Million Meter Club, and online ranking.

The Model D is also notably comfortable, with an ergonomic handle that allows for a natural arm and hand position; an aluminum rail capped with a stainless-steel track for smooth seat movements; and adjustable Flex-foot footrests. Other details include a removable LogCard that stores your workout data and personal preferences; built-in heart rate monitoring with an optional Polar receiver (sold separately); a USB interface for easy data transfer to a PC or Mac; caster wheels for quick mobility; and a collapsible design for efficient transport and storage.

The Model D requires a footprint of 9 by 4 feet for use and offers a weight capacity of 500 pounds. It also carries a five-year warranty on frame parts and a two-year warranty on moving parts and the monitor.

Manufactured by the company that set the standard in rowing, the Concept2 Model D Indoor Rower delivers proven performance and fitness benefits. Concept2 Indoor Rowers are used worldwide by Olympic athletes, cardiac rehab patients, and every caliber of rower in between. Rowing provides superb total-body cardiovascular conditioning in a smooth impact-free exercise. A great investment, this commercial-grade machine is recommended for home use and supported with free online motivational tools such as the Concept2 online logbook, rowing challenges and training forum. The self-calibrating Performance Monitor (PM3), included with each Model D, displays workout data, five display options, a LogCard to record results, games and more! Every Concept2 Indoor Rower comes with a 30-day money back guarantee and limited 2-year parts, 5-year frame warranty.

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Snoring and obstructive sleep apnoea syndrome are common sleep disorders caused by the collapse of the upper airways. Continuous positive airway pressure therapy is effective, but is not suitable for many patients.

Reports of didgeridoo players experiencing reduced daytime sleepiness and snoring after practising, led experts in Switzerland to test the theory that training of the upper airways by didgeridoo playing can improve these disorders.

They identified 25 patients with moderate obstructive sleep apnoea syndrome and who complained about snoring. Patients were randomly allocated to an intervention group (didgeridoo lessons and daily practice at home for four months) or a control group (remained on a waiting list for lessons).

Compared with the control group, daytime sleepiness and apnoea scores improved significantly in the didgeridoo group. Partners of patients in the didgeridoo group also reported much less sleep disturbance.

Although overall quality of sleep did not differ significantly between groups, a combined analysis of sleep related measures showed a moderate to large effect of didgeridoo playing.

The authors conclude that regular training of the upper airways by didgeridoo playing reduces daytime sleepiness and snoring in people with moderate obstructive sleep apnoea syndrome and also improves the sleep quality of partners.

“Larger trials are needed to confirm our preliminary findings, but our results may give hope to the many people with moderate obstructive sleep apnoea syndrome and snoring, as well as to their partners,” they say.

http://www.bmj.com/cgi/content/full/332/7536/266

The basis of Tabata Training is 4 minutes of intense interval training/circuit training. What you are doing is taking an exercise we’ll use sprints as an example here.

• Sprint as hard as you can for 20 seconds
• Walk for 10 seconds
• Repeat 7 more times for a total of 8 sets.

So what you have is a total of 4 minutes workout time.

Tabata Training can be done with a number of different exercises the idea is to use an exercise that gets the whole body involved or at least the major muscle groups.TabataTraining can be done with Barbells, Dumbells, Kettlebells or just Bodyweight exercises. I’ll give you some other exercises and routines to try in a minute but first let me give you some background and how Tabatas work.

Tabata Training was developed by Izumi Tabata (imagine that) at the National Institute of Fitness and Sports in Tokyo, Japan. They did a study on comparing the effects of moderate intensity endurance(aerobics) and high endurance intermittenttraining(tabata training intervals) on VO2 max and anerobic capacity.

To cut to the results of the study: the moderate intensity group training program produced a significant increase in VO2 max of about 10%, but had no effect on anaerobic capacity. The high intensity group improved their VO2 max by about 14% while anaerobic capacity improved by 28%. The study was done over a six week period. Both groups working out 5 days per week.

It seems athletic performance is better later in the day.

“In the afternoon and evening,” Dr. Smolensky said, “you are in a different biological state.”

http://www.nytimes.com/2009/12/10/health/nutrition/10best.html

One recent study, by the late Thomas Reilly and his colleagues at the Research Institute for Sport and Exercise Sciences at Liverpool John Moores University in England, found that people’s maximum heart rates and sub-maximal heart rates were lower in the morning but that their perception of how hard they were working was the same in the morning as it was later in the day.

Dr. Reilly and his colleague Jim Waterhouse, in a review published this year, also noted that athletes’ best performances, including world records, were typically set in the late afternoon or early evening.

It’s been a while since I posted here on paunchiness.

I’ve been spending my blogging time working on Adventure Canoe. I’ll get back to this blog as the weather gets colder and there is less time for paddling.

Low amounts of vitamin C correlates with increased body fat and waist measurements. Nutrition researchers at Arizona State University report that the amount of vitamin C in the blood is directly related to fat oxidation during both exercise and at rest.

The study shows that those who consume adequate quantities of vitamin C oxidize 30% more fat while doing normal exercises than individuals with an inadequate quantity of Vitamin C consumption.

The research however, does not imply that vitamin C can be considered the new remedy for obesity and the new means of causing weight loss. Rather, it establishes that consuming insufficient quantities of vitamin C is liable to hamper any efforts of weight loss.

Before beginning a controlled four-week diet, 20 obese men and women were randomized by gender and body weight into a Vitamin C group, taking a 500 mg vitamin C daily and a control group taking a placebo. All participants consumed a diet adjusted to promote slow weight loss. The diet contained 67% of the RDA for vitamin C.

At the beginning of the study, participants with the lowest blood concentrations of vitamin C exhibited a higher body fat mass and tended not to oxidize fat well compared to their less obese counterparts. As the participants moved through the four week diet, with a steady amount of vitamin C being consumed, blood vitamin C concentrations increased 30 percent in those taking vitamins and fell 27 percent in the control group whose only vitamin C intake was the 67 percent of the USRDA contained in the food. As vitamin C blood concentrations fell, so did the participants’ ability to oxidize fat.

Vitamin C is an essential cofactor for the biosynthesis of a small protein-like molecule known as carnitine. Carnitine functions to shuttle fat molecules to the site of fat oxidation in tissue cells. When cells do not have access to fat molecules, feelings of fatigue ensue since energy metabolism is affected. Moreover, fat tends to accumulate in tissues when carnitine concentrations are reduced.

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Caitlin started a blog http://www.generalplatitude.com

Check it out for her latest quips about life, watching other people’s babies and getting out of jury duty.

ACA Canoe Instructor Training – Level 3: River Canoeing

I found an interesting article on WebMD today about Fish Oil and Omega-3. I’ve been a long time reader of Mens Health Magazine and they’ve touted the merits of fish oil for a long time.

Check out the following and let me know what you think.

Think all dietary fat is the same? Guess again
By Colette Bouchez
WebMD Weight Loss Clinic-Feature

If you ask folks what food group they should avoid, most will probably answer “fats.” While it’s true that, in large amounts, some types of fat are bad for your health (not to mention your waistline), there are some we simply can’t live without.

Among them are the omega-3 fatty acids, found in foods including walnuts, some fruits and vegetables, and coldwater fish such as herring, mackerel, sturgeon, and anchovies.

“It not only plays a vital role in the health of the membrane of every cell in our body, it also helps protect us from a number of key health threats,” says Laurie Tansman, MS, RD, CDN, a nutritionist at Mount Sinai Medical Center in New York.

The benefits of omega-3s include reducing the risk of heart disease and stroke while helping to reduce symptoms of hypertension, depression, attention deficit hyperactivity disorder (ADHD), joint pain and other rheumatoid problems, as well as certain skin ailments. Some research has even shown that omega-3s can boost the immune system and help protect us from an array of illnesses including Alzheimer’s disease.

Just how do omega-3s perform so many health “miracles” in people? One way, experts say, is by encouraging the production of body chemicals that help control inflammation — in the joints, the bloodstream, and the tissues.

But even as important is their ability to reduce the negative impact of yet another essential type of fatty acid known as omega-6s. Found in foods such as eggs, poultry, cereals, vegetable oils, baked goods, and margarine, omega-6s are also considered essential. They support skin health, lower cholesterol, and help make our blood “sticky” so it is able to clot. But when omega-6s aren’t balanced with sufficient amounts of omega-3s, problems can ensue.

