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I consume a lot of cholesterol. For three months straight, I consumed around 6-8 eggs a day with Feta cheese, and about a third of a gallon of milk each day. I got my cholesterol tested before and after this regime, and my overall cholesterol decreased, and my ratio of HDL/LDL became more favorable.

I know there is serious debate about the Lipid Hypothesis, with research on both sides claiming statistical significance one way or another.

From the Harvard Public Health repository:

And the biggest influence on blood cholesterol level is the mix of fats and carbohydrates in your diet—not the amount of cholesterol you eat from food.

An aggressive, competing claim on HowStuffWorks:

It's because the level of cholesterol already present in your blood can be increased by high consumption of cholesterol and saturated fat in your diet. This increase in dietary cholesterol has been associated with atherosclerosis, the build-up of plaques that can narrow or block blood vessels. (Think about what happens to your kitchen drain pipes when you pour chicken fat down the sink.) If the coronary arteries of the heart become blocked, a heart attack can occur. The blocked artery can also develop rough edges. This can cause plaques to break off and travel, obstructing blood vessels elsewhere in the body. A blocked blood vessel in the brain can trigger a stroke.

In response to people arguing that the HowStuffWorks link is outdated, here is an academic source, from J.D. Spence, D.J. Jenkins, J. Davignon, "Dietary cholesterol and egg yolks: not for patients at risk of vascular disease", Can J Cardiol, 26 (2010), pp. e336–e339

There is also no doubt that cholesterol feeding is a causal factor in animal models of atherosclerosis. Such models include rhesus monkeys fed a diet rich in egg yolks that developed hypercholesterolemia, xanthomatosis and atherosclerosis (46,47). In 1908, Ignatowski showed that meat – containing the pro-oxidant iron – fed to adult rabbits, or milk and egg yolks fed to weanling rabbits, induced atherosclerosis (48). In 1913, Anitschkov established the cholesterol-fed rabbit as a model for dietary atherosclerosis (49). Cholesterol feeding in rabbits not only causes cholesterol accumulation in plasma and the arterial wall but also promotes inflammation and cell proliferation, which may be blocked by the anti-inflammatory agent cortisone to prevent the formation of raised atherosclerotic lesions (50).

Dietary cholesterol increased coronary risk in both the Ireland Boston Diet-Heart Study (53) and the Western Electric study (54). These results showed good agreement between the Keys dietary score, which emphasized saturated fat, and the Hegsted score, which emphasized dietary cholesterol. Possible confounding of cholesterol intake from eggs with other risk factors, such as smoking, have been raised as a concern. However, the careful work of Markus et al (55) showed that cholesterol intake, independent of smoking and other risk factors, increased carotid intima-media thickness.

I have two questions:

  1. What is the best scientific understanding of the relationship between dietary cholesterol and blood-level cholesterol?

  2. How, exactly, does the mix of fats and carbohydrates affect cholesterol?

  • 1
    Welcome to Skeptics! I am confused about what the claim is that you are skeptical about. You should find a claim of someone who who suggests there is a relationship between dietary cholesterol and blood cholesterol, because at the moment your answer contains no claims that you express skepticism about. – Oddthinking Jun 27 '13 at 15:39
  • 1
    Sorry about that. I thought that it was the mainstream view that dietary cholesterol impacts blood cholesterol, so I didn't think I needed to cite it. I've since edited by answer to reflect the opinion I'm skeptical of. – Parseltongue Jun 27 '13 at 17:33
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    @Parseltongue the 1st link you cited is the correct one. The last one appears to be from the early 1900s and "monkeys fed a diet rich in egg yolks" isn't a diet 100% cholesterol, but still, what were the other components of the diet besides eggs? Pasta??? Even still, correlation does not equal causation, though its not clear what the correlation would have been in that case. I'd tend to value publications made 2011 (my link in Cambridge) rather than something from 100yrs ago. Can you supply something more recent that indicates dietary cholesterol affects blood cholesterol? – Randy Jun 29 '13 at 1:47
  • @Parseltongue these links may be of interest to you. nytimes.com/2008/01/27/opinion/27taubes.html?_r=0 garytaubes.com/2011/04/… life.gaiam.com/article/… – Randy Jul 4 '13 at 19:10
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Cambridge journals - "Dietary cholesterol: from physiology to cardiovascular risk"

Dietary cholesterol comes exclusively from animal sources, thus it is naturally present in our diet and tissues. It is an important component of cell membranes and a precursor of bile acids, steroid hormones and vitamin D. Contrary to phytosterols (originated from plants), cholesterol is synthesised in the human body in order to maintain a stable pool when dietary intake is low. Given the necessity for cholesterol, very effective intestinal uptake mechanisms and enterohepatic bile acid and cholesterol reabsorption cycles exist; conversely, phytosterols are poorly absorbed and, indeed, rapidly excreted. Dietary cholesterol content does not significantly influence plasma cholesterol values, which are regulated by different genetic and nutritional factors that influence cholesterol absorption or synthesis. Some subjects are hyper-absorbers and others are hyper-responders, which implies new therapeutic issues. Epidemiological data do not support a link between dietary cholesterol and CVD. Recent biological data concerning the effect of dietary cholesterol on LDL receptor-related protein may explain the complexity of the effect of cholesterol on CVD risk.

Wikipedia on Cholestorol

Most ingested cholesterol is esterified, and esterified cholesterol is poorly absorbed. The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis.[8] For these reasons, cholesterol intake in food has little, if any, effect on total body cholesterol content or concentrations of cholesterol in the blood.

