Heart disease: one of science-based medicine’s great successes

Sixty years ago, the world was full of miracles. Western Europe was recovering from the devastation of World War II, an agricultural revolution promised to banish the fear of starvation in large parts of the world, and the mythical Mad Men era gave Americans a taste of technology-dependent peace and prosperity unlike any in the past. Despite the technological progress that would soon send animals into space and return them relatively unharmed, Americans, and westerners in general, were still dying of heart disease at a frightening rate. If you, as a middle aged American, experienced chest pain and were lucky enough to make it to a hospital (about 20% of all sufferers would die immediately), you would probably be given nitroglycerin and morphine to control you pain, put on bed rest, and could expect to live a few more years, with limited physical activity.

Heart disease continues to be a top killer of Americans, but there has been a dramatic decline in heart disease mortality in the last 60 years, with age-specific mortality rates dropping 60%. Fewer people are developing heart disease, and those that have it are living longer. It is estimated that in 2000 alone, there were 341,745 fewer heart disease deaths than would have been expected if rates had remained unchanged.  This decline has not been driven by a renaissance of alternative medicine.  It has been driven by science.

The trend has been going on for many decades, and has been accelerating, although current trends in diabetes and obesity put us at risk for more overall cases of heart disease in the future. So what are we doing right? How have we managed to cut the death rate from heart disease so dramatically?

So-called alternative medicine practitioners seem hell-bent on finding evidence-free ways to prevent and fight disease. No lie is too blatant in the pursuit of their ideology. For example, one chiropractic website claims that everything we think we know about prevention of heart disease is wrong:

The tyical risk factors include high cholesterol, smoking, high blood pressure, and diabetes.  Prescription drugs serve as these programs’ centerpiece, with counseling and education as adjunct treatments.  They are spearheaded by the American Heart Association, the American Medical Association, local and state governments, and even the federal government.

Yet 10 years ago study results by the Cochrane Heart Group and The Cochrane Collaboration ( showed that treating risk factors was “ineffective in achieving reductions in total or cardiovascular disease mortality (death).”

Of course, we don’t get a real citation to follow.    One of the most offensive investigations into heart disease prevention is the TACT trial, an unethical trial asking a question that doesn’t require an ethics-free clinical trial to answer.  We know a lot about heart disease.  And we know this because of well-designed trials and studies that ask the right questions.  The medical literature over the last 30 years has seen a flood of studies of heart disease. As would be expected, most are incomplete, answering only one or two questions, and studies often conflict.  But over time, trends emerge, and the truth precipitates from the noise.

In reducing heart disease mortality, there have been different relative contributions from primary prevention (preventing new cases of heart disease) and secondary prevention (preventing recurrent cases).  A recent study in the American Journal of Public Health analysed data from 1980-2000. The authors found that most of the reduction in deaths from heart disease (nearly 80%) were due to primary prevention, specifically decreasing smoking rates, and improvements in blood pressure and cholesterol levels. Society-wide reductions in smoking, blood pressure, and cholesterol are saving hundreds of thousands of lives in the U.S. every year.  This is a different conclusion than that of the Virginia chiropractors who once read an un-citable Cochrane review.

What’s best about these data is they give us guidance;  real science gives us real predictions.  The smoking rate in the US is still hovering around 24%. More than half of people with known high blood pressure do not have their blood pressure under control. Evidence shows us that we can easily prevent more heart attack deaths through education and through better adherence to extant treatment guidelines.  Behavioral changes such as smoking cessation, diet and exercise, and the proper use of medications can all contribute to the fight against heart disease.  Reducing heart disease deaths isn’t all that complicated, and it won’t take miracles. We just have to follow the evidence.

*Similar trends have been seen in other English-speaking countries


Hurlburt CW (1927). THE CARDIAC CRIPPLE. Canadian Medical Association journal, 17 (11), 1305-9 PMID: 20316574

Sytkowski PA, Kannel WB, & D’Agostino RB (1990). Changes in risk factors and the decline in mortality from cardiovascular disease. The Framingham Heart Study. The New England journal of medicine, 322 (23), 1635-41 PMID: 2288563

FRY J (1964). CORONARY HEART DISEASE IN GENERAL PRACTICE: NATURAL HISTORY OVER TWELVE YEARS (1950-1961). Proceedings of the Royal Society of Medicine, 57, 39-42 PMID: 14114173

Centers for Disease Control and Prevention (CDC) (1999). Decline in deaths from heart disease and stroke–United States, 1900-1999. MMWR. Morbidity and mortality weekly report, 48 (30), 649-56 PMID: 10488780

Young, F., Capewell, S., Ford, E., & Critchley, J. (2010). Coronary Mortality Declines in the U.S. Between 1980 and 2000 Quantifying the Contributions from Primary and Secondary Prevention American Journal of Preventive Medicine, 39 (3), 228-234 DOI: 10.1016/j.amepre.2010.05.009

Wijeysundera HC, Machado M, Farahati F, Wang X, Witteman W, van der Velde G, Tu JV, Lee DS, Goodman SG, Petrella R, O’Flaherty M, Krahn M, & Capewell S (2010). Association of temporal trends in risk factors and treatment uptake with coronary heart disease mortality, 1994-2005. JAMA : the journal of the American Medical Association, 303 (18), 1841-7 PMID: 20460623

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81 thoughts on “Heart disease: one of science-based medicine’s great successes

  1. tuck says:

    Science is also about correctly measuring successes. Picking the bottom of the Great Depression as a start point for measuring GDP might give you the mistaken impression that certain policies had a beneficial effect on GDP.

    Here is a post on Heart disease which moves the measuring point back closer to what ought to be the null hypothesis: the point at which heart disease was extremely rare, prior to the great increase of the 20th century.

    You’ll see that while the successes of the last 60 years remain, they look far less impressive, and reflect primarily an increase in the effectiveness of treatment, not a decrease in incidence. Pretty clearly the low heart disease rates of the 18th and 19th centuries were not caused by Lipitor, or heart procedures that could not be performed at that time.

    Until science-based medicine can answer the question about what caused this epidemic, and how can it be prevented, the “success” looks much less impressive.

  2. I seem to remember a kerfuffle a few years back about statins lowering risk factors but not mortality, but a brief glance at google wasn’t reflecting that. Can you refresh my memory? Because it sounds as though that is what the chiropractic website might be alluding to.

  3. Peter Lipson says:

    Actually, tuck, if you look at the references heart disease increased in incidence in the early part of the 20th century, perhaps for a number of reasons, including changing diagnostic methods and increasing life-span. There are lifestyle contributions as well, and heart disease incidence and prevalence (but not mortality) may be increasing (i’ll have to check that). The incidence will probably go up as obesity and its complications (hypertension and diabetes) increase.

    Data show that improving hypertension and diabetes, through lifestyle change and/or medication, are beneficial.

    I’m not sure what your overall point is.

  4. Todd W. says:


    A few questions to keep in mind, though, as you look at 18th and 19th century stats:

    1) How accurate was the reporting? Were cases underreported?
    2) What were the average lifespans?
    3) What age were the reported cases?
    4) How does all of that compare to reporting/lifespans/age at incidence today?

