CT heart scans and radiation: The real story

 
CT heart scans and radiation: The real story “My personal opinion is that many patients today who are receiving multiple CT scans may well be getting at least comparable doses to subjects that have now developed malignancies from x-ray radiation received in the 1930s and '40s. And, similar to those days when the doses were unknown, the dose that patients receive today over a course of years of multiple CT scans is also completely unknown . . .

“I recommend that all healthcare providers become familiar with the concept that 1 in 1000 CT studies of the chest, abdomen, or pelvis may result in cancer.”
Richard C. Semelka, MD
Professor and Vice Chairman, Department of Radiology
University of North Carolina–Chapel Hill
Is this just hype to generate headlines? Or is the truth buried in the enormous marketing clout of the medical device industry, among which the imaging device manufacturers reign supreme?
It’s been over 110 years since radiation was first used for medical imaging. Over those years, it has had its share of misadventures.

In the 1930s and 1940s, before the dangers of radiation were recognized, shoe shoppers had shoes fitted using an x-ray device of the foot to assess fit. High doses of radiation were used to shrink enlarged tonsils and extinguish overactive thyroid glands. Attitudes towards radiation were so lax that doctors commonly permitted themselves to be exposed without protection day after day, year after year, until an unexpected rise in blood cancers like leukemia was observed. As recently as the 1970s and 1980s, cancers like Hodgkins’ disease were treated with high doses of radiation, also leading to radiation-induced diseases decades later.

Not all radiation is bad. Radiation can also be used as a therapeutic tool and even today remains a useful and reasonably effective method to reduce the size, sometimes eliminate, certain types of cancer. Forty percent of people with cancer now receive some form of radiation as part of their treatment (Ron E 2003).

Just how much does medical radiation add to our exposure?  Estimates vary, but most experts estimate that medical imaging provides approximately 15% of total lifetime exposure. In other words, radiation exposure from medical imaging is simply a small portion of total exposure that develops over the years of life. Exposure can be much higher, however, in a specific individual who undergoes repeated radiation imaging or treatment of one sort or another.

For all of us, exposure to medical radiation is part of lifetime exposure from multiple sources, added to the radiation we receive from the world around us. Just by living on earth, we are exposed to radiation from space and naturally-occurring radioactive compounds, and receive somewhere around 3.0 mSv per year (U.S. Nuclear Regulatory Commission). (Doses for radiation exposure are commonly expressed in milliSieverts, mSv, a measure that reflects whole-body radiation exposure.) People living in high-altitude locales like Colorado get exposed to an additional 30–50% ambient radiation (1.0–1.5 mSv more per year).

Much of the information on radiation exposure comes from studies like the Life Span Study that, since 1961, has tracked 120,000 Japanese exposed to radiation from the atomic bombs dropped in 1945 (Preston DL et al 2003). Although regarded as a high-dose exposure study for obvious reasons, there are actually thousands of people in this study who were exposed to lesser quantities of radiation (because of distance from the bomb sites) who still display a “dose-response” increased risk for cancer many years later in life. Radiation exposures of as little as 5–20 mSv showed a slight increase in lifetime risk.

Occupational and excessive medical exposure to radiation also provides a “laboratory” to examine radiation risk. Miners exposed to radon gas; patients exposed to the imaging agent, Thorotrast, containing radioactive isotope thorium dioxide and used as an x-ray contrast agent in the 1930s and 1940s and possesses the curious property of lingering in the body for over 30 years after administration; radium injections administered between 1945 and 1955 to treat diseases like ankylosing spondylitis and tuberculosis, all provide researchers an opportunity to study the long-term effects of various types of radiation exposure over many years (Harrison JD et al 2003).

The excess exposure of workers and several hundred thousand nearby residents to the Mayak nuclear plant in Russia has also revealed a “dose-response” relationship, with increasing exposure leading to more cancers, including leukemia and solid cancers of the bone, liver, and lung (Shilnikova NS et al 2003). Nuclear waste released into the Techa river between 1948 and 1956 contaminated drinking water used by over 100,000 Russians. A plant explosion in 1957 also released an excess of radiation into the atmosphere, yielding exposure via inhalation.

Some sources estimate that at least 272,000 people have been affected by radiation from the Mayak plant. This unfortunate situation has, however, yielded plenty of data on radiation exposure and its long-term effects.

It’s also been known for several decades that people who receive therapeutic radiation for treatment of cancer, even with the reduced doses now employed, are subject to increased risk of a second cancer consequent to the radiation treatment.

From experiences like this, radiation experts estimate that an exposure of 10 mSv increases a population’s risk for cancer by 1 in 1000 (Semelka RC et al 2007).

This question was recently thrust into the spotlight with publication of a study from Columbia University in New York suggesting that a 20-year old woman would be exposed to a lifetime risk of cancer as high as 1 in 143 consequent to the radiation received during a CT coronary angiogram. (Important note: This was estimated risk from a CT coronary angiogram, not a simple heart scan that we advocate for the Track Your Plaque program.) The risk at the low end of the spectrum would be in an 80-year old man (because of the shorter period of time to develop cancer), with a risk of 1 in 5017. If “gating” to the EKG is added (which many scan centers do indeed perform nowadays), risk for a 60-year old woman is estimated at 1 in 715; risk for a 60-year old male, 1 in 1911 (Einstein AJ et al 2007). This study generated some criticism, since it did not directly involve human subjects, but used “phantoms” or x-ray dummies to simulate x-ray exposure. Nonetheless, the point was made: CT coronary angiograms in current practice do indeed expose the patient to substantial quantities of radiation, sufficient to pose a lifetime risk of cancer.

The media frenzy  The NY Times ran an article called With Rise in Radiation Exposure, Experts Urge Caution on Tests in which they stated:

"According to a new study, the per-capita dose of ionizing radiation from clinical imaging exams in the United States increased almost 600 percent from 1980 to 2006. In the past, natural background radiation was the leading source of human exposure; that has been displaced by diagnostic imaging procedures, the authors said."

“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”

Radiation is a widely used imaging tool in medicine. Although CT scans of the brain, bones, chest, abdomen, and pelvis account for only 5% of all medical radiation procedures, they are responsible for nearly 50% of medical radiation used. It’s been known for years that increasing radiation exposure increases cancer risk over many years, but the boom of newer, faster devices that provide more detailed images has opened the floodgates to expanded use of CT scanners.

But before we join in the hysteria, let's first take a look at exposure measured for different sorts of tests:

Typical effective radiation dose values for common tests

Computed Tomography
Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv

Non-CT
Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv
Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN  A plain, everyday chest x-ray, providing less than 0.1 mSv exposure, provides about the same quantity of radiation exposure as flying in an airplane for four hours, or the same amount of radiation from exposure to our surroundings for 11–12 days. Similar exposure arises from dental x-rays.

If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

With a heart scan on a 16- or 64-slice multidetector device, exposure is around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 chest x-rays or 20 mammograms. Now, that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legitimate medical questions. They are not screening tests to be applied broadly and used year after year.

It’s also worth giving second thought to any full body scan you might be considering. These screening studies include scans of the chest, abdomen, and pelvis. These scans, performed for screening, expose the recipient to approximately 10 mSv of radiation (Radiological Society of North American, 2007). Debate continues on whether the radiation exposure is justified, given the generally asymptomatic people who generally undergo these tests.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.

Heart scans, CT coronary angiograms and the future  Unfortunately, practicing physicians and those involved in providing CT scans are generally unconcerned with radiation exposure. The majority, in fact, are entirely unaware of the dose of radiation required for most CT scan studies and unaware of the cancer risk involved. It is therefore up to the individual to insist on a discussion of the type of scanner being used, the radiation dose delivered (at least in general terms), the necessity of the test, alternative methods to obtain the same diagnostic information, all in the context of lifetime radiation exposure.

