envoy510

The chocolate ration is being increased to 25 grammes per week.

Monthly Archives: February 2008

Review: The Great Cholesterol Con, Part 1

I saw a reference to The Great Cholesterol Con: The Truth About What Really Causes Heart Disease and How to Avoid It by Dr. Malcolm Kendrick on the web somewhere and decided to give it a try. I ordered it from amazon.com and waited more than 2 months for it to ship.

Before I get into looking at specific things about the ideas presented in the book, I’d like to say a few words about the style. He uses a very informal tone throughout the book and very often includes humor, most often sarcasm. At first I was a little put off by this, since in some instances he really goes over the top (entire paragraphs can be sarcastic screeds). However, the first time I was deep in the middle of understanding something which I thought was a contradiction of something said in earlier paragraphs only to find that he was being sarcastic, I was not amused. He had purposefully taken the other side of the argument to make it look silly, but because the subject was complex it wasn’t that silly, so I was confused. For my tastes, it would have been much better to forgo this style for a more direct, humorless approach.

I’ll get to the evidence itself, I will say that at some points in the book there is a lot of repetition. I think some of the later, repeated examples could be compressed a little. It would make the book a little short and give room to fix my next criticism…

There are basically, two parts to the book: debunking the cholesterol causes heart disease theory and offering his theory on the cause of heart disease. The first part is very thorough, but the second part is short and left me wanting more.

I probably seem pretty negative on the book. The problems above, with the exception of the short second part, are pretty superficial. I believe the book successfully makes the case that cholesterol does not cause heart disease. I really hope the evidence in the book is picked up by other researchers and that it sparks a debate that will result in more sane views of heart disease. While I do believe his conclusions from looking at publicly available data, I strongly believe that Dr. Kendrick’s book is the first step in a long process of changing the medical establishment. Let’s hope that process starts sooner rather than later.

Chapter 1: What is heart disease, anyway? I learned a lot in the first part of chapter, a sort of refresher on what causes a heart attack. Plaque builds up in the arteries and is covered by a fibrous cap. When this fibrous cap ruptures the body’s blood-clotting system rushes to repair itself by encapsulating the plaque now in the blood stream. This clotting action is what can block the artery, causing the heart muscle fed by the artery to be starved of oxygen. At this point the muscle may infarct, or undergo local cell death. If a narrowing of the artery is discovered before it ruptures, then an angioplasty can be performed to widen the artery with a stent and balloon. The disease of the heart, called atherosclerosis, is really a disease of the arteries.

What I did not know is that plaques can also build up in arteries other than the ones leading to the heart, such as the neck. In these cases, the process of rupturing causes a stroke, or an infarction in the brain.

I appreciated the last section which discussed issues with even the simple process described above. He lists three facts which seem puzzling, and seem to belie a more complex explanation. He then goes on to describe in more detail the cell death:

… heart muscle does not actually become necrotic, or die, following a heart attack. Instead, what happens is a process of cell alteration, or adaptation – which means that, at some point, the cells affected by a lack of blood supply are deciding whether or not to ‘infarct’ and change into scar tissue or, instead, to remain as fully functioning heart muscle. How and why do they make this decision? Who knows.

Chapter 2: What is cholesterol, anyway? A very good question, one that I have personally never seen explained anywhere, even though I have been aware of the medical term for a good 20 years. As he puts it, “cholesterol is absolutely essential for life” and “one of the key functions of the liver is to synthesize” it. He enumerates the things in our bodies which require cholesterol, such as brain synapses, vitamin D production, cell membranes, sex hormones and bile.

A lesson in biochemistry is next, specifically one all about fats. Bad saturated fats. Good unsaturated fats, such as Omega 3 fatty acids. Polyunsaturated fats, such as olive oil. And, the final form of fat, the hydrogenated unsaturated fat, which does not appear in nature. This is our dreaded trans-fatty acid, or what is called trans-fat in popular culture.