    While there probably has been an overall increase in incidence over the past several centuries, picking your starting point is not necessarily as accurate as you portray, either. Lifestyle factors almost certainly play a large part in incidence (e.g., smoking, poor diet, lack of exercise, etc.).

    @Dr. Lipson

    I’m curious if you read the recent piece in Skeptical Inquirer examining surgical vs. medical treatment and prevention of heart disease. If you have, what is your take on it?

  5. Peter Lipson says:

    That’s an enormous question (not the “did you read” part—i haven’t but i will).

    “Treatment of heart disease” means lots of different things, including:

    Primary prevention
    Secondary prevention

    Treatment of acute ischemia/revascularization.

    Revascularization is an area of active research an conflict, esp regarding CABG vs. PCI.

  6. tuck, the biggest factor identified in the first two posts in series you linked to was tobacco smoking. Which SBM has been virgorously attacking for quite some time and is mentioned prominently in the post above.

  7. WilliamOBLivion says:

    If I may speak for Tuck, I believe his point is twofold:

    1) If you pick (as he said) the 1930s for GDP comparisons or 1979 for temperature comparisons you are artificially supporting your argument by comparing “worst case” with “current”. The 1930s were a period of extremely depressed economic activity, and 1979 was a particularly cold year.

    2) Until we accurately know what causes CHD–which Dr. Guyenet thinks is caused in large part by the modern industrial diet–heavily refined foods and modern cooking practices taking a lot of the “good stuff” out of food (micro-nutrients, vitamin K2, omega-3s) resulting in a need to supplement them back, and modern cooking practices (short fermentation times on breads, etc.) leaving the bad stuff (phytic acid etc.) in. Also the use of lots of refined sugars and stuff like high fructose corn syrup (which is now in EVERYTHING, including Robotussin. Along with sucrolose, WTF?)

    The problem as I see it–and not just in Medicine, but in many contentious areas–that the further back in time we go, the worse our records are. We have data that says that there were fewer cases of CHD “Back in the day”, but how valid is that data? If you were looking just at a given area maybe there were diet and lifestyle indicators THERE that were not generalized etc. etc.

    I think Tuck’s criticism is unfair in one regard, we don’t “know” that Dr. Guyenet is right about the causes of CHD. We’re pretty sure that bad diet isn’t the only cause.

    We don’t have data of the same quailty as todays to compare against, and we know there are LOTS of variables. One is (and this may have been disproven while my back is turned) what really is the link between gum disease and CHD? How much has brushing and flossing delayed the onset of CHD? How much has good antibiotics allowed people to survive random other infections long enough to develop CHD.

    Since this article wasn’t about something slightly different I think it was a sort of cheap shot.

  8. dr.cosa says:

    Another great post about a controversial topic.

    Yes there is no shortage of quackery on the topic, though posting a chiropractor’s take on CHD is disingenuous, it portrays opposition to the accepted notions as lacking merit. Instead why not delve into the many facets of the concepts behind heart attacks and it’s connection to diet, exercise, medication and high BP?

    Its difficult to quantify the effects of any one lifestyle factor in prevention of and reduction of CHD because often they are adopted at the same time. The proto-typical 50 year old alpha-male working 60 hour weeks finds himself in hospital after a heart-attack is scared out of his mind to now quit smoking, eat ‘healthier’ and adopt a stress-reducing lifestyle. Is it any wonder he might improve his chances from experiencing a second attack?

    Does the reduction in smoking refer to the amount smoked or the number of people who smoke anything from 1 cigarette to 1 pack a day? is there a tapering off of risk for those who smoke significantly less per day than others?

    with the cross hairs focused on medications, we need to avoid sweeping generalizations about “medication” regiments that “work”, we know that some do and some dont, and much of the success may be marred by too many factors to single out one particular modality.

    is the science really settled on the efficacy of the current generation of cholesterol lowering medications?

    is the science really settled on the best approaches to avoid a heart attack, have we accurately estimated genetic variables to the point where success on the part of lifestyle changes are given so much credit to the reduction of heart disease?

    it is problematic comparing multi-generational trends in something like CHD due to the sheer difficulty in diagnosing and recording these deaths prior to modernized medicine. men may have more often than not died during one of the many wars or of other diseases. how accurately these would have been diagnosed is difficult for all but the most modern locations in the early part of the 20th century and late 19th century.

    is the very term “heart attack” too broad, when a 40 year old suffers one vs. an 80 year old, or when an otherwise healthy man suffers one vs. a morbidly obese smoker? should we consider CHD a multi-faceted, spectrum of diseases?

  9. Angora Rabbit says:

    Re: Tuck, the respondents have nailed it IMO. We actually do know why CHD rates rose. It’s that combination of longevity, energy expenditure and diet changes. Having said that there are real questions about diagnostic accuracy in the early data set, so the claim of “reduced incidence in previous centuries” is a soft claim.

    Dr. Guyenet’s claim about dietary contributions is an overly simplistic and incomplete portrait of CHD cause and progression. For example, mean U.S. energy expenditure has significantly declined, 700 kcal/d since 1900 and 100 kcal/d since 1980. Dietary added fat consumption increased from 32 lbs to 66 lbs per person per yar from 1909 to 1998. Both exercise and fat intake are significant modifiers of CHD risk.

    It’s also interesting that while the role of some dietary risk factors are very clear and solid (e.g. cholesterol intake, total fat intake), others that looked good in the epidemiology studies (e.g. vitamin E, B6) are not coming so clean in the human intervention trials. This may well be because the interventions are coming too late, for too short a period, and need multiple dietary changes instead of a single nutient intervention.

    Here in the nutrition field we agree with Dr. Lipson that the reduction in CHD is a very real success thanks to the multipronged approach of prevention, diagnosis and treatment. Go blow those trumpets loudly!

    I am puzzled by the CHD-deniers and those who claim diet has no role. I think Skeptic had an article about it some years ago. That claim leaves me baffled.

  10. weing says:

    Excellent post. We’ve come a long way, and we still have a long way to go. Of course, the anti-science cultists and the arrogantly ignorant will always be trying to slow down progress with claims that they know better. No cure for stupidity.

  11. weing says:

    “I am puzzled by the CHD-deniers and those who claim diet has no role.”

    I would guess that they assume that we all have protective PCSK9 mutations.

  12. Angora Rabbit says:

    Dr. Cosa I think is making a good point that science and medicine are moving targets. We can have the best but we really mean “the best with current knowledge.” There is always room for improvement. As you point out, there are genetic and other modifiers such that treatments have to be mindful of the individual and tailor accordingly. We talk about prevention but what we really mean is reduced risk. Sadly these are nuances that are not always conveyed well or heard correctly.

  13. Angora Rabbit says:

    “I would guess that they assume that we all have protective PCSK9 mutations.”

    LOL. The gene de jour.

  14. jmd says:

    I may be way off here, but in the 18th and 19th centuries, weren’t people more likely to die because of something like an infectious disease or injury before they could live long enough to even get heart disease? (Or am I thinking of cancer?)

