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| Healthcare rankings. |
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| I highlighted Great Britain in green. |
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| Cancer mortality. |
Sunday, 29 June 2014
Some fascinating healthcare statistics: Article by Ezra Klein.
Spotted on Twitter. From Is America better at treating cancer than Europe? , by Ezra Klein.
Friday, 27 June 2014
Saturated fats Saturated fats Saturated fats.
George Henderson left the following comment. I think that the information in it deserves a bigger audience.
Saturated fats seem to get the blame for everything nowadays. "Saturated fats clogged my arteries". "Saturated fats gave me cancer". "Saturated fats stole my job". O.K, I've done that joke before.
There are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats and there are saturated fats. Saturated fats are an ester of Glycerol (a 3-carbon alcohol) and three saturated fatty acids (SFA's). There are roughly six categories of SFA's.
1) Short chain SFA's such as Acetic acid, Propionic acid, Butyric acid (found in butter and also what soluble fibre ferments into in the colon) and Caproic acid.
2) Medium chain SFA's such as Caprylic acid, Capric acid, Lauric acid and Myristic acid.
3) Long chain SFA's such as Stearic acid.
4) SFA's behaving like Palmitic acid.
5) Odd chain SFA's such as Pentadecylic acid and Margaric acid.
6) Very long chain SFA's such as Behenic acid.
See http://en.wikipedia.org/wiki/List_of_saturated_fatty_acids
In foods, the above SFA's are associated with different things.
1) and 2) don't get associated with much polyunsaturated fatty acids (PUFA's), e.g. dairy and tropical nuts.
3) and 4) are more likely to be associated with long-chain PUFA's, e.g. meats, poultry, temperate nuts.
5) is associated with CLA and not much PUFA's, e.g. dairy from grass-fed animals.
See also Siri-Tarino et al, Forests & Trees and "Eureka!" moments and Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.
Saturated fats seem to get the blame for everything nowadays. "Saturated fats clogged my arteries". "Saturated fats gave me cancer". "Saturated fats stole my job". O.K, I've done that joke before.
There are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats and there are saturated fats. Saturated fats are an ester of Glycerol (a 3-carbon alcohol) and three saturated fatty acids (SFA's). There are roughly six categories of SFA's.
1) Short chain SFA's such as Acetic acid, Propionic acid, Butyric acid (found in butter and also what soluble fibre ferments into in the colon) and Caproic acid.
2) Medium chain SFA's such as Caprylic acid, Capric acid, Lauric acid and Myristic acid.
3) Long chain SFA's such as Stearic acid.
4) SFA's behaving like Palmitic acid.
5) Odd chain SFA's such as Pentadecylic acid and Margaric acid.
6) Very long chain SFA's such as Behenic acid.
See http://en.wikipedia.org/wiki/List_of_saturated_fatty_acids
In foods, the above SFA's are associated with different things.
1) and 2) don't get associated with much polyunsaturated fatty acids (PUFA's), e.g. dairy and tropical nuts.
3) and 4) are more likely to be associated with long-chain PUFA's, e.g. meats, poultry, temperate nuts.
5) is associated with CLA and not much PUFA's, e.g. dairy from grass-fed animals.
See also Siri-Tarino et al, Forests & Trees and "Eureka!" moments and Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.
Thursday, 26 June 2014
How a B.Sc.(Hons) in Electronic Engineering is relevant to Diet & Nutrition.
The human body regulates various processes using negative feedback loops. Here's blood glucose regulation.
Here's a generic Hypothalamus-Pituitary-X Axis loop, where X may be thyroid, adrenal, gonadal etc.
Electronic Engineers understand how negative feedback systems work, such as phase-locked loops & amplifiers.
Negative feedback control systems can overshoot, especially if there's a delay in the feedback path that's longer than the rise time of the input step.
An example of this is the first-phase insulin response. Loss of the first-phase insulin response occurs in over-fat people who are hyperinsulinaemic. Without the first-phase insulin response, there's a delay between an increase in blood glucose and an increase in insulin secretion. A rapid upwards step in blood glucose (say, from eating a high-GL meal) causes a massive overshoot in insulin secretion, resulting in postprandial sleepiness, also down-regulation of insulin receptor activity in the appetite centres of the brain, causing ravenous hunger when the insulin level falls to normal.
See also Blood Glucose, Insulin & Diabetes.
People shouldn't be too quick to write-off the knowledge of an Electronic Engineer who's delving into the mysteries of the human body.
 |
| From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387 |
Here's a generic Hypothalamus-Pituitary-X Axis loop, where X may be thyroid, adrenal, gonadal etc.
 |
| From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387 |
Negative feedback control systems can overshoot, especially if there's a delay in the feedback path that's longer than the rise time of the input step.
An example of this is the first-phase insulin response. Loss of the first-phase insulin response occurs in over-fat people who are hyperinsulinaemic. Without the first-phase insulin response, there's a delay between an increase in blood glucose and an increase in insulin secretion. A rapid upwards step in blood glucose (say, from eating a high-GL meal) causes a massive overshoot in insulin secretion, resulting in postprandial sleepiness, also down-regulation of insulin receptor activity in the appetite centres of the brain, causing ravenous hunger when the insulin level falls to normal.
See also Blood Glucose, Insulin & Diabetes.
People shouldn't be too quick to write-off the knowledge of an Electronic Engineer who's delving into the mysteries of the human body.
Wednesday, 25 June 2014
The Conflation Game.
Li-i-ife, is the name of the game, and I wanna play the game with you.....
People have been "grinding my gears" by conflating carbohydrates with sugars. All sugars are carbohydrates, but not all carbohydrates are sugars. See Carbs Carbs Carbs. to find out about the five basic different types of carbohydrates.
Krauss et al has been "at it" again. In Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia, at the bottom of Table 1 is "carbohydrate, 50% simple and 50% complex". The carbohydrates consisted of half simple (probably fructose, as that has the worst effect on particle size) and half starches (probably maltodextrin, as it rapidly hydrolyses into glucose).
The effect of such a sugary diet is as follows:-
The percentage of pattern B (small, dense) LDL particles increases significantly in proportion to the percentage of Dietary "carbohydrate". The implication of this study (also A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins ) is that high-carb, low-fat diets are atherogenic.
