Evidence debunking low sodium diet

[Raryn]

Wow. I love this thread. Catching up has been a hoot. (I'm back after taking my shelf )

Let's summarize how it's gone so far:

1. CaptainSSO starts the thread by citing an article that Na doesn't have anything to do with HTN, thus "debunking" low sodium diets.
2. The "myth" that low-fat diets help obesity is brought up.
3. One small RCT that shows a low salt diet for 7 days might increase some measures of insulin resistance is cited.
4. Large, evidence based studies are brought up on the above points regarding that lowering Na intake is associated with a decrease in BP, even a modest decrease in BP is significant, and that both population trials and randomized controlled trials show that at least some sodium restriction lowers your risk of death. No further discussion of sodium has really taken place after this point.
5. Evidence-based randomized controlled trials of diets were brought up and show that there is no significant advantage to either low-fat or low-carb diets for weight loss after 1-2 years. Each have advantages for various metabolic measures, but it's impossible to call one "better". None of the strict low-carb proponents have cited any studies that suggest otherwise, though we've gotten several youtube videos.
6. Rothbard brings up the "uselessness" of statins.
7. Huge evidence-based trials are brought up that show statins reduce all-cause mortality significantly in primary prevention and secondary prevention as well as doing so cost effectively. It is acknowledged that there are possible arguments against using statins for primary prevention related to side effects, but there is absolutely no argument against secondary prevention.
8. Rothbard continues to dig himself into a hole by arguing against the evidence (as provided by the medical establishment). The crux of his argument seems to be that citing the experts of the exact field we're discussing is an "appeal to authority" (note: appealing to an authority in a field is only a fallacy if the authorities being appealed to aren't experts in the subject of discussion but are in fact random authorities. Such as citing the of a group of engineers in a discussion on climatology or something.)
9. Rothbard continues to dig himself into a hole by saying that "Detoxification, avoidance of pro-inflammatory foods, supplementation with antioxidants, stress reduction, etc." is the way to cure all that ails our patients. All of these things have either no evidence behind them or have evidence that they are actively harmful to our patients health (supplementation with antioxidants increases your risk of all-cause mortality)
10. The diabetes/statin link is hashed out. Does the evidence indicate that the two are linked? Yes. No one denies that, and arguments on whether something is barely statistically significant are useless. If it's significant, it's significant, unless you have a study with more power that shows it isn't. I'd rather have one extra at-risk patient develop diabetes than three patients die.
11.

Think about all the problems we have today-almost EVERYONE has to have braces--why is that? It can't be normal, nature would NEVER select for crooked teeth.

Think about what all the plastic surgeons we have today are doing-SO MANY people are getting boob jobs--why is that? It can't be normal, nature would NEVER select for small breasts.

Also, apparently people just started eating grains and sugar sometime in the 1950s, because that's when the incidence of diabetes went up. (Note: Pretty much all autoimmune conditions currently have increasing incidences. Do I know why? If I did, I'd publish it and get a Nobel. Lots of theories though, including related to hygiene. There's another factor with type I diabetes though: Before the 1920s it was damn near 100% fatal. Afterwards, it wasn't. Afflicted individuals survived to have children. There's a huge genetic association with type I)
12. Claims that hunter gatherers lived modern life expectancies while citing papers that say the exact opposite. (Note: The life expectancy at birth isn't a good measure anyway, too skewed by infant mortality. But look at the "life expectancy at age 45" numbers cited above. Right now, your average 45 year old american is expected to live to be 80. The numbers cited there range from 57-72)

In even more short: Four or five times in this thread, claims have been made that were the opposite of what is taught in medical school. Every time, evidence was cited supporting common medical practice. No convincing evidence has been cited a single time refuting the supporting evidence.

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[jdh71]

5. Evidence-based randomized controlled trials of diets were brought up and show that there is no significant advantage to either low-fat or low-carb diets for weight loss after 1-2 years. Each have advantages for various metabolic measures, but it's impossible to call one "better". None of the strict low-carb proponents have cited any studies that suggest otherwise, though we've gotten several youtube videos.

There is this one

The problem when you look at these studies though are really the end points. For me weight isn't as much of an important endpoint as body modification. What you really want your patients to do is cut fat, not just proportionately decrease in overall size, so now you're just a smaller fat guy. Ultimately, you'd like your patients to keep as much muscle as possible as this is better for overall metabolism and doesn't contribute to the hormonal milieu that same way the extra fat does.

The other problem with the low carb diets is that they've tended to run too low, and thereby are difficult to keep up with.

What I'd love to do someday if I can could ever get funding for it is to randomize patient's to a "usual care arm" - ie low fat, low calorie diet, exercise encouraged with a low carb arm that is around 75-100grams of carbs per day (you could have a single sammich), same calories, adding resistance training and walking.

But there's no money in prevention, just pills.

