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tammyp
07-24-2009, 06:40 AM
i have it, genetic. i take red yeast rice, omegas, and 10co enzyme. i hear this is hard on your liver as if it were an actual statin drug. since we discuss liver support here, what do any of you suggest to go along with this to help keep my liver healthy? btw....this cocktail got me down 180 points.

Rattbones
07-24-2009, 07:12 AM
I don't normally post anything in the womens sections but I wanted to pass this on. Super Human Radio just had a show on "the Cholesterol Myth Exposed" especially the use of statins. It's episode 333
http://www.superhumanradio.com/mp3/player.htm

tammyp
07-24-2009, 08:19 AM
sweet ! thanks!

triceptor
07-24-2009, 08:46 AM
I don't normally post anything in the womens sections but I wanted to pass this on. Super Human Radio just had a show on "the Cholesterol Myth Exposed" especially the use of statins. It's episode 333
http://www.superhumanradio.com/mp3/player.htm


damn... you beat me too it LOL

Here's a permalink. The player rotates the older shows down the list...

:: The Cholesterol Myth Exposed :: Guest: Sally Fallon :: Fallon is the founding president of the Weston A Price Foundation and works tirelessly to expose the dangerous myths promoted by the food and pharmaceutical industry. If you are on statin drugs or know someone who is you absolutely need to listen to this episode. The cholesterol myth and the use of statin drugs are hurting more people than they are saving. ::

http://www.superhumanradio.com/rss/2009/SHR_Show_333.mp3


Thanks Rattbones :bowdown:

sassy69
07-24-2009, 08:57 AM
*NOTE TO SELF* I need to listen to this -- my dad is also genetically high cholesterol as well. He loves his Lipitor.

triceptor
07-24-2009, 09:04 AM
*NOTE TO SELF* I need to listen to this -- my dad is also genetically high cholesterol as well. He loves his Lipitor.

one of the things we discuss is a recent study published in the Lancet that shows older individuals with the highest total cholesterol LIVE THE LONGEST!!!! Tell your dad. The Lancet is the oldest and most respected medical journal in the world.

Choleostatin drug manufacturers already see the writing on the wall. They're in phase I, II and III clinical trails to show that statin drugs have "other" benefits like anti inflammation. The number of people who get heart attacks WHILE on statins is alarming and shoots holes in their use.

Older adults who are genetically "gifted" to have higher cholesterol will live longer. do you have a great great grandfather or great great uncle who lived into his 7th or 8th decade of life on your father's side?

NubianBeauty
07-24-2009, 09:50 AM
I take red yeast rice only. Was prescribed Zetia refused to use it... now suffering from high lipids again Dr gave me Zocor but I'm just gonna start the RYR again since it works. He never knew the diff. My high CHO is from TSH & thyroid issues.

heavyiron
07-24-2009, 11:01 AM
i have it, genetic. i take red yeast rice, omegas, and 10co enzyme. i hear this is hard on your liver as if it were an actual statin drug. since we discuss liver support here, what do any of you suggest to go along with this to help keep my liver healthy? btw....this cocktail got me down 180 points.
Are you saying these OTC sups are like a statin drug?

CQ-10 is an antioxidant for the heart that lowers BP.

Plant sterols are another good way to lower LDL.

Liv 52 is excellent for the liver with proper hydration.

Tatyana
07-24-2009, 11:25 AM
one of the things we discuss is a recent study published in the Lancet that shows older individuals with the highest total cholesterol LIVE THE LONGEST!!!! Tell your dad. The Lancet is the oldest and most respected medical journal in the world.

Choleostatin drug manufacturers already see the writing on the wall. They're in phase I, II and III clinical trails to show that statin drugs have "other" benefits like anti inflammation. The number of people who get heart attacks WHILE on statins is alarming and shoots holes in their use.

Older adults who are genetically "gifted" to have higher cholesterol will live longer. do you have a great great grandfather or great great uncle who lived into his 7th or 8th decade of life on your father's side?

There are quite a few points I agree with you on statins, I think they are used far too commonly.

What exactly is considered 'genetically high cholesterol' in the US, as I have heard a few of the lads talking about having high cholesterol and by UK standards it was perfectly normal.

If someone has familial hypercholesterolaemia, then yes I can understand a statin. If someone has several risk factors, including high blood pressure, obesity, diabetes, smoking, advanced age, bad diet, and they don't want to do anything to help themselves, or even if they do, then yes, I can see the use of a statin.

Familial hypercholesterolaemia is not that common, and there are some very distinctive symptoms.

For example Tammy, your cholesterol at 180 mg/dl is 4.7 mmol/L, which is perfectly acceptable.

What was it before?


There is also an issue if your cholesterol is too low, for example, if your cholesterol is around 3 mmol/L - 116 mg/dl, it is in that range we refer to as the 'suicide range' as our brains are mostly fat, cholesterol is essential in maintaining membrane fluidity, and low cholesterol impacts this.

This is also the sort of level I see quite a bit in the elderly, and it is because they are malnourished.

There is a study that has demonstrated that just lowering your cholesterol to any significant amount can precipitate incidences of violence as well as depression.

This paper will raise your blood pressure Carl, the storm over statins, the pharmacological treatment of children

http://content.nejm.org/cgi/content/short/359/13/1309

Statins also have an impact on other important functions in the body.

http://content.nejm.org/content/vol359/issue13/images/medium/01f1.gif (http://content.nejm.org/content/vol359/issue13/images/large/01f1.jpeg)

Steroid Synthesis Pathway.

Inhibition of this steroid pathway by a statin (red) may have pleiotropic effects:

influencing antioxidant activity (pink);
intracellular processes (blue), including signal transduction, cell proliferation, and apoptosis;
structural components (green);
and steroid hormones (yellow).

FPP denotes farnesyl pyrophosphate, GGPP geranylgeranyl pyrophosphate, and HMG-CoA 3-hydroxy-3-methylglutaryl coenzyme A. Arrows may reflect more than one enzymatic reaction.

Quadsweep
07-24-2009, 03:37 PM
I have heard that policosanol works well as it appears to lower LDL and raise HDL. It is said to work as well as Lipitor without the liver sides at lowering total cholesterol.

Quadsweep

triceptor
07-24-2009, 04:41 PM
I have heard that policosanol works well as it appears to lower LDL and raise HDL. It is said to work as well as Lipitor without the liver sides at lowering total cholesterol.

Quadsweep


One of the best things for increasing HDL while lowering LDL is a $2 bottle of nicotinic acid (Niacin). Numerous studies show it is Superior 90% of statins because it increases LDL receptor in the liver while reducing HDL receptor. No need to go crazy with it either . 300mgs split over 3 x 100mg doses a day for about two weeks will have a profound effect. Oh BTW the flush has something to do with it because the "flush-free" potassium salt version don't work.

One warning... too much Niacin Is no good. It causes hepatic stress. Stay low dose (< 500mgs a day) and let it work over time.

badfish51581
07-24-2009, 05:21 PM
Here's a great paper for everybody:

http://www.jpands.org/vol10no3/colpo.pdf

badfish51581
07-24-2009, 05:36 PM
More interesting reading...


Cholesterol is NOT the Cause of Heart Disease

By Ron Rosedale, MD

Cholesterol is not the major culprit in heart disease or any disease. If it becomes oxidized it can irritate/inflame tissues in which it is lodged in, such as the endothelium (lining of the arteries). This would be one of numerous causes of chronic inflammation that can injure the lining of arteries. However, many good fats are easily oxidized such as omega-3 fatty acids, but it does not mean that you should avoid it at all costs.

Common sense would indicate that we should avoid the oxidation (rancidity) of cholesterol and fatty acids and not get rid of important life-giving molecules. Using the same conventional medical thinking that is being used for cholesterol would lead one to believe that doctors should reduce the risk of Alzheimer's disease by taking out everybody's brain. In fact, cholesterol is being transported to tissues as part of an inflammatory response that is there to repair damage.

The fixation on cholesterol as a major cause of heart disease defies the last 15 years of science and deflects from real causes such as the damage (via glycation) that sugars such as glucose and fructose inflict on tissues, including the lining of arteries, causing chronic inflammation and resultant plaque.

Insulin & Leptin Resistance

Hundreds of excellent scientific articles have linked insulin resistance and more recently leptin resistance to cardiovascular disease much more strongly than cholesterol, and they are in fact at least partially responsible for cholesterol abnormalities. For instance, insulin and leptin resistance result in "small dense" LDL particles and a greater number of particles.

This is much more important than the total cholesterol number. Because of particle size shift to small and dense, the total LDL cholesterol could still be low even though the number of particles and the density of the particles is greater. Small, dense LDL particles can squeeze between the cells lining the inside of the arteries, the "gap junction" of the endothelium, where they can get stuck and potentially oxidize, turn rancid, and cause inflammation of the lining of the arteries and plaque formation.

Importantly, many solid scientific studies have shown a mechanistic, causal effect of elevated insulin and leptin on heart and vascular disease, whereas almost all studies with cholesterol misleadingly only show an association. Association does not imply cause. For instance, something else may be causing lipid abnormalities such as elevated cholesterol and triglycerides, and also causing heart disease.

This "something else" is improper insulin and leptin signaling. Similarly, sugar does not cause diabetes; sugar is just listening to orders. Improper insulin and leptin signaling is the cause of diabetes. Likewise, cholesterol does not cause heart disease, but improper metabolic signals including improper signals to cholesterol (causing it to oxidize) and perhaps to the liver that manufactures the cholesterol, will cause heart and vascular disease and hypertension.

Removing cholesterol will do nothing to improve the underlying problems, the real roots of chronic disease, which will always have to do with improper communication, and the generals of metabolic communication are insulin and leptin. They are really what must be treated to reverse heart disease, diabetes, osteoporosis, obesity, and to some extent aging itself.

Cholesterol; Wrongly Accused?

Before we can begin to talk about the real cause and effective treatment for heart and blood vessel disease, we must first look at what is known, or I should say what we think we know. The first thing that comes to mind when one hears about heart disease is almost always cholesterol. Cholesterol and heart disease has been almost synonymous for the last half-century. Cholesterol has been portrayed as the Darth Vader to our arteries and our heart.

The latest recommendation given by a so-called panel of "experts" recommends that a person's cholesterol be as low as possible, in fact to a level so low they say it cannot be achieved by diet, exercise, or any known lifestyle modification. Therefore, they say cholesterol-lowering drugs; particularly the so-called "statins" need to be given to anyone at high risk of heart disease. Since heart disease is the number one killer in this country that would include most adults and even many children. The fact that this might add to the $26 billion in sales of statin drugs last year I'm sure played no role in their recommendations.

