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Hamster, where's that from?The characteristic opacity of aged skin is the result of an accumulation of layers of dead cells on the surface. While the vital underlying skin cells contain much less cholesterol than normal, the inert cells contain an increased amount of choles- terol sulfate. When the skin’s free cholesterol content is increased experimentally, the skin regains its ability to shed the dead superficial cells. When it’s lowered experimentally, as with a statin, the skin takes on the structure and appearance of old skin. Aging seems to be a state of cholesterol starvation.
WTF?! What's your background man? (sorry if you've answered it before...)I as a recipient of Kobayashi Award
Only during development? What happens in adulthood?cerebellar and pineal neurosteroids and their biological actions on the growth and survival of Purkinje cells during development
Saturated fats aren’t superior. It’s more complicated than a black or white situation based from Petri dish studies.
That's because it is.
@haidut curious about fatty acid esters like the SFA esters. How come they are beneficial vs. Cholesterol esters?
Most SFA esters are easily metabolized back into their SFA + ester components but I don't think the same happens with cholesterol
Would you suggest taking lidocaine orally? Would you suggest orally for progesterone?In addition to progesterone and lidocaine mentioned in the newsletter, pregnenolone may help as well. The study below suggests pregnenolone could be a competitor for the ACAT enzyme that creates cholesteryl esters and as such inhibit the formation of those esters, as pregnenolone had 50-100 fold higher affinity for ACAT than cholesterol does. So far there is no evidence that pregnenolone esters are harmful and at least one of them (pregnenolone sulfate) is known to serve as the long term storage form of pregnenolone.
Cellular Pregnenolone Esterification by Acyl-CoA:Cholesterol Acyltransferase
"...Pregnenolone (PREG) can be converted to PREG esters (PE) by the plasma enzyme lecithin: cholesterol acyltransferase (LCAT), and by other enzyme(s) with unknown identity. Acyl-CoA:cholesterol acyltransferase 1 and 2 (ACAT1 and ACAT2) convert various sterols to steryl esters; their activities are activated by cholesterol. PREG is a sterol-like molecule, with 3-β-hydroxy moiety at steroid ring A, but with much shorter side chain at steroid ring D. Here we show that without cholesterol, PREG is a poor ACAT substrate; with cholesterol, the Vmax for PREG esterification increases by 100-fold. The binding affinity of ACAT1 for PREG is 30–50-fold stronger than that for cholesterol; however, PREG is only a substrate but not an activator, while cholesterol is both a substrate and an activator. These results indicate that the sterol substrate site in ACAT1 does not involve significant sterol-phospholipid interaction, while the sterol activator site does. Studies utilizing small molecule ACAT inhibitors show that ACAT plays a key role in PREG esterification in various cell types examined. Mice lacking ACAT1 or ACAT2 do not have decreased PREG ester contents in adrenals, nor do they have altered levels of the three major secreted adrenal steroids in serum. Mice lacking LCAT have decreased levels of PREG esters in the adrenals. These results suggest LCAT along with ACAT1/ACAT2 contribute to control pregnenolone ester content in different cell types and tissues."
Lowering blood cholesterol VIA DRUGS or PUFAs. You make it sound like higher cholesterol is superior than normal cholesterol.
Classification and cause
Lysosomal acid lipase deficiency is a genetic disease that is autosomal recessive. It is an inborn error of metabolism that causes a lysosomal storage disease.[3] The condition is caused by a mutation of the LIPA gene, which is responsible for the gene coding of the lysosomal lipase protein (also called lysosomal acid lipase or LAL), which results in a loss of the protein's normal function.[2] When LAL functions normally, it breaks down cholesteryl esters and triglycerides in low density lipoprotein particles into free cholesterol and free fatty acids that the body can reuse; when LAL doesn't function, cholesteryl esters and triglycerides build up in the liver, spleen and other organs.[3][4] The accumulation of fat in the walls of the gut and other organs in leads to serious digestive problems including malabsorption, a condition in which the gut fails to absorb nutrients and calories from food, persistent and often forceful vomiting, frequent diarrhea, foul-smelling and fatty stools (steatorrhea), and failure to grow.[3]
It appear to me that a shortage or some malfunctioning of this pancreatic enzyme is THE ISSUE in heart disease and liver disease and nearly every other fatty problem in the human body. The genetic explanation may be true in infants but I doubt it's the issue in everyone else. Something blocks the production or inactivates this enzyme as we age and bad things happen. It's up to us to solve the mystery because big pharma would not be interested in doing so.
