Here’s a journal article the anti-fat hysterics at the USDA, American Heart Association, American Diabetes Association, etc. all should read. (Of course if they did, they’d dismiss it.) The article, published in Advances in Nutrition, is titled Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence. Let’s look at some quotes:

Although early studies showed that saturated fat diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease (CAD), the evidence of dietary saturated fats increasing CAD or causing premature death was weak.

The evidence was weak because the anti-fat hysterics relied on teleoanalysis: saturated fat raises cholesterol (in some people) and cholesterol is associated with heart disease, therefore saturated fat must cause heart disease.  Bad logic leads to bad theories.

Numerous reports and reviews in recent years have begun to call the perceived pernicious effects of dietary saturated fatty acids (SFAs) into question.

And yet few of those reports have changed the thinking of your average health reporter … not to mention the goofballs who write those annoying Eat This, Not That books and articles.

The purpose of this review is to summarize the scientific understanding as it relates to dietary fats in health and disease, particularly with regard to the innocuous nature of SFAs and the physiological effects that have implicated PUFAs in numerous disorders and diseases. The role of dietary fats in cardiovascular disease (CVD) and many other diseases is complex, yet there is a powerful inertia that has allowed the saturated fat doctrine to endure.

I don’t think powerful inertia is the correct phrase here. More like powerful vested interests.

Human food preferences tend to favor foods with both fats and sugars, which complicates any attempts to correlate saturated fats with disease.

Well, that should complicate any attempts at correlation, but the geniuses at the American Heart Association and other promoters of arterycloggingsaturatefat! hysteria found a simple solution: if people who eat saturated fats mixed with sugars get heart disease, blame the fat. (After all, you can’t blame sugar and still put your seal of approval on boxes of Cocoa Puffs.)

Because dietary saturated fats do not promote inflammation, it may be wiser to minimize omega-6 PUFAs and consume more SFAs to reduce various types of inflammation.

But … but … but the American Heart Association says corn oil is good for you.

Investigators often seem to have a particular bias against saturated fats.

That’s a polite way of saying “Scientists are freakin’ liars.”

Campaigns were waged against tropical oils (palm and coconut oils) in the early 1980s because of their high levels of SFAs, even though palm oil contains about as much MUFAs acids as SFAs and has an ample amount of PUFAs to keep serum cholesterol low …. Claims that tropical oils with a high SFA content increase the risk of CAD lack clear scientific evidence to that effect. Indeed, countries with high intake of tropical oils have some of the lowest rates of heart disease in the world.

Quick, somebody call The Guy From CSPI. He was behind those campaigns waged against tropical oils, which caused coconut oil to be replaced with trans fats – which he declared safe at the time. Given the success (ahem, ahem) of his campaigns, I’d like him to comment on that last paragraph.

Many of the shorter chain fatty acids found in milk fat and coconut oil have beneficial health effects. The shorter chain SFA in milk (C4–C12) are not only metabolized rapidly for energy in infants, but have been found to have important antiviral, antimicrobial, antitumor, and immune response functions. Lauric acid, which is present in milk and the most abundant fatty acid in coconut oil, is effective in preventing tooth decay and plaque buildup. Diets rich in coconut oils have also been shown to lower other risk factors for CAD, such as tissue plasminogen activator antigen and Lp(a).

Aren’t you glad the USDA has decided kids in school can’t drink whole milk, but sugar-laden skim milk is fine and dandy?

It should not be surprising that substitution of carbohydrates (starches) for saturated fats in the diet has relatively little effect on serum lipids. Excess carbohydrates are converted to fats for efficient energy storage, and the human body synthesizes primarily SFAs from excess carbohydrates, although MUFAs are also formed. Consequently, from a physiological viewpoint, there is no reason to believe that replacing fat in the diet with carbohydrate at a constant caloric intake will improve the serum lipid profile significantly. Indeed, a low-fat, high-carbohydrate diet causes an increase in serum triglycerides and small, dense LDL particles, which are more strongly associated with CAD than serum total cholesterol or LDL-C.

So skip the bacon and eggs and eat your Cheerios. The American Heart Association says those processed grains are good for your heart.

The meager effect that saturated fats have on serum cholesterol levels when modest but adequate amounts of polyunsaturated oils are included in the diet, and the lack of any clear evidence that saturated fats are promoting any of the conditions that can be attributed to PUFA makes one wonder how saturated fats got such a bad reputation in the health literature. The influence of dietary fats on serum cholesterol has been overstated, and a physiological mechanism for saturated fats causing heart disease is still missing.