Or did it?

Expert Conflict of Interests

Major consumer groups think so. They found out that eight of the nine "experts" that made the recommendations were on the payroll of pharmaceutical companies that manufacture those drugs. Major scientific organizations have chastised medical journals for allowing the pharmaceutical industry to publish misleading results and half-truths. There is a major push under way to force the pharmaceutical industry (and others) to publish results of all of their studies, and not just the ones that appear positive. The studies that showed negative results would be forced to be published also.

It could be that lowering cholesterol might not be as healthy as we are being told. More and more studies are coming out showing just how unhealthy lowering cholesterol might be, particularly by the use of statin drugs. In particular, statin drugs have been shown to be harmful to muscles causing considerable damage. A common symptom of this damage is muscular aches and pains that many patients experience on cholesterol-lowering drugs, however most do not realize that these drugs are to blame.

Hmm...isn't the heart a muscle?

Statin Drugs Actually Increase Heart Disease

Indeed, low cholesterol levels have been shown to worsen patients with congestive heart failure, a life-threatening condition where the heart becomes too weak to effectively pump blood. Statin drugs have been shown to also cause nerve damage and to greatly impair memory. One reason that statin drugs have these various serious side effects is that they work by inhibiting a vital enzyme that manufactures cholesterol in the liver. However, the same enzyme is used to manufacture coenzyme Q10, which is a biochemical needed to transfer energy from food to our cells to be used for the work of staying alive and healthy.

Statin drugs are known to inhibit our very important production of coenzyme Q10. Importantly, while many cardiologists insist that lowering cholesterol is correlated with a reduction in the risk of heart attacks; few can say that there is a reduction in the risk of mortality (death). That has been much harder to show. In other words it has never been conclusively shown that lowering cholesterol saves lives. In fact, several large studies have shown that lowering cholesterol into the range currently recommended is correlated with an increased risk of dying, especially of cancer.

No Such Thing as Good and Bad Cholesterol

Because the correlation of total cholesterol with heart disease is so weak, many years ago a stronger correlation was sought. It was found that there is so-called "good cholesterol" called HDL, and that the so-called "bad cholesterol" was LDL. HDL stands for high-density lipoprotein, and LDL stands for low-density lipoprotein. Notice please that LDL and HDL are lipoproteins -- fats combined with proteins. There is only one cholesterol.

There is no such thing as a good or a bad cholesterol. Cholesterol is just cholesterol. It combines with other fats and proteins to be carried through the bloodstream, since fat and our watery blood do not mix very well. Fatty substances therefore must be shuttled to and from our tissues and cells using proteins. LDL and HDL are forms of proteins and are far from being just cholesterol. In fact we now know there are many types of these fat and protein particles. LDL particles come in many sizes and large LDL particles are not a problem. Only the so-called small dense LDL particles can potentially be a problem, because they can squeeze through the lining of the arteries and if they oxidize, otherwise known as turning rancid, they can cause damage and inflammation. Thus, you might say that there is "good LDL" and "bad LDL." Also, some HDL particles are better than others.

Knowing just your total cholesterol tells you very little. Even knowing your LDL and HDL levels do not tell you very much.

A mistake that is rarely made in the hard-core sciences such as physics seems to be frequently made in medicine. This is confusing correlation with cause. There may be a weak correlation of elevated cholesterol with heart attacks, however this does not mean it is the cholesterol that caused the heart attack. Certainly gray hair is correlated with getting older; however one could hardly say that the gray hair caused one to get old. Using hair dye to reduce the gray hair would not really make you any younger. Neither it appears would just lowering your cholesterol.

Perhaps something else is causing both the gray hair and aging. Even if elevated cholesterol were significant and heart disease (which I question) perhaps something else is causing the elevated cholesterol and also causing the heart disease.

Let's look little more at cholesterol or, as Paul Harvey was fond of saying, "the rest of the story." First and foremost, cholesterol is a vital component of every cell membrane on Earth. In other words, there is no life on Earth they can live without cholesterol. They will automatically tell you that, in of itself, it cannot be evil. In fact it is one of our best friends. We would not be here without it. No wonder lowering cholesterol too much increases one's risk of dying. Cholesterol also is a precursor to all of the steroid hormones. You cannot make estrogen, testosterone, cortisone, and a host of other vital hormones without cholesterol.

Cholesterol Is The Hero, Not The Villain.

It was determined many years ago that the majority of cholesterol in your bloodstream comes from what your liver is manufacturing and distributing. The amount of cholesterol that one eats plays little role in determining your cholesterol levels. It is also known that HDL shuttles cholesterol away from tissues, and away from your arteries, back to your liver. That is why HDL is called the "good cholesterol;" because it is supposedly taking cholesterol away from your arteries. But let's think about that.


Why does your liver make sure that you have plenty of cholesterol?
Why is HDL taking cholesterol back to your liver?
Why not take it right to your kidneys, or your intestines to get rid of it?

It is taking it back to your liver so that your liver can recycle it; put it back into other particles to be taken to tissues and cells that need it. Your body is trying to make and conserve the cholesterol for the precise reason that it is so important, indeed vital, for health.

One function of cholesterol is to keep your cell membranes from falling apart. As such, you might consider cholesterol your cells "superglue." It is a necessary ingredient in any sort of cellular repair. The coronary disease associated with heart attacks is now known to be caused from damage to the lining of those arteries. That damage causes inflammation. The coronary disease that causes heart attacks is now considered to be caused mostly from chronic inflammation.

What Is Inflammation?

Think of what happens if you were to cut your hand. Within a fraction of a second, chemicals are released by the damaged tissue to initiate the process known as inflammation. Inflammation will allow that little cut to heal, and indeed to keep you from dying. The cut blood vessels constrict to keep you from bleeding too much. Blood becomes "thicker" so that it can clot. Cells and chemicals from the immune system are alerted to come to the area to keep intruders such as viruses and bacteria from invading the cut. Other cells are told to multiply to repair the damage so that you can heal. When the repair is completed, you have lived to be careless another day, though you may have a small scar to show for your troubles.

We now know that similar events take place within the lining of our arteries. When damage occurs to the lining of our arteries (or even elsewhere) chemicals are released to initiate the process of inflammation. Arteries constrict, blood becomes more prone to clot, white blood cells are called to the area to gobble up damaged debris, and cells adjacent to those damaged are told to multiply. Ultimately, scars form, however inside our arteries we call it plaque. And the constriction of our arteries and the "thickening" of our blood further predisposes us to high blood pressure and heart attacks.

So Where Might Cholesterol Fit Into All Of This?

When damage is occurring and inflammation is being initiated, chemicals are being released so that that damage can be repaired. One could speculate that to replace damaged, old and worn-out cells the liver needs to be notified to either recycle or manufacture cholesterol since no cell, human or otherwise, can be made without it. In this case, cholesterol is being manufactured and distributed in your bloodstream to help you repair damaged tissue and in fact to keep you alive.

If excessive damage is occurring such that it is necessary to distribute extra cholesterol through the bloodstream, it would not seem very wise to merely lower the cholesterol and forget about why it is there in the first place. It would seem much smarter to reduce the extra need for the cholesterol -- the excessive damage that is occurring, the reason for the chronic inflammation.

So Why Take Cholesterol-Lowering Drugs?

The pharmaceutical companies thought that you might think that. They went back to the drawing board. They did more "research" and found (coincidentally) that statin drugs had anti-inflammatory effects. Therefore we're currently being told to stay on our cholesterol-lowering drugs because now they work by reducing inflammation and perhaps not even by reducing cholesterol, and in fact perhaps in spite of it. Aspirin reduces inflammation for a lot less money. So does vitamin E, and fish oil, and dietary changes without the dangers of drugs and having many other benefits instead.

What About Triglycerides?

Triglycerides are just medical terminology for fat. A person with high triglycerides has a lot of fat in the bloodstream. Triglycerides are generally measured when a person has fasted overnight. High fasting triglycerides are either from manufacturing too much, or using (burning) too little. In other words, what high triglycerides are telling you is that you are making too much fat and you are unable to burn it. This indeed is a major problem. The inability to burn fat underlies virtually all of the chronic diseases of aging, and in fact may contribute to the rate of aging itself.

As such, one might think that the control of fat burning and storage might be very important in heart disease, and the other diseases of aging such as diabetes, obesity, osteoporosis, and even cancer. Indeed, this appears to very much be the case. The two hormones that to a major extent control our ability to burn and store fat, insulin and leptin, appear to play a major role in all of the chronic diseases of aging. I would call them the most important hormones, indeed chemicals in the entire body. But that is a story for next time.

badfish51581
07-24-2009, 05:49 PM
One more...


Insulin Resistance: The Real Culprit

By Ron Rosedale (http://nourishedmagazine.com.au/blog/articles/author/rrosdale/)

Letís talk about a couple of case histories. These are actual patients that Iíve seen Patient A saw me one afternoon and said that he had literally just signed himself out of the hospital ďAMA,Ē or against medical advice. Like in the movies, he had ripped out his IVís. The next day he was scheduled to have his second by-pass surgery. He had been told that if he did not follow through with this by-pass surgery, within two weeks he would be dead. He couldnít walk from the car to the office without severe chest pain. He was on eight different medications for various things. But his first by-pass surgery was such a miserable experience he said he would rather just die than have to go through the second one and had heard that I might be able to prevent that.

To make a long story short, this gentleman right now is on no insulin. I first saw him three and a half years ago. He plays golf four or five times a week. He is on no medications whatsoever, he has no chest pain, and he has not had any surgery.

Patient B had a triglyceride level of 2200. Patient B was referred by patient A. His cholesterol was 950. He was on maximum doses of all of his medications. He was 42 years old, and he was told that he had familial hyperlipidema and that he had better get his affairs in order, that if that was what his lipids were despite the best medications with the highest doses, he was in trouble.

He was not fat at all, he was fairly thin. Whenever I see a patient on any of those medications, theyíre off the very first visit. They have no place in medicine. He was taken off the medications and in six weeks his lipid levels, both his Triglycerides and his cholesterol were hovering around 220. Six more weeks they were both under 200.

I should mention that this patient had a CPK (creatine phosphokinase, an enzyme found mainly in the heart, brain, and skeletal muscle) that was quite elevated. It was circled on the lab report that he brought in initially with a question mark by it because they didnít know why. The reason why was because he was eating off his muscles, because if you take (gyinfibrozole) and any of the HMG co-enzyme reductase inhibitors (cholesterol lowering drugs) together, that is a common side effect, and they shouldnít be given together. So he was chewing up his muscles, including his heart which they were trying to treat. So if indeed he was going to die, it was the treatment that was going to kill him.

