My Version of Eggs Benedict

Poached EggsAn apology to all you purists out there, I poached the eggs hard and obviously forgo the English muffin.

It is possible to poach eggs without the special pan…it’s easier with it. I brushed in some coconut oil and gave each cup a quarter twist from the pepper and salt mill. These were left to simmer to my desired consistency.

Once the eggs are done I used the poaching pan as a double boiler with a smaller pan to make the hollandaise sauce. Two egg yolks, a healthy pat of butter and salt whisked together with ground cayenne pepper, lemon juice and a bit of Tapatio. This step has to be done at very low temperature for the precise amount of time or you’ll end up with spicy egg yolk scrambled eggs.

The bacon was cooked on a half-sheet pan lined with parchment for about 20 minutes at 410. Every time you get really good bacon at a restaurant they’ve cooked it in the oven, just do it that way from now on.

Plate it up and enjoy.

Saturated Fat – What if Bad Fat is Actually Good for You?

Today someone caught me eating cheese. I got a disappointed look that said “you’ve come so far, don’t screw it up now.”

So, I opened up my browser and Googled saturated fat. Here’s what Men’s Health had to say:

What if Bad Fat is Actually Good for You?

For decades, Americans have been told that saturated fat clogs arteries and causes heart disease. But there’s just one problem: No one’s ever proved it

Suppose you were forced to live on a diet of red meat and whole milk. A diet that, all told, was at least 60 percent fat — about half of it saturated. If your first thoughts are of statins and stents, you may want to consider the curious case of the Masai, a nomadic tribe in Kenya and Tanzania.

In the 1960s, a Vanderbilt University scientist named George Mann, M.D., found that Masai men consumed this very diet (supplemented with blood from the cattle they herded). Yet these nomads, who were also very lean, had some of the lowest levels of cholesterol ever measured and were virtually free of heart disease.

Scientists, confused by the finding, argued that the tribe must have certain genetic protections against developing high cholesterol. But when British researchers monitored a group of Masai men who moved to Nairobi and began consuming a more modern diet, they discovered that the men’s cholesterol subsequently skyrocketed.

Similar observations were made of the Samburu — another Kenyan tribe — as well as the Fulani of Nigeria. While the findings from these cultures seem to contradict the fact that eating saturated fat leads to heart disease, it may surprise you to know that this “fact” isn’t a fact at all. It is, more accurately, a hypothesis from the 1950s that’s never been proved.

The first scientific indictment of saturated fat came in 1953. That’s the year a physiologist named Ancel Keys, Ph.D., published a highly influential paper titled “Atherosclerosis, a Problem in Newer Public Health.” Keys wrote that while the total death rate in the United States was declining, the number of deaths due to heart disease was steadily climbing. And to explain why, he presented a comparison of fat intake and heart disease mortality in six countries: the United States, Canada, Australia, England, Italy, and Japan.

The Americans ate the most fat and had the greatest number of deaths from heart disease; the Japanese ate the least fat and had the fewest deaths from heart disease. The other countries fell neatly in between. The higher the fat intake, according to national diet surveys, the higher the rate of heart disease. And vice versa. Keys called this correlation a “remarkable relationship” and began to publicly hypothesize that consumption of fat- causes heart disease. This became known as the diet-heart hypothesis.

At the time, plenty of scientists were skeptical of Keys’s assertions. One such critic was Jacob Yerushalmy, Ph.D., founder of the biostatistics graduate program at the University of California at Berkeley. In a 1957 paper, Yerushalmy pointed out that while data from the six countries Keys examined seemed to support the diet-heart hypothesis, statistics were actually available for 22 countries. And when all 22 were analyzed, the apparent link between fat consumption and heart disease disappeared. For example, the death rate from heart disease in Finland was 24 times that of Mexico, even though fat-consumption rates in the two nations were similar.
The other salient criticism of Keys’s study was that he had observed only a correlation between two phenomena, not a clear causative link. So this left open the possibility that something else — unmeasured or unimagined — was leading to heart disease. After all, Americans did eat more fat than the Japanese, but perhaps they also consumed more sugar and white bread, and watched more television.

