The straight dope on Cholesterol– Part 1 (Attia)

The straight dope on Cholesterol– Part 1

Posted by Peter Attia on Apr 25, 2012

Concept #1 – What is cholesterol?

Cholesterol is a 27-carbon molecule shown in the figure below. Each line in this figure represents a bond between two carbon atoms. Sorry, I’ve got to get it out there. That’s it. Mystery over.

All this talk about “cholesterol” and most people don’t actually know what it is. So there you have it. Cholesterol is “just” another organic molecule in our body.

I need to make one important distinction that will be very important later. Cholesterol, a steroid alcohol, can be “free” or “unesterified” (“UC” as we say, which stands for unesterified cholesterol) which is its active form, or it can exist in its “esterified” or storage form which we call a cholesterol ester (“CE”). The diagram above shows a free (i.e., UC) molecule of cholesterol. An esterified variant (i.e., CE) would have an “attachment” where the arrow is pointing to the hydroxyl group on carbon #3, aptly named the “esterification site.”

Since cholesterol can only be produced by organisms in the Animal Kingdom it is termed a zoosterol. In a subsequent post I will write about a cousin of cholesterol called phytosterol, but at this time I think the introduction would only confuse matters. So, if you have a question about phytosterols, please hang on.

Concept #2 – What is the relationship between the cholesterol we eat and the cholesterol in our body?

We ingest (i.e., take in) cholesterol in many of the foods we eat and our body produces (“synthesizes”) cholesterol de novo from various precursors. About 25% of our daily “intake” of cholesterol – roughly 300 to 500 mg — comes from what we eat (called exogenous cholesterol), and the remaining 75% of our “intake” of cholesterol — roughly 800 to 1,200 mg – is made by our body (called endogenous production). To put these amounts in context, consider that total body stores of cholesterol are about 30 to 40 gm (i.e., 30,000 to 40,000 mg) and most of this resides within our cell membranes. Every cell in the body can produce cholesterol and thus very few cells actually require a delivery of cholesterol. Cholesterol is required by all cell membranes and to produce steroid hormones and bile acids.

Of this “made” or “synthesized” cholesterol, our liver synthesizes about 20% of it and the remaining 80% is synthesized by other cells in our bodies. The synthesis of cholesterol is a complex four-step process (with 37 individual steps) that I will not cover here (though I will revisit), but I want to point out how tightly regulated this process is, with multiple feedback loops. In other words, the body works very hard (and very “smart”) to ensure cellular cholesterol levels are within a pretty narrow band (the overall process is called cholesterol homeostasis). Excess cellular cholesterol will crystalize and cause cellular apoptosis (programmed cell death). Plasma cholesterol levels (which is what clinicians measure with standard cholesterol tests) often have little to do with cellular cholesterol, especially artery cholesterol, which is what we really care about. For example, when cholesterol intake is decreased, the body will synthesize more cholesterol and/or absorb (i.e., recycle) more cholesterol from our gut. The way our body absorbs cholesterol is so amazing, so I want to spend a bit of time discussing it.

In medical school, whenever we had to study physiology or pathology I always had a tendency to want to anthropomorphize everything. It’s just how my brain works, I guess, and understanding cholesterol absorption is a great example of this sort of thinking. The figure below shows a cross-section of a cell in our small intestine (i.e., our “gut”) called an enterocyte that governs how stuff in our gut actually gets absorbed. The left side with the fuzzy border is the side facing the “lumen” (the inside of the “tube” that makes up our gut). You’ll notice two circles on that side of the cell, a blue one and a pink one.

[What follows is a bit more technical than I would have liked, but I think it’s very important to understand how this process of cholesterol absorption works. It’s certainly worth reading this a few times to make sure it sinks in.]

• The blue circle represents something called a Niemann-Pick C1-like 1 protein (NPC1L1). It sits at the apical surface of enterocytes and it promotes active influx (i.e., bringing in) of gut luminal unesterified cholesterol (UC) as well as unesterified phytosterols into the enterocyte. Think of this NPC1L1 as the ticket-taker at the door of the bar (where the enterocyte is the “bar”); he lets most cholesterol (“people”) in. However, NPC1L1 cannot distinguish between cholesterol (“good people”) and phytosterol (“bad people” – I will discuss these guys later, so no need to worry about it now) or even too much cholesterol (“too many people”). [I can’t take any credit for this anthropomorphization – this is how Tom Dayspring explained it to me!]

• The pink circle represents an adenosine triphosphate (ATP)-binding cassette (ABC) transporters ABCG5 and ABCG8. This complex promotes active efflux (i.e., kicking out) of unesterified sterols (cholesterol and plant sterols – of which over 40 exist) from enterocytes back into the intestinal lumen for excretion. Think of ABCG5,G8 as the bouncer at the bar; he gets rid of the really bad people (e.g., phytosterols as they serve no purpose in humans) you don’t want in the bar who snuck past the ticket-taker (NPC1L1). Of course in cases of hyperabsorption (i.e., in cases where the gut absorbs too much of a good thing) they can also efflux out un-needed cholesterol. Along this analogy, once too many “good people” get in the bar, fire laws are violated and some have to go. The enterocyte has “sterol-excess sensors” (a nuclear transcription factor called LXR) that do the monitoring and these sensors activate the genes that regulate NPC1L1 and ABCG5,G8).

There is another nuance to this, which is where the CE versus UC distinction comes in:

• Only free or unesterified cholesterol (UC) can be absorbed through gut enterocytes. In other words, cholesterol esters (CE) cannot be absorbed because of the bulky side chains they carry.