We get a peek at the first topic for debunking: there is no connection between fats and cholesterol. Kendrick contends that Ancel Keys single handedly turned medical science against saturated fat. Keys did say there was no connection between cholesterol in food and cholesterol in the blood, but Kendrick claims there is no evidence for fats increasing cholesterol in the blood. The chapter ends with his statement that “when the liver makes fats, it makes saturated fats, and saturated fats alone.”

Chapter 3: You cannot have a cholesterol level. Cholesterol is not soluble in blood and as a result it must be transported in molecules known as lipoproteins. Fats are also transported by lipoproteins, and this is the first valid connection between fat and cholesterol. There are different types of lipoproteins, all named because of their size:

  1. The largest is called chylomicron, which it turns out is not a lipoprotein.
  2. The next smaller lipoprotein is called VLDL (very low density lipoprotein). To again confuse matters, VLDL are referred to as triglycerides.
  3. IDL or intermediate density lipoprotein.
  4. LDL, or low density lipoprotein. This is “bad” cholesterol.
  5. HDL, or high density lipoprotein. This is “good” cholesterol.

All types but LDL and HDL are ignored from this point forward. HDL is good because it is believed to remove “cholesterol from plaques in arteries and transports it back to the liver for reprocessing”.

It was certainly news to me that HDL and LDL are not cholesterol itself, but rather the mechanism by which cholesterol is transported. The implication is that if you have too much LDL it must be transporting cholesterol in your blood, but doesn’t this lipoprotein also transport fat? Couldn’t some of them just be transporting fats? Kendrick doesn’t say this explicitly, and I was a little disappointed that he did not.

He points out that the cholesterol hypothesis has evolved over the years to deal with various attacks. At first, it was eating cholesterol that raised blood levels of cholesterol, but when that was found to be incorrect, the hypothesis changed to blame lipoproteins. Kendricks says it well:

Indeed, the closer you look, the more you find that the cholesterol hypothesis is a truly amazing beast. It is in a process of constant adaption in order to encompass all contradictory data without keeling over and expiring.

This is a theme that comes up over and over again in future chapters.

Where does LDL come from? It is what is left from VLDL after it has lost some fats (p32-33). This leads to the obvious logical inference: since LDL comes from VLDL, saturated fat must cause a rise in LDL, right? Wrong (p33, source being the American Journal of Medicine):

The thing that raises VLDL levels is eating carbohydrates… On the other hand, a high-fat diet lowers VLDL levels.

A study by the American Heart Association found (here) says when you eat more fat the VLDL level drops, in one study by 50%. I’ll let Kendrick take it from here (p34):

This should mean that eating fat will, in turn, lower LDL levels, shouldn’t it? Well, actually it doesn’t. A high-fat diet neither raises nor lowers LDL levels. … there is absolutely no connection whatsoever between the VLDL level and the LDL level.

He goes on to say that LDL levels are fairly constant in the blood and there are not daily fluctuations of it. This leads to the conclusion that “the system controlling LDL levels is unaffected by what you eat, or the amount of VLDL manufactured by the liver.” He said, that in fact, there is no proof that eating an increasing amount of saturated fat increases LDL levels in the blood. Some studies have show a correlation, but some have shown the opposite. The largest and longest running study, called the Framingham Study, found this:

… the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol [by which he means LDL]. -Dr William Castelli, Director of the Framingham Study, 1992

However, if you look at the Framingham website, on the
Emerging Risk Factors page, they still list LDL as a risk factor, along with two very new ones:

  • “Homocysteine — Framingham investigations indicate that high levels of this amino acid may contribute to heart disease, stroke, and a reduced flow of blood to the hands and feet. Researchers believe that homocysteine may contribute to the buildup of fatty substances in the arteries, increase the stickiness of blood platelets (clotting), and make blood vessels less flexible, less able to widen to permit increased blood flow. Levels of the amino acid are related partly to a genetic mechanism and diet. The good news is that diet, especially one high in folic acid and B vitamins, favorably affects the levels of homocysteine.”
  • “Infectious Agents — Viruses and other infectious agents may harm blood vessel walls, starting the atherosclerotic process. Framingham researchers are investigating whether cytomegalovirus (CMV), chlamydia, and H. pylori, a bacterium that causes stomach ulcers, play a role in damaging healthy blood vessels.”

