whaddaya mean double blind? Just feed some poor guy 50 big macs and see what happens to him. Unless, of course, you're willing to make assumptions as to the rest of his diet and the functionality of his digestive and endocrine systems.
Big macs contain a large amount of carbs.
Feed him just the meat and cheese and nothing bad will happen.
Big macs also have an absurd amount of sodium in them
Meat, cheese and blood pressure that would make a 55 year old diabetic overweight sedentary black male feel good about himself
Excess dietary sodium is bad only if you have a pre-existing condition. If your doctor determines that you're under high risk of stroke/CVD, then avoid it. If you have chronic high blood pressure, avoid it. If you have other conditions, avoid it.
But if you're a healthy individual, then there is no reason to avoid it.
Excess dietary sodium is bad only if you have a pre-existing condition. If your doctor determines that you're under high risk of stroke/CVD, then avoid it. If you have chronic high blood pressure, avoid it. If you have other conditions, avoid it.
But if you're a healthy individual, then there is no reason to avoid it.
but drink enough water, says the peanut gallery in perfect unison
Paladin on
Marty: The future, it's where you're going? Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
There is nothing to disagree on since you're objectively wrong. You can review the sodium research if you want, although I have to warn you that it's quite extensive. The only time sodium becomes dangerous is when it reaches amounts close to 1g per body weight in lbs, which is why people out in the sea die without fresh water, or why the ancient Chinese committed suicide by eating salt tablets. Nothing in the modern diet comes even close to those amounts though.
There is nothing to disagree on since you're objectively wrong. You can review the sodium research if you want, although I have to warn you that it's quite extensive. The only time sodium becomes dangerous is when it reaches amounts close to 1g per body weight in lbs, which is why people out in the sea die without fresh water, or why the ancient Chinese committed suicide by eating salt tablets. Nothing in the modern diet comes even close to those amounts though.
well I mean, plenty of things could happen before you actually die, like renal failure and brain shrinkage and heart failure
I don't know why I'm picking on you I should probably take a break
Paladin on
Marty: The future, it's where you're going? Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
It would just be better if you provided citations for your claims rather than vomiting on the thread without even paying attention to basic grammar or punctuation.
seriously guy, reading your posts is just painful. Half the time I dont even know what you're talking about. And the other half of the time you still aren't making much sense.
There is nothing to disagree on since you're objectively wrong. You can review the sodium research if you want, although I have to warn you that it's quite extensive. The only time sodium becomes dangerous is when it reaches amounts close to 1g per body weight in lbs, which is why people out in the sea die without fresh water, or why the ancient Chinese committed suicide by eating salt tablets. Nothing in the modern diet comes even close to those amounts though.
As supporting proof, please read this article on the science and politics of dietary salt research (winner of the 1999 Science in Society Journalism Awards!)
tl;dr version: excess dietary salt has not conclusively been identified as the causative agent for high blood pressure.
It would just be better if you provided citations for your claims rather than vomiting on the thread without even paying attention to basic grammar or punctuation.
To tell you the truth I feel more comfortable discussing these topics in terms of biochemical pathways than macroscopic studies. But in order to get a good pathway going, you've got to cite several papers proving each link in the chain if you want to be thorough. I don't know about you, but I'd like the discussion to go in a direction where the initial idea is laid out as a grand diagram of fat metabolism to prove your point, and then we go after individual processes with cited references. Because while studies showing no correlation between ketotic fat consumption and heart disease are nice, they don't tell us anything that bulletproof the methods for general instruction, use, and exception.
But yes, I agree that my discourse has deteriorated, on my part due to lack of sleep resulting in bad judgment.
Paladin on
Marty: The future, it's where you're going? Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
There is nothing to disagree on since you're objectively wrong. You can review the sodium research if you want, although I have to warn you that it's quite extensive. The only time sodium becomes dangerous is when it reaches amounts close to 1g per body weight in lbs, which is why people out in the sea die without fresh water, or why the ancient Chinese committed suicide by eating salt tablets. Nothing in the modern diet comes even close to those amounts though.