Despite the apparent flaws in Keys’s argument, the diet-heart hypothesis was compelling, and it was soon heavily promoted by the American Heart Association (AHA) and the media. It offered the worried public a highly educated guess as to why the country was in the midst of a heart-disease epidemic. “People should know the facts,” Keys said in a 1961 interview with Time magazine, for which he appeared on the cover. “Then if they want to eat themselves to death, let them.”

The seven-countries study, published in 1970, is considered Ancel Keys’s landmark achievement. It seemed to lend further credence to the diet-heart hypothesis. In this study, Keys reported that in the seven countries he selected — the United States, Japan, Italy, Greece, Yugoslavia, Finland, and the Netherlands — animal-fat intake was a strong predictor of heart attacks over a 5-year period. Just as important, he noted an association between total cholesterol and heart-disease mortality. This prompted him to conclude that the saturated fats in animal foods — and not other types of fat — raise cholesterol and ultimately lead to heart disease.

Naturally, proponents of the diet-heart hypothesis hailed the study as proof that eating saturated fat leads to heart attacks. But the data was far from rock solid. That’s because in three countries (Finland, Greece, and Yugoslavia), the correlation wasn’t seen. For example, eastern Finland had five times as many heart-attack fatalities and twice as much heart disease as western Finland, despite only small differences between the two regions in animal-fat intake and cholesterol levels. And while Keys provided that raw data in his report, he glossed over it as a finding. Perhaps a larger problem, though, was his assumption that saturated fat has an unhealthy effect on cholesterol levels.

Although more than a dozen types of saturated fat exist, humans predominantly consume three: stearic acid, palmitic acid, and lauric acid. This trio comprises almost 95 percent of the saturated fat in a hunk of prime rib, a slice of bacon, or a piece of chicken skin, and nearly 70 percent of that in butter and whole milk.

Today, it’s well established that stearic acid has no effect on cholesterol levels. In fact, stearic acid — which is found in high amounts in cocoa as well as animal fat –i s converted to a monounsaturated fat called oleic acid in your liver. This is the same heart-healthy fat found in olive oil. As a result, scientists generally regard this saturated fatty acid as either benign or potentially beneficial to your health.
Palmitic and lauric acid, however, are known to raise total cholesterol. But here’s what’s rarely reported: Research shows that although both of these saturated fatty acids increase LDL (“bad”) cholesterol, they raise HDL (“good”) cholesterol just as much, if not more. And this lowers your risk of heart disease. That’s because it’s commonly believed that LDL cholesterol lays down plaque on your artery walls, while HDL removes it. So increasing both actually reduces the proportion of bad cholesterol in your blood to the good kind. This may explain why numerous studies have reported that this HDL/LDL ratio is a better predictor of future heart disease than LDL alone.

All of this muddies Keys’s claim of a clear connection between saturated-fat intake, cholesterol, and heart disease. If saturated fat doesn’t raise cholesterol in such a way that it increases heart-disease risk, then according to the scientific method, the diet-heart hypothesis must be rejected. However, in 1977 it was still a promising idea.

That was the year Congress made it government policy to recommend a low-fat diet, based primarily on the opinions of health experts who supported the diet-heart hypothesis. It was a decision met with much criticism from the scientific community, including the American Medical Association. After all, officially endorsing a low-fat diet could change the eating habits of millions of Americans, and the potential effects of this strategy were widely debated and certainly unproved.

We’ve spent billions of our tax dollars trying to prove the diet-heart hypothesis. Yet study after study has failed to provide definitive evidence that saturated-fat intake leads to heart disease. The most recent example is the Women’s Health Initiative, the government’s largest and most expensive ($725 million) diet study yet. The results, published last year, show that a diet low in total fat and saturated fat had no impact in reducing heart-disease and stroke rates in some 20,000 women who had adhered to the regimen for an average of 8 years.

But this paper, like many others, plays down its own findings and instead points to four studies that, many years ago, apparently did find a link between saturated fat and heart disease. Because of this, it’s worth taking a closer look at each.