Our concerns about radiation exposure all boil down to concern over lifetime risk for cancer, a disease that strikes approximately 20% of all Americans. Many factors contribute to cancer risk, including obesity, excessive saturated fat intake, low fiber intake, lack of vitamin D, repeated sunburns, excessive alcohol use, smoking, exposure to pesticides and other organochemicals, asbestos and other industrial exposures, electromagnetic wave exposure, and genetics. Radiation is just one source of risk, though to some degree a controllable one.

Some people, on hearing this somewhat disturbing discussion, refuse to ever have another medical test requiring radiation. That’s the wrong attitude. It makes no more sense than wearing lead shielding on your body 24 hours a day to reduce exposure from the atmosphere. Taken in the larger context of life, radiation exposure is just one item on a list of potentially harmful factors.

It is, however, worth some effort to minimize radiation exposure over your lifetime, particularly before age 60, and by submitting to high-dose testing only when truly necessary, or when the potential benefits outweigh the risks. Thus, with heart scans and CT coronary angiography, some thought to the potential benefits of knowing your score or the information gained from the CT angiogram need to be considered before undergoing the test. Often the practical difficulty, of course, is that your risk for heart disease simply cannot be known until after the test.

In our view, in the vast majority of instances a simple CT heart scan can serve the simple but crucial role of quantifying risk for heart attack and atherosclerotic plaque. CT heart scans yield this information with less than a tenth of the radiation exposure of a CT coronary angiogram. In people without symptoms and a normal stress test, there is rarely a need for CT coronary angiography with present day levels of radiation exposure. Perhaps as technology advances and the radiation required to generate images is reduced, then we should reconsider.

Early experiences are suggesting that the newest 256-slice scanners, now being developed but not yet available, will cut the dose exposure of 64-slice CT angiograms in half (from 27.8 mSv to 14.1 mSv in a recent Japanese study). The 256-slice scanners will allow scanning that is faster over a larger area in a given period of time.

Thankfully, the scanner manufacturers are increasingly sensitive to the radiation issue and have been working on methods to reduce radiation exposure. However, it still remains substantial.

References: Einstein AJ, Henzlova MJ, Rajagopalan S. Estimating risk of cancer associated with radiation exposure from 64-slice computed tomography coronary angiography. JAMA 2007 Jul 18;298(3):317–323.
Harrison JD, Muirhead CR. Quantitative comparisons of cancer induction in humans by internally deposited radionuclides and external radiation. Int J Radiat Biol 2003 Jan;79(1):1–13.
Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305–1310.
Kalra MK, Maher MM, Toth TL, Hamberg LM, Blake MA, Shepard J, Saini S. Strategies for CT radiation dose optimization. Radiology 2004;230:619–628.
Mayo JR, Aldrich J, Müller NL. Radiation exposure at chest CT: A statement of the Fleischner Society. Radiology 2003; 228:15–21.
Mori S, Nishizawa K, Kondo C, Ohno M, Akahane K, Endo M. Effective doses in subjects undergoing computed tomography cardiac imaging with the 256-multislice CT scanner. Eur J Radiol 2007 Jul 10; [Epub ahead of print].
Preston DL, Pierce DA, Shimizu Y, Ron E, Mabuchi K. Dose response and temporal patterns of radiation-associated solid cancer risks. Health Phys 2003 Jul;85(1):43–46.
Ron E. Cancer risks from medical radiation. Health Phys 2003 Jul;85(1):47–59.
Shilnikova NS, Preston DL, Ron E et al. Cancer mortality risk among workers at the Mayak nuclear complex. Radiation Res 2003 Jun;159(6):787–798.
Semelka RC, Armao DM, Elias J Jr, Huda W. Imaging strategies to reduce the risk of radiation in CT studies, including selective substitution with MRI. J Magn Reson Imaging 2007 May;25(5):900–9090.
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Confirmed Again: Statin Drugs Accelerate Cardiovascular Disease - Mercola

Confirmed Again: Statin Drugs Accelerate Cardiovascular Disease

October 15 2012

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By Dr. Mercola

Statins are the world's most-prescribed class of medications. A staggering one in four Americans over the age of 45 now take cholesterol-lowering drugs such as Pravachol, Mevacor, Lipitor, Zocor, Crestor, and others. A majority of them are taking these drugs for primary prevention of heart attacks and strokes.

However, mounting research suggests this could be a critical mistake.

Most recently, two separate studies have concluded that progression of coronary artery calcification, which is the hallmark of potentially lethal heart disease, is INCREASED with statin drug use.

Statins Increase Prevalence of Coronary Calcification by More than 50 Percent!

A new study in the journal Atherosclerosis¹ shows that statin use is associated with a 52 percent increased prevalence and extent of calcified coronary plaque compared to non-users. None of the participants in the study – 6,673 in all – had any known coronary artery disease at the time of undergoing coronary CT angiography (CCTA) – a non-invasive method that allows you to see coronary atherosclerotic features, including plaque composition.

Arterial plaque is a hallmark of cardiovascular disease and increases your risk of all-cause mortality, so clearly, anything that increases calcification and stiffening of your arteries is wisely avoided. And statins seem to fall into this category.

These disturbing findings come right on the heels of another study published in the journal Diabetes Care,² which discovered that type 2 diabetics with advanced atherosclerosis who are frequent statin users have significantly higher amounts of coronary artery calcification compared to less frequent users of the drug.

Furthermore, in a subgroup of participants who initially were not receiving statins, progression of both coronary artery calcification as well as abdominal aortic artery calcification was significantly increased when they began frequent statin use.
The authors concluded that:

"More frequent statin use is associated with accelerated coronary artery calcification in T2DM patients with advanced atherosclerosis."

So much for statins being the answer for diabetics... Diabetes is a risk factor for cardiovascular disease, which is why many diabetics are prescribed a statin drug to reduce their risk. Alas, as these studies show, statins actually accelerate the progression of disease!

Making matters worse, statins have also been shown to significantly increase your risk of developing type 2 diabetes³ if you don't have it already. This is a risk everyone needs to be aware of. In one study, statins increased the risk of type 2 diabetics in postmenopausal women by 48 percent.⁴

Few People Really Benefit from a Statin Drug

Statins, I believe, are one of the most unnecessary drugs on the market. A small group of people with familial hypercholesterolemia, a genetic defect that causes cholesterol levels above 325-350, do seem to benefit from statins. However, in my clinical experience over more than two decades and tens of thousands of patients, I had a grand total of three patients that fell into this category as it's a relatively uncommon genetic problem.
The fact that one in four Americans over the age of 45 is now taking a statin drug as a form of "preventive medicine" does not bode well when you consider the massive increases in disease risk these drugs are now associated with. It's downright shocking that doctors are so slow to realize the potential damage inflicted on their patients for no reward at all.

The research that led to statins being heavily promoted as a form of primary prevention of heart disease and stroke was funded by AstraZeneca, the maker of Crestor. Since the release of that study in 2008, none of their claims have turned out to hold water in subsequent research. On the contrary, as the two featured studies show, they actually worsen cardiovascular disease progression.

The drugs also come with an avalanche of other potential side effects, which tend to be dose dependent.⁵ In fact, as of 2009 there were well over 900 studies proving their adverse effects, which run the gamut from muscle problems to increased cancer risk. One of the primary mechanisms of harm appears to be CoQ10 depletion. If you take statin drugs without supplementing with CoQ10 (or ideally, the reduced form, called ubiquinol, which is far more effective), your health is at serious risk.

GreenMedInfo.com has compiled over 300 documented adverse health effects associated with statins,⁶ some of the most common of which include:

Muscle problems, polyneuropathy (nerve damage in the hands and feet), and rhabdomyolysis (a serious degenerative muscle tissue condition)	Anemia
Acidosis	Sexual dysfunction
Immune depression	Cataracts
Pancreas or liver dysfunction, including a potential increase in liver enzymes	Memory loss

What You Need to Know About Cholesterol in Order to Understand the Dangers of Statins

Statin drugs work by preventing the formation of cholesterol and reduce LDL cholesterol, which is considered the "bad" cholesterol. There is no argument that these drugs can effectively lower your cholesterol levels. However, what has NOT been proven is that they significantly lower your risk of dying from heart disease. In no way, shape or form do they treat the underlying cause of your problem. They are nothing more than a toxic band-aid.