I call "Shenanigans".
A high sugar diet is atherogenic, but carbohydrates from potatoes, rice, sweet potatoes/yams & beans (if not overcooked), actual whole grains (i.e not flour) & whole fruits aren't.
People have been "grinding my gears" by conflating carbohydrates with sugars. All sugars are carbohydrates, but not all carbohydrates are sugars. See Carbs Carbs Carbs. to find out about the five basic different types of carbohydrates.
Krauss et al has been "at it" again. In Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia, at the bottom of Table 1 is "carbohydrate, 50% simple and 50% complex". The carbohydrates consisted of half simple (probably fructose, as that has the worst effect on particle size) and half starches (probably maltodextrin, as it rapidly hydrolyses into glucose).
The effect of such a sugary diet is as follows:-
The percentage of pattern B (small, dense) LDL particles increases significantly in proportion to the percentage of Dietary "carbohydrate". The implication of this study (also A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins ) is that high-carb, low-fat diets are atherogenic.
I call "Shenanigans".
A high sugar diet is atherogenic, but carbohydrates from potatoes, rice, sweet potatoes/yams & beans (if not overcooked), actual whole grains (i.e not flour) & whole fruits aren't.
Guest post: Denialism as Pseudoscientific Thinking.
In pseudoscience there’s a subtype called Denialism. Denialism seeks to deny an established science and violate multiple principles of logic, and scientific methodology, this is mostly because of a priori beliefs and preconceptions. Typically the same cognitive and logical errors are committed in denialism reasoning.
The whole process starts with a desired conclusion, that a generally accepted scientific or historical claim is not true. Denialists have ideological reasons, and engage in motivated reasoning, rationalizing away the undesired claim.
In essence and practical terms, they work backward from their desired conclusion, filling in justifications.
In moving the goalposts, they always demand more evidence for a claim, even if currently available. However when that burden of evidence is met, the goalposts are moved and more evidence is demanded.
They may use vagueness in defining a certain term to move the goalpost away from any possible dis-confirming evidence.
Because science has gaps, they explore them as if it the specific scientific theory being discussed is invalid or not well established.
Let’s take the example of HIV denial. Deniers often demand a single study or scientific paper establishing HIV as the cause of AIDS. However, it is not established by a single study but rather by a large body of evidence.
In scientific reasoning we must see if the gaps are slowly being filled, and if predictions are met, and if it fits together with other lines of evidence, observational or experimental.
If a theory has been going around in circles and not progressing, that is a strong indication of pseudoscience.
Disagreements within a discipline are explored, often small details, as if the science in question is not solid.
Another strategy the narrowing of evidence that may count as “scientific”. The most common is using the logical fallacy of confusing correlation with causation.
Correlation is not the same as causation, not necessarily anyway. Correlations need to be used properly, and multiple correlations can triangulate a specific causal relationship observed in a correlation. Epidemiology is based on correlations and observational evidence, if they were invalid the entire field simply would vanish.
They can even deny all historical sciences such as astronomy, geology, or even forensics.
This is an argument from ignorance. If a version of events is not true then the alternate claim or version must be. However, they rarely provide positive evidence for their alternate claim.
Little factoids can be gathered and taken out of context. The goal is to sow doubt, uncertainty, and distrust, focusing on apparent inconsistencies, or gaps. However in healthy skepticism we consider all the evidence in the proper perspective, and even though knowledge is incomplete, reliable conclusions can be achieved.
As a last resort comes the conspiracy theory, claiming that the scientific evidence itself is fraudulent, a grand conspiracy. This tactic allows them to dismiss all the evidence and rationalize it away.
Grant, John. Denying Science. Amherst: Prometheus Books, 2011.
Novella, Steven. “More on God of the Gaps.” NeuroLogica Blog. http://theness.com/neurologicablog/index.php/more-on-god-of-the-gaps
Novella, Steven. “Skepticism and Denial.” The NESS. http://www.theness.com/index.php/skepticism-and-denial
Specter, Michael. Denialism: How Irrational Thinking Hinders Scientific Progress, Harms the Planet, and Threatens Our Lives. London: Penguin Press, 2009
Tokuno, Hajime. “Holocaust Denial.” The NESS. http://www.theness.com/index.php/holocaust-denial
For more information on Sérgio Fontinhas, see Big Fitness Project.
The whole process starts with a desired conclusion, that a generally accepted scientific or historical claim is not true. Denialists have ideological reasons, and engage in motivated reasoning, rationalizing away the undesired claim.
In essence and practical terms, they work backward from their desired conclusion, filling in justifications.
1. Moving the goalposts
In moving the goalposts, they always demand more evidence for a claim, even if currently available. However when that burden of evidence is met, the goalposts are moved and more evidence is demanded.
They may use vagueness in defining a certain term to move the goalpost away from any possible dis-confirming evidence.
2. Unreasonable demand for evidence
Because science has gaps, they explore them as if it the specific scientific theory being discussed is invalid or not well established.
Let’s take the example of HIV denial. Deniers often demand a single study or scientific paper establishing HIV as the cause of AIDS. However, it is not established by a single study but rather by a large body of evidence.
In scientific reasoning we must see if the gaps are slowly being filled, and if predictions are met, and if it fits together with other lines of evidence, observational or experimental.
If a theory has been going around in circles and not progressing, that is a strong indication of pseudoscience.
3. Pointing out disagreements
Disagreements within a discipline are explored, often small details, as if the science in question is not solid.
4. Denying entire categories of evidence
Another strategy the narrowing of evidence that may count as “scientific”. The most common is using the logical fallacy of confusing correlation with causation.
Correlation is not the same as causation, not necessarily anyway. Correlations need to be used properly, and multiple correlations can triangulate a specific causal relationship observed in a correlation. Epidemiology is based on correlations and observational evidence, if they were invalid the entire field simply would vanish.
They can even deny all historical sciences such as astronomy, geology, or even forensics.
5. False dichotomy
This is an argument from ignorance. If a version of events is not true then the alternate claim or version must be. However, they rarely provide positive evidence for their alternate claim.
6. Campaign of Doubt
Little factoids can be gathered and taken out of context. The goal is to sow doubt, uncertainty, and distrust, focusing on apparent inconsistencies, or gaps. However in healthy skepticism we consider all the evidence in the proper perspective, and even though knowledge is incomplete, reliable conclusions can be achieved.
