High-cholesterol diet improves immunity?

A Cholesterol-Rich Diet Accelerates Bacteriologic Sterilization in Pulmonary Tuberculosis

Background: Hypocholesterolemia is common among tuberculous patients and is associated with mortality in miliary cases. Some in vitro studies have shown that cholesterol is necessary for the good functioning of macrophages and lymphocytes.

Study objectives: To determine whether a cholesterol-rich diet could accelerate sputum sterilization in patients with pulmonary tuberculosis.

Design: An 8-week follow-up, randomized, controlled trial carried out from March 2001 to January 2002.

Setting: A third-level hospital for respiratory diseases in Mexico City.

Patients and interventions: Adult patients with newly diagnosed pulmonary tuberculosis were hospitalized for 8 weeks and randomly assigned to receive a cholesterol-rich diet (800 mg/d cholesterol [experimental group]) or a normal diet (250 mg/d cholesterol [control group]). All patients received the same four-drug antitubercular regimen (ie, isoniazid, rifampin, pyrazinamide, and ethambutol).

Measurements and results: Every week, a quantitative sputum culture and laboratory tests were done and respiratory symptoms were recorded. Patients in the experimental group (10 patients) and the control group (11 subjects) were HIV-negative and harbored Mycobacterium tuberculosis that was fully sensitive to antitubercular drugs. Sterilization of the sputum culture was achieved faster in the experimental group, as demonstrated either by the percentage of negative culture findings in week 2 (80%; control group, 9%; p = 0.0019) or by the Gehan-Breslow test for Kaplan-Meier curves (p = 0.0037). Likewise, the bacillary population decreased faster (p = 0.0002) in the experimental group. Respiratory symptoms improved in both groups, but sputum production decreased faster in the experimental group (p < 0.05). Laboratory test results did not differ between the groups. Conclusions: A cholesterol-rich diet accelerated the sterilization rate of sputum cultures in pulmonary tuberculosis patients, suggesting that cholesterol should be used as a complementary measure in antitubercular treatment.

It’s been speculated, notably by Dr. Uve Ravnskov, a noted skeptic of the cholesterol hypothesis of heart disease, that cholesterol protects against infections. There are good mechanistic reasons for thinking so; this passage from the first link explains:

Cholesterol constitutes up to 30% of the total lipid content in the cell membrane, and participates in the fluidity of this structure.10Consequently, cholesterol is involved in the activity of membrane-bound enzymes and membrane functions such as phagocytosis and cell growth.11In this context, Drabowsky et al12demonstrated that cholesterol content in the cell membrane of human lymphocytes is important for their cytotoxic function. Heiniger and Marshall13found that cholesterol participates in the differentiation and proliferation cycles that convert lymphocytes into cytotoxic cells. Moreover, in a work published by Gatfield and Pieters14a clear derangement of the ability of the macrophage to phagocytase mycobacteria was observed when they were depleted of cholesterol.

In TB patients, low cholesterol is strongly associated with mortality. The above study looks as if it proves a causal connection: more cholesterol, better immunity.


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