Homocysteine is not discussed in Kendrick’s book, but the issue of damage to blood vessels is discussed later in the book.

Chapter 4: What are stains [sic] and how do hey work? (That is an unfortunate typographical error.) Statins are a group of drugs that reduce the production of cholesterol. By reducing cholesterol production, they have the side-effect of reducing VLDL production. We have already established that when VLDLs shrink they form LDLs. So, it must be true that statins reduce LDLs because they reduce VLDLs? No. It has already been established there is no link between VLDL levels and HDL levels.

An important digression on LDL:

LDL levels are controlled by the number of LDL receptors in the body. The moreLDL receptors you have, the more LDL will be removed from the circulation. … Unlike VLDL, or IDL, LDLs do not shrink, thereby changing into other types of lipoprotein. LDLs wander about in the circulation, essentially unaltered, until they lock on to an LDL receptor. At this point, the LDL and all of its contents are pulled into cells and then broken down, along with the receptor itself. So, if you have a million LDL receptions waving about trying to attract some passing LDL, a million LDLs will be removed from the circulation. And if you want to remove more LDLs, more receptors must be manufactured, then transported to the surface of the cell – wherever in the body those cells may be.

So getting back to statins, they work to lower LDL because they lower cholesterol production in the liver, which causes the liver to run out of the building block of VLDL, which then prompts the production of LDL receptors to retrieve cholesterol from other parts of the body to make VLDLs. The increased number of LDL receptors causes LDL levels in the blood to fall.

Kendrick goes on to complain that statins are not surgical in their operation, but that it is a complex drug that is floating around in the blood that has a wide range of different actions (35 non-cholesterol lower side-effects of statins have been documented). Kendrick’s main point, however, is that lowering LDL isn’t why statins work, and that it has to be attributed to some of these 35 actions are actually responsible for protecting blood vessels against heart disease. He finishes the chapter with this nail in the coffin for the official line on statins:

After all, there were plenty of drugs around that lowered cholesterol before statins were discovered. But only statins showed any significant benefit in treating cadiovascular disease.

Chapter 5: The rise and rise of the cholesterol hypothesis. There is much interesting information on the rise of the hypothesis, going back as far as the mid-19th century. It was sort of a mental break from all the complexity of the previous chapters. It was very welcome.

Central to this discussion is Ancel Keys, who used data from seven countries to prove his hypothesis (a high correlation between saturated-fat intake, increased cholesterol and heart disease). They are Italy, Greece, (former) Yugoslavia, Netherlands, Finland, USA, and Japan. Then came the Framingham study (1948) and other research that piled on to validate the cholesterol hypothesis. Statins were just the icing on the cake. He ends the chapter with a cogent summary of the stepwise logic that leads us to the modern theory of cholesterol (p55-6).

Chapter 6: Eat whatever you like (diet has nothing to do with heart disease). Now comes the real work of the book, the deconstruction of the diet causes CHD (coronary heart disease). Kendrick’s believe there is no scientific evidence to prove the connection. Being rather difficult to prove a negative, he launches into the two main ideas of the first half of this chapter: failure of the US Surgeon General to establish a link and ideas from Professors Law and Wald. On the former, Kendrick says:

In 1988, the Surgeon General’s office decided to gather together all the evidence linking saturated fat to heart disease, and thus silence any remaining naysayers forever. Eleven years later, the project was killed. In a letter circulated in was stated that the office ‘Did not anticipate fully the magnitude of the additional expertise and staff resources that would be needed.’

