AAS - How to maintain cholesterol levels and stay healthy??

[Wayacrucis]

I'm sure all of you know, or maybe you don't, because I barely ever see threads addressing the topic of cholesterol. I've been cycling on and off for about two years now. Experimented with a lot of compounds... Tren , T3, Arimidex , etc...almost all the basics and the most used AI and fat burners. I've also been researching and reading a lot and taking the entire "constantly cycling life style" a lot more seriously. In the beginning I had the mind set of most people: Meh, whatever on cycle 2-3 months, I'll take my milk thistle do a good PCT, you know what could go wrong? And well not much can go wrong, unless you are constantly cycling and using the mind set.

So I have a couple of questions for you vets that costantly cycle:

RBC Levels - I'm aware that if RBC levels increase too much, blood becomes thick. Thick blood = increased chance of a heart attack or a stroke. A lot of people suggest donating blood. How often to donate?? and how much?? what is enough?

Cholesterol - This is the most detrimental side of AAS in my opinion. Increase bad cholesterol and decrease good. What does this mean? clogged arteries. Good way to die early. So how do you guys keep cholesterol in check? I try my best to eat very clean, consume lots of good fats, keep sodium low, lots of pottasium. What do you guys recommend doing to maitain cholesterol levels in the normal range? any supps? and specific good fats to consume more than others? etc...?

AI and Lipids - I've read that using Arimidex will also hinder cholesterol levels. Stack this with AAS and you must have some ****ed up lipids. How bad is Adex really on lipids? will using 0.5 E3D hinder lipids??
Also why does Adex even have this affect? I'd like to know is it the compound Adex itself that messes with lipipds or does it only have this affect when estrogen levels are below normal??



I'm sorry for asking so many questions, but there are so many threads on will stacking X,Y,G together make me big? how about X,L,Y will this make me bigger? and we have so many stickies on how to do a PCT, run a proper cycle, but what about us guys that aren't just about that 1-2 cycles?? Guys that are getting ready to compete and actually care about their health? I'd really appreciate some input on this.

[Brohim]

Competing as a BBer usually means high dose of AAS. High dose of AAS does not equal healthy. Who told you competing and using AAS (in large doses) is healthy?

You realize Testosterone is cholesterol. And you are injecting large quanities into your body. Of course your lipids are going to be hell! If you want good lipids don't do AAS and eat a balanced diet.

Your body is a wonderful organism. It alway's strives for balance. Injecting large doses of hormones upset the balance so of course your systems will be out of whack. (While using AAS)

[Wayacrucis]

Competing as a BBer usually means high dose of AAS. High dose of AAS does not equal healthy. Who told you competing and using AAS (in large doses) is healthy?

You realize Testosterone is cholesterol. And you are injecting large quanities into your body. Of course your lipids are going to be hell! If you want good lipids don't do AAS and eat a balanced diet.

Your body is a wonderful organism. It alway's strives for balance. Injecting large doses of hormones upset the balance so of course your systems will be out of whack. (While using AAS)

I never said it was healthy, but I'm sure there are ways to keep somewhat decent lipids. I have a friend that is on 750mg Test E, 600mg EQ and his cholesterol levels were in the normal range. He just stays very lean year round, barely eats junk. Though I'm sure everyone's body is different.I've never been in a big believer in huge doses = huge gains. I mean I've ran 1g of Test, with 500mg Tren weekly, but I'm not one of those guys that'll stack 6 drugs together all at medium high to high doses.

My dad had an open heart surgery at around 50 years old due to clogged arteries. This was mainly due to smoking, he never had anything to do with bodybuilding. So genetically, I might be predisposed to it a well. I cut down this summer, and was about 215lbs at 8% BF 6'0. Trying to compete next summer...and just wanna do my best to damage my body as least as possible..because I'm probably going to continue competing..

[Brohim]

I never said it was healthy, but I'm sure there are ways to keep somewhat decent lipids. I have a friend that is on 750mg Test E, 600mg EQ and his cholesterol levels were in the normal range. He just stays very lean year round, barely eats junk. Though I'm sure everyone's body is different.

Yeah best way is to keep a clean diet. Don't go dirty bulk and eat whatever you want. That is disgusting and vile. Keeping lean year around is the way to go

[Narkissos]

Bump for Swifto and some others... as I'm curious as well.