  15. Peter Lipson says:

    while it may be difficult to look at relative contributions of risk factors and interventions, that is exactly what these studies do. it’s sort of the point.

  16. -regarding Protective PCSK9 Mutations

    They’re my favorite band.

  17. Chris says:

    tuck, I don’t believe that heart disease did not exist in the early 20th century. That is because there is a genetic heart condition that runs in my family.

    My grandparents’ first child died in her first few weeks due to a genetic heart disorder. Their youngest child, my uncle, died in his mid-forties. My son was diagnosed with the condition when he was fourteen and has been on beta-blockers ever since.

    My stepmothers’ family all had a genetic form of hypertension, and typically died in their early forties (her father and one brother). When the early diuretic medication came out she and her remaining four siblings doubled that lifespan (between 70 and 95). My stepmother actually died from cancer when she was 82, most likely from smoking for over forty years (finally quit at age 60).

    We must have the wrong PCSK9 Mutations.

  18. Dawn says:

    We also have a different language from the 18th and 19th (even early 20th) centuries. If you read books from those eras, you won’t find references to heart attacks. You’ll read about “dropsy” (probably congestive heart failure), people who “died in their sleep”, people whose “heart just gave out”, rheumatic heart disease, apoplexy (which was more likely to be a stroke but use varied), “frail” people, etc.

    So you can’t compare apples (their terminology) to oranges (modern terminology) because we don’t know exactly what was meant always by those diagnoses. And, as was pointed out higher in the thread, people didn’t live as long. Injury, illness were more likely to kill you before you lived long enough to die from a heart attack.

    Back in the early 1940’s, my great-grandmother had high blood pressure and died around age 65 (young, compared to today). A cousin had malignant hypertension and died in her late 30s, leaving a teenage son. With improved treatment, other family members have lived to their 80s and 90s.

  19. tuck says:

    @Peter Lipson: My point is as stated in the comment: “Until science-based medicine can answer the question about what caused this epidemic, and how can it be prevented, the “success” looks much less impressive.”

    Medicine is treating the symptoms of heart disease, and has not in over 100 years figured out what caused the epidemic. Now treating symptoms is good, and essential, but it’s a low standard to set, IMHO.

    @Todd W: Guyenet address most of your questions in the post I linked to.

    @Allison Cummins: There are also cultures similar to ours where smoking does not cause the same rates of heart disease: France or Japan, for instance. Yet Japanese move to the United States and experience US-style rates heart disease. Smoking’s not the explanation, although obviously it contributes.

    @WilliamOBLivion: You’re not correctly summarizing Guyenet’s thesis, but folks can follow the link and it he can speak for himself, he has sections on coronary disease and diseases of civilization. And yes, we don’t know if he’s correct. Which is why I didn’t get into his theories of causation. I happen to think they’re pretty compelling (and scientific!), but that’s a different issue.

    I don’t think it’s a cheap shot. I don’t think the success is completely attributable to science-based medicine, any more than the low cardiac disease rates some societies experience are.

    @Angora Rabbit: “We actually do know why CHD rates rose. It’s that combination of longevity, energy expenditure and diet changes.” Look into each of those, and, except for the last one, you’ll see that they’re not accurate. Guyenet addresses the longevity issue in the post I presented above. And there’s so much disagreement in the medical profession over diet that claiming that as part of the “success” is a bit much. Saturated fat, for instance, has been blamed for cardiac disease for all of the last 60 years, yet in only the last two years have major researchers come out and stated that there is, in fact, no relation between saturated fat and heart disease, and that the medical advice to avoid saturated fat may have worsened the problem. Whoops.

    @jmd: The link I provided looks specifically at heart disease, and people did live long enough to get it. We have 20-year-olds getting heart attacks nowadays.

    Science and medicine have known that certain countries have high rates of heart disease, and certain other countries have lower (near-zero, in some cases) rates of heart disease for some time now. What are the differences? Many of the current theories have huge holes in them. And many of the theories that we’re operating under have huge holes.

    Science-based medicine is clearly the only way to effectively treat patients. But I don’t think that some of the points in this post are really addressing the root causes.

    If we really knew what was causing heart disease, it would be as common as rickets, or scurvy. The approaches that Dr. Lipson commends are commendable, for sure, but they’re palliative, at best. This is not to dismiss the efforts of the doctors who are working their hardest to care for patients, a operating as well as they can with imperfect information.

    My root complaint about this post is that many of the approaches that have been taken to address heart disease aren’t really science, and that therefore it’s a little early to be claiming success for science-based medicine in this field.

  20. weing says:

    “If we really knew what was causing heart disease, it would be as common as rickets, or scurvy.”

    I really don’t know what that means.

    “My root complaint about this post is that many of the approaches that have been taken to address heart disease aren’t really science, and that therefore it’s a little early to be claiming success for science-based medicine in this field.”

    Can you give examples, of the approaches to address heart disease, that you say are not really science?

  21. Todd W. says:


    Re: 18th and 19th c. heart disease rates

    The link you posted says nothing of 18th century heart disease rates, and very little about 19th century, other than some limited data from about 1870 on.

    As to accuracy, there was assertion that the records were accurate, but Dr. Guyenet gives us no way to verify that claim. Again, this only applies to the years he discussed (namely, 1870 on).

    Suffice to say, that picking a starting point of the 18th or 19th century, based on the link you provided, is not demonstrably more accurate than looking at a starting point around 1940.

    What we do know, however, is that, whether you start in 1940 or 1840, heart disease incidence has gone up. We also know that behavioral and medical interventions have played some role in lowering the mortality, if not the morbidity, of heart disease.

    I am, however, by no means a specialist in cardiac issues, and I understand that there is still scientific uncertainty regarding causes and best treatments/preventions. The choice of where you start is important, but the validity/accuracy of that starting point is just as important.

  22. Chris says:


    We have 20-year-olds getting heart attacks nowadays.

    That has happened for a long time. The week before my son was diagnosed with an echocardiogram a twelve year old girl died from the same condition at a track meet. It is one of the most common reason for sudden cardiac death in young people (there are other conditions, like Long QT Syndrome).

    If we really knew what was causing heart disease, it would be as common as rickets, or scurvy.


    Recent publications indicate that HCM is the most common of all genetic heart conditions affecting 1 in 500 people in the general population. Based on these data we may estimate that as many as 600,000 people in the United States have HCM. Subsequent studies have also proven that HCM has a prevalence of 1 in 500 in a wide variety of populations including, Native Americans, Chinese, Rural Midwestern US, and others. There is no gender, age or ethnic factor specific to HCM, HCM is an equal opportunity disease.

    Yah, sure:

    As of today (January 2009), a multitude of 500 mutations in 11 genes, which are necessary for the development and contraction of heart muscle cells (in units called sarcomeres), have been mapped to their respective chromosomes and isolated from members of families with HCM; (some of these mutations also exist in skeletal muscle, as well as heart muscle). The 11 genes presently regarded as causing HCM are known in scientific terms as: 1) beta-myosin heavy chain; 2) cardiac myosin-binding protein C; 3) cardiac troponin-T; 4) troponin I; 5) alpha-tropomyosin; 6 & 7) essential and regulatory myosin light chains; 8) actin; 9) alpha-myosin heavy chain; 10) titin; and 11) muscle LIM protein. In most patients, HCM is caused by the initial 3 genes on this list while the other 8 genes each account for only a small fraction of the patients.