7. Conspiracy theory
As a last resort comes the conspiracy theory, claiming that the scientific evidence itself is fraudulent, a grand conspiracy. This tactic allows them to dismiss all the evidence and rationalize it away.
Grant, John. Denying Science. Amherst: Prometheus Books, 2011.
Novella, Steven. “More on God of the Gaps.” NeuroLogica Blog. http://theness.com/neurologicablog/index.php/more-on-god-of-the-gaps
Novella, Steven. “Skepticism and Denial.” The NESS. http://www.theness.com/index.php/skepticism-and-denial
Specter, Michael. Denialism: How Irrational Thinking Hinders Scientific Progress, Harms the Planet, and Threatens Our Lives. London: Penguin Press, 2009
Tokuno, Hajime. “Holocaust Denial.” The NESS. http://www.theness.com/index.php/holocaust-denial
For more information on Sérgio Fontinhas, see Big Fitness Project.
Tuesday, 24 June 2014
Guest post: Science versus Pseudoscience.
Pseudoscience is so flawed that it cannot be considered legitimate science. Of course it is common to claim that one’s beliefs are scientific, but mostly they are not.
Pseudoscience lacks the true method of science and goes way beyond just a few errors, the methods themselves are so flawed that makes the theory suspicious.
Between the two extremes of science and pseudoscience there is a gray zone, but legitimate science and pseudosciences can still be identified. The denial of this two extremes in the continuum, is a false continuum logical fallacy, or philosophically called the demarcation problem.
The most prominent feature of this pathological science is working backward from desired results, or motivated reasoning. The result is that they make evidence fit into preconceived notions. They use biased logic and cherry-picked evidence in order to defend a desired conclusion. There’s no concern and effort to prove their own theories wrong.
This relates to the congruence bias, testing one’s own theory by looking for positive evidence and cherry-picked evidence.
They will only look for confirming evidence, avoid dis-confirming evidence, and may engage in special pleading and shifting the burden of proof.
In confirmation bias, they look for supportive evidence for their own desired conclusions, choosing only the evidence that supports their own theory, irrespective of quality, negative evidence.
Anecdotes are uncontrolled, or ad-hoc observations, and they are not systematic. They rely on confirmation bias and recall bias.
Low-grade evidence is often favored no matter how implausible it may be.
Emotional appeal is another typical tactic among pseudoscientists who try to defend their statements, claiming what people say is more important than actual numbers on paper.
Pseudoscientific belief may even be based upon a single case or observation, preliminary evidence, or even a single anecdote. This is the hasty generalization logical fallacy.
Pseudoscientific principles may also be based upon a philosophical idea, not been empirically tested or developed as a scientific theory.
This involves grandiose claims based upon preliminary evidence. Far-reaching claims overturn entire portions of well-established science, using very little research or tiny bits of evidence.
In extreme cases, pseudoscience leads to alternative science, all of science is replaced with an alternative version.
Pseudoscientists make bold claims that are often absolute and go way beyond the evidence. Pseudoscientists offer simple answers to complex questions, a theory of everything where one tiny casual source is used to explain the entire universe, if it comes to that.
Pseudoscientists generally cannot accept criticism and avoid the scientific community. They claim being victim of a conspiracy and stay away from mainstream science and community.
Pseudoscientists use vague terms and words to obfuscate, so they can shift the definition around, use it in different ways at different times when it suits them, to confuse others and avoid explaining their point. Vague terms such as “information” or “energy” are often used with no specificity as in a scientific discussion.
Pseudosciences fail to progress, and tend to be stagnant. They are ad nauseam trying to establish their theory rather than build a body of evidence for it.
Anomaly hunting is yet another common feature in which they search for anomalies trying to establish a conclusion, which does not seek to refute or explore other alternatives.
Nickerson, Raymond. “Confirmation Bias: A Ubiquitous Phenomenon in Many Guises.” Review of General Psychology 2, no. 2 (1998): 175–220.
Novella, Steven. “Anomaly Hunting.” NeuroLogica Blog. http://theness.com/neurologicablog/index.php/anomaly-hunting
Pigliucci, Massimo. Nonsense on Stilts: How to Tell Science from Bunk. Chicago: University of Chicago Press, 2010
Shermer, Michael, The Borderlands of Science: Where Sense Meets Nonsense. New York: Oxford University Press, 2001.
Gardner, Martin. Fads and Fallacies in the Name of Science. Mineola: Dover Publications, 1957
Shermer, Michael. Why People Believe Weird Things. New York: Henry Holt/Times Books, 1997.
For more information on Sérgio Fontinhas, see Big Fitness Project.
See also Guest post: Denialism as Pseudoscientific Thinking.
Pseudoscience lacks the true method of science and goes way beyond just a few errors, the methods themselves are so flawed that makes the theory suspicious.
Between the two extremes of science and pseudoscience there is a gray zone, but legitimate science and pseudosciences can still be identified. The denial of this two extremes in the continuum, is a false continuum logical fallacy, or philosophically called the demarcation problem.
Features of Pseudoscience
1. Motivated reasoning
The most prominent feature of this pathological science is working backward from desired results, or motivated reasoning. The result is that they make evidence fit into preconceived notions. They use biased logic and cherry-picked evidence in order to defend a desired conclusion. There’s no concern and effort to prove their own theories wrong.
This relates to the congruence bias, testing one’s own theory by looking for positive evidence and cherry-picked evidence.
2. Burden of proof and confirmation bias
They will only look for confirming evidence, avoid dis-confirming evidence, and may engage in special pleading and shifting the burden of proof.
In confirmation bias, they look for supportive evidence for their own desired conclusions, choosing only the evidence that supports their own theory, irrespective of quality, negative evidence.
3. Anecdotal evidence
Anecdotes are uncontrolled, or ad-hoc observations, and they are not systematic. They rely on confirmation bias and recall bias.
Low-grade evidence is often favored no matter how implausible it may be.
Emotional appeal is another typical tactic among pseudoscientists who try to defend their statements, claiming what people say is more important than actual numbers on paper.
Pseudoscientific belief may even be based upon a single case or observation, preliminary evidence, or even a single anecdote. This is the hasty generalization logical fallacy.