“When blood is too ’sticky,’ it promotes clot formation, and this can increase the risk of heart attack and stroke,” says nutritionist Lona Sandon, RD, a spokeswoman for the American Dietetic Association. But once you add omega-3s to the mix, the risk of heart problems goes down, she tells WebMD.

The latest research shows that the most promising health effects of essential fatty acids are achieved through a proper balance between omega-3s and omega-6s. The ratio to shoot for, experts say, is roughly 4 parts omega-3s to 1 part omega-6s.

Most of us, they say, come up dangerously short.

“The typical American diet has a ratio of around 20 to 1 — 20 omega-6’s to 1 omega-3 — and that spells trouble,” says Sandon, an assistant professor of nutrition at University of Texas Southwestern Medical Center in Dallas. While reducing your intake of omega-6s can help, getting more omega-3s from food is an even better way to go.

How to Get What You Need

Omega-3 fatty acids are not one single nutrient, but a collection of several, including eicosapentaenic acid (EPA) and docosahexanoic acid (DHA). Both are found in greatest abundance in coldwater fish — and that, say experts, is one reason so many of us are deficient.
How to Get What You Need continued…

Over the past several years, the Food and Drug Administration and other groups have issued warnings about mercury and other harmful chemicals found in fish. This has led many people to stop eating fish — a big mistake, Tansman says.

“People have taken the whole FDA advisory out of context including who it’s for, which is primarily pregnant women, and small children,” she says. Moreover, Tansman says, even if you obey the FDA warnings in the strictest sense, the latest advisory says that up to 12 ounces of a variety of fish each week is safe for everyone. That amount, Tansman reminds us, is roughly half of what we need to get enough omega-3s.

“The recommendation [for omega-3s] is two servings of fish a week,” Tansman says. “At 3 to 4 ounces per serving, that’s well below the FDA’s safe limit of 12 ounces per week.”

According to the American Heart Association, those looking to protect their hearts should eat a variety of types of fatty fish (such as salmon, tuna, and mackerel) at least twice a week. Those with heart disease should get 1 gram of omega-3s (containing both EPA and DHA) per day, preferably from fatty fish. About 1.5 ounces of fish contains 1 gram of omega-3s.

But even if you don’t like fish (or choose not to eat it), you can still get what you need from dietary sources. WebMD Weight Loss Clinic “Recipe Doctor” Elaine Magee, MPH, RD, says one answer lies in plants rich in omega-3s — particularly flaxseed.

“It’s safe to say this is the most potent plant source of omega-3,” says Magee, author of The Flax Cookbook. While flaxseed contains no EPA or DHA, Magee says, it’s a rich source of another omega-3 known as alpha-linolenic acid (ALA), which the body can use to make EPA and DHA.

Flaxseed is available in health food stores and many supermarkets, sold as whole seeds, ground seeds, or oil. Although flaxseed oil contains ALA, Magee says ground flaxseed is a much better choice because it also contains 3 grams of fiber per tablespoon, as well as healthy phytoestrogens. Other sources of omega-3s include canola oil, broccoli, cantaloupe, kidney beans, spinach, grape leaves, Chinese cabbage, cauliflower, and walnuts.

“About an ounce — or one handful — of walnuts have about 2.5 grams of omega-3s,” says Sandon. “That’s equal to about 3.5 ounces of salmon.”

Besides getting more omega-3s, you can also help your heart by replacing some omega-6s from cooking oils with a third fatty acid known as omega-9 (oleonic acid). This is a monounsaturated fat found primarily in olive oil.

Though it is not considered “essential” (the body can make some omega-9), by substituting it for oils rich in omega-6s, you can help restore the balance between omega-3s and omega-6s, plus gain some additional health benefits.

“Factors found in olive oil can also help boost the good cholesterol, which can also help your heart,” says Magee.

Supplements vs. Foods

If you’re thinking that maybe the easiest and most low-cal way to get omega-3s is with fish oil capsules, not so fast. Many nutritionists say it’s a bad idea.

“There is something about whole food that when it goes into the body it’s more than 90% absorbed, while [with] a supplement you absorb only about 50%,” says Sandon.

Moreover, says Sandon, because the components of different foods work together, they may offer a more complete and balanced source of nutrients.

“It could be something more than just the omega-3s in fish that make it so healthy,” says Sandon. “It could be the amino acids that provide benefits we are not going to see in fish-oil supplements alone.”

And if you’re thinking fish-oil capsules will help you avoid the contamination risks of fresh fish, think again. Because supplements are not regulated in the U.S., Sandon says, some may contain concentrated amounts of the same toxins found in fresh fish. And because the oil is so concentrated, the supplements can also produce an unpleasant body odor.

More important, experts say, there is a danger of overdosing on fish-oil supplements, particularly if you take more than the recommended amount. Doing so can increase your risk of bleeding or bruising. This isn’t likely to happen when you get your intake from foods.

The one-time fish oil supplements can really help is if you need to reduce your levels of triglycerides, a dangerous blood fat linked to heart disease. The American Heart Association recommends that people with extremely high triglycerides get 2 to 4 daily grams of omega-3s (containing EPA and DHA) in capsules — but only in consultation with their doctors.

“The key here is to never take these supplements without your doctor’s consent,” says Magee. “This is not something you want to fool with on your own.”

The millions that view flab as the most disgusting ingredient of human flesh have, for years, waged war against its presence. Yet, through all their clashes, fat has emerged victorious a dreadful number of times, only to foster the same frustration that ignited so many ill-advised attempts to destroy it. This inevitably has led dieters down two seemingly different paths – one of indulgence, the other, starvation.

The destructive forces of overeating are well chronicled. After numerous failed attempts with dieting gimmicks and bogus potions, succumbing to fast-food fantasies casually becomes a justifiable alternative. In time, a healthy meal plan is as automatic as Homer Simpson’s exercise regimen, and a steady diet of McDonald’s combo platters is an insurmountable addiction. Thus, it is not surprising that America exhibits such extraordinary health problems, the likes of which have done little to avert those whose diets contribute to the soaring obesity that shackles an appreciable physique. If you truly are what you eat, then 50 million Americans are a Big Mac with extra cheese and a large side of fries.

Deceive the Body, and the Body Strikes Back

Though the above example reaches the extremes of a hopeless, carefree cuisine, the results of a starvation diet can also be a disaster of catastrophic proportions. The logic behind it is intuitive: fat is hideous, so eliminate it (and all calories for that matter) from the diet. By this rationale, the dieter assumes that the body has no choice but to begin slashing inches off its carcass. In reality, this is hardly the case. In fact, just the opposite is usually true, such that the body responds by administering its fat strangle-hold even tighter, making the process of weight loss almost impossible.

If the human body could list its top ten most efficient processes, adaptation would probably rank number one. Evolution’s millions of years have shaped the body into a species that is geared not for the production of a slim waist or muscular arms, but for survival. In ages prior, when restaurants were about as plentiful as the wheel, periods of famine prevailed. Yet, so did the human race. The catch, unfortunately, is that those with a considerable propensity to store fat survived. Thus, the twentieth-century version of our ancestors is one that has adapted to years of food shortages through a nauseating ability to maintain a pear-shaped torso. So much for “Survival of the fittest.”

When the innocent dieter initiates a restrictive diet, the conditioned response by the body is to kick into the aforementioned survival mode. This, in essence, is a signal to store fat to offset an anticipated period of deficient caloric intake. Compounding matters is a gradual decline of the body’s metabolism, rendering the process of fat loss even more difficult. The process is no different than any other the body performs when encountering change – it adapts. Instead of perceiving food as the culprit, it should rather be viewed as fuel. Food is fuel for an increasing metabolism, fuel for the release of fat-burning and muscle-building hormones, and finally, fuel for a healthy diet and a normal lifestyle. When food is eaten in the precise amounts, the body again must adapt. This time, however, it adapts to the notion that its needed energy will be granted. When this gift is awarded, the body responds with its own goodwill gesture, a liberation of its suddenly unnecessary fat stores.