[austinite]

I had a hard time with cholesterol levels and tried everything naturally/OTC to no avail. Finally got some Crestor and take 5mg nightly. This little pill brought me back and I don't cycle without it. I also take Metformin HCL extended release @ 500mg nightly to control blood sugar (although I am not diabetic)

[Sgt. Hartman]

I don't worry too much about cholesterol levels (hdl and ldl) on cycle. There's little to no evidence that supports the idea that lower LDL cholesterol reduces cardiovascular events in people who don't already have heart disease. And I damn sure wouldn't take a statin to lower my ldl. Blood pressure is the most important stat to monitor while on cycle imo and there are many ways to control it even on aggressive cycles. I've used low dose cialis with great success.

Here's a long article that nobody will probably read lol but here it is anyway.




Why has there never been a record of cholesterol having blocked a vein in the body! What is it about arteries that makes cholesterol attach itself to their walls, while leaving the veins alone? It is really the sticky nature of cholesterol that is behind the blockage of healthy blood vessel walls?

The answers to these questions may surprise you. The body actually uses the lipoprotein cholesterol as a kind of bandage to cover abrasions and tears in damaged arterial walls just as it does it for any other wound. Cholesterol is nothing less than a life-saver. However, for the past thirty-eight years, this lipoprotein has been stigmatized to be the number one cause of deaths in the rich nations - heart disease.

This is how the theory goes: For reasons not really known, a form of cholesterol that has earned the name "bad" somehow increases in the bloodstream of millions of people today; it sticks to the walls of arteries, and eventually, it will starve the heart muscle of oxygen and nutrients. Accordingly, the masses are urged to reduce or ban cholesterol-containing fats from their diet so that they can live without the fear of arterial occlusion and dying from a heart attack.

The tremendous concern of being attacked by this "vicious" lipoprotein has finally led to ********** technologies that can even extract cholesterol from cheese, eggs, and sausages, thus making these "deadly" foods "consumer-safe." Products that claim to be low in cholesterol, such as margarine and light-foods, have become a popular choice of "healthy eating."

Cholesterol is Not the Culprit After All

But as INTERHEART and other studies have shown, cholesterol isn't a serious risk factor for heart disease at all. An earlier study sponsored by the German Ministry of Research and Technology showed that no exact link exists between food cholesterol and blood cholesterol. Even more surprising, in Japan, the cholesterol levels have risen during recent years, yet the number of heart attacks has dropped. The largest health study ever conducted on the risks of heart disease took place in China. Like so many similar studies, the Chinese study found no connection between heart disease and the consumption of animal fats.

In an 8-year long heart study, researchers observed 10,000 people with high cholesterol levels. Half of them received a best-selling statin drug. The other half were simply told to eat a normal diet and get enough exercise. The results stunned the researchers. Although the statin drug did indeed lower serum cholesterol, this had no impact whatsoever on death rate, non-fatal heart attacks and fatal arterial disease. In other words, the statin-users had zero advantage over those who received no treatment at all. However, they had just spent eight years taking a costly drug with hideous side effects - risking liver failure, muscle wasting, even sudden death. Lowering cholesterol either through drugs or low fat diets does not lower the risk of developing heart disease.

All the major European long-term cholesterol studies have confirmed that a low-fat diet did not reduce cholesterol levels by more than 4 percent, in most cases merely 1-2 percent. Since measurement mistakes are usually higher than 4 percent and cholesterol levels naturally increase by 20 percent in autumn and drop again during the wintertime, the anti-cholesterol campaigns since the late 1980s have been very misleading, to say the least. A more recent study from Denmark involving 20,000 men and women, in fact, demonstrated that most heart disease patients have normal cholesterol levels. The bottom line is that cholesterol hasn't been proved a risk factor for anything.

The current medical understanding of the cholesterol issue is more than incomplete. The argument that animal tests on rabbits have confirmed that fatty foods cause hardening of the arteries sounds convincing, but only when the following facts are omitted:

* Rabbits respond 3,000 times more sensitively to cholesterol than humans do.

* Rabbits, which are non-carnivorous animals by nature, are force-fed excessive quantities of egg yolk and brain for the sake of proving that cholesterol-containing foods are harmful.

* The DNA and enzyme systems of rabbits are not designed for consumption of fatty foods, and if given a choice, these animals would never eat eggs or brains.

It is obvious that the arteries of these animals have only an extremely limited ability to respond to the damage caused by such unsuitable diets. For over three and half decades, Western civilization assumed that animal fats were the main cause of dietary heart disease. This misinformation is highlighted by the fact that heart attacks began to rise when consumption of animal fats actually decreased. This was verified by British research, which revealed that those areas in the U.K. where people consumed more margarine and less butter had the highest numbers of heart attacks. Further studies revealed that heart attack patients had consumed the least amounts of animal fats.