• Much (> 50%) of the cholesterol we ingest from food is esterified (CE), hence we don’t actually absorb much, if any, exogenous cholesterol (i.e., cholesterol in food). CE can be de-esterified by pancreatic lipases and esterolases – enzymes that break off the side branches and render CE back to UC — so some ingested CE can be converted to UC.

• Furthermore, most of the unesterified cholesterol (UC) in our gut (on the order of about 85%) is actually of endogenous origin (meaning it was synthesized in bodily cells and returned to the liver), which ends up in the gut via biliary secretion and ultimately gets re-absorbed by the gut enterocyte. The liver is only able to efflux (send out via bile into the gut) UC, but not CE, from hepatocytes (liver cells) to the biliary system. Liver CE cannot be excreted into bile. So, if the liver is going to excrete CE into bile and ultimately the gut, it needs to de-esterify it using enzymes called cholesterol esterolases which can convert liver CE to UC.

• Also realize that the number one way for the liver to rid itself of cholesterol is to convert the cholesterol into a bile acid, efflux that to the bile (via a transporter called ABCB11) and excrete the bile acids in the stool (typically most bile acids are reabsorbed at the ileum).

Concept #3 – Is cholesterol bad?

One of the biggest misconceptions out there (maybe second only to the idea that eating fat makes you fat) is that cholesterol is “bad.” This could not be further from the truth. Cholesterol is very good!

 In fact, there are (fortunately rare) genetic disorders in which people cannot properly synthesize cholesterol. Once such disease is Smith-Lemli-Opitz syndrome (also called “SLOS,” or 7-dehydrocholesterol reductase deficiency) which is a metabolic and congenital disorder leading to a number of problems including autism, mental retardation, lack of muscle, and many others.

Cholesterol is absolutely vital for our existence. Let me repeat: Cholesterol is absolutely vital for our existence. Every cell in our body is surrounded by a membrane. These membranes are largely responsible for fluidity and permeability, which essentially control how a cell moves, how it interacts with other cells, and how it transports “important” things in and out. Cholesterol is one of the main building blocks used to make cell membranes (in particular, the ever-important “lipid bilayer” of the cell membrane).

Beyond cholesterol’s role in allowing cells to even exist, it also serves an important role in the synthesis of vitamins and steroid hormones, including sex hormones and bile acids. Make sure you take a look at the picture of steroid hormones synthesis and compare it to that of cholesterol (above). If this comparison doesn’t convince you of the vital importance of cholesterol, nothing I say will.
One of the unfortunate results of the eternal need to simplify everything is that we (i.e., the medical establishment) have done the public a disservice by failing to communicate that there is no such thing as “bad” cholesterol or “good” cholesterol. All cholesterol is good!

The only “bad” outcome is when cholesterol ends up inside of the wall of an artery, most famously the inside of a coronary artery or a carotid artery, AND leads to an inflammatory cascade which results in the obstruction of that artery (make sure you check out the pictures in the links, above). When one measures cholesterol in the blood – we really do not know the final destination of those cholesterol molecules!

And that’s where we’ll pick it up next time – how does “good” cholesterol end up in places it doesn’t belong and cause “bad” problems? If anyone is looking for a little extra understanding on this topic, please, please, please check out my absolute favorite reference for all of my cholesterol needs, LecturePad. It’s designed primarily for physicians, but I suspect many of you out there will find it helpful, if not now, certainly once we’re done with this series.

To summarize this somewhat complex issue

1. Cholesterol is “just” another fancy organic molecule in our body, but with an interesting distinction: we eat it, we make it, we store it, and we excrete it – all in different amounts.
2. The pool of cholesterol in our body is essential for life. No cholesterol = no life.
3. Cholesterol exists in 2 forms – UC and CE – and the form determines if we can absorb it or not, or store it or not (among other things).
4. Most of the cholesterol we eat is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason is it not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.
5. Re-absorption of the cholesterol we synthesize in our body is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.
6. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control. I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.
7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up.

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How to increase your risk of heart disease

August 5, 2008   Chris Kresser

Easy! Just follow Dr. Steinberg’s recent recommendations.

Dr. Daniel Steinberg, author of “The Cholesterol Wars”, has just issued new recommendations proposing that “aggressive intervention to lower cholesterol levels as early as childhood is the best approach available today to reducing the incidence of coronary heart disease.”

In a review article published in the August 5, 2008 issue of the American Heart Association journal Circulation, Steinberg and his colleagues state that “with a large body of evidence proving that low cholesterol levels equate with low rates of heart disease, “…our long-term goal should be to alter our lifestyle accordingly, beginning in infancy or early childhood” and that “…instituting a low-saturated fat, low-cholesterol diet in infancy (7 months) is perfectly safe, without adverse effects…”

I don’t know whether to scream or cry when I read this stuff. Or both. Why? Because Dr. Steinberg’s dietary recommendations – if embraced by parents – are sure to increase the risk of heart disease and cause developmental problems in the children unfortunate enough to adopt them.

Let’s take a closer look at each part of the article on ScienceDaily.com describing the new recommendations and see if Steinberg’s claims make any sense.

According to Steinberg, progress has been made in the treatment of coronary heart disease in adults with cholesterol lowering drugs like statins. However, while studies show a 30% decrease in death and disability from heart disease in patients treated with statins, 70% of patients have cardiac events while on statin therapy.

Progress in treating heart disease? What progress? Heart disease is the #1 cause of death in the U.S. today. In the early part of the 20th Century, heart disease was relatively unknown. I would hardly call that progress.