It seems believable to me that if the evidence was there they would have been able to collate it and produce a report that proved the link once and for all. They could not. This is, however, merely circumstantial evidence for the cholesterol hypothesis being complete garbage. About the effort, Bill Harlan of the Oversight Committee and Assicate Director of the Office of Disease Prevention at the National Institute of Health had this to say:

The report was initiated with a preconceived opinion of the conclusions, but the science behind those opinions was clearly not holding up.

History is littered with people starting out with notions of how something works and conducting a study to prove it, only later to be found completely false. Other information on this can be obtained from Gary Taubes’ New York Times Magazine article What if It’s All Been a Big Fat Lie?” , which was predictably attacked. Gary Taubes responds here to one such attack.

The Law and Wald part of the chapter focuses on their controversial use of teleoanalysis to prove the saturated-fat/CHD link. The main idea of teleoanalysis is to combine data from different types of studies. Kendrick quotes Law and Wald directly (emphasis mine):

… provide the answer to studies that would be obtained from studies that have not been done and often, for ethical and financial reasons, could never be done.

Kendrick does a good job of shredding the Law and Wald ideas. From the direct quotes and ideas presented, they do seem like typical bad science.

The rest of the chapter is devoted to presenting evidence contrary to the idea that saturated fat causes CHD. A summary of the evidence:

  1. Rationing in the UK during WWII, when 50 million people were put on a low-saturated fat diet for 12 years, is used to prove the saturated fat/CHD hypothesis, yet CHD was already falling before rationing even started and CHD increased nearly tripled during the 12 years.
  2. The French paradox. The French, compared with the British, eat more saturated fat, smoke more, exercise less, and have the same measurable LDL and HDL levels, yet they have 25% the CHD as the British. The ad-hoc explanation for this is they eat more garlic and drink more red wine, but that has never been proven.
  3. Emigrant Asian Indians in the UK have a high rate of CHD, yet as a population they have a low intake of saturated fat. The ad-hoc explanation for this is they are genetically predisposed to CHD, but there is no explanation of how this predisposition is supposed to act to cause CHD. In other words, there is no proof of this ad-hoc explanation.
  4. The Inuit have a very high intake of saturated fat, but a low incidence of CHD. The ad-hoc explanation for this is they consume a lot of Omega 3 fatty acids from fish.
  5. The Israeli Paradox. Israel has one of the highest polyunsaturated/saturated fat raions in the world, yet a high prevalence of CHD. The ad-hoc explanation is their higher consumption of Omega-6 fatty acids, for which there is no evidence.
  6. After WWII in Switzerland, saturated fat consumption increased 20%, yet CHD fell in the same 25 year period. The ad-hoc explanation had to do with milk from grass-fed alpine cows protected them.

Kendrick gives a couple of more examples, but you get the point.

Next is Dr Kendrick’s 14-country study. The data is from the WHO and is for 1998 (or nearly so when data for that year is not available). In his words:

Every single one of the seven countries with the lowest saturated-fat consumption has significantly higher rates of heart disease than every single one of the seven countries with the highest saturated-fat consumption.

Kendrick claims to be able “to fill an entire book with studies that have been done contradicting the diet-heart hypothesis.” He then suggests looking at these resources: The International Network of Cholesterol Skeptics, this website, or Second Opinions.

According to research, Kendrick believes there are two dietary substances which do afford protection against CHD, and they are: Omega 3 fatty acids and alcohol. He grudgingly lists Omega 3 fatty acids. In fact, it does seem to contradict his “contrary” evidence of the Inuit. Perhaps the issue is that the Inuit have such high intake of saturated fats and such a low incidence of CHD that Omega 3 fatty acids could not explain the paradox.

The postscript to this chapter lists some of his favorite quotes. Kendrick points out that the researchers from the Framingham Study had already found that “a high saturated fat intake consumption reduced the rate of strokes.” However, the researchers discounted it saying:

This hypothesis, however, depends on the presence of a strong direct association of fat intake with CHD. Since we found no such association, competing mortality from CHD is very unlikely to explain our results.

