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Random Health thoughts - SWD version

metranger8694

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^ nice strawman.
Yes he is. A very smart man indeed who backs up his subject matter with science and thought. I think that many folks would love to be as in good physical condition, health and smarts as Mark at his age.

Any time you feel like posting corroborating articles/studies that support your erroneous articulations and beliefs here would be more than welcome.
 

hendrix

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Harvard school of public health days that for most people cholesterol from eggs doesn't make a difference. It should be noted that they have a premier program in health epidemiology. People who have high cholesterol mostly have it because their livers generate it. This as far as I can tell has become accepted as fact. Certainly eating 5+ eggs a day is probably not good for you but the evidence that an egg a day harms to is just not there

To add on, recent meta analyses have found no association with egg consumption and heart disease or stroke.

Saturated fats and trans fats are the dietary factors of concern with regard to serum cholesterol.

Eggs are also great for choline

@Benesyed No adverse effects associated with GMO consumption as far as we can tell. Whether monoculture and Monsanto et al should exist is another discussion.

I'm looking into this maybe I'm wrong but I do trust hms. More than health by style forun

These recent meta-analyses which have indeed caused somewhat of a stir have been based on flawed methodology. The reasons for this are outlined below.

1. Physiology and biochemistry. As we know, HDL and LDL are lipid transporters. Therefore, any time someone is losing weight they will have an improvement in the HDL:LDL ratio and general lipids. This makes sense and you can easily test it for yourself. The opposite is also true - any time you put on significant amounts of body fat your ratios will worsen - hence why sugary foods, even if they're low fat, are also bad for you from the CVD standpoint. This is also why someone's ratios can improve on a twinky diet so long as it's below maintenance calories.

TAKE AWAY: Study design needs to be ISOCALORIC. It is no use adding and removing eggs from a diet if its not substituted with something of the same caloric value. Moreover, if you're removing eggs and replacing with bacon, of course you're not going to see a result.


Here is an example of a meta-analysis done THE RIGHT WAY - using studies that controlled calorie content.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2125600/
OBJECTIVE: To determine the quantitative importance of dietary ***** acids and dietary cholesterol to blood concentrations of total, low density lipoprotein, and high density lipoprotein cholesterol. DESIGN: Meta-analysis of metabolic ward studies of solid food diets in healthy volunteers. SUBJECTS: 395 dietary experiments (median duration 1 month) among 129 groups of individuals. RESULTS: Isocaloric replacement of saturated fats by complex carbohydrates for 10% of dietary calories resulted in blood total cholesterol falling by 0.52 (SE 0.03) mmol/l and low density lipoprotein cholesterol falling by 0.36 (0.05) mmol/l. Isocaloric replacement of complex carbohydrates by polyunsaturated fats for 5% of dietary calories resulted in total cholesterol falling by a further 0.13 (0.02) mmol/l and low density lipoprotein cholesterol falling by 0.11 (0.02) mmol/l. Similar replacement of carbohydrates by monounsaturated fats produced no significant effect on total or low density lipoprotein cholesterol. Avoiding 200 mg/day dietary cholesterol further decreased blood total cholesterol by 0.13 (0.02) mmol/l and low density lipoprotein cholesterol by 0.10 (0.02) mmol/l. CONCLUSIONS: In typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol.

2. Variability and lack of statistical power. There is high amounts of variability between people. Two people who eat the exact same diet may have very different blood cholesterol. One can quite easily make a snapshot picture of lipids and diets and find no correlation with anything. This does not mean that correlation does not exist. It is the same with how poorly designed studies managed to find that bicycle helmets don't protect people: clearly they do protect people, based on actual physical, mechanical and physiological evidence. Just poor statistics can't find this.

Secondary to this point, there must be a baseline from which cholesterol changes are observed. Otherwise you're not assessing dietary effects, all you're assessing is population variability.

TAKE AWAY: Studies need to be INTERVENTION studies, which people's diets are met with an intervention and then outcomes are observed from that point, rather than cross-sectional studies where there is no statistical power.