The Los Angeles VA Hospital Study (1969) This UCLA study of 850 men reported that those who replaced saturated fats with polyunsaturated fats were less likely to die of heart disease and stroke over a 5-year period than were men who didn’t alter their diets. However, more of those who changed their diets died of cancer, and the average age of death was the same in both groups. What’s more, “through an oversight,” the study authors neglected to collect crucial data on smoking habits from about 100 men. They also reported that the men successfully adhered to the diet only half the time.

The Oslo Diet-Heart Study (1970) Two hundred men followed a diet low in saturated fat for 5 years while another group ate as they pleased. The dieters had fewer heart attacks, but there was no difference in total deaths between the two groups.

The Finnish Mental Hospital Study (1979) This trial took place from 1959 to 1971 and appeared to document a reduction in heart disease in psychiatric patients following a “cholesterol-lowering” diet. But the experiment was poorly controlled: Almost half of the 700 participants joined or left the study over its 12-year duration.
The St. Thomas’ Atherosclerosis Regression Study (1992) Only 74 men completed this 3-year study conducted at St. Thomas’ Hospital, in London. It found a reduction in cardiac events among men with heart disease who adopted a low-fat diet. There’s a major caveat, though: Their prescribed diets were also low in sugar.

These four studies, even though they have serious flaws and are tiny compared with the Women’s Health Initiative, are often cited as definitive proof that saturated fats cause heart disease. Many other more recent trials cast doubt on the diet-heart hypothesis. These studies should be considered in the context of all the other research.

In 2000, a respected international group of scientists called the Cochrane Collaboration conducted a “meta-analysis” of the scientific literature on cholesterol-lowering diets. After applying rigorous selection criteria (219 trials were excluded), the group examined 27 studies involving more than 18,000 participants. Although the authors concluded that cutting back on dietary fat may help reduce heart disease, their published data actually shows that diets low in saturated fats have no significant effect on mortality, or even on deaths due to heart attacks.

“I was disappointed that we didn’t find something more definitive,” says Lee Hooper, Ph.D., who led the Cochrane review. If this exhaustive analysis didn’t provide evidence of the dangers of saturated fat, says Hooper, it was probably because the studies reviewed didn’t last long enough, or perhaps because the participants didn’t lower their saturated-fat intake enough. Of course, there is a third possibility, which Hooper doesn’t mention: The diet-heart hypothesis is incorrect.

Ronald Krauss, M.D., won’t say saturated fats are good for you. “But,” he concedes, “we don’t have convincing evidence that they’re bad, either.”

For 30 years, Dr. Krauss — an adjunct professor of nutritional sciences at the University of California at Berkeley — has been studying the effect of diet and blood lipids on cardiovascular disease. He points out that while some studies show that replacing saturated fats with unsaturated fats lowers heart-disease risk, this doesn’t mean that saturated fats lead to clogged arteries. “It may simply suggest that unsaturated fats are an even healthier option,” he says.

But there’s more to this story: In 1980, Dr. Krauss and his colleagues discovered that LDL cholesterol is far from the simple “bad” particle it’s commonly thought to be. It actually comes in a series of different sizes, known as subfractions. Some LDL subfractions are large and fluffy. Others are small and dense. This distinction is important.

A decade ago, Canadian researchers reported that men with the highest number of small, dense LDL subfractions had four times the risk of developing clogged arteries than those with the fewest. Yet they found no such association for the large, fluffy particles. These findings were confirmed in subsequent studies.

Now here’s the saturated-fat connection: Dr. Krauss found that when people replace the carbohydrates in their diet with fat–saturated or unsaturated — the number of small, dense LDL particles decreases. This leads to the highly counterintuitive notion that replacing your breakfast cereal with eggs and bacon could actually reduce your risk of heart disease.
Men, more than women, are predisposed to having small, dense LDL. However, the propensity is highly flexible and, according to Dr. Krauss, can be switched on when people eat high-carb, low-fat diets or switched off when they reduce carbs and eat diets high in fat, including the saturated variety. “There’s a subgroup of people at high risk of heart disease who may respond well to diets low in fat,” says Dr. Krauss. “But the majority of healthy people seem to derive very little benefit from these low-fat diets, in terms of heart-disease risk factors, unless they also lose weight and exercise. And if a low-fat diet is also loaded with carbs, it can actually result in adverse changes in blood lipids.”

