Erin Thomson, MPH
Project Manager
Jefferson School of Population Health
As Congress is working to pass a health reform bill, efforts should be made to ensure that the legislation includes provisions to improve the quality of health care. This would require quality reporting by all members of the health care system, including pharmacy practice. Pharmacists are an integral component of the health care team and provide valuable knowledge and skills that increase the quality of patient outcomes.
The Pharmacy Quality Alliance (PQA) partnered with the National Committee for Quality Assurance (NCQA) in the development of 15 pharmacy performance measures. The measures are aimed at improving medication adherence, ensuring adequate drug therapy for patients with diabetes and asthma, and helping to ensure appropriate drug therapy in the elderly population. During 2007, PQA developed and pilot‐tested a questionnaire to gather consumer feedback on the quality of pharmacy services. This questionnaire was developed in accordance with the Agency for Healthcare Research and Quality guidelines for development of Consumer Assessment of Healthcare Providers and Systems surveys.
In order to determine the resource requirements for collecting and aggregating prescription claims data and calculating the 15 PQA-endorsed measures, PQA funded 5 Phase I Demonstration Projects. The demonstration sites included a health plan, a community pharmacy corporation and three health plan coalitions. The demonstration project was focused on generating pharmacy performance reports using the measures and collecting patient experiences with pharmacy services using the PQA-sponsored survey. The sites anticipate completion of Phase I by the end of 2009.
The Jefferson School of Population Health, in partnership with CNA, was awarded an AHRQ grant to conduct an independent external evaluation of the PQA Phase I Demonstration Project. Two survey instruments, including a Qualitative Interview Guide and a Quantitative Pharmacist Survey, were developed and pilot-tested. The instruments were designed to assess the challenges, issues, and technical problems that were encountered during the project as well as the operational costs and non-financial burdens encountered in collecting the data, generating reports, and using the performance data.
JSPH staff are currently conducting the qualitative on-site interviews of demonstration project staff and will be disseminating the quantitative pharmacist survey to field pharmacists early in the New Year. We are eagerly anticipating the results as we seek to determine the feasibility of engaging pharmacy in quality measurement strategies and look forward to sharing our results later next year. If you have questions or would like additional information about this initiative, please contact Erin Thomson, MPH (erin.thomson@jefferson.edu) or Laura Pizzi, PharmD, MPH (laura.pizzi@jefferson.edu).
Wednesday, January 6, 2010
Stop Measuring and Start Thinking
Sam Taylor-Wood, Still Life, 2001, Edition of 6, 35 mm Film/DVD
(Thanks to Sam Taylor-Wood for permission to use this image)
(Thanks to Sam Taylor-Wood for permission to use this image)
Saturday, January 2, 2010
Eating fish whole: Smelts
Since different parts of a fish have different types of nutrients that are important for our health, it makes sense to consume the fish whole. This is easier to do with small than big fish.
One of my favorite types of small fish is the smelt; the photo below shows a batch of smelts that I prepared using the recipe below. Another small fish favorite is the sardine. Small fish are usually low in the food chain, and thus have very low concentrations of metals that can be toxic to humans.
Many people dislike the taste of smelts, but will eat them if they are well seasoned and their texture is somewhat hard. Here is a recipe that will get you that.
- Steam cook the smelts for 30 minutes to 1 hour (less time = harder texture).
- Spread the steam cooked smelts on a sheet pan covered with aluminum foil; use light olive oil to prevent the fish from sticking to the foil.
- Preheat oven to 350 degrees Fahrenheit.
- Season the steam cooked smelts to taste; I suggest using salt, chili powder, garlic powder, and herbs.
- Bake the smelts for 30 minutes, turn the oven off, and leave them there for 1 hour.
There is no need to clean, or gut, the smelts for the recipe above. Since they feed primarily on plant matter, and have a very small digestive tract, there is not much to be “cleaned” off of them anyway.
They will be ready to store or eat cold. There are several variations of this recipe. For example, you can bake them for 40 minutes, and then serve them hot.
One of my favorite types of small fish is the smelt; the photo below shows a batch of smelts that I prepared using the recipe below. Another small fish favorite is the sardine. Small fish are usually low in the food chain, and thus have very low concentrations of metals that can be toxic to humans.