By the way, this effect has been known about for YEARS: e.g. summarised in the paper below from 1979!
https://www.ncbi.nlm.nih.gov/pubmed/313701

"The confounding that results from the uncontrolled conditions under which most epidemiologic observations are made is sufficient to undermine their validity with respect to investigation of the relationship between diet and serum cholesterol. In this paper, the authors show, using both a mathematical model and referring to empirical data, that if certain variances are sufficiently great, even when there is cause and effect, correlation coefficients close to zero would be expected from the actual data of a cross-sectional study. Cross-sectional designs are therefore not suitable for studying this relationship."

3. Similar to point 2, although there's a near linear relationship between saturated fat/cholesterol and blood cholesterol, at some point the line turns into a curve: i.e. small changes for someone who already has very high cholesterol aren't going to find a correlation. Unfortunately, heart disease is the number 1 killer in most developed countries, and most of us have higher than optimal blood cholesterol: normal is getting a heart attack. Therefore studies where the control and the intervention group eat the standard american diet with minor modifications aren't going to find anything.
 

metranger8694

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These recent meta-analyses which have indeed caused somewhat of a stir have been based on flawed methodology. The reasons for this are outlined below.

1. Physiology and biochemistry. As we know, HDL and LDL are lipid transporters. Therefore, any time someone is losing weight they will have an improvement in the HDL:LDL ratio and general lipids. This makes sense and you can easily test it for yourself. The opposite is also true - any time you put on significant amounts of body fat your ratios will worsen - hence why sugary foods, even if they're low fat, are also bad for you from the CVD standpoint. This is also why someone's ratios can improve on a twinky diet so long as it's below maintenance calories.

TAKE AWAY: Study design needs to be ISOCALORIC. It is no use adding and removing eggs from a diet if its not substituted with something of the same caloric value. Moreover, if you're removing eggs and replacing with bacon, of course you're not going to see a result.


Here is an example of a meta-analysis done THE RIGHT WAY - using studies that controlled calorie content.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2125600/
OBJECTIVE: To determine the quantitative importance of dietary ***** acids and dietary cholesterol to blood concentrations of total, low density lipoprotein, and high density lipoprotein cholesterol. DESIGN: Meta-analysis of metabolic ward studies of solid food diets in healthy volunteers. SUBJECTS: 395 dietary experiments (median duration 1 month) among 129 groups of individuals. RESULTS: Isocaloric replacement of saturated fats by complex carbohydrates for 10% of dietary calories resulted in blood total cholesterol falling by 0.52 (SE 0.03) mmol/l and low density lipoprotein cholesterol falling by 0.36 (0.05) mmol/l. Isocaloric replacement of complex carbohydrates by polyunsaturated fats for 5% of dietary calories resulted in total cholesterol falling by a further 0.13 (0.02) mmol/l and low density lipoprotein cholesterol falling by 0.11 (0.02) mmol/l. Similar replacement of carbohydrates by monounsaturated fats produced no significant effect on total or low density lipoprotein cholesterol. Avoiding 200 mg/day dietary cholesterol further decreased blood total cholesterol by 0.13 (0.02) mmol/l and low density lipoprotein cholesterol by 0.10 (0.02) mmol/l. CONCLUSIONS: In typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol.

2. Variability and lack of statistical power. There is high amounts of variability between people. Two people who eat the exact same diet may have very different blood cholesterol. One can quite easily make a snapshot picture of lipids and diets and find no correlation with anything. This does not mean that correlation does not exist. It is the same with how poorly designed studies managed to find that bicycle helmets don't protect people: clearly they do protect people, based on actual physical, mechanical and physiological evidence. Just poor statistics can't find this.

Secondary to this point, there must be a baseline from which cholesterol changes are observed. Otherwise you're not assessing dietary effects, all you're assessing is population variability.

TAKE AWAY: Studies need to be INTERVENTION studies, which people's diets are met with an intervention and then outcomes are observed from that point, rather than cross-sectional studies where there is no statistical power.

By the way, this effect has been known about for YEARS: e.g. summarised in the paper below from 1979!
https://www.ncbi.nlm.nih.gov/pubmed/313701

"The confounding that results from the uncontrolled conditions under which most epidemiologic observations are made is sufficient to undermine their validity with respect to investigation of the relationship between diet and serum cholesterol. In this paper, the authors show, using both a mathematical model and referring to empirical data, that if certain variances are sufficiently great, even when there is cause and effect, correlation coefficients close to zero would be expected from the actual data of a cross-sectional study. Cross-sectional designs are therefore not suitable for studying this relationship."