Patient C: a lady with severe osteoporosis. A fairly young woman and she was put on a high carbohydrate diet and told that would be of benefit, and placed on estrogen, which is a fairly typical treatment. They wanted to put her on some other medicines which she didnít want, she wanted to know if there was an alternative. Although we didnít have as dramatic a turn around, we got her to one standard deviation below the norm in a year, taking her off the estrogen she was on.

Insulin in Chronic Disease

What would be the typical treatment of cardiovascular disease? First they check the cholesterol. High cholesterol over 200, they put you on cholesterol lowering drugs and what does it do? It shuts off your CoQ10. What does CoQ10 do? It is involved in the energy production and protection of little energy furnaces in every cell, so energy production goes way down. A common side effect of people who are on all these HMG co-enzyme reductase inhibitors is that they tell you their arms feel heavy. Well, the heart is a muscle too, and itís going to feel heavy too. One of the best treatments for a weak heart is CoQ10 for congestive heart failure. But medicine has no trouble shutting CoQ10 production off so that they can treat a number (cholesterol figure).

The common therapies for osteoporosis are drugs
For cancer reduction there is nothing.
But all of these have a common cause.
The same cause as Aging.

Aging

There are three major centenarian studies going on around the world. They are trying to find the variable that would confer longevity among these people. Why do centenarians become centenarians? Why are they so lucky? Is it because they have low cholesterol, exercise a lot, live a healthy, clean life? Well the longest recorded known person who has ever lived, Jean Calumet of France who died last year at 122 years, smoked all of her life and drank. What they are finding on these major centenarian studies is that there is hardly anything in common among them. They have high cholesterol and low cholesterol, some exercise and some donít, some smoke, some donít. Some are nasty and ornery as can be and some calm and nice.

But one thing is common, they all have low sugar, relatively for their age. They all have low triglycerides for their age. And they all have relatively low insulin. Insulin is the common denominator in everything Iíve just talked about. The way to treat cardiovascular disease, the way I treated the high risk cancer patient, and osteoporosis, high blood pressure, the way to treat virtually all the so-called chronic diseases of aging is to treat insulin itself.

The other major avenue of research in aging has to do with genetic studies of so-called lower organisms. Weíve the entire genes mapped out for several species of yeast and worms.

We think of life span as being fixed but in lower forms of life it is very plastic. Life span is strictly a variable depending on the environment. If there is a lot of food around they are going to reproduce quickly and die quickly, if not they will just bide their time until conditions are better.
We know now that the variability in life span is regulated by insulin.
Insulin is found as in even single celled organisms. It has been around for several billion years. And its purpose in some organisms is to regulate life span. The way genetics works is that genes are not replaced, they are built upon. We have the same genes as everything that came before us. We just have more of them. We have added books to our genetic library, but our base is the same. What we are finding is that we can use insulin to regulate lifespan too.

If there is a single marker for lifespan, as they are finding in the centenarian studies, it is insulin, specifically, insulin sensitivity or insulin resistance.

Insulin Resistance

Insulin resistance is the basis of all of the chronic diseases of aging.
In almost all cases if you treat a symptom, you are going to make the disease worse because the symptom is there as your bodyís attempt to heal itself. The medical profession calls the symptoms diseases. Using Ear Nose and Throat medicine for example, that patient will walk out of there with a diagnosis of Rhinitis which is inflammation of the nose. Is there a reason that patient has inflammation of the nose? I think so. Wouldnít that underlying cause be the disease as opposed to the descriptive term of Rhinitis or Pharyngitis? Some one can have the same virus and have Rhinitis or Pharyngitis, or Sinusitis, they can have all sorts of ďitisesĒ which is a descriptive term for inflammation. They treat what they think is the disease which is just a symptom.

It is the same thing with cholesterol. If you have high cholesterol it is called hypercholesterolemia. Hypercholesterolemia has become the code for the disease when it is only the symptom. So they treat that symptom and what are they doing to the heart? Messing it up.

If you are going to treat any disease, you need to get to the root of the disease. If you keep pulling a dandelion out by itís leaves, you are not going to get very far. But the problem is that we donít know what the root is, or we havenít. They know what it is in many other areas of science, but the problem is that medicine really isnít a science, it is a business.
It doesnít matter what disease you are talking about, whether you are talking about a common cold or about cardiovascular disease, or osteoporosis or cancer, the root is always going to be at the molecular and cellular level, and I will tell you that insulin is going to have its hand in it, if not totally controlling it.

The Purpose of Insulin

As I mentioned, in some organisms it is to control their lifespan, which is important. What is the purpose of insulin in humans? If you ask your doctor, they will say that itís to lower blood sugar and I will tell you right now, that is a trivial side effect. Insulinís evolutionary purpose is to store excess nutrients.

Storing Fat

We come from a time of feast and famine and if we couldnít store the excess energy during times of feasting, we would all not be here, because we all have had ancestors that encountered famine. So we are only here because our ancestors were able to store nutrients, and they were able to store nutrients because they were able to elevate their insulin in response to any elevation in energy rich foods that the organism encountered. When your body notices that the sugar is elevated, it is a sign that youíve got more than you need right now, you are not burning it so it is accumulating in your blood. So insulin will be released to take that sugar and store it.

How does it store it? Glycogen. Do you know how much glycogen you have in your body at any one time? Very little. All the glycogen stored in your liver and all the glycogen stored in your muscle if you had an active day wouldnít last you the day. Once you fill up your glycogen stores how that sugar is stored? Saturated fat.

So the idea of the medical profession to go on a high complex carbohydrate, low saturated-fat diet is an absolute oxymoron, because those high complex carbohydrate diets are nothing but a high glucose diet, or a high sugar diet, and your body is just going to store it as saturated fat. The body makes it into saturated fat quite readily.

Building Muscle

It is an anabolic hormone. Body builders are using insulin now because it is legal, so they are injecting themselves with insulin because it builds muscle, it stores protein too.

Storing Magnesium

A lesser known fact is that insulin also stores magnesium. If your cells become resistant to insulin, since you canít store magnesium so you lose it, in the urine. What is one of magnesiumís major roles? To relax muscles. Intracellular magnesium relaxes muscles. You lose magnesium and your blood vessels constrict, which increases blood pressure, and reduces energy since intracellular magnesium is required for all energy producing reactions that take place in the cell. But most importantly, magnesium is also necessary for the action of insulin. It is also necessary for the manufacture of insulin. So then you raise your insulin, you lose magnesium, and the cells become even more insulin resistant. Blood vessels constrict, glucose and insulin canít get to the tissues, which makes them more insulin resistant, so the insulin levels go up and you lose more magnesium. This is the vicious cycle that goes on from before you were born.
Insulin sensitivity is going to start being determined from the moment the sperm combines with the egg. If your mother, while you were in the womb was eating a high carbohydrate diet which is turning into sugar, we have been able to show that the fetus in animals becomes more insulin resistant. Worse yet, we are able to use sophisticated measurements, and if that fetus happens to be a female, they find that the eggs of that fetus are more insulin resistant.

Retaining Sodium

What else does insulin do? We mentioned high blood pressure, if your magnesium levels go down you get high blood pressure. We mentioned that the blood vessels constrict and you get high blood pressure. Insulin also causes the retention of sodium, which causes the retention of fluid, which causes high blood pressure and fluid retention: congestive heart failure.
One of the strongest stimulants of the sympathetic nervous system is high levels of insulin. What does all of this do to the heart? Not very good things.

There was a study done a couple of years ago, that showed that heart attacks are two to three times more likely to happen after a high carbohydrate meal. They said specifically NOT after a high fat meal. Why is that? Because the immediate effects of raising your blood sugar from a high carbohydrate meal is to raise insulin and that immediately triggers the sympathetic nervous system which will cause arterial spasm, constriction of the arteries. If you take anybody prone to a heart attack and that is when they are going to get it.

Mediating blood lipids.

The way you control blood lipids is by controlling insulin. We wonít go into a lot of detail, but we now know that LDL cholesterol comes in several fractions, and it is the small, dense LDL that plays the largest role in initiating plaque. Itís the most oxidizable. It is the most able to actually fit through the small cracks in the endothelium. And thatís the one that insulin actually raises the most. When I say insulin, I should say insulin resistance.

It is insulin resistance that is causing this.

Cells become insulin resistant because they are trying to protect themselves from the toxic effects of high insulin. They down regulate their receptor activity and number of receptors so that they donít have to listen to that noxious stimuli all the time. It is like having this loud, disgusting rap music played and you want to turn the volume down. You might think of insulin resistance as like sitting in a smelly room and pretty soon you donít smell it anymore because you get desensitized. Itís like you are starting to go deaf and your are telling others to speak up because you canít hear them, so if I was your pancreas, I would just start talking louder, and what does that do to your hearing? You would become deafer.

Insulin Restistance Role in Heart Disease, Cancer and Osteoporosis

Insulin stimulates cells to divide. If all of the cells were to become resistant to insulin we wouldnít have that much of a problem. The problem is that all of the cells donít become resistant. Some cells are incapable of becoming very resistant. The liver becomes resistant first, then the muscle tissue, then the fat. When the liver becomes resistant insulin suppresses its production of sugar. When you wake up in the morning it is a reflection of how much sugar your liver has made. If your liver is listening to insulin properly it wonít make much sugar in the middle of the night. If your liver is resistant, those brakes are lifted and your liver starts making a bunch of sugar so you wake up with a bunch of sugar.

The next tissue to become resistant is the muscle tissue. Insulin allows your muscles to burn sugar for so if your muscles become resistant to insulin it canít burn that sugar that was just manufactured by the liver. So the liver is producing too much, the muscles canít burn it, and this raises your blood sugar.

Fat cells also become resistant, but not for a while. It is only after a while that they become resistant. It takes them longer. Liver first, muscle second, and then your fat cells. So for a while your fat cells retain their sensitivity. As people become more and more insulin resistant, their weight goes up. But eventually they plateau.

As all these major tissues become resistant, your liver, muscles and fat, your pancreas is putting out more insulin to compensate, so you are hyperinsulinemic and youíve got insulin floating around all the time, 90 units, more. But there are certain tissues that arenít becoming resistant such as your endothelium, the lining of the arteries do not become resistant very readily. So all that insulin is effecting the lining of your arteries.

Insulin floating around in the blood causes a plaque build up. Insulin causes endothelial proliferation, thatís the first step, it causes a tumor, an endothelial tumor. Insulin also causes the blood to clot too readily. Every step of the way, insulinís got its fingers in it and is causing cardiovascular disease. It fills it with plaque, it constricts the arteries, it stimulates the sympathetic nervous system, it increases platelet adhesiveness and coaguability of the blood. Any known cause of cardiovascular disease, insulin is a part of.