In this context, it is important to differentiate between processed and unprocessed fats. It has been discovered that people who died from a heart attack were found to have many more of the harmful fatty acids derived from the partially hydrogenated vegetable oils in their fat tissue than those who survived. These so-called "faulty" fats (trans-fatty acids) envelop and congest the membranes of cells, including those that make up the heart and coronary arteries. This practically starves the cells of oxygen, nutrients, and water, and eventually kills them.

In another more comprehensive study, 85,000 nurses working in American hospitals observed a higher risk for heart disease in patients who consumed margarine, crisps, potato chips, biscuits, cookies, cakes, and white bread, all of which contain trans fats.

Eating margarine can increase heart disease in women by 53 percent over eating the same amount of butter, according to a recent Harvard Medical Study. While actually increasing LDL cholesterol, margarine lowers the beneficial HDL cholesterol. It also increases the risk of cancers up to five times. Margarine suppresses both the immune response and insulin response. This highly processed and artificial product is practically resistant to destruction, being one molecule away from plastic. Flies, bacteria, fungi, etc. won't go near it because it has no nutritional value and cannot be broken down by them. It can last for years, not just outside the body, but inside as well.

It is very apparent that eating damaged, rancid fats or trans-fats can destroy any healthy organism and should be avoided by anyone. In 2007 New York City banned the use of trans fats in its restaurants; however, the trans fats are merely being replaced with new artificial fats that have the same or worse effects.

Healthy Today - Sick Tomorrow

Unfortunately, high cholesterol (hypercholesterolemia) has become the dominating health concern of the 21st century. It is actually an invented disease that doesn't show up as one. Even the healthiest people may have elevated serum cholesterol and yet their health remains perfect. But they are instantly turned into patients when a routine blood test reveals that they have a "cholesterol problem."

Since feeling good is actually a symptom of high cholesterol, the cholesterol issue has confused millions of people. To be declared sick when you actually feel great is a hard nut to swallow. So it may take a lot of effort on behalf of a practicing physician to convince his patients that they are sick and need to take one or more expensive drugs for the rest of their lives. These healthy individuals may become depressed when they are being told they will need to take potentially harmful drugs to lower their cholesterol levels on a long-term, daily basis. When they also learn that they will require regular checkups and blood tests, their worry-free, good life is now over.

These doctors cannot be blamed for the blunder of converting healthy people into patients. Behind them stands the full force of the U.S. government, the media, the medical establishment, agencies, and of course, the pharmaceutical companies. All of them have collaborated to create relentless pressure in disseminating the cholesterol myth and convincing the population that high cholesterol is its number one enemy. We are told that we need to combat it by all means possible to keep us safe from the dreadful consequences of hypercholesterolemia.

The definition of a "healthy" level of cholesterol has been repeatedly adjusted during the past 30 years, which certainly does not give me much confidence in a system of medicine that professes to be founded on sound scientific principles. In the early days of measuring cholesterol levels, a person at risk was any middle-aged man whose cholesterol was over 240 and possessed other risk factors, such as smoking or being overweight.

After the adjustment of parameters during the Cholesterol Consensus Conference in 1984, the population was hit by a shock wave. Now, anyone (male or female) with overall cholesterol readings of 200 mg percent (200mg per 100 ml) could receive the dreaded diagnosis and a prescription for pills. The claim that 200 blood serum cholesterol is normal and everything above is dangerous was scientifically unfounded, though. At least, this was the consensus of all the major cholesterol studies. In fact, a report in a 1995 issue of the Journal of the American Medical Association showed no evidence linking high cholesterol levels in women with heart conditions later in life.

Although it is considered completely normal for a 55-year-old woman to have a cholesterol level of 260 mg percent, most women that age are not told about this. Also healthy employees are found to have an average of 250 mg percent with high fluctuations in both directions.

The lack of evidence linking elevated cholesterol with increased risk of heart disease, however, didn't stop the brainwashing of the masses. In the U.S. 84 percent of all men and 93 percent of all women aged 50-59 with high cholesterol levels were suddenly told they needed treatment for heart disease. The totally unproved but aggressively promoted cholesterol theories turned most of us into patients for a disease that we probably will never develop. Fortunately, not everyone has followed the advice to have their cholesterol levels checked but, unfortunately, millions of people have fallen into the trap of misinformation.

To make matters worse, the official, acceptable cholesterol level has now been moved down to 180. If you have already had one heart attack, your cardiologist will tell you to take cholesterol-lowering statins even if your cholesterol is very low. From the viewpoint of conventional medicine, having a heart attack implies that your cholesterol must be too high. Hence you are being sentenced to a lifetime of statins and a boring low-fat diet. But even if you have not experienced any heart trouble yet, you are already being considered for possible treatment.

