Cholesterol
| Cholesterol | |
|---|---|
 | |
| Molecular formula | C₂₇H₄₆O |
| Type | Sterol |
| Saturation | N/A (sterol, not a fatty acid) |
| Melting point | |
| Food sources | Eggs, liver, dairy, meat; also synthesized endogenously (mostly liver) |
| Synonyms | |
| Ray's verdict | Generally helps Precursor for membranes, bile acids, vitamin D, and all steroid hormones; diet shifts levels only modestly in most people |
Cholesterol is a sterol. Cells use it for membranes, bile acids, vitamin D, and steroid hormones (pregnenolone, progesterone, cortisol, androgens). The liver makes most circulating cholesterol. Diet shifts levels modestly in many people.
Mainstream cardiology treats high LDL as the main cause of atherosclerosis. The seed-oil and statin story misses hypothyroid metabolism, oxidized fats, and cholesterol's protective roles.[1]
Longevity and centenarians
[edit]In a 35-year follow-up of the Swedish AMORIS cohort (44,636 people, 1,224 of whom reached 100), higher iron and lower glucose distinguished future centenarians from non-centenarians. For total cholesterol, only the lowest quintile carried reduced odds of reaching 100.[2] A published correction to that analysis, after the reference quintile used in the original figure was found to be miscoded, states plainly that having high cholesterol "neither increases nor decreases the probability of living to 100 years of age" once that floor is cleared.[3] So the real finding is narrower than "centenarians all have high cholesterol": chronically low cholesterol tracks with worse odds of reaching 100, but cholesterol on the high side of normal isn't itself doing the work, an important distinction from claims that elevated cholesterol directly drives longevity. Other centenarian cohort studies similarly find a U-shaped mortality curve where mid-200s mg/dL total cholesterol tracks lowest mortality risk in people over 75. Some of this advantage may reflect lipid particle size and composition rather than raw cholesterol concentration; centenarians tend to have larger, more buoyant, less easily oxidized lipoprotein particles.
Thyroid and conversion
[edit]Cholesterol was a thyroid marker before it became a cardiovascular risk marker. By the mid-1930s, high blood cholesterol was used as a sign of low thyroid. Raising thyroid activity brought cholesterol down as the basal metabolic rate rose.[4] Lewis Hurxthal, working at the Lahey Clinic where many hyperthyroid patients underwent thyroidectomy, documented the same pattern directly in his surgical patients: those with excess thyroid secretion ran below-normal serum cholesterol, cholesterol climbed after surgery, and administering thyroid hormone brought it back down, sensitive enough that he proposed serum cholesterol itself as a diagnostic test for thyroid function.[5]
A modern randomized, double-blind crossover trial directly compared T3 (liothyronine) against T4 (levothyroxine) in hypothyroid patients, dosing each to produce the same TSH suppression so the comparison wasn't confounded by under- or over-replacement. Switching to T3 dropped total cholesterol by 10.9%, LDL by 13.3%, and apolipoprotein B by 18.3% versus T4, with no significant difference in HDL, heart rate, blood pressure, exercise tolerance, or insulin sensitivity; T3 also produced significant weight loss, consistent with a genuine increase in metabolic rate rather than reduced food intake.[6]
T3 regulates cholesterol and lipoprotein metabolism. Low thyroid activity reduces LDL clearance and leaves more cholesterol circulating instead of being converted into steroid hormones and bile acids.[7]
A study of 25,862 people found that total and LDL cholesterol increased progressively as thyroid function declined. The difference was already significant with TSH between 5.1 and 10 mIU/L.[8]
I think of people as being lucky if they have cholesterol of 250 ... brought their cholesterol down to about 170 or so.
Adequate cholesterol provides material for pregnenolone, progesterone, and DHEA. Thyroid hormone and vitamin A support that conversion. Stress that suppresses thyroid activity leaves cholesterol high as conversion slows. See Hypothyroidism and Basal temperature.
PUFA and vessels
[edit]The cholesterol-as-poison doctrine revived in the 1950s when polyunsaturated seed oils lowered serum cholesterol. Many toxins lower cholesterol without protecting the heart.[1] Oxidized polyunsaturated fats and low thyroid damage vessels while cholesterol itself is raw material for repair and steroid defense. A crossover trial found vitamin E (200–400 mg/day for 50 days) increased the oxidation-resistance lag phase of both LDL and HDL by roughly 45–90%, and raised cholesteryl ester transfer activity, evidence that antioxidant status, not lipoprotein type, governs cholesterol's atherogenic potential.[10] See PUFA, Saturated fat.
Statins and low cholesterol
[edit]Statins lower cholesterol by blocking synthesis. Side effects and calcification patterns in the wider literature sit next to the point that very low cholesterol associates with other risks. Protective roles of cholesterol for membranes, immunity, and hormone production set a floor. See Progesterone, Pregnenolone.
A 12-year Japanese cohort of 12,334 adults found low total cholesterol (below roughly 160 mg/dL) carried about 50% higher all-cause mortality than moderate levels (age-adjusted hazard ratio 1.49 in men, 1.50 in women), driven by higher stroke, heart-failure, and cancer deaths in the low-cholesterol group; high cholesterol (above roughly 240 mg/dL) was not associated with excess mortality in the same cohort.[11]
See also
[edit]References
[edit]- ↑ 1.0 1.1 Ray Peat, "Cholesterol, longevity, intelligence, and health," raypeat.com.
- ↑ Murata S, Ebeling M, Meyer AC, Schmidt-Mende K, Hammar N, Modig K. "Blood biomarker profiles and exceptional longevity: comparison of centenarians and non-centenarians in a 35-year follow-up of the Swedish AMORIS cohort," GeroScience. 2023. doi:10.1007/s11357-023-00936-w.
- ↑ Murata S, et al. "Correction to: Blood biomarker profiles and exceptional longevity, GeroScience. 2023. doi:10.1007/s11357-023-00996-y.
- ↑ K. B. Turner and A. Steiner, "A long term study of the variation of serum cholesterol in man," Journal of Clinical Investigation 18, no. 1 (1939): 45–49.
- ↑ Hurxthal LM. "Blood cholesterol and thyroid disease. III. Myxedema and hypercholesteremia," Arch Intern Med. 1934;53(5):762-781.
- ↑ Celi FS, Zemskova M, Linderman JD, et al. "Metabolic effects of liothyronine therapy in hypothyroidism: a randomized, double-blind, crossover trial of liothyronine versus levothyroxine," J Clin Endocrinol Metab. 2011;96(11):3466-3474. doi:10.1210/jc.2011-1329.
- ↑ L. H. Duntas and G. Brenta, "The effect of thyroid disorders on lipid levels and metabolism," Medical Clinics of North America 96, no. 2 (2012): 269–281.
- ↑ G. J. Canaris et al., "The Colorado thyroid disease prevalence study," Archives of Internal Medicine 160, no. 4 (2000): 526–534.
- ↑ Ray Peat, "Thyroid/Progesterone and Diet", Your Own Health And Fitness, 27:35
- ↑ Arrol S, Mackness MI, Durrington PN. "Vitamin E supplementation increases the resistance of both LDL and HDL to oxidation and increases cholesteryl ester transfer activity," Atherosclerosis. 2000;150(1):129-34. doi:10.1016/s0021-9150(99)00353-6. PMID 10781643.
- ↑ Nago N, Ishikawa S, Goto T, Kayaba K. "Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study," J Epidemiol. 2011;21(1):67-74. doi:10.2188/jea.je20100065.