Well sugar is sugar but added sugars are often excessive in foods. I think you are referring to my sugar-cancer comment? Naturally occurring sugars in unprocessed foods usually are within certain ranges and paired with fiber other good things so not the bad thing. Added sugars and the carb content in processed foods is what is "abused" leading to most metabolic syndrome issues. The daily amount of sugar people take in currently, natural or added, far exceeds healthy levels.
The high sugar content we ALL absorbed as kids is not the same as when we intake later in life. Those young metabolic engines we had as kids were pretty good at absorbing and burning off that sugar. Bouncing off the walls right? It is our bodies that begin to slow down and start feeling the effects of our diet as we get into our 30s and 40s. Better diet and exercise and reverse a lot and certainly those two have already been proven to lower cholesterol and triglycerodes. I have to find the studies that show how those things can also break down plaque build up on artery linings over time. Dest probably has it at his finger tips but as a kid your body was not converting it to fat so easily because we had race car engines. Now with my Pruis motor that excessive crap turns to crap. But plaque can be reduced naturally by the body unless you get to point of some people with 80% blockage or the lining has hardened so much and they need to use the little balloon to pop ot open. Have to go look it up again
That's kind of what I had been hoping to hear and recall reading some material that suggested it. But I also read years ago about young (overweight) kids on bad diets whose arteries were already 50% blocked. So I guess their race car engines were parked in front of video games rather than doing the stuff we did as kids. I realize that diet and lifestyle can reverse some of the effects of plaque buildup and prevent excess additional buildup going forward. But can it undo most of the buildup that had already occurred or just make something of a dent in it?
Yeah with some kids who eat like adults and are obese I have to think there is already something faulty in their metabolism. Or 2 kids eat like a horses and one is chubby and one is a stick. I always feel sad when I see/hear about kids in that condition because you and I have an understanding/choice but that kid does not. So where was the doctor/parents in all of that? I always hated the kids with furnaces with metabolisms haha. Let me see if I can find the studies info. I doubt you can make a 50% blocked arterty go to 0% but I think it can be ameliorated quite a bit. The issue is the thickening of the lining and blood pressure to get through that narrowing. Let me see if I can pull it up.
VLDL is produced from fruit as well, just not as efficiently as HFCS. You cannot reverse the damage done in youth, but eating clean will limit further blockage.
Trying to find more detailed research but plaque built up is there to stay for the most part. I doubt the way you ate as a kid caused severe plaque buildup but at older ages it is way more important since you don't feel symptoms of plaque build up. I.e., I have no idea the level of plaque build up I have but eating better is to avoid it leading to further blockage. As indicated above you have dense and fluffy LDL lipoproteins. The fluffy ones do not get stuck to your artery lining or enter the lining as easily so a high LDL number ALONE is not telling. Need a LDL-P test to test particle size. "There's no simple, direct way to measure VLDL cholesterol, which is why it's normally not mentioned during a routine cholesterol screening. VLDL cholesterol is usually estimated as a percentage of your triglyceride value. An elevated VLDL cholesterol level is more than 30 milligrams per deciliter (0.77 millimole/liter). The best way to lower your VLDL cholesterol is to lower your triglycerides. Losing weight and exercising regularly are key, and you might also want to avoid sugary food and alcohol in particular." More info: The many types of lipoproteins Cholesterol, a waxy, yellowish fat found in cells throughout the body, travels through your bloodstream in tiny, protein-covered particles called lipoproteins. The lipid part of these particles contains both cholesterol and triglycerides, a type of fat used to store energy and deliver it to your muscles. The smallest and densest particles are high-density lipoproteins (HDL), also known as "good" cholesterol. They remove cholesterol from artery walls and return it to the liver for excretion. Low-density lipoprotein (LDL) particles are known as "bad" cholesterol. They deliver cholesterol to cells in the artery wall, creating artery-clogging plaque that can trigger a heart attack or stroke. A standard lipid panel measures levels of HDL, LDL, total cholesterol, and triglycerides in your blood. It may also include a measurement of very-low-density lipoprotein (VLDL)—particles made by the liver that carry a large amount of triglyceride. LDL: Larger vs. smaller particles Most clinicians focus on LDL because it's a good way to predict heart attack risk. But many people diagnosed with heart disease have LDL levels that aren't especially high. It turns out that LDL particles are not all created equal. Smaller, more tightly packed LDL has an easier time getting into arteries. Larger, fluffier particles may be less dangerous. Also, research suggests that a key protein on LDL called apolipoprotein B (apoB) is an important contributor for heart disease risk. Advanced lipoprotein testing measures the size, distribution, and number of these subparticles as well as apoB. It may also include lipoprotein (a) and apolipoprotein A-1, the main protein on HDL.