Facts and Fallacies of Food

The constituents of all food can be separated into three types: protein, carbohydrates, and fats. Together they form the basis of all diets and, along with exercise, ultimately determine changes in body composition. This is achieved through hormonal release, an increase in metabolism, and the preservation and enhancement of muscle tissue.

Proteins are considered the body’s building blocks for repair, maintenance, and muscular growth. Adequate protein intake ensures the preservation of muscle tissue and enhances recovery from both strenuous workouts and daily activities. Since exercise causes significant damage to muscular tissue and subsequent growth requires adequate recovery, a lack of protein is often the missing factor. Without it, muscle may be spared and appreciable decreases in metabolism will soon follow. This, as illustrated previously, is a splendid method for accumulating a fatty midsection.

Fallacy #1: The RDA for Protein is Sufficient

The recommended daily allowance (RDA) for protein is approximately .36 grams per pound of body weight. Therefore, according to the RDA, a 200 lb. man would require a mere 72 grams of protein daily. This may be sufficient for a sedentary individual like the vice president, but when factoring in strenuous activity such as endurance or weight training, the RDA is grossly inadequate. In fact, research studies have suggested that consuming the RDA for protein during periods of intense training may lead to loss of muscular tissue (17, 10). It is apparent that protein requirements depend on an individualFs activity level, such that a range between .64 and .91g of protein per pound of body weight is appropriate (17, 10).

The body’s primary fuel for energy is derived from carbohydrates. They are especially important for aerobic activities and high-volume weight training, and are also utilized during periods of recovery. As was the case with protein, inadequate intake of carbohydrates can compromise exercise performance and duration. However, carbohydrates have also demonstrated an air of infallibility in the recommendations of most dieticians, though perils do exist even with this vaunted energy source.

Fallacy #2: The More Carbs the Better

Contrary to what is often uttered about the wonderful merits of carbohydrates, the fact remains that excess carbs lead to excess inches. With the exception of the overly lean individual with a speedy metabolism, where weight gain is often the goal, overindulgence of high carbohydrate foods can be as detrimental to waistlines as excess fat. It is often stated that spare carbohydrates are, in large part, stored for energy. However, it is more likely that excess carbohydrates will be converted to body fat (3). Furthermore, studies have shown that identical improvements in body composition, strength, and muscular endurance can be achieved with diets that derive as little as 40% of their calories from carbohydrates versus those that contained over 60% (15, 19). Studies have also repeatedly demonstrated that the sum caloric intake is the predominant factor in weight loss and an elevated carbohydrate intake is not advantageous (1, 7).

It is obvious that fats have endured more than their share of abuse. Saturated fats, in particular, are considered a key contributor to heart disease, an epidemic that has claimed more lives than the flood in Genesis. Fats also carry over twice as many calories per gram than both carbohydrates and protein. Though it is true that an excessive fat intake is the best way to resemble a blimp, it’s also a fact that fat is necessary for proper metabolic function, hormone production, and as an energy source.

Fallacy #3: Avoid Fats Entirely

Most American diets are either too deficient or too abundant in fat intake. As stated previously, neither method is a successful tactic for weight loss. When examining the habits of most restrictive diets, there is a prevailing assumption that all dietary fat can only be deposited to adipose tissue. This is an absurd misconception. In reality, the body utilizes dietary fat for energy in a state of negative energy balance (21). As long as the total caloric intake is less than what is expended, the percentage of fat in the diet is not as significant as once thought. Studies have also affirmed that equivalent differences in weight loss can be achieved with diets consisting of approximately 10-50% fat, as long as the total calorie consumption was identical (1, 7).

With these menacing fallacies of food exposed, it is evident that the low calorie, low fat, high carbohydrate diets that have been advocated for years are in fact fallacies themselves. A long-standing, correct approach to weight loss is the procedure whereby more calories are expended than ingested. Unfortunately, this has formed the basis of extremely low calorie diets, diets that result in the loss of vital muscle tissue and a striking decrease in metabolism. Take, for example, the Slim-Fast diet. This is a nice, convenient drink that is akin to a small cup of milk and copious helpings of sugar. With few calories, a meager appearance by protein, and no fat, the body exhibits a ruthless preservation of adipose tissue, a greater propensity for fat accumulation, and a yearning for real food and a normal life. The low-calorie deception offered by such diets is further augmented by an overload of sugar and similar carbohydrates, yet another frustrating contributor to ballooning belt sizes.

All Carbohydrates are not Created Equal
Now that it’s intuitive to avoid excess carbohydrates, the type of carb must also endure similar scrutiny. Though all carbohydrates are broken down into glucose and released into the bloodstream, the speed at which this process occurs varies drastically with different carbohydrates. Interestingly, this absorption rate is a critical factor in energy levels, fat reduction, and overall health. Fortunately, foods have been assigned a glycemic index, a measure of how fast their carbohydrates enter the bloodstream to be utilized as energy or stored as glycogen (a preserved energy form). High-glycemic foods, therefore, are available quickly for use as energy. Though this may seem optimal, in actuality they trigger a hormonal reaction that has reverse effects.

High-glycemic carbohydrates produce a rush of glucose into the bloodstream, elevating blood sugar levels dramatically. This sudden rise stimulates a release of the hormone insulin, which essentially negates the high-energy effects of glucose. The rapid surge of insulin shuttles the glucose out of the bloodstream, effectively dropping energy levels to lethargic lows. To make matters worse, the insulin also takes the fatty acid energy source with it, shoveling it into fat cells for storage. High-glycemic foods, therefore, exhibit a double curse, keeping consumers fat and lazy.

In the past, it was recommended that foods high in simple sugars (candy, cookies, soft drinks) be avoided for the aforementioned reasons. This is true; however, many revered energy sources are also considered high-glycemic foods. Surprisingly, many kinds of pasta, rice, and potatoes rank rather high on the glycemic index. Many breads and cereals are also offensive, fast enough to zap energy levels and hoard fat like the good-ol’ days of famine and starvation.

The opposite results, fortunately, are available with the ingestion of low-glycemic foods. They provide for more stable energy levels and an attenuated insulin response, favoring the probability of productive workouts and sustained vitality. These foods rank in the below 70 category on the glycemic index chart, which is provided below. All foods are rated according to white bread, which receives a very speedy score of 100. The following is a list of common foods and their respective scores, categorized into three accommodating lists:

High Moderate Low
Instant Rice (128) Ice Cream (87) Grapefruit juice (69)
Crispix cereal (124) Cheese Pizza (86) Green peas (68)
Baked Potato (121) White Rice (83) Grapes (66)
Cornflakes cereal (119) Popcorn (79) Linguine (65)
Rice Krispies cereal (117) Oatmeal Cookies (79) Macaroni (64)
Pretzels (116) Brown Rice (79) Orange (63)
Total cereal (109) Spaghetti, durum (78) Peach (60)
Donut (108) Sweet corn (78) All-Bran cereal (60)
Watermelon (103) Oat Bran (78) Spaghetti, white (59)
Bagel (103) Sweet Potato (77) Apple juice (58)
Cream of Wheat (100) Banana (77) Apple (54)
Grapenuts cereal (96) Special K cereal (77) Vermicelli (50)
Nutri-grain bar (94) Orange juice (74) Barley (49)
Macaroni and Cheese (92) Cheese tortellini (71) Fettucine (46)
Raisins (91) Chocolate (70) Lentils (41)

Table adapted from reference 6.

Since foods are usually eaten in combinations, note that the glycemic index of a meal is usually lower than the glycemic index of the highest constituent. For instance, if equal calories of a bagel and an apple are combined, the glycemic index of that meal becomes a more acceptable 79. Protein also helps matters, such that they efficiently decrease the total glycemic index by slowing the absorption rate of carbohydrates. This emphasizes the importance of combining protein and carbohydrates in each meal.

Food: A Potent Hormone Trigger

As stated, the hazards of one hormone, insulin, are encouraged by the ingestion of high-glycemic foods. While insulin promotes fat storage, a substance known as growth hormone (GH) effectively burns fat, builds muscle, and improves the immune system. This provides another advantage to low-glycemic foods. If low-glycemic foods are emphasized and blood sugar levels remain stable, a positive environment exists for GH to exert its effects (13).