From the Multiple Risk Factor Intervention Trial:

The overall results do not show a beneficial effect on CHD or total mortality from this multifactor intervention.

The multifactor intervention they speak of is cutting cholesterol consumption by 42% and saturated fat consumption by 28%, with no effect on CHD.

Lastly, I prefer Kendrick’s paraphrasing of Professor Michael Oliver commenting on a Finish study:

In a ten-year follow-up to the initial study (hailed as a success) it found that those people who continued to follow the carefully controlled cholesterol-lowering diet were twice as likely to die of heart disease as those who didn’t.

Really, all I can say is… wow.

Chapter 7: A raised cholesterol/LDL level does not cause heart disease. Here Kendrick immediately acknowledges that there are cracks in the foundation of the diet part of the diet-heart hypothesis, but that he is “in the wilderness” when it comes to attacking the raised cholesterol causes CHD. He even complains that the people on his side in this argument tend to be a little nutty.

This chapter is really the second and main blow to the mainstream ideas of the cholesterol/CHD theory. He starts off with the mainstream evidence:

  1. “Atherosclerotic plaques contain a lot of cholesterol, which must have come from the blood. So heart disease had to have something to do with cholesterol-containing lipoproteins.
  2. People with familial hypercholesterolaemia (FH) die very young from heart disease, sometimes as young as five.
  3. Statins lower cholesterol levels and protect against heart disease.
  4. ‘Normal’ people (without HF) with higher cholesterol levels are more likely to die from heart disease.”

In other words, these are the usual suspects that appear time and again in medical journals. Kendrick contends that these facts are at best partial truths. He makes a good analogy between the above facts and a Western movie set: look at the buildings from the street, they look real, but move around to the side and you can tell they are just facades.

The next attack on the status quo comes from a 1995 study in The Lancet. It included 450,000 people over a period of 16 years, who suffered 13,000 strokes. The conclusion was there is no association between blood cholesterol and stroke. Remember, many strokes are due to arterial plaque in the carotid arteries. He then quotes a European study that yielded a similar conclusion. Then, Kendrick points out:

So, you have two conditions – stroke and heart disease – that are both fundamentally a form of arterial disease. Yet, raised cholesterol is a risk factor for one, but not the other.

After listing the risk factors for stroke (form the American Stroke Association) are the same as those for CHD, he asks:

… where is cholesterol in list? … how can lowering cholesterol with statins reduce the risk of stroke (which they do), if a raised cholesterol level isn’t a risk factor for stroke?

Kendrick points out that this would only make sense in a world where the benefit from taking a statin has nothing to do with its cholesterol lowering ability. Kendrick then goes on to refute an ad-hoc explanation of the above inconvenient truth.

In fact, it gets even better. A low cholesterol level is actually associated with a huge increase in death from stroke, and Kendrick believes it may even cause it. The best evidence for this comes from a Japanese study published in Stroke in 2004:

The risk of death from [cerebral] infarction [AKA stroke] was reduced by 64% in the high cholesterol consumption group.

I don’t know when I learned it, but I know that the Japanese have a very high rate of strokes, compared to the US. At least, that’s what I had read over and over again. Kendrick lists the data for death rates for stroke in Japanese men (p88, Fig. 21) and it is quite stunning: from 1965 to 1995 the number of deaths plummeted from 1,334 to 226 deaths per 100,000/year (a reduction of 5.9x), while at the same time their saturated fat intake quadrupled. Kendrick summarizes it well:

According to mainstream thinking, ischaemic strokes are caused by raised cholesterol levels, and ischaemic strokes represent 75% of all strokes. However, over the last 50 years, cholesterol levels have risen by 20% in Japan, and the rate of stroke has fallen off the edge of a cliff – dropping 600%. And the rate of heart disease has also fallen dramatically.