So just what makes statins so dangerous, and why are they not the answer for managing your cholesterol levels?

First you need to understand the biological workings of cholesterol. In fact, there is no such thing as "good" or "bad" cholesterol. Both HDL and LDL cholesterol perform vital functions in your body, which is why it's actually dangerous to bring your LDL levels down too low.

HDL (high density lipoprotein) and LDL (low density lipoprotein) are actually proteins that transport the cholesterol to and from your tissues. Cholesterol in turn is a precursor to your steroid hormones, bile acids, cell membrane walls and vitamin D. For example, cholesterol is essential for you to make testosterone or estrogen, cortisol, DHEA or pregnenolone, or a multitude of other steroid hormones that are necessary for health, without cholesterol. Even more importantly, your cells cannot regenerate their membranes without it.

The reason you have LDL to begin with is to transport the cholesterol to the tissues in order to make new cells and repair damaged ones. However, there are different sizes of LDL particles and it's the LDL particle size that is relevant, and statins do not modulate the size of the particles. Unfortunately, most people still don't know about that part, and very rarely, if ever, get tested for particle size. The particles are sticky, so very small LDL's can easily get stuck in different areas, and the build-up eventually causes inflammation and damage.

The only way to make sure your LDL particles are large enough to not cause damage is through your diet. In fact, it's one of the major functions of insulin.

Conveniently enough, a healthy diet is also the answer for type 2 diabetes, so by focusing on what you eat, you're treating both your diabetes and your cholesterol levels, and reducing your associated risk of heart disease. If you eat properly, which is really the only known good way to regulate LDL particle size, then it does the right thing; it takes the cholesterol to your tissues, the HDL takes it back to your liver, and no plaque is formed.

The Critical Importance of CoQ10

Again, if you're on a statin drug, you MUST take at least 100-200 mg of ubiquinol or CoQ10 per day. Ubiquinol is also beneficial for those not taking statins. If you're not on a statin drug, the amount of CoQ10 or ubiquinol you might need depends on how sick you are. The sicker you are, the more you need. As a general guideline if you're not ill, taking 50-100 mg per day would probably be sufficient. If you're over the age of 70, double that dose, or up to 200 mg per day. This is because your natural CoQ10 levels begin to drop after the age of 40, and by the age of 70, levels begin to precipitously drop.
Ideally, you'll want to split the dose up to two or three times a day, rather than taking it all at once, as this will result in higher blood levels. Other dosing guidelines include:

Hypertension 200 mg/day	World class athletes who need extra ATP turnover, 300-600 mg/day	Heart transplant or severe CHF, 300-600 mg/day in divided doses
Arrhythmia 200 mg/day	Typical athlete 100-300 mg/day	Mitral valve prolapse, a combination of 400 mg magnesium and 100-200 mg of CoQ10

How to Help Lower Your Cholesterol Naturally

There's really virtually NO reason to take statins and suffer the consequences from these ill-conceived drugs. If you truly want to normalize your cholesterol levels, following these simple lifestyle changes can help get you there:

• First, normalize your insulin levels by eliminating sugar (particularly fructose) and grains. A fasting insulin level is easy to draw and is very inexpensive. It should be below 3.
• Take a high-quality animal-based omega-3 supplement, such as krill oil.
• Eat a good portion of your food raw (ideally organic to avoid agricultural chemicals).
• Eat healthy, preferably raw, fats, such as:
  
  

  Olive oil	Coconut and coconut oil	Organic raw dairy products	Avocados
  Raw organic nuts	Seeds	Pastured eggs (raw, or lightly cooked with yolks intact)	Organic, grass-fed meats

• Regular exercise is another important tool. When you exercise you increase your circulation and the blood flow throughout your body. The components of your immune system are also better circulated, which means your immune system has a better chance of fighting an illness before it has the opportunity to spread.
• If you are a man, or a woman who is in menopause, you should check your iron levels, as elevated levels of iron can cause major oxidative damage in the blood vessels, heart and other organs. Excess iron is also one of the major contributing factors of cancer risk.
• Avoid smoking and drinking alcohol excessively.

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Read the complete article here.

Results of my second serial CAC Scan just in.

I have been working hard on slowing plaque growth for several years but mostly in the last year and a half because I had my first viable CAC scan to provide a measuring point baseline for reference.

Other comments on the report follow.

• IMPRESSION: Stable exam compared to Sept 15, 2011

• PATIENT: 69 year old man with no cardiac symptoms but a past history of cardiovascular disease resulting in 6 MI events over a 17 year period. His current stress level is low. He has a history of prior cardiac procedures including CABG (1x), Angiography and Coronary Stent (3x). He has a family history of stroke and heart disease in a first or second degree relative.

• YOUR AGATSTON CALCIUM SCORE IS: 1072.3

• Your current EBT heart was compared to your most recent prior scan and the progression of calcified plaque is less than 15% annually. This is a very good result and is consistent with a low risk for coronary event over the next few years.

Encouraging but no resting on my laurels. The 22% annualized plaque growth in the RCA is a matter of concern reminding me that further improvement is necessary so adjustments may have to be made in my diet etc.


Prior Scan was Sept 15, 2011
Current Scan Oct 5, 2012
My assessment is that it looks pretty good except for % change on LMCA and the RCA
That line below the chart that ends with 4% is good.
Have consult with doctor tomorrow (10/15/2012). Stay tuned for a more qualified analysis.




Note my treatment plan which seems to be paying off is that of the Track Your Plaque Program. It primarily consists of diet and supplements with minimal drug intervention (especially 'no statins' which I do not tolerate). It includes advanced lipid analysis then treating atherogenic ones such as Lp(a) and apo B or LDL particle number and particle size.

Important safety label changes to cholesterol-lowering statin drugs

FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs

Facts about statins

A class of prescription drugs used together with diet and exercise to reduce blood levels of low-density lipoprotein (LDL) cholesterol (“bad cholesterol”) Marketed as single-ingredient products, including Lipitor (atorvastatin), Lescol (fluvastatin), Mevacor (lovastatin), Altoprev (lovastatin extended-release), Livalo (pitavastatin), Pravachol (pravastatin), Crestor (rosuvastatin), and Zocor (simvastatin) Also marketed as combination products, including Advicor (lovastatin/niacin extended-release), Simcor (simvastatin/niacin extended-release), and Vytorin (simvastatin/ezetimibe)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Safety Announcement

[2-28-2012] The U.S. Food and Drug Administration (FDA) has approved important safety label changes for the class of cholesterol-lowering drugs known as statins. These changes were made to provide the public with more information for the safe and effective use of statins and are based on FDA’s comprehensive review of the statin class of drugs (see Data Summary below). The changes include the following:

Infographic About Cholesterol and Statins1 2

Monitoring Liver Enzymes
Labels have been revised to remove the need for routine periodic monitoring of liver enzymes in patients taking statins. The labels now recommend that liver enzyme tests should be performed before starting statin therapy and as clinically indicated thereafter. FDA has concluded that serious liver injury with statins is rare and unpredictable in individual patients, and that routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.

Adverse Event Information
Information about the potential for generally non-serious and reversible cognitive side effects (memory loss, confusion, etc.) and reports of increased blood sugar and glycosylated hemoglobin (HbA1c) levels has been added to the statin labels. FDA continues to believe that the cardiovascular benefits of statins outweigh these small increased risks.

Drug Interactions
The lovastatin label has been extensively updated with new contraindications (situations when the drug should not be used) and dose limitations when it is taken with certain medicines that can increase the risk for muscle injury (see Lovastatin Dose Limitations below).

Healthcare professionals should refer to the drug labels for the latest recommendations for prescribing statins (also see Additional Information for Healthcare Professionals below). Patients should contact their healthcare professional if they have any questions or concerns about statins.

