Welcome to a new month

Monday WOD

For Time:


Run 800M
100 Wall Balls (20M/14W)
Run 800M

Holy Cherry Pickers

I hope that everyone is not broken from the deployment WOD. I was told that class load today was a little light. Sprinting is a key part to preparing for the unknown and unknowable. For those of you who showed up awsome.

Here is a great WOD for Friday

Cindy
AMRAP in 20 min
5 Pull ups
10 Push ups
15 Squats

Scale as needed.

Next week starts WODs planned by Jenn, I will be posting but she has developed her own WODs. Trainers now get 2 weeks of WOD development/programing (with a little coaching), this is a great training opertunity for our younger trainers as they grow and develop. Please provide them feed back on how the upcoming WODs affect you. You are our gage on where to go.

Thursday

Great job for deployment WOD. That was a real smoker

After such a hard WOD that here is a WOD that will give the weight lifting a break

run/rest
60/60
60/50
60/40
60/30
60/20
60/10
60/20
60/30
60/40
60/50
60/Finished

Keep track of total distance
Rest can be walking or stopped

Farewell to a founder

Tomorrow will be Dons last WOD before he deploys. Post is supposed to open at 1000 so as long as it is still open this WOD is on as a farewell to Don. Seeing that he deploys for a year I took some of his best ideas and made them into this WOD to show you how fast 12 months can go by.

For Time
12 Pull Ups
12 Deadlifts – 265 - 165
12 Burpees
12 Hang Power Clean – 175 - 115
12 Double Unders
12 Front Squats – 125 - 85
12 Double Unders
12 Push Press – 75 - 65
12 Burpees
12 OHS – 55 - 45
12 Pull Ups
12 SDHP – 45 - 35



The bar is set up from inside to out with 5-10-15-35-45. Women it is 5-10-10-15-25. You drop off the bar as you move thru the wod. The numbers are short and the weights heavy power thru it and you can complete the deployment wod in no time.

No class

Due to weather class is on ur own. Please be safe

Deadlift for weight

1-1-1-1-1-1-1
Deadlift

You should reach Max load some where around rep 5

Monday's WOD

21-15-9
Box Jumps
Thrusters (95/65)
Burpees

No Classes Friday!

Due to the trainers meeting there will be no organized classes on Friday. If you wish to WOD on your own, you can do:

4 rounds for time of:
Run 400
50 Squats

Thursday's WOD

Push Press
1-1-1-1-1-1

http://media.crossfit.com/cf-video/cfj-nov-05/push-press.wmv

Sorry about the lack of posting this week. We had people cutting out some dead sod in our back yard and replacing it and they cut the buried coaxial cable line that runs to our house knocking out our internet for 3 days!

Tuesday WODel

5rds
9 wide grip deadlifts
6 hang power snatch
3 OHS
Men 95
Women 65

HP snatch is from waist and a short land

Bad cholesterol’: It’s not what you think

Finally, the mainstream media publishes something accurate on cholesterol and how the FDA recommended diet affects it.

It's time to rethink the halo-and-pitchfork view of our blood fat levels

Two laboratory machines have played a role in perhaps the greatest medical misadventure of our time: the indictment of a villain — LDL cholesterol — with the ultimate crime of the heart, coronary artery disease.

One machine delivered the early, misleading evidence of cholesterol's guilt, and another may have just nabbed the actual killer. And because the killer's likeliest and earliest targets are men, we'd all better pay attention to the new case being made against it.

The first machine, an early prototype of a device called an analytical ultracentrifuge, was crucial to the 1949 discovery of high-density lipoprotein (HDL) and low-density lipoprotein (LDL). These common blood fats would become cemented in people's minds by their angel/devil personas, "good" and "bad" cholesterol. But now the halo-and-pitchfork images seem a little simplistic. And hardly useful.

These cholesterol characterizations were spun out of a wall-size contraption that rotated plasma at 40,000 revolutions per minute from the late 1940s until the machine's retirement in 2004. When you consider its role in the powerful beliefs we hold about heart disease, the sprawling, rattling beast should be mounted under flattering light in the Smithsonian.

For decades, a tidy narrative about the relationship between LDL cholesterol and heart disease has affected everything from the food we eat to the drugs we take to the test results we track and the worries we harbor. This oversimplified view of cholesterol — that all LDL is the same and that all LDL is bad — has enabled the adoption of an accompanying oversimplified dietary belief, that all saturated-fat consumption raises your risk of heart disease.