Many people dislike the taste of smelts, but will eat them if they are well seasoned and their texture is somewhat hard. Here is a recipe that will get you that.
- Steam cook the smelts for 30 minutes to 1 hour (less time = harder texture).
- Spread the steam cooked smelts on a sheet pan covered with aluminum foil; use light olive oil to prevent the fish from sticking to the foil.
- Preheat oven to 350 degrees Fahrenheit.
- Season the steam cooked smelts to taste; I suggest using salt, chili powder, garlic powder, and herbs.
- Bake the smelts for 30 minutes, turn the oven off, and leave them there for 1 hour.
There is no need to clean, or gut, the smelts for the recipe above. Since they feed primarily on plant matter, and have a very small digestive tract, there is not much to be “cleaned” off of them anyway.
They will be ready to store or eat cold. There are several variations of this recipe. For example, you can bake them for 40 minutes, and then serve them hot.
Friday, January 1, 2010
Intermittent fasting and reduced inflammation
A recent post on the Primal Wisdom blog led me to do go back to some of the research on an approach to dieting that I tried myself, with some positive results. The approach is known as intermittent fasting (IF). I also found an excellent blog post by Dr. Michael Eades on IF (see here).
Typically IF involves fasting every other day. On the non-fasting days, food and water consumption is not restricted in any way. On fasting days, only water is consumed. Variations of this approach usually involve replacing water with juice, and having an eating window of only a few hours within longer periods – e.g., fasting 19 hours and then eating during a window of 5 hours, for each period of 24 hours.
IF is different from calorie restriction (CR), in that in the latter total daily calorie intake is restricted to a somewhat fixed amount, below one’s basal metabolic rate (the number of calories needed to maintain one’s current weight). In CR the calorie restriction is not normally achieved through fasting, but through careful portion size control and selection of foods based on calorie content. Having said that, some prominent CR practitioners also practice IF.
One interesting aspect of IF studies is that often they do not involve any calorie reduction in the participants' diet; that is, individuals consume the same amount of calories that they would if they were not fasting at all. In other words, they consume 2X outside their fasting window; where X would be their normal caloric consumption without fasting.
Yet, the benefits of IF are still achieved. For example, during Ramadan, the levels of inflammation markers and factors, such as C-reactive protein (CRP) and homocysteine, go down, and remain low for several weeks after IF is interrupted. These inflammation markers and factors are known to be strongly associated with heart disease.
In fact, animal studies suggest that virtually identical benefits can be obtained through IF in terms of increased lifespan and disease resistance, as those normally associated with CR. Again, this is somewhat surprising because often IF does not involve any reduction in calories consumed.
Fasting promotes increased levels of growth hormone in humans. A decline in growth hormone levels is associated with aging. Thus, increased circulating growth hormones may be one of the mechanisms by which IF may affect lifespan.
There have been some reports of IF being associated with negative effects on health, but I suspect that they are associated with gorging on refined carbohydrates and sugars during the eating window. Refined carbohydrates and sugars promote inflammation, and IF reduces inflammation. It is conceivable that a very high consumption of refined carbohydrates and sugars during the eating window may completely negate the benefits of IF, particularly if one is doing a half-hearted version of IF to start with.
A combination of IF and a diet low in refined carbohydrates and sugars probably makes sense in terms of our evolved physiology. Our Stone Age ancestors had to fast on a regular basis, based on the availability of food – there were no refrigerators or grocery stores during the vast majority of our evolutionary history as a species. When food was available, it was consumed to satiety. In other words, our Stone Age ancestors practiced IF, against their will. Because of that, this is the state in which our body evolved to operate optimally.
If you watch enough episodes of the TV show Survivorman, you will probably notice that it is very unlikely that our Stone Age ancestors had access to enough calories to survive on plant foods only, assuming that they faced problems similar to those in the show.
Our digestive tract has evolved over millions of years from a mostly vegetarian diet, practiced by our Australopithecine ancestors, to a primarily carnivorous diet, adopted by human ancestors as far back as Homo erectus, and probably Homo habilis. Given that, only the recent invention of refined carbohydrates and sugars has given us access to enough dense carbohydrate sources of calories.