The exploits of the muscle-building hormone testosterone are even more profound. Studies have demonstrated that testosterone is chiefly influenced by the ratios of food in the diet. Therefore, the percentages of protein, carbohydrates, and fat can have dramatic effects on changes in body composition. For instance, for the individual seeking added muscular mass, a low protein to carbohydrate ratio and a moderately high-fat intake are necessary for maximal testosterone output (20, 14). This is not to suggest a reduction in protein intake; rather the percentage of carbohydrates in the diet should be much greater than protein (20). Furthermore, the source of food also influences testosterone concentrations, such that a vegetarian diet produces much lower testosterone levels than a meat-rich diet (12).

A diet high in red-meat, however, is also an abundant source of saturated fat. Though the reasons for avoiding saturated fats are well established, such as their contribution to heart disease, other forms of fat can be quite beneficial for normal metabolism and hormone production. The fats contained in fish, for example, should be emphasized in the diet. In addition, olive, sunflower, and canola oils are rich in monounsaturated fatty acids, a form of fat that is a powerful stimulant of testosterone (20).

Planning the Metamorphosis

Before an appropriate, individualized diet can be incorporated, an accurate reading of body fat percentage must first be performed. Since daily calorie requirements depend both on the amount of lean body mass (all bodily constituents except fat) and activity level of an individual, this is a necessary estimation. This is because of the radically different metabolic processes required to maintain muscle as opposed to fat. Specifically, muscle requires a great deal of energy to sustain it, while fat basically sits (or hangs) there. As a result, the daily calorie intake should be sufficient to maintain muscle, not fat. Therefore, the differences in protein and calorie requirements of two men of the same weight, one at 10% fat and the other at 20%, are astounding.

Once body fat percentage is known, there are three primary stages in developing an ideal calorie level: 1) determine metabolic rate, 2) choose an appropriate protein intake depending on lean body mass, metabolic rate, and activity level, and 3) select a suitable nutrient ratio according to metabolic rate and body composition goals. The following tables provide the completion of all three stages.

Table 1. Fast, Moderate, and Slow Metabolic Rates.

1.Fast – Individuals with a fast metabolic rate exhibit low weight and body fat levels, have trouble gaining muscle, and can generally eat like pigs with no adverse consequences.

2.Moderate – These individuals generally desire to maintain body weight, decrease fat, and slightly increase muscle mass. Excess calorie intake usually results in mild weight increases.

3.Slow – A slow metabolic rate usually equates to a high propensity for weight and fat gain. These individuals desire extensive weight loss.

Note: These estimates are subjective and do not exactly encompass all types of metabolic rates. In reality, everyone is different. It should be emphasized also that varying degrees of all three rates exist. Namely, fast-moderate and moderate-slow metabolic rates are common and can be utilized as intermediaries in the following tables.

Grams of protein required per pound lean body mass Metabolic Rate No Exercise Light Exercise Strenuous Exercise Strenouus Exerices Intense Exercise Fast .6 .8 .9 1.0 1.2 Moederate .5 .7 .8 .9 1.1 Slow .4 .6 .7 .8 1.0

Percentage of Daily Caloric Intake Nutrition Fast Metabolism Moderate Metabolism Slow Metabolism
Protein 17% 22% 27%
Carbohydrates 58% 55% 55%
Fats 25% 23% 21%

Note: One gram of protein or carbohydrate equals four calories, while one gram of fat is equal to nine.

Two Examples

Example 1. This individual is a 5′9″, 140 lb. male with 5% body fat. He exhibits a fast metabolic rate and utilizes intense weight training 4-5 times a week (activity level 4) in an attempt to gain weight. To determine his caloric requirements, simply calculate lean body mass and choose an appropriate protein intake and nutrient ratio.

1. 140 lbs. x 95% lean body mass = 133 lbs. lean tissue
2. This individual would require approximately 1.0g of protein per pound of lean body mass, or 133g daily.
3. Protein would therefore account for 532 calories (133g x 4 calories per gram). He would then utilize a nutrient ratio where protein consisted of 17% of his daily calories, such that 532 divided by 17% would result in the daily calorie intake.
4. 532/.17 = 3129 total calories/day. To determine the amount of carbohydrates and fat, simply multiply this number by their respective percentages. For example, the daily carbohydrate intake would be 1814 calories (3129 x .58), or 454 grams (1814 calories/4 calories per gram). The daily fat intake is 782 calories (3129 x .25), or 87 grams (782 calories/9 calories per gram).
5. Optimally, this person should eat 5-6 meals per day. If 5 meals are consumed, each meal would average approximately 626 calories, in the same ratio of nutrients as described above. Of course, this number will vary, especially since post-workout meals should contain more calories.

Example 2. This individual is a 6′0″, 190 lb. male with 18% body fat. He desires to lose a little weight and a lot of fat to become “toned.” Since he gains weight rapidly if his calorie intake soars too high, he is considered to have a moderate-slow metabolism. He currently trains with weights and runs for thirty minutes five times per week. He would therefore fall between activity levels four and five, requiring approximately .85-1.05 grams of protein per pound of lean body mass.

1. 190 lbs. x 82% lean body mass = 156 lbs. lean tissue
2. 156 lbs. x .95g protein = 148g protein daily
3. Protein would therefore account for 592 calories (148g x 4 calories per gram). A nutrient ratio for an individual with a moderate-slow metabolism would be 24.5% protein, 53.5% carbohydrates, and 22% fat (percentages derived from using the average of moderate and slow metabolism ratios). This individual’s daily calorie intake is determined by dividing 592 by 24.5%, resulting in 2416 calories.

4. Utilizing the same method as outlined in example 1, the daily carbohydrate intake is 1292 calories, or 323 grams. The daily fat intake is 531 calories, or 59 grams.

The Importance of Nutrient Timing

The number and content of daily meals is an extremely important but overlooked facet of proper nutrition. The timing and quality of foods ingested, especially pre- and post-workout, is often the difference between a successful diet and another failed attempt at physique enhancement. Skipping breakfast, avoiding post-workout meals, and consuming high-glycemic carbohydrates before workouts can easily transform a sound meal plan into an unwitting disaster. Interestingly, however, even the most sensible diets ignore the crucial nature of nutrient timing.

As stated numerous times, elevating the metabolic rate is one of the most efficient ways to burn fat. The digestion of meals requires calories by itself, so the more often the body must break down food, the more efficient it becomes. Therefore, small meals should be consumed throughout the day to maximize the metabolic response. Related to this is breakfast, the “most important meal of the day.” Though the post-workout meal may be equally important, the consumption of a large breakfast has been shown to result in significantly greater fat losses than diets that avoided it (8). Since the metabolic rate is fastest in the morning and slows throughout the day, it is more likely that the calories consumed during breakfast will be utilized by the body and not stored as fat. Skipping breakfast, on the other hand, may result in vital losses of muscle and a subsequent decrease in metabolism.

For much the same reason, the post-workout meal is equally essential. Following exercise, the body exhibits an elevated metabolic rate, much like it does upon awakening. A lack of food following exercise, therefore, results in muscle tissue breakdown and, of course, a corresponding tumble of the metabolic rate. Research has proven that the synthetic rate of protein doubles following exercise and remains elevated for over 24 hours (11, 4). In other words, the body is primed for the acceptance of protein for muscle maintenance and growth. Equally important is the ample consumption of carbohydrates. Following exercise, the body is somewhat depleted of its glycogen stores. Remarkably, it has been shown that high-glycemic carbohydrates post-workout are the preferred source to replenish the body’s energy stores (5). Not only does this result in greater storage for recovery and subsequent workouts, but it also significantly decreases muscle breakdown (16).

To obtain the most optimal effects of the previous findings, post-workout meals should contain about twice the normal amount of carbohydrates and protein and should be ingested immediately following exercise. For example, an individual eating five meals per day and 3000 calories would consume a post-exercise meal of approximately 1000 calories, while the other four meals would average 500. All subsequent post-workout meals should also contain a larger percentage of protein than pre-workout meals to comply with the body’s elevated protein synthetic rate.