The LDL hypothesis has also encouraged many of us to swallow the most-prescribed class of drugs in recent history. Americans spent more than $14 billion on LDL-lowering medications in 2008. Whether that money came out of their own pockets — straight up, or through ever-escalating co-pays — or out of the hemorrhaging U.S. health-insurance system known as Medicare, it's a huge expenditure. Twenty-four million Americans take statins, and the latest health directives suggest that those numbers should be higher. And why stop at grown-ups? Some pediatricians want to start feeding Lipitor (and the like) to kids.


As John Abramson, M.D., writes in his book "Overdosed America," "Largely as a result of these guidelines, cholesterol control has become the main focus of preventive health care in the United States."

So it's more than a little disconcerting that the other machine in this story, a complex pile of gadgetry quietly clicking away on a countertop in Berkeley, California, is only the most recent breakthrough that has called the entire LDL cholesterol premise into question.

On a balmy Sunday last August, Ronald M. Krauss, M.D., the director of the department of atherosclerosis research at Children's Hospital Oakland Research Institute, showed me into his workplace to demonstrate a novel new system for tabulating LDL. Using a particle-spitting process known as ion mobility analysis, Dr. Krauss and his colleagues have developed the first device capable of counting LDL and other lipoproteins down to their smallest subcomponents. (Several other ways of analyzing LDL subparticles exist, but they involve indirect methods.)



A New Jersey company, Quest Diagnostics, worked for 7 years with Dr. Krauss — who is helping to set the new cholesterol recommendations from the NIH's National Cholesterol Education Program — to develop a method of analyzing cholesterol. Borrowing the same processes used for testing air pollution and residue from explosives, the quarter-million-dollar prototype is very sophisticated technology. "It determines the size of the particle based on physics," says Dr. Krauss with nerdy admiration, "on the speed at which it flies through the air."

In other words, this machine won't be coming to your community clinic anytime soon. But even if it's not ready for mass production, the information gleaned using technologies like ion mobility means that LDL cholesterol can no longer be identified as the single source of all heart trouble. Those pamphlets adorning your doctor's waiting room may portray LDL as a kind of lone gunman taking a bead on your heart, but they hide a basic fact of science: "Bad cholesterol" is at best a poor shorthand for four major types of independently behaving LDL, each with its own implications for heart disease. We ignore the distinctions at our peril.


Some of these forms of LDL are relatively safe and some are dangerous, and treating them all as one and the same — the way we do every time we pay our clinic for a three-part lipid panel that simplistically says "LDL: 125" — is telling us little about the LDL cholesterol that matters, all the while sending health costs through the roof. We may be medicating many people who have no clear need for medication, using drugs that don't target the right particles, and replacing foods that are benign with foods that are anything but. (this is why statins are so ineffective)

So in the heart-disease world, we've been stalking the devil we know instead of the devils we don't know. But we need to get to know them if we hope to dodge the number one killer of men.


LDL comes in four basic forms: a big, fluffy form known as large LDL, and three increasingly dense forms known as medium, small, and very small LDL. A diet high in saturated fat mainly boosts the numbers of large-LDL particles, while a low-fat diet high in carbohydrates propagates the smaller forms. The big, fluffy particles are largely benign, while the small, dense versions keep lipid-science researchers awake at night. (so basically the FDA recommended diet actually propagates the harmful LDL - shocker!)

But here's the problem: The typical LDL test doesn't distinguish between large and small LDL particles — it can't even spot the difference. And people can have mostly large LDL or mostly small LDL in their overall LDL, depending upon a host of genetic, lifestyle, and environmental factors. Your own personal mix may make all the difference between living to a heart-healthy old age and becoming a Monday-morning casualty at your desk.

Dr. Krauss and collaborators from Harvard and Malmo, Sweden, have helped identify what influences the difference. Working with blood samples from 4,600 healthy Swedish men and women, they used ion mobility analysis to count 11 forms of cholesterol subparticles for each person, and then ran the data through a complex statistical sorting program. After looking for relationships correlating with the 8 percent of people who went on to develop cardiovascular disease, they found three scenarios that predicted it, from the most powerful predictor to the least:

1. High levels of smaller and medium LDL combined with low HDL (a dreaded diabetes-linked syndrome Dr. Krauss had previously called atherogenic lipoprotein phenotype, or pattern B)
2. Low HDL levels
3. High total LDL levels

According to Dr. Krauss, the three risk factors appear to represent three separate processes that put your cardiovascular health at risk. For men, the first two scenarios are more predictive of heart disease, but the third — high total LDL — was only marginally predictive of heart disease in men. Nowhere to be seen, of course, is the "total cholesterol" number doctors have been bashing us over the head with for decades. Turns out that number is not as useful a predictor for individuals. "LDL cholesterol is used as a marker for heart-disease risk," Dr. Krauss explains. "It's not a perfect marker, and the particle story is part of the reason for that."