So, a combination of IF and a diet low in (or devoid of) refined carbohydrates and sugars makes evolutionary sense, and is probably why so many people who adopt Paleolithic diets see so many improvements in health markers such as inflammation markers, blood pressure, and HDL cholesterol.
Typically IF involves fasting every other day. On the non-fasting days, food and water consumption is not restricted in any way. On fasting days, only water is consumed. Variations of this approach usually involve replacing water with juice, and having an eating window of only a few hours within longer periods – e.g., fasting 19 hours and then eating during a window of 5 hours, for each period of 24 hours.
IF is different from calorie restriction (CR), in that in the latter total daily calorie intake is restricted to a somewhat fixed amount, below one’s basal metabolic rate (the number of calories needed to maintain one’s current weight). In CR the calorie restriction is not normally achieved through fasting, but through careful portion size control and selection of foods based on calorie content. Having said that, some prominent CR practitioners also practice IF.
One interesting aspect of IF studies is that often they do not involve any calorie reduction in the participants' diet; that is, individuals consume the same amount of calories that they would if they were not fasting at all. In other words, they consume 2X outside their fasting window; where X would be their normal caloric consumption without fasting.
Yet, the benefits of IF are still achieved. For example, during Ramadan, the levels of inflammation markers and factors, such as C-reactive protein (CRP) and homocysteine, go down, and remain low for several weeks after IF is interrupted. These inflammation markers and factors are known to be strongly associated with heart disease.
In fact, animal studies suggest that virtually identical benefits can be obtained through IF in terms of increased lifespan and disease resistance, as those normally associated with CR. Again, this is somewhat surprising because often IF does not involve any reduction in calories consumed.
Fasting promotes increased levels of growth hormone in humans. A decline in growth hormone levels is associated with aging. Thus, increased circulating growth hormones may be one of the mechanisms by which IF may affect lifespan.
There have been some reports of IF being associated with negative effects on health, but I suspect that they are associated with gorging on refined carbohydrates and sugars during the eating window. Refined carbohydrates and sugars promote inflammation, and IF reduces inflammation. It is conceivable that a very high consumption of refined carbohydrates and sugars during the eating window may completely negate the benefits of IF, particularly if one is doing a half-hearted version of IF to start with.
A combination of IF and a diet low in refined carbohydrates and sugars probably makes sense in terms of our evolved physiology. Our Stone Age ancestors had to fast on a regular basis, based on the availability of food – there were no refrigerators or grocery stores during the vast majority of our evolutionary history as a species. When food was available, it was consumed to satiety. In other words, our Stone Age ancestors practiced IF, against their will. Because of that, this is the state in which our body evolved to operate optimally.
If you watch enough episodes of the TV show Survivorman, you will probably notice that it is very unlikely that our Stone Age ancestors had access to enough calories to survive on plant foods only, assuming that they faced problems similar to those in the show.
Our digestive tract has evolved over millions of years from a mostly vegetarian diet, practiced by our Australopithecine ancestors, to a primarily carnivorous diet, adopted by human ancestors as far back as Homo erectus, and probably Homo habilis. Given that, only the recent invention of refined carbohydrates and sugars has given us access to enough dense carbohydrate sources of calories.
So, a combination of IF and a diet low in (or devoid of) refined carbohydrates and sugars makes evolutionary sense, and is probably why so many people who adopt Paleolithic diets see so many improvements in health markers such as inflammation markers, blood pressure, and HDL cholesterol.
Wednesday, December 23, 2009
Half-hearted Atkins diet and cardiovascular disease
I would like to comment on a recent article comparing the Atkins, Ornish and South Beach
An excellent post by Michael Eades clarifies a number of issues with the study, including what one could argue is the study's main flaw. Apparently the study compared a half-hearted Atkins diet, with probably equally half-hearted Ornish andSouth Beach
I refer to the study's Atkins diet as half-hearted because it seems to rely on a daily consumption of between 120 and 180 grams of carbohydrates. This is unlikely to lead to ketosis, the cornerstone of the Atkins diet, where the body uses ketone bodies (made from dietary as well as body fat) as a source of energy.