As supporting proof, please read this article on the science and politics of dietary salt research (winner of the 1999 Science in Society Journalism Awards!)
tl;dr version: excess dietary salt has not conclusively been identified as the causative agent for high blood pressure.
I'll read that in a bit thanks (even though it supports my views).
It would just be better if you provided citations for your claims rather than vomiting on the thread without even paying attention to basic grammar or punctuation.
To tell you the truth I feel more comfortable discussing these topics in terms of biochemical pathways than macroscopic studies. But in order to get a good pathway going, you've got to cite several papers proving each link in the chain if you want to be thorough. I don't know about you, but I'd like the discussion to go in a direction where the initial idea is laid out as a grand diagram of fat metabolism to prove your point, and then we go after individual processes with cited references. Because while studies showing no correlation between ketotic fat consumption and heart disease are nice, they don't tell us anything that bulletproof the methods for general instruction, use, and exception.
But yes, I agree that my discourse has deteriorated, on my part due to lack of sleep resulting in bad judgment.
I'm not sure where you're going with this. Double-blind clinical studies are considered the gold standard in medical research precisely because they are macroscopic. They give you information on the exact things we're interested in, ie growth rate, muscle synthesis, fat loss.
Research into biochemical pathways are fine in determining mechanisms, but don't usually translate well to whole organisms because they are so myopic. Yeah yeah, ketosis does a, b, c in pathway X, but who the fuck cares aside from scientists? As well, these are usually done in model animals, which may or may not translate to humans.
It would just be better if you provided citations for your claims rather than vomiting on the thread without even paying attention to basic grammar or punctuation.
To tell you the truth I feel more comfortable discussing these topics in terms of biochemical pathways than macroscopic studies. But in order to get a good pathway going, you've got to cite several papers proving each link in the chain if you want to be thorough. I don't know about you, but I'd like the discussion to go in a direction where the initial idea is laid out as a grand diagram of fat metabolism to prove your point, and then we go after individual processes with cited references. Because while studies showing no correlation between ketotic fat consumption and heart disease are nice, they don't tell us anything that bulletproof the methods for general instruction, use, and exception.
But yes, I agree that my discourse has deteriorated, on my part due to lack of sleep resulting in bad judgment.
I'm not sure where you're going with this. Double-blind clinical studies are considered the gold standard in medical research precisely because they are macroscopic. They give you information on the exact things we're interested in, ie growth rate, muscle synthesis, fat loss.
Research into biochemical pathways are fine in determining mechanisms, but don't usually translate well to whole organisms because they are so myopic. Yeah yeah, ketosis does a, b, c in pathway X, but who the fuck cares aside from scientists? As well, these are usually done in model animals, which may or may not translate to humans.
Who the fuck cares? Really? Do you know what happens when you bank on macro studies that aren't fully supported by the micro ones? Well a good example would be DDT. Macro it appeared great, until we started looking at the micro effect and then whoooops.
Now with regards to Sodium and blood pressure whoooops you're full of shit.
I draw you to the relevant paragraph here, written conveniently in plain language,
Sodium reduction alone from a high level to a low level reduced blood pressure by 8.3/4.4 mm Hg among individuals with hypertension and by 5.6/2.8 mm Hg among those without hypertension; the greatest reductions in blood pressure were seen in 2 groups at high levels of risk for developing hypertension, Blacks and older persons. The combination of this amount of salt reduction and the DASH diet lowered blood pressure levels by 11.5/5.7 mm Hg and 7.1/3.7 mm Hg, respectively, among those with and without hypertension. These findings reaffirm the benefit of recommending that sodium be limited to 2400 mg or less per day; they suggest that limiting sodium intake further to 1500 mg per day is feasible and would result in additional reductions in blood pressure levels without adverse effects.
and here,
Higher sodium intakes have negative effects in addition to that of increasing blood pressure levels. The National Health and Nutrition Examination Survey Epidemiologic Follow-up Study showed that, among participants aged 25 to 74 years who were overweight, a 100-mmol increase in intake of sodium was associated with an increase in relative risk of coronary heart disease mortality of 61%, an increase in stroke mortality of 89%, and an increase in all-cause mortality of 39%. Moreover, these effects were found after adjustment for blood pressure, age, body mass index, and other important variables.19 Given that more than 50% of adults are now considered to be overweight,20 this study has major implications in regard to the importance of reducing sodium intake above and beyond concerns about blood pressure.