No, no, no … I’ve heard nutritionists, doctors and dietitians on TV insisting that thousands of studies prove that saturated fat causes heart disease. Thousands!

It is time to reevaluate the dietary recommendations that focus on lowering serum cholesterol and to use a more holistic approach to dietary policy.

Well, the USDA dietary experts reevaluate their dietary recommendations every five years. Then, acting like the division of Monsanto the USDA has become, they recommend even less natural saturated fat and more mutant grains. But give them another 50 years or so, and they may actually pay attention to the science.

And another 50 years after that, the American Heart Association may do the same.

A reader asked me for some information on cancer and sugar, so I pulled up some items from my research database.  As long as I had the articles in front of me, I thought I’d share them.

Nothing listed here proves absolutely that sugars drive cancer or that a ketogenic diet will prevent cancer, but taken together, the articles do paint a picture.  Let’s take a look.

Cancer cells slurp up fructose, US study finds

Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same.

Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found.

They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types.

“These findings show that cancer cells can readily metabolize fructose to increase proliferation,” Dr. Anthony Heaney of UCLA’s Jonsson Cancer Center and colleagues wrote.

“They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.”

I found some suggested meal plans on the USDA’s official My Plate site, which I’ll share in another post.  Whole milk isn’t on the meal plan for breakfast, but orange juice and strawberry-flavored (i.e., sugary) skim milk are.  Remind me again … which of those drinks contains fructose and which doesn’t?

Compound That Blocks Sugar Pathway Slows Cancer Cell Growth

Scientists at Johns Hopkins have identified a compound that could be used to starve cancers of their sugar-based building blocks. The compound, called a glutaminase inhibitor, has been tested on laboratory-cultured, sugar-hungry brain cancer cells and, the scientists say, may have the potential to be used for many types of primary brain tumors.

The Johns Hopkins scientists, inventors on patent applications related to the discovery, caution that glutaminase inhibitors have not been tested in animals or humans, but their findings may spark new interest in the glutaminase pathway as a target for new therapies.

Glutaminase is an enzyme that controls how glucose-based nutrients are converted into the carbon skeleton of a cell. Additional enzymes that help construct the so-called “bricks” of the carbon skeleton are controlled by a gene called IDH1. In some brain cancer cells, IDH1 is mutated and the resulting enzyme grinds up the bricks into nutrients that feed cancer cells.

Yes, yes, I know what you’re thinking:  if blocking the glucose pathway slows cancer growth, why not just tell people to stop eating foods that spike glucose?  Well, I’m pretty sure the answer lies in the fact that scientists have applied for patents.  You can’t patent dietary advice, but you can patent a drug.

Diabetes Medication May Get New Life as Cancer Treatment

The drug metformin, a mainstay of diabetes care for 15 years, may have a new life as a cancer treatment, researchers said.

In a study in mice, low doses of the drug, combined with a widely used chemotherapy called doxorubicin, shrank breast-cancer tumors and prevented their recurrence more effectively than chemotherapy alone.

The findings add to a growing body of evidence that metformin, marketed as Glucophage by Bristol-Myers Squibb Co. and available in generic versions, could be a potent antitumor medicine.

In the report, being published in the Oct. 1 edition of Cancer Research, a journal of the American Association for Cancer Research, researchers said the combination of metformin and doxorubicin killed both regular cancer cells and cancer stem cells.

In contrast, doxorubicin alone had limited effect on the stem cells.

Mice that grew tumors generated from human breast-cancer cells have remained tumor-free for nearly three months on the combined treatment, while tumors have recurred in those not given the diabetes remedy.

Researchers said the results have potentially broad implications for cancer treatment.

Hmmm, now why would a drug given to type 2 diabetics be effective against cancer?  You have to read pretty far down the article to find out:

How metformin affects cancer isn’t certain, but one possibility is that it deprives tumor cells of sugar.

“Cancer cells are gluttons for glucose,” said George Prendergast, president and chief executive officer of Lankenau Institute for Medical Research, Wynnewood, Pa. “It is likely that metformin is taking advantage of this gluttony of the cancer cell in order to attack it.”

Cancer cells are gluttons for glucose … I’ll be sure to think about when I’m drinking my USDA-approved skim milk with added sugar.

