Saturated Fats, Cholesterol Lard and Vitamin D

[mcb]

I am curious if it is possible to stop taking certain drugs that are designed to lower cholesterol, specifically one called "Crestor" , I have been reading a lot of the info here and it sounds like these drugs are worse then the actual cholesterol itself.

I thought we had a thread that discussed Crestor, but I was unable to locate it, so it must have been a different medication. Here are some excerpts from Public Citizen's worstpills.org website, where they place it in their "Do not use" category.

Public Citizen Petition to Ban Rosuvastatin (CRESTOR)
Our concerns prior to approval about rhabdomyolysis and kidney toxicity have been confirmed in the results of the first year of marketing in the UK and Canada and in the first six months of marketing in the U.S. Data obtained from the U.S., the UK and Canada show that seven cases of rhabdomyolysis and nine cases of kidney damage or failure occurred after FDA approval. On the basis of this information, confirming the fact that the drug has the unique risks we were concerned with prior to its approval, we filed a petition in March 2004 asking the FDA to take the drug off the market. Major U.S. insurers, including WellPoint/Blue Cross, with 16 million beneficiaries, have refused to reimburse for the drug because of safety concerns.

Rosuvastatin (CRESTOR) is the most dangerous of the popular cholesterol-lowering statin drugs, according to a study published in the medical journal Circulation.

In summary, rosuvastatin has no proven health benefit in people with elevated cholesterol levels. As discussed above, it has caused potentially serious kidney toxicity that is not seen with the other statins; it is the only statin that caused rhabdomyolysis, a life-threatening adverse drug reaction, in preapproval clinical trials; and there are already four statins on the market that are safer than rosuvastatin and have demonstrated a health benefit to patients.

 

[mcb]

I should also mention that some of the books we have been reading here, such as Primal Body, Primal Mind, Deep Nutrition, and The Art and Science of Low Carbohydrate Living have quite a bit to say about statins and about indicators such as LDL and HDL test results. For example,

Study after study has demonstrated the potentially debilitating effects of statin drugs. There are over nine hundred studies to date showing the adverse potential effects of statin drugs on everything from cognitive functioning to immune-system functioning. One recent study showed that the statin drug simvastatin (Zocor and Simvacor) actually hinders the ability of the body’s immune system to kill pathogens! The same study showed that the use of these drugs also resulted in an increase in cytokine production, which increases damaging systemic inflammation (Hubbard 2010). Another review of nineteen large studies of more than sixty-eight thousand deaths by the Division of Epidemiology at the University of Minnesota found that low cholesterol levels predicted an increased risk of dying from gastrointestinal and respiratory diseases (Jacobs, Blackburn, Higgins, et al. 1992). Finally, the same University of Minnesota team did a study of more than one hundred thousand healthy individuals in the San Francisco area for fifteen years. At the end of the study, those who had low cholesterol levels at the start of the study had been admitted to the hospital more often because of an infectious disease. In other words, either low cholesterol made them more vulnerable to infection or high cholesterol protected those who did not become infected. The promotion of the low-cholesterol agenda and the use of statin drugs have been much more than wrong; they have been lethal.

Among numerous other things, the use of statin drugs can produce a confused state similar to that of Alzheimer’s disease. They have additionally even been linked with Lou Gehrig’s disease. A new study published in the Journal of the American College of Cardiology revealed that driving down cholesterol levels actually increases the risk of cancer (Alawi et al. 2007).

Gedgaudas, Nora T. (2011-06-22). Primal Body, Primal Mind: Beyond the Paleo Diet for Total Health and a Longer Life (pp. 78-79). Healing Arts Press. Kindle Edition.

 

[Rick Rowe]

I should also mention that some of the books we have been reading here, such as Primal Body, Primal Mind, Deep Nutrition, and The Art and Science of Low Carbohydrate Living have quite a bit to say about statins and about indicators such as LDL and HDL test results. For example,

Study after study has demonstrated the potentially debilitating effects of statin drugs. There are over nine hundred studies to date showing the adverse potential effects of statin drugs on everything from cognitive functioning to immune-system functioning. One recent study showed that the statin drug simvastatin (Zocor and Simvacor) actually hinders the ability of the body’s immune system to kill pathogens! The same study showed that the use of these drugs also resulted in an increase in cytokine production, which increases damaging systemic inflammation (Hubbard 2010). Another review of nineteen large studies of more than sixty-eight thousand deaths by the Division of Epidemiology at the University of Minnesota found that low cholesterol levels predicted an increased risk of dying from gastrointestinal and respiratory diseases (Jacobs, Blackburn, Higgins, et al. 1992). Finally, the same University of Minnesota team did a study of more than one hundred thousand healthy individuals in the San Francisco area for fifteen years. At the end of the study, those who had low cholesterol levels at the start of the study had been admitted to the hospital more often because of an infectious disease. In other words, either low cholesterol made them more vulnerable to infection or high cholesterol protected those who did not become infected. The promotion of the low-cholesterol agenda and the use of statin drugs have been much more than wrong; they have been lethal.