I mentioned that insulin increases cellular proliferation, what does that do to cancer? It increases it. And there are some pretty strong studies that show that one of the strongest correlations to breast and colon cancer are with levels of insulin.

Hyperinsulinemia causes the excretion of magnesium in the urine. What other big mineral does it cause the excretion of? Calcium. What is the cause of osteoporosis? There are two major causes, one is a high carbohydrate diet which causes hyperinsulinemia. People walking around with hyperinsulinemia can take all the calcium they want by mouth and itís all going to go out in their urine.

The medical profession just assume a Calcium supplement has a homing device and it knows to go into your bone. What happens if you high levels of insulin and you take a bunch of calcium? Most of it is just going to go out in your urine. You would be lucky if that were the case because that part which doesnít does not have the instructions to go to your bone because the anabolic hormones arenít working. This is first of all because of insulin, then because of the IGFís from growth hormone, also testosterone and progesterone, they are all controlled by insulin and when they are insulin resistant they canít listen to any of the anabolic hormones. So your body doesnít know how to build tissue anymore, so some of the calcium may end up in your bone, but a good deal of it will end up everywhere else. Metastatic calcifications, including in your arteries.

Causes of Insulin Resistance

High Carbohydrate Diets

Any time your cell is exposed to insulin it is going to become more insulin resistant. That is inevitable, we cannot stop that, but the rate we can control. An inevitable sign of aging is an increase in insulin resistance. That rate is variable, if you can slow down that rate you can become a centenarian, and a healthy one. You can slow the rate of aging. Not just even the rate of disease, but the actual rate of aging itself can be modulated by insulin. We should be living to be 130, 140 years old routinely.

We talk about simple and complex carbohydrates, that is totally irrelevant, it means absolutely nothing. Carbohydrates are fiber or non-fiber. If you have a carbohydrate that is not a fiber it is going to be turned into a sugar, whether it be glucose or not. It may be fructose and wonít necessarily raise your blood glucose, but fructose is worse for you than glucose.

Throughout most of the history of life on Earth there was no oxygen. Organisms had to develop very specific mechanisms of dealing with high levels of oxygen before there could ever be life with oxygen. So we evolved very quickly, as plants arose and developed a very easy means of acquiring energy, they could just lay back and catch rays, and they dealt with that oxygen with the carbon dioxide by spitting it out, they didnít want it around. So the oxygen in the atmosphere increased. All the other organisms then had to cope with that toxic oxygen. Many perished if they didnít have ways of dealing with it. One of the earliest ways of dealing with all that oxygen was for the cells to huddle together, so that at least the interior cells wouldnít be exposed to as much. So, multi-celled organisms arose after oxygen did. Of course, with that came the need for cellular communication.

Everyone knows that oxygen causes damage, but unfortunately, the press has not been as kind to publicize glycation. Glycation is the same as oxidation except substitute the word glucose. When you glycate something you combine it with glucose. Glucose combines with anything else really, itís a very sticky molecule. Just take sugar on your fingers. Itís very sticky. It sticks specifically to proteins. So the glycation of proteins is extremely important. If it sticks around a while it produces what are called advanced glycated end products: AGEs.

That acronym is not an accident. Glycation damages the protein to the extent that white blood cells will come around and gobble it up and get rid of it, so then you have to produce more, putting more of a strain on your ability to repair and maintain your body.

That is the best alternative; the worst alternative is when those proteins that canít turn over very rapidly get glycated , like collagen, or like a protein that makes up nerve tissue. These proteins cannot be gotten rid of, so the protein accumulates, and the AGEs accumulate and they continue to damage. That includes the collagen that makes up the matrix of your arteries. We know that there are receptors for AGEs, hundreds of receptors for every macrophage. They are designed to try to get rid of those AGEs, but what happens when a macrophage combines with an AGE product? It sets up an inflammatory reaction. We know that cardiovascular disease is an inflammatory process, any type of inflammation. You eat a diet that promotes elevated glucose, and you produce increased glycated proteins and AGEs, you are increasing your rate of inflammation of any kind. You get down to the roots of chronic illness, including arthritis, diabetes, headaches.

So we age and at least partially we accumulate damage by oxidation, and one of the most important types of tissues that oxygenate is the fatty component, the lipid, especially the poly-unsaturated fatty acids, they turn rancid. And they glycate, and the term for glycation in the food industry is carmelization. They use it all the time, that is how you make caramel. So the way we age is that we turn rancid and we carmelize.

Diet for Healing Insulin Resistance

Caloric Restriction. There are thousands of studies done since the fifties on caloric restriction. They restrict calories of laboratory animals. It has been known since the fifties that if you restrict calories but maintain a high level of nutrition, called ďC.R.O.N.ís:Ē Caloric restriction with optimal nutrition, these animals can live anywhere between thirty and two-hundred percent longer depending on the species. Theyíve done it on several dozen species and the results are uniform throughout. They are doing it on primates now and it is working with primates, we wonít know for sure for about another ten years, they are about half way through the experiment, our nearest relatives are also living much longer.

Nutrient Dense foods are key.

There are fifty-some essential nutrients to the human body. You know you need to breathe oxygen. It gives us life and it kills us. Same with glucose. Certain tissues require some glucose (which can be made from fat). It is essential. It gives us life and it kills us. We know that we have essential amino acids and we have essential fatty acids. They are essential for life, we better take them in as building blocks or we die. If we took all the essential nutrients that are known to man and computed the top ten foods that contain each nutrient that is required by the human body, grains would not come up in the top ten.

What is the minimum daily requirement for carbohydrates? ZERO. The food pyramid is based on a totally irrelevant nutrient.

Letís back up even further? Why do we eat?


To gather energy. The body stores excess energy as fat. Why does the body store it as fat? Because that is the bodyís desired fuel. That is the fuel the body wants to burn and that will sustain you and allow you to live. The body can store only a little bit of sugar. In an active day you would die if you had to rely one-hundred percent on sugar.
To replace tissue, to gather up building blocks for maintenance and repair.We need the building blocks and we need fuel, to have energy to obtain those building blocks and to fuel those chemical reactions to use those building blocks. So what are the building blocks that are needed? Proteins and Fatty acids. Not much in the way if carbohydrates. You can get all the carbohydrates you need from proteins and fats.

Sugar was never meant to be your primary energy source. Your brain will burn sugar, but it doesnít have to, it can burn by-products of fat metabolism called ketones. You can get enough sugar that your brain needs actually from fat; just eating one-hundred percent fat. Two triglycerides will give you a molecule of glucose. Glucose was meant to be fuel used if you had to, in an emergency situation, expend and extreme amount of energy, such as running from a saber tooth tiger. It is a turbo charger, a very hot burning fuel, if you need fuel over and above what fat can provide you will dig into your glycogen and burn sugar. But your primary energy source as we are here right now should be almost all fat.
But what happens if you eat sugar. Your bodyís main way of getting rid of it, because it is toxic, is to burn it. That which your body canít burn your body will get rid of by storing it as glycogen and when that gets filled up your body stores it as fat. If you eat sugar your body will burn it and you stop burning fat.

When you are insulin resistant and you have a bunch of insulin floating around all the time, you wake up in the morning with an insulin of 90. How much fat are you going to be burning? Virtually none. What are you going to burn if not fat? Sugar coming from your muscle. So you have all this fat that youíve accumulated over the years that your body is very adept at adding to. Every time you have any excess energy you are going to store it as fat, but if you donít eat, you will still burn sugar because that is all your body is capable of burning anymore. Where is it going to get the sugar? Well you donít store much of it in the form of sugar so it will take it from your muscle. Thatís your bodyís major depot of sugar. You just eat up your muscle tissue. Any time you have excess you store it as fat and any time you are deficient you burn up your muscle.

So where do carbohydrates come in? They donít. There is no essential need for carbohydrates. SO why are we all eating carbohydrates? To keep the rate of aging up, we donít want to pay social security to everyone..

I didnít say you canít have any carbs, I said fiber is good. Vegetables are great, I want you to eat vegetables. The practical aspect of it is that you are going to get carbs, but there is no essential need. The traditional Eskimo diet for most of the year subsists on almost no vegetables at all, but they get their vitamins from organ meats and things like eyeball which are a delicacy, or were. So, you donít really need it, but sure, vegetables are good for you and you should eat them. They are part of the diet that I would recommend, and that is where youíll get your vitamin C.

Fruit is a mixed blessing. You can divide food on a continuum. There are some foods that I really canít say anything good about since there is no reason really to recommend them. And the other end of the spectrum are foods that are totally essential, like:

Omega 3 fatty acids for instance which most people are very deficient in, and even those have a detriment because they are highly oxidizable, so you had better have the antioxidant capacity. So if you are going to supplement with cod liver oil you should supplement with Vitamin E too or it will actually do you more harm than good. Omega 3 oils can be a double edged sword. Most food is a double edged sword. Like oxygen and glucose, they keep us alive and they kill us, eating is the biggest stress we put on our body and that is why in caloric restriction experiments you can extend life as long as you maintain dense nutrition. This is the only proven way of actually reducing the rate of aging, not just the mortality rate, but the actual rate of aging, because eating is a big stress.

Chromium

Chromium, it depends on who you are dealing with, but are we talking about a diabetic patient which is supposed to be the topic of this talk, yes, all my diabetics go on 1,000 mcg. Of chromium, some a little bit more if they are really big people. Usually 500mcg for a non-diabetic. It depends on their insulin levels. I donít care so much what their sugar levels are, I care what their insulin levels are, which is a reflection of their insulin sensitivity.

Carnitine

Carnitine is a shuttle. It takes fatty acids into the cell. You canít burn fat without it. I say they should take as much carnitine as they can afford.

Co Q10

It is involved in the energy production of all cells. It protects the mitochondria from electron leakage and damage. Give anywhere from 100 to 500mg, depending on the kind of Q10, some are more absorbable than others.

Vanadyl Sulfate

An insulin mimic, so that it can basically do what insulin does by a different mechanism. If it went through the same insulin receptors, then it wouldnít offer any benefit, but it doesnít, it actually has been shown to go through a different mechanism to lower blood sugar, so it spares insulin and then it can help improve insulin sensitivity. On someone who I am trying to really get their insulin down I go 25mg 3X/day temporarily.

B Vitamins are necessary in the conversion of all energy, so they all get extra B Vitamins, usually in a multi.