Pseudoscientific principles may also be based upon a philosophical idea, not been empirically tested or developed as a scientific theory.
4. Grandiose claims (Galileo syndrome)
This involves grandiose claims based upon preliminary evidence. Far-reaching claims overturn entire portions of well-established science, using very little research or tiny bits of evidence.
5. Alternative science
In extreme cases, pseudoscience leads to alternative science, all of science is replaced with an alternative version.
6. Absolute claims
Pseudoscientists make bold claims that are often absolute and go way beyond the evidence. Pseudoscientists offer simple answers to complex questions, a theory of everything where one tiny casual source is used to explain the entire universe, if it comes to that.
7. Hostility
Pseudoscientists generally cannot accept criticism and avoid the scientific community. They claim being victim of a conspiracy and stay away from mainstream science and community.
8. Vagueness
Pseudoscientists use vague terms and words to obfuscate, so they can shift the definition around, use it in different ways at different times when it suits them, to confuse others and avoid explaining their point. Vague terms such as “information” or “energy” are often used with no specificity as in a scientific discussion.
9. Stagnation
Pseudosciences fail to progress, and tend to be stagnant. They are ad nauseam trying to establish their theory rather than build a body of evidence for it.
10. Anomaly hunting
Anomaly hunting is yet another common feature in which they search for anomalies trying to establish a conclusion, which does not seek to refute or explore other alternatives.
Nickerson, Raymond. “Confirmation Bias: A Ubiquitous Phenomenon in Many Guises.” Review of General Psychology 2, no. 2 (1998): 175–220.
Novella, Steven. “Anomaly Hunting.” NeuroLogica Blog. http://theness.com/neurologicablog/index.php/anomaly-hunting
Pigliucci, Massimo. Nonsense on Stilts: How to Tell Science from Bunk. Chicago: University of Chicago Press, 2010
Shermer, Michael, The Borderlands of Science: Where Sense Meets Nonsense. New York: Oxford University Press, 2001.
Gardner, Martin. Fads and Fallacies in the Name of Science. Mineola: Dover Publications, 1957
Shermer, Michael. Why People Believe Weird Things. New York: Henry Holt/Times Books, 1997.
For more information on Sérgio Fontinhas, see Big Fitness Project.
See also Guest post: Denialism as Pseudoscientific Thinking.
Friday, 20 June 2014
Another tasty analogy.
Here's a tasty analogy.
In Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy, I analogised the effect of carbohydrate consumption on mean serum glucose level with the effect of fat consumption on mean serum triglyceride level. Here's another one.
Chronic excessive consumption of carbohydrates relative to what are being burned results in excessive fat synthesis in the liver, resulting in excessively-high fasting serum triglyceride level, which is harmful.
Chronic excessive consumption of fats relative to what are being burned results in excessive cholesterol synthesis in the liver, resulting in excessively-high fasting VLDL, LDL & IDL level, which is harmful.
Seems legit.
 |
| From http://grannychoe.com/recipe3_Soup.php |
In Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy, I analogised the effect of carbohydrate consumption on mean serum glucose level with the effect of fat consumption on mean serum triglyceride level. Here's another one.
Chronic excessive consumption of carbohydrates relative to what are being burned results in excessive fat synthesis in the liver, resulting in excessively-high fasting serum triglyceride level, which is harmful.
Chronic excessive consumption of fats relative to what are being burned results in excessive cholesterol synthesis in the liver, resulting in excessively-high fasting VLDL, LDL & IDL level, which is harmful.
Seems legit.
Thursday, 19 June 2014
Siri-Tarino et al, Forests & Trees and "Eureka!" moments.
Here's Fig. 2 from Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease:-
The above "Forest" plot has a subtotal RR of 1.07 (95% CI 0.96 1.19). The overall conclusion is that there's no association between saturated fat intake and the RR for CHD. Hmmm.
I looked at the data in Table 3. Of the 16 studies contributing to the CHD results, only 3 of them specify high sat fat intakes over a wide range. The results from these 3 studies are as follows:-
Pietinen et al: RR=0.93 (95% CI 0.6, 1.44).
Mann et al: RR=2.77 (95% CI 1.25, 6.13).
Boniface et al: Pooled RR = 1.37 (95% CI 1.17, 1.65).
The results from Pietinen et al are statistically-insignificant (95% CI values are way above & below 1) with an overall slight protective effect. The results from Mann et al have a RR >> 1 with both 95% CI's >1 and the results from Boniface et al have a RR >1 with both 95% CI's >1.
Other studies either have sat fat intakes varying from very low to low, or specify mean/median sat fat intakes without values for highest & lowest tertiles/quartiles/quintiles etc. Other studies have results that are statistically-insignificant.
However, there are some studies that show a slight protective effect of small amounts of sat fats. How come?
Thanks to George Henderson, I had a "Eureka!" moment. He posted a link to Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis.
Here's Fig. 1 from that study.
The Meat SF plot has a net positive slope (bad news, but the range of intake is very small), the Butter & Plant SF plots are random, but the Dairy SF plot has a net negative slope (good news). Dairy saturated fats in amounts of up to 10g/day are protective against CHD. As the Dairy sat fat intake is too small to have a significant effect on lipids, what's the mechanism? I think that it's Vitamin K2. See Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.
When you average out the results from all studies, the result is null. This is data dilution statistics.
EDIT: See also Study: Saturated Fat as Bad as Sugar!
 |
| Risk ratios and 95% CIs for fully adjusted random-effects models examining associations between saturated fat intake in relation to coronary heart disease and stroke. |
The above "Forest" plot has a subtotal RR of 1.07 (95% CI 0.96 1.19). The overall conclusion is that there's no association between saturated fat intake and the RR for CHD. Hmmm.
I looked at the data in Table 3. Of the 16 studies contributing to the CHD results, only 3 of them specify high sat fat intakes over a wide range. The results from these 3 studies are as follows:-
Pietinen et al: RR=0.93 (95% CI 0.6, 1.44).
Mann et al: RR=2.77 (95% CI 1.25, 6.13).
Boniface et al: Pooled RR = 1.37 (95% CI 1.17, 1.65).