Among numerous other things, the use of statin drugs can produce a confused state similar to that of Alzheimer’s disease. They have additionally even been linked with Lou Gehrig’s disease. A new study published in the Journal of the American College of Cardiology revealed that driving down cholesterol levels actually increases the risk of cancer (Alawi et al. 2007).

Gedgaudas, Nora T. (2011-06-22). Primal Body, Primal Mind: Beyond the Paleo Diet for Total Health and a Longer Life (pp. 78-79). Healing Arts Press. Kindle Edition.

Thanks Megan for taking the time to locate this information for myself.
I find it mind boggling that this is being prescribed, that i am being prescribed this drug to combat cholesterol which was high again on my last doctors visit and he, my doctor! Who wanted to double my does and I said NO too him the last time.

I hate medication of any kind because I believe it's a loosing battle once started and from the research I have done both online and here at cassiopaea.org and it all seems to agree with my findings.

I don't like feeling toxic and or nauseous all the time, i had been on another medication of which I have recently switched from for another that is keeping me a live, I don't have the night sweats and nauseous feeling anymore or the dizziness! I hate being tide to having to take something that I will probably end up dying from it's side effects or from forgetting to take the meds and or my body building an resistance to the drug because of forgetting to take the medication itself.

I am starting to understand why some people have taken matters into there own hands and just went commando and stopped everything and allowed nature to take its course. This is not something I plan on doing, but I think when it comes to "crestor" I think its probably in my best interest to stay away from this drug.
I have been suffering since I have been on it with memory issues and I didn't realize this until I read the article you posted, it is what I know to be like Alzheimer’s disease, an extremely mild case! but never the less my memory is almost laughable at time because I can't remember the most basic of things that have happened and or I may have been leaving thing and not knowing where I left them and or I completely forget what I was doing and standing in the middle of the room and just trying to regain and or try to figure out what I was about to do.

I greatly appreciate you taking the time to comment on my post and the information.

 

[Nienna]

Hellfire, since you read this forum, you may know that the Medical schools here in the U.S. are funded by the pharmaceutical companies. So what has been taught to the med students is how to treat illnesses with pharmaceuticals. Not how to cure people. That wouldn't make any money for the pharmaceutical companies. Most doctors only read what these companies put out there for them. And, of course, most of the medical papers the doctors read are only those that are pretty much funded by these same pharmaceutical companyies.

Reading the books recommended in the Life Without Bread thread will show you how our bodies actually NEED cholesterol. But, hey, lowering cholesterol is big money for those pharmaceutical companies. And, like you said, all of the side effects alsoneed to be dealt with later on. So more money for them, and the doctors you go to to get those drugs.

 

[mcb]

Here is one piece of the history of how we arrived in our present situation, from Why We Get Fat. Mind boggling indeed.

Another reason to question the belief that saturated fat is bad for our health is that experimental evidence in support of the idea has always been surprisingly hard to come by. I know this seems difficult to believe, considering how forcefully we’ve been told that saturated fat is a killer. But what we’ve been told and what the evidence actually supports parted ways in 1984, when the National Heart, Lung, and Blood Institute launched its massive health campaign. At the time, the NHLBI experts lacked confidence in the fat/heart-disease connection, for good reason: the institute had spent $115 million on a huge, decade-long clinical trial to test the idea that eating less saturated fat would curb heart disease, but not a single heart attack had been prevented.

This could have been taken as reason to abandon the idea entirely, but the institute had also spent $150 million testing the benefits of a cholesterol-lowering drug, and this second trial had succeeded. So the institute’s administrators took a leap of faith, as one of them, Basil Rifkind, later described it: They had spent twenty years and an inordinate amount of money trying to demonstrate that cholesterol-lowering, low-fat diets would prevent heart disease, Rifkind explained, and they had, up until then, failed. Trying again would be too expensive and would take at least another decade, even if the institute could afford it. But once they had compelling evidence that lowering cholesterol with a drug would save lives, it seemed like a good bet that a low-fat, cholesterol-lowering diet would as well. “It’s an imperfect world,” Rifkind had said. “The data that would be definitive are ungettable, so you do your best with what is available.”

The ambition was admirable, but the results have been, as I said, disappointing. Researchers have continued to demonstrate that cholesterol-lowering drugs can prevent heart attacks and apparently allow some people to live longer (at least those who are at particularly high risk of a heart attack). But it has still not been demonstrated that either low-fat or low-saturated-fat diets will do the same.

Taubes, Gary (2010-12-28). Why We Get Fat: And What to Do About It. Knopf. Kindle Edition.

