Does Aspirin Stop Cancer

This is a very interesting and relatively brief summary of the topic - the short answer is - "we don't know who will get the most benefit for the new risks."
http://www.healthnewsreview.org/2014/08/aspirin-and-cancer-story-more-complicated-than-many-are-reporting/

Harper: "Thank God for Greg Glassman"

The link that follows is a video of a CF Journal interview with Bob Harper, of Biggest Loser fame. I've been enjoying this show for a couple of seasons, and for the same reason that I enjoy coaching people in nutrition and fitness - you can see them transform the defining reality of their lives. They are re-born, almost literally. The compelling element of the Biggest Loser is to see and experience what it's like to have life from death. This interview with Bob Harper is only 10 minutes but it's a remarkable manifestation of Greg Glassman's vision of elite fitness, and even of having CrossFit be the means to transform the state of what is called the "fitness industry" in our country. Here's the full CFJ link: http://journal.crossfit.com/2012/04/bopharper.tpl#comments

Here's a shorter, free version:
Mac: http://media.crossfit.com/cf-video/CrossFitJournal_BopHarper_PRE.mov
Windows: http://media.crossfit.com/cf-video/CrossFitJournal_BopHarper_PRE.wmv

If you can put a person that is 200 pounds overweight on a prescription of CrossFit and do better than other traditional training options for the obese - what other endorsement could CrossFit get? CrossFit for seasoned citizens? Yes, it's being done. CrossFit for Wounded Warriors? Absolutely. CrossFit for type 1 diabetics? Yes! CrossFit for kids? Uh huh!!

Why? Why do all these disparate populations train and love the same prescription (constantly varied functional movements at high intensity)? IT WORKS. IT'S THE RESULTS PEOPLE. What has been called fitness training for years is certainly better than nothing, but it pales in comparison to what happens to people who CrossFit. CrossFit makes them look better, sure, but more importantly it gives a practice field for participants to test limits, exceed perceived inability, and maybe more significant – CrossFit workouts seem to a trigger a hormonal cascade that makes us humans feel good. Were we born needing to feel the hormones we generate doing intense exercise? I think it’s at least possible. Jogging gives some of those hormones, as does any activity, but once you’ve tried a few CF workouts – it’s different.

I think Greg Glassman's vision of transforming the fitness industry is well on its way. Next up: the health care industry. Ambitious? Insanely ambitious. How could it be done? First, our health care system does a remarkable job of keeping sick people alive. But it is wretched at keeping people healthy, and at making sick people well. CrossFit can change that. The model of using drugs to treat symptoms of poor health - high blood pressure, dislipidemia, gout, pain/inflammation, blood sugar disregulation (IOW, metabolic derangement) - is a model that assumes the genome was build to fail. It's a model that makes sense if you think this much sickness is "normal." It would be easy to believe that if you were a physician applying the low fat, low salt, fad diet of the last 30 years, and noticing that your patients were not getting better as a result. From that experience, you could think "We have to use drugs, no one will do what it takes to take care of their health." Everyday, CrossFitters buck that set of obstacles and restore health, instead of treating the symptoms of their disease. Our health care system is collapsing under the weight of excessive government intervention, which has led to the low fat fad diet and worse - to the defacto subsidization of a food industry that is making us sick and at the same time the subsidization of the drug industry which helps us to survive (but hardly to thrive) our illness. If you think it's insane and absurd to suggest that CrossFit could save the nation's health care system and our national budget at the same time - well, I do too, but I'm not betting against it either. And I WILL do the microscopic amount that I can to support the potential for change.

I've been thinking "thank god for Greg Glassman" for years. Bob Harper, thank you, godspeed on your mission.

Athletes and Statins, Problems

http://healthydietsandscience.blogspot.com/2010/04/statins-and-muscle-problems-in-athletes.html?spref=tw
Bottom line for me is I wouldn't consider doing statins unless I have a heart issue.  There's good reason to believe almost anyone can avoid having to use these things if they don't eat like a USDA food-pyramid-moron.  This study shows what one would think it would show - if you take a powerful medicine that affects cellular energy production and short circuits your body's ability to operate normally, it's no free lunch.  The embedded video is also worth looking at.