As for statins, please refer to my previous article “The Truth About Statin Drugs” for a more accurate appraisal of the effectiveness (or lack thereof) of statins. In short, statins don’t reduce the risk of death in 95% of the population, including healthy men with no pre-existing heart disease, women of any age and the elderly. While statin drugs do reduce mortality for young and middle-aged males with pre-existing heart disease, the benefit is small and not without significant adverse effects, risks and costs.

For example, in the six largest studies done on statins and mortality to date, the absolute risk reduction ranged from -0.3% to 3.3%. In two of those studies, statins actually increased the risk of death. In an analysis of this data, the UK Medical Research Council determined that even if you were in the 5% of the population that statins benefit, you’d have to take a statin for 30 years at a cost of $42,000 just to add nine months (best case) to your life.

Even that scenario is entirely hypothetical, because statins cause cancer in lab animals. Although this hasn’t been shown in humans to date, the window between exposure to a carcinogen and development of cancer can be as long as 25 years for humans. Since no one has been on statins for that long, there is still reason to believe that they might have the same effect in humans that they do on animals.

Progress? I don’t think so.

In fact, they propose that lowering low-density lipoproteins (the so-called “bad cholesterol”) to less than 50 mg./dl. even in children and young adults is a safe and potentially life-saving standard, through lifestyle (diet and exercise) changes if possible. Drug treatment may also be necessary in those at very high risk.

“Bad cholesterol”? That’s so 1975. It is well accepted even within the mainstream scientific community today that normal LDL cholesterol (so-called “bad cholesterol”) is not a risk factor for heart disease. Instead, it is the oxidation of the polyunsaturated fatty acid in the membrane of the LDL particle (when the level of antioxidants in the diet is insufficient to protect them) that contributes to heart disease.

Therefore, the only LDL cholesterol that could be called “bad” is oxidized LDL.

And what promotes oxidation of the LDL particle? Eating polyunsaturated fat (found in vegetable oils, nuts and seeds and in almost all processed food). Of course, these are exactly the fats the American Heart Association has promoted as “heart-healthy” for decades.

In addition to promoting oxidation of LDL particles, polyunsaturated fats contribute directly to atherosclerosis and heart attacks. 75% of arterial plaque is made up of unsaturated fat, of which 50% is polyunsaturated (only 25% is saturated). The greater the concentration of polyunsaturated fat in the plaque, the more likely it is to rupture. Such ruptures, and the ensuing blood clots that form, are a primary cause of heart attacks.

Another well-established cause of heart disease is inflammation. Omega-6 polyunsaturated fats, which constitute a large percentage of caloric intake for most Americans, are known to promote inflammation. Indeed, excess linoleic acid (LA) in the diet from vegetable oil has been shown to contribute directly to heart disease.

So, the notion that saturated fat “clogs arteries” and causes heart attacks is totally false. It is actually polyunsaturated fat – the so-called “heart-healthy fat – which has those effects.

If people’s lives weren’t at stake the irony of such a situation might be almost funny. As it stands it’s one of the great public health tragedies of modern times.

And what about the notion that eating cholesterol raises cholesterol levels in the blood? It turns out to be false – and Steinberg even admits as much in his own book. There are two parts of the hypothesis that cholesterol causes heart disease. The first part, called the “diet-heart hypothesis”, is that eating cholesterol in the diet raises cholesterol levels in the blood. The second part, called the “lipid hypothesis”, holds that high cholesterol levels in the blood cause heart disease.

We’ve already addressed the “lipid hypothesis” above. As for the “diet-heart hypothesis”, Steinberg clearly states in his book that there is little evidence to support it. Tightly controlled egg-feeding studies have shown that eating cholesterol only raises cholesterol levels in about 30% of the population (“hyper-responders”).
However, these same studies showed that egg consumption led to an increase in “light, fluffy LDL” that was actually protective against heart disease. Why? Because these large, buoyant LDL particles are protected against oxidation.
Finally, what about saturated fat? Does it cause heart disease as Steinberg suggests? Once again, the evidence squarely contradicts Dr. Steinberg’s claim. In 22 of 26 published studies there was no significant relationship between saturated fat intake and either coronary or all-cause mortality.

Among the studies that Dr. Steinberg failed to mention in his book or in his recent recommendation:

• Rose, et al. (1965): Replacing animal fat with corn oil for two years lowered serum cholesterol by 23 mg/dL but quadrupled cardiac and total mortality.
• Sydney Diet-Heart Study (1978): Replacing animal fat with vegetable fat for five years lowered cholesterol by five percent but increased total mortality by 50 percent.

What’s more, in the few studies where saturated fat restriction did reduce deaths from heart disease, deaths from cancer, brain hemorrhage, suicide & violent death went up! In his book The Great Cholesterol Con, Anthony Colpo concludes:

“If saturated fats caused even a portion of the damage for which they are frequently blamed, their negative effects should be readily and repeatedly demonstrable in controlled clinical trials. However, after excluding the results of the poorly designed and sloppily conducted northern European studies, it quickly becomes apparent that there does not exist a single tightly controlled trial which shows that saturated fat restriction can save even a single life.”

There are two more claims made by Dr. Steinberg that I need to address.

“lowering low-density lipoproteins to less than 50mg/dL even in children and young adults is a safe and potentially life-saving standard.”

As stated above, there is absolutely no evidence that lowering LDL protects against heart disease. More than 40 trials have been performed to see if cholesterol lowering can prevent heat attacks. When all the results were pooled together, just as many died in the treatment groups as the control groups.