Since so many children now show signs of elevated cholesterol, we have a whole new generation of candidates for medical treatment. So yes, current edicts stipulate cholesterol testing and treatment for young adults and even children! The statin drugs that doctors use to push cholesterol levels down are LIPITOR (atorvastatin), Zocor (simvastatin), Mevacor (lovastatin), and Pravachol (pravastatin). If you decide to follow your doctor's advice and take one of these drugs, make certain to read the list of side effects so that you know the risks you are taking.

If you want to obtain objective and untainted information on cholesterol, agencies like the National Institutes of Health and the American College of Cardiology are certainly not the places from which to obtain it. Until recently, they wanted you to keep your overall cholesterol level below 150. Then, in 2001, they finally admitted that measuring overall cholesterol levels makes no sense at all, so they began recommending an LDL level below 100. Now their aim is to keep LDL lower than 70. Every time they lower the target, the number of "patients" requiring treatment jumps dramatically, much to the benefit of the drug producers. Being officially backed by these agencies, doctors feel motivated, if not obliged, to prescribe these expensive drugs to their new patients.

The extensive promotional campaigns by the pharmaceutical giants have already brainwashed the masses to believe they need these drugs to be safe from sudden heart attack. Even if a doctor knows the truth about the cholesterol deception, these anxious patients will demand a prescription from him. This is not just affecting their health, but everyone's economic future. The massive sales of these best-selling drugs of all time drive up health care costs to levels that undermine economic growth and make basic health care unaffordable to an ever-increasing number of people. The masses have been so brainwashed with misinformation that this lurking financial crisis doesn't seem to be their immediate concern.

In 2004, there were already 36 million statin candidates in the U.S., with 16 million using LIPITOR alone. When the official LDL target level drops to 70, another 5 million people will be eligible for their use. At the consumer markup price of $272.37 and an actual cost of $5.80 for a month supply of LIPITOR, you can understand the incentive that the pharmaceutical industry has to push their products and make them a mass commodity.


-Andreas Moritz-

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Primary Prevention of Acute Coronary Events With Lovastatin in Men and Women With Average Cholesterol Levels
Results of AFCAPS/TexCAPS
John R. Downs, MD; Michael Clearfield, DO; Stephen Weis, DO; Edwin Whitney, MD; Deborah R. Shapiro, DrPH; Polly A. Beere, MD, PhD; Alexandra Langendorfer, MS; Evan A. Stein, MD; William Kruyer, MD; Antonio M. Gotto, Jr, MD, DPhil; for the AFCAPS/TexCAPS Research Group
JAMA. 1998;279(20):1615-1622. doi:10.1001/jama.279.20.1615


ABSTRACT
ABSTRACT | METHODS | RESULTS | COMMENT | REFERENCES

Context.— Although cholesterol-reducing treatment has been shown to reduce fatal and nonfatal coronary disease in patients with coronary heart disease (CHD), it is unknown whether benefit from the reduction of low-density lipoprotein cholesterol (LDL-C) in patients without CHD extends to individuals with average serum cholesterol levels, women, and older persons.

Objective.— To compare lovastatin with placebo for prevention of the first acute major coronary event in men and women without clinically evident atherosclerotic cardiovascular disease with average total cholesterol (TC) and LDL-C levels and below-average high-density lipoprotein cholesterol (HDL-C) levels.

Design.— A randomized, double-blind, placebo-controlled trial.

Setting.— Outpatient clinics in Texas.

Participants.— A total of 5608 men and 997 women with average TC and LDL-C and below-average HDL-C (as characterized by lipid percentiles for an age- and sex-matched cohort without cardiovascular disease from the National Health and Nutrition Examination Survey [NHANES] III). Mean (SD) TC level was 5.71 (0.54) mmol/L (221 [21] mg/dL) (51st percentile), mean (SD) LDL-C level was 3.89 (0.43) mmol/L (150 [17] mg/dL) (60th percentile), mean (SD) HDL-C level was 0.94 (0.14) mmol/L (36 [5] mg/dL) for men and 1.03 (0.14) mmol/L (40 [5] mg/dL) for women (25th and 16th percentiles, respectively), and median (SD) triglyceride levels were 1.78 (0.86) mmol/L (158 [76] mg/dL) (63rd percentile).

Intervention.— Lovastatin (20-40 mg daily) or placebo in addition to a low–saturated fat, low-cholesterol diet.