I see Lipitor commercials frequently as we track the Grizzly's through the NBA tournament - this is a novel experience for me, by the way, as I've never watched an NBA game before - and the language is remarkably and deliberately vague.  They go way out of their way to avoid making detailed claims, and rely heavily on innuendo like "80% of people who die from heart disease have high cholesterol."  That makes me go "hmmmm."  Why not say "people who take our medicine get well" or "people who use statins, even young, lean and fit people without currently diagnosed heart disease (like the model on this commercial), show a reduction in all cause mortality"?  There's a reason they don't say things like that, and I'm sure you can figure it out.

I also have to let out a moan when the commercial protagonist complains that "diet and exercise didn't do it for me."  Well, if you eat the moron low fat USDA food pyramid junk with 11 servings of whole grains daily, that's not going to help you, your family or me stay off of statins either.  If that's your plan, skip all the agony of eating that nonsense and just get the statin Rx filled.  Better yet - eat meat, vegetables, some nuts and seeds, little fruit or starch, and no sugar/wheat and be healthy.

Heartscan on the Statin Killers

"With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.
"More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.
"As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.
"Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record."
http://feedproxy.google.com/~r/blogspot/mnKK/~3/jzWpx9i4710/statin-buster.html?utm_source=feedburner&utm_medium=email

Lipoprotein Lesson

From Dr. Davis at www.heartscanblog.blogger.com:

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).
Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.
When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.
Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).
Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?
Easy: Because the treatments are nutritional and inexpensive.
The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.
Treatments for Lp(a) include (in order of my current preference):
1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3
Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.
In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.
That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)
Now you know better.

Mike Eades, More on Statins 2

"The only evidence that statins produce any decrease in all-cause mortality is in men under the age of 65 who have established heart disease. For women of all ages with and without heart disease and for men of all ages without heart disease, these drugs don’t bring about a decrease in all-cause mortality.

And in that small subset of people for whom they do work – men under the age or 65 with a history of heart disease (not a history of high cholesterol, but a documented history of having experienced a heart attack), the evidence is that they don’t work all that well.

What do you mean they don’t work all that well? Robert Jarvik tells us in the ubiquitous Lipitor ads that the drug reduces the risk of heart disease by 36 percent in these people.

The dramatic 36% figure has an asterisk. Read the smaller type. It says: “That means in a large clinical study, 3% of patients taking a sugar pill or placebo had a heart attack compared to 2% of patients taking Lipitor.”

Now do some simple math. The numbers in that sentence mean that for every 100 people in the trial, which lasted 3 1/3 years, three people on placebos and two people on Lipitor had heart attacks. The difference credited to the drug? One fewer heart attack per 100 people. So to spare one person a heart attack, 100 people had to take Lipitor for more than three years. The other 99 got no measurable benefit. Or to put it in terms of a little-known but useful statistic, the number needed to treat (or NNT) for one person to benefit is 100.

Compare that with, say, today’s standard antibiotic therapy to eradicate ulcer-causing H. pylori stomach bacteria. The NNT is 1.1. Give the drugs to 11 people, and 10 will be cured.

A low NNT is the sort of effective response many patients expect from the drugs they take. When Wright and others explain to patients without prior heart disease that only 1 in 100 is likely to benefit from taking statins for years, most are astonished. Many, like Winn, choose to opt out."

In clinical trials of statins, side effects were relatively rare. But many doctors believe they are more common in the real world, afflicting perhaps as many as 15% of patients. After muscle aches, prominently mentioned on Lipitor’s label, common complaints include cognitive problems ranging from mild confusion to loss of memory. Former astronaut and retired family doctor Duane Graveline says that he “descended into the black pit of amnesia” both times he was put on Lipitor, prompting him to write a book and set up a Web site on statins’ side effects.
http://www.proteinpower.com/drmike/statins/a-bad-week-for-statins/

Mike Eades, More on Statins

Do they have enough "critical thinking skills to wonder about the hypothesis that LDL-cholesterol is really a problem.

The next day the New York Times, in an article that wasn’t all that anti-statin, started thusly:

For decades, the theory that lowering cholesterol is always beneficial has been a core principle of cardiology. It has been accepted by doctors and used by drug makers to win quick approval for new medicines to reduce cholesterol.