 

[SpecterGT260]

^Part of it is due to modern medicine, you're right, in that we have antimicrobials and trauma surgeons, incubators for babies, etc. I have a couple articles dealing with the subject, not with mortality per se, but rather with the lack of diseases of civilization found in hunter gatherer remains. I'll have to find them though. But a large factor in mortality was due to death from trauma/infections, and that by itself brings down the life expectancy. However, of those who DIDN'T succumb to infections/trauma/infant mortality their life expectancy was quite long. I'll need to find my sources though because I realize that is pretty counterintuitive. But the main point here is that they typically didn't suffer from the diseases of civilization that are so common today.

then the part about cancer was a logical extension. the 2 hit hypothesis is pretty solid right? not gunna get someone jumping down my throat for that one? if 2 hits occur randomly over a given time, then likelihood of a 2nd hit is somewhat time dependent. it follows that an increase in median age of death will bring with it an increased incidence of cancers.

but the main point was that homeopaths and naturopaths forget that before modern medicine and modern technological advances were around that people dropped like flies of all manner of things.... they attack the few short comings while ignoring the many short comings of their approach and also ignoring the many strengths. And however we want to slice this.... the natural/organic hippie crowd just gets to me... adoption of all of the "natural" BS across the globe would effectively kill about a third of humanity (since we've got ball busters in here im being conservative.... I think the number was higher than that)

 

[CaptainSSO]

Wow. I love this thread. Catching up has been a hoot. (I'm back after taking my shelf )

Let's summarize how it's gone so far:


4. Large, evidence based studies are brought up on the above points regarding that lowering Na intake is associated with a decrease in BP, even a modest decrease in BP is significant, and that both population trials and randomized controlled trials show that at least some sodium restriction lowers your risk of death. No further discussion of sodium has really taken place after this point.
5. Evidence-based randomized controlled trials of diets were brought up and show that there is no significant advantage to either low-fat or low-carb diets for weight loss after 1-2 years. Each have advantages for various metabolic measures, but it's impossible to call one "better". None of the strict low-carb proponents have cited any studies that suggest otherwise, though we've gotten several youtube videos.
6. Rothbard brings up the "uselessness" of statins.
7. Huge evidence-based trials are brought up that show statins reduce all-cause mortality significantly in primary prevention and secondary prevention as well as doing so cost effectively. It is acknowledged that there are possible arguments against using statins for primary prevention related to side effects, but there is absolutely no argument against secondary prevention.

11. Think about what all the plastic surgeons we have today are doing-SO MANY people are getting boob jobs--why is that? It can't be normal, nature would NEVER select for small breasts..

As far as the sodium is concerned, first I never conceded on that. It's just not worth arguing anymore. To cause the drop of 7 mmHg (7 mmHg was the figure you yourself stated) required a drop in HALF of sodium consumption. This is for people with Type 2 hypertension. For BP less than that, the drops are even less. We're not talking about not salting your eggs in the morning. We're talking about cutting out half of sodium consumption. 7 mmHg systolic drops for people with Type 2 hypertension is not significant--even it lowers their risk by 1.1 or whatever the number is (much less than 2x). Their risk is already way up. That's like telling someone with stage 4 lung cancer to stop smoking--it's not really going to make a difference at that point. Or here's a better analogy--it's like putting a band-aid on someone with a gash that needs 15 stitches.

The low carb diet study you cited was not even a low-carb diet, the percentages varied between like 30 and 40% or something ridiculous like that.

The study done with the Na+ and mortality had four cohorts showing the INVERSE relationship. You cannot just ignore that. If it was 10 cohorts showing a positive correlation and 4 showing no correlation, ok, that's a little different. But that's not what it was. I don't care if you think this study is so "notoriously hard" to do--you readily accept the results, except you throw out the parts you don't like because "they're hard to do." If they're so hard to do than I would be hesitant to accept the results anyway, irrespective of those 4 cohorts showing the inverse relationship.

I'm not going to address your comment about plastic surgery. You've got to be ****ing kidding me. If you can't see the difference between those 2 I don't know what to tell you.
Here's a picture of some teeth of aborigines in work done by Weston Price.

http://www.google.com/search?tbm=is...s&sa=N&biw=320&bih=356&q=aboriginal teeth#i=1

Anyway, this was a good discussion, not sure why you had to start being a smart ass.

Edit: No, people didn't just start eating flour and sugar in the 1950s, but that's when Ancel Keys and his buds were finally beginning to really get the ball rolling on low fat diets. Since we can't get most of our energy from proteins, low-fat by default means high carb.

http://www.google.com/search?tbm=is...disease 20th century&sa=N&biw=320&bih=356#i=1

Interesting, look at that chart and think about the percentages of all these diseases that are increasing. Animal fat consumption starts dropping around 1950s, which means, by default, carb consumption is increasing.

As far as questioning the current medical doctrine, you're right, that should never be done.

 

[SpecterGT260]

i really think the plastic surgery thing was sarcastic....

There is only 1 person in this thread dumb enough to actually think that is a valid point, and he's busy neverminding

 

[CaptainSSO]

i really think the plastic surgery thing was sarcastic....

There is only 1 person in this thread dumb enough to actually think that is a valid point, and he's busy neverminding

Hahaha.

 

[facetguy]

On the issue of long-term diet studies (>2 yrs), the evidence starts to thin out and trends toward equalization between diet types. However, we should keep in mind that there are plenty of studies that have shown that low-carb diets do stand up well when compared to other diets, including low fat diets, and not just for weight loss but for improvements in various metabolic endpoints (TGs, HDL, etc.). With that in mind, dogmatic adherence to solely the low fat diet is not evidence based, and patients (particularly patients with insulin issues) should be offered a low carb diet as a viable choice; this is not generally happening today.

