Well I am NOT an expert but I do know that cholesterol is something that your body makes naturalyl and it will NEVER OVER make it. Cholesterol is something that you have but NEVER need anymore of it ,,like a supplement ,,,you just don't need it. Well cholestrol is ONLY found in animal products. If you never ate any animal product you would NEVER have high cholesterol. So generaly most animal product eaters will have high cholestrol. It is basically like plaque clogging your veins,,,so it prevents the blood from moving like it should. My grandma has problems and I keep telling her to stop eating meat and it will go down. But ya know how people get stuck in their ways with food ,,,, so she takes medication.
You NEED cholesterol to live. Your nerves, brain and other organs need it. The problem comes in when your body can't dispose of excesses of it. Then it clogs your circulatory system, and can trigger a heart attack, a stroke or other heart and blood events. Some people can eat tons of cholesterol in their diets and have NO change in their blood levels, others can be on a low cholesterol diet and still have problems.(And the other way around, too. Breastfed individuals (ones who were breastfed for a significant time as children) have much less problem with cholesterol, as breast milk has lots of cholesterol in it (as well as other things good for the circulatory system) and it "primes" the body to deal with cholesterol in a healthy manner later. Formula had NO cholesterol in it, and the body never learns how to deal with this substance. Keeping and eye on your "good" and "bad" cholesterol is a good idea. It is easier to prevent a circulatory disease, by keeping yourself healthy, than to treat one once you have it.
Interesting article about Cholesterol "Only 20% of the cholestrol found in your blood is a direct result of the foods you eat. The remaining amount is produced by your liver from the excess sugars (carbohydrates). Although it seems logical that cutting back on fatty foods will decrease your total cholestrol levels, in actuality, the less fat you eat, the higher the rate of cholestrol production in the liver. Cholestrol and fat are absolutely essential to good health. They are used by the body as building materials and are in need of constant replenishment to make important hormones such as estrogen, DHEA, and the antistress hormones coritsol. When we deprive our body of cholestrol, the compound the body uses to make these hormones, cell membrane structure is altered and cell growth is disrupted. This causes an increased risk of cancer because cancer arises from the abnormal division of cells. In addition, a lack of cholestrol in our diets can lead to depression and irritability. If we do not include cholestrol in our diets, our body will produce it's own cholestrol by converting the carbohydrates we eat into cholestrol. Insulin plays an important role in the cholestrol equation. Insulin activates an enzyme in your liver called MGH co-AReductase, which causes your liver to overproduce cholestrol from the carbohydrates you eat. When the insulin levels are high, the liver produces more cholestrol. It is this internal overproduction of cholestrol that contributes to the formation of damaging artery plaque that can lead to heart attacks and strokes. Eating a balanced diet including a moderate amount of fruits, protein, and complex carbs, in proper combination, keeps your blood sugar levels balanced. Eating real foods such as olive oil, whole, unsalted butter (not margarine because it's loaded with trans fats), and fish (as opposed to fat free, high sugar foods) increases your HDL, the good cholestrol in your blood stream. This good cholestrol is responsible for fighting off heart disease. Eating a diet too low in fats has been shown to lower your HDL. This controls your insulin levels, which is the key to controlling cholestral levels." Information based on research done by Dr. Diana Schwarzbein. An endocrinologist from Santa Barbra, California
Heres what I know: HDL cholesterol is good. LDL cholesterol is bad. Ive also read some things on plaque buildup in arteries and stuff. Doesn't really sound like cholesterol is the main enemy when it comes to artery clogging. It starts with like tissue damage on the wall of the blood vessel then white blood cells gathering, along with calcium and clotting(fibrinogen?). So yea... dunno where cholesterol comes into the picture.
It's actually more complex than that. There are actually two kinds of LDL. There is the small, dense LDL, and then there is the large, fluffy LDL particles, which are mostly harmless. When a person's cholesterol is tested, the test does not discern between the two types of LDL. A person who eats a lot of coconut oil and eggs might have elevated HDL, which is considered to be the good cholesterol, but they might also have elevated levels of LDL, except these LDL particles are the harmless ones. But if a person's inflammatory markers (blood glucose, CRP, etc.) are in check, it really doesn't matter how high a person's numbers are, which I will explain in the next paragraph. Yes, in order for there to be plaque buildup, there must first be inflammation, which causes the arteries to harden and then crack. The cholesterol comes into play as a repair mechanism for these cracks in the arterial walls. Heart attacks and strokes occur when pieces of that plaque break away and create a blockage. The notion that cholesterol simply clings to the walls of the healthy arteries in the absence of inflammation is simply not true. So the culprit in heart disease and strokes is not cholesterol. Cholesterol simply is not a contributing factor in heart disease. Inflammation is, and what causes inflammation is a diet high in sugar and refined carbohydrates. Furthermore, there is a direct correlation with fructose consumption and triglycerides, since fructose is processed in the liver, which is where most of the cholesterol in the blood comes from -- not from dietary intake of saturated fat and cholesterol. This is why fructose is the most dangerous of all the sugars. It was initially billed as the healthiest sugar because of its low glycemic response, without taking into account its affect on the liver.
Perhaps anecdotally but I have been tracking my cholesterol for decades with annual physicals and every time I donated blood. As I got older it seemed the higher numbers were more prevalent (tho LDL & HDL were in good ratio). I am ovo/lacto vegetarian and use 2% milk and reduced fat cheeses. But the cholesterol kept going over 200 mg/dl. So, I went with fat free milk,(I consume a lot of milk) rationed my eggs to one a day and rationed my daily cheese (that I like with red wine) to a 1 inch cube. My cholesterol went down from 200 or more to the 180s and has been at that for over a year. So, I think there is a correlation between animal product/cholesterol intake and the amount in blood. BTW, I don't drink soft drinks and avoid a lot of sugars.