Glutamine

I put people on glutamine powder. Glutamine can act really as a brain fuel, so it helps eliminate carbohydrate cravings while they are in that transition period. I like to give it to them at night and I tell them to use it whenever they feel they are craving carbohydrates. They can put several grams into a little water and drink it and it helps eliminate carbohydrate cravings between meals.

Other therapeutic doses of nutrients include:

Elemental magnesium 300 to 400 depending on what their gut can tolerate. I like I.V. magnesium to replenish them.

Vitamin E, big fan of Vitamin E, I would go to 2000mg.

Zinc, 30 to sixty mg, balanced with 2mg of copper per 15 mg of zinc, usually 4mg of copper sebacate.

Taurine: 1gm twice a day.

Vanadium 25mg for about two to three months. Then down to 71/2 mg three times a day, then Iíll go down further, then I take them off completely once they are better. They can have as much glutamine as they want and as much carnitine as they can afford. The more the better

I use gymnema sylvestre a lot.

Sardines are a very good therapeutic food. They are baby fish so they havenít had time to accumulate a bunch of metal. They are smoked so they are not cooked and the oil is not spoiled in them. You have to eat the whole thing. Not the boneless and skinless. You need to eat all the organs and they are high in vitamins and magnesium.

DNA glycates. So if people are worried about chromosomal damage from chromium, what they should really be worried about instead is high blood sugar. DNA repair enzymes glycate as well. Insulin is by far your biggest poison. .

Insulin should be tested on everybody repeatedly, and why it is not is only strictly because there hasnít been drugs till recently that could effect insulin, so there is no way to make money off of it. Fasting insulin is one way to look at it, not necessarily the best way. But it is the way that everybody could do it. Any family doctor can measure a fasting insulin. There are other ways to measure insulin sensitivity that are more complex that we do sometimes. We use intravenous insulin and watch how rapidly their blood sugar crashes in a fasting state in 15 minutes and that assesses insulin sensitivity, then you give them dextrose to make sure they donít crash any further. There are other ways that are utilized to directly assess insulin sensitivity, but you can get a pretty good idea just by doing a fasting insulin.

Related Information

Acid/Alkaline

It is a high protein diet that will increase an acid load in the body, but not necessarily a high fat diet. Vegetables and greens are alkalinizing, so if you are eating a lot of vegetables along with your protein it equalizes the acidifying effect of the protein. I donít recommend a high protein diet. I recommend an adequate protein diet. I think you should be using fat as your primary energy source, and fat is kind of neutral when it comes to acidifying or alkalinizing. In general, over 50% of the calories should come from fat. When we get to fat, the carbohydrates are clear cut, no scientist out there is really going to dispute what Iíve said about carbohydrates. There is the science behind it. You canít dispute it. There is a little bit of a dispute as to how much protein a person requires. When you get to fat, there is a big grey area within science as to which fat a person requires. We just have one name for fat, we call it fat or oil. Eskimos have dozens of names for snow and east Indians have dozens of names for curry. We should have dozens of names for fat because they do many different things. And how much of which fat to take is still open to a lot of investigation and controversy.

My take on fat is that if I am treating a patient who is generally hyperinsulinemic or overweight, I want them on a low saturated fat diet. Because most of the fat they are storing is saturated fat. When their insulin goes down and they are able to start releasing triglycerides to burn as fat, what they are going to be releasing mostly is saturated fat. So you donít want to take anymore orally. There is a ration of fatty acids that is desirable, if you took them from the moment you were born, but we donít, we are dealing with an imbalance here that we are trying to correct as rapidly as we can. You have plenty of saturated fat. Most of us here have enough saturated fat to last the rest of our life. Truthfully. Your cell membranes require a balance of saturated and poly-unsaturated fat, and it is that balance that determines the fluidity. As I mentioned, your cells can become over-fluid if they donít have any saturated fat. Saturated fat is a hard fat. We can get the fats from foods to come mostly from nuts. Nuts are a great food because it is mostly mono-unsaturated. Your primary energy source ideally would come mostly from mono-unsaturated fat. Itís a good compromise. It is not an essential fat, but it is a more fluid fat. Your body can utilize it very well as an energy source.

Sugar and Hormones

We only have one hormone that lowers sugar, and thatís insulin. Its primary use was never to lower sugar. Weíve got a bunch of hormones that raise sugar, cortisone being one and growth hormone another, and epinephrine, and glucagon. Our primary evolutionary problem was to raise blood sugar to give your brain enough and your nerves enough and primarily red blood cells, which require glucose. So from an evolutionary sense if something is important we have redundant mechanisms. The fact that we only have one hormone that lowers sugar tells us that it was never something important in the past.

So you get this rush of sugar and your body panics, your pancreas panics and it stores, when it is healthy, insulin in these granules, ready to be released. It lets these granules out and it pours out a bunch of insulin to deal with this onslaught of sugar and what does that do? Well the pancreas generally overcompensates, and it causes your sugar to go down, and just as I mentioned, you have got a bunch of hormones then to raise your blood sugar, they are then released, including cortisone. The biggest stress on your body is eating a big glucose load. Then Epinephrine is released too, so it makes your nervous and it also stimulates your brain to crave carbohydrates, to seek out some sugar, my sugar is low. So you are craving carbohydrates, so you eat another bowl of cereal, or a big piece of fruit, you eat something else so that after your sugar goes low, and with the hormone release, and with the sugar cravings and carbohydrate craving your sugars go way up again which causes your pancreas to release more insulin and then it goes way down. Now you are in to this sinusoidal wave of blood sugar, which causes insulin resistance. Your body canít stand that for very long. So you are constantly putting out cortisone.

The more hormones your cells are exposed to, the more resistant they will become to almost any hormone. Certain cells more than others, so there is a discrepancy. The problem with hormone resistance is that there is a dichotomy of resistance, that all the cells donít become resistant at the same time. And different hormones affect different cells, and the rate of hormone is different among different cells and this causes lots of problems with the feedback mechanisms. We know that one of the major areas of the body that becomes resistant to many feedback loops is the hypothalamus.

Hypothalamic resistance to feedback signals plays a very important role in aging and insulin resistance because the hypothalamus has receptors for insulin too. I mentioned that insulin stimulates sympathetic nervous system, it does so through the hypothalamus, which is the center of it all.

heavyiron
07-24-2009, 06:32 PM
One of the best things for increasing HDL while lowering LDL is a $2 bottle of nicotinic acid (Niacin). Numerous studies show it is Superior 90% of statins because it increases LDL receptor in the liver while reducing HDL receptor. No need to go crazy with it either . 300mgs split over 3 x 100mg doses a day for about two weeks will have a profound effect. Oh BTW the flush has something to do with it because the "flush-free" potassium salt version don't work.

One warning... too much Niacin Is no good. It causes hepatic stress. Stay low dose (< 500mgs a day) and let it work over time.

Clinical profiles of plain versus sustained-release niacin (Niaspan) and the physiologic rationale for nighttime dosing.

Knopp RH (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Knopp%20RH%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
University of Washington and Northwest Lipid Research Clinic, Seattle 98104, USA.
Niacin is the oldest and most versatile agent in use for the treatment of dyslipidemia. It has beneficial effects on low-density lipoprotein cholesterol; high-density lipoprotein cholesterol; the apolipoproteins B and A-I constituting these fractions; triglyceride; and lipoprotein(a). Together, these benefits lead to a diminished incidence of coronary artery disease among niacin users. The chief constraints against niacin use have been flushing, gastrointestinal discomfort, and metabolic effects including hepatotoxicity. Time-release niacin has been developed in part to limit flushing, and now a nighttime formulation (Niaspan) has been developed that assists in containing this untoward effect. In a pivotal metabolic study, bed-time administration of 1.5 g time-release niacin was shown to have the same beneficial effects as 1.5 g plain niacin in 3 divided doses and to be well tolerated. Previous studies suggest that bedtime niacin administration diminishes lipolysis and release of free fatty acids to the liver; this, in turn, leads to an abolition of the usual diurnal increase in plasma triglyceride, which may result in diminished formation and secretion of triglyceride in the very-low-density lipoprotein fraction.



Effects of extended-release niacin on lipid profile and adipocyte biology in patients with impaired glucose tolerance.

Linke A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Linke%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Sonnabend M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sonnabend%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Fasshauer M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Fasshauer%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), HŲllriegel R (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22H%C3%B6llriegel%20R%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Schuler G (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Schuler%20G%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Niebauer J (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Niebauer%20J%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Stumvoll M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Stumvoll%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), BlŁher M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Bl%C3%BCher%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Department of Cardiology, Heart Center, University of Leipzig, Leipzig, Germany.
BACKGROUND: Low high-density lipoprotein cholesterol (HDL-C) serum concentrations are independent risk factors for the development of coronary artery disease. In patients with the metabolic syndrome, low HDL-C can contribute to premature atherosclerosis. Extended-release (ER) niacin increases HDL-C and was shown to slow the progression of atherosclerosis. Adipose tissue is an important site of niacin action. Here we sought to determine potential pleiotropic effects of ER niacin on adipose tissue biology in patients with impaired glucose tolerance (IGT). METHODS AND RESULTS: Thirty patients with IGT (mean age=45.2+/-3.9 years), low HDL-C serum concentrations (HDL-C <1.0 mmol/l), but no additional comorbidities were treated once-daily with ER niacin (1000 mg) in a randomized open-label controlled (n=30) study for 6 months. During the first 4 weeks, daily dose was increased from 375 to 1000 mg in weekly intervals. At baseline and after 6 months, subcutaneous adipose tissue biopsies were taken, body fat mass, insulin sensitivity (euglycemic-hyperinsulinemic clamp), and adipokine serum concentrations were measured. After 6 months of ER niacin treatment, HDL-C increased significantly by 24% and adiponectin by 35%. In addition, ER niacin significantly reduced circulating lipoprotein (a) by 38% (p<0.001) and fasting triglycerides by 12% (p<0.05). Whole-body insulin sensitivity increased in the ER niacin treatment group, although this trend was not statistically significant (p=0.085). Six months ER niacin led to a significant reduction in mean adipocyte size associated with increased insulin sensitivity in isolated adipocytes and gene expression changes including increased adiponectin, C/EBPalpha, C/EBPdelta, PPARgamma and decreased carnitine palmitoyl transferase 2, hormone sensitive lipase, nicotinic acid receptor (GPR109B) and fatty-acid synthase mRNA expression. CONCLUSION: Treatment with ER niacin significantly improves atherogenic lipid profile in patients with IGT. These beneficial effects could at least in part be due to pleiotropic niacin effects in adipose tissue, characterized by decreased mean adipocyte size, increased insulin sensitivity and altered mRNA expression profile.

triceptor
07-25-2009, 01:05 AM
Clinical profiles of plain versus sustained-release niacin (Niaspan) and the physiologic rationale for nighttime dosing.