Additional Information for Patients

• The statin drug labels have been revised to provide patients with more information on the safe and effective use of statins. Patients should be aware of the following information:
  • There have been rare reports of serious liver problems in patients taking statins. Patients should notify their healthcare professional right away if they have the following symptoms: unusual fatigue or weakness; loss of appetite; upper belly pain; dark-colored urine; or yellowing of the skin or the whites of the eyes.
  • Memory loss and confusion have been reported with statin use. These reported events were generally not serious and went away once the drug was no longer being taken.
  • Increases in blood sugar levels have been reported with statin use.
  • Certain medicines should never be taken (are contraindicated) with lovastatin (Mevacor) (see Lovastatin Dose Limitations below).
• Patients should contact their healthcare professional if they have any questions or concerns about statins.
• Patients should report side effects from the use of statins to the FDA MedWatch program, using the information in the "Contact FDA" box at the bottom of the page.
  

Additional Information for Healthcare Professionals

• Healthcare professionals should perform liver enzyme tests before initiating statin therapy in patients and as clinically indicated thereafter. If serious liver injury with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment, therapy should be interrupted. If an alternate etiology is not found, the statin should not be restarted.
• There have been rare post-marketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These reported symptoms are generally not serious and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks).
• Increases in glycosylated hemoglobin (HbA1c) and fasting serum glucose levels have been reported with statin use.
• Healthcare professionals should follow the recommendations in the lovastatin label regarding drugs that may increase the risk of myopathy/rhabdomyolysis when used with lovastatin (see Lovastatin Dose Limitations below).
• Healthcare professionals should report adverse events involving statins to the FDA MedWatch program using the information in the "Contact FDA" box at the bottom of this page.
  

Data Summary

Removal of routine monitoring of liver enzymes from drug labels

FDA reviewed current monitoring guidelines, including the National Lipid Association’s Liver Expert Panel and Statin Safety Task Force recommendations.^{1, 2} The Liver Expert Panel stated that the available scientific evidence does not support the routine monitoring of liver biochemistries in asymptomatic patients receiving statins. The Panel made this recommendation because (1) irreversible liver damage resulting from statins is exceptionally rare and is likely idiosyncratic in nature, and (2) no data exist to show that routine periodic monitoring of liver biochemistries is effective in identifying the very rare individual who may develop significant liver injury from ongoing statin therapy. The Panel believed that routine periodic monitoring will instead identify patients with isolated increased aminotransferase levels, which could motivate physicians to alter or discontinue statin therapy, thereby placing patients at increased risk for cardiovascular events.¹ The National Lipid Association’s Statin Task Force also stated that routine monitoring of liver function tests is not supported by the available evidence.²

FDA reviewed post-marketing data to evaluate the risk of clinically serious hepatotoxicity associated with statins. FDA had conducted several post-marketing reviews of statins and hepatotoxicity between years 2000 and 2009 by searching the Agency’s Adverse Event Reporting System (AERS) database. Those reviews consistently noted that reporting of statin-associated serious liver injury to the AERS database was extremely low (reporting rate of ≤2 per one million patient-years). FDA’s updated review focused on cases of severe liver injury, defined as a 4 (severe liver injury) or a 5 (death or liver transplant) using the Drug Induced Liver Injury Network (DILIN) liver injury severity scale, which were reported to AERS from marketing of each statin through 2009. Cases meeting those criteria were further assessed for causality. Seventy-five cases (27 cases with a severity score of 4, and 48 cases with a severity score of 5 (37 deaths and 11 liver transplants) were assessed for causality. Thirty of the 75 cases (14 deaths, 7 liver transplantations, and 9 severe liver injury) were assessed as possibly or probably associated with statin therapy. No cases were assessed as highly likely or definitely associated with statin therapy. FDA concluded that, despite a rising use of statins as a class since the late 1990s, there has not been a detectable increase in the annual rates of fatal or severe liver injury cases possibly or probably causally associated with statin use.

FDA also reviewed cases from the DILIN and Acute Liver Failure Study Group (ALFSG), organizations that have been submitting reports to FDA of drug-associated liver injury in their liver injury outcome studies. As of January 1, 2011, DILIN had submitted 25 reports of statin-associated liver injury to FDA, 12 of which gave hospitalization as an outcome. A 2010 article from ALFSG included 133 prospectively identified cases of idiopathic drug-induced liver injury resulting in acute liver failure.³ Of these 133 patients, 15 were taking statins, and in six of these 15 individuals a statin was identified as the only potential drug to cause drug-induced liver injury.

Based on all available data, FDA has determined that all currently marketed statins appear to be associated with a very low risk of serious liver injury and that routine periodic monitoring of serum alanine aminotransferase (ALT) does not appear to detect or prevent serious liver injury in association with statins.

Cognitive adverse events

FDA reviewed the AERS database, the published medical literature (case reports and observational studies),^4-13 and randomized clinical trials to evaluate the effect of statins on cognition.^14-17

The post-marketing adverse event reports generally described individuals over the age of 50 years who experienced notable, but ill-defined memory loss or impairment that was reversible upon discontinuation of statin therapy. Time to onset of the event was highly variable, ranging from one day to years after statin exposure. The cases did not appear to be associated with fixed or progressive dementia, such as Alzheimer’s disease. The review did not reveal an association between the adverse event and the specific statin, the age of the individual, the statin dose, or concomitant medication use.

Data from the observational studies and clinical trials did not suggest that cognitive changes associated with statin use are common or lead to clinically significant cognitive decline.

Increases in glycosylated hemoglobin (HbA1c) and fasting plasma glucose

FDA’s review of the results from the Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) reported a 27% increase in investigator-reported diabetes mellitus in rosuvastatin-treated patients compared to placebo-treated patients. High-dose atorvastatin had also been associated with worsening glycemic control in the Pravastatin or Atorvastatin Evaluation and Infection Therapy – Thrombolysis In Myocardial Infarction 22 (PROVE-IT TIMI 22) substudy.¹⁸

FDA also reviewed the published medical literature.^19-26 A meta-analysis by Sattar et al.,19 which included 13 statin trials with 91,140 participants, reported that statin therapy was associated with a 9% increased risk for incident diabetes (odds ratio [OR] 1.09; 95% confidence interval [CI] 1.02-1.17), with little heterogeneity (I2=11%) between trials. A meta-analysis by Rajpathak et al.,²⁰ which included 6 statin trials with 57,593 participants, also reported a small increase in diabetes risk (relative risk [RR] 1.13; 95% CI 1.03-1.23), with no evidence of heterogeneity across trials. A recent study by Culver et al.,²⁶ using data from the Women’s Health Initiative, reported that statin use conveys an increased risk of new-onset diabetes in postmenopausal women, and noted that the effect appears to be a medication class effect, unrelated to potency or to individual statin.

Based on clinical trial meta-analyses and epidemiological data from the published literature, information concerning an effect of statins on incident diabetes and increases in HbA1c and/or fasting plasma glucose was added to statin labels.

Lovastatin drug-drug interactions

Information regarding drug-drug interactions and contraindications and dose limitations has been added to the lovastatin label. Subsequent to the June 2011 label revisions to the simvastatin-containing products, which were based largely on the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) trial,²⁷ a review of drug-drug interactions with lovastatin was conducted because the physicochemical and pharmacokinetic properties of lovastatin are comparable to those of simvastatin.

Lovastatin is a sensitive in vivo cytochrome P450 3A4 (CYP3A4) substrate. Strong CYP3A4 inhibitors are predicted to significantly increase lovastatin exposure. A literature review indicates that itraconazole, a strong CYP3A4 inhibitor, increases lovastatin exposure up to 20-fold and the drug interaction appears to result in rhabdomyolysis.²⁸ The effect of itraconazole on lovastatin exposure can therefore be extrapolated to other strong CYP3A4 inhibitors, including ketoconazole, posaconazole, erythromycin, clarithromycin, telithromycin, human immunodeficiency virus (HIV) protease inhibitors, boceprevir, telaprevir, and nefazodone.