The results from Pietinen et al are statistically-insignificant (95% CI values are way above & below 1) with an overall slight protective effect. The results from Mann et al have a RR >> 1 with both 95% CI's >1 and the results from Boniface et al have a RR >1 with both 95% CI's >1.
Other studies either have sat fat intakes varying from very low to low, or specify mean/median sat fat intakes without values for highest & lowest tertiles/quartiles/quintiles etc. Other studies have results that are statistically-insignificant.
However, there are some studies that show a slight protective effect of small amounts of sat fats. How come?
Thanks to George Henderson, I had a "Eureka!" moment. He posted a link to Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis.
Here's Fig. 1 from that study.
 |
| HRs and 95% CI's of CVD risk according to quintiles of energy-adjusted SF from different sources (n = 5209). |
The Meat SF plot has a net positive slope (bad news, but the range of intake is very small), the Butter & Plant SF plots are random, but the Dairy SF plot has a net negative slope (good news). Dairy saturated fats in amounts of up to 10g/day are protective against CHD. As the Dairy sat fat intake is too small to have a significant effect on lipids, what's the mechanism? I think that it's Vitamin K2. See Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.
When you average out the results from all studies, the result is null. This is data dilution statistics.
EDIT: See also Study: Saturated Fat as Bad as Sugar!
Sunday, 15 June 2014
I'm NOT a lipophobe, I'm a very naughty boy!
First, postprandial triglycerides again. From Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women, here's a plot of HR for future CHD vs TG's at various times after eating.
Notice how the HR falls with increasing time from last meal. As TG's ≥12 hours after eating are a surrogate for Insulin Resistance (IR) and the HR is only 1.04 (95% CI 0.79 - 1.38), this strongly suggests that IR is not a significant factor.
It's been suggested that IR might increase PP TG's in the 2 - 4 hour period due to impaired clearance. According to Fig. 3B in Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism, TG clearance in healthy men doesn't significantly start until after 4 hours has elapsed. Therefore, an impairment in TG clearance isn't going to make a significant difference to TG level in the 2 - 4 hour period.
Second, the reason why I'm having to repeat myself is due to Cholesterol: Do chylomicrons clog your arteries? (2), where I've been called "my resident lipophobe". As I drink Gold Top milk (5.2g of fat/100mL) and eat pork including belly slices (you know, those strips of pork with a lot of fat on them), I'm being attacked for something that I'm not.
What I'm criticising is dietary extremism. Eating fats in foods is fine by me, but eating sticks of Kerrygold butter and/or dumping loads of butter and/or MCT oil into coffee to achieve "Nutritional Ketosis" is not a good idea. Anyway, here's an amusing spoof on Bulletproof coffee.
 |
| Hazard ratio (HR) and 95% confidence interval (CI) for highest vs lowest tertiles of triglyceride level (see Table 3 for values), adjusted for age, blood pressure, smoking, hormone use, levels of total and high-density lipoprotein cholesterol, diabetes mellitus, body mass index, and high-sensitivity C-reactive protein level. |
Notice how the HR falls with increasing time from last meal. As TG's ≥12 hours after eating are a surrogate for Insulin Resistance (IR) and the HR is only 1.04 (95% CI 0.79 - 1.38), this strongly suggests that IR is not a significant factor.
It's been suggested that IR might increase PP TG's in the 2 - 4 hour period due to impaired clearance. According to Fig. 3B in Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism, TG clearance in healthy men doesn't significantly start until after 4 hours has elapsed. Therefore, an impairment in TG clearance isn't going to make a significant difference to TG level in the 2 - 4 hour period.
Second, the reason why I'm having to repeat myself is due to Cholesterol: Do chylomicrons clog your arteries? (2), where I've been called "my resident lipophobe". As I drink Gold Top milk (5.2g of fat/100mL) and eat pork including belly slices (you know, those strips of pork with a lot of fat on them), I'm being attacked for something that I'm not.
What I'm criticising is dietary extremism. Eating fats in foods is fine by me, but eating sticks of Kerrygold butter and/or dumping loads of butter and/or MCT oil into coffee to achieve "Nutritional Ketosis" is not a good idea. Anyway, here's an amusing spoof on Bulletproof coffee.
Saturday, 14 June 2014
Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.
Julianne Taylor of Paleo & Zone Nutrition posted the following excellent lecture on Facebook:-
Eating Through The Myths: Food, Health and Happiness - Taylor, Prof. R., Berlin, 28-Sep-12
EDIT: The link above needs Flash. If Flash isn't available, see YouTube video below.
Salient points:
1) It's a chronic calorie excess (of carbohydrates and/or fats) that causes problems.
2) Motivation, motivation, motivation!
3) Both diet and exercise are important. See Move More: Solutions to problems.
4) You can't outrun your fork. See The 5th Myth of Modern Day Dieting: You Can Outrun Your Fork.
5) Underlying Insulin Resistance needs to be addressed. See Insulin Resistance: Solutions to problems.
See also Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol, and Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause (PDF).
For more information on Prof. Taylor's work, see Reversing Type 2 Diabetes.
EDIT: Long-term results are now in. See Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The full study is behind a pay-wall, but here are a couple of Figures from it.
86% of participants who completed all 3 phases of the trial maintained over 15kg of weight loss and achieved remission from diabetes. Participants who dropped-out at various points achieved less weight loss at the 1 year point and achieved a lower % of remission. It's not easy for people who are consuming 15% fewer kcals/day of healthy foods to maintain motivation when they're constantly being bombarded by persuasive marketing encouraging them to eat yummy Food Products.
If beta cells have been irreversibly damaged and the above approach doesn't work, improved glycaemic control can be achieved using a LCHF diet.
Eating Through The Myths: Food, Health and Happiness - Taylor, Prof. R., Berlin, 28-Sep-12
EDIT: The link above needs Flash. If Flash isn't available, see YouTube video below.
Salient points:
1) It's a chronic calorie excess (of carbohydrates and/or fats) that causes problems.
2) Motivation, motivation, motivation!
3) Both diet and exercise are important. See Move More: Solutions to problems.
4) You can't outrun your fork. See The 5th Myth of Modern Day Dieting: You Can Outrun Your Fork.
5) Underlying Insulin Resistance needs to be addressed. See Insulin Resistance: Solutions to problems.
See also Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol, and Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause (PDF).
