"Krauss discovered that LDL actually comes in distinct subspecies, all characterized by still finer gradations in density and size. “It was blazingly obvious. Unignorable,” says Krauss.*49 Eventually, Krauss identified seven discrete subclasses of LDL. He also noted that the smallest and densest of the low-density lipoproteins had two significant properties: it had a strong negative correlation with HDL, and it was the subspecies that was elevated in patients with heart disease."
"What would now become apparent was that LDL cholesterol is little more than an arbitrary concept that oversimplifies its own complex diversity. The fact that LDL and LDL cholesterol are not synonymous complicates the science."
"Total cholesterol gave way to HDL and LDL cholesterol and even triglycerides. All fat gave way to animal and vegetable fat, which gave way to saturated, monounsaturated, and polyunsaturated fat, and then polyunsaturated fats branched into omega-three and omega-six polyunsaturated fats. By the mid-1980s, these new levels of complexity had still not deterred the AHA and NIH from promoting carbohydrates as effectively the antidote to heart disease, and either all fats or just saturated fats as the dietary cause."
"Everything should be made as simple as possible,” Albert Einstein once supposedly said, “but no simpler.” Our understanding of the nutritional causes of heart disease started with Keys’s original oversimplification that heart disease is caused by the effect of all dietary fat on total serum cholesterol."
Gary Taubes from chapter nine of "Good Calories, Bad Calories"
This book is a tough, magnificent read. I kept reading and re-reading this section to try to nail it down. The takeaways - LDL cholesterol is an imprecise term. Diabetics and heart disease patients are most likely to have this profile: high triglycerides, high levels of small dense LDL and low HDL. The easiest way to treat this profile is through carbohydrate restriction. Even those with the genetic predisposition to this 'atherogenic profile' can see a reduction in the severity of their profile through sensible carbohydrate intake.
Unlike statins, carbohydrate restriction has no known adverse side effects.
Sunday, January 9, 2011
Saturday, January 8, 2011
What Works Best - Statins or a Porterhouse?
Worried about your health, your heart disease risk and your blood lipids? You gotta get a steak tonight ...
"Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein.*48 Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.) The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon."
Gary Taubes, "Good Calories Bad Calories"
"Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein.*48 Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.) The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon."
Gary Taubes, "Good Calories Bad Calories"
Friday, January 7, 2011
Early to Bed, Early to Rise ... Part 1
http://www.ncbi.nlm.nih.gov/pubmed/20837645
This is a great example of how complicated it is to do good science on humans, including how assumptions can confound an otherwise interesting study.
The abstract starts off with this interesting assumption: "A fat-rich energy-dense diet is an important cause of insulin resistance." I don't have the subscription to the publication journal, but I would really love to see how they justify this statement. What's their definition of "fat rich"? What exactly are the parameters of "energy dense"? What's interesting about these terms is the implications in a real person's diet. For example, try to eat a fat rich, low carb diet, and you find you don't eat a great deal of total "energy". Why? Hunger is very well controlled on a fat rich, carb restricted (50g/day or less) diet. If you eat a small amount of an "energy dense" food like coconut oil, that WILL NOT make you insulin resistant. Ever eat a large quantity of butter without any sugar? Probably not, with the possible exception of macadamia nuts! (In fact, if you overeat fat by too large a margin, you'll have enough diarrhea to discourage this practice). I'd venture a guess that, assuming you could eat "too much" coconut oil/butter/cheese/full fat dairy, it still would not make you insulin resistant (by the way, I'm betting my life on this answer because that's how I eat). What makes a person insulin resistant is eating a bunch of grain products, whole or otherwise, and/or food laden in sugars (and fructose is specifically implicated in the genesis of insulin resistance - beautiful explanation of why is available at this link: Lustig on Fructose). The fact is that we often eat a lot of fat when we're eating a lot of grains/sugars, but that's a different case entirely than when one eats low carb (50g/day or less), adequate protein (minimum 60g/day), and good fats to satiety.