But what is most disturbing to me about Steinberg’s statement is the idea that lowering LDL to such unnatural levels is a “safe and potentially life-saving standard”. Cholesterol is a vital substance in our bodies. 50% of all cell membranes are made up of cholesterol; it is a precursor to sex hormones which govern fertility, reproduction and sexual development; it is an antioxidant that helps prevent free radical damage; and it is needed particularly by infants and children to ensure proper development of the brain and nervous system.

In fact, evidence in adults shows that low cholesterol levels can be dangerous and even life-threatening:

• Low cholesterol is associated with increased total mortality in elderly people.
• Framingham (1987): “There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years.” In other words, as cholesterol fell death rates went up.
• Honolulu Heart Program (2001): “long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”
• J-LIT (2002): The highest death rate was observed among those with lowest cholesterol (under 160mg/dl); the lowest death rate was observed with those whose cholesterol was between 200-259mg/dl.

Low cholesterol has also been associated with increased rates of cancer, depression, violent and aggressive behavior, and suicide.

With that in mind, how could anyone possibly claim that reducing cholesterol to extremely low levels in children is “safe”?

“Drug treatment may also be necessary in those [children] at very high risk.

I’m not even sure where to start with this one, except to recommend that people like Dr. Steinberg be prosecuted for making such unfounded, irresponsible and dangerous recommendations.

According to the American Academy of Pediatrics:

“Also, data supporting a particular level of childhood cholesterol that predicts risk of adult CVD do not exist, which makes the prospect of a firm evidence-based recommendation for cholesterol screening for children elusive.

It is difficult to develop an evidence-based approach for the specific age at which pharmacologic treatment should be implemented. . . . It is not known whether there is an age at which development of the atherosclerotic process is accelerated.”

Which is to say there is no evidence suggesting that cholesterol levels in kids are a risk factor for adult heart disease.

Furthermore, as we have already discussed, cholesterol is absolutely essential for brain development. Lowering brain levels of cholesterol in children, whose brains are still developing at a rapid rate, could have dire consequences.

Surely Dr. Steinberg must be aware of this? There is nothing controversial about the role of cholesterol in brain development. You can find this information in any physiology or biochemistry textbook. So why – especially in light of the lack of evidence linking cholesterol to heart disease in kids – is he suggesting that we give statins to children?

I really have no idea. In all likelihood Dr. Steinberg means well and believes he’s acting in the interest of our children. But I cannot understand how a respected medical doctor and researcher could overlook such an elementary and important fact and ignore the weight of scientific evidence.

We’ve all heard the saying “when all you’ve got is a hammer, everything looks like a nail.” When someone like Dr. Steinberg has invested so much of their life and energy into the theory that cholesterol causes heart disease, I guess it’s hard to let it go.
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The hidden truth about statins

June 12, 2010   by Chris Kresser

 

Statins are the most popular drugs in history. Drug companies made $26 billion selling statins alone in 2008. 25 million Americans take them, and the number is growing each year.

One reason why statins are the best-selling drug category by far is that 92% of people taking them are healthy. The FDA has approved the prescription of statins to people at low risk for heart disease and stroke, who don’t even have high cholesterol. Two years ago the American Academy of Pediatricians recommended that statins be prescribed for kids as young as eight years old.

With sales statistics like this, you’d think statins are wonder drugs. But when you look closely at the research, a different story emerges. Statins have never been shown to be effective for women of any age, men over 65, or men without pre-existing heart disease. Early studies did suggest that statins are effective for men under 65 with pre-existing heart disease, but later, more rigorous clinical trials has not confirmed this benefit.

In addition, statins have been shown to have serious side effects and complications in up to 30% of people who take them. Studies have also shown that the majority of these adverse events go unreported, because doctors are largely unaware of the risks of statins.

Watch the two videos below to learn the whole story. Or, you can read this article for a concise summary of the evidence.

Video Presentation

link

Handouts

• Statin research summary: lists the eight statin studies performed in 2008 – 2009, including the drugs and populations studied and the results. If you’re currently taking a statin, you might consider printing this out and taking it to your doctor as a springboard for a conversation about whether statins are right for you.

References

ENHANCE
KasteleinJJ, AkdimF, StroesES, for ENHANCE investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358:1431-43
CASHMERE
O’Riordan M. CASHMERE: no IMT effect with atorvastatin over 12 months. (link)
ACHIEVE
O’Riordan M. ACHIEVE stopped: IMT study with Niacin/Laropiprant halted by Merck & Co. (link)
SEAS
Rossebø AB, Pedersen TR, Boman K, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med 2008;359:1343-56
GISSI-HF
GISSI-HF Investigators, Tavazzi L, Maggioni AP, Marchioli R, et al. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomized, double-blind, placebo-controlled trial. Lancet 2008;372:1231-9
CORONA
Kjekshus J, Apetrei E, Barrios V, et al. Rosuvastatin in older patients with systolic heart failure. N Engl J Med 2007;357:2248-61
AURORA
Fellström BC, Jardine AG, Schmieder ME, et al for the AURORA study group. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med 2009;360:1395-407
JUPITER
Ridker PM, Danielson E, Fonseca FA, et al, for the JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-Reactive protein. N Engl J Med 2008;359:2195-207

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How to prevent diabetes and heart disease for $16

November 26, 2010   Chris Kresser

In the last article we discovered that the blood sugar targets established by the American Diabetes Association are far too high, and do not protect people from developing heart disease, diabetes or other complications. And we looked at what the scientific literature indicates are safer targets for fasting blood sugar, hemoglobin A1c and either OGTT or post-meal blood sugar.