In other words, when you tease apart the subsets of LDL that are preferentially involved in heart disease, total LDL is a less reliable bio-marker. It's like the sniffles that could signal allergies, or the onset of swine flu, or nothing at all. This ambiguity works both ways. Just because you have less of the symptom (statin users take note) doesn't mean you'll have less of the disease. A drop in your total LDL cholesterol might mean nothing at all. A higher LDL cholesterol reading, for that matter, could simply mean you are a healthy person who has learned how to build an amazing sauce out of wine, garlic, shallots, butter, and heavy cream.

We currently test for a number that tells us less about our health than we think it does, and then we busily (and expensively) medicate it downward. It would be more effective to test the numbers that do matter, of course, and then to learn how we can keep those meaningful numbers in check, whether we do it through different meals, more miles on the pedometer, or better-targeted medications.

Cholesterol is a natural substance your body produces for a variety of uses. It is carried through the body in three containers — LDL, HDL, and VLDL — that deliver it to cells along with triglycerides. The average man reasons that the cholesterol in his scrambled eggs must surely end up in his arteries somehow, and this makes him do things like order egg-white omelets for breakfast.


There is indeed a link between the cholesterol you eat and the cholesterol in your arteries. It's just not the "eat more, have more" worry that's been drummed into you for years. In fact, your body's production and uptake of cholesterol is highly regulated; eat a six-egg omelet and your body simply produces less cholesterol because of the dietary onslaught. "There is a very weak connection between the LDL cholesterol we measure and dietary cholesterol," Dr. Krauss says. "I spend a lot of time talking to reporters and trying to explain that dietary cholesterol is not the same as blood cholesterol." He adds that the 200 milligrams of cholesterol most people eat every day is nothing compared with the 800 milligrams their bodies produce. But you don't have to take his word for it. "It is now acknowledged that the original studies purporting to show a linear relation between cholesterol intake and coronary heart disease may have contained fundamental study design flaws," wrote the author of a recent review in the International Journal of Clinical Practice.




So eggs are off the heart-disease hook. But what about saturated fat? One of the major types of saturated fat we eat — the stearic acid that makes up one-third of the saturated fat in beef — has little or no impact on blood cholesterol. And you may well imagine that pizza grease and butter are magically transported from your gut to your arteries, but that's like using sock puppets to explain the workings of a supercomputer. Other types of saturated fat do increase LDL, it turns out (sometimes HDL, too), and high LDL is modestly associated with heart disease, but the saturated fat on your plate never goes anywhere near your arteries. Saturated fat increases bad-cholesterol levels by interfering with receptors responsible for removing LDL from the blood. Whether or not that's a health concern is anyone's guess.

"If you substitute polyunsaturated [good] fat for saturated fat, you see a reduction in heart-disease risk," Dr. Krauss says, casting more doubt on four decades of diet advice. "The interpretation of that finding has been that saturated fat is bad. My view, based on the data I have seen, is that it means polyunsaturated fat is good; it doesn't necessarily say anything about saturated fats being bad... Does that mean saturated fat is bad fat? Or just that saturated fat is not a good fat?"

Of course, that isn't the message we're all accustomed to hearing.

And for that you can blame the analytical ultracentrifuge — or, more specifically, the fact that so many heart-disease authorities weren't ready for what it discovered. The first one ever used in the United States arrived in Berkeley thanks to the efforts of John Gofman, Ph.D., M.D., a physicist-turned-physician previously employed by the Manhattan Project. After the war, Dr. Gofman wanted to cure heart disease in the worst way, and he thought the answer might lie in the newly discovered particles known as lipoproteins, the fat-protein particles that encircled cholesterol and triglycerides to shepherd them through the bloodstream. He took plasma samples from people with and without heart disease and used his new machine to spin the samples like nobody's business. Because of the physical properties of the plasma, the fatty lipoprotein particles separated and floated, with the lightest ones making it to the top first. Thanks to his analytical ultracentrifuge, Dr. Gofman discovered three major classes of lipoproteins. He named the lightest lipoproteins VLDL, for very-low-density lipoproteins (chicken-fat-type globules carrying triglycerides); the next most buoyant came to be known as LDL, and the heaviest were called HDL.