Main Outcome Measures.— First acute major coronary event defined as fatal or nonfatal myocardial infarction, unstable angina, or sudden cardiac death.

Results.— After an average follow-up of 5.2 years, lovastatin reduced the incidence of first acute major coronary events (183 vs 116 first events; relative risk [RR], 0.63; 95% confidence interval [CI], 0.50-0.79; P<.001), myocardial infarction (95 vs 57 myocardial infarctions; RR, 0.60; 95% CI, 0.43-0.83; P=.002), unstable angina (87 vs 60 first unstable angina events; RR, 0.68; 95% CI, 0.49-0.95; P=.02), coronary revascularization procedures (157 vs 106 procedures; RR, 0.67; 95% CI, 0.52-0.85; P=.001), coronary events (215 vs 163 coronary events; RR, 0.75; 95% CI, 0.61-0.92; P=.006), and cardiovascular events (255 vs 194 cardiovascular events; RR, 0.75; 95% CI, 0.62-0.91; P=.003). Lovastatin (20-40 mg daily) reduced LDL-C by 25% to 2.96 mmol/L (115 mg/dL) and increased HDL-C by 6% to 1.02 mmol/L (39 mg/dL). There were no clinically relevant differences in safety parameters between treatment groups.

Conclusions.— Lovastatin reduces the risk for the first acute major coronary event in men and women with average TC and LDL-C levels and below-average HDL-C levels. These findings support the inclusion of HDL-C in risk-factor assessment, confirm the benefit of LDL-C reduction to a target goal, and suggest the need for reassessment of the National Cholesterol Education Program guidelines regarding pharmacological intervention.

[Sgt. Hartman]

I'm not trying to change anyone's mind, just giving an different point of view. What was Lovastatin's role in the study (funding, etc.)?

I'd still like to hear an explanation of exactly how high LDL causes CHD?

[AD]

It might be inevitable that some research funds come from big pharma companies. But we can sieve out biased studies by looking at design and methodology of studies.

[AD]

http://www.mayoclinic.com/health/cor...SECTION=causes

The way you asked that question makes me want to be extra cautious with my answer. High chol causes narrowing and blockage of blood vessels by the process of artherosclerosis.

[AD]

I'm not trying to change anyone's mind, just giving an different point of view. What was Lovastatin's role in the study (funding, etc.)?

In the same way that you suspect big pharma of overstating the need to lower chol, why aren't you suspicious of Moritz over-promoting his homeopathic non-pharmacological ways?

[The Bear 79]

I use triple fish oil with co q 10, + 3 - 4 cloves of garlic & two cups of oats everyday, my cholesterol has never been in an unhealthy / dangerous range.

[Sgt. Hartman]

The last thing I want is for people to ignore their high cholesterol simply because imo it's relatively unimportant and wind up having health implications because of it. This is merely my opinion.

I don't think that high cholesterol alone increases the risk of stroke:


Background: Controversy remains on the relation between serum lipids levels and stroke risk. This paper investigated the association of total and HDL cholesterol level to fatal and non-fatal, and haemorrhagic and ischaemic stroke in four European cohorts participating in EUROSTROKE.

Methods: EUROSTROKE is a collaborative project among ongoing European cohort studies on incidence and risk factors of stroke. EUROSTROKE is designed as a nested case-control study. For each stroke case, two controls were sampled. Strokes were classified according to MONICA criteria or reviewed by a panel of four neurologists. At present, data on stroke and risk factors were available from cohorts in Cardiff (84 cases), Kuopio (74 cases), Rotterdam (157 cases), and Novosibirsk (79 cases).

Results: Pooled analyses showed no significant association between total cholesterol and risk of stroke (odds ratio for increase of 1 mmol/l in cholesterol of 0.98 (95% CI 0.88 to 1.09)). Analyses for haemorrhagic stroke and cerebral infarction revealed odds ratios of 0.80 (95% CI 0.61 to 1.05) and 1.06 (95% CI 0.94 to 1.19), respectively. The association of HDL cholesterol to stroke was different in men compared with women. In men, there was a general trend towards a lower risk of stroke with an increase in HDL (odds ratio per 1 mmol/l increase in HDL cholesterol 0.68 (95% CI 0.40 to 1.16)). In women, however, an increase in HDL was associated with a significant increased risk of non-fatal stroke and of cerebral infarction (odds ratios of 2.46 (95% 0.1.20 to 5.04) and 2.52 (95% CI 1.15 to 5.50), respectively. The difference between men and women in the association of HDL with stroke seemed to differ mainly in smokers and never smokers, but not among ex smokers.