    So, oh wise tuck, please tell me how we were supposed to prevent the abnormal growth of heart muscle that happened when my son hit puberty? We will be monitoring his siblings until they are at least in their mid-30s, but you must have an alternative method to actually predict and prevent any problems.

  23. Peter Lipson says:

    Part of tuck’s reasoning is a reductio ad absurdum regarding “cause”. Often in science, cause=association. Heart disease is strongly associated with higher cholesterol, with higher blood pressures, etc. It is also associated with certain pathological changes in blood vessels and with increased markers of inflammation. So, while we may not be able to say “x always is the cause of y”, we can say “a,b, and c are usually associated with y, and fixing a, b, and c prevents y”. That’s pretty good. Tuck’s argument is much more of an angels/pinheads thing.

  24. weing says:

    It’s worthwhile remembering the term “essential hypertension” once meant that it was actually needed and not treated. I don’t think that was based on any science either. Check out FDRs blood pressures:

  25. We’re able to prevent the vitamin deficiency diseases of scurvy and rickets through a combination of public education, medical recommendations and legislated food supplementation. These are conditions with simple causes and simple fixes.

    Heart disease (tuck linked to a blog post specifically about coronary artery disease) is multifactorial and doesn’t have simple fixes. Let’s say that we knew all the causes today and they were reducible to only two, smoking and sedentary lifestyles. No other factors have any effect. Getting older isn’t bad for our hearts; neither is being heavier; neither is being male; neither are doughnuts.

    Now that we know the Two True Causes of all heart disease, explain how it would be as easy to eradicate as scurvy and rickets.

    Scurvy — This one’s easy. Eat a fruit or vegetable every day. A 6 oz glass of orange juice is great but french fries will do the trick. If you can’t or won’t, take a multivitamin. People like these things. The people who don’t eat them tend to be people who can’t, like sailors or prisoners. Give people a little education, give the Florida Orange Growers a little nudge and off we go.

    Rickets — This one’s trickier. Get a little sun but not too much. Use dairy products (the law requires that they contain vitamin D, through fortification if necessary) and eggs or fish. If you can’t or won’t, take a multivitamin. Most people will do these things if they can without being told, but dark-skinned children living at southern or northern latitudes (especially in sulphurous smog) and who don’t eat fish or dairy are at risk, so formula is fortified with vitamin D and pediatricians recommend vitamin D supplements for breastfed babies. Getting vitamin D is complicated enough that it requires a combination of legislation, public education and doctor’s prescriptions to prevent rickets.

    Heart Disease — ???
    I’ve made it Real Easy for you by whittling it down to only two causes.

  26. Calli Arcale says:


    Also the use of lots of refined sugars and stuff like high fructose corn syrup (which is now in EVERYTHING, including Robotussin. Along with sucrolose, WTF?)

    Frankly, I think any marginal worseness of HFCS is overwhelmed by the simple fact that we get waaaaay too much sugar (of all kinds) in our diet. Picking a marginally healthier form of sugar is probably not significant when so many people are getting several times the RDA for sugar. But I’m not a doctor; that’s just my opinion.

    The reason it’s in Robitussin is because Robitussin tastes *nasty*. And if a person is taking enough Robitussin to worry about the HFCS in it, they’ve probably got bigger problems (like a drug overdose).


    @jmd: The link I provided looks specifically at heart disease, and people did live long enough to get it. We have 20-year-olds getting heart attacks nowadays.

    It’s not exactly common, though, and the ones who do usually have congenital defects that had gone undiagnosed and consequently untreated.

    If we really knew what was causing heart disease, it would be as common as rickets, or scurvy.

    That’s only true if the cause is something preventable. Rickets is preventable with Vitamin D supplementation, and scurvy is preventable with adequate vitamin C intake (and it’s usually not difficult to get it through diet). Consider malaria; we know exactly what causes that, but it’s still a major global health problem. More to the point, “heart disease” is a pretty broad term. It encompasses everything from congenital defects to bacterial damage (my grandpa has two bad valves thanks to staph infections) to viral infections to cancer to coronary disease and more. It clearly doesn’t have a single cause, therefore finding a known cause of heart disease cannot eliminate heart disease altogether.

    (Random tidbit: scurvy rates are actually increasing in the US, in a particular subgroup: college freshmen, who sometimes learn the hard way why man cannot live on bread alone.)

  27. Harriet Hall says:

    weing said “the term “essential hypertension” once meant that it was actually needed and not treated.”

    I don’t think “essential” meant it was needed or not treated. I think “essential” was a synonym for what we would call “idiopathic” today: i.e. no identifiable cause.

  28. Peter Lipson says:

    Essential HTN also meant “not secondary”, another words, primary hypertension not known to be due to some other medical condition.

  29. weing says:

    I think we have to find some textbooks from the early 20th century to settle this. I think that was before your time too, Harriet.

  30. Peter Lipson says:

    I have one at home: my dad’s Cecil’s from 1944. I’ll dig it up later.

  31. Harriet Hall says:

    I googled “essential hypertension” and everything I could find, from Wikipedia to the dictionary, agreed with my interpretation. I couldn’t find anything to support weing’s interpretation. I am old enough to remember the term being used and to have reached my understanding of what it meant several decades ago.

    I’m always open to persuasion by good evidence. I couldn’t find any, but maybe you can.

  32. Stuartg says:

    I note that using ICD10 to code my patients’ discharges, the condition is described as “Essential (primary) hypertension.”

    It appears that there has been a terminology change over the decades but the condition remains the same.

  33. daedalus2u says:

    I went to a talk by Thomas Insel today, and he brought up the issue of the change in death rates for CHD. The change is not small.

    It is all due to prevention, and to treatment of symptoms before the damage gets too bad.

    Life expectancy has gone up by ~25+ years of life in the past century.

  34. weing says:

    I found a paper of Osler’s from 1912, in the BMJ, that talks about the advantages and disadvantages of hypertension. Just a cursory reading left me with the impression that, in some cases at least, it was not something to avoid.

  35. tuck says:

    @Peter Lipson: “‘a,b, and c are usually associated with y, and fixing a, b, and c prevents y’.”

    Except that in this case you’re not ‘fixing’ anything. You’re reducing the evidence of symptoms (in the case of cholestorol and palliative surgical procedures like the stent) and you’re not preventing it, the incidence of it has declined. This is similar to the 55 mile-an-hour speed limit. The year after it was introduced, fatalities declined. The year after it was eliminated, fatalities declined. In our case, “diseases” associated with heart disease, your “a” and “b” above (diabetes and obesity) continue to increase. Heart disease mortality has declined, through the the hard efforts of the medical profession, but obviously the problem is not “fixed”.

    I’m going to use an engineer’s definition of “fix” here, which is a bit more rigourous. If you fix something in engineering, you remove the cause of breakage. Medicine has not done this in the case of heart disease.