Arterial plaque reduction does occur (disease regression), obviously I want to avoid it in the first place; I am not going to be good as new. For example, patients on statins have been shown to have atheroma volume reductions. Here is the killer (pun intended unfortunately): more patients died in the statinated group (even though they had plaque reductions) than in non-statinated grp.
This is really interesting study, my comments afterwards: Apolipoprotein CIII links dyslipidemia with atherosclerosis. Kawakami A1, Yoshida M. Author information Abstract Plasma levels of lipoproteins that contain apolipoprotein (apo) CIII predict coronary heart disease (CHD), and associate with contributors to metabolic syndrome such as type 2 diabetes and hypertriglyceridemia. ApoCIII causes hypertriglyceridemia by inhibiting the catabolism and the clearance of TG-rich lipoproteins (TLRs), and the association of apoCIII with CHD has been commonly attributed to these properties; however, it has been untested whether apoCIII itself or in association with lipoproteins directly affects atherogenic mechanisms in vascular cells. This review describes the proatherogenic effect of apoCIII-containing lipoproteins. In brief, apoCIII-rich VLDL (VLDL CIII+) increased the adhesion of human monocytes to vascular endothelial cells (ECs). ApoCIII alone also increased monocyte adhesion to vascular ECs. Interestingly, apoCIII-rich HDL did not reduce the adhesion of monocytes to vascular ECs, whereas HDL without apoCIII decreased their adhesion, suggesting that apoCIII in HDL counteracts the anti-inflammatory property of HDL. ApoCIII alone as well as VLDL CIII+also activated vascular ECs through the activation of NF-kappaB, and induced the recruitment of monocytes to vascular ECs. Moreover, apoCIII induced insulin resistance in vascular ECs and caused endothelial dysfunction. These findings indicate that apoCIII in TLRs not only modulates their metabolism, but also may directly contribute to the development of atherosclerosis by activating the proinflammatory signal transduction of vascular cells. Here, we propose a novel role for apoCIII that links dyslipidemia with atherosclerosis." This study looked to isolate a spedcific lipoprotein that contributes greatly to plaque buildup and they isolated Apo CIII. Apo-CIII is a component of very low density lipoprotein (VLDL). An increase in apoC-III levels induces the development of hypertriglyceridemia. In persons with type 2 diabetes, elevated plasma Apo-CIII is associated with higher plasma triglycerides and greater coronary artery calcification (a measure of subclinical atherosclerosis). Apo-CIII delays the catabolism of triglyceride rich particles. HDL cholesterol particles that bear Apo-CIII are associated with increased, rather than decreased, risk for coronary heart disease. So even in HDL levels that are healthy, existence of the ApoCIII protein counters the good effect of HDL. What I found is that Apc-CIII is directly involved in artherogenesis! https://lipidworld.biomedcentral.com/articles/10.1186/s12944-016-0352-y
So the question of the day...how do we reduce Apoc-III lipoproteins? First obvious answer is reducing blood triglycerdies levels. However reasing that ApoCIII exists in HDL and LDL I am looking for studies that show how to attack ApoCIII directly without medication. I.e. what type of diet increases ApocIII production and how to avoid that. However there are now studies looking to target ApocIII with treatments to reduce the risk in serious cases.
http://clinchem.aaccjnls.org/content/55/7/1274 Highlights: In part, the increased recognition of the importance of lowering triglycerides has been a result of increased recognition of the metabolic syndrome (MS). Although the diagnosis of MS is based on meeting at least 3 of the 5 criteria (increased triglycerides, low HDL-C, abdominal obesity, high blood pressure, and increased fasting glucose concentrations), by far the majority of individuals with MS have increased triglycerides. ...it has long been demonstrated that increased serum triglycerides are associated with lowered HDL-C concentrations and decreased HDL and LDL particle sizes. Moreover, treatment of patients with triglyceride-lowering therapies such as fibric acid derivatives not only lowers serum triglycerides but also increases HDL-C concentrations. In particular, reducing serum triglycerides is known to be associated with increased HDL2, the larger HDL particles thought to be more protective than the smaller HDL3 particles. Similarly, although increased triglycerides may not be the only mechanism for decreased average particle size of LDL, it is a major mechanism involved in increasing the proportion of small, dense LDL particles. Lowering triglycerides is almost always associated with the reduction of small, dense LDL particles, thereby further rendering an individual’s lipid profile to be less atherogenic. What I found interesting about rest of the article is that people with a mutation where they do not produce the ApocIII lipoprotein had lower cholesterol and lower triglyceride levels. Makes me wonder if those of us with family histories of higher cholesterol (absolute numbers) come from an overexpression of the APOCIII gene? Either way, it gives some substanc to triglycerdies and cholesteral particle size and maybe future tests to see levels of APOCIII lipoproteins in fasting individuals....