While Dr. Krauss is much published and highly respected — he has served twice as chairman of the writing committee of the AHA’s dietary guidelines — the far-reaching implications of his work have not been generally acknowledged. “Academic scientists believe saturated fat is bad for you,” says Penny Kris-Etherton, Ph.D., a distinguished professor of nutritional studies at Penn State University, citing as evidence the “many studies” she believes show it to be true. But not everyone accepts those studies, and their proponents find it hard to be heard. Kris-Etherton acknowledges that “there’s a good deal of reluctance toward accepting evidence suggesting the contrary.”

Take, for example, a 2004 Harvard University study of older women with heart disease. Researchers found that the more saturated fat these women consumed, the less likely it was their condition would worsen. Lead study author Dariush Mozaffarian, Ph.D., an assistant professor at Harvard’s school of public health, recalls that before the paper was published in the American Journal of Clinical Nutrition, he encountered formidable politics from other journals.

“In the nutrition field, it’s very difficult to get something published that goes against  established dogma,” says Mozaffarian. “The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence.” Mozaffarian says he believes it’s critical that scientists remain open minded. “Our finding was surprising to us. And when there’s a discovery that goes against what’s established, it shouldn’t be suppressed but rather disseminated and explored as much as possible.”

Perhaps the apparent bias against saturated fat is most evident in studies on low-carbohydrate diets. Many versions of this approach are controversial because they place no limitations on saturated-fat intake. As a result, supporters of the diet-heart hypothesis have argued that low-carb diets will increase the risk of heart disease. But published research doesn’t show this to be the case. When people on low-carb diets have been compared head-to-head with those on low-fat diets, the low-carb dieters typically scored significantly better on markers of heart disease, including small, dense LDL cholesterol, HDL/LDL ratio, and triglycerides, which are a measure of the amount of fat circulating in your blood.

For example, in a new 12-week study, University of Connecticut scientists placed overweight men and women on either a low-carb or low-fat diet. Those who followed the low-carb diet consumed 36 grams of saturated fat per day (22 percent of total calories), which represented more than three times the amount in the low-fat diet. Yet despite this considerably greater intake of saturated fat, the low-carb dieters reduced both their number of small, dense LDL cholesterol and their HDL/LDL ratio to a greater degree than those who ate a low-fat diet. In addition, triglycerides decreased by 51 percent in the low-carb group–compared with 19 percent in the low-fat group.
This finding is worth noting, because even though cholesterol is the most commonly cited risk factor for heart disease, triglyceride levels may be equally relevant. In a 40-year study at the University of Hawaii, scientists found that low triglyceride levels at middle age best predicted “exceptional survival” — defined as living until age 85 without suffering from a major disease.

According to lead study author Jeff Volek, Ph.D., R.D., two factors influence the amount of fat coursing through your veins. The first, of course, is the amount of fat you eat. But the more important factor is less obvious. Turns out, your body makes fat from carbohydrates. It works like this: The carbs you eat (particularly starches and sugar) are absorbed into your bloodstream as sugar. As your carb intake rises, so does your blood sugar. This causes your body to release the hormone insulin. Insulin’s job is to return your blood sugar to normal, but it also signals your body to store fat. As a result, your liver starts converting excess blood sugar to triglycerides, or fat.

All of which helps explain why the low-carb dieters in Volek’s study had a greater loss of fat in their blood. Restricting carbs keeps insulin levels low, which lowers your internal production of fat and allows more of the fat you do eat to be burned for energy.

Yet even with this emerging data and the lack of scientific support for the diet-heart hypothesis, the latest AHA dietary guidelines have reduced the recommended amount of saturated fat from 10 percent of daily calories to 7 percent or less. “The idea was to encourage people to decrease their saturated-fat intake even further, because there’s a linear relationship between saturated-fat intake and LDL cholesterol,” says Alice H. Lichtenstein, Ph.D., Sc.D., who led the AHA nutrition committee that wrote the recommendation.