Then Dr. Gofman asked people about their health and diet. He learned that having high LDL or high triglycerides correlated with an increased risk of heart disease, high HDL correlated with a low risk of heart disease, and that the two profiles responded entirely differently to foods in the diet. (He also learned that cholesterol could be packaged either tightly clustered or loosely assembled within LDL; measuring it did little to reflect this risk.) Saturated fat raised LDL, while carbohydrates raised triglycerides, ultimately lowering HDL (this is what you should be concerned about - controlling your carbs and keeping your triglycerides down). (Dr. Gofman even recognized that LDL was made up of subtypes, although the meaning of the diversity was unclear at first.) It was groundbreaking work, but too advanced for the movement it ultimately spawned. With so few analytical ultracentrifuges available, researchers began using cheaper methods of counting lipoproteins, methods now offered during routine physicals. One form of cholesterol became "good," the other "bad."

"It sort of lost the details," says Dr. Krauss.


By the time Dr. Krauss arrived at Berkeley in 1976, the ideas of Dr. Gofman, who had left for greener pastures, began attracting support. A 1977 NIH study — an early set of papers from the now legendary Framingham Heart Study — confirmed that high HDL is associated with a reduced risk of heart disease. It also confirmed that LDL and "total cholesterol" tells us little about the risk of having a heart attack, language that heart-disease authorities would downplay years later. Given this finding, as Gary Taubes writes in "Good Calories, Bad Calories," we would have been better off to start testing for HDL — or even triglycerides — and nothing else.

Dr. Krauss was working part-time in Dr. Gofman's old lab and flipping through some data cards when he noticed a correlation that would change everything. As he combed through a recently completed study of 80 men and 54 women in Modesto, California, Dr. Krauss noticed that the people with low HDL tended to have high LDL. But not just any LDL was elevated; only the smaller forms observable to Dr. Gofman's analytical ultracentrifuge.

"I started studying these readouts, and what popped out were some amazingly strong inverse correlations," he says, still amazed at his good fortune. "It was just sitting there in the data." Dr. Krauss had found that small, dense LDL particles were the evil twin of good cholesterol. HDL and small LDL tended to move at the same time, he discovered, but in opposite directions. If your smaller forms of LDL were high, your HDL was low; if your smaller forms of LDL were low, your HDL was high. Whether one was the cause and the other was the effect was unclear, but given the newly discovered importance of HDL, the importance of smaller forms of LDL was now real.

This created a practical problem. Lumping all forms of LDL cholesterol together, as labs currently do when they count it in your basic blood draw, tells us little about how much of that LDL is small and how much is large. "Everyone doesn't necessarily have the same amount of very small LDL in their LDL," Dr. Krauss explains. Some people have mostly large LDL, a group Dr. Krauss would describe as "pattern A," while others have mostly small LDL (and usually, low HDL and high triglycerides), a group Dr. Krauss would label "pattern B." The second group has an increased risk of heart disease (a finding suggested again this year through the use of ion mobility). Large LDL, on the other hand — and large LDL is usually the majority of the LDL that shows up in a standard blood profile — is mostly benign.

The heart-disease community was not impressed. "It took me 4 years to publish that paper," he says, recalling his early work on subparticles in the late 1970s. "That's beginning to tell you some of the obstacles I was going to face."


The cost of that resistance had become apparent by the mid-1980s and into the 1990s as Dr. Krauss began to test whether changes in diet could change a person's LDL profile from good to bad, or from pattern A to pattern B. Using data from the Framingham Heart Study — the longest-running study of its kind — health organizations had begun to roll out the message of "good" and "bad" cholesterol, a message that in turn created the concept of good fats and bad fats. But during experiments, Dr. Krauss discovered that while a diet high in saturated fat from dairy products would indeed make your LDL levels rise, "saturated fat intake results in an increase of larger LDL rather than smaller LDL particles," as he wrote in an American Journal of Clinical Nutrition review he co-authored in 2006. A diet heavy in full-fat cheese and butter — but not overloaded in calories — triggered the relatively harmless health profile described as pattern A. (Having demonstrated the benign consequences for cholesterol from consuming dairy fat, he is currently conducting studies to find out if the same holds true for diets high in saturated fat from beef.)

Not only is dairy fat unlikely to increase heart-disease risk, Dr. Krauss and others have learned, but reducing saturated fat in a way that increases carbohydrates in a diet can shift a person's LDL profile from safe to dangerous. (let's see how long it takes for the FDA to make any changes.....) That's pretty much what happens whenever some well-meaning person with "high LDL" starts eating "low-fat" frozen dinners filled out with corn-derived additives, all the while engaging in the customary ravaging of a basket filled with dinner rolls.

"I like Ron Krauss and admire his work," says Dean Ornish, M.D., a fellow Bay Area heart-disease researcher and surely the most visible proponent of the idea that a diet low in saturated fat and high in carbohydrates can help reduce the risk of heart disease. But Dr. Ornish says Dr. Krauss shifted his study participants from pattern A to pattern B by having them eat more of the processed carbohydrates. "The carbohydrates they fed people were predominantly refined, like sugar and white flour," says Dr. Ornish. "That's not what I've been recommending."