The next bit goes into a detailed discussion of cholesterol/LDL and total mortality, which Kendrick believes is more important than just taking into account deaths from CHD. It seems possible to me that an increased level of cholesterol might kill people in other ways, or not.

Fig. 22 (p90) shows the risk of death in the next 5 years, at various cholesterol levels. For the American readers, this is where the problem of units hits home. The data for the table is in mmol/l, which mean nothing to me. So, google to the rescue. To convert mmol/l of HDL or LDL cholesterol to mg/dl, multiply by 39. So, getting back to Fig. 22, the lowest risk of death is at 195-234 mg/dl. Cholesterol levels lower and above this have a higher risk of death.

Fig. 23 does the treatment for men, and the sweet spot for cholesterol is 156-195 mg/dl, with 195-234 mg/dl being only slightly higher, but both less than 156 and more than 234 mg/dl having a much higher risk of death.

Fig. 24 shows the non-cancer, non-cadiovascular death at various cholesterol levels in the next 5 years for women. The higher the cholesterol the lower the risk of death.

The Framingham Study confirmed this:

There is a direct association between falling cholesterol levels over th fist 14 years [of the study] and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1mg/dl per year drop in cholesterol levels).

In other words, Kendrick says:

If your total cholesterol were to fall from 5 to 4 mmol/l [or fall from 195 to 156 mg/dl], your risk of dying would increase by more than 400%. Not only that, but your risk of dying of a cardiovascular disease would increase by … 546%.

The reference for this is the Journal of the American Medical Association, April 24, 1987, pages 2176 to 2180. Not exactly a fly-by-night publication. Kendrick then goes on to quote a study of mortality in older people, published in The Lancet in 2001:

Our data accord with previous findings of increased mortality in elderly people with low serum cholesterol, and show that long term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier that patients start to have lower cholesterol concentrations, the greater the risk of death.

We have been unable to explain our results. These data cast doubt on the scientific justification for lowering cholesterol to very low concentrations.

Did this change the opinion of the scientific community? No. The authors were merely attacked for being “irresponsible”.

An Austrian study is more inclusive in the group put at risk for low cholesterol. It was published in the Journal of Women’s Health, even though it included 150,000 people and lasted for 15 years, with more than 450,000 examinations. The study confirmed “that a low cholesterol level after the age of 50 (and under 50, if you are a man) is significantly associated with all-cause mortality.” (Kendrick, p94)

Kendrick then goes on to cite a British and Finish study, and another one done on the very old (over 85) published in The Lancet. All confirm either increased mortality for low cholesterol or decreased mortality for increased cholesterol. Kendrick summarizes where we are:

  • “Under the age of 50, your cholesterol level doesn’t really make much difference to your risk of dying. However, if your cholesterol level starts falling, watch out. You are at a terrible risk – a 429% increased risk of death per 1 mmol/l [or 39 mg/dl] drop, according to the Framingham Study.
  • After the age of 50, a low cholesterol level is associated with a significantly greater overall mortality. The older you get, the more dangerous it is to have a low cholesterol level.”

There is a long discussion of how a low cholesterol might be an indication of a serious underlying disease, which is why low cholesterol is associated with higher mortality. Kendrick does a good job of destroying this ad-hoc explanation of why people shouldn’t be worried about low cholesterol.

The next section is dedicated to the female paradox (women suffer from much less CHD but have higher cholesterol levels), and the ad-hoc explanation of female sex hormones offer protection from CHD. In a study of women who had two types of hysterectomies, those that have their ovaries removed (and as a result they no longer manufacture female sex hormones) and those that do not, there was no difference in the two groups, with respect to CHD. What about women that have hormone replacement therapy after menopause? Their rate of CHD increases. So, the sex hormone ad-hoc hypothesis is clearly incorrect.