Knopp RH (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Knopp%20RH%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
University of Washington and Northwest Lipid Research Clinic, Seattle 98104, USA.
Niacin is the oldest and most versatile agent in use for the treatment of dyslipidemia. It has beneficial effects on low-density lipoprotein cholesterol; high-density lipoprotein cholesterol; the apolipoproteins B and A-I constituting these fractions; triglyceride; and lipoprotein(a). Together, these benefits lead to a diminished incidence of coronary artery disease among niacin users. The chief constraints against niacin use have been flushing, gastrointestinal discomfort, and metabolic effects including hepatotoxicity. Time-release niacin has been developed in part to limit flushing, and now a nighttime formulation (Niaspan) has been developed that assists in containing this untoward effect. In a pivotal metabolic study, bed-time administration of 1.5 g time-release niacin was shown to have the same beneficial effects as 1.5 g plain niacin in 3 divided doses and to be well tolerated. Previous studies suggest that bedtime niacin administration diminishes lipolysis and release of free fatty acids to the liver; this, in turn, leads to an abolition of the usual diurnal increase in plasma triglyceride, which may result in diminished formation and secretion of triglyceride in the very-low-density lipoprotein fraction.



Effects of extended-release niacin on lipid profile and adipocyte biology in patients with impaired glucose tolerance.

Linke A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Linke%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Sonnabend M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sonnabend%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Fasshauer M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Fasshauer%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), HŲllriegel R (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22H%C3%B6llriegel%20R%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Schuler G (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Schuler%20G%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Niebauer J (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Niebauer%20J%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Stumvoll M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Stumvoll%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), BlŁher M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Bl%C3%BCher%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Department of Cardiology, Heart Center, University of Leipzig, Leipzig, Germany.
BACKGROUND: Low high-density lipoprotein cholesterol (HDL-C) serum concentrations are independent risk factors for the development of coronary artery disease. In patients with the metabolic syndrome, low HDL-C can contribute to premature atherosclerosis. Extended-release (ER) niacin increases HDL-C and was shown to slow the progression of atherosclerosis. Adipose tissue is an important site of niacin action. Here we sought to determine potential pleiotropic effects of ER niacin on adipose tissue biology in patients with impaired glucose tolerance (IGT). METHODS AND RESULTS: Thirty patients with IGT (mean age=45.2+/-3.9 years), low HDL-C serum concentrations (HDL-C <1.0 mmol/l), but no additional comorbidities were treated once-daily with ER niacin (1000 mg) in a randomized open-label controlled (n=30) study for 6 months. During the first 4 weeks, daily dose was increased from 375 to 1000 mg in weekly intervals. At baseline and after 6 months, subcutaneous adipose tissue biopsies were taken, body fat mass, insulin sensitivity (euglycemic-hyperinsulinemic clamp), and adipokine serum concentrations were measured. After 6 months of ER niacin treatment, HDL-C increased significantly by 24% and adiponectin by 35%. In addition, ER niacin significantly reduced circulating lipoprotein (a) by 38% (p<0.001) and fasting triglycerides by 12% (p<0.05). Whole-body insulin sensitivity increased in the ER niacin treatment group, although this trend was not statistically significant (p=0.085). Six months ER niacin led to a significant reduction in mean adipocyte size associated with increased insulin sensitivity in isolated adipocytes and gene expression changes including increased adiponectin, C/EBPalpha, C/EBPdelta, PPARgamma and decreased carnitine palmitoyl transferase 2, hormone sensitive lipase, nicotinic acid receptor (GPR109B) and fatty-acid synthase mRNA expression. CONCLUSION: Treatment with ER niacin significantly improves atherogenic lipid profile in patients with IGT. These beneficial effects could at least in part be due to pleiotropic niacin effects in adipose tissue, characterized by decreased mean adipocyte size, increased insulin sensitivity and altered mRNA expression profile.

the problem is that sustained release is more taxing to the liver and should only be used by those who have no other alternatives. I've used 300mgs of plain old nicotinic acid for years now and it keeps my HDL high and I don't get the flush any longer when I take it...

triceptor
07-25-2009, 01:15 AM
Clinical profiles of plain versus sustained-release niacin (Niaspan) and the physiologic rationale for nighttime dosing.

Knopp RH (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Knopp%20RH%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
University of Washington and Northwest Lipid Research Clinic, Seattle 98104, USA.
Niacin is the oldest and most versatile agent in use for the treatment of dyslipidemia. It has beneficial effects on low-density lipoprotein cholesterol; high-density lipoprotein cholesterol; the apolipoproteins B and A-I constituting these fractions; triglyceride; and lipoprotein(a). Together, these benefits lead to a diminished incidence of coronary artery disease among niacin users. The chief constraints against niacin use have been flushing, gastrointestinal discomfort, and metabolic effects including hepatotoxicity. Time-release niacin has been developed in part to limit flushing, and now a nighttime formulation (Niaspan) has been developed that assists in containing this untoward effect. In a pivotal metabolic study, bed-time administration of 1.5 g time-release niacin was shown to have the same beneficial effects as 1.5 g plain niacin in 3 divided doses and to be well tolerated. Previous studies suggest that bedtime niacin administration diminishes lipolysis and release of free fatty acids to the liver; this, in turn, leads to an abolition of the usual diurnal increase in plasma triglyceride, which may result in diminished formation and secretion of triglyceride in the very-low-density lipoprotein fraction.



Effects of extended-release niacin on lipid profile and adipocyte biology in patients with impaired glucose tolerance.

Linke A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Linke%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Sonnabend M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sonnabend%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Fasshauer M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Fasshauer%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), HŲllriegel R (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22H%C3%B6llriegel%20R%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Schuler G (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Schuler%20G%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Niebauer J (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Niebauer%20J%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Stumvoll M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Stumvoll%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), BlŁher M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Bl%C3%BCher%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Department of Cardiology, Heart Center, University of Leipzig, Leipzig, Germany.
BACKGROUND: Low high-density lipoprotein cholesterol (HDL-C) serum concentrations are independent risk factors for the development of coronary artery disease. In patients with the metabolic syndrome, low HDL-C can contribute to premature atherosclerosis. Extended-release (ER) niacin increases HDL-C and was shown to slow the progression of atherosclerosis. Adipose tissue is an important site of niacin action. Here we sought to determine potential pleiotropic effects of ER niacin on adipose tissue biology in patients with impaired glucose tolerance (IGT). METHODS AND RESULTS: Thirty patients with IGT (mean age=45.2+/-3.9 years), low HDL-C serum concentrations (HDL-C <1.0 mmol/l), but no additional comorbidities were treated once-daily with ER niacin (1000 mg) in a randomized open-label controlled (n=30) study for 6 months. During the first 4 weeks, daily dose was increased from 375 to 1000 mg in weekly intervals. At baseline and after 6 months, subcutaneous adipose tissue biopsies were taken, body fat mass, insulin sensitivity (euglycemic-hyperinsulinemic clamp), and adipokine serum concentrations were measured. After 6 months of ER niacin treatment, HDL-C increased significantly by 24% and adiponectin by 35%. In addition, ER niacin significantly reduced circulating lipoprotein (a) by 38% (p<0.001) and fasting triglycerides by 12% (p<0.05). Whole-body insulin sensitivity increased in the ER niacin treatment group, although this trend was not statistically significant (p=0.085). Six months ER niacin led to a significant reduction in mean adipocyte size associated with increased insulin sensitivity in isolated adipocytes and gene expression changes including increased adiponectin, C/EBPalpha, C/EBPdelta, PPARgamma and decreased carnitine palmitoyl transferase 2, hormone sensitive lipase, nicotinic acid receptor (GPR109B) and fatty-acid synthase mRNA expression. CONCLUSION: Treatment with ER niacin significantly improves atherogenic lipid profile in patients with IGT. These beneficial effects could at least in part be due to pleiotropic niacin effects in adipose tissue, characterized by decreased mean adipocyte size, increased insulin sensitivity and altered mRNA expression profile.

the problem is that sustained release is more taxing to the liver and should only be used by those who have no other alternatives. I've used 300mgs of plain old nicotinic acid for years now and it keeps my HDL high and I don't get the flush any longer when I take it...

heavyiron
07-25-2009, 09:28 AM
One of the best things for increasing HDL while lowering LDL is a $2 bottle of nicotinic acid (Niacin). Numerous studies show it is Superior 90% of statins because it increases LDL receptor in the liver while reducing HDL receptor. No need to go crazy with it either . 300mgs split over 3 x 100mg doses a day for about two weeks will have a profound effect. Oh BTW the flush has something to do with it because the "flush-free" potassium salt version don't work.

One warning... too much Niacin Is no good. It causes hepatic stress. Stay low dose (< 500mgs a day) and let it work over time.


the problem is that sustained release is more taxing to the liver and should only be used by those who have no other alternatives. I've used 300mgs of plain old nicotinic acid for years now and it keeps my HDL high and I don't get the flush any longer when I take it...

Your statement originally was "flush free don't work" My point is it does work and the more it is studied the more data we have to confirm this. Secondly your dosage is low even for regular Niacin. I don't think I have ever read a study where 300mg was used daily showing a "profound effect" as you stated earlier. If you have a study at that dose I would love to read it.

I do agree that liver stress is possible with Niacin however.

Tatyana
07-25-2009, 10:39 AM
What would be the typical treatment of cardiovascular disease? First they check the cholesterol. High cholesterol over 200,


I just checked, and it seems that 200-240 ng/dl is what is considered high in the US.

That is only 5.17-6.12 mmol/L which is average in the UK.

My cholesterol has been up to 8 mmol/L or 300 mg/dL at least twice when I have checked it when I am playing with my diet and my GP doesn't bat an eyelid at that.

My normal cholesterol is always between 4.9-5.6 mmol/L.





In the UK, the average total cholesterol level is 5.7mmol/l.

The levels of total cholesterol fall into the following categories:

ideal level: cholesterol level in the blood less than 5mmol/l.
mildly high cholesterol level: between 5 to 6.4mmol/l.
moderately high cholesterol level: between 6.5 to 7.8mmol/l.
very high cholesterol level: above 7.8mmol/l.
As well as this figure, doctors also have to take into account:

the ratio between good and bad cholesterol
the presence of other risk factors for cardiovascular disease, such as smoking, diabetes and high blood pressure.
It is possible for someone to have a high level of total cholesterol and still have a relatively low cardiovascular risk because of an absence of other risk factors or because their family history is free from coronary disease.

triceptor
07-25-2009, 11:35 AM
I just checked, and it seems that 200-240 ng/dl is what is considered high in the US.