Dietary glycemic load and colorectal cancer risk

The link above is to an observational study based on food questionnaires, so it doesn’t exactly meet the gold standard for research.  Nonetheless, here’s the conclusion:

The positive associations of glycemic index and load with colorectal cancer suggest a detrimental role of refined carbohydrates in the etiology of the disease.

The next time some vegan zealot trots out an observational study showing a weak association between meat and cancer, you can reply with this one and explain that since glycemic load is strongly associated with colorectal cancer, you’re sticking with a low-glycemic diet – meat included.  If the vegan zealot starts quoting the China Study, you can reply with this (sort of) China study of Chinese Americans:

Carbohydrates and colorectal cancer risk among Chinese in North America

Here’s the conclusion:

These data indicate that increased eCarb (non-fiber carb) and total carbohydrate consumption are both associated with increased risk of colorectal cancer in both sexes, and that among women, relative risk appears greatest for the right colon, whereas among men, relative risk appears greatest for the rectum.

So get T. Colin Campbell’s high-carb diet out of my face.

Effects of a ketogenic diet on tumor metabolism

This one isn’t a study; it’s a case report from 1995 of two pediatric cancer patients put on ketogenic diets.  Here are some quotes from the abstact:

OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient’s overall nutritional status.

So all the way back in 1995, at least some doctors suspected that depriving cancers of glucose might help.  Sheesh.  Anyway …

RESULTS:  Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression.

Improvements in mood and skill development?  No, no, no … low-carb diets make you depressed and irritable.  I know that’s true, because I read it on Yahoo Health.

Glucose deprivation activates feedback loop that kills cancer cells

Compared to normal cells, cancer cells have a prodigious appetite for glucose, the result of a shift in cell metabolism known as aerobic glycolysis or the “Warburg effect.” Researchers focusing on this effect as a possible target for cancer therapies have examined how biochemical signals present in cancer cells regulate the altered metabolic state.

Now, in a unique study, a UCLA research team led by Thomas Graeber, a professor of molecular and medical pharmacology, has investigated the reverse aspect: how the metabolism of glucose affects the biochemical signals present in cancer cells.

In research published June 26 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation — that is, depriving cancer cells of glucose —activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species, the cell-damaging molecules and ions targeted by antioxidants like vitamin C.

Hey, I don’t care if it’s an amplification loop that does the job or if the cancer cells just die off from a lack of fuel.  The point is, once again we see that depriving cancer cells of sugars can kill them.

Keep starving those cancer cells, folks.

Well, I am shocked: researchers recently discovered some lost data from a 40-year-old study on heart disease, analyzed the lost data, and discovered … wait for it … the animal fats we’ve been consuming for hundreds of thousands of years appear to be better for our health than the chemically extracted vegetable oils we’ve only been consuming for the past 100 years.

I know, I know … you can’t believe it either, can you? The new analysis has (fortunately) been making a bit of a splash in the media. Here are some quotes from an article published in the online edition of Forbes:

In an exceedingly strange turn of events, data from a clinical trial dating from the 1960s, long thought to be lost, has now been resurrected and may contribute important new information to the very contemporary controversy over recommendations about dietary fat composition.

The American Heart Association has long urged people to increase their consumption of polyunsaturated fatty acids (PUFAs), including omega 6 PUFAs, and reduce their consumption of saturated fatty acids. The recommendations are based on the simple observation that PUFAs lower total and LDL cholesterol while SFAs have the opposite effect. However, the cardiovascular effects of substituting PUFAs for SFAs have never been tested in randomized, well-controlled clinical trials, and a growing proportion of experts now suspect that simple changes in total cholesterol and LDL cholesterol may not tell the whole story.

Let’s just stop and re-read part of that paragraph.

However, the cardiovascular effects of substituting PUFAs for SFAs have never been tested in randomized, well-controlled clinical trials …

We’ve never had anything remotely resembling actual proof that substituting vegetable oils for animal fats prevents heart disease. But the lack of proof didn’t stop an entire industry from building up around the belief that vegetable oils are better for our health – just visit your grocery store and look at all the tubs of Smart Balance and other butter substitutes touting the fact that they contain less saturated fat.