For more information on Prof. Taylor's work, see Reversing Type 2 Diabetes.
EDIT: Long-term results are now in. See Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The full study is behind a pay-wall, but here are a couple of Figures from it.
86% of participants who completed all 3 phases of the trial maintained over 15kg of weight loss and achieved remission from diabetes. Participants who dropped-out at various points achieved less weight loss at the 1 year point and achieved a lower % of remission. It's not easy for people who are consuming 15% fewer kcals/day of healthy foods to maintain motivation when they're constantly being bombarded by persuasive marketing encouraging them to eat yummy Food Products.
If beta cells have been irreversibly damaged and the above approach doesn't work, improved glycaemic control can be achieved using a LCHF diet.
Thursday, 12 June 2014
Carbs, Carbs, Carbs, Carbs and Carbs.
Carbohydrates seem to get the blame for everything nowadays. "Carbohydrates made me fat". "Carbohydrates burned-out my pancreas". "Carbohydrates raised my blood glucose". "Carbohydrates raised my blood triglycerides". "Carbohydrates stole mer jerb!". O.K, I made the last one up!
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.
Also, Blue Zone populations eat a diet with a high percentage of total energy (%E) from carbohydrates. See Low serum insulin in traditional Pacific Islanders--the Kitava Study and The Kitava Study. The Kitavans eat ~70%E from carbohydrates, ~20%E from fats and ~10%E from proteins. They don't eat a significant amount of Western crap-in-a-bag/box/bottle.
Maybe it has something to do with the type of carbohydrates and with what they're eaten. In A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins , (emphasis, mine) "The very-low-fat, high-carbohydrate experimental diet was designed to supply less than 10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein." Simple carbohydrates are sugars.
The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!
1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.
2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very high glycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.
3. There are oligosachharides e.g. FOS.
4. There are polysaccharides e.g. inulin.
5. There is soluble fibre/fiber e.g. cellulose.
Although overeating sugars containing fructose & starches that rapidly hydrolyse into glucose makes the liver fatty, overeating fats also makes the liver fatty. See Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.
It's the chronic over-consumption of crap-in-a-bag/box/bottle (high in sugars and/or starches and/or fats), not just carbohydrates, that causes over-fatness and other health problems.
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.
Also, Blue Zone populations eat a diet with a high percentage of total energy (%E) from carbohydrates. See Low serum insulin in traditional Pacific Islanders--the Kitava Study and The Kitava Study. The Kitavans eat ~70%E from carbohydrates, ~20%E from fats and ~10%E from proteins. They don't eat a significant amount of Western crap-in-a-bag/box/bottle.
Maybe it has something to do with the type of carbohydrates and with what they're eaten. In A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins , (emphasis, mine) "The very-low-fat, high-carbohydrate experimental diet was designed to supply less than 10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein." Simple carbohydrates are sugars.
The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!
1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.
2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very high glycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.
3. There are oligosachharides e.g. FOS.
4. There are polysaccharides e.g. inulin.
5. There is soluble fibre/fiber e.g. cellulose.
Although overeating sugars containing fructose & starches that rapidly hydrolyse into glucose makes the liver fatty, overeating fats also makes the liver fatty. See Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.
It's the chronic over-consumption of crap-in-a-bag/box/bottle (high in sugars and/or starches and/or fats), not just carbohydrates, that causes over-fatness and other health problems.
Wednesday, 11 June 2014
Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy.
Fat storage:
Here's a plot of mean (±SEM) plasma insulin concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal. |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
100g of glucose produces a large spike in insulin concentration and 40g of fat produces no significant spike in insulin concentration. According to Gary Taubes' insulin hypothesis of obesity, in the absence of a significant spike in insulin concentration, fat cannot be stored.
Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post).
 |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
Plasma triacylglycerol concentration falls to baseline between 240min and 360min. OGTT's and OFTT's are performed with the subjects at rest for the duration of the test.
Referring to It's all in a day's work (as measured in Joules) , at rest the subject is burning ~1kcal/min with ~95% of it coming from fat, making a fat-burning rate of ~0.11g/min.
At a fat-burning rate of ~0.11g/min, it would take ~360min for plasma triacylglycerol to fall to baseline if the 40g of fat from the OFTT was only being burned and not being stored. As shown above, it only takes ~120min to fall to baseline. Therefore, fat from the OFTT that isn't burned is stored in ~120min in the absence of a significant insulin spike. Q.E.D.
A delicious analogy:
Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post). | ||
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
The OGTT (100g of glucose) produces a large spike in plasma glucose concentration which lasts for ~210min before returning to baseline. Higher plasma glucose concentrations glycate more than lower plasma glucose concentrations. Average plasma glucose concentration over 0 to 360min is higher with the OGTT than with the OFTT, therefore there is more glycation damage with the OGTT than with the OFTT. Don't regularly consume 100g or more of glucose!
Here's a plot of Mean (±SEM) plasma triacylglycerol concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal.
 |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
Although the plasma triacylglycerol concentration after consuming a high-carbohydrate evening meal is slightly higher than after consuming a high-fat evening meal, the two plots above are essentially flat, indicating that none of the 100g of glucose consumed was turned into fat by de novo lipogenesis (DNL) within 6 hours.
As discussed in the previous post, higher plasma triacylglycerol concentrations are more atherogenic than lower plasma triacylglycerol concentrations. Average plasma triacylglycerol concentration over 0 to 360min is higher with the OFTT than with the OGTT, therefore there is more atherogenicity with the OFTT than with the OGTT.
Don't regularly consume 40g or more of fat!
An interesting study that involved humongous fat consumption was Response of body weight to a low carbohydrate, high fat diet in normal and obese subjects , which used up to 600g of fat/day. It's possible to lose weight on an ultra-high-fat diet, but average plasma triacylglycerol concentrations would have been extremely high. Fasting TG's reduce on an ultra-high-fat diet, probably due to suppression of endogenous TG synthesis by exogenous TG intake.
Tuesday, 10 June 2014
Ultra-high-fat (~80%) diets: The good, the bad and the ugly.
The good:
Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (Fig. 1). |
| Fig. 1 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
An OGTT (100g of glucose dissolved in water) causes a short-term increase in blood glucose level. Ditto for insulin (see Fig. 2 ▪ & □ below).
 |
| Fig. 2 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
An OFTT (40g of fat as cream) doesn't cause a significant increase in blood glucose level (see Fig. 1 • & ○ above). Ditto for blood insulin (see Fig. 2 • & ○ above).