That is only 5.17-6.12 mmol/L which is average in the UK.

My cholesterol has been up to 8 mmol/L or 300 mg/dL at least twice when I have checked it when I am playing with my diet and my GP doesn't bat an eyelid at that.

My normal cholesterol is always between 4.9-5.6 mmol/L.

What's worst is that the medical orthodoxy at the prodding of Big Pharma here in the United States of Consumption are trying to artificially push the "safe" upper limits to 160 ng/dl in an attempt to get everyone on choleostatin drugs..... it makes me sick to see the value of life placed so far below self interests and corporate profits.

triceptor
07-25-2009, 11:49 AM
Your statement originally was "flush free don't work" My point is it does work and the more it is studied the more data we have to confirm this. Secondly your dosage is low even for regular Niacin. I don't think I have ever read a study where 300mg was used daily showing a "profound effect" as you stated earlier. If you have a study at that dose I would love to read it.

I do agree that liver stress is possible with Niacin however.

Those examples you use are not "flush free" as are marketed as flush free OTC niacin. Those are flush free because they are released slowly. Niaspan is still nicotinic acid just a modified version that releases slowly.

And yes it doesn't take 1.5 grams of niacin to cause a change in total cholesterol in a normally functioning liver. I experimented with this three years ago. Using 300mgs a day of OTC niacin for 6 weeks and my total cholesterol went from 240 to 190. I did this as an experiment using an in-home cholesterol tester that anyone can purchase a their local pharmacy.

I also had my then 80 year old mother do to get her off of statins with her physicians agreement. She stopped teh statins and began taking 300 mgs of nicotinic acid a day instead and after 6 months she returned for a regularly scheduled exam and her total cholesterol numbers had not changed and her HDL was higher.

I also did an interview with a physician on Lipoprotein (a) being a better predictor than LDL as a risk of atherosclerosis and he confirmed my statement that there seems to a link between teh flushing and the effectiveness of the niacin. I'll dig it up and post it here.

Tatyana
07-25-2009, 11:54 AM
What's worst is that the medical orthodoxy at the prodding of Big Pharma here in the United States of Consumption are trying to artificially push the "safe" upper limits to 160 ng/dl in an attempt to get everyone on choleostatin drugs..... it makes me sick to see the value of life placed so far below self interests and corporate profits.

Let's say 'yah' for universal health care where we have groups of scientists, clinicians and medical ethics experts overseeing some of the general guidelines for treatment (NICE - National Institute for Clinical Excellence).

There are some bonuses to having a national program, it does cost a lot of money, and the prevention of disease is far cheaper.

This is a HUGE report, there are shortened guidelines on their site.

You can google search NICE guidelines on X and see what they have to say about just about any disease.

The diet advice isn't as advanced as some of the things that we know to be beneficial, but the majority of the population is not going to change their diets in a radical manner.

This is a huge document, I took out a few bits that might interest you.
From NICE guidelines for lipid modification:



1.1 Management
Strategies for the prevention of CVD are threefold. First are interventions to reduce the prevalence of CVD risk factors in the general population. The largest number of CVD events will occur in those at low risk. Smoking cessation combined with changes in mean blood pressure and cholesterol through national reductions in salt intake, saturated fat consumption and increases in physical activity are fundamental to the national strategy for improvement.
The second strategy is interventions in individual people at high risk of developing CVD and focusing health service resources on those at greatest risk with most to gain. This strategy, largely based in primary care, includes smoking cessation and the identification and assessment of those at high risk with appropriate advice on diet, physical activity and treatment for high blood pressure and lipid modification.


1.1 Recommendations for lifestyle
Cardioprotective diet
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section53)1.1.1 People at high risk of or with CVD should be advised to eat a diet in which total fat intake is 30% or less of total energy intake, saturated fats are 10% or less of total energy intake, intake of dietary cholesterol is less than 300 mg/day and where possible saturated fats are replaced by monounsaturated and polyunsaturated fats. It may be helpful to suggest they look at www.eatwell.gov.uk/healthydiet for further practical advice.
1.1.2 People at high risk of or with CVD should be advised to eat at least five portions of fruit and vegetables per day, in line with national guidance for the general population. Examples of what constitutes a portion can be found at www.eatwell.gov.uk/healthydiet and www.5aday.nhs.uk
1.1.3 People at high risk of or with CVD should be advised to consume at least two portions of fish per week, including a portion of oily fish. Further information and advice on healthy cooking methods can be found at www.eatwell.gov.uk/healthydiet
1.1.4 Pregnant women should be advised to limit their oily fish to no more than two portions per week. Further information and advice on oily fish consumption can be found at www.eatwell.gov.uk/healthydiet
1.1.5 People should not routinely be recommended to take omega-3 fatty acid supplements for the primary prevention of CVD.
Plant stanols and sterols recommendations
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section54)1.1.6 People should not routinely be recommended to take plant sterols and stanols for the primary prevention of CVD.

Physical activity
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section55)1.1.7 People at high risk of or with CVD should be advised to take 30 minutes of physical activity a day, of at least moderate intensity, at least 5 days a week, in line with national guidance for the general population[1] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#_ftn1).
1.1.8 People who are unable to perform moderate-intensity physical activity at least 5 days a week because of comorbidity, medical conditions or personal circumstances should be encouraged to exercise at their maximum safe capacity.
1.1.9 Recommended types of physical activity include those that can be incorporated into everyday life, such as brisk walking, using stairs and cycling (see 'At least five a week')16.
1.1.10 People should be advised that bouts of physical activity of 10 minutes or more accumulated throughout the day are as effective as longer sessions (see 'At least five a week')16.
1.1.11 Advice about physical activity should take into account the personís needs, preferences and circumstances. Goals should be agreed and the person should be provided with written information about the benefits of activity and local opportunities to be active, in line with íPhysical activity' (NICE public health intervention guidance 2).

Combined interventions (diet and physical activity)
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section56)1.1.12 Advice on diet[2] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#_ftn2) and physical activity[3] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#_ftn3) should be given in line with national recommendations.

Weight management
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section58)1.1.13 People at high risk of or with CVD who are overweight or obese should be offered appropriate advice and support to work towards achieving and maintaining a healthy weight in line with 'Obesity' (NICE clinical guideline 43).

Alcohol consumption
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section57)1.1.14 Alcohol consumption for men should be limited to up to 3Ė4 units a day. For women, alcohol consumption should be limited to up to 2Ė3 units a day. People should avoid binge drinking. Further information can be found at www.eatwell.gov.uk/healthydiet.

Smoking cessation
[Hyperlink to Evidence Statements & Narratives] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#section59)1.1.15 All people who smoke should be advised to stop, in line with 'Smoking cessation servicesí (NICE public health guidance 10).
1.1.16 People who want to stop smoking should be offered support and advice, and referral to an intensive support service (for example, the NHS Stop Smoking Services).
1.1.17 If a person is unable or unwilling to accept a referral to an intensive support service they should be offered pharmacotherapy in line with ' Smoking cessation servicesí (NICE public health guidance 10) and 'Varenicline for smoking cessation' (NICE technology appraisal guidance 123).

1.2 Introduction Ė lifestyle modification for the primary and secondary prevention of CVD
There is a substantive and consistent body of epidemiological, physiological and observational evidence demonstrating that changes in diet modify blood lipids and other risk factors and that these changes are associated with reductions in morbidity and mortality from CVD. Similarly epidemiological, physiological and observational evidence supports the association between cardiovascular health and levels of moderate or greater physical activity and associates a sedentary lifestyle with increased cardiovascular risk.
It is difficult to design, fund or organise randomised trials sufficiently large and rigorous that can yield evidence for the effect of diet, physical activity, smoking cessation or multifactorial lifestyle interventions on cardiovascular events. The observational literature on diet, dietary modification and physical activity provides a large body of evidence that has been periodically reviewed for major national initiatives. It is beyond the resources of this guideline to attempt such a review and we have referenced national reports and systematic reviews and cross referred to appropriate national advice.

[1] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#_ftnref1) Department of Health (2004) At least five a week: evidence on the impact of physical activity and its relationship to health. A report from the Chief Medical Officer. London: Department of Health. Available from www.dh.gov.uk (http://www.dh.gov.uk/)

[2] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#_ftnref2) See www. eatwell.gov.uk/healthydiet

[3] (http://forums.rxmuscle.com/newreply.php?do=newreply&p=399509#_ftnref3) Department of Health (2004) At least five a week: evidence on the impact of physical activity and its relationship to health. A report from the Chief Medical Officer. London: Department of Health. Available from www.dh.gov.uk (http://www.dh.gov.uk/)

tammyp
07-25-2009, 12:06 PM
Are you saying these OTC sups are like a statin drug?

CQ-10 is an antioxidant for the heart that lowers BP.

Plant sterols are another good way to lower LDL.

Liv 52 is excellent for the liver with proper hydration.

statins are derived from RYR. i lowered from 400 to 220, a drop of 180. my dr was shocked since nothing usually helps genetic but meds.

heavyiron
07-25-2009, 12:25 PM
Those examples you use are not "flush free" as are marketed as flush free OTC niacin. Those are flush free because they are released slowly. Niaspan is still nicotinic acid just a modified version that releases slowly.

And yes it doesn't take 1.5 grams of niacin to cause a change in total cholesterol in a normally functioning liver. I experimented with this three years ago. Using 300mgs a day of OTC niacin for 6 weeks and my total cholesterol went from 240 to 190. I did this as an experiment using an in-home cholesterol tester that anyone can purchase a their local pharmacy.

I also had my then 80 year old mother do to get her off of statins with her physicians agreement. She stopped teh statins and began taking 300 mgs of nicotinic acid a day instead and after 6 months she returned for a regularly scheduled exam and her total cholesterol numbers had not changed and her HDL was higher.

I also did an interview with a physician on Lipoprotein (a) being a better predictor than LDL as a risk of atherosclerosis and he confirmed my statement that there seems to a link between teh flushing and the effectiveness of the niacin. I'll dig it up and post it here.
Maybe it is semantics but the abstracts I gave do not cause flushing therefore they can be termed flush free :p

I look forward to any studies demonstrating 300mg of niacin daily causes profound effects in lipids.

JayV
07-25-2009, 12:34 PM
Maybe it is semantics but the abstracts I gave do not cause flushing therefore they can be termed flush free :p

I look forward to any studies demonstrating 300mg of niacin daily causes profound effects in lipids.