Someone mentioned (I think somewhat tongue-in-cheek) that perhaps we've all started eating grains 50 years ago. Obviously, grains date back a little farther than that. But what has changed, at least according to some evidence, is the grain itself, particularly wheat which has been engineered for greater yield. These intentional alterations to wheat may be what has proven problematic, at least according to this book by cardiologist Wm. Davis:
http://www.amazon.com/Wheat-Belly-L...1543/ref=sr_1_1?ie=UTF8&qid=1330566643&sr=8-1

There is a new documentary film called "In Search of the Perfect Human Diet" which I haven't seen yet but explores many of the anthropological/evolutionary issues vis-a-vis diet. It's pro-Paleo diet if I'm not mistaken. In it, Cordain (those of you into this stuff know Cordain's work) apparently uses a football field analogy to explain how long 'we' ate a Paleo diet vs. our current post-agriculture diet; it's shown briefly in this trailer:
http://perfecthumandiet.us/

 

[SpecterGT260]

I gotta be honest... the whole "you are what you eat" thing strikes me as a little naive... maybe I am missing something, but the chemist in me wants to say "protein is protein" regardless of where it comes from. Most compounds are broken down in the GI system enough that I really don't think it matters how inbred it is... id want to see information in exactly which compounds are absorbed without complete breakdown before we start blaming crossbred grains

 

[facetguy]

I gotta be honest... the whole "you are what you eat" thing strikes me as a little naive... maybe I am missing something, but the chemist in me wants to say "protein is protein" regardless of where it comes from. Most compounds are broken down in the GI system enough that I really don't think it matters how inbred it is... id want to see information in exactly which compounds are absorbed without complete breakdown before we start blaming crossbred grains

I'll admit I haven't read Davis's book yet, but I've heard him on a couple of podcasts and he goes into quite a bit of detail.

 

[SpecterGT260]

ya, there is a lot about the GI system I don't know yet. Much of my assumption is based on things like "well you can drink snake venom with no ill effects" so a direct MHC-I style from inside to outside pathway really doesnt make sense. however.... flamingos are pink.... I dunno

 

[SpecterGT260]

As far as questioning the current medical doctrine, you're right, that should never be done.

I don't think anyone is saying we should not question current medical practice. there is a difference between being critical and being alarmist. I am one of the most critical people I know - to the eternal frustration of my classmates because I ask questions until I get an answer that satisfies me. none of this "that's just how it is" crap. But if I am critical of established practice, I am even more critical of those that challenge it. And IMO that is how it should be. There are plenty of eyes doing peer review, it is normal to be suspicious of some new research out of left field which contradicts current thinking supported by a pedigree of research.

be critical of everything you hear - but that isnt the same thing as rejecting everything you hear. somewhere along the lines people started blurring the distinction between the two words.

 

[Rothbard]

nm

 

[phltz]

and unless I am reading your link incorrectly I am not sure how I am "talking out of my ass". huntergatherers avg life expectancy at birth was 21-37 years... and I said "you;'d be lucky to hit 40".... its a hell of a long read so I maybe I missed something but your response is a straw man tactic for one, and doesn't exactly agree with your statement preceding it.

Life expectancy at birth is skewed by the large infant mortality rate. It might be worth saying "You'd be lucky to hit puberty". But once hunter gatherers make it to adulthood, an appreciable number of them made it to what we would recognize today as old age. 60 year olds are certainly more common now than they would have been 10,000 years ago, but they're far from unprecedented.

I'm not sure how this thread turned into a big discussion of the benefits of fat/carbs/protein/paleo diets. But seeing as how a lot of it has gone that way, it's worth pointing out that people evolved for the most part in conditions of sodium scarcity. The hunter-gatherer diet probably had much less sodium than the modern American gets. Additionally, our paleolithic forbears generally did a lot more sweating as they ran down game on the savanna, so they presumably had higher sodium losses as well. Plus there's evidence that the Na+/K+ ratio is as, if not more, significant than absolute Na+ intake, and our paleolithic ancestors almost certainly had a higher potassium consumption.

Pretty much every line of evidence and reasoning points to saying that the typical American would be very well served by cutting sodium consumption, and possibly getting more potassium as well. Is cutting sodium hard? Sure. But it's free, safe, and effective, so even if most of your patients don't cut it as much as you'd like, it's still worth recommending to them.

 

[CaptainSSO]

^Pretty much every line of evidence? Here's another one to the contrary. Bottom line is that there's not much good evidence that cutting sodium reduces disease, and evidence is even beginning to emerge supporting the opposite, re: the initial article I posted, the insulin resistance and Na+ article, and the one below. Are the conclusions definitive? Of course not, but we'll have to wait for more studies. In the meantime I'm not going to worry about adding salt to my popcorn.

http://www.ncbi.nlm.nih.gov/m/pubmed/16490476/


"The inverse relationship of sodium to CVD mortality seen here..."

 

[phltz]

^Pretty much every line of evidence? Here's another one to the contrary. Bottom line is that there's not much good evidence that cutting sodium reduces disease, and evidence is even beginning to emerge supporting the opposite, re: the initial article I posted, the insulin resistance and Na+ article, and the one below. Are the conclusions definitive? Of course not, but we'll have to wait for more studies. In the meantime I'm not going to worry about adding salt to my popcorn.

http://www.ncbi.nlm.nih.gov/m/pubmed/16490476/


"The inverse relationship of sodium to CVD mortality seen here..."

This is particularly uncompelling. This is an observational study, so the results could easily stem from some confounde, such as having been told to limit sodium consumption due to preexisting heart problems. Couple that with sodium consumption being estimated from a self-reported 24-hour recall of food consumption, and you're pretty much asking for people who know they should be eating less sodium to lie about their sodium intake.

