The relationship between the cholesterol we eat and the cholesterol levels in our blood is complex and highly individualized. On one extreme, some believe dietary cholesterol is completely harmless while others consider it highly damaging. As usual, the truth lies somewhere in the middle and depends greatly on the individual.
So let’s dive to topics from cholesterol absorption in the intestines to the tests available for assessing your absorption status. By the end, you’ll have a more nuanced understanding of how dietary cholesterol influences blood cholesterol as well as actionable advice tailored to your individual variability.
Cholesterol Absorption in the Intestine
The Absorption Process
When we eat foods containing cholesterol, it first travels to our small intestine. At this stage, most cholesterol is “esterified,” meaning bound to a fatty acid. Esterified cholesterol molecules are too large to be absorbed. However, enzymes from the pancreas called lipases can break apart some of the fatty acids, converting cholesterol esters into “free” or unesterified cholesterol. Free cholesterol can then be absorbed by receptors in intestinal lining cells called enterocytes.
The main receptor responsible for cholesterol absorption is called Niemann-Pick C1 Like 1 (NPC1L1). This receptor specifically binds to free cholesterol, pulling it from the intestine into enterocytes.
However, anywhere from 75-90% of absorbable free cholesterol in our gut actually comes from our liver, not our diet. The liver packages cholesterol into bile which flows into the small intestine. The purpose is to ultimately excrete excess cholesterol, but NPC1L1 can’t tell the difference and absorbs some back into enterocytes.
The Effect on Blood Cholesterol Levels
Once inside enterocytes, cholesterol can take a few paths. One route packages cholesterol into large lipoproteins called chylomicrons. Chylomicrons mainly carry triglycerides but also transport cholesterol from enterocytes to the liver.
Alternatively, cholesterol can leave enterocytes directly via HDL particles. Intestinal absorption contributes somewhat to HDL cholesterol levels. Therefore, high HDL (e.g. >60 mg/dL) can indicate cholesterol hyperabsorption.
The liver receives absorbed cholesterol via chylomicron remnants and must decide what to do with it. Whether absorbed or synthesized in the body, the liver manages nearly all cholesterol. Therefore, even though we can absorb more cholesterol from a high dietary intake, our blood levels don’t rise proportionally because the liver removes excess.
Individual Variability in Absorption
Clearly absorption regulation is complex, involving pancreatic enzymes, various intestinal receptors, and the liver. Genetics influence each part of this process, meaning absorption ability varies considerably between people.
Ideally, we could test absorption ability before making blanket dietary recommendations for or against cholesterol. As mentioned, high HDL hints at excess intestinal absorption since enterocytes can export cholesterol on HDL particles. However, HDL levels have many influencing factors.
The most clinically useful and simplest test checks blood levels of plant sterols like sitosterol and campesterol. We normally absorb little to no plant sterols, allowing them to transit the intestine untouched. Sterol hyper-absorption, however, loads them into blood lipoproteins.
In summary, around 75% of people fall into an average absorption category where dietary cholesterol modestly impacts blood levels. Roughly 20% absorb so little that even radically high intake elicits little response. And about 20% absorb enough, likely due to genetic factors, for dietary intake to affect risk of high cholesterol issues. Objective testing can determine which group you fall into.
Implications for Management
The complexity around cholesterol absorption leads to vastly different dietary recommendations between individuals.
For hypo-absorbers, unlimited dietary cholesterol poses no concern. For hyper-absorbers, reducing cholesterol intake may provide benefit. Though challenging, testing absorption ability allows tailoring advice rather than blanket population-level guidelines.
Knowing absorption ability allows selecting the medication, or combination, targeting the specific metabolic defect elevating blood cholesterol. As an example, combining low dose statins and low dose ezetimibe balances reducing synthesis and absorption. This orchestrated approach often manages cholesterol more effectively than simply escalating statin dose alone.
In summary, balancing cholesterol production and absorption maintains healthy levels. Genetic factors can disrupt this equilibrium in either direction for different people. Therefore, both dietary advice and medical treatment must individualize based on the specific dominant metabolic abnormality rather than taking a generalized approach.
The complex physiology regulating cholesterol metabolism
Far from the extremes of eliminating dietary cholesterol or mindlessly consuming it, the best policy depends greatly on the individual. The complex physiology regulating cholesterol absorption provides insight into personalized recommendations and treatment approaches.
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