The lack of proof didn’t stop The Guy From CSPI from harassing the restaurant industry into substituting vegetable oils for the lard and tallow they once used to fry foods. (And a chicken-fried steak hasn’t tasted the same since.) The lack of proof didn’t stop schools, hospitals, company cafeterias, and just about every other institution that serves meals from dumping butter in favor of margarine.  The lack of proof doesn’t stop the average doctor, dietitian or nutritionist from believing that hundreds or even thousand of studies have shown that animal fats cause heart disease.

Let’s read on:

One trial that actually tested the hypothesis was the Sydney Diet Heart Study, which ran from 1966 through 1973. In the trial, 458 men with coronary disease were randomized to a diet rich in linoleic acid (the predominant omega 6 PUFA in most diets) or their usual diet. Although total cholesterol was reduced by 13% in the treatment group during the study, all-cause mortality was higher in the linoleic acid group than in the control group. However, in the original publications, and consistent with the practice at the time, deaths from cardiovascular (CVD) and coronary heart disease (CHD) deaths were not published.

Now, in a new paper published in BMJ, Christopher Ramsden and colleagues report that they were able to recover and analyze data from the original magnetic tape of the Sydney Diet Heart Study. The new mortality findings are consistent:

• All cause: 17.6% in the linoleic group versus 11.8% in the control group, HR 1.62, CI 1.00-2.64)
• CV disease: 17.2% versus 11%, HR 1.70, CI 1.03-2.80
• CHD: 16.3% versus 10.1%, HR 1.74, CI 1.04-2.92

Once again, let’s re-read part of the text above and let it sink in for a moment:

Although total cholesterol was reduced by 13% in the treatment group during the study, all-cause mortality was higher in the linoleic acid group than in the control group.

One of the goals of the original study was to lower cholesterol levels by swapping vegetable oils for animal fats. That goal was achieved – yahoo! Open the champagne.

And then the study subjects had to go and ruin the party by dying prematurely at a higher rate — from both heart disease and all causes combined — despite their lower cholesterol levels. The operation was a success, but unfortunately the patient died.

I’ve read the full text of the study, which includes this paragraph in the discussion section:

The traditional diet-heart hypothesis predicts that these favorable, diet-induced changes in blood lipids will diminish deposition of cholesterol in the arterial wall, slow progression of atherosclerosis, reduce clinical cardiovascular risk, and eventually improve survival. As expected, increasing n-6 from safflower oil significantly reduced total cholesterol. However, these reductions were not associated with mortality outcomes. Moreover, the increased risk of death in the intervention group presented fairly rapidly and persisted throughout the trial. These observations, combined with recent progress in the field of fatty acid metabolism, point to a mechanism of cardiovascular disease pathogenesis independent of our traditional understanding of cholesterol lowering.

That’s the polite, academic way of putting it. Allow me to interpret for the non-academic masses:

The Lipid Hypothesis is a crock of @#$%. Cholesterol doesn’t cause heart disease. Saturated fat doesn’t cause heart disease. TIME magazine, your doctor, your government health officials, and everyone else who warned you to cut back on saturated fats, switch to vegetable oils, and lower you cholesterol to save yourself from heart disease had no @#$%ing clue what they were talking about.

This wasn’t some namby-pampy observational study based on food-recall surveys, by the way. It was a controlled clinical trial. The subjects in the intervention group were given the safflower-oil products to consume, they received ongoing dietary counseling, and they kept daily food diaries … until they died, anyway.

The explanation we’re given for the “lost” data just now being discovered and analyzed is that a computer data tape was misplaced back in the day. (For those of you who were born after 1970, that’s how digital data used to be stored – on magnetic tape.) The explanation is probably true … but given that the original study was completed around the time the arterycloggingsaturatedfat! theory was sweeping the medical world, I can imagine another scenario:

“Did you finish crunching the numbers, Jenkins?”

“Yes, sir. The men who switched to safflower oil lowered both their total cholesterol and their LDL by a significant amount. Thirteen percent, in fact.”

“Outstanding!”

“Yes, but … uh …”

“Well?  What are you waiting for?”

“How soon do I get tenure, sir?”

“Out with it, Jenkins!”

“The men who switched to the safflower oil also had significantly higher rates of cardiovascular disease, heart disease, and overall mortality.”

“Hmmm.  That’s not at all what we expected.”

“I know, sir.”

“Good thing you misplaced the data.”

“No, sir, I have it right—”

“I said, good thing you misplaced the data.”

“Oh. Right. And, uh, for how many years did I misplace it, sir?”

“I’d say … let’s see … about forty years.”