 

[facetguy]

I'm not sure how this thread turned into a big discussion of the benefits of fat/carbs/protein/paleo diets. But seeing as how a lot of it has gone that way, it's worth pointing out that people evolved for the most part in conditions of sodium scarcity. The hunter-gatherer diet probably had much less sodium than the modern American gets. Additionally, our paleolithic forbears generally did a lot more sweating as they ran down game on the savanna, so they presumably had higher sodium losses as well. Plus there's evidence that the Na+/K+ ratio is as, if not more, significant than absolute Na+ intake, and our paleolithic ancestors almost certainly had a higher potassium consumption.
.

From page 10 of this PDF http://www.ajcn.org/content/81/2/341.full.pdf+html
"Taken together, the addition of manufactured salt to the food supply and the displacement
of traditional potassium-rich foods by foods introduced during the Neolithic and Industrial periods caused a 400% decline in the potassium intake while simultaneously initiating a
400% increase in sodium ingestion (4, 12, 159)."

"The inversion of potassium and sodium concentrations in hominin diets had no evolutionary precedent and now plays an integral role in eliciting and contributing to numerous diseases of
civilization."

 

[tiedyeddog]

From page 10 of this PDF http://www.ajcn.org/content/81/2/341.full.pdf+html
"Taken together, the addition of manufactured salt to the food supply and the displacement
of traditional potassium-rich foods by foods introduced during the Neolithic and Industrial periods caused a 400% decline in the potassium intake while simultaneously initiating a
400% increase in sodium ingestion (4, 12, 159)."

"The inversion of potassium and sodium concentrations in hominin diets had no evolutionary precedent and now plays an integral role in eliciting and contributing to numerous diseases of
civilization."

The last statement sounds like pure conjecture?

 

[CaptainSSO]

This is particularly uncompelling. This is an observational study, so the results could easily stem from some confounde, such as having been told to limit sodium consumption due to preexisting heart problems. Couple that with sodium consumption being estimated from a self-reported 24-hour recall of food consumption, and you're pretty much asking for people who know they should be eating less sodium to lie about their sodium intake.

It was 78 million people. Your observation might hold water if if was a smaller sample size, but variables of the type you're discussing are essentially going to get diluted out. The longer and larger the study, the less chance of things like someone misjudging their intake for that day will matter.

(On top of that, purely from a psychological standpoint, that doesn't really make sense. It was a 13 year long study. So what, for 13 years these people are sneaking off to eat Pringles and thinking, "Ah, I know I'm not supposed to be eating too much salt, so maybe if I just lie about it to these people it won't affect my health at all." Anyway, this is a side point for fun, my real argument is above.)

 

[phltz]

It was 78 million people. Your observation might hold water if if was a smaller sample size, but variables of the type you're discussing are essentially going to get diluted out. The longer and larger the study, the less chance of things like someone misjudging their intake for that day will matter.

(On top of that, purely from a psychological standpoint, that doesn't really make sense. It was a 13 year long study. So what, for 13 years these people are sneaking off to eat Pringles and thinking, "Ah, I know I'm not supposed to be eating too much salt, so maybe if I just lie about it to these people it won't affect my health at all." Anyway, this is a side point for fun, my real argument is above.)

A larger sample size will reduce random errors. It does nothing to address a systematic error, such as the one I proposed. This is very basic stats.

 

[CaptainSSO]

A larger sample size will reduce random errors. It does nothing to address a systematic error, such as the one I proposed. This is very basic stats.

Except it's not a systematic error. This is very basic common sense.

You're discounting the study based on your own (probably ungrounded) systematic error.

A. It doesn't make a lot of sense for most people to lie. See my point above.

B. Even if we assume some of thesepeople do lie, it certainly won't be most, so it won't be a systematic error.

Since you like to tell other people what "very basic stats" are, let's address that. Since it's a pretty fair assumption that tens of millions of people aren't going to lie about their sodium consumptions, the people who do lie would be more of a random error than a systematic one, thus being diluted by the sample size.

This is the way these large scale, long term dietary studies have to be done, unless you want to lock them all up in a hospital for 13 years. To suggest that enough people (out of 78 million) are lying to completely throw off the results of the study is just ridiculous, and wishful thinking. Take your blinders off.

 

[CaptainSSO]

-/

 

[phltz]

Except it's not a systematic error. This is very basic common sense.

You're discounting the study based on your own (probably ungrounded) systematic error.

A. It doesn't make a lot of sense for most people to lie. See my point above.

B. Even if we assume some of thesepeople do lie, it certainly won't be most, so it won't be a systematic error.

Since you like to tell other people what "very basic stats" are, let's address that. Since it's a pretty fair assumption that tens of millions of people aren't going to lie about their sodium consumptions, the people who do lie would be more of a random error than a systematic one, thus being diluted by the sample size.

This is the way these large scale, long term dietary studies have to be done, unless you want to lock them all up in a hospital for 13 years. To suggest that enough people (out of 78 million) are lying to completely throw off the results of the study is just ridiculous, and wishful thinking. Take your blinders off.

Studies have shown that dieting overweight individuals systematically underestimate the calories they consume <source> and overestimate the exercise they get <source>. Why is it so hard to believe that hypertensive individuals who have been recommended to consume less sodium would also systematically underestimate their sodium consumption?