Conclusion: This analysis of the EUROSTROKE project could not disclose an association of total cholesterol with fatal, non-fatal, haemorrhagic or ischaemic stroke. HDL cholesterol however, seemed to be related to stroke differently in men than in women.



And again here:

Cholesterol, diastolic blood pressure, and stroke: 13 000 strokes in 450 000 people in 45 prospective cohorts

Prospective Studies Collaboration1 2
Abstract

Individual studies of stroke have not clearly answered two questions: on the relation, if any, between total blood cholesterol and stroke; and on how the strength of the relation between diastolic blood pressure and stroke varies with age. The associations of blood cholesterol and diastolic blood pressure with subsequent stroke rates were investigated by review of 45 prospective observational cohorts involving 450 000 individuals with 5-30 years of follow-up (mean 16 years, total 7·3 million person-years of observation), during which 13 397 participants were recorded as having had a stroke. Most of these were fatal strokes in studies that recorded only mortality and not incidence, but about one-quarter were from studies that recorded both fatal and non-fatal strokes. After standardisation for age, there was no association between blood cholesterol and stroke except, perhaps, in those under 45 years of age when screened. This lack of association was not influenced by adjustment for sex, diastolic blood pressure, history of coronary heart disease, or ethnicity (Asian or non-Asian). However, because the types of the strokes were not centrally available, the lack of any overall relation might conceal a positive association with ischaemic stroke together with a negative association with haemorrhagic stroke. When the highest and the lowest of the six blood pressure categories were compared, the difference in usual diastolic blood pressure was 27 mm Hg (102 vs 75 mm Hg), and there was a fivefold difference in stroke risk. This fivefold difference was seen both in those with a pre-existing history of coronary heart disease and in those without it. The proportional difference in stroke risk, however, was more extreme in middle than in old age. Among those aged <45, 45-64, and 65+ when screened, the differences in the relative risks of stroke (between the highest diastolic blood pressure category and a combination of the lowest two categories) were tenfold, fivefold, and twofold, respectively. However, because the absolute stroke risks are greater in old age, the absolute differences in the annual stroke rates showed an opposite pattern, being 2, 5, and 8 per thousand, respectively. This suggests that the effects of therapeutic blood pressure reductions should be assessed separately in middle age and in old age.

http://www.mayoclinic.com/health/cor...SECTION=causes

The way you asked that question makes me want to be extra cautious with my answer. High chol causes narrowing and blockage of blood vessels by the process of artherosclerosis.

According to this high cholesterol protects against atherosclerosis:

High cholesterol may protect against infections and atherosclerosis
U. Ravnskov
+ Author Affiliations

Independent researcher
Address correspondence to Dr U. Ravnskov, Magle Stora Kyrkogata 9, S-22350, Sweden. e-mail: [email protected]
Introduction

Many researchers have suggested that the blood lipids play a key role in the immune defence system.1–,21 There is also a growing understanding that an inflammatory response of the arterial intima to injury is a crucial step in the genesis of atherosclerosis. and that infections may be one type of such injury.22 These two concepts are difficult to harmonize with the low-density-lipoprotein (LDL) receptor hypothesis, according to which high LDL cholesterol is the most important cause of atherosclerosis. However, the many observations that conflict with the LDL receptor hypothesis, may be explained by the idea that high serum cholesterol and/or high LDL is protective against infection and atherosclerosis.

I will admit that there's a correlation between high cholesterol and CHD but I don't think it's the cause. There's a lot of books and info on this if you read up on it you'll see I'm not the only one who thinks this. Check out "The Great Cholesterol Con" by Malcom Hendrick or just google cholesterol myths and you'll see what I'm talking about.

[Swifto]

I want to share my opinion on certain aspects of cholesterol. I am sure there are some who disagree, but that's ok...I'm giving my thoughts anyway.

So LDL and total cholesterol readings...that is what we should focus on right?

My answer is hell no, and let me explain why in the simplest way i can.

- First of all there isn’t good or bad cholesterol at all. It’s all the same initially. The carriers of cholesterol, lipoproteins are where we get HDL and LDL. (It's just the name of the carriers that tote it around our blood).

Should we be happy when our LDL is in range. My opinion...not necessarily. Do you want to know what really matters?

Think of a road….cars (or carriers/lipoproteins) are carrying passengers (cholesterol). Does it matter how many people are in the cars? Nope. What causes traffic jams and accidents, are the number of cars on the road. The road is our arteries by the way in my analogy. This is called particle number/concentration. The more cars you have, the more danger there is.