In this article I’m going to introduce a simple technique that, when used properly, is one of the most effective ways to maintain healthy blood sugar and prevent cardiovascular and metabolic disease – without unnecessary drugs.

I love this technique because it’s:

• Cheap. You can buy the equipment you need for $16 online.
• Convenient. You can perform the tests in the comfort of your home, in your car, or wherever else you might be.
• Personalized. Instead of following some formula for how much carbohydrate you can safely eat, this method will tell you exactly what your carbohydrate tolerance is, and which carbs are “safe” and “unsafe” for you.
• Safe. Unlike the oral glucose tolerance test (OGTT), which can produce dangerous and horribly uncomfortable spikes in blood sugar, this strategy simply involves testing your blood sugar after your normal meals.

The strategy I’m referring to is using a glucometer to test your post-meal blood sugars. It’s simple, accessible and completely bypasses the medical establishment and pharmaceutical companies by putting the power of knowledge in your hands.

It’s one of the most powerful diagnostic tools available, and I use it with nearly all of my patients. Here’s how to do it.

Step one: buy a glucometer and test strips

A glucometer is a device that measures blood sugar. You’ve probably seen them before – they’re commonly used by diabetics. You prick your finger with a sterilized lancet, and then you apply the drop of blood to a “test strip” that has been inserted into the glucometer, and it measures your blood sugar.

There are literally hundreds of glucometers out there, and their accuracy, quality and price varies considerably. The one I recommend to my patients is called the Relion Ultima, which can be purchased with 20 test strips for $16.00 online at Walmart.com. (Note: as a rule I don’t like to support Walmart, but I haven’t been able to find this unit anywhere else at a similar price.) Even better, the test strips, which you’ll need on an ongoing basis to monitor your blood sugar, are relatively cheap for the Relion Ultima. You can get a 100 of them for $39 at Walmart online ($0.39/strip).

I’m sure there are many other choices that work well, but this is the unit I have the most experience with, and in general it is very reliable. Another good choice is the TrueTrack meter drugstores sell under their own brand name (i.e. Walgreens, Sav-on, etc.). Other models to consider are the One Touch Ultra or one of the Accu-Chek meters. The problem with these, however, is that the test strips tend to be more expensive than the Relion Ultima.

Step two: test your blood sugar

1. Test your blood sugar first thing in the morning after fasting for at least 12 hours. Drink a little bit of water just after rising, but don’t eat anything or exercise before the test. This is your fasting blood sugar level.
2. Test your blood sugar again just before lunch.
3. Eat your typical lunch. Do not eat anything for the next three hours.
Test your blood sugar one hour after lunch.
4. Test your blood sugar two hours after lunch.
5. Test your blood sugar three hours after lunch.

Record the results, along with what you ate for lunch. Do this for two days. This will tell you how the foods you normally eat affect your blood sugar levels.

On the third day, you’re going to do it a little differently. On step 3, instead of eating your typical lunch, you’re going to eat 60 – 70 grams of fast acting carbohydrate. A large (8 oz) boiled potato or a cup of cooked white rice will do. For the purposes of this test only, avoid eating any fat with your rice or potato because it will slow down the absorption of glucose.

Then follow steps 4-6 as described above, and record your results.

Step three: interpret your results

If you recall from the last article, healthy targets for blood sugar according to the scientific literature are as follows:

Marker	Ideal*
Fasting blood glucose (mg/dL)	<86
OGGT / post-meal (mg/dL after 1 hour)	<140
OGGT / post-meal (mg/dL after 2 hours)	<120
OGGT / post-meal (mg/dL after 3 hours)	Back to baseline
Hemoglobin A1c (%)	<5.3

*To convert these numbers to mmol/L, use this online calculator.
Hemoglobin A1c doesn’t apply here because you can’t test it using a glucometer. We’re concerned with the fasting blood sugar reading, and more importantly, the 1- and 2-hour post-meal readings.

The goal is to make sure your blood sugar never rises higher than 140 mg/dL an hour after a meal, drops below 120 mg/dL two hours after a meal, and returns to baseline (i.e. what it was before you ate) by three hours after a meal.

There are a few caveats to this kind of testing. First, even reliable glucometers have about a 10% margin of error. You need to take that into account when you interpret your results. A reading of 100 mg/dL could be anything between 90 mg/dL and 110 mg/dL if you had it tested in a lab. This is okay, because what we’re doing here is trying to identify patterns – not nit-pick over specific readings.

Second, if you normally eat low-carb (less than 75g/d), your post-meal readings on the third day following the simple carbohydrate (rice or potato) challenge will be abnormally high. I explained why this occurs in the last article, but in short when you are adapted to burning fat your tolerance for carbohydrates declines. That’s why your doctor would tell you to eat at least 150g/d of carbs for three days before an OGTT if you were having that test done in a lab.

If you’ve been eating low-carb for at least a couple of months before doing the carbohydrate challenge on day three of the test, you can subtract 10 mg/dL from your 1- and 2-hour readings.

This will give you a rough estimate of what your results would be like had you eaten more carbohydrates in the days and weeks leading up to the test. It’s not precise, but it is probably accurate enough for this kind of testing.

Step four: take action (if necessary)

So what if your numbers are higher than the guidelines above? Well, that means you have impaired glucose tolerance. The higher your numbers are, the further along you are on that spectrum. If you are going above 180 mg/dL after one hour, I’d recommend getting some help – especially if you’re already on a carb-restricted diet. It’s possible to bring numbers that high down with dietary changes alone, but other possible causes of such high blood sugar (beta cell destruction, autoimmunity, etc.) should be ruled out.