What about Krauss’s findings that not all LDL is equal? Lichtenstein says that her committee didn’t address them, but that it might in the future.

It could be that it’s not bad foods that cause heart disease, it’s bad habits. After all, in Volek’s study, participants who followed the low-fat diet — which was high in carbs — also decreased their triglycerides. “The key factor is that they weren’t overeating,” says Volek. “This allowed the carbohydrates to be used for energy rather than converted to fat.” Perhaps this is the most important point of all. If you consistently consume more calories than you burn, and you gain weight, your risk of heart disease will increase — whether you favor eating saturated fats, carbs, or both.

But if you’re living a healthy lifestyle — you aren’t overweight, you don’t smoke, you exercise regularly — then the composition of your diet may matter much less. And, based on the research of Volek and Dr. Krauss, a weight-loss or maintenance diet in which some carbohydrates are replaced with fat — even if it’s saturated — will reduce markers of heart-disease risk more than if you followed a low-fat, high-carb diet.

“The message isn’t that you should gorge on butter, bacon, and cheese,” says Volek. “It’s that there’s no scientific reason that natural foods containing saturated fat can’t, or shouldn’t, be part of a healthy diet.”

For more on this topic and a guide to foods you shouldn’t fear, check out “Fat Foods You Can Eat”.

Vitamin C Lowers Levels Of Heart Disease Biomarker C-reactive protein (CRP)

A new study led by researchers at the University of California, Berkeley, adds to the evidence that vitamin C supplements can lower concentrations of C-reactive protein (CRP), a central biomarker of inflammation that has been shown to be a powerful predictor of heart disease and diabetes. The same study found no benefit from daily doses of vitamin E, another antioxidant.

This study comes just days after a larger, eight-year clinical trial led by researchers at Boston’s Brigham and Women’s Hospital failed to show that vitamins C or E could cut the risk of heart attacks or strokes.

That trial does not necessarily close the books on the benefits of vitamin C for cardiovascular health, according to Gladys Block, UC Berkeley professor emeritus of epidemiology and public health nutrition and lead author of the study looking at vitamins C and E and their impact on CRP levels. She pointed out that the Brigham and Women’s Hospital study did not screen study participants for elevations in CRP – defined by the American Heart Association as 1 milligram per liter or greater – which is an important distinction in determining who might benefit from taking vitamin C.

The study led by Block, currently online and scheduled to appear in the Jan. 1 issue of the journal Free Radical Biology and Medicine, shows that for healthy, non-smoking adults with an elevated level of CRP, a daily dose of vitamin C lowered levels of the inflammation biomarker after two months compared with those who took a placebo. However, participants who did not start out with elevated CRP levels saw no benefit from vitamin C supplementation.

“This is an important distinction; treatment with vitamin C is ineffective in persons whose levels of CRP are less than 1 milligram per liter, but very effective for those with higher levels,” said Block. “Grouping people with elevated CRP levels with those who have lower levels can mask the effects of vitamin C. Common sense suggests, and our study confirms, that biomarkers are only likely to be reduced if they are not already low.”

The researchers said that for people with elevated CRP levels, the amount of CRP reduction achieved by taking vitamin C supplements in this study is comparable to that in many other studies of cholesterol-lowering drugs called statins. They noted that several larger statin trials lowered CRP levels by about 0.2 milligrams per liter; in this latest study, vitamin C lowered CRP by 0.25 milligrams per liter.

“This finding of an effect of vitamin C is important because it shows in a carefully conducted randomized, controlled trial that for people with moderately elevated levels of inflammation, vitamin C may be able to reduce CRP as much as statins have done in other studies,” said Block.

Evidence of the link between elevated CRP levels and a greater risk of heart disease has grown in recent years, but it had been unclear whether the beneficial effects of lowering CRP were independent of the effects of lowering cholesterol.