Wikipedia on Cholestorol

Isocalorically replacing dietary carbohydrates with monounsaturated and polyunsaturated fats has been shown to lower serum LDL and total cholesterol levels and increase serum HDL levels, while replacing carbohydrates with saturated fat was shown to increase HDL, LDL, and total cholesterol levels.

In summary:

  • Dietary cholesterol has "no significant" or "little if any" effect on blood serum cholesterol (except, for "some subjects who are hyper-absorbers or hyper-responders")
  • Increasing monounsaturated and polyunsaturated fats in the diet decreases blood serum cholesterol.
  • However saturated fats increase cholesterol (saturated fats include animals fats like butter, cheese, cream, and fatty meats; some vegetable oils including coconut, palm, and cottonseed; and various prepared foods).
  • 2
    @Wertilq what on earth did you do to my answer? You removed a reference and made references more obscure. The 3rd paragraph is text from wikipedia, with the reference being [27] atvb.ahajournals.org/content/12/8/911.short I wanted that in my answer specifically. – Randy Jun 28 '13 at 1:25
  • No it's not. [27] was not from [27] on wikipedia, ncbi.nlm.nih.gov/pubmed/1386252 was the exactly the same one. It's the same article, but it's another link. Overall mixing references from wikipedia with your own references is bad, since Skeptics uses a similar format for its links. If you edit your answer you notice your link is still there. But you never quoted anything from that link, and it was link to probably the worst abstract I've ever seen, so I couldn't find anything to link from it, I choose to omit it thus since it just didn't provide anything. – Wertilq Jun 28 '13 at 9:07
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    If you want to have the reference, then quote something from it. The reference was to an abstract that didn't have much of any non-terminology words in it, and was full of numbers. Overall your answer needs more words, and less quotes, all your quotes uses highly complex english, and you never make a point with your references. Explain with text what you've gotten from the links, one sentence can be enough. Quotes with advanced medicine terminology and tons of references does not make a good answer. – Wertilq Jun 28 '13 at 9:08
  • 1
    [27] is atvb.ahajournals.org/content/12/8/911.short and ncbi.nlm.nih.gov/pubmed/1386252 which is the same reference. Further, what "advanced medicine terminology"? My links are have less advanced terminology than the question. Tons of references? Its just cambidge and wiki which summarizes from aha. I need more words? Well, why didn't you add the words while you were editing? ;) Actually, I feel more words just clutter it up. I shouldn't need 1 sentence to explain 1 sentence. – Randy Jun 28 '13 at 18:57
3

What is the best scientific understanding of the relationship between dietary cholesterol and blood-level cholesterol?

This can be answered from another answer I have given to a similar question Does eating high cholesterol foods impact cholesterol blood levels of 30% of population based on Web MD article?

This meta-analysis from 1992 by Hopkins of 76 trials where food was supplied by a metabolic kitchen nicely answers this question. [1]

cholesterol kinetics

The rise in cholestrol on consuming cholesterol is closely tied to the baseline consumption of dietary cholesterol. So, you can see that if you're on a plant based diet ( or vegan ), with zero cholesterol intake, then consuming an egg containing 250 mg of cholesterol will raise your serum cholesterol by about 0.35 mmol/L (13.5 mg/dl) but if you're on an average american diet of 400 mg/day of cholesterol, then the rise is only 0.1 mmol/L (3.9 mg/dl). This is the reason why many studies were confused by the effect of eggs on dietary cholesterol as they didn't understand the relationship between baseline intake and added consumption.

and so for most people who are on high cholesterol diets ( eg. the Standard American Diet aka SAD ) of about 400 mg of cholesterol per day, then additional cholesterol has little impact on their blood levels.

One of the treatments for hyperlipidemia is to use plant phytosterols.

It is well-established that high intakes of plant sterols or stanols can lower serum total and LDL cholesterol concentrations in humans (see Cardiovascular Disease below) (10, 11). In the intestinal lumen, phytosterols displace cholesterol from mixed micelles and inhibit cholesterol absorption (12). In humans, the consumption of 1.5-1.8 g/d of plant sterols or stanols reduced cholesterol absorption by 30-40% (13, 14). At higher doses (2.2 g/d of plant sterols), cholesterol absorption was reduced by 60% (15). In response to decreased cholesterol absorption, tissue LDL-receptor expression was increased, resulting in increased clearance of circulating LDL (16). Decreased cholesterol absorption is also associated with increased cholesterol synthesis, and increasing phytosterol intake has been found to increase endogenous cholesterol synthesis in humans (13). Despite the increase in cholesterol synthesis induced by increasing phytosterol intake, the net result is a reduction in serum LDL cholesterol concentration.

So, it clear from the above the dietary cholesterol is important, and interrupting that absorption has beneficial effects on both total cholesterol and LDL-c.

How, exactly, does the mix of fats and carbohydrates affect cholesterol?

Many studies have shown that dietary fatty acids regulate plasma LDL-C levels by affecting LDL receptor activity, protein, and mRNA abundance [3]

You could read several books on the subject for further explanation.


[1] Hopkins PN. Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review. Am. J. Clin. Nutr. 1992 Jun;55(6):1060-70. PubMed PMID: 1534437.

[2] http://lpi.oregonstate.edu/infocenter/phytochemicals/sterols/#biological_activity

[3] Fernandez ML, West KL. Mechanisms by which dietary fatty acids modulate plasma lipids. J. Nutr. 2005 Sep;135(9):2075-8. PubMed PMID: 16140878.

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