Now either the APHA are full of shit and don't know their assholes from their elbows, or sodium is not a good thing to be gorging on and you're giving out some fucking reckless advice.
And there are literally dozens of papers showing how high levels of sodium are dangerous outside of high blood pressure,
It damages your blood vessels. It destroys your organs. It does systemic damage to your body. But oh yes, just drink a few glasses of water and you'll be OK.
Quick question- I am trying to hunt it down on my own, but does anyone (geckhan, protein, robman, others) have a review article of some sort handy that describes the biochemical action of insulin on lipid metabolization and storage?
NOTE: Do NOT just recommend me the books in the OP, I am trying to get at the actual academic research here
Quick question- I am trying to hunt it down on my own, but does anyone (geckhan, protein, robman, others) have a review article of some sort handy that describes the biochemical action of insulin on lipid metabolization and storage?
NOTE: Do NOT just recommend me the books in the OP, I am trying to get at the actual academic research here
I'm not so much hot on the biochemistry of lipid digestion, my research focus is cardiac & large blood vessel remodeling.
I am not either, but I want to learn where these cats learned so much about it. I am doin' a literature crawl right now, but it is slow going and I was just curious if any of them had it on hand.
My copy of good calories, bad calories is lent out, so I won't be too much help here. Someone who does have it though could list out the sources for the insulin / fat regulation chapters though.
A caveat of this study was its reliance on the accuracy of the
dietary assessments of the component studies, which may vary
depending on the method used (25). Underreporting of calories
has often contributed to the error associated with dietary
assessments, particularly in overweight individuals. Generally, 4-
to 7-d food records are considered to be the most accurate means
of dietary assessment, but such methods are generally not feasible
in large cohort studies. A single 24-h recall is relatively easy to
collect, but the information does not reflect long-term dietary
patterns. FFQs have become the method of choice in large epidemiologic
studies because they are inexpensive and can assess
long-term diets (25); however, this method is also subject to
random and systematic errors.
This, again, goes back to my original statement. Going back on data that doesn't have a selective criteria and agreed upon method of obtaining results is horse shit. You can make claims all you want, but the fact that they can't fucking agree on how to collectively obtain dietary intake makes this paper plausible and only a theory. This is exactly why genomics tests are neither proof or fact of disease assessments because they can't agree on how to fucking judge/measure/whatever the fuck you want to call it on taking measurements. I mean, it's annoying that you cite this shit and the end result is that they make claims on data they obtained by asking them fucking questions. Patients LIE and everyone knows it. Dietary measurements by asking questions is beyond stupid and not worthy of any amount of time spent reading hte paper. You can get any answer with statistics, doesn't mean it's right.
Most recently, however, an analysis
conducted in a pooled cohort of studies showed a lower CHD risk
when saturated fat was replaced with polyunsaturated fat and
increased nonfatal myocardial infarction, but not fatal CHD, risk
when saturated fat was replaced with carbohydrate (24).
Inverse associations of polyunsaturated fat and CVD risk have
previously been reported (41, 42). Replacement of 5% of total
energy from saturated fat with polyunsaturated fat has been
estimated to reduce CHD risk by 42% (43). Notably, the amount
of dietary polyunsaturated fat in relation to saturated fat (ie, the P:
S ratio) has been reported to be more significantly associated with
CVD than saturated fat alone, with a reduced CHD risk found
with P:S ratios 0.49
This is from your conclusion...which is admittedly inconclusive
It damages your blood vessels. It destroys your organs. It does systemic damage to your body. But oh yes, just drink a few glasses of water and you'll be OK.
It may be doing some of those things in great excess. The studies you linked basically say:
* in large amounts sodium is bad for you. oookaaaay
* The only evidence with regards to damage to organs is in patients who are very sensitive to sodium. Quoting from one of your links, "There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries." (i.e. exactly what i said with regards to pre-existing conditions)
* the greatest benefit of sodium reduction was seen in patients with high blood pressure (i.e. almost exactly what i said with regards to pre-existing conditions)
etc.