Newly released results from a multinational clinical trial help answer that question. Led by researchers at Harvard Medical School, the study, known as the Jupiter trial, found that statins reduced cardiovascular mortality and morbidity among people whose cholesterol levels were normal, but whose levels of CRP were greater than 2 milligrams per liter. The Jupiter trial found that among people who had such high levels of CRP at baseline, levels of CRP were 37 percent lower with statins compared with a placebo.

“One of the strengths of the Jupiter trial is that only persons with CRP levels greater than 2 milligrams per liter were enrolled,” Block added. “Researchers found very important effects of lowering CRP in people who had high levels to begin with.”

In the UC Berkeley study on vitamin C, participants who started out with CRP levels greater than 2 milligrams per liter had 34 percent lower levels of CRP with vitamin C compared with a placebo.

The UC Berkeley study also found a strong link between obesity and elevated levels of CRP. The researchers found that while 25 percent of normal-weight people had elevated levels of CRP, those levels were found in 50 percent of overweight and 75 percent of obese participants.

“The low-grade inflammation that characterizes obesity is believed to contribute to a number of disorders, including atherosclerosis and insulin resistance,” said Nina Holland, adjunct professor at UC Berkeley’s Division of Environmental Health Sciences and co-investigator on the study. Holland’s biorepository at UC Berkeley processed and stored the thousands of blood samples involved in this study.

Notably, the American Heart Association and the U.S. Centers for Disease Control and Prevention recommends that clinicians measure CRP levels in patients who have a moderately elevated risk of cardiovascular problems, as determined by other established risk factors such as high cholesterol levels and smoking.

“Major studies have found that the level of CRP in the body predicts future risk of cardiovascular disease, including myocardial infarction, stroke and peripheral artery disease, as well as diabetes,” said Block. “Some believe CRP to be as important a predictor of future heart problems as high levels of LDL and low levels of HDL cholesterol.”

The UC Berkeley-led study looked at the separate effects of two antioxidants: vitamin C and vitamin E. The researchers randomly divided 396 healthy, non-smoking adults from the San Francisco Bay Area into groups taking daily doses of either 1,000 milligrams of vitamin C, 800 international units of vitamin E or a placebo. The recommended dietary allowance (RDA) for vitamin C is 90 milligrams per day for men and 75 milligrams per day for women. The researchers noted that the suggested upper limit for vitamin C is 2,000 milligrams per day, or twice the level used in the study.

They compared participants’ baseline CRP levels with their levels two months later, at the end of the study. Fewer than half of the participants in the study started with elevated levels of CRP.

Participants who had baseline CRP levels less than 1 milligram per liter saw no significant effect on CRP levels after taking vitamin C supplements. However, those who started off with CRP levels of 1 milligram per liter or higher saw a 16.7 percent drop in levels after two months of treatment with vitamin C.

The researchers found no significant results for those taking vitamin E. They are uncertain as to why vitamin E did not show an effect even though it is also an antioxidant. Block noted that these vitamins have other functions independent of their antioxidant properties. Or, perhaps the difference relates to the fact that vitamin E is fat soluble and thus found in cell membranes while vitamin C is water soluble and found in intercellular fluid, the researchers said.

Although this study ended at two months, Block noted that there is no evidence to date of adverse effects for longer-term use of vitamin C at high levels. At the same time, researchers acknowledged the need to study whether vitamin C’s beneficial impact on CRP levels continue past two months.

“This is clearly a line of research worth pursuing,” said Block. “It has recently been suggested by some researchers that people with elevated CRP should be put on statins as a preventive measure. For people who have elevated CRP but not elevated LDL cholesterol, our data suggest that vitamin C should be investigated as an alternative to statins, or as something to be used to delay the time when statin use becomes necessary.”

Kekwick Diet, Atkins Fat Fast Weight Loss Results

The Kekwick Diet was named after one of its developers, Alan Kekwick. It was documented in a study titled:

“Calorie Intake in Relation to Body Weight Changes in the Obese,” Lancet, July 28, 1956, 155-161 by Alan Kekwick and Gaston Pawan.