Switching back to the study, I'm skeptical when anyone starts off with terms like "energy dense" or "fat laden" because this is the language of those who have led the science of diet into demonstrably poor science for the last 30+ years, the same flavor of science that has, incredibly, accepted the conjecture that high fat diets cause heart disease, and that weight gain can be simplified to a restatement of the First Law of Thermodynamics (which is not relevant for determining causality in human weight gain).
The study took three groups, all of which were fed a "Healthy male volunteers (18-25 y) received a hyper-caloric (∼+30% kcal day(-1)) fat-rich (50% of kcal) diet for 6 weeks." In other words, they tried to over-feed the subjects by 30%, using a diet of 50% fat (which they think is a high level of fat).
In short, one group didn't exercise and gained six pounds. Another group exercised in a fasted state and gained almost no weight. The third group ingested carbs prior to exercise (IOW, exercised but not in a fasted state) and wound up about in the middle of the three groups. The three groups had similarly different outcomes in terms of other measures of health (insulin sensitivity, et al).
Interesting result - two groups had equal intake, and equal exercise but different outcomes for weight gain and health markers. Why? How could the "calorie is a calorie" model be true if this study proves repeatable (and therefore valid)?
In other words, what use can we make of the implications of this study? That's a tough question, because as is so often the case, there are many "complexifiers." For example - what would have happened had they used only protein/fat in the pre-workout "fast break"? What would have happened if they used 100g/day or less of carbohydrate? What if the long endurance training sessions had been either shorter, or shorter but more intense (anaerobic), or had incorporated resistance training? The mental experiments we could imagine would fill up a large chart with possible options to be tested. Unless you think it's a great idea to burn up four hours a week doing pointless and possibly injurious cardiovascular training, knowing that you can "overeat" by 30% if you train in the fasted state is not a useful data point.
In part 2, I'll superimpose this study result with the Paleolithic Model, to see if the two can be reconciled.
This is a great example of how complicated it is to do good science on humans, including how assumptions can confound an otherwise interesting study.
The abstract starts off with this interesting assumption: "A fat-rich energy-dense diet is an important cause of insulin resistance." I don't have the subscription to the publication journal, but I would really love to see how they justify this statement. What's their definition of "fat rich"? What exactly are the parameters of "energy dense"? What's interesting about these terms is the implications in a real person's diet. For example, try to eat a fat rich, low carb diet, and you find you don't eat a great deal of total "energy". Why? Hunger is very well controlled on a fat rich, carb restricted (50g/day or less) diet. If you eat a small amount of an "energy dense" food like coconut oil, that WILL NOT make you insulin resistant. Ever eat a large quantity of butter without any sugar? Probably not, with the possible exception of macadamia nuts! (In fact, if you overeat fat by too large a margin, you'll have enough diarrhea to discourage this practice). I'd venture a guess that, assuming you could eat "too much" coconut oil/butter/cheese/full fat dairy, it still would not make you insulin resistant (by the way, I'm betting my life on this answer because that's how I eat). What makes a person insulin resistant is eating a bunch of grain products, whole or otherwise, and/or food laden in sugars (and fructose is specifically implicated in the genesis of insulin resistance - beautiful explanation of why is available at this link: Lustig on Fructose). The fact is that we often eat a lot of fat when we're eating a lot of grains/sugars, but that's a different case entirely than when one eats low carb (50g/day or less), adequate protein (minimum 60g/day), and good fats to satiety.
Switching back to the study, I'm skeptical when anyone starts off with terms like "energy dense" or "fat laden" because this is the language of those who have led the science of diet into demonstrably poor science for the last 30+ years, the same flavor of science that has, incredibly, accepted the conjecture that high fat diets cause heart disease, and that weight gain can be simplified to a restatement of the First Law of Thermodynamics (which is not relevant for determining causality in human weight gain).