If your numbers are only moderately elevated, it’s time to make some dietary changes. In particular, eating fewer carbs and more fat. Most people get enough protein and don’t need to adjust that.

And the beauty of the glucometer testing is that you don’t need to rely on someone else’s idea of how much (or what type of) carbohydrate you can eat. The glucometer will tell you. If you eat a bowl of strawberries and it spikes your blood sugar to 160 mg/dL an hour later, sorry to say, no strawberries for you. (Though you should try eating them with full-fat cream before you give up!) Likewise, if you’ve been told you can’t eat sweet potatoes because they have too much carbohydrate, but you eat one with butter and your blood sugar stays below 140 mg/dL after an hour, they’re probably safe for you. Of course if you’re trying to lose weight, you may need to avoid them anyways.

You can continue to periodically test your blood sugar this way to see how you’re progressing. You’ll probably notice that many other factors – like stress, lack of sleep and certain medications – affect your blood sugar. In any case, the glucometer is one of your most powerful tools for preventing degenerative disease and promoting optimal function.

Resources

If you haven’t already, check out Jenny Ruhl’s excellent Blood Sugar 101 site. Jenny won’t tell you this herself, but she’s an authority on blood sugar and probably knows more about it than 99.9% of health care practitioners (she’s an author). In particular, check out the “Painless Blood Sugar Testing”, “Frequently Asked Questions” and “How to Lower Your Blood Sugar” sections. I’d link to them directly, but her site uses frames and doesn’t allow it.
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Tough sell: Preventive cardiology

Tough sell: Course coaxes trainees toward preventive cardiology

April 18, 2012 Shelley Wood
                                       

Dubai, UAE - It's a tricky question: how to convince young doctors to get involved in CVD prevention, when other areas of cardiology are so alluring—and more lucrative? That conundrum was, in part, the impetus for a three-part preventive-cardiology session aimed at students and cardiology trainees that opened the World Congress of Cardiology (WCC) 2012.

It's a tough sell in a part of the world where salaries and cost of living are high, prestige and reputation are paramount, and other specialties pay better. The UAE has one of the highest per-capita incomes in the world, according to 2011 figures from the International Monetary Fund, with doctors earning some of the highest salaries; there is no income taxation in the UAE.

"Prevention does not in the mind of the public carry the charisma of invasive cardiologists or cardiac surgery," Dr JM Muscat-Baron (Department of Health and Medical Sciences, Dubai) acknowledged to his young audience at the start of the first session. "[But] you are the future and the catalysts for change; you are the teachers of tomorrow."

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"We believe that it is our young trainees who need to be taught how to practice preventive cardiology," Bazargani said. "Unfortunately, preventive cardiology is not well known in our region, and we believe that only way we can reduce the burden of CVD is through preventing it."

This is the first time the WCC has included a preventive-cardiology session specifically aimed at general medical students and cardiology trainees, one of the WCC 2012 program committee members, Dr Nooshin Mohd Bazargani (Dubai Hospital), told heartwire. Preventive cardiology, she pointed out, is not actually taught in many medical schools in the Middle East, despite the burgeoning need.

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Heart failure and vitamin D. But what about sunlight?

Heart failure and vitamin D. But what about sunlight?

18 April 2012 Barry Groves

 

Supports Chapter Eleven: Our irrational fear of sunlight
Vitamin D, just like all other vitamins, is essential not just to our health, but to life itself. Vitamin D is actually not really a vitamin, because our bodies can synthsize it from cholesterol in our skin with the action of the ultra-violet end of the spectrum of sunlight. But as the specific wavelength - UVB - is attenuated by the atmosphere, there is no point in sunbathing when the sun is low in the sky. We have to be in the sun, with as little clothing on as possible, and no sunscreen, when the sun is so high in the sky that our shadow is no longer than we are. In other words, in the middle of the day. But that is exactly what we are told by the 'experts' not to do!

There is very little food which contains vitamin D. And vitamin D is one of the four fat-soluble vitamins (the others are A, E, and K). But fat is 'bad for us', isn't it! So the incompetent 'experts' also advise us to shun the only foods which can help.

It should come as no surprise, therefore, that severe vitamin D deficiency is a widespread health problem throughout the industrialised world.
Now a study just published in the European Journal of Heart Failure points out a growing serious health issue caused by this misguided advice. The Abstract of that study is below:

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Israel Gotsman, Ayelet Shauer, Donna R. Zwas, et al. Vitamin D deficiency is a predictor of reduced survival in patients with heart failure; vitamin D supplementation improves outcome. Eur J Heart Fail (2012) 14 (4):357-366.doi: 10.1093/eurjhf/hfr175

Abstract

Aims Vitamin D deficiency is a highly prevalent, global phenomenon. The prevalence in heart failure (HF) patients and its effect on outcome are less clear. We evaluated vitamin D levels and vitamin D supplementation in patients with HF and its effect on mortality.

Methods and results 25-Hydroxyvitamin D [25(OH)D] levels were evaluated in HF patients from a health maintenance organization (HMO), and compared them with those of the rest of the members of the HMO. Patients with HF (n = 3009) had a lower median 25(OH)D level compared with the control group (n = 46 825): 36.9 nmol/L (interquartile range 23.2–55.9) vs. 40.7 nmol/L (26.7–56.9), respectively, P < 0.00001. The percentage of patients with vitamin D deficiency [25(OH)D <25 nmol/L] was higher in patients with HF compared with the control group (28% vs. 22%, P < 0.00001). Only 8.8% of the HF patients had optimal 25(OH)D levels (≥75 nmol/L). Median clinical follow-up was 518 days. Cox regression analysis demonstrated that vitamin D deficiency was an independent predictor of increased mortality in patients with HF [hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.21–1.92, P < 0.001] and in the control group (HR 1.91, 95% CI 1.48–2.46, P < 0.00001). Vitamin D supplementation was independently associated with reduced mortality in HF patients (HR 0.68, 95% CI 0.54–0.85, P < 0.0001). Parameters associated with vitamin D deficiency in HF patients were decreased previous solar radiation exposure, body mass index, diabetes, female gender, pulse, and decreased calcium and haemoglobin levels.