As I see it, the main findings of the study were that the participants in the half-hearted Atkins diet, after a period of 4 weeks on the diet, and when compared with the participants in the other diets, had: (a) greater levels of total cholesterol and LDL cholesterol, with only a small improvement in their HDL cholesterol and triglycerides levels; and (b) greater levels of markers for inflammation (e.g., C-reactive protein).
The participants were young and healthy. Their average age was 30.6 years, and their average body mass index was 22.6. On average, their total cholesterol was 184.9 mg/dL, triglycerides were 78.1 mg/dL, LDL cholesterol was 107.2 mg/dL, and HDL cholesterol was 62.2 mg/dL. These are arguably fairly healthy numbers; although quite a few doctors might want to put most of these folks preventively on statins because of their LDL being greater than 100.
What I find interesting about this study, and consistent with both my own experience and also a theory that I have, is that it suggests that a low carb. diet has to really be low carb. in order to bring about the benefits that one normally sees as a result of a diet that induces ketosis. A diet with, say, > 150 g of refined grains per day, is not really a low carb. diet.
Again, in my experience, and that of many other people, a truly low carb. diet (very low in, if not devoid of, refined carbs and sugars), will lead to an impressive increase in HDL cholesterol (especially for those who have low HDL to start with), an equally impressive decrease in triglycerides, increased insulin sensitivity, and possibly a decrease in LDL.
However, a half-hearted Atkins diet may actually lead to elevated LDL (of the small-dense type), and more inflammation, just like this study suggests it does, without the benefits regarding HDL and trigs. The reason is that the still relatively high level of carbohydrate intake, especially if it comes in the form of refined carbs. and sugars, will lead to higher levels of insulin being secreted into the bloodstream. This will promote increased body fat deposition. The extra saturated fat being consumed will be turned into body fat, and not used as energy, starving the cells and leading to increased hunger.
A diet rich in saturated fat may indeed be bad when it is also a diet even moderately rich in insulin-boosting, easily digestible carbs. This may be one of the main reasons why there have been so many studies in the past showing a correlation between saturated fat consumption and heart disease; studies that typically did not control for carbohydrate consumption.
In a recent interview on the Livin' La Vida Low-Carb Blog, Dr. John Salerno goes into more detail regarding this issue, recommending a much more rigid adoption of the Atkins diet than many think is okay. (In fact, I often talk to people who think that if they cut a very high carb. intake in half - e.g., from 400 to 200 grams per day - replacing the carbs with fat, they will be halfway into a full blown Atkins diet.) Dr. Salerno has worked in the past with Dr. Atkins. He calls his diet the Silver Cloud Diet. I am not sure I agree with all that Dr. Salerno had to say, but his argument in favor of a diet very low in carbs. does make sense to me.
Finally, I think that it is dangerous to extrapolate the results of any study, no matter how comprehensive, to the population in general. Each individual is unique in terms of his or her genetic makeup and life history; the latter also influences metabolic patterns. (Even identical twins raised together may display different metabolic patterns, because of their different life histories.) So, while a low carb. diet may work well for a lot of people, it may have very negative effects on a few. Increases in inflammation markers and adverse effects on LDL cholesterol (especially when LDL is measured directly, accounting for particle numbers and sizes) are warning signs that any low carb. dieter should pay attention to.
Reference:
Miller, M. et al. (2009). Comparative effects of three popular diets on lipids, endothelial function, and c-reactive protein during weight maintenance. Journal of the American Dietetic Association, 109, 713-717.
An excellent post by Michael Eades clarifies a number of issues with the study, including what one could argue is the study's main flaw. Apparently the study compared a half-hearted Atkins diet, with probably equally half-hearted Ornish and
I refer to the study's Atkins diet as half-hearted because it seems to rely on a daily consumption of between 120 and 180 grams of carbohydrates. This is unlikely to lead to ketosis, the cornerstone of the Atkins diet, where the body uses ketone bodies (made from dietary as well as body fat) as a source of energy.
As I see it, the main findings of the study were that the participants in the half-hearted Atkins diet, after a period of 4 weeks on the diet, and when compared with the participants in the other diets, had: (a) greater levels of total cholesterol and LDL cholesterol, with only a small improvement in their HDL cholesterol and triglycerides levels; and (b) greater levels of markers for inflammation (e.g., C-reactive protein).