    The problem with giving the credit to “science-based medicine” for reducing the heart disease rate is that we don’t know what caused it in the first place (we have hypotheses, several of which, including some which have been disproven are repeated in the comments here). Clearly the heart disease rate did not go up because medical care was lacking. Something else caused it to go up, and the development of cardiovascular medical care was merely a reaction.

    Since we don’t know why it went up, we can’t say with certainty why it’s going down. It could be because of medicine, true, or it could be because the initial conditions are improving themselves.

    You’re putting yourself in the position of the witch doctor who takes credit for a rainy day, without knowing why the rain occurrs in the first place.

    I like this site a lot. But picking on accupuncturists and the like, who are grossly and obviously unscientific, is too easy. If you want to really do some good, turn your gimlet eye on the “science-based” medical profession, which is often grossly unscientific itself.

  36. weing says:


    We all know that there is no single cause of CHD. You have knowledge of the one true cause? Share your wisdom, please. Please give examples of the unscientific approaches to prevent and treat CHD. You make an accusation but “Where’s the beef?”

  37. tuck says:

    @daedelus2u: that’s an excellent bit. All three of the dietary causes of heart disease that they cite have since been debunked. Saturated fat does not cause heart disease, salt does not cause high blood pressure, and dietary cholesterol does not cause increased blood cholesterol. Some hat trick.

    They mention dietary fat and cholesterol consumption peaking in 1909 and yet heart disease continued to increase until 1950! So fat and cholesterol consumption cause heart disease, and yet heart disease continued to increase for 41 years, two generations, after fat consumption peaked?

    They mention smoking as a cause, yet heart disease declined for 14 years before the smoking rate declined.

    They also mention that heart disease intervention studies started in the ’60s, 10+ years after heart disease rates had started to decline.

    Isn’t the old line that ‘half of what you learn in medical school is obsolete in 7 years, but you won’t know what half’?

    God bless the Doctors, they have the toughest job in the world.

  38. Chris says:


    I’m going to use an engineer’s definition of “fix” here, which is a bit more rigourous. If you fix something in engineering, you remove the cause of breakage. Medicine has not done this in the case of heart disease.

    Okay, other than a heart transplant, how do you “fix” hypertrophic cardiomyopathy? Do a gene transplant?

  39. windriven says:

    @weing, Todd, Dr. Lipson, et al

    tuck is playing you. His, ahem, argument is classic sophistry: begin with an erroneous assumption and proceed merrily along to its logical conclusion. In this case it is tuck’s lame and unsubstantiated assertion that “heart disease was extremely rare, prior to the great increase of the 20th century.”

    Hey tuck, so was living past 45. So was meaningful medical record keeping. So, for that matter, was consistently high quality diagnosis. Dufus.

    Todd W picked this up and confronted it early in the comment stream. That tuck now brays on oblivious to the challenges to his fundamental assertion betrays a lack of seriousness on his part. Answering gibberish with reasoned analysis is like trying to teach a pig to sing. It wastes your time. And it irritates the pig.

  40. Peter Lipson says:

    Yeah but you’ve got to love pure gold like:

    Except that in this case you’re not ‘fixing’ anything. You’re reducing the evidence of symptoms

    Tell you what…next time someone thanks me for “reducing the evidence of symptoms” of their heart attack, i’ll make sure to tell them i know a guy on the internet who’s an idiot.

  41. weing says:

    I don’t know where you get your information but I would not rush to eat saturated fat, smoke, and abuse salt if I were you. Oh, perish the thought! In a lot of people, those factors are the main contributors to their disease. I’ll be the first to admit, not in everyone.

  42. Peter Lipson says:

    What would be interesting is an actual refutation of the data in the citations. These aren’t perfect studies, although I obviously think they’re pretty good. Right now it’s ex culo assertions vs. actual data.

    C’mon: bring it. The study says these three factors were important. Why are they wrong?

  43. David Gorski says:

    Essential HTN also meant “not secondary”, another words, primary hypertension not known to be due to some other medical condition.

    That is what I remember being taught in medical school in the 1980s, namely that “essential” hypertension was a wastebasket term for hypertension not clearly caused by something like renal artery stenosis, pheochromocytoma, etc.

  44. Reductionist Nurse says:

    Somewhat of a digression but in curiosity of the “Essential hypertension” claim, I’ve got a 1935 copy of the Modern Home Physician in front of me, I thought its entry on Hypertension was interesting:

    For the proper circulation of the blood a sufficient degree of blood pressure (q.v.) is necessary. Clinically the blood pressure is estimated by an instrument called a sphygmomanometer, which is generally used on a brachial artery. It is estimated in terms of millimeters of mercury which it would support, in the same way as air pressure is measured in a mercurial barometer, though the sphygmomanometer may be of an aneroid type, like some barometers. The blood pressure in the brachial artery is found to vary normally from 130 to 140 in those above forty years of age.
    An increased pressure, judged according to what is usual at the person’s age, is described as hyperpiesis. This may be a temporary occurrence, as as during excitement or muscular exertion. It may occur, for example, merely from excitement due to the fact that a doctor is applying a sphygmomanometer. Some people are found to have hyperpiesis, however, in conjunction with weakening of the arterial walls, involves a risk of rupture of the vessels, such weakening being caused, as a rule, by microorganisms or their poisons.
    Hyperpiesis leads in time to hypertrophy of the heart and of the muscle coat of the arteries. About middle age hyperpiesis may occur and be associated with indefinite illness, but the increased presure may not be dependent on kidney disease or narrowing of the blood vessels by arteriosclerosis (q.v.). The condition underlying this rise of blood pressure, or hyperpiesis, is called hyperpiesia. It can be remedied by taking a simple diet, moderate in amount, and sufficient open-air exercise. It is important, also, to get rid of worries, including worry over the increased blood pressure, should this fact be known to the patient. The bowels should be kept open. Bromides are often useful. ”

    I thought it was very interesting in such that going all the way back to the 1930’s they recognized both white-coat hypertension and the importance to reduce psychological stress. Now who says old school doctors weren’t “holistic”? :)

  45. daedalus2u says:

    What your tissues actually need is not “blood pressure”, but “blood flow”.

    In the short term, there is a fixed quantity of blood, and the heart has a limited pumping capacity. Blood flow to the peripheral tissues is regulated by changing the cross section of the various blood vessels to and from those tissue compartments and by changing the pressure difference between the outlet of the heart and the inlet of the heart.

    When you need more blood flow in the short term, physiology responds by increasing the blood pressure difference between the outlet and inlet of the heart, dilating vessels leading to the tissues that need more, and constricting the vessels leading to the tissues that need less.

    When you are “running from a bear”, your blood pressure may go up 2x or more. This is adaptive in the short term, but maladaptive in the long term. The ideal blood pressure is only sufficient to give the correct flow, and the right dynamic range to account for relative changes in blood delivery needs.

    Raising blood pressure is only for short term compensation. For long term compensation (as for example when a muscle grows bigger and needs more blood flow to support it), you want to remodel the vasculature to keep the basal flow appropriate and to allow for the correct dynamic range by constricting other vessels when blood flow to them is not needed.