Now.....key point here...

The number you get for your LDL is just the amount being carried around in your LDL carriers we'll call them, not the number of carriers/cars on the road - again, that is called particle concentration.

Now, here is another part I want to drive home.

Ok so now think about this. Let’s say we have 10 gallons of Karboload, in 10 containers. Now let’s say we have 10 gallons of Karboload in 100 containers. It’s still the SAME amount of karboload (cholesterol), but in the second case, you have 100 gallons so MORE PARTICLES! You could have a traditionally great LDL number. It does NOT matter. What does matter is how many particles are carrying it around. The more you have, the more the risk of crashing on the road (lodging in the lumen in an artery). Typically people with insulin resistance have this problem or people that eat junk carbs frequently.

Why is this? Because their carriers/lipoprotiens have much more triglycerides in them. So there is less cholesterol due to this in the carrier.....so we need more carriers...again, not good. If you want to increase particle concentration or the number of carriers, just go to 7/11 and drink a load of HFCS laden Big Gulps every day.

Another factor that is really important is Apo B. If people seem interested in this thread and topic, we can go down that road, cause it's important as well. We can also get into fibrinogen, C-reactive protein, measures that really matter.....not total cholesterol.....

Moral of this, you want to get a test done that measures LDL concentration (number of carriers) and LDL particle size..as there does seem to be alot of evidence that smaller cars on the road crash easier and aren't as bouyant.

Sorry if this doesn't make sense...it's later, but all this cholesterol nonsense being perpetuated just annoys me.

- John Meadows.

Rather than post the link, I have PM'd a link where this is discussed at length on another forum by nutritionists and some very bright minds and it taught me a thing or two.

[Swifto]

There are a lot of myths on cholesterol, the main one being animal fats cause high lipids, or any fatty foods for that matter. Some of the worls highest consuming animal fat cultures, such as African tribes and Eskimo's have the most favourable lipid profiles.

Emphasis on ratio, too low LDL will also cause problems.

I think there is without doubt a link between lipid profile and CHD as well. One cannot argue its not applicable and as its applicable, it should be something we monitor when using androgens.

[AD]

if anyone look hard enough, no doubt some studies can be found to contradict conventional wisdom. but here is the WHO guidelines on cholesterol:

http://www.policy-centre.com/downloa...idelines07.pdf

here's the last paragraph





Conclusions
The direction of travel is clear. Clinical
trial evidence is widening the scope of
cholesterol management in the prevention
and treatment of CVD, particularly in
the inclusion of most or all people with
diabetes. It is also leading to increasingly
aggressive targets for those at most risk.
Whilst improvements in diet and lifestyle
remain the first option for cholesterol
reduction, assisted by developments in
plant sterol-enhanced foods, the focus of
guidelines remain on reducing LDL-C with
lipid lowering drugs as the first line of
therapy when this proves necessary in the
achievement of cholesterol targets. There
is a clear and significant time lag between
the incorporation of clinical trial evidence
into pan-European standards of best practice,
widely endorsed by lipid experts and
their national associations, and their
incorporation into national and local
practice across Europe. Thus CVD remains
a leading cause of avoidable death and
disability in Europe.


may have to read the whole article (too big for me to cut and paste) to see the whole picture, but surely the guideline by the worldwide authority in medical science should carry some weight.

[Swifto]

High HDL Cholesterol (Hyperalphalipoproteinemia)

High-density lipoprotein (HDL) is positively associated with a decreased risk of coronary heart disease (CHD). As defined by the US National Cholesterol Education Program Adult Treatment Panel III guidelines, an HDL cholesterol level (HDL-C) of 60 mg/dL or greater is a negative (protective) risk factor.[1] On the other hand, a high-risk HDL cholesterol level is described as one that is below 40 mg/dL. Randomized, controlled clinical trials have demonstrated that interventions to raise HDL cholesterol levels are associated with reduced CHD events. A prospective analysis by Mora et al investigated the link between cholesterol and cardiovascular events in women and found baseline HDL-C level was consistently and inversely associated with incident coronary and coronary vascular disease events across a range of low-density lipoprotein-cholesterol (LDL-C) values.[2]

The major apolipoproteins of HDL are apolipoprotein (apo) A-I and apo A-II, the alpha lipoproteins. An elevated concentration of apo A-I and apo A-II is called hyperalphalipoproteinemia (HALP), which is associated with a lower risk CHD. Conversely, hypoalphalipoproteinemia increases the risk of CHD. The levels at which HDL confers benefit or risk are not discrete, and the cut points are somewhat arbitrary, especially considering that HDL levels are, on average, higher in US women compared with men and higher in blacks compared with whites.