The participants were young and healthy. Their average age was 30.6 years, and their average body mass index was 22.6. On average, their total cholesterol was 184.9 mg/dL, triglycerides were 78.1 mg/dL, LDL cholesterol was 107.2 mg/dL, and HDL cholesterol was 62.2 mg/dL. These are arguably fairly healthy numbers; although quite a few doctors might want to put most of these folks preventively on statins because of their LDL being greater than 100.
What I find interesting about this study, and consistent with both my own experience and also a theory that I have, is that it suggests that a low carb. diet has to really be low carb. in order to bring about the benefits that one normally sees as a result of a diet that induces ketosis. A diet with, say, > 150 g of refined grains per day, is not really a low carb. diet.
Again, in my experience, and that of many other people, a truly low carb. diet (very low in, if not devoid of, refined carbs and sugars), will lead to an impressive increase in HDL cholesterol (especially for those who have low HDL to start with), an equally impressive decrease in triglycerides, increased insulin sensitivity, and possibly a decrease in LDL.
However, a half-hearted Atkins diet may actually lead to elevated LDL (of the small-dense type), and more inflammation, just like this study suggests it does, without the benefits regarding HDL and trigs. The reason is that the still relatively high level of carbohydrate intake, especially if it comes in the form of refined carbs. and sugars, will lead to higher levels of insulin being secreted into the bloodstream. This will promote increased body fat deposition. The extra saturated fat being consumed will be turned into body fat, and not used as energy, starving the cells and leading to increased hunger.
A diet rich in saturated fat may indeed be bad when it is also a diet even moderately rich in insulin-boosting, easily digestible carbs. This may be one of the main reasons why there have been so many studies in the past showing a correlation between saturated fat consumption and heart disease; studies that typically did not control for carbohydrate consumption.
In a recent interview on the Livin' La Vida Low-Carb Blog, Dr. John Salerno goes into more detail regarding this issue, recommending a much more rigid adoption of the Atkins diet than many think is okay. (In fact, I often talk to people who think that if they cut a very high carb. intake in half - e.g., from 400 to 200 grams per day - replacing the carbs with fat, they will be halfway into a full blown Atkins diet.) Dr. Salerno has worked in the past with Dr. Atkins. He calls his diet the Silver Cloud Diet. I am not sure I agree with all that Dr. Salerno had to say, but his argument in favor of a diet very low in carbs. does make sense to me.
Finally, I think that it is dangerous to extrapolate the results of any study, no matter how comprehensive, to the population in general. Each individual is unique in terms of his or her genetic makeup and life history; the latter also influences metabolic patterns. (Even identical twins raised together may display different metabolic patterns, because of their different life histories.) So, while a low carb. diet may work well for a lot of people, it may have very negative effects on a few. Increases in inflammation markers and adverse effects on LDL cholesterol (especially when LDL is measured directly, accounting for particle numbers and sizes) are warning signs that any low carb. dieter should pay attention to.
Reference:
Miller, M. et al. (2009). Comparative effects of three popular diets on lipids, endothelial function, and c-reactive protein during weight maintenance. Journal of the American Dietetic Association, 109, 713-717.
Tuesday, December 22, 2009
Guest Commentary: Where are Nurse Practitioners in Health Care Reform?
Theresa Pluth Yeo, PhD, MPH, MSN, CRNP, AOCNP
Coordinator, Advanced Practice Oncology Nursing Program
Assistant Professor, Jefferson Schools of Nursing and Population Health
(Former President of the Nurse Practitioner Association of Maryland)
Cortese and Korsmo, in their September 23, 2009 article in the NEJM, observed that, “Americans do not consistently receive high-value health care. Collectively, our country spends more on health care than any other nation, but our people do not receive the best outcomes, safety, service, or access (to health care) in return.”
Our health care system is largely dominated by a plethora of specialists but deficient in primary care physicians. At a time when only 247 residency positions in primary care are available for graduating medical students per year (down 328 residency positions since 1999), over 6,000 nurse practitioners (NPs) are educated each year at more than 325 colleges and universities. Most of these NPs choose primary care or family practice settings for employment. (For the uninitiated, NPs are fully-trained and licensed registered nurses who complete a Master’s or doctoral degree as an advanced practice nurse and pass a certifying examination administered by a national board, which allows them to be licensed by state boards of nursing as a NP).