    Blood pressure as a diagnostic tool is measured at rest. It should be a certain range at rest because that is the default state, where the various tissue compartments have their normal “at rest” blood flow needs.

    A deviation from that “at rest” blood pressure indicates something is wrong. What is “wrong” is that the vasculature has not remodeled itself to produce the appropriate blood flow “at rest” using the appropriate pressure gradient between the outlet and inlet of the heart.

    What you really want in cases of high blood pressure at rest is for physiology to reconfigure the vasculature to return to a normal “at rest” blood pressure (I think this nuance is not well appreciated). If you lower blood pressure via drugs, you remove that degree of freedom from physiology, so physiology responds by changing something else, by increasing vascular remodeling.

    A large part of vascular remodeling is regulated by nitric oxide, so low NO leads to insufficient vascularization (aka capillary rarefaction) and high blood pressure at rest. Increasing the basal NO level all by itself increases vascular remodeling and decreases blood pressure because there is more blood vessel cross section available for flow, so it takes less pressure to drive the appropriate amount of blood through it.

    “Essential” hypertension simply means hypertension that is not secondary to something else that is known to cause hypertension. It does not mean that it is helpful. High blood pressure at rest is never helpful, it is a sign of dysregulation of the vasculature. It needs to be corrected.

  46. windriven says:

    CHD. Coronary heart disease. I am not a physician but isn’t all heart disease coronary? Does coronary heart disease imply some subtle distinction that I don’t apprehend?

  47. Angora Rabbit says:

    The problem is, as Tuck’s use of language makes abundantly clear, that he is not versed in biomedical research and how we conduct these studies and interpret their findings. As Drs. Lipson and Gorski are both pointing out but with politer language than I am using here. It takes our own grad students four years of biology and another year of graduate study before they can even tackle Nutritional Epidemiology, and a full semester of three credits before they are comfortable in reading the papers and correctly interpreting their conclusions. It is not clear to me how we can teach a person outside the field, like Tuck, these concepts in a blog or two. On my more discouraging days, I suspect the internet has created a situation where, just because a person can read something, they think they “understand” it and do not appreciate how superficial that understanding really is. I encounter this regularly in my own field, and I’m sure other writers here have the same experiences in their own areas. There is a reason that the 10,000 hour rule makes sense.

    College was supposed to give us a smarter populace, but the cynic in me wonders if instead it gives us a populace fooled into thinking they are smarter and more critical thinking than they really are. Which as an academic is a depressing thought.

  48. windriven says:

    @ Angora

    Your overall point is well-taken. I would argue further that the push for near-universal college education has led to a sad decline in the standards for and therefore the value of a baccalaureate degree. I encounter graduates of (perhaps formerly) respected programs who cannot write a coherent paragraph.

    But on the issue of tuck I would disagree on the particulars. Anyone with a secondary school science education should understand the general principles of the scientific method and have developed some basic skills in critical thinking.

    I am guessing that tuck knows better and is, for whatever reasons, just trying to provoke a response. Accepting at face value an assertion that heart disease was “extremely rare” prior to the 20th century demands a degree of credulity that one associates with a drool cup.

  49. Harriet Hall says:


    The term “coronary heart disease” is confusing. It is used to refer to disease of the coronary arteries that supply blood to the heart muscle. As opposed to diseases of the heart muscle, the valves, the electrical conducting system, etc.
    It would be more accurate to call it “coronary artery disease.”

  50. nory says:

    It seems to me weing could be right on the early meaning of the “essential hypertension”. None of us is old enough – Google included :) – to rely only on personal memories in this case.

    Here is what Gary D. Goldberg, PhD, (Clinical Professor of Medical Education, Angeles College of Nursing, Los Angeles, Ca) mentions in an article published online in the RN Journal.

    “Some early authorities concluded that such hypertension was not merely “primary” but “essential,” because brusque pressure reductions were deleterious (e.g., harmful to health). ”

    Unfortunately he doesn’t give the reference for this (his email adress is posted on the site; he might provide the reference if asked).

    Here is the link where the article can be accessed:

  51. daedalus2u says:

    Nory, what the body needs is blood flow, not blood pressure. Blood pressure is the mechanism by which physiology generates the appropriate blood flow. If blood pressure is high, what is needed is to lower blood pressure while maintaining the same blood flow. Lowering the pressure and not maintaining blood flow is always deleterious.

    There are a number of ways that could be used to lower blood pressure. If you reduce blood volume enough, you will acutely lower blood pressure. This is not recommended except in certain circumstances because it also reduces blood flow. If blood pressure is so high there is risk of hemorrhage, then reduced flow may be tolerable because hemorrhage may be worse than short term reduced flow while physiology adjusts.

    The idea that some hypertension might be “essential”, or “necessary” is not correct. It is not a property of the “hypertension”, it is a property of the physiology of the individual with hypertension. If the pressure-flow characteristics of their vasculature are such that appropriate flow cannot be maintained without some level of hypertension, that does not mean the hypertension should not be treated, it means that it must be treated carefully so that the vasculature can remodel itself over the course of treatment so as blood pressure goes down, appropriate blood flow is maintained.

    There are no non-invasive ways of measuring blood flow. What is done instead is measure blood pressure, and assume that if blood pressure is in the “normal” range, that then there is appropriate blood flow. This works if the vasculature is “normal”, and has a “normal” pressure-flow characteristic. The problem in hypertension is that the pressure-flow characteristic is not “normal”. In hypertension, the blood flow is “normal”, but the pressure-flow characteristics are not normal and that shows up as elevated blood pressure. The goal of treatment is to restore a “normal” pressure-flow characteristic, when blood pressure becomes “normal”, that goal has been achieved.

  52. weing says:


    We all know what the current usage of the term “essential hypertension” is. We are talking about history of medicine here. Unlike CAM, where the sum of all knowledge is revealed from on high to someone in the past like the founders of homeopathy and chiropractic, SBM is constantly evolving and we see how the great Osler and others were wrong. That is one reason why FDR’s BP was not treated. Another reason was that big pharma hadn’t made the drugs to treat it. Once the drugs were made big pharma invented the disease of hypertension. :)

    1. Harriet Hall says:

      I think the discussion has gotten sidetracked. In the past, higher levels of BP were accepted as normal, the risks of lowering BP too rapidly were recognized, and the available treatments were problematic. That is very different from saying doctors thought a high BP was “essential” to health. After all, they called it hypertension: it was a diagnosis saying the BP was higher than normal. If they had thought it was essential to health, they would have simply defined high BPs as normal and would have diagnosed lower BPs as the disease “hypotension.”
      There are two meanings of “essential,” one related to necessity and the other related to the essence of something. I maintain that the meaning of essential hypertension has always been the current meaning: hypertension by its own essence as opposed to hypertension due to identifiable causes. Big Pharma did not invent the disease hypertension: science discovered that lower BPs improve patient outcome, and so the definition of a normal BP has been repeatedly adjusted downward since I graduated from medical school in 1970. And Big Pharma treatments have on occasion been rejected when science found that those who had lowered their BP with a specific drug had a worse outcome.