 

[CaptainSSO]

Studies have shown that dieting overweight individuals systematically underestimate the calories they consume <source> and overestimate the exercise they get <source>. Why is it so hard to believe that hypertensive individuals who have been recommended to consume less sodium would also systematically underestimate their sodium consumption?

Those are different types of studies. Every participant in each of those studies has an active goal in mind--they're trying to lose weight. It makes sense that they'll inflate their numbers a little bit--it's like asking a high school kid how much he can bench press. You're assuming that the majority of the people in the 78 million person study are trying to eat less salt to reduce hypertension, and thus will underestimate their consumption. That's a huge assumption.

The Na+ study was just simply measuring values. If the goal of the Na+ study was specifically to cut salt in order to reduce hypertension, than ok I could agree that perhaps the results were swayed by people fudging numbers. But that wasn't what this study was.

But even so, it doesn't really make sense that the results would be off so bad that they were inversed. I can see maybe no correlation. But not inversed. That just doesn't make sense.

By the way, if you're so opposed to observational studies that you'll discount this entire study on your own largely unfounded assumption, how do you think a lot of the other Na+ studies were done--showing a direct relationship b/w Na+ and CVD? I bet a lot of those were observational as well.

Also, if you look at the full article, it says they excluded people with pre-existing heart disease as well as people on a low sodium diet for medical reasons.

http://www.amjmed.com/article/S0002-9343(05)01046-6/fulltext

Anyway, like I said before, I'm not suggesting that reduced sodium consumption = instant death. Clearly more studies need to be done in this area. But at the least they do show that the low sodium dietary recommendation is shaky at best--it's not founded on solid science. It was just a hypothesis that gained a large amount of momentum despite only tenuous evidence supporting it. It seems to me that at this point in time, we really can't say rather a reduced sodium diet is a good or bad idea. Instead of getting people to worry about eating less salt, I think we should get them to worry about eating less sugar and refined carbohydrates.

By the way, I forgot to bring up an important point about the low-carb diets. First, it's not carbohydrates per se that are the problem, it's refined carbohydrates (which for all intents and purposes are just the same as eating sugar), sucrose, HFCS, etc. These are the main problem. And my support of these diets is mainly for health reasons, not for weight loss (although they do work well for weight loss). You can definitely lose weight by eating less and exercising, but just because you're not overweight doesn't mean you're healthy.

 

[CaptainSSO]

Come at me Raryn.

OK, I seriously need to study now.

 

[CaptainSSO]

///

 

[CaptainSSO]

Let me pose a question: For those of you who don't believe that high carbohydrate diets are responsible for atherosclerosis, why exactly do you think those with diabetes have vastly increased risk of cardiovascular disease?

 

[SpecterGT260]

Let me pose a question: For those of you who don't believe that high carbohydrate diets are responsible for atherosclerosis, why exactly do you think those with diabetes have vastly increased risk of cardiovascular disease?

diabetes - Insulin dysfunction or insensitivity - either way.

The liver is largely insulin independant having mostly GLUT2 transporters which operate with a high Km - that is, it takes a buildup of glucose for GLUT2 to work at high capacity. Or a more functional way of thinking about it - GLUT2 does not allow transient leakage of glucose back and forth across a membrane. If glucose wants to get past it has to really want it (high gradient across membrane)

In situations of increased blood glucose, the GLUT2 of the liver will import glucose into hepatocytes which are not directly affected by the pathophysiology of diabetes (at least as far as glucose uptake goes).

Within the hepatocytes, the upstream pressure of increased [Glc] will cause glycolysis with a buildup at AcCoA due to the limited uptake abilities of the Krebs cycle. When AcCoA builds up, it can spontaneously react to form ketone bodies and it also triggers synthesis of fatty acids -

Fatty acid synthesis uses acetyl CoA and AcAcCoA to make saturated fatty acids (typically palmitate I believe...)

AcAcCoA is also directly involved in cholesterol synthesis, and barring any allosteric inhibition of pathway proteins, cholesterol synthesis will increase.

In essense, the upstream pressure of the buildup of AcCoA from increased blood glucose will ultimately result increased synthesis of both cholesterol and fatty acids which will be returned to the blood

 

[Kevin Baker]

I didn't see this posted yet but I found the Australian paradox to be an interesting critique to the Cult of Taubes.

http://www.mdpi.com/2072-6643/3/4/491

"Abstract: Ecological research from the USA has demonstrated a positive relationship between sugars consumption and prevalence of obesity; however, the relationship in other nations is not well described. The aim of this study was to analyze the trends in obesity and sugar consumption in Australia over the past 30 years and to compare and contrast obesity trends and sugar consumption patterns in Australia with the UK and USA. Data on consumption of sugar in Australia, the UK and USA were obtained from the Food and Agriculture Organization for the years 1980–2003. The prevalence of obesity has increased 3 fold in Australians since 1980. In Australia, the UK and USA, per capita consumption of refined sucrose decreased by 23%, 10% and 20% respectively from 1980 to 2003. When all sources of nutritive sweeteners, including high fructose corn syrups, were considered, per capita consumption decreased in Australia (&#8722;16%) and the UK (&#8722;5%), but increased in the USA (+23%). In Australia, there was a reduction in sales of nutritively sweetened beverages by 64 million liters from 2002 to 2006 and a reduction in percentage of children consuming sugar-sweetened beverages between 1995 and 2007. The findings confirm an “Australian Paradox”—a substantial decline in refined sugars intake over the same timeframe that obesity has increased. The implication is that efforts to reduce sugar intake may reduce consumption but may not reduce the prevalence of obesity."