NP educational programs provide training in the diagnosis and treatment of acute minor illnesses, disease prevention, and management of stable chronic conditions. Nurse practitioners are part of the solution in health care reform and fill an important niche in providing access to a qualified health care provider for millions of Americans. NPs are a win-win for patients – NPs bring their education, compassion and experience as RNs to bear on patient care, yet they are paid less than physicians. An ever growing body of evidence points to comparable quality care – and often higher patient satisfaction – with NPs as primary health care providers. Currently there are 139,000 NPs practicing in the US.
So why is the AMA threatened by NPs? In October 2009 the AMA launched an offensive, targeting NP practice in a document entitled: AMA Scope of Practice Data Series – Nurse practitioners. The document states in part that: “The physician is responsible for the supervision of nurse practitioners and other advanced practice nurses in all settings and that the physician is responsible for managing the health care of patients in all practice settings.” This is blatantly untrue. Nursing has been a self-regulating and self-licensing profession for as long as medicine has. Why has the leadership of the AMA decided that physicians and only physicians have the “right” to assess, diagnose and treat ill persons and that all “non-physician providers” should be supervised by a physician?
The American Nurses’ Association recently issued a response to this AMA document, voicing its objection to the AMA’s attempts to change the public’s perception of NP practice as anything other than fully qualified professionals working within a legally established scope of practice. As America struggles to reconstruct its health care delivery “system,” it is unproductive for one profession to attempt to marginalize another. NPs stand ready to help meet the nation’s health care needs as collaborating partners, not as physician supervised providers. Health care reformers look our way!
Coordinator, Advanced Practice Oncology Nursing Program
Assistant Professor, Jefferson Schools of Nursing and Population Health
(Former President of the Nurse Practitioner Association of Maryland)
Cortese and Korsmo, in their September 23, 2009 article in the NEJM, observed that, “Americans do not consistently receive high-value health care. Collectively, our country spends more on health care than any other nation, but our people do not receive the best outcomes, safety, service, or access (to health care) in return.”
Our health care system is largely dominated by a plethora of specialists but deficient in primary care physicians. At a time when only 247 residency positions in primary care are available for graduating medical students per year (down 328 residency positions since 1999), over 6,000 nurse practitioners (NPs) are educated each year at more than 325 colleges and universities. Most of these NPs choose primary care or family practice settings for employment. (For the uninitiated, NPs are fully-trained and licensed registered nurses who complete a Master’s or doctoral degree as an advanced practice nurse and pass a certifying examination administered by a national board, which allows them to be licensed by state boards of nursing as a NP).
NP educational programs provide training in the diagnosis and treatment of acute minor illnesses, disease prevention, and management of stable chronic conditions. Nurse practitioners are part of the solution in health care reform and fill an important niche in providing access to a qualified health care provider for millions of Americans. NPs are a win-win for patients – NPs bring their education, compassion and experience as RNs to bear on patient care, yet they are paid less than physicians. An ever growing body of evidence points to comparable quality care – and often higher patient satisfaction – with NPs as primary health care providers. Currently there are 139,000 NPs practicing in the US.
So why is the AMA threatened by NPs? In October 2009 the AMA launched an offensive, targeting NP practice in a document entitled: AMA Scope of Practice Data Series – Nurse practitioners. The document states in part that: “The physician is responsible for the supervision of nurse practitioners and other advanced practice nurses in all settings and that the physician is responsible for managing the health care of patients in all practice settings.” This is blatantly untrue. Nursing has been a self-regulating and self-licensing profession for as long as medicine has. Why has the leadership of the AMA decided that physicians and only physicians have the “right” to assess, diagnose and treat ill persons and that all “non-physician providers” should be supervised by a physician?
The American Nurses’ Association recently issued a response to this AMA document, voicing its objection to the AMA’s attempts to change the public’s perception of NP practice as anything other than fully qualified professionals working within a legally established scope of practice. As America struggles to reconstruct its health care delivery “system,” it is unproductive for one profession to attempt to marginalize another. NPs stand ready to help meet the nation’s health care needs as collaborating partners, not as physician supervised providers. Health care reformers look our way!