The bad:
Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (Fig. 3). |
| Fig. 3 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
An OFTT (40g of fat as cream) causes a significant increase in blood triacylglycerol (a.k.a. TAG a.k.a. triglyceride a.k.a. TG) level for 3 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG is only +0.1mmol/L. Is high postprandial TG a problem? Definitely, maybe. From Cholesterol And Coronary Heart Disease , "Cholesterol-depleted particles oxidise faster than large, cholesterol-rich ones." Chylomicrons, chylomicron remnants & VLDL-C are triglyceride-rich, cholesterol-poor, as that's the composition of the fat in the diet.
The ugly:
Here's evidence that high postprandial TG is atherogenic. See Fig. 1 in Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.People who have Insulin Resistance &/or type 2 diabetes have impaired postprandial clearance of glucose and TG, which is atherogenic. Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity.
Here's evidence that postprandial saturated fat TG is atherogenic. Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling.
See also:-
Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.,
Effect of a single high-fat meal on endothelial function in healthy subjects.,
Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins.,
Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.,
Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects.,
Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes.,
Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress.,
High-energy diets, fatty acids and endothelial cell function: implications for atherosclerosis.,
Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.,
[Influence of postprandial hypertriglyceridemia on the endothelial function in elderly patients with coronary heart disease].,
Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size.,
Association between fasting and postprandial triglyceride levels and carotid intima-media thickness in type 2 diabetes patients.,
[Correlation of lipemia level after fat loading with manifestation of atherosclerosis in coronary arteries].,
Postprandial hypertriglyceridemia and carotid intima-media thickness in north Indian type 2 diabetic subjects.,
Association between postprandial remnant-like particle triglyceride (RLP-TG) levels and carotid intima-media thickness (IMT) in Japanese patients with type 2 diabetes: assessment by meal tolerance tests (MTT).,
Postprandial lipemia and remnant lipoproteins.,
Elevated levels of platelet microparticles in carotid atherosclerosis and during the postprandial state.,
Postprandial metabolic and hormonal responses of obese dyslipidemic subjects with metabolic syndrome to test meals, rich in carbohydrate, fat or protein.,
Atherosclerosis, diabetes and lipoproteins.,
Clinical relevance of non-fasting and postprandial hypertriglyceridemia and remnant cholesterol.,
Post-prandial hypertriglyceridemia in patients with type 2 diabetes mellitus with and without macrovascular disease.,
A hypertriglyceridemic state increases high sensitivity C-reactive protein of Japanese men with normal glucose tolerance.,
CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis.,
[Trends of evaluation of hypertriglyceridemia -from fasting to postprandial hypertriglyceridemia-].,
The effects of dietary fatty acids on the postprandial triglyceride-rich lipoprotein/apoB48 receptor axis in human monocyte/macrophage cells.
See also What Is the Significance of Postprandial Triglycerides Compared With Fasting Triglycerides? and Uncovering a Hidden Source of Cardiovascular Disease Risk.
A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG isn't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrates, there is still glucose in the blood, thanks to the liver and kidneys. Also, some carbohydrates don't spike blood glucose (or fructose) level. It's pure speculation that the subjects in the above studies had high blood glucose at the same time as high postprandial TG. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG, and there was no significant association between fasting TG and the risk factor for CHD, this suggests that the subjects had no significant metabolic derangement and were not eating excessive amounts of sugar.
According to Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in Overweight Men, there's a ~50% reduction in postprandial TG after adaptation to a low-carb, high-fat diet. However, mean energy intake was 1,850kcals/day, the subjects were in a 500kcal/day energy deficit and %E from fat was 60%.
Some people's LDL becomes very high on low-carbohydrate high-fat diets. See Some Metabolic Changes Induced by Low Carbohydrate Diets.
It's possible to get Coronary Artery Calcium (CAC) scans, to measure the amount of calcified plaque in coronary arteries. While a high CAC value means lots of plaque, a zero CAC value doesn't necessarily mean zero plaque, as young people and people with a high Vitamin K2 intake don't have significant calcification. See Stenosis Can Still Exist in Absence of Coronary Calcium.
See also Page 10 of HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD - Nathan Pritikin.
"Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?"
The answer is "Yes."
Saturday, 7 June 2014
Bray et al shows that a calorie *is* a calorie (where weight change is concerned).
Continued from Everyone is Different, Part 3.
EDIT: I made an error in stating that all of the extra calories came from fat, in the fat overfeeding phase. Thanks to commenter CynicalEng for pointing that out. It doesn't change the conclusion at all.
At 01:17 on 6th June, during a Facebook discussion, Fred Hahn told me:-
"Nigel Kinbrum - read this please.
Bray, et al. Shows that a Calorie is Not a Calorie and that Dietary Carbohydrate Controls Fat Storage.
Perhaps you'll learn something from a real expert who teaches metabolism to medical students at the largest medical school in the country."
So I did.
At 02:22, I replied:-
"Thanks for that. I read Feinman's blog post about Bray et al https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/ some time ago.
There's a fundamental error in Feinman's analysis. As LeonRover pointed out in his comment https://feinmantheother.com/.../bray-et-al-shows-that.../...
In Diets:- "Absolute carbohydrate intake was kept constant throughout the study."
Also, in COMMENT:- "The extra calories in our study were fed as fat, as in several other studies, and were stored as fat..."
Oh, whoops! That may be why it was rejected by the editor."
Here's Figure 6 from Bray's study.
Some Definitions:-
LBM = Lean Body Mass
FM = Fat Mass = Body Fat
Weight change = (LBM change + FM change)
Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).
(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36
∴ A calorie *is* a calorie (where weight change is concerned) ± some inter-personal variation.
∴ Insufficient protein can result in LBM loss (this is bad).
As LBM has a lower Energy Density (~600kcals/lb) than FM (~3,500kcals/lb), LBM loss can increase weight loss, when in a Caloric Deficit.
See The Energy Balance Equation, for a simple explanation, and The Dynamics of Human Body Weight Change, for an incredibly complicated one!