But that has been constant and has not changed over the reduction in animal fat and the lowered cholesterol numbers. On the body producing its own cholesterol: In my notes, from 1987 (age 43) to 2000 (age 56) my total cholesterol was always below 200 except for 3 occasions. I made a note on those three times that I had fasted then exercised, such as biking to the blood donation site. I assumed it was my own cholesterol from my body assimilating fat for fuel. (the LDL/HDL ratio was excellent).
The notion that large LDL particles are harmless resulted in part from a lack of proper analysis of the particle distribution and confounding risk factors in patients. It was an oversight in the medical community. It was quickly picked up by promoters of high-fat, low-carb diets who tend to have higher LDL cholesterol and larger LDL particle size. Such people would naturally want to believe that large LDL particles are harmless. It's known that people with familial hypercholesterolemia have large LDL particles, yet they are at a very high risk for CVD, even as children and teenagers. This fact alone makes it clear that large LDL particles can't be considered harmless in all cases.
The following paper describes some of the nuances in the interpretation that can make people mistakenly believe that large LDL are harmless. The details can be difficult to read and understand, but they are important. Advanced Lipoprotein Testing and Subfractionation Are Not (Yet) Ready for Routine Clinical Use Samia Mora, MD, MHS Circulation. Author manuscript; available in PMC 2010 May 5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735461/ From the paper: "First, pathophysiological data supporting the view that small LDL particles may be more atherogenic than large particles include the greater oxidation potential of small particles, their association with endothelial dysfunction and multiple metabolic abnormalities, and impaired clearance from the circulation.1,41 However, several mechanisms may underlie the atherosclerotic effect of large LDL.1 At both extremes of LDL size, decreased receptor-binding affinity for LDL receptors is present.42 Large LDL particles also have higher core cholesterol ester content, potentially delivering more cholesterol per particle to arterial walls.43 Large LDL particles predominate in patients with familial hypercholesterolemia and those consuming high-saturated-fat diets.44 Second, epidemiological data for small LDL particles being more atherogenic than large ones are derived from studies that found that small LDL size was associated with higher CVD risk, although not all studies found this association to be independent of other risk factors such as triglycerides or apoB, with which small LDL particles are strongly associated.45–47 Other studies found that large LDL size was associated with CVD.48,49 An important limitation of these studies is that LDL size was often measured by GGE, which determines the predominant distribution of LDL size (ie, average LDL size; large versus small) but does not quantifythe number of large and small LDL particles."
Additional excerpt from the paper: "This distinction is important because a decrease in average LDL size does not necessarily translate into a greater number of small LDL particles because it could also result from having fewer large LDL particles (Figure 3). Thus, small LDL size may potentially confound the association of LDL particle concentration (number) with CVD. A confounding variable is both associated with the risk factor and causally associated with the outcome. A potential confounder (eg, smaller LDL size) may mask the relationship between the risk factor (eg, LDL particle concentration) and the outcome (eg, CVD). A study population may have a mix of individuals, some with predominantly large LDL, such as those with familial hypercholesterolemia, and others with predominantly small LDL, such as those with diabetes mellitus or insulin resistance. These individuals would also be expected to differ in their concentration of LDL particles. For example, we may not know if risk in the diabetic patient is due to the diabetes mellitus or the small LDL particles, but if the risk is predicted correctly by knowing that the person has diabetes mellitus, high LDL particle concentration, high triglycerides, and low HDL cholesterol, it may not be useful to also measure LDL size. This is demonstrated by 2 case examples outlined in Figure 4. For the same serum concentration of LDL cholesterol, individual B has smaller average LDL particle size and concomitantly more LDL particles than individual A, who has larger average LDL size. Small LDL particles contain less cholesterol than large ones. Thus, individual B must have a higher concentration of total LDL particles, as measured either by NMR (LDL particle concentration) or immunoassay (apoB), for the same LDL cholesterol as individual A. Prior studies that suggested that smaller LDL particles were more “atherogenic” did not adequately control for the inverse correlation between small and large LDL particle concentrations and potential confounding due to their differing associations with other lipoproteins, lipids, and cardiovascular risk factors.16,20,50 A report from 5500 asymptomatic individuals in the Multi-Ethnic Study of Atherosclerosis (MESA) compared the per-particle associations of small and large LDL with carotid intima-media thickness, a direct and well-validated measure of subclinical atherosclerosis.28 To unmask the association of large LDL with IMT, participants were classified into categories of small LDL particle concentration (Figure 5). In these stratified analyses, higher concentrations of large LDL were significantly associated with intima-media thickness within any particular category of small LDL. This was also confirmed by regression analysis: After particle correlations were accounted for, both small and large LDL were “atherogenic” to a similar extent."
there is no proof whatsoever that cholesterol is bad. Cholesterol is a healing hormone. Whenever you injure yourself, one of the first hormones that go to the wound is cholesterol. The older you get the more cholesterol your body needs. There is no "one-for-all cholesterol guideline" because everybody is different. If your stress level is high then your cholesterol level is also high. If you suffered an injury or surgery lately then your cholesterol levels will be high (temporarily). Therefore it is very useless and misleading to get your cholesterol levels checked. Btw cholesterol lowering drugs are one of the most lucrative products of the pharma industry.
Our body needs cholesterol and brains FOR SURE...probably why so much dementia now as so many are taking statins for what their docs tell them is needed to lower cholesterol. Very pathetic, $$$$$$. I got wise probably 20 yrs ago, and I'm 82. Don't overdose but don't worry. Have had my doctor test homocysteine levels and they were elevated so have been taking supplements to lower these levels. Read the Cholesterol Myth The Cholesterol Myths - Uffe Ravnskov There are other books written as well.....