Now, I'm not one to claim causation from correlation but it seems to me, there is something more to the issue than simple sugars/carbs.

 

[CaptainSSO]

diabetes - Insulin dysfunction or insensitivity - either way.

The liver is largely insulin independant having mostly GLUT2 transporters which operate with a high Km - that is, it takes a buildup of glucose for GLUT2 to work at high capacity. Or a more functional way of thinking about it - GLUT2 does not allow transient leakage of glucose back and forth across a membrane. If glucose wants to get past it has to really want it (high gradient across membrane)

In situations of increased blood glucose, the GLUT2 of the liver will import glucose into hepatocytes which are not directly affected by the pathophysiology of diabetes (at least as far as glucose uptake goes).

Within the hepatocytes, the upstream pressure of increased [Glc] will cause glycolysis with a buildup at AcCoA due to the limited uptake abilities of the Krebs cycle. When AcCoA builds up, it can spontaneously react to form ketone bodies and it also triggers synthesis of fatty acids -

Fatty acid synthesis uses acetyl CoA and AcAcCoA to make saturated fatty acids (typically palmitate I believe...)

AcAcCoA is also directly involved in cholesterol synthesis, and barring any allosteric inhibition of pathway proteins, cholesterol synthesis will increase.

In essense, the upstream pressure of the buildup of AcCoA from increased blood glucose will ultimately result increased synthesis of both cholesterol and fatty acids which will be returned to the blood

That's one of the mechanisms, you are correct. Advanced glycation end products, insulin resistance, hyperinsulinemia, increased blood glucose likely all play a role. Excess carbs --> insulin secretion ---> acetyl CoA carboxylase ---> fatty acid synthesis ---> VLDL secreted by the liver ---> metabolized into LDL. But all these processes happen in people who aren't diabetic as well, just not to the same extent. There is a huge disjoint between our ideas of why diabetics get heart disease and why non diabetics get heart disease, whereas the most likely explanation is that there is a similar mechanism. We tend to think of diabetics as a separate class, whereas it's more of a continuum from a healthy person to a diabetic, with several steps along the process.

^Kevin Baker, it's not just sweeteners. It's refined carbohydrates in general. So if I stop drinking so much soda and start eating more bread and pasta, that's not going to ameliorate the problem. So if you were to show me a study like that where the consumption of all refined carbohydrates and sugar decreased, then that would be worth exploring further, and I'd be more likely to reevaluate my ideas. You can avoid eating a single milligram of sugar, but if the other types of carb consumption don't drop it won't mean a thing.

It would be like doing a study on gun murder and saying "Well, the sale of 9 mm's are down, but murder rates haven't changed." But unless you're looking at .38's, .45's, and .22's, you're not getting the big picture.

 

[SpecterGT260]

That's one of the mechanisms, you are correct. Advanced glycation end products, insulin resistance, hyperinsulinemia, increased blood glucose likely all play a role. Excess carbs --> insulin secretion ---> acetyl CoA carboxylase ---> fatty acid synthesis ---> VLDL secreted by the liver ---> metabolized into LDL. But all these processes happen in people who aren't diabetic as well, just not to the same extent. There is a huge disjoint between our ideas of why diabetics get heart disease and why non diabetics get heart disease, whereas the most likely explanation is that there is a similar mechanism. We tend to think of diabetics as a separate class, whereas it's more of a continuum from a healthy person to a diabetic, with several steps along the process.

^Kevin Baker, it's not just sweeteners. It's refined carbohydrates in general. So if I stop drinking so much soda and start eating more bread and pasta, that's not going to ameliorate the problem. So if you were to show me a study like that where the consumption of all refined carbohydrates and sugar decreased, then that would be worth exploring further, and I'd be more likely to reevaluate my ideas. You can avoid eating a single milligram of sugar, but if the other types of carb consumption don't drop it won't mean a thing.

It would be like doing a study on gun murder and saying "Well, the sale of 9 mm's are down, but murder rates haven't changed." But unless you're looking at .38's, .45's, and .22's, you're not getting the big picture.

insulin resistance (which is probably what is most relevant here) will mean that glucose levels are chronically elevated. When this happens in healthy people it is post-meal and insulin clears the glucose. DM2 is the equivalent (in this example) of rush hour and closing down all roads except 1 - the liver. and the only way out of the liver is to come out as a VW beetl...er.... I mean fat

EDIT: I've always found it counter intuitive to consider diabetics separately in terms of metabolism vs non-diabetics. Most of the same pathways will be intact in diabetics..... its just that the outputs will be abnormal with abnormal inputs.

 

[CaptainSSO]

Importantly here, the mechanism we discussed, endogenous triglyceride synthesis and subsequent VLDL increases, will apply to anyone, diabetic or not, eating a high carbohydrate meal. The blood glucose is cleared post meal, but the way in which that blood glucose is cleared leads to problems.

Edit: It is also worth noting that despite good control of chronic blood glucose levels with exogenous insulin and other pharmaceuticals, the incidence of atherosclerosis and CVD is still way up for diabetics than for non-diabetics.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144314/?tool=pmcentrez

 

[SpecterGT260]

Are.... are we agreeing then?

 

[CaptainSSO]

We are if you are agreeing that the primary mechanism of atherosclerosis for the vast majority of the population (of the US that is, since Kevin Baker has apparently established that Australians are immune to the influence of sugar) is indeed via high carbohydrate consumption?