Interleukin-1 Beta as a Target for Atherosclerosis Therapy: The Biological Basis of CANTOS and BeyondThe major one is PUFA being the main precursor to inflammatory mediators like prostaglanding and leukotrienes, as well as promoting cortisol, estrogen, serotonin and NO. SFA have largely the opposite of those effects. CVD is an inflammatory disease, just like all other chronic ones and as such the role of PUFA is pretty clear.
Interleukin-1 Beta as a Target for Atherosclerosis Therapy: The Biological Basis of CANTOS and Beyond
Condensed Abstract
“Inflammatory pathways drive atherogenesis and link traditional risk factors to atherosclerosis and its complications. Interleukin-1 beta (IL-1β) has emerged as an actionable mediator in prevention of recurrent cardiovascular events. Intrinsic vascular wall cells and lesional leukocytes alike can produce this pro-inflammatory cytokine. Local stimuli in the plaque boost the generation of active IL-1β through the action of a molecular assembly known as the inflammasome. Therapies that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. Biomarker-directed application of anti-inflammatory interventions promise to personalize allocation of therapy for our cardiovascular patients.”
Interleukin-1 Beta as a Target for Atherosclerosis Therapy: The Biological Basis of CANTOS and Beyond
Thank youI think Sour is just a troll. If somebody is that contrarian to everything we are discussing on the forum then why be here??? Either a troll or a paid agent provocateur.
I would not waste time with him/her.
Most SFA esters are easily metabolized back into their SFA + ester components but I don't think the same happens with cholesterol. Also, there are many studies with SFA esters on mammals showing their beneficial effects while studies with the cholesteryl esters are invariably negative.
Thanks.
I am beginning to suspect the cholesterol strawman was invented deliberately to keep people distracted from the real cause (inflammation) and what drives inflammation. The cholesterol hypothesis came long before statins were even conceptualized, so there must have been some other impetus to propose this ruse. And that something was sales of omega-6 and omega-3, which are the main byproducts of the agricultural and maritime industries. Those industries were the dominant ones in most Western countries at the turn of the 20th century when the cholesterol ruse first started, and to this day are some of the most heavily subsidized ones.
Would progesterone also reverse existing cholesteryl esters, or only slow down their production?I guess the easiest thing would be to supplement with some digestive enzymes and pregnenolone/progesterone could help with the cortisol/estrogen and also by competing with cholesterol for esterification.
Perhaps, but it's too much trouble for a dubious gain.@haidut @ecstatichamster @lampofred @Hugh Johnson @jamies33 @yerrag @Mito
Maybe this is one of the larger, currently unsung, benefits of sulfur amino acid restriction (SAAR, =methionine+cysteine restriction) with respect to longevity and healthspan
Low sulfur intake > less substrate for cholesterol sulfation
On top of that, SAAR diets tend to lower stearoyl-CoA desaturase-1 (SCD1) activity, lowering the endogenous synthesis of unsaturated fatty acids > less substrate for cholesterol esterification to unsaturated fats
Would progesterone also reverse existing cholesteryl esters, or only slow down their production?
I don't know if you've ever read Anthony Colpo's book "The Great Cholesterol Con," but there are three chapters that deal with this very issue. Chapter 10 "Money, Politics, and Cholesterol" Chapter 11 "Creating a 'Consensus'" and Chapter 12 "If We Want Your Opinion, We'll Give It To You!"
He specifically talks about that infamous Time Magazine with "Cholesterol: And Now The Bad News...." on the cover, and the Consensus Development Conference in Bethesda Maryland in 1984, and how it was clearly pre-planned agenda, to spread the idea of Cholesterol being bad. He also discusses how the Vegetable Oil industry profited off this "Consensus" before statins.