Lovastatin Dose Limitations

Previous lovastatin label	New lovastatin label
Avoid lovastatin with: Itraconazole Ketoconazole Erythromycin Clarithromycin Telithromycin HIV protease inhibitors Nefazodone	Contraindicated with lovastatin: Itraconazole Ketoconazole Posaconazole Erythromycin Clarithromycin Telithromycin HIV protease inhibitors Boceprevir Telaprevir Nefazodone
Do not exceed 20 mg lovastatin daily with: Gemfibrozil Other fibrates Lipid-lowering doses (≥1 g/day) of niacin Cyclosporine Danazol	Avoid with lovastatin: Cyclosporine Gemfibrozil
	Do not exceed 20 mg lovastatin daily with: Danazol Diltiazem Verapamil
Do not exceed 40 mg lovastatin daily with: Amiodarone Verapamil	Do not exceed 40 mg lovastatin daily with: Amiodarone
Avoid large quantities of grapefruit juice (>1 quart daily)	Avoid large quantities of grapefruit juice (>1 quart daily)

References

1. Cohen DE, Anania FA, Chalasani N; for the National Lipid Association Statin Safety Task Force Liver Expert Panel. An assessment of statin safety by hepatologists. Am J Cardiol. 2006;97(8A):77C-81C.
2. McKenney JM, Davidson MH, Jacobson TA, Guyton JR. Final conclusions and recommendations of the National Lipid Association Statin Safety Assessment Task Force. Am J Cardiol. 2006;97(8A):89C-94C.
3. Reuben A, Koch DG, Lee WM; for the Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatology. 2010;52(6):2065-2076.
4. Orsi A, Sherman O, Woldeselassie Z. Simvastatin-associated memory loss. Pharmacotherapy. 2001;21:767-9.
5. Wagstaff LR, Mitton MW, Arvik BM, Doraiswamy PM. Statin-associated memory loss: analysis of 60 case reports and review of the literature. Pharmacotherapy. 2003;23:871-80.
6. Evans MA, Golomb BA. Statin-associated adverse cognitive effects: survey results from 171 patients. Pharmacotherapy. 2009;29:800-811.
7. Parker BA, Polk DM, Rabdiya V, et al. Changes in memory function and neuronal activation associated with atorvastatin therapy. Pharmacotherapy. 2010;30(6):236e-240e.
8. Zamrini E, McGwin G, Roseman JM. Association between statin use and Alzheimer's disease. Neuroepidemiology. 2004;23:94-98.
9. Zandi PP, Sparks DL, Khachaturian AS, et al. Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study. Arch Gen Psychiatry. 2005;62:217-224.
10. Zhou B, Teramukai S, Fukushima M. Prevention and treatment of dementia or Alzheimer's disease by statins: a meta-analysis. Dement Geriatr Cogn Disord. 2007;23:194-201.
11. Beydoun MA, Beason-Held LL, Kitner-Triolo MH, et al. Statins and serum cholesterol's associations with incident dementia and mild cognitive impairment. J Epidemiol Community Health. 2011;65:949-957.
12. Bettermann K, Arnold AM, Williamson J, et al. Statins, risk of dementia, and cognitive function: secondary analysis of the Ginkgo Evaluation of Memory Study. J Stroke Cerebrovasc Dis. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2010.11.002³. Accessed January 31, 2012.
13. Benito-León J, Louis ED, Vega S, Bermejo-Pareja F. Statins and cognitive functioning in the elderly: a population-based study. J Alzheimers Dis. 2010;21:95-102.
14. Muldoon MF, Barger SD, Ryan CM, et al. Effects of lovastatin on cognitive function and psychological well-being. Am J Med. 2000;108:538-546.
15. Muldoon MF, Ryan CM, Sereika SM, Flory JD, Manuck SB. Randomized trial of the effects of simvastatin on cognitive functioning in hypercholesterolemic adults. Am J Med. 2004;117:823-829.
16. Trompet S, van Vliet P, de Craen AJ, et al. Pravastatin and cognitive function in the elderly. Results of the PROSPER study. J Neurol. 2010;257:85-90.
17. Feldman HH, Doody RS, Kivipelto M, et al. Randomized controlled trial of atorvastatin in mild to moderate Alzheimer disease: LEADe. Neurology. 2010;74:956-964.
18. Sabatine MS, Wiviott SD, Morrow DA, McCabe CH, Cannon CP. High-dose atorvastatin associated with worse glycemic control: a PROVE-IT TIMI 22 substudy. Circulation. 2004;110(Suppl I):S834.
19. Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010;375(9716):735-742.
20. Rajpathak SN, Kumbhani DJ, Crandall J, Barzilai N, Alderman M, Ridker PM. Statin therapy and risk of developing type 2 diabetes: a meta-analysis. Diabetes Care. 2009;32(10):1924-1929.
21. Sukhija R, Prayaga S, Marashdeh M, et al. Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients. J Investig Med. 2009;57:495-499.
22. Koh KK, Quon MJ, Han SH, Lee Y, Kim SJ, Shin EK. Atorvastatin causes insulin resistance and increases ambient glycemia in hypercholesterolemic patients. J Am Coll Cardiol. 2010;55:1209-1216.
23. Thongtang N, Ai M, Otokozawa S, et al. Effects of maximal atorvastatin and rosuvastatin treatment on markers of glucose homeostasis and inflammation. Am J Cardiol. 2011;107:387-392.
24. Kostapanos MS, Liamis GL, Milionis HJ, Elisaf MS. Do statins beneficially or adversely affect glucose homeostasis? Curr Vasc Pharmacol. 2010;8:612-631.
25. Mills EJ, Wu P, Chong G, et al. Efficacy and safety of statin treatment for cardiovascular disease: a network meta-analysis of 170,255 patients from 76 randomized trials. QJM. 2011;104:109-124.
26. Culver AL, Ockene IS, Balasubramanian R, et al. Statin use and risk of diabetes mellitus in postmenopausal women in the Women's Health Initiative. Arch Intern Med. 2012;172(2):144-152.
27. Armitage J, Bowman L, Wallendszus K; for the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) Collaborative Group. , et al. Intensive lowering of LDL cholesterol with 80 mg versus 20 mg simvastatin daily in 12,064 survivors of myocardial infarction: a double-blind randomised trial. Lancet. 2010;376:1658-1669.
28. Lees RS, Lees AM. Rhabdomyolysis from the coadministration of lovastatin and the antifungal agent itraconazole. N Engl J Med. 1995;333:664-555.

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Read the complete article here.

New JAMA Study Bakes Fish Oils- Don’t Believe It! - Cohen

New JAMA Study Bakes Fish Oils- Don’t Believe It!

 

 

Dear Pharmacist,

 

I just heard about the new study that says fish oil supplements don’t prevent heart attacks, and may not help us. Should I keep taking fish oils? –S.S., Chicago

Answer: Yes, if they’re high-quality. The “study” wasn’t a study at all, it was a meta-analysis, which means researchers examine results from a bunch of trials and draw their own conclusions based on the collective data. The meta-analysis you refer to appeared in the September 2012 issue of JAMA and included 68,000 participants in 20 different studies that covered a time frame 24 years. I have some problems with their opinion that fish oils are fairly worthless. The research I know of suggests strong benefits to the heart and arteries when you take high-quality fish oils. These are my problems with the JAMA article:

1. The researchers only reviewed 20 studies, but there are thousands that suggest cardiovascular protection by fish oils, particularly the EPA and DHA components. You’re not going getting the full picture from 20 studies.
2. How much fish oil was used? Most people were taking 1,000mg per day, but you need about 2,000 mg per day (total daily dose of EPA and DHA) to truly impact coronary heart disease. We come up therapeutically short! What about the ratio of EPA to DHA; ideally, I’d like it to be 3:2; for example, 600mg of EPA to 400mg DHA is a 3:2 ratio.

3. The looked at chronically ill people who had serious conditions, like they had already suffered a heart attack and stroke, not folks taking it for prevention. Fish oils are not intended to prevent heart attack or stroke. Plus, it’s super hard to prevent more health catastrophes, once you’ve had one. Feeling skewed?