  53. JMB says:


    Medicine’s goals are to save lives and stamp out disease. We are happy anytime we save a life (or help save a life), or stamp out a disease. There are relatively few diseases we have actually stamped out (most are infectious diseases stamped out by vaccines, but even those may have some risk of resurgence), but that does not diminish the accomplishment of saving lives.

    Science’s goal is knowledge (different from medicine’s goals). Medicine uses science as a tool to save lives and stamp out disease (but medicine is still an art). Our scientific knowledge may be incomplete, but medicine still celebrate the success of saving lives thus far achieved . Our scientific knowledge is far more advanced than tuck gives us credit for, it is just that the factors experimentally validated are far more complex than can be reduced to a simple thesis for consumption in a book or on a website.

    An engineer can close down the traffic on a bridge while a complete fix is implemented, SBM must fix the bridge while the bridge is still in use. SBM must deal with the cards already dealt to the patient. As much as we would like to eliminate the bad cards in the deck being dealt, that is not going to help the patient already holding the bad cards.

    The value of scientific principles applied in medicine isn’t determined based on compelling arguments (that may be reason for research grants to be awarded), it is about what hypothesized factors will result in a measurable change in outcomes. This isn’t a debate where the best argument wins, this is a calculation in which we determine the weighted value of each of the factors in the outcome. When our calculations are accurate enough, and the weights of the altered factors are heavy enough to reduce the expected mortality, then we have success in SBM.

    We cannot know before the scientific knowledge in a particular disease is complete (if it ever will be), what the best strategy was for devoting resources (time and money) to the goals of saving lives and stamping out disease. If we devote all of our resources to stamping out disease, we may watch a lot of people die unnecessarily before we find the cause and eliminate the disease.

  54. weing says:

    According to Kaplan, the word essential comes from the German word that means idiopathic. The better term would be idiopathic. On reading Osler’s November of 1912 paper in the BMJ, I got the distinct impression that it was not such a bad thing. I could see how some physicians from the 1930s and 1940s could view it as meaning necessary. The ICD-9 still lists benign hypertension as a diagnosis, which should have been buried with the patients that had it. I was always taught that essential meant idiopathic also and I graduated in 1980. The comments about big pharma were and are tongue in cheek as indicated by the emoticon to rattle the big pharma conspiracy theorists.

  55. nory says:

    Harriet, I agree that the comments about the original meaning of “essential hypertension” are collateral. I just thought it would be nice to find out which one of the two opinions is the documented one. After all we are on SBM where referencing is essential :) I think you’ve missed the point that Goldberg was trying to make: “such hypertension was NOT MERELY “primary” but “essential”. We need a real proof about the historical use of the term in case to conclude in one way or the other.

  56. Peter Lipson says:

    We still don’t have a primary source on it. I’m not yet convinced that this isn’t myth, but i’m willing to be convinced.

  57. Peter Lipson says:

    According to Cecil’s 1947 ed:

    Essential hypertension is a term employed to indicate the existence of abnormally high systolic and diastolic arterial blood pressure in individuals who have neither inflammatory kidney disease, urinary tract obstruction or other disorders which are known to result in elevation of the blood pressure…

    He goes on to talk about malignant essential htn vs other, etc. there is no indication in this text that essential ever meant “needed”.

  58. nory says:

    Peter, I really admit that it can be a myth. Cecil’s is truly an excellent textbook but is not the kind of source to help us getting the final answer to this question which is clearly of historical /theoretical interest. I really appreciate all of you taking time to answer the issue.

  59. nory says:

    Finally, I got the kind of paper I was looking for. “Pathogenesis of essential hypertension: historical paradigms and modern insights.”
    The article can be accessed on PMC at this link:

    The paragraph of interest reads like this:

    “The observation that many cases of hypertension had no clinical evidence of kidney disease and was often asymptomatic led to the term ‘benign’ hypertension to characterize those individuals [14]. In this context, some authorities suggested that the rise in blood pressure might be necessary or ‘essential’ in order to provide blood supply to its destination sites through the thickened blood vessels [15].

    And the reference for it is:

    15. Volhard F. Discussion of Bright’s disease [in German]. Verh Deutsch Pathol Gesell. 1905;9:111–114.

    1. Harriet Hall says:

      “some authorities suggested that the rise in blood pressure might be necessary or ‘essential’ in order to provide blood supply to its destination sites through the thickened blood vessels”

      I don’t think the fact that “some authorities suggested” is evidence that the original meaning of essential hypertension was that elevated BP was essential to health. I think it means that some authorities suggested that some cases of idiopathic hypertension might not be idiopathic but might be a response to a pathological condition.

  60. Th1Th2 says:

    Good article.

    I always thought that an ‘essential’ HTN is a normal physiological response but to label it being a primary or idiopathic disease is erroneous. The only ‘primary’ problem lies with the physician on how they manage such condition because they are clearly ‘deficient’ in knowledge about human physiology while the patient suffers from unnecessary interventions.

    Now can someone discuss about drug-induced and iatrogenic HTN? In this drug-oriented society, I guess this is more of an epidemic than the so-called essential HTN.

  61. nory says:

    There are indeed drugs that induce high blood pressure as adverse effect (corticosteroids) but these cases are not as prevalent as to justify labeling it as an epidemic.

  62. Th1Th2 says:

    Harriet Hall,

    “I think it means that some authorities suggested that some cases of idiopathic hypertension might not be idiopathic but might be a response to a pathological condition.”

    But then you wouldn’t call it idiopathic if the cause is pathological. The reason for the increase in BP is attributed to the increased sympathetic nervous system activity for example, as a response to stress , hence, the term ‘essential’ since it is a normal reaction.

  63. Harriet Hall says:

    Me “might not be idiopathic”
    Th1Th2 “then you wouldn’t call it idiopathic”

    No, I wouldn’t. Gee, Th1Th2 finally got something right!

  64. Chris says:

    This evening I listened to a 60 Second Science episode on a repeat of a thirty year old study on the cognitive ability of 70 year old people. It should not be a surprise that the 70 year olds born in the 1930s did better than the earlier generation. Here is the quote of interest:

    They also had better nutrition, a higher quality education, and better treatment of high blood pressure and cholesterol.

  65. JMB says:

    College was supposed to give us a smarter populace, but the cynic in me wonders if instead it gives us a populace fooled into thinking they are smarter and more critical thinking than they really are.

    I think that is so very true. I remember only two science courses in college that attempted to assess a student’s ability to critically analyze and utilize information (beyond simple use of formula). Both courses were hated by students, and had very small enrollment (and many 4.0 students dropped out of them to maintain their 4.0). Students in science courses almost always wanted to be tested on their memorization of “scientific facts”. The question that students of science should be asked over and over is the following, “Here is the result of this experiment in which (fill in discourse on methods) showed (fill in the discourse on results). Now given this information, what might you be able to conclude would likely happen in this scenario (describe situation)?”

  66. JMB says:

    But then you wouldn’t call it idiopathic if the cause is pathological. The reason for the increase in BP is attributed to the increased sympathetic nervous system activity for example, as a response to stress , hence, the term ‘essential’ since it is a normal reaction.