I mean, you can try to paint sodium as this big bad evil micro-nutrient, but it isn't. Yes, it is bad for you if you have other health problems, as it will just exacerbate them. If you're healthy though, excess sodium won't hurt you in any noticeable way.
Furthermore, there was insufficient statistical power for this
meta-analysis to assess the effects on CVD risk of replacing
specific amounts of saturated fat with either polyunsaturated fat
or carbohydrate.
It damages your blood vessels. It destroys your organs. It does systemic damage to your body. But oh yes, just drink a few glasses of water and you'll be OK.
It may be doing some of those things in great excess. The studies you linked basically say:
* in large amounts sodium is bad for you. oookaaaay
* The only evidence with regards to damage to organs is in patients who are very sensitive to sodium. Quoting from one of your links, "There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries." (i.e. exactly what i said with regards to pre-existing conditions)
* the greatest benefit of sodium reduction was seen in patients with high blood pressure (i.e. almost exactly what i said with regards to pre-existing conditions)
etc.
I mean, you can try to paint sodium as this big bad evil micro-nutrient, but it isn't. Yes, it is bad for you if you have other health problems, as it will just exacerbate them. If you're healthy though, excess sodium won't hurt you in any noticeable way.
It damages your blood vessels. It destroys your organs. It does systemic damage to your body. But oh yes, just drink a few glasses of water and you'll be OK.
It may be doing some of those things in great excess. The studies you linked basically say:
* in large amounts sodium is bad for you. oookaaaay
* The only evidence with regards to damage to organs is in patients who are very sensitive to sodium. Quoting from one of your links, "There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries." (i.e. exactly what i said with regards to pre-existing conditions)
* the greatest benefit of sodium reduction was seen in patients with high blood pressure (i.e. almost exactly what i said with regards to pre-existing conditions)
etc.
I mean, you can try to paint sodium as this big bad evil micro-nutrient, but it isn't. Yes, it is bad for you if you have other health problems, as it will just exacerbate them. If you're healthy though, excess sodium won't hurt you in any noticeable way.
It damages your blood vessels. It destroys your organs. It does systemic damage to your body. But oh yes, just drink a few glasses of water and you'll be OK.
It may be doing some of those things in great excess. The studies you linked basically say:
* in large amounts sodium is bad for you. oookaaaay
* The only evidence with regards to damage to organs is in patients who are very sensitive to sodium. Quoting from one of your links, "There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries." (i.e. exactly what i said with regards to pre-existing conditions)
* the greatest benefit of sodium reduction was seen in patients with high blood pressure (i.e. almost exactly what i said with regards to pre-existing conditions)
etc.
I mean, you can try to paint sodium as this big bad evil micro-nutrient, but it isn't. Yes, it is bad for you if you have other health problems, as it will just exacerbate them. If you're healthy though, excess sodium won't hurt you in any noticeable way.
It cuts your statement in about half, as a pound is roughly equal to two kilograms, which would make the LD50 of sodium chloride in humans about 500mg/lbs
Who the fuck cares? Really? Do you know what happens when you bank on macro studies that aren't fully supported by the micro ones? Well a good example would be DDT. Macro it appeared great, until we started looking at the micro effect and then whoooops.
Wee, strawman. If they did the proper macro studies in the 1940's, they would've realized that it was completely fucked without even going into the mechanistic stuff. They never thought to do (the now commonplace) chronic exposure studies on fish or other model animals. They just figured, "Hey it kills bugs! Cool!"
On the other hand, ketogenic diets are safe on both macro and micro scales. It's just that when you get into something that's as complex as nutrition, micro studies are of limited benefit imo.
Now with regards to Sodium and blood pressure whoooops you're full of shit.