4. What about the medications these folks were taking? The participants were taking all sorts of blood pressure pills and diuretics, most of which just so happen to be drug muggers of magnesium! Do you realize that serious uncorrected magnesium deficiency can cause a heart attack, no matter how much fish oil you take! To me, this is a huge gap in their premature conclusion.
5. What about Gamma Linolenic Acid or “GLA” status? When you take fish oils, an omega 3 fatty acid, you have to also supplement with GLA (an omega 6 fatty acid) because high doses of fish oils will cause drug mugging of GLA. For example, if you take 1,000 mg of fish oil (EPA and DHA totaled together), you need 500mg GLA at the same time. Evening primrose oil supplements can provide this GLA. This is important because GLA deficiency can increase your tendency to form clots (bad). GLA is known to protect the heart, without adequate amounts, you could suffer cardiac consequences, and this was not even addressed.

Even the American Heart Association approves of fish oils for heart health. Think smart and don’t be fooled by a single study intended to sway you away from decades of positive research.
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READ THE COMPLETE ARTICLE HERE.
Also watch Suzy's video discussing this here.

Low Cholesterol Leads to an Early Death - Evans/Naughton

Book Review: Low Cholesterol Leads to an Early Death Posted by Tom Naughton  Oct082012

 

Back in April I reviewed and recommended Cholesterol and Saturated Fat Prevent Heart Disease – Evidence from 101 Scientific Papers, a book by David Evans, who somehow manages to maintain and constantly update a huge collection of study abstracts and synopses on his Healthy Diets and Science website.

After I posted that review, David asked me if I’d write the foreword for his next book, another collection of 101 studies which suggest that low cholesterol – despite everything we’ve been told – isn’t good for us. I agreed, wrote the forward, then forgot about it until I received a copy of the new book this week. I was actually a bit surprised when I saw Foreword by Tom Naughton in the table of contents. Must be my advancing age.

Anyway, I like Low Cholesterol Leads to an Early Death — Evidence From 101 Scientific Papers for all the same reasons I like the previous one. It’s not a book you’ll sit down and read for pleasure, but it’s an excellent, easy-to-use reference to keep on your bookshelf. I frequently receive emails from readers asking me to point them to research they can wave in front of worried family or friends and say, “See? Saturated fat isn’t going to kill me, and no, I don’t need to take the @#$%ing statin the doctor is pushing on me!” (Or words that effect. ) If 101 studies won’t do the trick, nothing will.
As in the previous book, for each of the 101 studies there’s a title, a citation so you can look up the study yourself, and a brief summary with occasional commentary by Evans. Papers published in medical journals tend to have sleep-inducing titles along the lines of Low-density lipoprotein as a predictor of mortality in a cohort of elderly Scandinavian patients, so Evans provides more colorful titles that get to the point. You’ve got to love opening a book and seeing titles like these:

Heart attack survivors live longer if they have high cholesterol
Low cholesterol levels increase the risk of death from stroke, cancer and all causes
Low cholesterol levels predict death in patients with bacteria in the blood
Colon cancer deaths increase in men with low cholesterol

Many of these studies (and there are many of them) have been around for decades. I doubt most doctors have ever read the studies or even heard of them. If they had, I don’t see how they could possibly believe prescribing statins to beat down an elderly patient’s “high” cholesterol is a good idea. As Evans writes in the book’s introduction:

The “high cholesterol is bad for your health” myth has survived for five or six decades. The myth is why health-care practitioners, media advertisements and family and friends keep pressing home the message we should lower our cholesterol. The myth is why, despite mounting scientific evidence showing the opposite, we are still advised to lower our cholesterol. The myth is why we are told we should eat tasteless, manufactured low-fat products to lower our cholesterol. The myth is why millions of healthy people are subjected to statins drugs (and their many side effects) that will lower our cholesterol.

The myth survives largely because the millions of people buying cholesterol-lowering cereals and swallowing cholesterol-lowering drugs represent billions of dollars in revenues. We can’t change that. But we can arm ourselves with evidence and hope to convince a few loved ones that lowering our cholesterol isn’t necessary or even a good idea.

If you’re arming yourself, this book is a great addition to your arsenal.
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Read the complete article here.

Book Review: Don’t Die Early - Rocky Angelucci (Naughton reviewed)

Sep062012

Book Review: Don’t Die Early

Posted by Tom Naughton

Lying on the gurney in the emergency room, I shielded my eyes from the glaring overhead lights and tried to remember exactly when my heart went wacko. I remember being anxious and out of sorts all evening. Looking back, I realized that during dinner my chest felt fluttery and strange inside, and I recall snapping at my wife, Laura, over nothing as I left the kitchen to go upstairs.

By the time I reached the top of the stairs, I knew something was very wrong— I could barely breathe and when I placed my fingers to the side of my neck, my pulse felt very unusual. Not the rhythmic beating I would have expected, but more like an indistinct, squishy fluttering. Walking into our spare bedroom, I retrieved the pulse meter from the shelf next to the treadmill. I slipped the meter on my finger and looked at the readout. The effort seemed exhausting. Sitting on the edge of the bed, I called for Laura. When she arrived a moment later, I handed her the pulse meter.

The display read 195 beats per minute and I knew my life had just changed forever. The old carefree way of taking care of my body that had worked fine in my youth and young adulthood wasn’t working anymore. I now had to become a conscious advocate of my own health.

That’s the opening from Don’t Die Early, an educational and very well-written book by Rocky Angelucci – who did nearly die early. Finding yourself lying on a gurney should certainly put a scare into you, but unfortunately many people respond to that scare by following their well-meaning doctor’s orders … you know, cut back on the eggs and saturated fats, eat your hearthealthywholegrains, etc.

Rocky didn’t go that route, partly (and I’m delighted to say this) because of Fat Head. As he explained in an email some months ago:

I have been a fan of yours since discovering a snippet of Fat Head on YouTube the evening I returned home from the hospital following a life-changing episode of atrial fibrillation. I was only 45 years old at the time, but had just been rudely awakened by the realization that the carefree lifestyle of my youth had become increasingly harmful. Fat Head’s discussion of insulin resistance and fat storage resonated very well with my pre-med college days studying life sciences and my experiences with the Zone diet and the hormonal implications of foods. Fat Head also catalyzed my growing displeasure at a procedure-driven medical system and gave substance to my vague feeling that politics, not science, has infiltrated medical care.

Because my underlying cardiac problem ultimately turned out to be an alarming plaque burden, my research quickly lead me to Dr. William Davis’ Track Your Plaque forum, where I have been a very active member for the past two years. I became so impressed with Dr. Davis that he has been my cardiologist for the past year. His warmth and prevention-minded attitude makes the journey from Dallas to Wisconsin entirely worthwhile. Thanks to my radical lifestyle changes, most of them flying in the face of conventional wisdom, I’m fortunate to be one of the TYP members who has shown dramatic plaque reversal, recently showing a 24% six-month decrease immediately following a horrific 83% increase the year before.

If I had heart disease, there’s no one in the world I’d rather have treating me than Dr. Davis. Rocky’s in good hands.

His email continued:
Emboldened by a background as a technical writer in the fields of software, nanotechnology, and medical devices, I’ve spent the past year writing a book on preventive health that captures what I’ve learned and applied to my own condition.

I read the book before it was published and again last week, and it’s excellent. When I consider recommending a book (publishers send me books I don’t recommend, by the way), I ask myself two questions: 1) Is the information useful to people who want to lose weight or become healthier? 2) Does it pass my “Aunt Martha” test … that is, could your Aunt Martha read it and understand it?
The answer to both questions in this case is an enthusiastic yes. Rocky has a gift for taking the science of nutrition and health and explaining it clearly, and it’s obvious from the many topics he covers and how well he covers them that he jumped into that science head-first. I learned more from this book than I thought I would, which is always a pleasure.

As the title indicates, Don’t Die Early isn’t about weight loss. It’s about how to live to a ripe old age and remain healthy along the way. Weight loss is covered in a section about dietary fallacies, but Rocky’s goals for the reader are the same goals he set for himself: 1) understand the true causes of heart disease, diabetes and inflammation; 2) learn how to reliably measure and track the instigators or markers of those diseases, such as LDL particle size and A1C; and 3) take specific actions to reverse disease or prevent it from developing in the first place.