(That was my main point regarding diabetics--you elucidated the mechanism yourself, I was just implying that the same mechanism is the impetus for CVD in healthy individuals, as well--simply at a slower rate).

 

[SpecterGT260]

well.... I don't know if I would go that far. Fat and cholesterol synthesis are not free-energy processes and glucose metabolism is usually pretty well regulated via insulin production (same GLUT2 transporters are on pancreas cells which import glucose only in high concentration states thereby triggering insulin release).

As a chemist via undergrad - I tend to think of nearly everything as a continuum so I do not disagree at all that sugar consumption alone can lead to atherosclerosis.

but as for a primary mechanism in healthy individuals..... The major reason I have trouble with that is because with proper GLUT4/insulin activity we have lots of places other than fat and cholesterol for glycolytic processes to go. ANY system can be overwhelmed - true, and after seeing the house of the CEO of PepsiCo I can imagine how much sugar is coursing through our veins at any given moment lol....

however, I suspect we eat just as much foods already high in cholesterol and fats. Cholesterol itself is pretty highly conserved in the body through bile re-uptake, so all in all I don't see carbs being the major contributor as compared to the more effecient process of simple fat and cholesterol absorption.

When it gets to pts with diabetes, the dietary lipids are assumed to be the same (unless they are diagnosed and acting accordingly) and now the glycolytic buildup has a pronounced effect independent from a normal unhealthy diet. One thing that supports this idea for me is that normal people do not become ketoacidotic without crash dieting. But diabetic ketoacidosis represents an overwhelmed system where even fat production cant keep up with the sugar levels - so they go to circulating ketone bodies and are excreted in urine. again, it is all on a continuum, but significant increases in a side product of a reaction typically represents a primary system that is approaching being overwhelmed.
--the continuum comment there is meant to illustrate that in chemistry you rarely really max out a process. So thinking about metabolic reacitions in terms of "this happens first, then this happens, then this" is sufficient for most purposes but it largely inaccurate. A better way is usually to think of it in terms of "component X has a processing rate of n%*[X]" whereby ALL possible processes are happening simultaneously and the substrate concentration interplays with various Km's to determine how much of which processes are happening. GLUT2, even with its high Km, will have a finite positive net activity even at trace glucose levels - it is just the nature of how affinities work. "all or none" is really not a valid chemical concept in the majority of cases except in situations where enzymes are allosterically or covalently inactivated

TL;DR
anything you put into your body (carb, lipid, protein) will provide a given % contribution to circulating cholesterol and therefore risk of athero. We (as in you and I, or maybe just I.... depending on if the research is out there) need more information to decide where the major contributing factors are.

 

[CaptainSSO]

^There is in fact a lot of research out there. You are correct in that our diet will increase the % of circulating cholesterol; however, circulating cholesterol (more specifically, the different lipoproteins which ferry it) is quite a heterogeneous group. One thing worth mentioning is that not all low density lipoproteins are equivalent, and the two different types increase or decrease depending on diet. I'll try to dig up a couple articles. The small, dense kind is the bitch of the bunch, and tends to be elevated in those with heart disease, metabolic syndrome, diabetes, etc. And there is good evidence that carbs are what do it.

You really should read Good Calories, Bad Calories though. He spent a few years doing all the research, so he really sorted everything out pretty damn well. You're the first person I've talked to who I've actually felt I have a decent shot at convincing (that's a compliment), and the book would just do a much better job than I am.

 

[moosetracks]

Excellent video. Taubes is the single best thing to happen to nutritional science in the last few years. I've been in contact with him trying to get him to come to my school. I'm so frustrated when I'm in clinic and obese patients (like 75% of our patient population) come in and the doctor or PA goes "you should make some lifestyle changes. Eat less and exercise more. Eat low fat foods." Ughhhh. How's that worked so far? Last I checked, the country got fatter as dietary fat consumption has gone down, per the recommendations of the 'experts'. I wish I could speak up, but I'm just the lowly med student. What I usually do is write down Why We Get Fat by Gary Taubes on a piece of paper and tell the patient to read it as they leave the room. I don't know how many have, but I'm hoping it's a couple.

Good discussion guys. Keep it up. It's amazing how much nutritional 'science' is obscured by hypotheses that certain people want to be true but the evidence doesn't support. It's 2012. We should know by now what optimal eating should consist of.

I have been on a low carb diet for about 6 months now and was trying to persuade my friends to get on it as well. I submitted to blood and urine test and my lab results were good. I was finally able to get them on the diet until one of them decided to ask a professor of food science who works on the production of grains asked them what he thinks about it. They each had lost about 5 lbs after 2 weeks but his words which went along the lines of "don't do it" without any evidence and they were off it. He stated cognitive deficits but every paper i've found has shown the opposite.

God I hate the ignorance with a passion.

 

[Kevin Baker]

I have been on a low carb diet for about 6 months now and was trying to persuade my friends to get on it as well. I submitted to blood and urine test and my lab results were good. I was finally able to get them on the diet until one of them decided to ask a professor of food science who works on the production of grains asked them what he thinks about it. They each had lost about 5 lbs after 2 weeks but his words which went along the lines of "don't do it" without any evidence and they were off it. He stated cognitive deficits but every paper i've found has shown the opposite.

God I hate the ignorance with a passion.