If you read the article I posted earlier, yes, the APHA is full of shit. The salt debate is highly politicized on both sides, and the effects of salt consumption on blood pressure is not conclusive. Much of the evidence for the salt-blood pressure link that forms the basis of the APHA recommendations are based on research by guys like Cutler, Stamler, et al (see the references section). Apparently, their research is silly goosery. There's no causal link between salt intake and blood pressure. In fact, this whole debate is reminiscent of the saturated fat "debate" that we're just getting over.
Spoilered for wall o' quotes
... By the same logic, cutting salt consumption a small amount might have little effect on a single individual — just as going from 20 cigarettes to 19 would — but a major impact on mortality across an entire population.
Although Rose’s proposition made intuitive sense, it still rested on the unproven conjecture that avoiding salt could reduce blood pressure, a conjecture that was beginning to seem extraordinarily resistant to any findings that might negate it. In 1979, for instance, Stamler and his Northwestern colleagues tested the hypothesis in an intrapopulation study of Chicago schoolchildren. They compared blood pressure in 72 children to salt intake, estimated from seven consecutive 24-hour urine samples, enough to reliably reflect habitual sodium intake. They reported a "clear-cut" relationship between sodium and blood pressure in the children but then tried twice to reproduce the result and failed twice.
"A variety of potential explanations of this phenomenon could be advanced," the authors wrote, one of which was the obvious: "No relationship in fact exists between sodium and [blood pressure]. ..." They then listed five reasons why they might have missed the expected relationship — insensitive measurement techniques, for instance, or genetic variability obscuring the role of sodium, or the possibility that "the true relationship is not yet evident in children." Because the first of the three studies was positive, Stamler and his colleagues concluded that their data were "not wholly negative" and "do in fact suggest a weak and inconsistent relationship."
This logic served to manifest what Simpson called "the resilience and virtual indestructibility of the salt-hypertension hypothesis. Negative data can always be explained away."
After years of work by nearly 150 researchers, the results appeared in the same 1988 BMJ issue that included the Scottish Heart Health Study. Intersalt had failed to confirm its primary hypothesis, which was the existence of a linear relationship between salt intake and blood pressure. Of the 52 populations, four were primitive societies like the Yanomamo with low blood pressure and daily salt intake below 3.5 grams. They also differed, however, in virtually every other imaginable way from the 48 industrialized societies that had higher blood pressure. The remaining 48 revealed no relationship between sodium intake and blood pressure. The population with the highest salt intake, for instance — in Tianjin, China, consuming roughly 14 grams a day — had a median blood pressure of 119/70 mmHg, while the one with the lowest salt intake — a Chicago African-American population at 6 grams a day — had a median blood pressure of 119/76 mmHg. Only body mass and alcohol intake correlated with blood pressure in this comparison.
The Intersalt researchers did derive two positive correlations between salt and blood pressure. One weak association appeared when they treated the 10,000-plus subjects as a single large population rather than 52 distinct populations. It implied that cutting salt intake from 10 grams a day to four would reduce blood pressure by 2.2/0.1 mmHg. The more potent association was between salt intake and the rise in blood pressure with age: Populations that ate less salt experienced a smaller rise than did populations that ate more salt. If this relationship was causal, Intersalt estimated, then cutting salt intake by 6 grams a day would reduce the average rise in blood pressure between the ages of 25 and 55 by 9/4.5 mmHg.
These findings made Intersalt Rorschach-like in its ability to generate conflicting interpretations. John Swales wrote off the results in an accompanying BMJ editorial, saying the potential benefit, if any, was so small it "would hardly seem likely to take nutritionists to the barricades (except perhaps the ones already there)." Today, the majority of the researchers interviewed by Science, including Intersalt members such as Daan Kromhout and Lennart Hansson, see it as a negative study. Says Hansson, "It did not show blood pressure increases if you eat a lot of salt."
As Davey Smith explained to Science, their commentary identified a litany of problems with Intersalt Revisited, from "O-level mathematical mistakes" to basing their statistical corrections on assumptions unsupported by data. For instance, in order to correct for regression dilution bias, Stamler and his colleagues assumed that changes in sodium intake and blood pressure in any individual were independent of each other over periods of a few weeks. But if blood pressure and salt intake did fluctuate together, Davey Smith and Phillips noted, then the Intersalt corrections would result in "an inappropriately inflated estimate." The two epidemiologists cited studies concluding that blood pressure and salt intake are related in the short term and pointed out that "the very hypothesis under test — that sodium intake ... is related to blood pressure — would predict [these] associations."