Next is a detailed analysis of HDL and its protective properties as the good cholesterol. I’m going to go straight to the conclusions on this one, that contradict the conventional wisdom that “people with high HDL levels tend to have a lower rate of heart disease”:

  • “In the … only study done in which proper outcomes where measured, e.g. death from heart disease – when HDL levels went up so did the rate of heart disease.
  • You can find populations with a high HDL level and a high rate of heart disease, and vice versa.
  • It is clear that HDL levels reflect other things, e.g. alcohol consumption, which do have a direct [positive] effect on heart disease.”

Kendrick then goes on to compare different groups of men and women, and says “there is only one conclusion that can be drawn from this unholy mess [of data]: cholesterol levels have no effect on heart diesease rates in women.”

Before proceeding, he stops to summarize where we’ve been:

  • A raised cholesterol level doesn’t cause strokes, but a low cholesterol level may well do.
  • A raised cholesterol level doesn’t increase overall mortality, but a low cholesterol level does.
  • A raised cholesterol level does not cause heart disease in women.

What is left is to answer what happens in men. Kendrick starts by saying what he does agree with:

  1. In men under the age of 50, a raised cholesterol level is associated with an increased risk of heart disease. (Note that I didn’t say ’caused’, I said ‘associated’.)
  2. Within countries/populations, a higher cholesterol level in men is associated with a higher rate of heart disease.

Enter the MONICA study, from which comes Fig. 26 (p119), which shows a comparison between heart-disease rates in men aged 35-74 and average cholesterol levels, from 15 populations around the world. The data is all over the place, making it difficult to correlate cholesterol and death rates from heart disease. Though, the countries with the highest cholesterol do have the lowest incidence of death from heart disease.

Kendrick then turns to exceptional groups of men. The Australian Aboriginals, for example, who have a high rate of CHD but a low average cholesterol. Or, Emigrant Asians (anyone who emigrates from Pakistan, India, Sri Lanka and/or Bangladesh) suffer very high rates of heart disease, no matter where they emigrate to. What about their risk factors for CHD? As a group and compared to the surrounding non-Emigrant Asian population they had lower total cholesterol levels, lower LDL levels, lower blood pressure, they smoked less and they were slightly less obese. In other words, most of their important risk factors were lower, yet they have dramatically more CHD. In fact, nearly 50% of this group are life-long vegetarians, according to Enas A Clin Cardiol, March 1995.

Kendrick summarizes it well:

So, Australian Aboriginals, Native Americans, Emigrant Asian Indians and a large percentage of Russian men have low cholesterol levels and high rates of heart disease. Hmmm. And the Swiss and the French have very high cholesterol levels and very low rates of heart disease.

Then:

Heart disease is primarily a disease of older poeple. The rate of heart disease in 65-year-old men is approximately 10 times that of 45-year-old men. Yet, while a raised cholesterol level is associated with heart disease in younger men, the association disappears as men get older.

A study published in the Journal of the American Geriatric Society in 1991 said: elevated total cholesterol was not found to be associated with CHD mortality in older men. As Kendrick says, elevated cholesterol is a risk factor, but these studies say it is not a risk factor when the disease kills the most people.

Kendrick now pauses to summarize where we are:

  • A raised cholesterol level is associated with heart disease in younger men – within a country.
  • There is no association at all between average cholesterol levels and the heart disease rate between countries.
  • Over the age of about 50, the association between cholesterol levels and hear disease disappears.
  • A falling cholesterol level is associated with a greater risk of heart disease.

He then goes into a detailed description of familial hypercholesterolaemia (FH), or people with extremely high levels of LDL in their bloodstream. He shows how statistical games are played to inflate the actual death rate from FH.

What I found really fascinating was his digression into the response to injury hypothesis cause for CHD:

  • “A factor (or more likely, several factors acting in unison), damages the endotheluim (single-celld lining of he artery wall).
  • This stumulates a small blood clot to form over the area of damage.
  • Endothelium re-grows over the blood clot, ‘repairing’ the area of damage.
  • With endothelium on top of it, the blood clot is effectively down into the artery wall, and is them broken down by white blood cells – thus disappearing.”