That’s what Rocky did, and was rewarded with excellent results:
In the first six months after embracing a preventive lifestyle, I accomplished the following:

• Lowered my body fat percentage from 20% to 11%
• Lowered my inflammatory markers by as much as 75% (you’ll learn about inflammation later)
• Reduced my triglycerides by more than 90% (this happened in the first 30 days)
• Improved every measurable aspect of my cholesterol
• Improved my fasting glucose by 25%
• Improved my muscle tone and stamina
• Lowered my blood pressure from an average of 145/90 to an average of 115/70
• Reduced my resting heart rate by more than 13 points

As impressive as these results might appear, I’m not revealing them so that you’ll invite me to your next party. They are to show you what is very attainable for anyone who makes the proper lifestyle changes.

The book is divided into two parts. Part One, titled The Major Players, provides in-depth explanations of heart disease, diabetes and inflammation. The message Rocky pounds home in these chapters is that it’s important not only to understand what these diseases actually are and what causes them, but to know specifically what to measure so you can tell if you’re developing them. Sadly (but not surprisingly), the tests your doctor orders often add up to too little, too late:

Imagine having the following conversation with your child’s teacher:

You: How is my daughter doing in school this semester? Is she learning the required material?

Teacher: Based upon her age, and what we infer her socioeconomic status to be, as well as her assertions that she does homework on a regular basis, we believe she has a very high likelihood of having mastered this semester’s materials acceptably.

You: Excuse me? What does this mean? Have you tested her on the material?

Teacher: No, we compared her socioeconomic status, apparent nutritional health, and her testimony that she does her homework regularly to a statistical model we have and there’s a strong correlation between your daughter’s parameters and students who mastered the coursework. Oh, and we measured the callouses on her writing fingers and they indicate that she’s likely doing quite a bit of writing, which our statistical model shows increases by 22% her chances of having mastered the material. Overall, we feel very confident that she has mastered this semester’s material.

You: I don’t understand why you’re comparing her to a statistical model instead of testing her. Do you ever plan on testing her?

Teacher: Only if she shows clear signs of having failed to master the material would we test her. As long as her parameters correlate acceptably to the statistical models of a successful population, we will assume that she is mastering the material.

Does this sound like a school you would like your child to attend? Does estimating your child’s performance by comparing indirect parameters to a statistical model sound like an ideal way to gauge her mastery of the subject matter? It certainly doesn’t to me.

Yet this is how our medical culture typically measures the risk of coronary artery disease during routine preventive exams.

That’s why Rocky didn’t know he was developing plaque in his arteries. He quotes Dr. William Davis, who says that the traditional methods of identifying people at risk for heart disease miss 90 percent of the people who eventually have a heart attack. If you want to know if you’re developing plaque, you should (surprise!) measure plaque.

The standard test for measuring diabetes often misses those who are developing it as well:
Many of the clinical guidelines in use today encourage a physician to use fasting glucose as the sole indicator of one’s diabetic health. Seeing a fasting glucose level within the laboratory “normal” range, both patient and physician are satisfied that the patient is at low risk of Type 2 diabetes.

Now that you know more about how diabetes progresses, you can see that gauging the risk of Type 2 diabetes solely on fasting glucose is terribly ineffective. An abnormal fasting glucose is typically the last commonly used indicator to show the presence of diabetes. In fact, by the time your fasting glucose is no longer in the normal range, you are already diabetic.

Throughout these chapters, Rocky explains which health markers you should be actually measuring and which specific tests you can request from your doctor or order online and perform at home.
Fat Head fans will be familiar with much of material on heart disease and diabetes, including how much of the standard advice from so-called experts is wrong. But even though I’ve read quite a bit on those topics, I kept coming across information in Don’t Die Early that was either new to me or struck me as particularly well-explained. Here are a couple of sample bits:

Perhaps the biggest problem with insulin being a growth hormone is that not all of the tissues in the body become desensitized to increasing levels of insulin at the same rate. As a person becomes more and more insulin-resistant, cells that are much less affected continue to respond to the ever-increasing levels of insulin, growing and multiplying more rapidly as insulin levels increase. What cells exhibit this behavior? The endothelial cells that form the lining of your arteries, for one. As these arterial cells multiply more rapidly, the lining of an insulin-resistant person’s arteries thicken and grow inward, hastening coronary artery disease. This is one of the reasons why so many diabetics die from heart disease.
…
A typical cell membrane is composed of a lipid bilayer, which is just what it sounds like: two layers of fatty acid molecules, sandwiched together to give cell membranes their much-needed strength. This bilayer also forms an effective barrier to foreign substances, through the use of embedded receptors that are designed to transfer only specific things into and out of the cell. The impermeable lipid layers and their receptors serve as gatekeepers to help ensure the health of a cell by transferring only what the cell needs, in the right amounts, into the cell and removing unwanted substances from within the cell. Virtually anything that the cell consumes or produces is transported this way, ensuring that only the proper substances ever reach the interior of the cell.

As with most structures of the body, the cell’s lipid bilayer needs to be constantly maintained, which the body does by constantly replenishing the crucial fatty acids that comprise the cell membranes. What happens if a person eats a trivial amount of healthy omega-3 fatty acids and an abundance of unhealthy omega-6 fatty acid? Simple, the body does its best with what you give it and will use the omega-6 fatty acids instead.

What this means is that in addition to their role in promoting inflammatory chemical messengers, omega-6 fatty acids become incorporated into virtually every cell in your body.

Part two of the book, Lifestyle Changes, includes chapters on dietary truths and fallacies, setting goals, and taking action. Again, the chapter on diet covers ground that’s largely familiar for Fat Heads (Gary Taubes and Dr. William Davis are quoted several times), but it’s well written and worth the read.

In the final two chapters, Rocky urges the reader to do enough testing to establish several baseline measurements (blood sugar, fasting insulin, vitamin D concentration, LDL particle size, etc.), set specific and attainable goals for improving those markers, then work to meet them. If you’ve ever wondered what your fasting insulin level or vitamin D concentration should be (ideally, anyway) this chapter will tell you. Rocky also gives advice on how to improve your odds of meeting each goal. For example, to achieve optimum triglyceride levels:

In summary, the best approach to reducing one’s triglycerides is

• Eliminate grains, replacing them with vegetables, nuts, and berries.
• Minimize carbohydrates (especially fructose), eating them in sufficient moderation so as to never cause unfavorable glucose levels.
• Consider supplementing your diet with omega-3 fatty acids from fish oil.
• Speak to your physician about supplementing with niacin to help optimize your triglycerides.
• All of the above steps will very effectively control your fasting triglycerides. To really take it to the next level, buy a Cardio-Chek triglyceride meter to measure your body’s response to different types of meals to identify exactly how sensitive your body is to specific types and quantities of fats. If you perform a small series of these carefully controlled tests, you’ll have infinitely more clarity on how to optimize your diet for the best possible postprandial triglyceride production (this will be especially valuable in determining whether saturated fat is good for you and at what level).

Near the very end of the book, there’s a section I’m sure many of you will relate to … the sub-chapter heading is Prepare To Be An Outcast. Here’s chunk of that section:

You may find yourself biting your tongue every time you see a friend, colleague, or loved one wolf down a low-fat, grain-based meal, laden with vegetable oil, as they complain about having acid reflux or autoimmune disorders.

You may see friends and loved ones struggle with weight problems while they eat low-fat foods that constantly elevate their blood glucose level, ensuring that they live life as the “walking starving,” trying unsuccessfully to lose weight.

Even your more health-conscious friends may not appreciate your one-upping them on matters of health and nutrition. Responding to their enthusiasm for fish oil with “Yes, but do you track your daily intake of omega-3 and omega-6 fatty acids and have you ever checked your Omega-3 Index?” will make you sound like a know-it-all.