I hear ya bro. I hate ignorance. One time, I was in this thread where people were debating the benefits of low carb versus regular diets and after much debate, both sides settled on no long term proven evidence of one diet being better over another in regards to weight. Then some ignorant person came in and professed how his sample size of 1 experience proved what all the scientific papers previously presented failed to find.

 

[CaptainSSO]

Come to the dark side, Specter. It is delicious.

This was my dinner tonight. Minus the french fries, of course.

 

[facetguy]

I hear ya bro. I hate ignorance. One time, I was in this thread where people were debating the benefits of low carb versus regular diets and after much debate, both sides settled on no long term proven evidence of one diet being better over another in regards to weight. Then some ignorant person came in and professed how his sample size of 1 experience proved what all the scientific papers previously presented failed to find.

What are your suggestions?

 

[SpecterGT260]

I'm eating Mac and cheese with chilli on it and a cookie for dessert. Am I doing this right?

 

[valkener]

I have to say Im fortunate to be blessed with a superior metabolism so I can't speak from personal experience. However, as other people have said loosing weight is not only a question of diet but of lifestyle. Exercise should always accompany any weight-loss efforts.

Just as in drug addictions, people tend to find substitutions for their "drug" and if they pass on carbs (I'm not saying that it's effective or not) they eat something else afterwards. I suppose in the no carbs diet it would be another sugar-free sausage fest or Big Mac minus the buns.

We all know how hard it is to kick a bad habit and so it takes more than just substituting..

 

[facetguy]

http://www.theatlantic.com/health/archive/2012/03/whats-really-making-us-fat/254087/1/
Atlantic article on calories in/out and obesity. Also nice intro to topic of obesogens, which right now gets very little play.

 

[phltz]

http://www.theatlantic.com/health/archive/2012/03/whats-really-making-us-fat/254087/1/
Atlantic article on calories in/out and obesity. Also nice intro to topic of obesogens, which right now gets very little play.

This article is a disaster. The idea of obesogens only makes sense insofar as they mess with the homeostatic or metabolic mechanisms that control the calories you take in or the calories you put out. These aren't conflicting theories about how weight gain/loss works, they are two different ways of understanding and thinking about the same phenomenon. Neither point of view disproves or argues against the other. The author consistently misses the point here. It's hard to tell if that's because she's dumb or the scientists and physicians she talked to were all disingenuous. I'm guessing the fault lies with the author.

 

[facetguy]

This article is a disaster. The idea of obesogens only makes sense insofar as they mess with the homeostatic or metabolic mechanisms that control the calories you take in or the calories you put out. These aren't conflicting theories about how weight gain/loss works, they are two different ways of understanding and thinking about the same phenomenon. Neither point of view disproves or argues against the other. The author consistently misses the point here. It's hard to tell if that's because she's dumb or the scientists and physicians she talked to were all disingenuous. I'm guessing the fault lies with the author.

When you say '2 different ways of thinking about the same phenomenon', if you mean obesity then yes. If you mean simply 'calories in/out' then no; there's that black box in-between the in and the out that we call metabolism, and if obesogens are affecting metabolism then it becomes an important concept (yes, one of many important factors but important nonetheless).

 

[NightSwim]

CaptainSSO: You're over-looking the clinical implications of these research findings. You're right that this research is interesting and somewhat contrary to previous notion about a low-salt diet's effect on HTN. However, it's not like a low-salt diet is used in your standard treatment of essential hypertension. It's primary use is in CKD and CHF. Maintaining a low-salt diet isn't easy, especially when we're surrounded by processed food, but it's still very doable.

 

[CaptainSSO]

^I know it's not a first line treatment option, but it IS still recommended--just the other day a friend of mine told me his GP recommended a low salt diet (for HTN). But more importantly, there's a wide-spread public notion that salt is unhealthy. And so I believe it falls within the realm of physicians to address it--and at the least say, "We don't really know that sodium restriction is such a good idea for the general population."

 

[NightSwim]

^I know it's not a first line treatment option, but it IS still recommended--just the other day a friend of mine told me his GP recommended a low salt diet (for HTN). But more importantly, there's a wide-spread public notion that salt is unhealthy. And so I believe it falls within the realm of physicians to address it--and at the least say, "We don't really know that sodium restriction is such a good idea for the general population."

It's certainly an interesting issue you've brought up, to say the least, and well worth discussing. Didn't they tell you on the 1st day of medical school that something like half the stuff they'll teach you will turn out wrong. With issues like this, it will take way more than a few studies to come to a consensus, especially if recent evidence goes against past evidence. Excessive salt intake is still likely something you want to try to avoid.

 

[Morsetlis]

maybe some day we can feed all this science into a computer and we won't even need doctors anymore

Can't come soon enough.

Butlerian Jihad!

 

[facetguy]

NYT opinion piece:
http://opinionator.blogs.nytimes.com/2012/03/20/is-a-calorie-a-calorie/?src=tp

Key points:
“We need a farm bill that’s designed from top to bottom to support healthier diets, one that supports growing fruits and vegetables and making them cheaper. We need to fix school lunches so they’re based on fresh foods, and fix food assistance programs so people have greater access to healthier foods.”

“Stop marketing food to kids. Period. Just make it go away.”

 

[Raryn]

A couple of interesting letters in a recent JAMA regarding the sodium excretion/mortality study:

http://jama.ama-assn.org/content/307/11/1138.2.full and the reply from the original authors http://jama.ama-assn.org/content/307/11/1139.full