Elevated HDL levels are associated with low levels of very low-density lipoprotein cholesterol (VLDL) and triglyceride (TG) levels. LDL-C levels may be within the reference range or elevated. Persons with HALP do not have any unusual clinical features, and the condition should not be considered a disease entity but rather a fortuitous condition that can increase longevity because of the associated decreased incidence of CHD.[3]

HDL is more tightly controlled by genetic factors than are the other lipoproteins (ie, LDL, VLDL, intermediate-density lipoprotein [IDL], and chylomicrons). For example, in certain families, especially some families with Japanese ancestry, a genetic deficiency of cholesteryl ester transfer protein (CETP) is associated with strikingly elevated HDL cholesterol levels.[4]

However, environmental factors also have a significant impact on HDL levels. Factors that elevate HDL concentrations include chronic alcoholism, treatment with oral estrogen repla***ent therapy, extensive aerobic exercise, and treatment with niacin, statins, or fibrates.[5, 6, 7] On the other hand, smoking reduces levels of HDL cholesterol, while quitting smoking leads to a rise in the plasma HDL level.

Very high levels of HDL cholesterol have been reported to be atherogenic. The mechanism of this paradoxical effect is not entirely clear.


Longevity


The aging process involves damage to the body and DNA so the key to longevity in the short term is limiting that damage, in the long term it involves repairing the body and DNA.

- Resveratol stimulates sirtuin genes linked to DNA repair. (fruit flies living 30-50% longer)
- *Good cholesterol HDL* is linked to longevity. (*people living to 100*)
- Low insoline is linked to longevity. (worms and fruit flies living longer)
- Sleep is linked to DNA repair.
- The secret of red wine. (resveratol and alcohol)
- Alcohol. (HDL boost and reduced dementia)
- Reduced stress and DNA damage
- Social networks and friends
- Digestion and supplements
- Sex and hormones
- Exercise and growth hormone
- The Legend (cholesterol and inflammation)
- A good diet and lower risk of disease

Sirtuin Genes and Resveratol

The sirtuin genes are part of an intricate stretch response or survival mode response. When times are tough they kick in and increase DNA repair or prevent cell death. Some people use calorie restriction in order to trigger the survival mode response and stimulate the sirtuin genes.

Resveratol also stimulates the sirtuin genes without the calorie restriction or survival mode response.
It is similar to calorie restriction but without the calorie restriction.

DAF2 Genes and Insoline

Decreased or low levels of insoline are also linked to longevity.
So a diet the keeps insoline levels low leads to a longer life similar to calorie restriction.

Good Cholesterol (HDL)

High levels of good cholesterol (HDL) are linked to longevity. (people living to 100)

Exercise is linked to higher HDL levels.

- Aerobic exercise, walking, jogging, exercise that raises your heart rate for 20 - 30 minutes at a time may be the most effective way to increase HDL levels. (duration)

A good diet can also reduce bad cholesterol (LDL) and increase good cholesterol (HDL).

- Vitamin B, B3 Niacin, can help lower bad cholesterol (LDL) and boost good (HDL) cholesterol.
- Alcohol, one or two drinks per day can significantly increase HDL levels.
- Omega-3 fatty acids can also increase HDL levels.
- Monounsaturated fats such as olive oil can increase HDL levels without increasing the total cholesterol.
- Soluble fibers such as oats, fruits, vegetables, and legumes can reduction LDL and an increase HDL levels.
- Calcium supplementation can increase HDL levels. (postmenopausal women)
- Cranberry juice has been shown to increase HDL levels.

- Trans fatty acids, partially hydrogenated vegetable oils, can increase LDL and reduce HDL levels.
- Sugar can decrease HDL and increase triglycerides levels.

Lose weight, obesity can increase LDL and reduced HDL levels.

Stop smoking, giving up tobacco will increase HDL levels.

Ultra-low-fat diets have been reported to result in a significant reduction in HDL in some individuals.

Cancer risk is reduced with increased HDL levels.

Detoxification and reduced plaque in blood vessels is linked to HDL cholestrol, the higher the better. (heart disease)

?Bad? LDL Cholesterol May Protect Us Against Cancer | The ******** for Natural Health USA

Above

[Amur Tiger]

Brohim,
I want to start Anavar Cycle for fat reductions even i dont have too much fats only some waistline. I hear Anavar affect sperm count and even quality. can you please help me how to safely use for better results. i am not fat guy.

[kelkel]

6 year old thread Amur. Start a new thread and guys will respond to you.