Dr. Krauss concedes that it's possible that refined carbohydrates are the problem when it comes to small LDL, but adds that his study used both complex and simple carbohydrates "in a manner consistent with many people's dietary practices when they adopt a low-fat diet." Low-fat diets are old news, you say? Try telling that to the makers of, say, Baked Lays. It will take us years to shake off the damage done by broadly implicating fat in the diet. "Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake," says Dr. Krauss.

Dr. Krauss learned about the safety of saturated fat from dairy thanks to a grant from — guess who? — the dairy industry. He also receives royalties on patents for two of the five methods for measuring small forms of LDL, including ion mobility. These are no small details, of course, and to his credit, he readily places his conflicts of interest on the table when the talk turns to heavy cream or particle-measurement technology. You could raise an eyebrow at these potential biases, but if you did, you'd also have to rethink the guidelines we now follow about healthy LDL. Their authors, nearly to a person, have taken money from a drug industry that's made a lucrative mission out of LDL mythology. (this is one of the issues with almost all major nutrition research - most is sponsored by either food companies or drug companies, casting questions on the validity of the research)


Then there is this: Dr. Krauss is not sure we should all race out to have our small LDL measured just yet. "I have not been an advocate of widespread testing for small LDL to assess heart-attack risk," he says. "It would be hard to justify the added expense for many people." At this point, he sees a role for small-LDL testing primarily in the management of people with heart disease or people who have a high risk of developing it. More research needs to be conducted before national guidelines make tests routine, he says. Until then, we have to live with the knowledge that the tests most commonly offered tell us only part of the story.

But what about statins? Dr. Krauss believes statins probably offer beneficial effects on heart-disease risk beyond those of lowering LDL (anti-inflammatory properties, for example). Interestingly, statins may help men who want to reduce their small-LDL levels. However, because they increase the removal of LDL from the blood (a process partial to larger LDL), "the benefit may be less than what you would expect from the drop in total LDL," he says.

So with small-LDL testing far from standard (your doctor can request an ion mobility analysis from Quest Diagnostics), the surest way you can reduce your numbers of the LDL that matters is to rely on time-tested advice. Eating fewer carbohydrates, losing weight, and engaging in more physical activity have all been shown to reduce small LDL. Weight loss, in fact, has been demonstrated to reverse the dreaded pattern B all by itself. In other words, worry less about eggs or butter and their effect on LDL, and focus more on eating fewer processed foods and staying in motion. "I am very much an advocate of starting with lifestyle first," Dr. Krauss says. (eat Paleo!!!!!)


Standing over his ion-spitting device quietly tabulating microscopic blood particles as the weekend wears on, Dr. Krauss invokes his admiration for Dr. Gofman, who died of heart failure at the age of 88. Dr. Gofman spent the second half of his career sounding the alarm about the dangers of low-level ionizing radiation, the type emitted from CT scans. (He was years ahead of his time on that subject, too.)

"Like the analytical ultracentrifuge, this process of ion mobility is based on first principles of physics," says Dr. Krauss. "So it's my attempt to leave a legacy, I hope, having been around to put Dr. Gofman's ultracentrifuge out to pasture."

It's in a warehouse, actually. Next door to a carpet store.

URL: http://www.msnbc.msn.com/id/35058896/ns/health-heart_health/page/2/

President's Day Schedule

There will be no noon class Friday February 12th. The 0800 and 0930 classes will still take place Friday.

There will be no CrossFit classes at all on Monday February 15th.

We will resume our normal class schedule Tuesday February 16th.

And now for some good nutritional info from CrossFit Blaboa (http://www.socalsc.com/)

Whey Protein is a by-product of cheese manufactured from cow's milk.It has the highest biological value of any protein. Meaning that it crosses the stomach quickly and is rapidly absorbed by the intestines. For years it has been the staple of many athletes/bodybuilders supplement program.

Why is this particular type of protein important?

Well the protein fraction in whey (approximately 10% of the total dry solids within whey) comprises four major protein fractions and six minor protein fractions. The major protein fractions in whey are beta-lactoglobulin, alpha-lactalbumin, bovine serum albumin and immunoglobulins. Each of these components has important body strengthening effects thanks to:

• A high protein efficiency ratio
o One study showed that milk protein elicits greater increase in branched chain amino acid concentrations in peripheral tissues as compared to soy.

• Lactose (found in whey but not whey concentrate) which is broken down into galacto-oligosaccharides that are used by intestinal bacteria leading to better functioning of the digestive tract.