Conclusions Vitamin D deficiency is highly prevalent in HF patients and is a significant predictor of reduced survival. Vitamin D supplementation was associated with improved outcome.

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CommentNote the last sentence. "Vitamin D supplementation" improves survival. So they only consider treating the problem after it has been caused. What's wrong with advising people to get out in the sun more?

Incidentally, I do get out in the sun as much as possible. It doesn't need a lot: half an hour a day at midday is sufficient. I had my serum vitamin D checked a couple of weeks ago. It was 150.8nmol/L. And I aim to keep it that way.
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Read the complete article here.
Barry's blog is here.

Risk of high-dose simvastatin

April 17, 2012 Michael O'Riordan

inShare0

 

Seattle, WA - Statins were responsible for rhabdomyolysis in 7.5% of patients diagnosed with the skeletal muscle condition, according to a review of International Classification of Disease, Ninth Edition (ICD-9) codes from a large nonprofit healthcare system in Seattle, WA.

Publishing their findings as a letter to the editor in the Journal of the American Medical Association, Dr James Floyd (University of Washington, Seattle) and colleagues also confirmed a significantly higher risk of rhabdomyolysis in patients treated with high doses of simvastatin.

Incidence rates of statin-related rhabdomyolysis

Statin	Person-years of use	Validated rhabdomyolysis cases, n	Incidence rates per 100 000 person-years
Simvastatin <20 mg/d	21 832	0	0
Simvastatin 20-39 mg/d	75 082	4	5.3
Simvastatin 40-79 mg/d	56 703	8	14.1
Simvastatin >80 mg/d	16 876	1	64.8
All doses	170 605	23	13.5
Other statins	116 54	6	5.2
All statins	286 756	29	10.1

In total, 22 cases of statin-related rhabdomyolysis were validated among 292 statin users with an ICD-9 code for rhabdomyolysis (positive predictive value 7.5%). Seven other patients were confirmed as having statin-related rhabdomyolysis using other criteria. Overall, the risk of rhabdomyolysis was significantly elevated among patients treated with simvastatin. The incidence rate ratio (IRR) for simvastatin compared with other statins was 2.61 (95% 1.03-7.84) using all validated cases of rhabdomyolysis.

"These results confirm in a community setting findings from a recent clinical trial that prompted the US Food and Drug Administration to issue a warning about the use of high-dose simvastatin," write the researchers.

Source

1. Floyd JS, Keckbert SR, Weiss SR, Carrel DS, Psaty BM. Use of administrative data to estimate the incidence of statin-related rhabdomyolysis. JAMA 2012; 307:1580-1583.

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Evidence based medicine

Following quoted from Chris Kresser.
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The myth of evidence-based medicine

I was talking with a colleague the other day (let’s call her M). M related a story one of her patients told her. This patient is a nurse at Kaiser. The nurse was telling M about a meeting she recently attended with the rest of the clinical staff at Kaiser. The purpose of the meeting was to inform all of the doctors and nurses about new clinical guidelines for preventing heart disease.

And what were these clinicians told? To encourage their patients to eat fewer refined carbs, less vegetable oil and less sugar? To engage in a stress management program? To get a moderate amount of physical activity?

Hardly. They were told, in a nutshell, to give everyone statins. The idea communicated to them was that statins are “like vitamins” (a direct quote), and should be distributed in a similar manner.
This got me thinking about the concept of “evidence-based medicine”. I’m all for it, by the way. Evidence-based medicine, that is. The problem is that it doesn’t really exist in the conventional medical model.

Actually, I take that back. It does exist. But to be more accurate we’d have to call it “20-or-30-year-old-evidence-based medicine”. That’s a more representative term for the kind of medicine being practiced today.

The story above is a perfect case in point. The evidence is clear that statins don’t work. (If you don’t believe that, watch this presentation.) Furthermore, the evidence is also clear that the low-fat, high carbohydrate, vegetable oil-fueled diet promoted for decades by the American Heart Association (AHA) has not only failed to prevent heart disease, it has promoted it.

Anyone who actually reads the scientific literature with an open mind and a critical eye could reach these conclusions. The studies aren’t top secret. They’re not kept in an underground fortress. They’re readily available online or at your local medical library.

Yet in spite of the overwhelming evidence against statins and the low-fat AHA diet, this is still the standard of care for heart disease in the medical profession.

I wish I could say this is an isolated case. But you see the same thing in just about every disease or health condition. The standard of care for hypothyroidism is a complete joke. (More on this after I pass my licensing exam, I promise!) Type II diabetes can, for the vast majority of people, be managed and prevented by a low-carb diet. GERD is treated with PPIs and acid stopping drugs, in spite of the evidence that it is actually caused by low stomach acid in most cases.

Maybe the best example, though, is the 2010 dietary guidelines recently published by the USDA. Tom Naughton over at Fat Head published a post on this recently, so I’ll just crib from that:

I started reading the USDA’s 2010 Dietary Guidelines this week. For those of you who hoped the federal government would finally wise up and dump the high-carb/low-fat nonsense … come on, you didn’t really expect that, did you?