Basically, what they did was to take a group of overweight subjects and put them in three groups. Each group received 1000 calories per day. One group was fed 90% carbohydrates, the second group 90% protein, and the third group 90% fat.

The group receiving 90% carbohydrates gained an average of 0,24 pounds per day of the study. The group receiving 90 protein lost an average of 0,6 pounds per day of the study, and the group receiving 90% fat lost an average of 0,9 pounds per day of the study.

This clearly demonstrates the superiority of diets high in protein and fats over diets high in carbohydrates. Note that each group received only 1000 calories per day. It’s interesting to note that even at the very restricted level of 1000 calories per day, subjects fed 90% carbohydrates actually GAINED weight.

A 1000 calorie per day diet of 90% fat is not a very exciting diet, but it can achieve the fat loss you apparently wish to achieve.

Do please note that the Kekwick is a diet designed by doctors and tested in clinical trials, so don’t be in too much of a hurry to dismiss it outright. It certainly isn’t a diet that should be widely used, however.

Finally, the Kekwick diet isn’t recommended unless you are extremely insulin resistant and have not been able to lose body fat on any other diet, including a more conventional low-carbohydrate diet.

In the book, Dr. Atkins New Diet Revolution, Dr. Atkins wrote that the Fat Fast is for the people who are severely resistant to weight loss. It’s not to “speed up” the rate of your loss because you believe you are losing too slowly.

According to Dr. Atkins you can be severely metabolically resistant to weight loss for a number of reasons. But you have to rule out any weight loss “stallers” that can be reversed or alleviated.

Before considering doing the Fat Fast:

1. Did you follow the book exactly during Induction and still didn’t lose any weight?

In other words, did you only eat what was listed on the Induction Acceptable Foods list, followed the rules of Induction, exercised, took your vitamin supplements, etc. If you didn’t do any or all of these things, your lack of weight loss might not be due to metabolic resistance to weight loss at all and you should really consider doing the diet properly before considering to do the Fat Fast.

2. Did you go to your doctor to have tests done for the following: hyperinsulinism, thyroid problems, and yeast overgrowth?

If any of these things apply to you, then your doctor should be able to give you treatments to help you with these problems and once these problems are solved your weight loss, typically, will improve.

3. Are you on any medications that can interfere with your weight loss?

Dr. Atkins cites anti-arthritis medications, steroids, hormones (birth control pills, HRTs), anti-depressants, diuretics and beta-blockers as some of the medications that can interfere with weight loss. If you are on any of these medications, you should sit down with your doctor and try to figure out if any alternatives can be given to you instead.

If you have gone through this list and have ruled out these things with your doctor, then Fat Fast might be an option for you.

Fat Fast/Kekwick diet isn’t for you if:

  1. You “cheated” through your Induction phase by not strictly following the Rules and/or eating foods not on the Acceptable Foods List or not in the quantities allowed during Induction. Those sneaks, cheats, and one bites can severely derail weight loss in some people.
  2. You are losing weight and want to break a stall.
  3. You want to speed up your metabolism to lose weight faster.
  4. You want to lose weight faster.

Chocolate Milk is the Best Recovery Drink

I love a tall glass of chocolate milk but until a few months ago I rarely thought to make it. Now I have a great excuse to drink it all the time.

I did some quick research on the best post workout recovery drink. Turns it’s not some fancy laboratory concoction or even even Gatorade. You get the best recovery from plain old chocolate milk. According to a 2006 sports nutrition study, “The findings suggest that chocolate milk has an optimal ratio of carbohydrates to protein to help refuel tired muscles”.

From CBSNews.com

During a 2004 Summer Olympics awash in controversies over steroids and supplements, one sportswriter wryly noticed that top American swimmer Michael Phelps was playing it safe — he preferred to drink Carnation Instant Breakfast between races.

Now it appears that the six-time gold medalist may have been onto something. A new study shows that plain old chocolate milk may be as good — or better — than sports drinks like Gatorade at helping athletes recover from strenuous exercise.