But now some prominent cardiologists say the results of two recent clinical trials have raised serious questions about that theory — and the value of two widely used cholesterol-lowering medicines, Zetia and its sister drug, Vytorin. Other new cholesterol-fighting drugs, including one that Merck hopes to begin selling this year, may also require closer scrutiny, they say.

Dr. Steven E. Nissen weighed in with his interview with Katie Couric on CBS that I posted earlier.

And the Wall Street Journal in it’s Health Blog anticipated a slew of lawsuits against the makers of Vytorin and maybe other statins to follow.

But the big daddy of them all has yet to hit the newsstands but has already been blasted over the internet. The next issue of Business Week, due to hit the stands next Monday, has been up online for the past few days, and it contains several articles, including the cover article, that are devastating for the makers of statin drugs.

The cover article titled Do Cholesterol Drugs Do Any Good starts right off in lock step with what I wrote in my Queen Mother of all statin posts a year or so ago. The Business Week piece starts with an interview with James M. Wright, a professor at the University of British Columbia and the director of the Canadian government-funded Therapeutics Initiative, an agency that analyzes drug data to see how well they actually work. Dr. Wright had one of his patients – Martin Winn – on a statin for a mildly elevated cholesterol level when the light bulb flashed on.

Wright saw, the drugs can be life-saving in patients who already have suffered heart attacks, somewhat reducing the chances of a recurrence that could lead to an early death. But Wright had a surprise when he looked at the data for the majority of patients, like Winn, who don’t have heart disease. He found no benefit in people over the age of 65, no matter how much their cholesterol declines, and no benefit in women of any age. He did see a small reduction in the number of heart attacks for middle-aged men taking statins in clinical trials. But even for these men, there was no overall reduction in total deaths or illnesses requiring hospitalization—despite big reductions in “bad” cholesterol. “Most people are taking something with no chance of benefit and a risk of harm,” says Wright. Based on the evidence, and the fact that Winn didn’t actually have angina, Wright changed his mind about treating him with statins—and Winn, too, was persuaded. “Because there’s no apparent benefit,” he says, “I don’t take them anymore.”

As I reported in my post the only evidence that statins produce any decrease in all-cause mortality is in men under the age of 65 who have established heart disease. For women of all ages with and without heart disease and for men of all ages without heart disease, these drugs don’t bring about a decrease in all-cause mortality.

http://www.proteinpower.com/drmike/statins/a-bad-week-for-statins/

Low Fat Long Term

As you consider this study, also consider the ground we've covered as regards LDL, small dense LDL, LDL measurement error, and relevance of LDL as a CVD risk factor (vice HDL/Total Chol. ratio, or TG/HDL ratio).  The low carb group lost ~3 kilos more weight, 2 kilos more fat, showed a greater reduction in triglycerides, greater increase in HDL, and also a predictable increase in LDL.  The only number that surprises or would concern me is the 'insignificantly' greater increase in apolipoprotein B.  These numbers are otherwise "all good," and comport well with what my experience shows happens when folks use carbohydrate restriction.  I would have liked seeing the numbers for fasting insulin levels and fasting blood sugars in the abstract.

BLUF:  "Eat meat and vegetables, nuts and seeds some fruit little starch and no sugar." www.crossfit.com

Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo^1,2,3,4

Design: Men and women (n = 118) with abdominal obesity and at least one additional metabolic syndrome risk factor were randomly assigned to either an energy-restricted (6–7 MJ) LC diet (4%, 35%, and 61% of energy as carbohydrate, protein, and fat, respectively) or an isocaloric LF diet (46%, 24%, and 30% of energy as carbohydrate, protein, and fat, respectively) for 1 y. Weight, body composition, and cardiometabolic risk markers were assessed.

Conclusions: Under planned isoenergetic conditions, as expected, both dietary patterns resulted in similar weight loss and changes in body composition. The LC diet may offer clinical benefits to obese persons with insulin resistance. However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored. This trial was registered with the Australian New Zealand Clinical Trials Registry at http://www.anzctr.org.au as ACTR 12606000203550.

http://www.ajcn.org/cgi/content/abstract/90/1/23

More From "Your Unstoppable Heart"

"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.