The study took three groups, all of which were fed a "Healthy male volunteers (18-25 y) received a hyper-caloric (∼+30% kcal day(-1)) fat-rich (50% of kcal) diet for 6 weeks." In other words, they tried to over-feed the subjects by 30%, using a diet of 50% fat (which they think is a high level of fat).
In short, one group didn't exercise and gained six pounds. Another group exercised in a fasted state and gained almost no weight. The third group ingested carbs prior to exercise (IOW, exercised but not in a fasted state) and wound up about in the middle of the three groups. The three groups had similarly different outcomes in terms of other measures of health (insulin sensitivity, et al).
Interesting result - two groups had equal intake, and equal exercise but different outcomes for weight gain and health markers. Why? How could the "calorie is a calorie" model be true if this study proves repeatable (and therefore valid)?
In other words, what use can we make of the implications of this study? That's a tough question, because as is so often the case, there are many "complexifiers." For example - what would have happened had they used only protein/fat in the pre-workout "fast break"? What would have happened if they used 100g/day or less of carbohydrate? What if the long endurance training sessions had been either shorter, or shorter but more intense (anaerobic), or had incorporated resistance training? The mental experiments we could imagine would fill up a large chart with possible options to be tested. Unless you think it's a great idea to burn up four hours a week doing pointless and possibly injurious cardiovascular training, knowing that you can "overeat" by 30% if you train in the fasted state is not a useful data point.
In part 2, I'll superimpose this study result with the Paleolithic Model, to see if the two can be reconciled.
Wednesday, January 5, 2011
More on D from Dr. Dowd
"Vitamin D replacement is suggested in patients with levels less than 30 ng/mL with a target of 40-65 ng/mL as would be found in wild primates and in life guards and non-mechanized farmers who work in the sun. Nobody is suggesting replacing vitamin D in people with normal levels. Based on data compiled by Dr. Reinhold Vieth, there are no credible reports of toxicity in adults with levels under 200 ng/mL. The safety window for vitamin D is seven times greater than the threshold of normal. We are vitamin D deficient because we spend no time outside in the sun unprotected by clothing or sun screen, like our Paleolithic ancestors. Moreover, we do not eat the wild animal protein, wild seafood, and particularly organ meat that we evolved on, which was high in vitamin D.
"Vitamin D supplementation is required by most Americans because we are rarely exposed to sun and our diets are filled with grain-based carbohydrates that are devoid of nutrition. Moreover, vitamin D is stored in fat and only liberated with moderate or intense exercise, something that most Americans do not do. Our lifestyle is a perfect storm for vitamin D deficiency."
http://www.thevitamindcure.com/blog/?p=151
Keep in mind that vitamin D supplementation is VERY inexpensive, but only gel caps will provide benefit; tablets can work, but require that you take them with a fat source. Also, most tablets seem to give a very small dose in a relatively large tablet, so they are much harder to take, especially for children.
How much do you need? Enough to get your measured blood levels where you want them, and there's really no shortcut here - you have to get measurements if you want to know how much you need. 6000 iu gets me to the low end of the desired range - I'm going to remeasure at the end of winter, and adjust my intake next winter accordingly.
Tuesday, January 4, 2011
Favorites from the Past Year
Evidence about saturated fat: http://tierneylab.blogs.nytimes.com/2008/07/21/good-news-on-saturated-fat/?pagemode=print
About calcium, and/or osteoporosis:
More about the cancer v. sun exposure math problem:
Vitamin D Supplementation, Critical: Getting vitamin D right
Best summary of why one change - carb restriction to help you become a fat burner vice a sugar burner - will positively effect every aspect of your health and life, and help you steer clear of the diseases of the west:
http://articles.mercola.com/sites/articles/archive/2001/07/14/insulin-part-one.aspx This transcript of a speech by Dr. Rosedale is almost ten years old, but the only part that's dated is his fear of saturated fat.