Semantics and brand naming aside, what is normally marketed as flush-free niacin is Inositol hexaniacinate and it is useless for lipid control. Nicotinic acid is what is needed if you are using niacin.
BTW Carl, I have been on 1.5-2 grams daily for several years. I get blood work done every 6 months and have had no problems.

triceptor
07-25-2009, 12:45 PM
Maybe it is semantics but the abstracts I gave do not cause flushing therefore they can be termed flush free :p

I look forward to any studies demonstrating 300mg of niacin daily causes profound effects in lipids.

Not semantics. OTC niacin supps marketed as "flush free" are not timed release or sustained release. They are generally potassium salts of nicotinic acid. The others in the abstracts are prescription only and not marketed as flush free.

saiyajinali
07-25-2009, 12:48 PM
i have it, genetic. i take red yeast rice, omegas, and 10co enzyme. i hear this is hard on your liver as if it were an actual statin drug. since we discuss liver support here, what do any of you suggest to go along with this to help keep my liver healthy? btw....this cocktail got me down 180 points.

Tammy,
1000 to 2000mg of flush free Niacin is very effective for lowering cholesterol... But you have to use flush free. The normal flush niacin is toxic on the liver & will set your skin on fire. The flkush free is time released. I had a mis step years ago that sent me to a cardiologist. previous to this, my dr did my bloodwork & noticed my cholesterol was high because of synthetic test raises cholesterol. He suggested me take the F.F. Niacin & it worked.
Anyway when I had that mis-step & I made my visit to the cardiologist, they ran the in depth tests on me to make sure I was ok, my cholesterol was excellent & I had no blockage... But I was diagnosed with testosterone induced hypertension lol..

Anyway, try starting off with 2000mg of Flush free niacin. This should help. Then, if you get your numbers where you want, lower your doseage to 1000mg. You can get this from walmart or any vitamin isle in 500mg capsules. Its cheap too..

saiyajinali
07-25-2009, 12:55 PM
Your statement originally was "flush free don't work" My point is it does work and the more it is studied the more data we have to confirm this. Secondly your dosage is low even for regular Niacin. I don't think I have ever read a study where 300mg was used daily showing a "profound effect" as you stated earlier. If you have a study at that dose I would love to read it.

I do agree that liver stress is possible with Niacin however.
Since 2003, I have taken 1000mg of flush free Niacin everyday & my liver enzymes are always good when I get my bloodwork done. And I have never experienced a flush either.. And during that time I eat a diet high in fat with lots of red meat & whole eggs, & have taken testosterone, & my cholesterol has always been great.

heavyiron
07-25-2009, 12:59 PM
Since 2003, I have taken 1000mg of flush free Niacin everyday & my liver enzymes are always good when I get my bloodwork done. And I have never experienced a flush either.. And during that time I eat a diet high in fat with lots of red meat & whole eggs, & have taken testosterone, & my cholesterol has always been great.
Do you take any liver sups or was this with no liver support?

heavyiron
07-25-2009, 01:04 PM
statins are derived from RYR. i lowered from 400 to 220, a drop of 180. my dr was shocked since nothing usually helps genetic but meds.
OK, I see. Do you have elevated liver enzymes? Because ryr can be used in healthy adults without damaging the liver.

saiyajinali
07-25-2009, 01:06 PM
Do you take any liver sups or was this with no liver support?
I never take orals so I never use any liver support supps. Unless Evening Primrose Oil counts as liver support.

heavyiron
07-25-2009, 01:14 PM
I never take orals so I never use any liver support supps. Unless Evening Primrose Oil counts as liver support.
Thank you

tammyp
07-25-2009, 04:55 PM
great read. my dr agrees with this. he said im healthy with diet blood pressure, etc..thats hes not worried. id

tammyp
07-26-2009, 01:50 PM
Is Fish Oil & Red Yeast Rice Better Than Statins in Cholesterol Treatment?
July 8, 2008 ∑ Filed Under General
University studies and private hospital studies are frequently deemed as difficult for Joe Q. Public to get in on from an investment or financial angle. But sometimes there is an opportunity to go against other established drug companies with blockbuster or mega-blockbuster drugs.

What if you were absolutely convinced scientifically that Red Rice Yeast & Fish Oil administered in certain controlled doses combined with education and regular habit reviews was as effective or more effective than traditional statins and pharmaceutical grade cholesterol treatments. While this is likely going to depend heavily on genetics and depend heavily upon the trial groups, a study is out that showed some phenomenal results that compared this head to head with patients taking Zocor, the statin from Merck & Co. (NYSE: MRK).

We want to stipulate that this is a small group and that it really looks like the results may be skewed because of behavior. But the results area start and in an extreme could lead to many forms of alternative treatments.

The Mayo Clinic has issued some data that will at worst lead to much broader study comparisons. The extreme case could be catastrophic for major pharmaceutical drug makers of statins as these are billions of dollars per year in the U.S. alone.

In the July issue of Mayo Clinic Proceedings, a group of researchers from Pennsylvania examine whether an alternative approach to treating high blood cholesterol may provide an effective treatment option for patients who are unable or unwilling to take statins.

Researchers followed 74 patients with high blood cholesterol who met standard criteria for using statin therapy, and they were then randomly assigned to either the alternative treatment group or the statin group and followed for three months.

The alternative treatment group participants received daily fish oil and red yeast rice supplements, AND they were enrolled in a 12-week multidisciplinary lifestyle program that involved weekly 3.5-hour educational meetings led by a cardiologist, dietitian, exercise physiologist and several alternative or relaxation practitioners. The statin group received 40 milligrams of Zocor daily, as well as printed materials about diet and exercise recommendations.

At the end of the three-month period, participants from both groups underwent blood cholesterol testing to determine the percentage change in LDL cholesterol. There was a reduction in LDL cholesterol levels in both groups, but here is the breakdown of the results:

The alternative treatment group saw a 42.4% reduction, and the statin group saw a 39.6% reduction.
Members of the alternative therapy group also had a substantial reduction in triglycerides, another form of fat found in the blood, and lost more weight.
The doctor quoted acknowledged that a larger, multi-center trial with longer follow-up is necessary to determine long-term compliance with the alternative regimen. It noted that previous studies involving diet and exercise have found a high rate of patients are either unable to or unwilling to follow lifestyle recommendations. This study also noted that the “excellent adherence” in the alternative group was undoubtedly related to the intensive follow-up, education and support provided for this group.

This is an interesting finding when you consider the behavioral aspect. Those who have to attend meetings and those who stick to a regimen do well. But giving prescription drugs and just some educational material might not be the best bets here. How many of us are lazy? Many. How many of us get around to reading everything we are supposed to read? How many of us don’t want to bother? Many, on both counts.

I am no doctor but there are certain things that become evident if you have gotten the chance to deal with doctors and medicine. Without trying to damn an entire nation’s habits, it has grown more and more obvious that Americans would rather just take a magic pill rather than get to the heart of the matter (no pun intended). Diet and exercise alone unfortunately doesn’t work for everyone. Some are just pre-disposed to high cholesterol, high blood pressure, or heart and arterial problems.

What percentage of those with high cholesterol and other physical diseases or issues would be helped with diet and exercise? The answer is many, albeit an undefined amount. Those will vary greatly depending on many factors from your race, your weight, your family history, your occupation, your general health levels, your activity, and your diet.

Regardless of how effective fish oil and red rice yeast combined with follow-on education and monitoring works, it is highly unlikely that Joe Public in America is going to make such a huge jump where everyone becomes fit and where everyone actually does what they are supposed to do (even what the KNOW they should do).

But this leaves a real opening here, and one that isn’t good for Big Pharma. Zocor is off of its exclusivity, but Merck recorded $876.5 million in 2007 sales from it (down from $2.8 Billion in 2006 when it had exclusivity). Merck’s Cozaar/Hyzaar to treat blood pressure saw $3.35 Billion in 2007 sales, and while that isn’t part of this study you know that many of the benefits in other regimens can further aid in this fight as well. Guess how much Pfizer (NYSE: PFE) shows Lipitor’s 2007 sales to lower LDL cholesterol. The answer is $12.675 Billion. Over at AstraZeneca (NYSE: AZN), Crestor counted for nearly $2.8 Billion in 2007 sales.

It would be highly unlikely that such a study, even of broadened out significantly and even if results continued to show superiority, would kill drugs in the statin class to lower LDL cholesterol. We are a nation addicted to prescriptions. But the key here seems to be the rigorous “behavior modification” on top of the use of “alternative regimens” or traditional prescription medicines is key.

Now imagine if we could apply the same theory over to Type II diabetes. OK, time to get off the soapbox.

Jon Ogg
July 8, 2008

Tags: AstraZeneca, chjolesterol, Crestor, high cholesterol, Lipitot, lowering cholesterol, merck, pfizer, statins

Tami Bellon
07-26-2009, 04:20 PM
statins are derived from RYR. i lowered from 400 to 220, a drop of 180. my dr was shocked since nothing usually helps genetic but meds.

Tam, have you listened to the SMR segment yet? If not.....take a listen. My dad has high cholesterol and I'm forwarding all kinds of stuff to him now because of what I heard.

Listen while cooking or cleaning or taking a shower. It's def worth it!

http://www.superhumanradio.com/rss/2009/SHR_Show_333.mp3

Shawn Bellon
07-26-2009, 04:38 PM
There is a thread in the mens chem section about Niacin lowering the bad and increasing the good.

tammyp
07-26-2009, 05:02 PM
i will..just havent gotten to it yet!

I.C.P.
07-29-2009, 06:51 AM
There is a thread in the mens chem section about Niacin lowering the bad and increasing the good.I just saw that in the men's section yesterday.I was pissed that the doctor in that thread said flush free does not work.I just bought a bottle of flush free.Then i hear that flush free and slow release and extended release are different.So,i say my doctor today and she said flush free is a scam for the most part.She said it may work in some people,but not all.I figure fcuk it,iam just gonna take straight up niacin and have comfort knowing it's doing what it's supposed to.

saiyajinali
07-29-2009, 11:36 AM
I just saw that in the men's section yesterday.I was pissed that the doctor in that thread said flush free does not work.I just bought a bottle of flush free.Then i hear that flush free and slow release and extended release are different.So,i say my doctor today and she said flush free is a scam for the most part.She said it may work in some people,but not all.I figure fcuk it,iam just gonna take straight up niacin and have comfort knowing it's doing what it's supposed to.

It DOES work. I had two doctors tell me to take it. My cholesterol was borderline, I took it while doing everything else the same(homestasis) went back got my blood work done, my cholesterol dropped.
So if it doesnt work, I guess it was a coincidence or aliens abducted me & ran a tube in my arteries & cleaned them out for me..