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 insaturated 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.

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."

http://www.menshealth.com/men/health/heart-disease/understanding-cholesterol-and-heart-disease/article/34cf5983f7a75210vgnvcm10000030281eac/6#

Interesting Heart Disease Predictive Model

http://circ.ahajournals.org/cgi/content/abstract/120/24/2448

What do you need to know to predict heart disease more accurately? Contrary to what all the statin advocates would have you believe, NOT LDL levels.

Men's Health on Heart Health - And Correct!

http://www.menshealth.com/men/health/heart-disease/understanding-cholesterol-and-heart-disease/article/34cf5983f7a75210vgnvcm10000030281eac
This is an easy to digest summarization of the work of folks like Gary Taubes. 

Bottom line - lower carb intake equals lower triglycerides and higher HDLs and better heart health.

Statins For Women - Ladies, Do Your Homework!

After a cursory Google search, I turned up these relevant links:

From http://www.cure-guide.com/Natural_Health_Newsletter/Statin_Drugs/statin_drugs.html
Excerpt: "The same week that the US Government decreed that 17 percent of its population should take statin drugs, another study was released that showed lowering cholesterol in women had no effect on mortality. Yet the government would still like men, women, and children to line up for prescriptions.

A study published by the American Medical Association in May examined the results of 13 clinical trials looking at the effect of statin drugs on women. They found that lowering cholesterol with drugs had no effect on mortality regardless of whether they had heart disease or not.

Walsh JM, Pignone M. Drug treatment of hyperlipidemia in women. JAMA 2004 May 12;291(18):2243-52."

Read on here:
WHY DON'T STATIN DRUGS WORK FOR WOMEN?
http://majidali.com/why_dont_statin_drugs_work_for_women.htm

Cholesterol Lowering Statin Drugs for Women, Just Say No by Jeffrey Dach MD
http://jeffreydach.com/2008/01/27/cholesterol-lowering-statin-drugs-for-women-just-say-no-by-jeffrey-dach-md.aspx
Quick excerpt: "The title of this chapter asks a crucially important question for women who are taking statin drugs for the primary prevention of heart attacks and stroke. Simply stated, such women are spending thousands of dollars on statin drugs only to buy a real risk of poisoning their livers, muscles, and other body organs for preventing diseases that they do not have."

Why The Cholesterol-Heart Disease Theory Is Wrong
http://www.becomehealthynow.com/ebookprint.php?id=1112
Quick excerpt: "First little problem - dietary intake of cholesterol has no impact on the level of cholesterol in your blood. If we look at two major long-term studies, Framingham and Tecumseh, it is clear that those who ate the most cholesterol had exactly the same level of cholesterol in their blood as those who ate the least cholesterol"

"‘But, hold on, that doesn’t matter,’ (the sound of goalposts being desperately moved fills the air) ‘It is not cholesterol in the diet that causes the cholesterol level to rise, it is the consumption of saturated fat?’Look again at the Tecumseh study. To explain that table in a little more detail. Basically, it divides people into thirds with high, average or low blood cholesterol levels. The absolute values are not important.Having done this we can examine the level of saturated fat consumed by these three groups. As can be seen:
Those in the lowest third of cholesterol levels consumed 52g/day of saturated fat
Those in the mid-range consumed 54g/day of saturated fat
Those with the highest levels consumed 54g/day of saturated fat
Which lead to the conclusion, from the authors that:
‘Serum cholesterol and triglyceride values were not positively correlated with selection of dietary constituents.’
I shall translate those weasel words into plain English. ‘You can eat as much saturated fat as you like and it makes no difference whatsoever to your blood cholesterol levels.’"

If you wonder why your doctor prescribed statins for you, and you should given their side effects (easily found on Google also), by all means ask him/her!! I am not qualified to give medical advice, but given what I know about heard disease, the cholesterol myths and side effects of medications, my doctor would have to be very, very convincing to get me to take statins, male or female, but especially if I was a female!

Note: I do not advocate for the accuracy of these links, and in fact disagree with many of the conclusions therein. These links are useful to the extent that they highlight that absurdity of prescribing statins to women, when there's no evidence that women benefit from the use of these drugs!