    Just because the cause is not pathologic does not mean the result won’t be pathologic. The natural selection of evolutionary pressure has equipped us with bodies to maximize the survival of the genome, not to live an active and healthy life to age 100. Our physiologic responses to stress will help us survive to reproduce. But our physiologic responses to stress may be a factor in death past reproductive age. It is known that there are risks associated with lowering blood pressure too fast or too low in older patients. It is also known that hardening of the arteries may be associated with spuriously high readings of blood pressure. Other than that, the old concept that hypertension is desirable in some patients with hardening of the arteries has long been discarded. I guess being ancient and discredited makes it fair game for woo meisters.

  67. nory says:

    I admit the quote doesn’t prove what the “original” meaning was but it does document that “essential” did not mean always what it does today. So far we can say that “some” authorities at the beginning of the XXth century suggested that in “many” hypertensives the rise in blood pressure was necessary to supply the blood flow. Probably that German article would bring a little more light.

  68. Earlier in the thread angora rabbit said that cholesterol intake was a factor in CHD, but I’ve been reading in the popular press that dietary cholesterol is NOT a factor. High blood cholesterol is apparently caused by dietary fat, not dietary cholesterol. Foods like eggs and prawns (shrimp) are supposedly OK now.

    I’m also rather puzzled about salt, because it seems to be such a given in the popular press that everyone is supposed to reduce their salt intake. The DASH study is usually cited, but the magnitude of the effect they cite on normal BP is very small, and I find nothing about what those of us at the low end of normal BP or hypotension should do.

    I vaguely recall reading that only some people respond to increased salt with hypertension, possibly due to genetic factors. So it could well be an epidemiological factor – reduces risk in a substantial proportion of the population, and hence the overall numbers – but it doesn’t necessarily apply to everyone.

    Can any of the medical research people out there confirm or deny these?

  69. Peter Lipson says:

    There are reasonable data pointing toward a correlation between salt consumpton and mortality

  70. Th1Th2 says:


    “Just because the cause is not pathologic does not mean the result won’t be pathologic. ”

    Basically it’s a shot in the dark approach being applied here by doctors in dealing with patients with essential HTN. Patients are being placed on medications unnecessarily with complete disregard to the systemic side-effects thus worsening of HTN. Hence, it opens up the gateway for multiple drug and long-term use. Voltaire was right, “Doctors are men who give drugs of which they know little, into bodies of which they know less… for diseases of which they know nothing at all.”

  71. Always Curious says:

    A few years ago, I read an author who mentioned the same pattern of new heart attack patients of “epidemic” proportions in the 50’s & 60’s that Tuck alluded to. Except this author proposed that the cause might be a heretofore unidentified pathogen. Such a pathogen could explain the sudden increase and dropping off (pre-intervention) in the incidence rate [errors in reporting notwithstanding]. Under this model, elevated fat & cholesterol levels are symptoms of infection and not primary causes. Searching for cholesterol lowering drugs to solve heart problems in his view was the same as using cough syrup to help a cold–you’ll feel better, have less severe symptoms, fewer complications, but the underlying problem remains.

    Does anyone with a better background in heart health have a better understanding on this? I’ve glanced through the literature once or twice on this topic & people have tried to correlate heart disease to various infectious agents (Helicobacter Pylori and Chlamydia pneumoniae), but it seems very preliminary to me.

  72. My goodness, we are branching out and moving from some sort of DSM diagnosis involving fear of contamination, to straighforward arrogance of ignorance in medicine generally. As Freud said,* this is progress!

    *“…much will be gained if we succeed in transforming your hysterical misery into common unhappiness. With a mental life that has been restored to health, you will be better armed against that unhappiness.”

  73. Chris says:

    That is an interesting question, Always Curious. I only know that infections have damaged hearts (one reason why my son gets prophylactic antibiotics before going to the dentist… yes, I know that policy changed, just not for him for various reasons).

  74. weing says:

    Always Curious,

    One of the arms of the PROVE IT study looked at a possible infectious cause of coronary artery disease. It didn’t pan out.

  75. Alison – I was thinking ‘oh shoot, the fire just jumped the river.’ Glad you have a more positive interpretation.

  76. nory says:

    Just one more reference, on our little side track about the historical turns of “essential hypertension”.

    “Primary hypertension has always been referred to as essential hypertension. The word ‘‘essential’’ was used because it was believed that higher pressures were needed to pump blood through arteries that were narrowed for some unknown reason. The use of the word has been so ingrained that it cannot be easily removed.”
    Encyclopedia of Heart Diseases, M Gabriel Kahn, Elsevier, 2006, p 472.

  77. Peter, thanks for the reply which unfortunately did not answer my question about salt. I’m in no way denying that there is a correlation between reducing salt and reducing blood pressure, and reducing blood pressure and reducing heart disease.

    My question is whether the correlation is meaningful on an individual level. Generalising from a population study to individuals in that population is known as the ecological fallacy, and it’s a hugely important stumbling block for social science, including epidemiology. All good researchers have to address this.

    If a goodly proportion of people with high blood pressure get better, that can produce a statistically significant effect without anyone else changing anything. The denialism blog entry seems to confirm this impression, actually: “Some people with hypertension are more sensitive to salt than others, and African Americans in general benefit more from salt reduction than other ethnic groups.” Confusingly, the AmJMed abstract notes that in their study there were definite effects relating mortality to salt intake – but “no such associations were observed for those <55 years old, non-whites, or the obese."

    So who are these "some people" who benefit? Is it worth staging a public health intervention targetted to "everyone" when only "some people" will benefit? Maybe yes, maybe no. I'd want more info on the magnitude and distribution of the effect first. Yes, if it's as significant as cigarette smoking; no if it's like breast cancer screening. You obviously wouldn't market breast cancer screening to everyone, male or female, from birth. Why market salt reduction that way? Should it be marketed to older people the way cancer screening is?

    And are there other groups of "some people" who might be disadvantaged? For a person with low blood pressure, prone to dizziness and fainting when standing up suddenly, I'm not sure it would be a good idea to reduce it any further. (That used to be me when I was younger. Now at last – thanks to being 20 years older, overweight, and less fit – I'm finally up to the low end of normal.)

  78. JMB says:

    @Cath of Canberra

    My question is whether the correlation is meaningful on an individual level.

    Dr Lipson is far more qualified to answer this than I am. But in lieu of a more direct answer, I would offer hearing one study that suggested that in an experiment comparing excess levels of dietary intake to urinary excretion of sodium, 2/3 ‘s of the normotensive population would simply excrete excess sodium the same day as the intake. However, I’m unaware of any test available to classify your individual response. Testing your own blood pressure response ifs difficult because of the variability of blood pressure from one minute to the next, and the precision of measurement required to detect a 2-8mm Hg drop due to sodium restriction. I think the current thinking is that the lower your resting blood pressure, even in the normotensive range, the lower your risk of heart attack and stroke. If you are told your blood pressure is unusually low, then you might not have to worry about the benefit of restricting salt intake.

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