A final fitness faux pas is the pre-workout meal. How many fitness enthusiasts eat a bagel before exercise? It seems that this is one of the most common pre-workout foods due to its alleged energy benefits. However, look at its glycemic index – it’s a whopping 103. The detrimental effects of this are monumental. The corresponding insulin response will not only decrease energy stores for exercise; it will also prevent fat breakdown at the same time. Fortunately, low-glycemic foods have much the opposite effect. They exhibit the ability to improve exercise performance without significantly compromising energy stores after a workout (9, 18). This, in turn, leads to enhanced recovery and accelerated progress.

A Word About Consistency

A suggested meal plan is not perfect, and individual tinkering will be required to determine the ideal diet. Losing weight too quickly is a sign of muscular and water loss, not necessarily fat loss. Therefore, those individuals should increase their caloric intake slightly. The same is true for similar imperfections; slight modifications are required and variety is encouraged. Remember that the body adapts to all changes, so an identical food and daily caloric intake will not only drive one to insanity, but also to stagnation.

If there is one truth about building an improved physique, it’s that it takes time, dedication, and consistency. Losing or gaining weight should be a slow, gradual process to ensure the changes are of the appropriate type. This is one of the reasons so many diets fail and the gimmicks appear. In the future, everything short of chemotherapy will be offered as the new miracle in weight loss. In time, it too will fall by the wayside and fat will settle hideously to the waistline. And all the while, lurking in reality, is everything short of quitting, the true miracle in physique excellence.

About the Author
Dr. Stout has a diversified background in exercise science. His primary fields of expertise are sports supplements, neuromuscular fatigue, and body composition analysis. He has over 70 published manuscripts, abstracts, and national presentations in nationally and internationally recognized journals. Dr. Stout currently serves as assistant professor at Creighton University and is the director of the Human Performance Research Laboratory. His current teaching responsibilities include courses in exercise physiology, statistics, research design, and biomechanics.

REFERENCES
1. Alford, B., A. Blankenship, R. Hagen. The effects of variations in carbohydrate, protein, and fat content of the diet upon weight loss, blood values, and nutrient intake of adult obese women. J Am Diet Assoc. 90(4):534-540. 1990

2. Anderson, K., et al. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sci. 40: 1761-1768. 1987

3. Baechle, T. Essentials of Strength Training and Conditioning. Human Kinetics: Champaign, IL. 1994. p. 215

4. Biolo, G., et al. Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans. Am J Physiol. 268(3 Pt 1): E514-520. 1995

5. Burke, L., M. Hargreaves, G. Collier. Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings. J Appl Physiol. 74: 1019-1023. 1993

6. Foster-Powell, K., J. Miller. International tables of glycemic index. Am J Clin Nutr. 62(1): 871S-890S. 1995

7. Golay, A., et al. Similar weight loss with low- or high-carbohydrate diets. Am J Clin Nutr. 63(2):174-178. 1996

8. Keim, N., et al. Weight loss is greater with consumption of large morning meals and fat-free mass is preserved with large evening meals in women on a controlled weight reduction regimen. J Nutr. 127(1): 75-82. 1997

9. Kirwan, J., et al. A low glycemic meal 45 minutes before exercise improves performance. Med Sci Sports Exerc. 28(5 S): S768. 1996

10. Lemon, R. Protein and amino acid needs of the strength athlete. Int J Sport Nutr. 1:127-145. 1991

11. MacDougall, J., et al. The time course for elevated muscle protein synthesis following heavy resistance exercise. Can J Appl Physiol. 20(4): 480-486. 1995

12. Raben, A., et al. Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet. Med Sci Sports Exerc. 24: 1290-1297. 1997

13. Rabinowitz, D., L. Ziebler. Suggested variations in plasma insulin and HGH concentrations during one feast-famine cycle. Nature. 199: 913-915. 1963

14. Reed, M., et al. Dietary lipids: an additional regulator of plasma levels of sex hormone binding globulin. J Clin Endocrinol Metab. 64: 1083-1085. 1987

15. Rinehardt, K. Effects of diet on muscle strength gains during resistive training. In: Muscle Development: Nutritional Alternatives to Anabolic Steroids. Columbus, OH: Ross Laboratories, 1988. pp. 78-82

16. Roy, B., et al. The effect of oral glucose supplements on muscle protein synthesis following resistance training. Med Sci Sports Exerc. 28(5 S): S769. 1996

17. Tarnopolsky, M., J. MacDougall, S. Atkinson. Influence of protein intake and training status on nitrogen balance and lean mass. J Appl Physiol. 64:187-193. 1988

18. Thomas, D., J. Brotherhood, J. Miller. Plasma glucose levels after prolonged strenuous exercise correlate inversely with glycemic response to food consumed before exercise. Int J Sport Nutr. 4(4): 361-373. 1994

19. Van Zant, R., J. Conway, J. Seale. Effects of dietary carbohydrate restriction on high intensity exercise performance. Med Sci Sports Exerc. 24:S71. 1992

20. Volek, J., W. Kraemer, J. Bush, T. Incledon, M. Boetes. Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. J Appl Physiol. 82(1): 49-54. 1997

21. Walberg-Rankin, J. A review of nutritional practices and needs of bodybuilders. J Strength and
Cond Research. 9(2):116-124. 1995

by Jeffrey R. Stout, from Peakhealth.com

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I found an interesting article about chest pain and Vitamin C. The theory is that heart disease is a form of mild scurvy brought on by a lack of Vitamin C or Ascorbate Acid. Humans, other primates and guinea pigs are unable to metabolize Ascorbate in their livers and thus need to take it in through diet or supplements.

Case Report: Lysine/Ascorbate-Related Amelioration of Angina Pectoris

Linus Pauling

Abstract 
It is gratifying to report the first observation of the amelioration of effort angina by the use of high-dose L-lysine and ascorbate in a man with severe coronary artery disease (CAD). This regimen was based on the hypothesis that, in thrombotic atherosclerosis, lipoprotein(a) [Lp(a)]‹ size-heterogeneous, LDL- like particles d displaying independent risk activity for CAD ‹initiates plaque formation by binding to fibrin in the damaged arterial wall. This postulated mechanism correlates with the findings that apoliprotein(a) [apo(a)] has a striking homology to plasminogen and the Lp(a) accumulates in atherosclerotic lesions in the arteries of man (Rath et al., 1989)and the hypoascorbic guinea pig (Rath and Pauling, 1990a, 1990b) and in occluded bypass venous grafts (Cushing et al., 1989). It is hoped that the remarkable outcome in this single case will motivate clinicians to examine the efficacy of lysine and ascorbate in additional cases of refractory angina. 

Coronary Heart Disease Case History 
In late April 1991, a biochemist National Science Medalist* with a familial trait of CAD told me that he experiences effort angina, in spite of medication and three coronary bypass operations. His father and a brother both died of CAD at age 62 he had his first angina attack at age 38. Now aged 71, this biochemist has fought CAD also by reducing risk factors (i.e., not smoking, exercising moderately, and diet/ weight control‹134 Ibs. at 5′5″). His first operation in 1978 (two vein grafts and one LIMA graft) precipitated a second operation (a parallel vein graft) five months later. Stripping of saphenous veins in the first operation induced massive swelling, thrombi, and infection in his leg; bilateral pulmonary emboli; and loss of patency in a vein graft. In 1987, following an attack of unstable angina, he was hospitalized for coronary angiography, adjustment of medications, and a Tl-stress test. A third operation in April 1990 followed attacks of unstable angina, a small MI, and angiography that revealed total occlusion of his right coronary artery and all bypass grafts except for a patent LIMA graft. Unfortunately, this LIMA was lacerated while freeing dense adhesions early in the third operation and required urgent heart-lung bypass cannulation and vein-patch repair; additionally, three venous grafts were made to left coronary arteries. The operation, which diminished but did not eliminate effort angina, left him with 1.8 liters of left-sided pleural effusate that was resistant to diuretics and tapping, and took 10 months to resorb. Medication with beta-receptor and calcium-channel blockers and lovastatin was reinstated; also, 325 mg of aspirin given initially was reduced to 81 mg following bilateral eye hemorrhages and adhesions that impair his peripheral vision. To this medication, he added 6 g of ascorbate (acid form), 60 mg CoQ-10; a multivitamin tablet with minerals; additional vitamins A, E and a B-complex; lecithin; and niacin, on advice of his cardiologist to try to raise his HDL level. Nevertheless, he still had to take nitroglycerin sublingually to suppress angina during a daily two mile walk and when working in his yard. This effort angina continued to worsen, imparting a feeling of impending doom that was reinforced by his cardiologist’s admonition during a check-up in March 1991 that a fifth angiographic test and a fourth bypass operation were no longer options. Also, the saphenous veins from his groin regions and legs had all been used for previous grafts. 