• Calcium (a minimal component of whey protein) decreases accumulation of body fat and accelerates weight and fat loss. The proposed mechanism is thought to be that parathyroid hormone and 1,25-(OH)2-D respond to low calcium diets and promote fat storage. High calcium diets inhibit these hormones and thus inhibit fat storage and promote increased fat breakdown and energy partitioning from fat to lean.

• Cystine: a conditionally essential amino acid, which is the rate-limiting factor for the body's production of glutathione an important antioxidant.

• An excellent source of branched-chain amino acids (leucine, isoleucine, valine)
o Leucine is a both a key signal molecule for initiation and an important substrate for new protein synthesis.

• It’s usage as a source of glutamine

• In one study it was found that whey supplements may prevent blood sugar spikes after high-carbohydrate meals.

Why should you care? Simple, the body is highly sensitive to insulin after exercise and shuttles carbohydrates and proteins into muscle cells instead of fat cells. This sensitivity declines post-workout until ~2 hours at which point it reaches baseline. Furthermore, the anabolic effects of insulin are synergistic with amino acids.11 Given the rapid absorption of whey, it is the ideal choice for post-workout to take advantage of the insulin-amino acid synergistic effect. This means that whey protein is going to rebuild the damage and replenish the muscle that your body has been using up as you constantly CRUSH yourself with daily WODS. Basically reversing the catabolic state that your body is in after a tough workout, meaning that you start to make the necessary adaptations to the overload that you submit your body to in your quest to become fit (and look better naked).

Friday's WOD

For time:

150 Burpees

Wednesday's WOD

AMRAP in 25 min:
10 Thrusters (m - 115# / w - 80#)
20 walking lunges

Tuesday's WOD - Strength Training!

Back Squat
5-5-3-3-3-1-1

Monday's WOD

5 rounds for time of:
7 KB thrusters (m – 1.5 pood / w – 1 pood)
11 Burpees

Gluten: What You Don't Know Might Kill You

Something you're eating may be killing you, and you probably don't even know it!

If you eat cheeseburgers or French fries all the time or drink six sodas a day, you likely know you are shortening your life. But eating a nice dark, crunchy slice of whole wheat bread--how could that be bad for you?

Well, bread contains gluten, a protein found in wheat, barley, rye, spelt, kamut, and oats. It is hidden in pizza, pasta, bread, wraps, rolls, and most processed foods. Clearly, gluten is a staple of the American diet.

What most people don't know is that gluten can cause serious health complications for many. You may be at risk even if you don't have full blown celiac disease.

In today's blog I want to reveal the truth about gluten, explain the dangers, and provide you with a simple system that will help you determine whether or not gluten is a problem for you.

The Dangers of Gluten

A recent large study in the Journal of the American Medical Association found that people with diagnosed, undiagnosed, and "latent" celiac disease or gluten sensitivity had a higher risk of death, mostly from heart disease and cancer. (i)

This study looked at almost 30,00 patients from 1969 to 2008 and examined deaths in three groups: Those with full-blown celiac disease, those with inflammation of their intestine but not full-blown celiac disease, and those with latent celiac disease or gluten sensitivity (elevated gluten antibodies but negative intestinal biopsy).

The findings were dramatic. There was a 39 percent increased risk of death in those with celiac disease, 72 percent increased risk in those with gut inflammation related to gluten, and 35 percent increased risk in those with gluten sensitivity but no celiac disease.

This is ground-breaking research that proves you don't have to have full-blown celiac disease with a positive intestinal biopsy (which is what conventional thinking tells us) to have serious health problems and complications--even death--from eating gluten.

Yet an estimated 99 percent of people who have a problem with eating gluten don't even know it. They ascribe their ill health or symptoms to something else--not gluten sensitivity, which is 100 percent curable.

And here's some more shocking news ...

Another study comparing the blood of 10,000 people from 50 years ago to 10,000 people today found that the incidences of full-blown celiac disease increased by 400 percent (elevated TTG antibodies) during that time period. (ii) If we saw a 400 percent increase in heart disease or cancer, this would be headline news. But we hear almost nothing about this. I will explain why I think that increase has occurred in a moment. First, let's explore the economic cost of this hidden epidemic.

Undiagnosed gluten problems cost the American healthcare system oodles of money. Dr. Peter Green, Professor of Clinical Medicine for the College of Physicians and Surgeons at Columbia University studied all 10 million subscribers to CIGNA and found those who were correctly diagnosed with celiac disease used fewer medical services and reduced their healthcare costs by more than 30 perecnt. (iii) The problem is that only one percent of those with the problem were actually diagnosed. That means 99 percent are walking around suffering without knowing it, costing the healthcare system millions of dollars.