In their response, published in the same issue, Stamler and his colleagues insisted that their corrections were legitimate because the "totality of the evidence — the only sound basis for judgment on this matter — supports the conclusion that this association is causal." They cited the "independent expert groups, national and international," that had concluded habitual high salt intake was a causal factor of high blood pressure, although they neglected to mention that those groups had all relied on Intersalt circa 1988 to reach their conclusions. Intersalt also listed seven reasons why their original estimate was "probably underestimated" but seemed to make no attempt to find reasons why it might have been overestimated. "It was embarrassing to read," Harvard School of Public Health epidemiologist Jamie Robins told Science, while describing Intersalt’s arguments as "arcane, bizarre, and special pleading."
There's so many hundreds of manuscripts on the salt-blood pressure link that you can easily find evidence for either side. In my mind, there's no consensus on this issue.
As for salt's other effects, I don't know anything on those subjects, so I'll pass.
The only reason I'm doing this is because you're not giving out concrete facts. You reference papers, but you shouldn't be doing this since you're not qualified.
I may not be at my sharpest right now, but I'm pretty sure this argument right here is exactly what I didn't want to happen
Instead of trading papers, I think it would be more helpful for us all to take a breather and investigate how the system works - do the biological math. Arguing about hormone regulated fat metabolism was exciting, because it was conducive to independent learning. Plus, establishing a "metabolic story" for these diets is a good way to show the strengths and potential weaknesses of each - not to mention any published evidence you produce will be a lot more black and white. Plus, at least there will be portions of each theory that everyone can agree on, like hyperinsulinemia is conducive to fat storage. For instance I can easily introduce a productive bone of contention: Insulin is one of the hormones necessary for fetal growth in pregnant women and lactation in nursing women: will its levels be enough on a ketotic diet? It's a practical argument respectful of each party's side and has a definite conclusion, ergo progress.
Paladin on
Marty: The future, it's where you're going? Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
Wait braincow, I don't know that it is fair to use an article by Gary Taubes as your source to prove that the APHA is full of shit.
Not saying he is wrong, but this is a bit like asking Don Quixote to write a paper on why windmills are evil
dude is the most accomplished science journalist in the world.
show some fucking respect.
Appeal to authority lols
But seriously, I understand he is a very respected figure. But to use the initiator of a debate as your source to prove that the "other side" is full of shit seems...tree housey.
EDIT: Because in this case I can easily just say the APHA is the oldest and most diverse organization of public health professionals in the world. (to quote their website and wikipedia)
Wait braincow, I don't know that it is fair to use an article by Gary Taubes as your source to prove that the APHA is full of shit.
Not saying he is wrong, but this is a bit like asking Don Quixote to write a paper on why windmills are evil
dude is the most accomplished science journalist in the world.
show some fucking respect.
Appeal to authority lols
But seriously, I understand he is a very respected figure. But to use the initiator of a debate as your source to prove that the "other side" is full of shit seems...tree housey.
that is not an appeal to authority. You are dismissing an entire argument, and refusing to read it, because you dont like the authors name.
Wait braincow, I don't know that it is fair to use an article by Gary Taubes as your source to prove that the APHA is full of shit.
Not saying he is wrong, but this is a bit like asking Don Quixote to write a paper on why windmills are evil
dude is the most accomplished science journalist in the world.
show some fucking respect.
Appeal to authority lols
But seriously, I understand he is a very respected figure. But to use the initiator of a debate as your source to prove that the "other side" is full of shit seems...tree housey.
EDIT: Because in this case I can easily just say the APHA is the oldest and most diverse organization of public health professionals in the world. (to quote their website and wikipedia)
That's fair. I'm a bit too busy to dig out the relevant primary articles, so this will have to do for now. But anyways, this doesn't mean that the information in the article is incorrect.