The above is thought to be the healthy response to injury. He continues:

However, if the endothelium keeps getting damaged (for whatever reason), clots keep forming, and more and more blood clots keep getting drawn into the artery wall. At which point the healing responses cannot cope. The area of damage becomes permanent. A plaqu forms that can grow and grow. In many cases a fibrous ‘cap’ forms over the plaque. This can rupture, triggering such a big blood clot that it fully blocks the artery.

This hypothesis has been around for more than 150 years, too.

More to come in Part 2.

Advertisements

William F. Buckley Jr. RIP


I’m a liberal, and have been since my earliest memories. When I was a kid (not sure how old, but probably 10ish), I watches lots of TV. Back in those days there were few channels. Like 4. Hey, I’m not that old! I have strong memories of watching William F. Buckley, Jr. What a strange man. What a strange manor. What a strange facility with the English language. While I didn’t always (often?) agree with him, I was only 10ish, so what did I know? I do remember being oddly unable to change the channel. I mean, Bewitched! was probably on, right, so why didn’t I just change the channel?!

Update: really like this.

Nintendo DS tracker notifier

The following script notifies me via a text message when either a Cobalt Blue or Crimson Nintendo DS Lite are available. It uses dstracker.com‘s XML feed.

Required software: Allegro CL 8.1 Express on Linux (though it could be adapted to Windows fairly easily by not trying to detach-from-terminal).


#! /usr/local/bin/mlisp -#C

;; Nintendo DS Lite tracker notifier.

(in-package :user)

(eval-when (compile eval load)
(require :osi)
(use-package :excl.osi)
(require :aserve)
(use-package :net.aserve.client)
(require :sax)
(use-package :net.xml.dom)
(require :smtp)
(use-package :net.post-office))

(defparameter *dstracker-url* "http://dstracker.com/rss.xml")
(defparameter *email* "...@txt.att.net")
(defparameter *re*
;; I only want to be notified of the Crimson and Cobalt versions:
"(cobalt|crimson)")

(defun read-feed (url)
(logit "reading feed from ~a" url)
(multiple-value-bind (content code headers)
(do-http-request url)
(declare (ignore headers))
(if* (not (eq 200 code))
then (error "Accessing url ~s gave http response code ~s" url code))
content))

(defun notify-user (to body ht)
(when (not (gethash body ht))
(setf (gethash body ht) t)
(logit "notify ~a" to)
(send-smtp "localhost" "dstracker" to body)))

(defun parse-feed-and-notify (xml ht)
(let* ((doc (parse-to-dom xml))
(root (dom-document-element doc))
(items (dom-list-elements-by-tag-name root "item")))
(dolist (item items)
(let* ((title (dom-list-elements-by-tag-name item "title"))
(text (dom-child-node-list (car title)))
(data (dom-data (car text))))
(when (match-re *re* data :case-fold t)
(notify-user *email* data ht))))))

(defun logit (format-string &rest format-arguments)
(format t "~@/locale-format-time/" (get-universal-time))
(apply #'format t format-string format-arguments)
(format t "~&"))

(defun doit ()
(let ((ht (make-hash-table :size 101 :test #'equalp)))
(loop
(parse-feed-and-notify (read-feed *dstracker-url*) ht)
(sleep #.(* 60 10)))))

(system:with-command-line-arguments ("l:" logfile)
(rest)
(declare (ignore rest))
(when (not logfile) (error "Must supply a log file via -l argument."))
(with-open-file (s logfile :direction :output :if-exists :always-append
:if-does-not-exist :create)
(if* (= (excl.osi:fork) 0)
then ;; child
(excl.osi:detach-from-terminal :output-stream s
:error-output-stream s)
(loop
(logit "starting up")
(doit))
else (exit 0 :quiet t))))

Image courtesy of imageshack.