It’s painful to realize that some people just don’t want to hear that there’s a better future available to them if they just abandon the current thinking on what’s healthy and what’s not. Many refuse to believe that they could ever get bad advice from a physician or from a “trusted” source like the USDA, the American Dietetic Association, or the American Diabetes Association. In such cases, you may just need to silently watch them continue on their path.

Sadly, that’s true. But for people who are open to trying a new path to health, Don’t Die Early is an excellent guidebook.
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Read the full article here.

What Your Doctors Don’t Know About the Drugs They Prescribe - Ben Goldacre

What Your Doctors Don’t Know About the Drugs They Prescribe
 Ben “Bad Science” Goldacre

We don’t really know if the drugs we use work. We just believe that we know.

Goldacre has just published a book on the subject, called Bad Pharma. You can read the foreword on his blog.

Quotes:

"A cancer at the core of evidence based medicine"

"This is a disaster. We cannot know the true effect of the medicines that we prescribe if we do not have access to all of the information."

 

..................................................................

Comments to the video.

1. eddie watts
   
   
   scary stuff, but not surprising really.
2. Ted Hutchinson
   
   
   High reprint orders in medical journals and pharmaceutical industry funding
   Here is a free full text paper in which Ben Goldacre was a co author.
   You may also enjoy.
   Ben Goldacre keynote Strata Conference London 2012
   I think we should also insist that all medical research conducted with public funds or using data collected from publicly funded hospitals/universities is made available free online six months from journal publication.
3. 
   
   Ted Hutchinson
   
   
   
   
   He was also on You and Yours today
   Talking about the way pharmaceutical companies influence prescribing practice and make huge donations to Charities purporting to help patients with particular diseases lobby for expensive medications.

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Watch this excellent Ted talk video here.

Know All 10 Heart Disease Risk Factors? - Alan Watson

Do You & Your Doctor Know All 10 Heart Disease Risk Factors?

 March 7, 2012 by Alan Watson

If you're new here, you may want to subscribe to my RSS feed. Thanks for visiting!

 

Heart disease is the #1 cause of death. About 50 percent of all people who die suddenly from heart disease have low or normal cholesterol. To protect yourself from heart disease, ask your doctor for a complete lipid evaluation. Fast 10-12 hours before blood is drawn (you can drink water). Because Total Cholesterol (TC) and LDL cholesterol are not the most reliable predictors of heart disease, they are not posted in the following chart.

 

QUICK SUMMARY:

Focus on Fasting Glucose, HDL, Triglycerides (TG) and the all important TG:HDL ratio. Keep in mind that before the advent of cholesterol-lowering statin drugs, the normal range for Total Cholesterol (TC) was: 180 mg/dl to 340 mg/dl. Also, it’s important to note that LDL is actually a family of particles. A discussion about LDL subclasses and LDL subclass testing follows in the summary of this article.

 

1. C-reactive protein (CRP) is produced by the liver in response to inflammation in the body. If monitored early enough, elevated CRP can be an early warning of a heart attack several years in advance. Optimum levels are below 1 mg/l. (You will have to request this test with most doctors.)

2. Fasting Glucose (FG) measures fasting blood sugar. Lowest all-cause mortality is associated with fasting glucose in the range of 80-89 mg/dl. According to the clinical experience of Dr. Robert Atkins, the risk of heart disease increases in linear manner as your Fasting Glucose goes over 100 mg/dl. (Specifically ask for this inexpensive test.)

3. Fibrinogen is a protein that in excess promotes blood clots. Elevated fibrinogen = thicker blood. Thicker blood flows less easily through partially blocked arteries. Consistent elevated fibrinogen (over 350 mg/dl) conveys a 250 percent increased risk of heart disease compared to people with fibrinogen levels below 235. (People who have recently suffered a heart attack will have elevated fibrinogen levels.)

4. Homocysteine is normally rapidly cleared from the bloodstream. Elevated homocysteine is a result of B-vitamin deficiencies, particularly folic acid, B-6 and B-12. Elevated homocysteine is associated with increased risk of heart attack, stroke, and all cause mortality. Levels less than 8 mmol/L are associated with longevity. (Again, you may have to request this test.)

5. Lipoprotein(a) has been called the “heart attack cholesterol.” Lipoprotein(a) is a sticky protein that attaches to LDL and accumulates rapidly at the site of arterial lesions or ruptured plaque. Readings of 30 mg/dl or more indicate serious increased risk of heart disease, especially in the presence of elevated fibrinogen (>350). While the Lp(a) level is largely genetically determined, it can be influenced by nutritional factors, such as high blood sugar and trans fatty acid consumption. (This test may not be as important as the rest and is seldom done routinely.)

6. HDL is made in the liver and acts as a cholesterol mop, scavenging loose cholesterol and transporting it back to the liver for recycling. HDL is associated with protection from heart disease. You want as much HDL as possible. HDL of 60 or more is associated with protection for men—70 or more for women.

7. Triglycerides (TG) should be under 100 mg/dl. Triglycerides are blood fats made in the liver from excess energy – especially carbohydrates. Risk is linear—the higher the number, the greater the risk, especially for women. While doctors may insist that a reading up to 150 is okay, Dr. Atkins’ clinical experience suggested otherwise.

8. TG:HDL ratio is the most reliable predictor of heart disease. Calculate your ratio by dividing TG by HDL. As an example, if TG = 80 and HDL = 80, your ratio is 1:1 representing low risk of heart disease. If your TG = 200 and your HDL = 50, your ratio is 4:1 representing serious risk of heart disease.

9. VLDL – Increasingly, Very Low Density Lipoprotein is measured/calculated. VLDL is sent out from the liver to deliver those liver made fats (Triglycerides) – as opposed to a Chylomicron that delivers dietary fat from the gut. Generally, VLDL is one fifth of your triglyceride level, although this is less accurate if your triglyceride level is greater than 400 mg/dl. (Beyond the scope of this article, LDL is the offspring of VLDL – they are closely-related.)

LDL particle size: Small dense Pattern B/Large fluffy Pattern A

An illustration from the Berkeley Heart Labs showing these particles

LDL – low density lipoprotein – is a family of particles. A lot of people with elevated LDL do not develop coronary artery disease, while individuals with low or modest levels often develop serious disease. This can be explained by the LDL particle number and size. Routine cholesterol testing only reveals the amount of LDL; not the quality of LDL.

We now know (my doctor didn’t) that there are different subclasses of LDL (and HDL). Under an electron microscope, some LDL particles appear large and fluffy; others small and dense. The big, fluffy particles are benign, while the small dense particles are strongly associated with increased risk of heart disease.

In excess, small dense LDL is toxic to the artery lining (the endothelium), and much more likely to enter the vessel wall – become oxidized – and trigger atherosclerosis. It’s becoming consensus medical opinion that only oxidized LDL can enter the macrophages in the lining of the arteries and contribute to plaque buildup.

HOW DO YOU KNOW WHAT LDL YOU HAVE? Certain clinical factors predict the presence of small dense LDL. These markers include HDL below 40 in men; below 50 in women – and Triglycerides (TG) higher than 120 mg/dl. Diabetes or pre-diabetes also predicts small dense LDL (Pattern B).

To determine LDL particle size, ask your doctor for a VAP (Vertical Auto Profile) test, which separates lipoprotein particles using a high speed centrifuge. The VAP test measures the basic information provided by a routine cholesterol test, but also identifies lipoprotein subclasses, LDL and HDL. (Go to http://thevaptest.com for more information.)

There are other tests as well. The NMR LipoProfile analyzes the number and size of lipoprotein particles by measuring their magnetic properties (http://theparticletest.com). Also Berkeley HeartLab’s LDL Segmented Gradient Gel Electrophoresis test measures all seven subclasses of LDL. (http://bhlinc.com).

If you don’t have insurance and can pay for just one test, get your fasting blood sugar checked. Any number over 100 – over 95 according to the late Dr. Atkins – is an early warning of diabetes, metabolic syndrome, and heart disease. If you have insurance or can afford a complete lipid panel, consider additional testing to determine the size and number of LDL particles. “A stitch in time saves nine.”
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