And it's not just a few who suffer, but millions. Far more people have gluten sensitivity than you think--especially those who are chronically ill. The most serious form of allergy to gluten, celiac disease, affects one in 100 people, or three million Americans, most of who don't know they have it. But milder forms of gluten sensitivity are even more common and may affect up to one-third of the American population.

Why haven't you heard much about this?

Well, actually you have, but you just don't realize it. Celiac disease and gluten sensitivity masquerade as dozens and dozens of other diseases with different names.

Gluten Sensitivity: One Cause, Many Diseases

A review paper in The New England Journal of Medicine listed 55 "diseases" that can be caused by eating gluten. (iv) These include osteoporosis, irritable bowel disease, inflammatory bowel disease, anemia, cancer, fatigue, canker sores, (v) and rheumatoid arthritis, lupus, multiple sclerosis, and almost all other autoimmune diseases. Gluten is also linked to many psychiatric (vi) and neurological diseases, including anxiety, depression, (vii) schizophrenia, (viii) dementia, (ix) migraines, epilepsy, and neuropathy (nerve damage). (x) It has also been linked to autism.(ix)

We used to think that gluten problems or celiac disease were confined to children who had diarrhea, weight loss, and failure to thrive. Now we know you can be old, fat, and constipated and still have celiac disease or gluten sensitivity.

Gluten sensitivity is actually an autoimmune disease that creates inflammation throughout the body, with wide-ranging effects across all organ systems including your brain, heart, joints, digestive tract, and more. It can be the single cause behind many different "diseases." To correct these diseases, you need to treat the cause--which is often gluten sensitivity--not just the symptoms.

Of course, that doesn't mean that ALL cases of depression or autoimmune disease or any of these other problems are caused by gluten in everyone--but it is important to look for it if you have any chronic illness.

By failing to identify gluten sensitivity and celiac disease, we create needless suffering and death for millions of Americans. Health problems caused by gluten sensitivity cannot be treated with better medication. They can only be resolved by eliminating 100 percent of the gluten from your diet.

The question that remains is: Why are we so sensitive to this "staff of life," the staple of our diet?

There are many reasons ...

They include our lack of genetic adaptation to grasses, and particularly gluten, in our diet. Wheat was introduced into Europe during the Middle Ages, and 30 percent of people of European descent carry the gene for celiac disease (HLA DQ2 or HLA DQ8), (xii) which increases susceptibility to health problems from eating gluten.

American strains of wheat have a much higher gluten content (which is needed to make light, fluffy Wonder Bread and giant bagels) than those traditionally found in Europe. This super-gluten was recently introduced into our agricultural food supply and now has "infected" nearly all wheat strains in America.

To find out if you are one of the millions of people suffering from an unidentified gluten sensitivity, just follow this simple procedure.

The Elimination/Reintegration Diet

While testing can help identify gluten sensivity, the only way you will know if this is really a problem for you is to eliminate all gluten for a short period of time (2 to 4 weeks) and see how you feel. Get rid of the following foods:

• Gluten (barley, rye, oats, spelt, kamut, wheat, triticale--see www.celiac.com for a complete list of foods that contain gluten, as well as often surprising and hidden sources of gluten.)

• Hidden sources (soup mixes, salad dressings, sauces, as well as lipstick, certain vitamins, medications, stamps and envelopes you have to lick, and even Play-Doh.)

For this test to work you MUST eliminate 100 percent of the gluten from your diet--no exceptions, no hidden gluten, and not a single crumb of bread.

Then eat it again and see what happens. If you feel bad at all, you need to stay off gluten permanently. This will teach you better than any test about the impact gluten has on your body.

But if you are still interested in testing, here are some things to keep in mind.

Testing for Gluten Sensitivity or Celiac Disease

There are gluten allergy/celiac disease tests that are available through Labcorp or Quest Diagnostics. All these tests help identify various forms of allergy or sensitivity to gluten or wheat. They will look for:

• IgA anti-gliadin antibodies

• IgG anti-gliadin antibodies

• IgA anti-endomysial antibodies

• Tissue transglutaminase antibody (IgA and IgG in questionable cases)

• Total IgA antibodies

• HLA DQ2 and DQ8 genotyping for celiac disease (used occasionally to detect genetic suspectibility).

• Intestinal biopsy (rarely needed if gluten antibodies are positive--based on my interpretation of the recent study)

When you get these tests, there are a few things to keep in mind.