Did you honestly believe the government would put together a panel of so-called experts who would announce that the government has been wrong for the past 40 years? That the food pyramid was a disaster? That billions of taxpayer dollars are subsidizing the same foods that are making us fat and diabetic?

Of course not. The new guidelines are, if anything, a perfect example of something I’ve said in previous posts (which I believe I may have borrowed from Milton Friedman): when a government program produces disastrous results, those results are offered as proof that we need to do the same thing again … only bigger!

That’s mostly what the new guidelines are: the same old $#@%, only bigger. Bigger reductions in saturated fat, bigger reductions in salt, bigger reductions in cholesterol, and of course (this is a government committee, after all) lots of “calls to action” … otherwise known as BIG federal programs to convince us poor fools in the public to finally start heeding their advice.

Everywhere you look, you see medicine that isn’t evidence-based – or medicine that’s based on evidence that’s ten, twenty and even fifty years old.

The truth is we don’t have evidence-based medicine. We have profit-based medicine. And as long as the insurance and pharmaceutical companies are running the show, that’s what we’ll continue to have.

Did you know Big Pharma is the second-most profitable industry in the world, behind only the oil industry? Did you know that these companies fund 2/3 of all medical research? Do you really think honest-to-goodness evidence-based medicine is even a possibility in this environment?

Luckily we’ve got the Internet, and some conscientious and intelligent researchers and medical professionals that are willing to look beneath the veil and share what they find with the rest of us.

These days that’s really our only hope as people trying to live healthy lives: to be our own advocates, to seek out information that comes from people without a vested financial interest in selling you something, to maintain a “healthy skepticism” (if I may use the term) about any claims made, whether they come from the conventional or alternative world.

Because let’s face it, evidence-based medicine is a myth.
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Why statin side effects are likely to be much more common than official statistics suggest

 Why statin side effects are likely to be much more common than official statistics suggest

By : Dr John Briffa

In the UK, the most popular ‘drugs bible’ goes by the name of the British National Formulary (BNF). Within its pages is found a wealth of information about pills and potions that are available over-the-counter and by prescription, including indications and advice of dosages. A significant proportion of the pages in the BNF are taken up with information about contraindications (situations where the drug should be avoided or used with caution) and side-effects. This information is now to be found as part of the packet insert which comes with medication. I’ve known many, many people to read this information and decide that they’ll give the medication a miss.

One class of medication with a range of known side-effects are the statins. These cholesterol-reducing drugs are known to have the potential to cause symptoms such as muscle pain and fatigue, as well as cause damage to organs such as the liver and kidneys. About a year ago I was at a medical lecture, and one (doctor) member of the audience commented that he felt his patients experienced side effects from taking statins far more commonly than official statistics suggested. My own experience supports this observation.

Could there be an explanation for this phenomenon?

One explanation has to do with the design of statin studies. Quite often, individuals who are in poor health and perhaps at increased risk of side-effects are automatically barred from entering a study. Yet, in the real world, even people who are poor candidates in this respect may end up being prescribed a statin. Individuals with a history of problems such as muscular pain or damage to the liver or kidneys (all of which can be exacerbated by statins) are typically excluded from studies too, further reducing the chance that side-effects will arise.

Even those who make it through this screening process, however, may be subjected to what is known as an ‘run in’ period prior to the study. Here, individuals may be treated with a statin with idea being that individuals who are ‘non-compliant’ (do not take their medication as instructed) are weeded out. However, the run-in period also affords the researchers the opportunity to detect individuals who are susceptible to statin side-effects and stop them getting into the study proper.

In other words, in formal studies participants are often at a significantly lower risk of side-effects than those in the general population.

Another problem with conventional studies is how side-effects are defined. Muscle pain is a quite-frequent side-effect of statins. In extreme cases, statins can cause a break-down of muscle tissue known as ‘rhabdomyolysis’ which can have potentially fatal consequences. In some studies, the focus has been on rhabdomyolysis, which means less severe side-effects such as muscle pain or fatigue may ‘go missing’.

Another way in which the bar for side-effects can be set very high concerns the blood parameters used to detect damage. For instance, in a recent study muscle damage was only deemed to have occurred when muscle enzyme levels (a marker for muscle damage) were at least 5 times the upper limit of normal [1]. In this same study, liver damage (another potential hazard of statins) was only deemed to have occurred when liver enzymes were at least 3 times the upper limit of normal. In both cases, a more logical approach would be to regard a rise of any amount above the top end of the normal range as abnormal and significant. This would be more how it is in actual clinical practice.
The elimination of individuals prone to side-effects and the setting of the bar very high for abnormalities help explain why the side-effects from statins seem much more common in the real world than officially quoted statistics.

However, even in the real world, there might be under-recognition of the damage statins can do. That’s because, quite often, doctors will dismiss the idea that statins might be the cause for someone’s symptoms, even when scientific evidence supports such as link. For more on this, see here.

References:
1. Nicholls S, et al. Effect of Two Intensive Statin Regimens on Progression of Coronary Disease. NEJM 2011;365(22):2078-87
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Truth About High Cholesterol

Watch this good video on cholesterol


Truth About High Cholesterol - Austin Wellness Institute

Should you take medications for high cholesterol?
Is high cholesterol even a bad thing?

Common Statin drugs include Lipitor, Crestor, Zocor, Lipex, Torvast, Lipobay, Lescol, Mevacor, Altocor, Livalo, Pitava.

Visit Dr. Bellonzi's website at
http://www.bewellrx.com
http://www.austinwellnessinstitute.com