Effect of the Addition of Lysine 
In this predicament and with his history of restenosis, I suggested that he continue ascorbate and add 5 g of L-lysine daily (ca., six times the lysine derived from dietary protein) to try to mitigate the atherosclerotic acitivity of Lp(a). After reading the 1990 Rath and Pauling reports and their manuscript titled “Solution to the puzzle of human cardiovascular disease”, he began taking I g of lysine in early May 1991 and reached 5 g (in divided doses eight hours apart) by mid-June. In mid-July, his HDL was, as usual, a low 28 mg/dl. A low-normal 0.9 mg/dl blood creatinine indicated that lysine could be increased, if needed. He could now walk the same two miles and do yard work without angina pain and wrote, “the effect of the lysine borders on the miraculous”. By late August, he cut up a tree with a chain saw, and in early September started painting his house. By late September, possibly from over-exertion, he again began to have angina symptoms during his walks, but after stopping strenuous work and increasing lysine to 6 g [calculated to provide a peak 280,000 molar excess in the blood over his then 6 mg/dl of Lp(a) to help compensate for the relatively high dissociation constant of lysine-Lp(a)] these symptoms stopped entirely by mid-October. His blood creatinine was still a normal 1.2 mg/dl. He attributes his newfound wellbeing to the addition of lysine to his other medications and vitamins. His wife and friends comment on his renewed vigor. 

Discussion 
This severe case of restenosing CAD was a difficult challenge to try to ameliorate by the addition of lysine. While a positive effect was anticipated, lysine had not been tested for activity in inhibiting or reversing Lp(a)-laden atherosclerotic plaques in hypoascorbemic guinea pigs (Rath and Pauling, 1990b). However, it was known that Lp(a) binds to lysine-Sepharose, immobilized fibrin and fibrinogen (Harpel et al., 1989); and the epithelial-cell receptor for plasminogen ( Gonzalez-Gronow et al., 1989). This binding specificity correlates with the genetic linkage on chromosome six and striking homology of apo(a) and plasminogen‹highly conserved multiple kringle-four domains, a kringle-five domain, and a protease domain (McLean et al., 1987). Moreover, using the molecular evolutionary clock, the loss in primates of the ability to synthesize ascorbate (Zuckerkandl and Pauling, 1962; Rath and Pauling, 1990a) and acquisition of Lp(a) (Maeda et al., 1983) both appear to have occurred about 40 million years ago. These observations and the presence of Lp(a) in sclerotic arteries (Rath et al., 1989; Rath and Pauling, 1990b) and in venous grafts (Cushing et al., 1989) indicate that atherosclerosis may be initiated by excess binding of Lp(a) to fibrin in vascular wall clots, thus interfering with normal fibrinolysis by plasmin. This thrombogenic activity, which is postulated to reside in plasmin-homologous domains of Lp(a), may help to stabilize the damaged vascular wall, especially in ascorbate deficiency (Scanu, Lawn, and Berg, 1991; Rath and Pauling, 1990a). Once bound to fibrin, the LDL-like domain of Lp(a) could promote atheromas (Scanu, Lawn, and Berg, 1991). In this scenario, high-dosage lysine could inhibit or reverse plaque accretion by binding to Lp(a). Independently, lysine benefits the heart as a precursor with methionine in the synthesis of L-carnitine, the molecule that carries fat into mitochondria for the synthesis of adenosine triphosphate (ATP) bond energy needed for muscular and other cellular activities (Cederblad and Linstedt, 1976). While his intake of 60 mg of CoQ-10, also required for ATP synthesis, prior to the addition of lysine improved his sense of wellbeing, it did not suppress his angina. Ascorbate without lysine also did not ameliorate angina, but it is needed as an antioxidant to protect the vascular wall against peroxidative damage and in hydroxylation reactions both in the synthesis of carnitine and in the conversion of procollagen to collagen (hydroxylation of prolyl and Iysyl residues) (Myllyla et al., 1984) to strengthen the extracellular matrix of the wall. 
Whatever the pathomechanisms of atherosclerosis, the addition of lysine to medications and vitamins, including ascorbate, markedly suppressed angina pectoris in this intractable case of CAD. While a single case is anecdotal, it is hoped that its remarkable success will motivate clinicians to commence studies as soon as possible of the general applicability of lysine and ascorbate in relieving angina pectoris, so as to decrease greatly the amount of human suffering with less dependence on surgical intervention. 

Footnote (p. 144) *The biochemist patient made a major contribution to this report, but wishes anonymity. 

References 
1. Cederblad G and Linstedt S: Metabolism of labeled carnitine in the rat. Archives of Biochemistry and Biophysics 175:173-182, 1976. 
2. Cushing GL, Gaubatz JW, Nava ML, Burdick BJ, Bocan TMA, Guyton JR, Weilbaecher D, DeBakey ME, Lawrie GM and Morrisett JD: Quantitation and localization of lipoprotein(a) and B in coronary artery bypass vein grafts resected at re-operation. Arteriosclerosis 9:593-603, 1989. 
3. Gonzalez-Gronow M, Edelberg J M and Pizzo SV: Further characterization of the cellular plasminogen binding site: Evidence that plasminogen 2 and lipoprotein(a) compete for the same site. Biochemistry 28:2374-2377, 1989. 
4. Harpel PC, Gordon BR and Parker TS: Plasminogen catalyzes binding of lipoprotein(a) to immobilized fibrinogen and fibrin. Proc. Natl. Acad. Sci. USA 86:3847-3851, 1989. 
5. Maeda N, Bliska JB and Smithies O: Recombination and balanced chromosome polymorphism suggested by DNA sequences 5′ to the human deltaglobin gene. Proc. Natl. Acad. Sci. USA 80:5012-5016, 1983. 
6. McLean JW, Tomlinson JE, Kuang WJ et al.: cDNA sequence of human apolipoprotein(a) is homologous to plasminogen. Nature 330:132-137, 1987. 
7. Myllyla R, Majamaa K, Gunzler V, Hanuska-Abel HM and Kivirikko KI: Ascorbate is consumed stoichiometrically in the uncoupled reactions catalyzed by prolyl-4-hydroxylase and Iysyl hydroxylase. Journal of Biological Chemistry 259:5403-5405, 1984. 
8. Rath M, Niendorf A, Reblin T, Dietel M, Krebber HJ and Beisiegel U: Detection and quantification of lipoprotein(a) in the arterial wall of 107 coronary bypass patients. Arteriosclerosis 9:579-592, 1989. 
9. Rath M and Pauling L: Hypothesis: Lipoprotein(a) is a surrogate for ascorbate. Proc.. Natl. Acad. Sci. USA 87:6204-6207, 1990a. 
10. Rath M and Pauling L: Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. Proc. Natl. Acad. Sci. USA 87:9388-9390, 1990b. 
11. Scanu M, Lawn RM and Berg K: Lipoprotein(a) and atherosclerosis. Annals of Internal Medicine 115:209-218, 1991. 
12.Zuckerkandl E and Pauling L: Molecular disease, evolution, and genic heterogeneity. In: Horizons in Biochemistry, eds. Kasha M. and Pullman B. (Academic Press, New York) pp. 189-225, 196

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Vitamin C may be a life-saver

Mega-doses of Vitamin C can counter avian flu, hepatitis and herpes, and can even control the advance of Aids

Read the original article at The Independent

By Jane Feinmann

Imagine that a deadly virus is sweeping the world, killing and maiming hundreds of thousands of children. Nothing seems able to stop it – until a doctor stands up at the American Medical Association and reports on 60 cases involving severely infected children, all of whom have been cured. Yet his work, subsequently reported in a peer-review journal, is ignored, leaving the virus to wreak havoc for decades.