The study, published in the International Journal of Sport Nutrition and Exercise Metabolism, was small in scale; it was partially funded by the dairy industry. But dietitians say the study should help to counter the notion that high-tech, expensive supplements are better than whole foods when it comes to athletic performance. They also note that milk contains key nutrients, such as calcium and vitamin D, in quantities that sports drinks can’t match.

“[Milk] is a sports drink ‘plus,’” Keith Ayoob, EdD, a registered dietitian and associate professor of pediatrics at the Albert Einstein College of Medicine, tells WebMD. “It will supply you with things you need whether or not you’re working out.”

The study builds on findings that intense endurance exercise reduces the muscles’ supply of stored glucose, or glycogen, a key source of fuel for exercise. To maximize glycogen replacement, the American College of Sports Medicine and the American Dietetic Association recommend taking in a serving of carbohydrates within 30 minutes after a long and vigorous workout.

Milk vs. Sports Drinks

Common sports drinks such as Gatorade supply those carbs, as well as fluids and electrolytes lost through sweat. However, more recent research suggests that adding protein to the mix may further hasten recovery. Hence the new wave of drinks such as Endurox R4 that include protein as well as higher doses of carbs.

In the study, nine male cyclists rode until their muscles were depleted of energy, then rested four hours and biked again until exhaustion. During the rest period, the cyclists drank low-fat chocolate milk, Gatorade, or Endurox R4. During a second round of exercise, the cyclists who drank the chocolate milk were able to bike about 50% longer than those who drank Endurox, and about as long as those who drank the Gatorade.

The findings suggest that chocolate milk has an optimal ratio of carbohydrates to protein to help refuel tired muscles, researcher Joel M. Stager, PhD, Indiana University kinesiology professor, tells WebMD.

But the most puzzling result of the study, experts say, was why Endurox — which has the same carb-to-protein ratio as the chocolate milk — fared so poorly. Researcher Jeanne D. Johnston, MA, tells WebMD it may have to do with the different composition of the sugars in the milk. Another theory is that the sugars in the milk may be better absorbed in the gut than those in the Endurox.

Edward F. Coyle, PhD, a researcher on exercise and hydration at the University of Texas, tells WebMD the trial would have been stronger if the researchers had also tested the effect of flavored water or another dummy (placebo) drink.

The study was partly funded by the Dairy and Nutrition Council, an industry group. Coyle says that the study’s reliance on industry funding is not unusual in the world of sports research, as federal funding for such research is hard to come by.

A Cheaper Alternative?

While rapid nutrient replacement may not be important for casual exercisers, it can make a big difference in performance for competitive athletes who work out vigorously once or twice a day, says Roberta Anding, a sports dietitian and spokeswoman for the American Dietetic Association.

Anding has long recommended chocolate milk for young athletes who come to her practice at Texas Children’s Hospital in Houston. For children and teenagers from lower-income families, it doesn’t make sense to spend serious money on sports drinks when they can get milk as part of a subsidized lunch program, she tells WebMD. The only advantage of sports drinks, she notes, is that they never spoil.

Ayoob estimates that more than two-thirds of teenagers should be drinking more milk anyway because they don’t get enough calcium in their diets. He also recommends milk for its vitamin D and potassium content. “For me, this is a no-brainer,” he says.

Sources: Karp, J. International Journal of Sport Nutrition and Exercise Metabolism, 2006; (16: 78-91). “Nutrition and athletic performance — Position of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine,” http://www.eatright.org/cps/rde/xchg/ada/hs.xsl/adap1200.cfm. Svrluga, Barry, “Olympics Swim Trials,” Washington Post, July 13, 2004, http://www.washingtonpost.com/wp-dyn/articles/A44785-2004Jul12.html. Jeanne Johnston, department of kinesiology, Indiana University at Bloomington. Joel M. Stager, PhD, department of kinesiology, Indiana University at Bloomington; Keith Ayoob, EdD, RD, associate professor of pediatrics, Albert Einstein College of Medicine. Edward F. Coyle, PhD, professor, kinesiology and health education, University of Texas. Roberta Anding, clinical and sports dietitian, Texas Children’s Hospital, Houston.