I was rather chuffed when Alan Aragon left the following comment at 04:34:-
"Nigel is correct. From Bray et al's text:
"The extra calories in our study were fed as fat, as in several other studies [33,34], and stored as fat with the lower percentage of excess calories appearing as fat in the high (25%) protein diet group. The higher fat intake in the low protein group probably reduced nutrient absorption (metabolizable energy) relative to the other groups and this would have brought the intake and expenditure closer together in this group.""
Feinman has deleted his blog post. However, his post I Told George Bray How to do it Right is still there. I believe that Dr. George A. Bray M.D. sort-of did it right.
Dr. George A. Bray used a "weight maintenance formula" in all three groups for the weight maintenance phase. He then changed the formula in all three groups to low-P, med-P and high-P formulas, for the fat overfeeding phase. Carbohydrate grams remained constant in all three groups for all phases, but additional fat grams were fewer in the high-P group than in the low-P group, for the fat overfeeding phase.
I would have used the low-P, med-P and high-P formulas for the weight maintenance phase and for the fat overfeeding phase, to equalise the additional fat grams in all three groups.
Continued on Everyone is different Part 4, Fallacies and another rant!
EDIT: I made an error in stating that all of the extra calories came from fat, in the fat overfeeding phase. Thanks to commenter CynicalEng for pointing that out. It doesn't change the conclusion at all.
At 01:17 on 6th June, during a Facebook discussion, Fred Hahn told me:-
"Nigel Kinbrum - read this please.
Bray, et al. Shows that a Calorie is Not a Calorie and that Dietary Carbohydrate Controls Fat Storage.
Perhaps you'll learn something from a real expert who teaches metabolism to medical students at the largest medical school in the country."
So I did.
At 02:22, I replied:-
"Thanks for that. I read Feinman's blog post about Bray et al https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/ some time ago.
There's a fundamental error in Feinman's analysis. As LeonRover pointed out in his comment https://feinmantheother.com/.../bray-et-al-shows-that.../...
In Diets:- "Absolute carbohydrate intake was kept constant throughout the study."
Also, in COMMENT:- "The extra calories in our study were fed as fat, as in several other studies, and were stored as fat..."
Oh, whoops! That may be why it was rejected by the editor."
Here's Figure 6 from Bray's study.
Some Definitions:-
LBM = Lean Body Mass
FM = Fat Mass = Body Fat
Weight change = (LBM change + FM change)
Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).
(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36
∴ A calorie *is* a calorie (where weight change is concerned) ± some inter-personal variation.
∴ Insufficient protein can result in LBM loss (this is bad).
As LBM has a lower Energy Density (~600kcals/lb) than FM (~3,500kcals/lb), LBM loss can increase weight loss, when in a Caloric Deficit.
See The Energy Balance Equation, for a simple explanation, and The Dynamics of Human Body Weight Change, for an incredibly complicated one!
I was rather chuffed when Alan Aragon left the following comment at 04:34:-
"Nigel is correct. From Bray et al's text:
"The extra calories in our study were fed as fat, as in several other studies [33,34], and stored as fat with the lower percentage of excess calories appearing as fat in the high (25%) protein diet group. The higher fat intake in the low protein group probably reduced nutrient absorption (metabolizable energy) relative to the other groups and this would have brought the intake and expenditure closer together in this group.""
Feinman has deleted his blog post. However, his post I Told George Bray How to do it Right is still there. I believe that Dr. George A. Bray M.D. sort-of did it right.
Dr. George A. Bray used a "weight maintenance formula" in all three groups for the weight maintenance phase. He then changed the formula in all three groups to low-P, med-P and high-P formulas, for the fat overfeeding phase. Carbohydrate grams remained constant in all three groups for all phases, but additional fat grams were fewer in the high-P group than in the low-P group, for the fat overfeeding phase.
I would have used the low-P, med-P and high-P formulas for the weight maintenance phase and for the fat overfeeding phase, to equalise the additional fat grams in all three groups.
Continued on Everyone is different Part 4, Fallacies and another rant!
Saturday silliness.
Now that I have resumed annoying people discussing diet & nutrition on the internet, the following chart should be used by non-English people, to allow them to understand what I write.
For a laugh, I created the superhero of Diet & Nutrition "The Nigeepoo".
Have a nice weekend!
 |
| From http://www.thepoke.co.uk/2011/05/17/anglo-eu-translation-guide/ |
For a laugh, I created the superhero of Diet & Nutrition "The Nigeepoo".
 |
| Using http://www.heromachine.com/heromachine-2-5-character-portrait-creator/ |
Monday, 2 June 2014
False dichotomies: cot'd.
I'm talking about the "What causes Z, X or Y?" & "What is best, X or Y" type statements.
Some people believe that hormonal disruption causes obesity, rather than energy excess. The vast majority of people who are overweight or obese weren't born with hormonal disruption. It's years of chronic energy excess (see Determinants of the Variability in Human Body-fat Percentage for the many reasons causing it) that make people too heavy/fat than is healthy. Once too heavy/fat than is healthy, various hormones become disrupted, causing even more energy excess. Therefore, the cause of obesity is not one thing or another, it's both (plus lots of others), which is why reversing it is so difficult.
On Peter D's blog, the title reads "You need to get calories from somewhere, should it be from carbohydrate or fat?" I say "Both. And some protein. And a bit of alcohol, too!" And I know that I shouldn't start sentences with And.
It's been a while since I posted a video of me singing. Here's one from February this year.
 |
| From http://johnbarban.com/fitness-vs-fatness-a-false-dichotomy/ |
Some people believe that hormonal disruption causes obesity, rather than energy excess. The vast majority of people who are overweight or obese weren't born with hormonal disruption. It's years of chronic energy excess (see Determinants of the Variability in Human Body-fat Percentage for the many reasons causing it) that make people too heavy/fat than is healthy. Once too heavy/fat than is healthy, various hormones become disrupted, causing even more energy excess. Therefore, the cause of obesity is not one thing or another, it's both (plus lots of others), which is why reversing it is so difficult.
On Peter D's blog, the title reads "You need to get calories from somewhere, should it be from carbohydrate or fat?" I say "Both. And some protein. And a bit of alcohol, too!" And I know that I shouldn't start sentences with And.
It's been a while since I posted a video of me singing. Here's one from February this year.
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