In the past I've been told multiple times that if you don't eat foods containing cholesterol, your body will increase its production of cholesterol to balance out the lack of nutritional cholesterol. On the other hand, if you eat sufficiently much cholesterol, the body will adapt its production of cholesterol in the other direction.
What evidence is there to support this statement?
Here's a study in which they measured a decrease in endogenous cholesterol synthesis after various amounts of dietary cholesterol: Dietary Cholesterol Feeding Suppresses Human Cholesterol Synthesis Measured by Deuterium Incorporation and Urinary Mevalonic Acid Levels (Arteriosclerosis, Thrombosis, and Vascular Biology, 1996):
The objective of this study was to measure the response of cholesterol biosynthesis in subjects to three different amounts of dietary cholesterol: 50 (low), 350 (medium), and 650 (high) mg cholesterol per 2800 kcal. Individuals with low (n=7), normal (n=12), and elevated (n=11) plasma cholesterol concentrations consumed in random order solid-food test diets (15%, 55%, and 30% of energy as protein, carbohydrate, and fat, respectively) at each dietary cholesterol level. The three diets were consumed for 4 weeks each, and each dietary phase was separated by a 4-week washout period. During the final week of each diet, 0.7 g D2O was given per kilogram of body water and deuterium incorporation into the erythrocyte cholesterol pool was measured for 24 hours. Urinary mevalonate levels were also determined in samples obtained during two consecutive 24-hour periods. Both techniques provided measurements of whole-body cholesterol biosynthesis. In all subjects the cholesterol synthesis rate as measured by deuterium incorporation was significantly lower (P<.05) after the transition from low- to medium- and low- to high-cholesterol diets. Urinary mevalonate excretion decreased after the change from the medium- to high- (P<.05) and low- to high- (P<.01) cholesterol diets. Although correspondence between the two methods was poor, they both indicated some suppression of cholesterol synthesis by dietary cholesterol. The response of cholesterogenesis to different amounts of dietary cholesterol was related to the rate of synthesis under depressed conditions of the low-cholesterol diet. These findings indicate modest downregulation of synthesis in response to dietary cholesterol in humans, independent of plasma cholesterol levels.
Metabolic responses to increased dietary cholesterol potentially include reduced endogenous synthesis, decreased absorption, and increased biliary excretion of cholesterol.
In some people, who are cholesterol hyperresponders, dietary cholesterol does not effectively suppress endogenous cholesterol synthesis, so it results in elevated blood cholesterol levels (Comprehensive Biotechnology, 2011). In one study, a decrease in dietary cholesterol intake resulted in a decrease of blood cholesterol in hyperresponders but not in hyporesponders: Endogenous cholesterol synthesis, fecal steroid excretion and serum lanosterol in subjects with high or low response of serum cholesterol to dietary cholesterol (Clinical Nutrition, 1986):
In this study we addressed the question whether hypo- and hyper-responders to dietary cholesterol differ with regard to the flexibility of endogenous cholesterol synthesis after changes in cholesterol intake. Whole-body cholesterol synthesis was measured as faecal excretion of neutral steroids and bile acids minus cholesterol intake. In addition, we determined serum concentrations of lanosterol, a precursor of cholesterol and a possible indicator of cholesterol biosynthetic activity. The study was carried out with 2 hyper- and 4 hypo-responders; these subjects had shown a consistently high or low response of serum cholesterol to a decrease in dietary cholesterol in two previous experiments.
The subjects received controlled high- (on average 697 mg of cholesterol per day) and low-cholesterol (109 mg/day) diets for periods of 4 weeks in succession; cholesterol was the only dietary variable. The two hyper-responders again showed a significant decrease in serum cholesterol. There was essentially no decrease in serum cholesterol in three of the four hypo-responders. The decrease in cholesterol intake caused an increase in cholesterol synthesis in five out of the six subjects.
In conclusion, in most people, dietary intake of cholesterol does not increase blood cholesterol levels because of decreased absorption and endogenous synthesis and increased excretion of cholesterol.
This question has also been answered on MedicalSciences.SE:
"The net daily synthesis of cholesterol is equal to the amount of cholesterol lost in the feces minus the dietary cholesterol"
The body synthesizes an amount approximately equal to the amount it absorbs
Source: Balancing Cholesterol Synthesis and Absorption in the Gastrointestinal Tract David E. Cohen, M.D., Ph.D.
copied from this answer https://medicalsciences.stackexchange.com/a/17712
Your question asks if/how "the body will adapt its production of cholesterol". Literally, any cell - that should include the hepatocytes of the liver - of "the body" produces cholesterol, as it is an essential part of the membrane (of animal cells, by the way, by a factor of 100 more so than of plant cell walls), and it should be empirically well ascertained that there is adaption of cholesterol production to dietary input (reflected, especially, by delivery of cholesterol by - so called "remnants" of cholesterol transporting lipoproteins and chylomicrones, which may very much seen as a regulatory system that balances production between specialized cholesterol producing cells, i.e. especially hepatocytes of the liver and adipocytes of the tissue).
However, refering to any mechanism your question may be about, there are still open questions. See quote below, last sentence.
Here's the only pertaining quote I found.
Takizawa, Cellular control of cholesterol:
"When cells are faced with low cholesterol levels, they respond by increasing the gene expression of proteins that stimulate biosynthesis of cholesterol, such as HMG-CoA reductase, and proteins that increase the uptake up cholesterol from the external environment, LDL receptor. These genes contain a common upstream regulatory element called the sterol response element that binds a transcriptional activator, called the sterol response element binding protein.
When bound to the element, the binding proteins turns on transcription of downstream gene. So, a key question is how the cell regulates the binding of the binding protein to the response element and how that regulation is sensitive to cholesterol levels."