“Why forty years, sir?”

“Because we’ll all be retired by then.”

Okay, I was dishonest in the title of this post.  Not all Norwegians have heart disease.  But almost all Norwegian men are (if we believe the prevailing guidelines) at high risk for heart disease.

Like most Americans, I spend very little time thinking about Norwegians.  The great Chicago columnist Mike Royko once pointed that in the ethnic melting pot of Chicago, you can hear jokes about the Irish, Jews, Italians, Poles, African-Americans, Mexicans, Puerto Ricans, French, British, Russians and Germans.  He even remembered some jokes about Swedes.  But when he asked around, nobody could remember ever hearing a joke about Norwegians.  Royko even tracked down a Norwegian-American acquaintance who confirmed, “Naw, nobody tells jokes about us.  We’re too nice.”

I got thinking about the Norwegians this weekend while answering comments on my post about the Spanish Paradox.  I remembered logging a study about Norwegians and their risk of heart disease into my database and pulled it up.  Here are some quotes from the study:

Since the first US Framingham model for predicting heart disease risk was published in 1991, it has become ever more widely recommended that doctors in primary care carry out risk assessment by combining several risk factors for cardiovascular disease using algorithms. Until recently most risk equations have been derived from the Framingham study, but these calculations tended to overestimate risk in the European context.

Actually, the Framingham model is lousy at predicting heart disease in the American context as well.  But let’s move on.

A new European risk scoring system for cardiovascular disease, based on the first phase of the systematic coronary risk evaluation (SCORE) project, was presented in 2003. The system is based on a pooled dataset of cohort studies from 12 European countries, among these Norway, and offers a format for estimating fatal cardiovascular disease risk that is suitable for clinical practice.

After explaining those guidelines, the researchers report on the results of applying them to data collected from several thousand Norwegians.  Here’s what they found:

At age 40, 22.5% of women and 85.9% of men were at high risk of cardiovascular disease. Corresponding numbers at age 50 were 39.5% and 88.7%, and at age 65 were 84.0% and 91.6%.  At age 40, one out of 10 women and no men would be classified at low risk for cardiovascular disease.

Hmmm … people in Norway must be dropping like flies from heart disease, at least according to the prevailing guidelines for estimating heart-disease risk … you know, cholesterol levels and all that stuff.

Here again is the American Heart Association’s chart showing rates of cardiovascular disease around the world:

You’ll notice Norway is down toward the lower end of the scale – not as low as France or Spain, but lower than the U.S., U.K. or Germany.

For once, the researchers recognize that the current guidelines are poppycock.  They don’t put it quite that way, of course.  Their language is more academic and polite:

Implementation of European guidelines to prevent cardiovascular disease would label most people in an unselected Norwegian population at high risk of fatal disease from age 40

The validity of the evidence base of the guidelines is questionable and predicts practical and ethical dilemmas related to resource allocation and clinical counselling.

Any overestimation of a person’s risk for cardiovascular disease can have important implications. Apart from causing unnecessary concern, it undermines the patient’s informed choice for intervention. It is also likely to increase prescribing costs and affect life insurance premiums.

Yup.  First thing you know, your doctor is scaring the bejeezus out of you and talking you into taking statins.

Over the weekend, I also had a mini-debate on Twitter with someone who insisted the French paradox is probably a matter of genetics.  I pointed out that waves of French moved to England to become landowners after the Norman Conquest and that the French and English have been intermarrying for hundreds of years.  I doubt that there’s a big difference between French DNA and British DNA.  He didn’t buy it and tweeted a link to a document detailing the marked genetic differences among Europeans.  He apparently didn’t notice that the document he linked described differences among Europeans separated by the Alps for most of history.

Look at the AHA chart one more time.  Scotland and Ireland are near the top.  England and Wales are near the middle.  Now go find Australia.  I’ll give you minute …

… Find it?  Yup, Australia is near the bottom.  My Australian readers can correct me if I’m wrong, but I’m pretty sure we can’t explain away the “Australian Paradox” by suggesting Australians are genetically distinct from the Irish, Scots and Brits.

So we have the Spanish, who are in “poor cardiovascular health” according to current guidelines, but have a low rate of heart disease.  We have the Norwegians, nearly all of whom are at a high risk of heart disease according to current guidelines, but have a relatively low rate of heart disease.

I’m thinking the problem is with the current guidelines.  Nice to see some researchers say as much.