Imagine that a deadly virus is sweeping the world, killing and maiming hundreds of thousands of children. Nothing seems able to stop it – until a doctor stands up at the American Medical Association and reports on 60 cases involving severely infected children, all of whom have been cured. Yet his work, subsequently reported in a peer-review journal, is ignored, leaving the virus to wreak havoc for decades.

This isn’t a docudrama about some futuristic plague – it’s a true story about what happened in June 1949 when polio was at its peak. Dr Frederick Klenner, a clinical researcher from Reidsville, North Carolina, reported that a massive intravenous dose of Vitamin C – up to 20,000mg daily for three days (today’s recommended daily allowance is 60mg) – had cured 60 of his patients. The findings were published in a medical journal, yet there was virtually no interest. Apart from a couple of minor trials, no attempt was made to find out if they had any scientific substance.

Relating this curious incident in a new book, Vitamin C, Infectious Diseases & Toxins: Curing the Incurable, Dr Thomas Levy, a US cardiologist, admits to being gripped by a range of emotions when he came across Klenner’s work and other studies that replicated it. “To know that polio had been easily cured yet so many people continued to die, or survived to be permanently crippled by it, was difficult to accept.”

Levy argues that the medical profession has routinely ignored research showing that high doses of Vitamin C can combat bacteria, toxins and severe viral infections including avian flu, SARS, hepatitis and herpes. And this is not a case of doctors sniffing at anecdotal evidence from a handful of enthusiasts. “Vitamin C is possibly the best-researched substance in the world. There are more than 24,000 papers and articles on the authoritative clinical website, Medline. Yet virtually the all the evidence has been dismissed.” Levy even claims that Aids can be controlled if a high enough dosage of Vitamin C is maintained.

This is not the first time doctors have had their cages rattled over the benefits of Vitamin C. The controversy has been simmering since 1753, when just a couple of sucks of a lime were shown to prevent scurvy. In the 1950s the chemist Linus Pauling, a double Nobel prize-winner, promoted the use of mega-doses of Vitamin C, but his research was rubbished by clinicians.

Recently, the anti-Vitamin C sentiment has grown. It has been blamed for causing the formation of kidney stones, and a study published in the journal Science in 2001 found that even 200mg doses of Vitamin C “facilitated the production of DNA-damaging agents associated with a variety of cancers”. This finding was widely interpreted as proving that Vitamin C causes cancer.

Britain’s Food Standards Agency recommends taking a maximum of 1,000mg of Vitamin C a day. But a directive going through the European Parliament aims to reduce this to less than 100mg in an attempt to harmonise dosages across the Continent. Despite being dubbed “illegal” by the advocate general of the European Court of Justice last week, the directive could still be passed.

The controversy has not put off consumers, many of whom take Vitamin C to ward off colds. The 1,000 mg capsule is the most popular single vitamin in Britain, with the 500mg version second.

Some people argue that we can get sufficient Vitamin C from a diet rich in fruit and vegetables, but Levy disagrees. The problem, he says, is that a genetic design fault makes us unable to synthesise our own Vitamin C. Levy claims that while recommended daily allowances of 60mg are enough to prevent the development of scurvy in otherwise healthy people, much higher levels are required to maintain health when an infection strikes. At such times, the body begins to “metabolise unusually large amounts of vitamin C, keeping stores so depleted that the recommended daily allowance will not even prevent many of the symptoms of scurvy from developing”.

Levy claims that the reason why most animals stay healthy throughout their lives, while humans spend years coping with one or more chronic diseases, is that animals make their own Vitamin C. The wild goat, for instance, makes around 13,000mg a day, rising to 100,000mg when faced with life-threatening infectious or toxic stress, according to a 1961 study published in the Annals of the New York Academy of Sciences.

So, is Levy right? Should everyone be taking mega-doses every day and having intravenous infusions when they fall ill? Possibly.

Dr Rodney Adeniyi-Jones regularly gives 20,000mg doses to people with arterial disease and as part of a flu treatment protocol, describing its effects as “beneficial… but not miraculous”. And Professor George Lewith of the Centre for Complementary and Integrated Medicine says that while Vitamin C is not a panacea, it does have clinical benefits depending on the dosage. “There may be doses that are therapeutic, while another dose may be damaging for the same condition. It is not a dose-response curve as with pharmaceuticals, and we need to be cautious until this is better understood.”

But he also warns that: “Many of the [Vitamin C] trials have been badly done and what evidence exists is mixed. Both those in favour and against high doses frequently misinterpret the data.”

Levy may well be seen to have an axe to grind, yet the evidence seems to support his view that apart from causing diarrhoea, mega-doses of Vitamin C are not toxic. He says that a series of studies published in leading journals have shown that, far from causing cancer, Vitamin C is a safe supplement for chronic cancer patients. Further large studies suggest that supplements do not put a normal person at greater risk of developing kidney stones.

According to Levy, the problem is not that people might take too much, but that they won’t take enough – and thus won’t get the desired effects. “There’s a popular medical view that taking Vitamin C just makes expensive urine. Some of it is lost in urine, but the more you consume, the more stays in your body.”

With a new book on the way claiming that Vitamin C deficiency is also a primary cause of cardiovascular disease, Levy cannot be accused of underselling his case. Nor can he overcome the fact that proper clinical trials are still desperately needed. Considering its overall safety, there appears to be no good reason why anyone with a chronic or acute health problem should not try, at the very least, a couple of week’s regime of two or three 1,000mg tablets of Vitamin C a day.

Need to Know: So how much should you take?

* For a cold

Three 1,000mg doses a day, according to the campaign group Consumers for Health Choice.

* For flu

Although it’s more serious, the viral load is similar, according to research, and taking up to 20,000mg a day could be beneficial.

* For shingles

Research has shown that this painful post-viral condition can be pretty well cured by an injection of 3,000mg of vitamin C. Taking four 1,000mg tablets orally for three days could be worthwhile as well.

* For a hangover

Taking 1,000mg daily in the week before a booze-up reduces stress on the liver. If you’re drunk and want to look sober, a large dose of vitamin C will prevent drunken behaviour, according to a 1986 study, “Alcohol and Alcoholism”.

* To maintain your health

A 1,000mg daily dose is regarded as safe by the Food Standards Agency, and adequate to keep sufficient vitamin C in the plasma and tissues. “We believe this is absolutely safe and definitely beneficial to people’s health,” says Sue Croft of Consumers for Health Choice.

What are ketones?

Ketones are a normal and efficient source of fuel and energy for the human body. They are produced by the liver from fatty acids, which result from the breakdown of body fat in response to the absence of glucose/sugar. In a ketogenic diet, such as Atkins … or diets used for treating epilepsy in children, the tiny amounts of glucose required for some select functions can be met by consuming a minimum amount of carbs – or can be manufactured in the liver from PROTEIN. When your body is producing ketones, and using them for fuel, this is called “ketosis”.

How will ketosis help me to lose weight?

Most reducing diets restrict calorie intake, so you lose weight but some of that is fat and some of it is lean muscle tissue as well. Less muscle means slowed metabolism, which makes losing weight more difficult and gaining it back all too easy. Ketosis will help you to lose FAT.

Being in ketosis means that your body’s primary source of energy is fat (in the form of ketones). When you consume adequate protein as well, there’s no need for the body to break down its muscle tissue. Ketosis also tends to accelerate fat loss — once the liver converts fat to ketones, it can’t be converted back to fat, and so is excreted.

But, isn’t ketosis dangerous?

Being in ketosis by following a low carbohydrate diet is NOT dangerous. The human body was designed to use ketones very efficiently as fuel in the absence of glucose. However, the word ketosis is often confused with a similar word, ketoacidosis.

Ketoacidosis is a dangerous condition for diabetics, and the main element is ACID not ketones. The blood pH becomes dangerously acidic because of an extremely high blood SUGAR level (the diabetic has no insulin, or doesn’t respond to insulin …. so blood sugar rises … ketones are produced by the body to provide the fuel necessary for life, since the cells can’t use the sugar). It’s the high blood sugar, and the acid condition that is so dangerous. Ketones just happen to be a part of the picture, and are a RESULT of the condition, not the CAUSE. Diabetics can safely follow a ketogenic diet to lose fat weight … but they must be closely monitored by their health care provider, and blood sugars need to be kept low, and stable.

How do the ketone test strips work, and where can I get them?