In light of the new research on the dangers of gluten sensitivity without full blown celiac disease, I consider any elevation of antibodies significant and worthy of a trial of gluten elimination. Many doctors consider elevated anti-gliadin antibodies in the absence of a positive intestinal biopsy showing damage to be "false positives." That means the test looks positive but really isn't significant.

We can no longer say that. Positive is positive and, as with all illness, there is a continuum of disease, from mild gluten sensitivity to full-blown celiac disease. If your antibodies are elevated, you should go off gluten and test to see if it is leading to your health problems.

So now you see--that piece of bread may not be so wholesome after all! Follow the advice I've shared with you today to find out if gluten may be the hidden cause of your health problems. Simply eliminating this insidious substnace from your diet, may help you achieve lifelong vibrant health.

That's all for today. Now I'd like to hear from you ...

Are you one of the millions that have been lead to believe gluten is perfectly safe to eat?

How do foods that contain gluten seem to affect you?

What tips can you share with others about eliminating gluten from your diet?

Please let me know your thoughts by posting a comment below.

To your good health,

Mark Hyman, MD

References

(i) Ludvigsson JF, Montgomery SM, Ekbom A, Brandt L, Granath F. Small-intestinal histopathology and mortality risk in celiac disease. JAMA. 2009 Sep 16;302(11):1171-8.

(ii) Rubio-Tapia A, Kyle RA, Kaplan EL, Johnson DR, Page W, Erdtmann F, Brantner TL, Kim WR, Phelps TK, Lahr BD, Zinsmeister AR, Melton LJ 3rd, Murray JA. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology. 2009 Jul;137(1):88-93

(iii) Green PH, Neugut AI, Naiyer AJ, Edwards ZC, Gabinelle S, Chinburapa V. Economic benefits of increased diagnosis of celiac disease in a national managed care population in the United States. J Insur Med. 2008;40(3-4):218-28.

(iv) Farrell RJ, Kelly CP. Celiac sprue. N Engl J Med. 2002 Jan 17;346(3):180-8. Review.

(v) Sedghizadeh PP, Shuler CF, Allen CM, Beck FM, Kalmar JR. Celiac disease and recurrent aphthous stomatitis: a report and review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;94(4):474-478.

(vi) Margutti P, Delunardo F, Ortona E. Autoantibodies associated with psychiatric disorders. Curr Neurovasc Res. 2006 May;3(2):149-57. Review.

(vii) Ludvigsson JF, Reutfors J, Osby U, Ekbom A, Montgomery SM. Coeliac disease and risk of mood disorders--a general population-based cohort study. J Affect Disord. 2007 Apr;99(1-3):117-26. Epub 2006 Oct 6.

(viii) Ludvigsson JF, Osby U, Ekbom A, Montgomery SM. Coeliac disease and risk of schizophrenia and other psychosis: a general population cohort study. Scand J Gastroenterol. 2007 Feb;42(2):179-85.

(ix) Hu WT, Murray JA, Greenaway MC, Parisi JE, Josephs KA. Cognitive impairment and celiac disease. Arch Neurol. 2006 Oct;63(10):1440-6.

(x) Bushara KO. Neurologic presentation of celiac disease. Gastroenterology. 2005 Apr;128(4 Suppl 1):S92-7. Review.

(xi) Millward C, Ferriter M, Calver S, Connell-Jones G. Gluten- and casein-free diets for autistic spectrum disorder. Cochrane Database Syst Rev. 2004;(2):CD003498. Review.

(xii) Green PH, Jabri B. Coeliac disease. Lancet. 2003 Aug 2;362(9381):383-91. Review.

Friday WOD

Man the deadlifts and Wallball were a smoker, but it was fast so today we'll go for a little bit longer

AMRAP in 20 min
5 L-Pull Ups
10 Box Jumps (20")
15 Knees to Elbows

If you cant do an L-pullup its ok just do the pull ups as you can. I suggest bands to slow down the rounds a little.

Thursday's Fun

21-15-9
Wall Ball (men 20lbs/women 14 lbs)
Deadlift (men 250bs/women 150 lbs)

Two hard WODs and now lets get strong

The Push Jerk
5-5-5-5-5

Post loads

Your should reach your 5 rep max by the last round. Focus on form and you can PR
Loads can move from behind or in front
Because its 5 reps Split Jerks are not allowed

Monday was a Great day for 24 - Jack Bauer

RX'd: Men - 1.5 pood (54 pounds); Women - 1 pood (36 pounds)

For Time:
21 Sumo Deadlift High Pull (SDHP) + 3 Kettlebell Swings (KB)
18 SDHP + 6 KB
15 SDHP + 9 KB
12 SDHP + 12 KB
9 SDHP + 15 KB
6 SDHP + 18 KB
3 SDHP + 21 KB