3. Similar to point 2, although there's a near linear relationship between saturated fat/cholesterol and blood cholesterol, at some point the line turns into a curve: i.e. small changes for someone who already has very high cholesterol aren't going to find a correlation. Unfortunately, heart disease is the number 1 killer in most developed countries, and most of us have higher than optimal blood cholesterol: normal is getting a heart attack. Therefore studies where the control and the intervention group eat the standard american diet with minor modifications aren't going to find anything.
Isocaloric? Blah blah blah.

What a bunch of jabberwocky nonsense.
 

metranger8694

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? choline is not a vitamin or nutrient of any particular benefit.
Choline no benefit?

You sir, are misinformed. As you are in most everything you've posted about fats, cholesterol and nutrition.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782876/
http://www.berkeleywellness.com/supplements/vitamins/article/should-you-boost-your-choline

I'd be curious to see what an average day of meals consists of for you.

Anyhow, I'm not sticking around to find out.

In good health,
Unsubscribed.
 

skeen7908

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That's a pretty juvenile response

I don't have a dog in this fight , but was hoping to learn something
 

MGoCrimson

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I blocked him long before he started with his pseudo science, "forensic anthropology" nonsense.

And LOL at isocaloric trials being nonsense.

@hendrix beyond its developmental and CNS roles, choline is pretty great at being a methyl donor for methylation of homocysteine and reduction of inflammatory factors of CVD.

You interpreted the cited studies correctly and rightly give more credence to interventional studies over epidemiological, but it does not seem you have put ratio and particle content/size of LDL into consideration -- both of which are stronger indicators of CVD risk than cholesterol counts.
 

hendrix

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Re: choline. From my ubderstanding its supposed benefits are tenuous and it also is potentially harmful, e.g. when it converts to TMAO. So I think we can say the jury is out as to whether it's legitimately a healthful component.

Re: the particle sizes. The way I see it the various different particle sizes are somewhat spectral in nature, imInot sure what relevance to ascribe here except to say that the low density ones (vldl, ldl etc) are bad and transport lipids to the tissue, and while HDL does the reverse, it's not actually protective.

Basically reduce your ldl (all low density) and your ratio will take care of itself automatically.

Attempts to increase HDL are far more tenuous and unproven in their protective effects.
 

hendrix

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Has research in the past year moved TMAO out of the realm of pure speculation?

It depends on your threshold. Without going through the literature IIRC TMAO:
- definitely causes atherosclerosis in experimental (mouse) models
- definitely is formed by gut bacteria when digesting choline-rich foods

YMMV, but to switch the question around:
Has research in the past year moved choline out of the realm of pure speculation?
 

MGoCrimson

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Yes, the mechanism by which choline contributes to methylation of homocysteine is well studied and several interventions verify its effect on lowering homocysteine levels.
 

hendrix

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Yes, the mechanism by which choline contributes to methylation of homocysteine is well studied and several interventions verify its effect on lowering homocysteine levels.

OK, but there are several studies finding negative outcomes of heart patients associated with choline (e.g. this one), and a few mechanistic studies showing that in mice at the least it definitely contributes to poor cardiovascular outcomes.
http://circheartfailure.ahajournals.org/content/9/1/e002314.short

I think there's not enough evidence to say that it's good or bad, the jury is out. In any case I don't think you should say "eggs are good cos choline", I think that's a little irresponsible.

Moreover, in any food you can list off several vitamins and nutrients, I'm sure you could do this with a Big Mac, this is not particularly informative. Instead if you compare the relative nutrition between an egg and the equivalent amount in another food (either by mass, calorie, or volume), that's more useful IMO.

1 large egg (50g) vs 50g walnuts, or chickpeas, or tofu, or hell even a spoonful of peanut butter - I think all of these options come out better, nutritionally than the egg.
 

Benesyed

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I ate a chocolate bar for lunch today
 

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