Ketone urine-testing strips, also called Ketostix or just ketone sticks … are small plastic strips that have a little absorptive pad on the end. This contains a special chemical that will change colour in the presence of ketones in the urine. The strips may change varying shades of pink to purple, or may not change colour at all. The container will have a scale on the label, with blocks of colour for you to compare the strip after a certain time lapse, usually 15 seconds. Most folks simply hold a strip in the flow of urine. Other folks argue that the force of the flow can “wash” some of the chemical away, and advise that a sample of urine be obtained in a cup or other container, then the strip dipped into it.

The chemical reagent is very sensitive to moisture, including what’s in the air. It’s important to keep the lid of the container tightly closed at all times, except for when you’re getting a strip to take a reading. Make sure your fingers are dry before you go digging in! They also have an expiry date, so make note of this when you purchase the strips … that’s for the UNopened package. Once opened, they have a shelf-life of about 6 months — you may wish to write the date you opened on the label for future reference.

Ketone test strips can be purchased at any pharmacy or at Amazon.com and are usually kept with the diabetic supplies. In some stores they’re kept behind the counter, so if you don’t see them on the shelf, just ask the pharmacist; you don’t need a prescription to buy them.

I’m following Induction strictly; why won’t my strips turn purple?

Ketones will spill into the urine ONLY when there is more in the blood than is being used as fuel by the body at that particular moment.

You may have exercised or worked a few hours previously, so your muscles would have used up the ketones as fuel, thus there will be no excess. You may have had a lot of liquids to drink, so the urine is more diluted. Perhaps the strips are not fresh, or the lid was not on tight and some moisture from the atmosphere got in.

Some low carbers NEVER show above trace or negative even … yet they burn fat and lose weight just fine. If you’re losing weight, and your clothes are getting looser, you’re feeling well and not hungry all the time .. then you are successfully in ketosis. Don’t get hung up on the strips; they’re just a guide, nothing more.

Will I lose weight faster if the strips show dark purple all the time?

No. Testing in the darkest purple range all the time is usually a sign of dehydration — the urine is too concentrated. You need to drink more water to dilute it, and keep the kidneys flushed.

The liver will make ketones from body fat, the fat you EAT, and from alcohol — the ketone strips have no way of distinguishing the source of the ketones. So, if you test every day after dinner, and dinner usually contains a lot of fat, then you may very well test for large amounts of ketones all the time. However this does not indicate that any BODY fat was burned.

The strips only indicate what’s happening in the urine. Ketosis happens in the blood and body tissues. If you’re showing even a small amount, then you are in ketosis, and fat-burning is taking place. Don’t get hung up on the ketone sticks.

Does caffeine affect ketosis?

This is questionable. There ARE a few studies that suggest caffeine may cause blood sugar to rise, with consequent effect on insulin … The studies involve consuming 50 gm glucose orally, followed by a dose of caffeine. This is quite different from a low carber, who is consuming only 20 gm carbs, in the form of high-fiber vegetables, spread throughout the day.

Many low carbers continue to enjoy caffeine-containing beverages with no serious impact on their weight-loss efforts. However, there are some sensitive individuals … and persons who are extremely insulin resistant may need to restrict or even eliminate all caffeine. If you have been losing successfully then find your weight loss stalled for a month or two, and you are following your program to the letter, you might consider stopping all caffeine for a while, to see if that will get things started again.

Will drinking alcohol affect ketosis?

No and yes. The liver can make ketones out of alcohol, so technically, when you drink you’ll continue to produce ketones and so will remain in ketosis. The problem is … alcohol converts more easily to ketones than fatty acids, so your liver will use the alcohol first, in preference to fat. Thus, when you drink, basically your FAT burning is put on hold until all the alcohol is out of your system.

This rapid breakdown of alcohol into ketones and acetaldehyde (the intoxicating by-product) … tends to put low carbers at risk for quicker intoxication … especially if no other food is consumed to slow absorption.

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I’ve been on low carb since Wednesday and have dropped 6lbs. This week I’m planning on getting to the gym at least three times and maybe thoqing in a bike ride or a game of raquetball.

I’ll keep you all posted. Currently at 260.

I am going to file this one under fad diets and throw in a word of caution. Ephedrine is a powerful drug and can have some serious side effects. Read and use this information at your own risk. I am posting this information because I’ve noticed a lot of my automatically generated Google adds are trying to lure you into buying different weight loss supplements and this is the only one with any sort of legitimate science to back it up.

I have used an ECA stack in the past but like Dumbo’s Feather (which if you remember helped him to fly) I think it had more of a placebo effect. Yes, I lost weight but I would attribute most of it to a good clean diet and an insane amount of grueling physical exercise. I am not advocating this method, nor am I using it myself. The FDA considered Ephedra dangerous enough to ban its sale as a supplement. It is still legal to buy over the counter for relief of asthma symptoms.  Anyway, on to how and why it works.

The following abstract is from an article by Nadir Yehya from the University of California, Los Angeles.

The field of obesity management is coming to appreciate the efficacy of pharmacological
treatments. For the past twenty years the thermogenic effects of sympathetic stimulation have been known and described. Recent studies have demonstrated that treating patients with a
drug combination including the sympathomimetic ephedrine, the stimulant caffeine, and the analgesic aspirin (ECA combination) will stimulate thermogenesis and result in lowered weight but maintained muscle mass. This protein-sparing lipolysis has been attributed to the elevated levels of cAMP generated by the ECA combination. In rat studies, the mechanism of action has been well characterized in vitro and although there is some discrepancy in humans, a similar mechanism seems to be active. Randomized placebo-controlled trials have demonstrated the short-term efficacy of the ECA combination, but long-term studies are lacking. Most studies have also demonstrated the incidence of short-term side effects associated with excessive sympathetic stimulation, and have shown them to be transient and mild. Future studies should focus on the long-term efficacy of the ECA combination, and the effects of stopping treatment on the maintenance of fat loss.

This research concludes that the ECA combination provides protein sparing lipolysis which translates to keeping muscle while burning fat. To lose wieght the body must break down and use fat. Typically, this catabolic activity burns both muscle and fat. Weight is lost but losing both fat and muscle is a bad thing. The ECA stack spares the protein or muscle in favor of fat.

So, the ECA stack burns fat and spares muscle. Let’s check the wiki to see how it works.

From a Wikipedia article:

The effects of the ECA stack in weight loss are primarily due to the ephedrine component. Ephedrine acts both as a beta agonist and stimulates the release of norepinephrine. Increased circulating norepinephrine in the body then acts on white adipose tissue by increasing cAMP levels. This causes a thermogenic effect, raising body temperature and increasing the user’s metabolism in conjunction with the rest of the stack.

However, the body’s negative feedback system then activates to normalize the metabolism. This is done via the production of phosphodiesterase inside the cells, and prostaglandins outside the cell, which both lower cAMP levels within the cell.

Caffeine inhibits the production of phosphodiesterase inside the cell and therefore slows cAMP breakdown. It also binds with and competitively inhibits adenosine receptors in the brain, triggering the release of epinephrine and increasing cAMP levels further.

Aspirin inhibits prostaglandin production outside of the cells, which, in conjunction with caffeine, greatly prolongs the thermogenic effects and increased metabolism by sustaining elevated cAMP levels.

Ephedrine also has an anorectic, or appetite-suppressing, effect. However, these effects only last for about two weeks if the stack is not cycled, as the body becomes tolerant to ephedrine to some degree. It is estimated that 60%–75% of the weight loss from using the ECA stack comes from the anorectic effect, and the remainder from thermogenesis.

The final component in weight loss of the ECA stack is that of a simple stimulant; the higher epinephrine and norepinephrine levels result in increased aerobic exercise performance and less fatigue.

Basically, the Ephedrine increases your metabolism and has a anorectic effect making you less hungry. The caffiene and asprin keep these effects going by blocking the body’s ability to compensate for these effects naturally.

Typically the ECA stack is consumed two or three times per day in a 1:10:10 or 1:10:15 ratio of ephedrine:caffeine:Aspirin. This translates to approximately 25 mg of ephedrine, 200 mg of caffeine and 325 mg of Aspirin for a single dose.

Once again, there are risks involved in taking this and it should be used with caution.