Posts
Big macs also have an absurd amount of sodium in them
Meat, cheese and blood pressure that would make a 55 year old diabetic overweight sedentary black male feel good about himself
But if you're a healthy individual, then there is no reason to avoid it.
but drink enough water, says the peanut gallery in perfect unison
Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
I don't think that's how science works
There is nothing to disagree on since you're objectively wrong. You can review the sodium research if you want, although I have to warn you that it's quite extensive. The only time sodium becomes dangerous is when it reaches amounts close to 1g per body weight in lbs, which is why people out in the sea die without fresh water, or why the ancient Chinese committed suicide by eating salt tablets. Nothing in the modern diet comes even close to those amounts though.
well I mean, plenty of things could happen before you actually die, like renal failure and brain shrinkage and heart failure
I don't know why I'm picking on you I should probably take a break
Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
So . . take a break, please.
As supporting proof, please read this article on the science and politics of dietary salt research (winner of the 1999 Science in Society Journalism Awards!)
tl;dr version: excess dietary salt has not conclusively been identified as the causative agent for high blood pressure.
To tell you the truth I feel more comfortable discussing these topics in terms of biochemical pathways than macroscopic studies. But in order to get a good pathway going, you've got to cite several papers proving each link in the chain if you want to be thorough. I don't know about you, but I'd like the discussion to go in a direction where the initial idea is laid out as a grand diagram of fat metabolism to prove your point, and then we go after individual processes with cited references. Because while studies showing no correlation between ketotic fat consumption and heart disease are nice, they don't tell us anything that bulletproof the methods for general instruction, use, and exception.
But yes, I agree that my discourse has deteriorated, on my part due to lack of sleep resulting in bad judgment.
Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
I'll read that in a bit thanks (even though it supports my views).
I'm not sure where you're going with this. Double-blind clinical studies are considered the gold standard in medical research precisely because they are macroscopic. They give you information on the exact things we're interested in, ie growth rate, muscle synthesis, fat loss.
Research into biochemical pathways are fine in determining mechanisms, but don't usually translate well to whole organisms because they are so myopic. Yeah yeah, ketosis does a, b, c in pathway X, but who the fuck cares aside from scientists? As well, these are usually done in model animals, which may or may not translate to humans.
Who the fuck cares? Really? Do you know what happens when you bank on macro studies that aren't fully supported by the micro ones? Well a good example would be DDT. Macro it appeared great, until we started looking at the micro effect and then whoooops.
Now with regards to Sodium and blood pressure whoooops you're full of shit.
http://ajph.aphapublications.org/cgi/content/full/94/1/19
I draw you to the relevant paragraph here, written conveniently in plain language,
and here,
Now either the APHA are full of shit and don't know their assholes from their elbows, or sodium is not a good thing to be gorging on and you're giving out some fucking reckless advice.
And there are literally dozens of papers showing how high levels of sodium are dangerous outside of high blood pressure,
http://hyper.ahajournals.org/cgi/content/abstract/15/6/900
http://ajprenal.physiology.org/cgi/content/abstract/297/2/F237
http://archinte.ama-assn.org/cgi/content/abstract/157/21/2449
It damages your blood vessels. It destroys your organs. It does systemic damage to your body. But oh yes, just drink a few glasses of water and you'll be OK.
NOTE: Do NOT just recommend me the books in the OP, I am trying to get at the actual academic research here
I'm not so much hot on the biochemistry of lipid digestion, my research focus is cardiac & large blood vessel remodeling.
I don't know if that link works or not.
This is from your conclusion...which is admittedly inconclusive
It may be doing some of those things in great excess. The studies you linked basically say:
* in large amounts sodium is bad for you. oookaaaay
* The only evidence with regards to damage to organs is in patients who are very sensitive to sodium. Quoting from one of your links, "There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries." (i.e. exactly what i said with regards to pre-existing conditions)
* the greatest benefit of sodium reduction was seen in patients with high blood pressure (i.e. almost exactly what i said with regards to pre-existing conditions)
etc.