Another Cat Skinner
http://heartscanblog.blogspot.com/2010/12/i-lost-37-lbs-with-fingerstick.html
Dr. Davis details how he's used a glucose meter to help folks get healthy, when they couldn't otherwise follow his dietary recommendations.
He starts folks off with nothing more than elimination of wheat and sugar. For those who cannot comply, sometimes the jolting reality of watching their blood sugar levels skyrocket one hour after ingestion of the food is the reality check needed to get a behavior change.
This is brilliant!!
"Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.
"What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.
"Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger."
Dr. Davis details how he's used a glucose meter to help folks get healthy, when they couldn't otherwise follow his dietary recommendations.
He starts folks off with nothing more than elimination of wheat and sugar. For those who cannot comply, sometimes the jolting reality of watching their blood sugar levels skyrocket one hour after ingestion of the food is the reality check needed to get a behavior change.
This is brilliant!!
"Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.
"What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.
"Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger."
The column is worth reading in entirety, and the glucose meters are an easy way to give yourself another tool in pursuit of renewed health.
Monday, January 3, 2011
Heart Scan On LDL Type
The two kinds of small LDL
Another home run from Dr. Davis in which he highlights the origins of small LDL (considered to be markers of atherosclerotic process, unlike large, fluffy LDL), which is either from a bad hand in the genetics department, or overconsumption of carbohydrates. He finds his patients see the most dramatic results by eliminating wheat, cornstarch, and sucrose.
Why are the small, dense LDL a worry? We don't know for sure. They just be a marker of an underlying, systemic inflammatory cascade. But as Dr. D reports, small LDL:
"--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.
--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.
--Small LDLs are more glycation-prone.
--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall."
What's the take away? You can measure the impact of carb over consumption via triglyceride levels, low HDL, high blood pressure, abdominal fat, hyper glycemia, a high A1c, AND by a large number of small, dense LDL. All of these markers are correlates with CVD and other diseases of civilization. They can all be down regulated by decreased carb consumption - 100g per day or less. The actual dose that will serve you best depends upon your genetic tolerance for carbs, the damage you've done to yourself from carb overdoses (how much, how long), and/or how long you've been restricting carb intake (the body heals, and over time folks seem to recover some carb tolerance).
Are you ready to change your health in 2011? Call me at 901-489-5856 and let's schedule a conference to assess your situation and decide if we can work together to maximize your health, physical performance and mental performance. It's an approach that works because you don't have to overcome hunger, and within a couple of weeks, you will look, feel and perform so much better, you'll work hard to sustain your success!
Another home run from Dr. Davis in which he highlights the origins of small LDL (considered to be markers of atherosclerotic process, unlike large, fluffy LDL), which is either from a bad hand in the genetics department, or overconsumption of carbohydrates. He finds his patients see the most dramatic results by eliminating wheat, cornstarch, and sucrose.
Why are the small, dense LDL a worry? We don't know for sure. They just be a marker of an underlying, systemic inflammatory cascade. But as Dr. D reports, small LDL:
"--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.
--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.
--Small LDLs are more glycation-prone.
--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall."
What's the take away? You can measure the impact of carb over consumption via triglyceride levels, low HDL, high blood pressure, abdominal fat, hyper glycemia, a high A1c, AND by a large number of small, dense LDL. All of these markers are correlates with CVD and other diseases of civilization. They can all be down regulated by decreased carb consumption - 100g per day or less. The actual dose that will serve you best depends upon your genetic tolerance for carbs, the damage you've done to yourself from carb overdoses (how much, how long), and/or how long you've been restricting carb intake (the body heals, and over time folks seem to recover some carb tolerance).
Are you ready to change your health in 2011? Call me at 901-489-5856 and let's schedule a conference to assess your situation and decide if we can work together to maximize your health, physical performance and mental performance. It's an approach that works because you don't have to overcome hunger, and within a couple of weeks, you will look, feel and perform so much better, you'll work hard to sustain your success!
Subscribe to:
Comments (Atom)