Saturday, December 19, 2009
Total cholesterol and cardiovascular disease: A U-curve relationship
The hypothesis that blood cholesterol levels are positively correlated with heart disease (the lipid hypothesis) dates back to Rudolph Virchow in the mid-1800s.
One famous study that supported this hypothesis was Ancel Keys's Seven Countries Study, conducted between the 1950s and 1970s. This study eventually served as the foundation on which much of the advice that we receive today from doctors is based, even though several other studies have been published since that provide little support for the lipid hypothesis.
The graph below (source: canibaisereis.com, with many thanks to O Primitivo) shows the results of one study, involving many more countries than Key's Seven Countries Study, that actually suggests a NEGATIVE linear correlation between total cholesterol and cardiovascular disease.
Now, most relationships in nature are nonlinear, with quite a few following a pattern that looks like a U-curve (plain or inverted); sometimes called a J-curve pattern. The graph below (source also: canibaisereis.com) shows the U-curve relationship between total cholesterol and mortality, with cardiovascular disease mortality indicated through a dotted red line at the bottom.
This graph has been obtained through a nonlinear analysis, and I think it provides a better picture of the relationship between total cholesterol (TC) and mortality. Based on this graph, the best range of TC that one can be at is somewhere between 210, where cardiovascular disease mortality is minimized; and 220, where total mortality is minimized.
The total mortality curve is the one indicated through the full blue line at the top. In fact, it suggests that mortality increases sharply as TC decreases below 200.
Now, these graphs relate TC with disease and mortality, and say nothing about LDL cholesterol (LDL). In my own experience, and that of many people I know, a TC of about 200 will typically be associated with a slightly elevated LDL (e.g., 110 to 150), even if one has a high HDL cholesterol (i.e., greater than 60).
Yet, most people who have a LDL greater than 100 will be told by their doctors, usually with the best of the intentions, to take statins, so that they can "keep their LDL under control". (LDL levels are usually calculated, not measured directly, which itself creates a whole new set of problems.)
Alas, reducing LDL to 100 or less will typically reduce TC below 200. If we go by the graphs above, especially the one showing the U-curves, these folks' risk for cardiovascular disease and mortality will go up - exactly the opposite effect that they and their doctors expected. And that will cost them financially as well, as statin drugs are expensive, in part to pay for all those TV ads.
One famous study that supported this hypothesis was Ancel Keys's Seven Countries Study, conducted between the 1950s and 1970s. This study eventually served as the foundation on which much of the advice that we receive today from doctors is based, even though several other studies have been published since that provide little support for the lipid hypothesis.
The graph below (source: canibaisereis.com, with many thanks to O Primitivo) shows the results of one study, involving many more countries than Key's Seven Countries Study, that actually suggests a NEGATIVE linear correlation between total cholesterol and cardiovascular disease.
Now, most relationships in nature are nonlinear, with quite a few following a pattern that looks like a U-curve (plain or inverted); sometimes called a J-curve pattern. The graph below (source also: canibaisereis.com) shows the U-curve relationship between total cholesterol and mortality, with cardiovascular disease mortality indicated through a dotted red line at the bottom.
The total mortality curve is the one indicated through the full blue line at the top. In fact, it suggests that mortality increases sharply as TC decreases below 200.
Now, these graphs relate TC with disease and mortality, and say nothing about LDL cholesterol (LDL). In my own experience, and that of many people I know, a TC of about 200 will typically be associated with a slightly elevated LDL (e.g., 110 to 150), even if one has a high HDL cholesterol (i.e., greater than 60).
Yet, most people who have a LDL greater than 100 will be told by their doctors, usually with the best of the intentions, to take statins, so that they can "keep their LDL under control". (LDL levels are usually calculated, not measured directly, which itself creates a whole new set of problems.)
Alas, reducing LDL to 100 or less will typically reduce TC below 200. If we go by the graphs above, especially the one showing the U-curves, these folks' risk for cardiovascular disease and mortality will go up - exactly the opposite effect that they and their doctors expected. And that will cost them financially as well, as statin drugs are expensive, in part to pay for all those TV ads.
Subscribe to:
Posts (Atom)