I mean, you can try to paint sodium as this big bad evil micro-nutrient, but it isn't. Yes, it is bad for you if you have other health problems, as it will just exacerbate them. If you're healthy though, excess sodium won't hurt you in any noticeable way.
Sorry, it was protein shakes paper
http://www.ajcn.org/cgi/content/abstract/ajcn.2009.27725v1
You said eating 1g of sodium is bad
http://www.annecollins.com/sodium_diet/sodium-hot-dogs.htm
And tell me people only eat one fucking hotdog
Actually - just look at this
http://www.fatcalories.com/results/rs_allthefacts.cfm?Rest3=Burger+King&Rest7=McDonald%27s&SortOrder=Sodmg&CatSearch=Sandwiches&SortAD=DESC&Submit=Search
Your lack of reading comprehension is astounding. I said eating 1g of sodium per 1lbs of bodyweight is fatal.
I wasn't done
http://news.ucsf.edu/releases/even-a-small-dietary-reduction-in-salt-could-mean-fewer-heart-attacks-strok/
It cuts your statement in about half, as a pound is roughly equal to two kilograms, which would make the LD50 of sodium chloride in humans about 500mg/lbs
Just pointing that out.
Wee, strawman. If they did the proper macro studies in the 1940's, they would've realized that it was completely fucked without even going into the mechanistic stuff. They never thought to do (the now commonplace) chronic exposure studies on fish or other model animals. They just figured, "Hey it kills bugs! Cool!"
On the other hand, ketogenic diets are safe on both macro and micro scales. It's just that when you get into something that's as complex as nutrition, micro studies are of limited benefit imo.
If you read the article I posted earlier, yes, the APHA is full of shit. The salt debate is highly politicized on both sides, and the effects of salt consumption on blood pressure is not conclusive. Much of the evidence for the salt-blood pressure link that forms the basis of the APHA recommendations are based on research by guys like Cutler, Stamler, et al (see the references section). Apparently, their research is silly goosery. There's no causal link between salt intake and blood pressure. In fact, this whole debate is reminiscent of the saturated fat "debate" that we're just getting over.
Spoilered for wall o' quotes
There's so many hundreds of manuscripts on the salt-blood pressure link that you can easily find evidence for either side. In my mind, there's no consensus on this issue.
As for salt's other effects, I don't know anything on those subjects, so I'll pass.
still, my statement stands
Not saying he is wrong, but this is a bit like asking Don Quixote to write a paper on why windmills are evil
dude is the most accomplished science journalist in the world.
show some fucking respect.
Instead of trading papers, I think it would be more helpful for us all to take a breather and investigate how the system works - do the biological math. Arguing about hormone regulated fat metabolism was exciting, because it was conducive to independent learning. Plus, establishing a "metabolic story" for these diets is a good way to show the strengths and potential weaknesses of each - not to mention any published evidence you produce will be a lot more black and white. Plus, at least there will be portions of each theory that everyone can agree on, like hyperinsulinemia is conducive to fat storage. For instance I can easily introduce a productive bone of contention: Insulin is one of the hormones necessary for fetal growth in pregnant women and lactation in nursing women: will its levels be enough on a ketotic diet? It's a practical argument respectful of each party's side and has a definite conclusion, ergo progress.
Doc: That's right, twenty five years into the future. I've always dreamed on seeing the future, looking beyond my years, seeing the progress of mankind. I'll also be able to see who wins the next twenty-five world series.
Appeal to authority lols
But seriously, I understand he is a very respected figure. But to use the initiator of a debate as your source to prove that the "other side" is full of shit seems...tree housey.
EDIT: Because in this case I can easily just say the APHA is the oldest and most diverse organization of public health professionals in the world. (to quote their website and wikipedia)
that is not an appeal to authority. You are dismissing an entire argument, and refusing to read it, because you dont like the authors name.
The argument is in his article.
That's fair. I'm a bit too busy to dig out the relevant primary articles, so this will have to do for now. But anyways, this doesn't mean that the information in the article is incorrect.
Twice!
This is in direct response to the quote from Taubes about Intersalt.
Like I said, don't use the progenitor of an argument as a source to prove the argument is valid okay?