A reader sent me a link to an interview with Dr. Robert Lustig, telling me that a registered dietitian called into the show to explain how it’s all about low-fat diets and calories in/calories out, which prompted Lustig to slap her down.

I listened to the entire interview, but if you only have time to enjoy hearing a dietitian put in her place, skip ahead to about 47 minutes in.  You can listen to the interview here.

If you’re a long-time reader, you may remember a post in which I recounted how a YouTube commenter I nicknamed “Cliffy” kept insisting that kids get fat because their parents feed them too much, period.  No amount of evidence or reason would budge Cliffy from this position.  Cliffy was (according to Cliffy) a lean, muscular gym rat — and therefore knew everything there is to know about the biochemistry of body composition.

I didn’t mention it in that post, but in another series of exchanges, Cliffy also insisted I did not (contrary to what my mirror and scale were telling me) become both leaner and more muscular after I tightened up my diet and switched to Fred Hahn’s Slow Burn workout method.  Cliffy explained that it’s physiologically impossible to gain muscle mass while losing fat mass, and in fact pretty much everyone who loses weight loses some muscle mass.  He knew this because some body-building guru he worships said as much.

I tried telling him that I did indeed put on muscle even while losing weight, that my arms and chest and thighs had become noticeably thicker while my waist shrank, but Cliffy explained that I’m an idiot (and a fat, lazy old man) and only thought I’d gained muscle because the weight loss gave me more definition.

So I looked up a clinical study in which women lost body fat while gaining muscle mass and posted the reference.  (YouTube won’t take links in comments.)  Cliffy read the study and replied that it’s sometimes possible for people who’ve never worked out and are therefore “untrained” to gain muscle while losing weight, but not for anyone who’s been regularly lifting weights – which I had been.  When I asked how being “untrained” makes the physiologically impossible become possible, he explained that I’m an idiot (and a fat, lazy old man) and must not have been “trained” even though I’d been lifting weights regularly before switching to Slow Burn.

I thought about Cliffy when Jimmy Moore posted the results of his nutritional ketosis experiment earlier this week.  When Jimmy started losing weight again after cutting back on protein and adding more fat to his diet, I was happy he’d reversed the creeping weight gain that had baffled him, but I wondered if the lower protein intake would lead to muscle loss.  That fear was put to rest when Jimmy and Christine visited us last week.  His arms looked thicker than when I saw him in July, not thinner. But of course Cliffy would insist that was just better definition creating the illusion of extra muscle mass.

Wrong once again, Cliffy.

If haven’t read Jimmy’s post, here’s the quick summary:  Two months ago he underwent a very accurate body-composition test called a DXA scan.  He had another DXA scan on Monday before leaving for Australia.  The test showed that during those two months, Jimmy shed just over 16 pounds of additional body fat while gaining just over six pounds of muscle.  He gained two pounds of muscle in his arms alone.  If that doesn’t sound like much, try this little thought experiment:  picture a one-pound lean steak.  That’s how much meat Jimmy put on each arm.  So yes, his arms are definitely thicker, not just better defined.

Cliffy would jump in at this point to insist that Jimmy was clearly “untrained” until recently.  Hogwash.  Jimmy’s been lifting weights for at least a couple of years, maybe longer.  I worked out with him on the low-carb cruise in May.  He was impressively strong.  “Untrained” muscles don’t push that much weight.  He may have been training harder lately, but he wasn’t “untrained” in May.

One of the speakers on the same low-carb cruise was Dr. Jeff Volek, who has conducted much of his research on athletes.  (It was Dr. Volek , along with Dr. Steve Phinney, who convinced Jimmy to try getting into nutritional ketosis to reverse his weight gain.)  I mentioned Cliffy’s theories to Dr. Volek one night and asked if it’s physiologically impossible to get leaner and more muscular over the same time period.  It’s not impossible at all, Dr. Volek replied; we’ve seen it happen over and over, even in athletes.  (Here’s a study in which athletes lost fat and gained lean body mass.)

So the bottom line:  don’t believe the myth that if you lose weight, you’re inevitably going to lose both muscle and fat.  If you work out and eat right, you can actually gain muscle.  I lost fat and gained muscle.  Jimmy lost fat and gained muscle, despite eating less protein than he did previously.  Athletes have lost fat while gaining muscle.

And Cliffy’s still an idiot, even if he’s not a fat, lazy old man.