 

[Rick Rowe]

Hellfire, since you read this forum, you may know that the Medical schools here in the U.S. are funded by the pharmaceutical companies. So what has been taught to the med students is how to treat illnesses with pharmaceuticals. Not how to cure people. That wouldn't make any money for the pharmaceutical companies. Most doctors only read what these companies put out there for them. And, of course, most of the medical papers the doctors read are only those that are pretty much funded by these same pharmaceutical companyies.

Reading the books recommended in the Life Without Bread thread will show you how our bodies actually NEED cholesterol. But, hey, lowering cholesterol is big money for those pharmaceutical companies. And, like you said, all of the side effects alsoneed to be dealt with later on. So more money for them, and the doctors you go to to get those drugs.

This is why I was getting so confused because I just started to read "Life Without Bread" book and it's findings are completely opposite so far from what I have been told and or advised. So I guess the million dollar question for me is do I stay on the Staten "Crestor" drug and hopefully dodge the bullet and or do what I feel is right and go off it completely. Or is the latter part insane thinking?

I have to see my homeopath next week and I am hoping because this isn't my area of expertise in any way shape. This is sad because i am seeking answers (the right ones) still from others to help me move on with my life and my decisions, it is very difficult because I am at a point where I love living and I would hate to do anything that could/would shorten whatever little bit I may have left.

My natural path has been amazing and giving me natural remedies that I would have normally taken pills from my doctor (prescribed of course) and been caught in that whole vicious cycle and feeling like crap.

Thank you, Nienna Eluch. for your response. :)

 

[mcb]

...it is very difficult because I am at a point where I love living and I would hate to do anything that could/would shorten whatever little bit I may have left.

Yes, it is difficult. There is evidence that statins can help certain people that are quite ill. On the other hand there is a lot of evidence that they are harming a lot of people that were not that ill. At the very least you might want to consider switching to a less toxic statin, and to investigate what you can do to improve your nutrition. You may be able, over time, be able to resolve any problems that statins may have been helping with.

While it isn't generally seen this way, Western countries (the US in particular) are malnourished, and weaker individuals (of which I am one) can find it difficult to survive. If you are in that kind of situation you may have to take dietary measures that other people you know don't have to take, just to stay alive.

Many health problems arise from various forms of inflammation. If you have these kinds of problems and want to be well, you need to find the causes of your inflammation and eliminate them. Doctors (at least here in the US) are trained to identify "diseases" and write prescriptions that do not address causes. There are financial incentives at every level to mask symptoms (using toxic drugs that create more disease) while ignoring causes, so that patients grow progressively more ill and need ever-increasing amounts of "health care."

There are a number of books you can read to help prepare to make better decisions. Here is a section of one book that may provide a useful perspective.

Statins and Low Carbohydrate Diets

Many physicians immediately turn to statins if a patient’s LDL-C level is above standard guidelines, but the decision to begin lipid lowering therapy deserves serious thought. Without question statins markedly lower LDL-C but the impact on decreasing coronary events is less clear cut. For instance, the original Lipids Research Clinics (LRC) cholesterol lowering study with binding resin (cholestyramine) reduced the number of heart attacks but not overall mortality[16]. And a recent study with a statin (the JUPITER Study) indicates that much of the benefit with this class of drug is due to reduced inflammation rather than reduced LDL-C[46]. Therefore, if a diet could reduce your level of inflammation (discussed in Chapter 14), perhaps there’s less need for the drug.

So in the big picture, the potential benefit of a statin drug needs to be weighed against the risk of side effects and cost of medication. The number of people who experience adverse side effects is not trivial, the most common being fatigue and muscle pain, and more recently there is concern with cognitive impairment and increased risk of diabetes. Furthermore, whether or not you make a personal or professional decision to begin statin therapy, there are still unique benefits associated with a low carbohydrate diet (see side bar – Restricting Carbohydrates has Benefits Beyond Statins).

In summary, if LDL-C is your sole intended target, a low fat diet and/or cholesterol-lowering drugs appear to make sense. But there is enough doubt to question whether LDL-C is the best target for everyone. If your target encompasses a broader range of potent biomarkers like triglycerides, HDL-C, LDL particle size, insulin resistance, or inflammatory markers, then using a low fat/high-carbohydrate diet is equivalent to dancing on the edge of a mine field, whereas a low carbohydrate diet improves all these blood borne risk markers.

Phinney, Stephen; Volek, Jeff (2011-07-08). The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-Saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable. Beyond Obesity LLC. Kindle Edition.

Here is the sidebar:

Restricting Carbohydrates has Benefits Beyond Statins

Statin therapy effectively lowers LDL-C, but if a patient presents with other risk factors the typical course of action is to prescribe additional drugs. In the case of atherogenicdyslipidemia, combining a statin with a fibrate and/or nicotinic acid is common. While this poly-pharmacy approach can be effective in reducing lipid biomarkers, there is an increased cost and greater likelihood of side effects with multiple drug use. Importantly, in contrast to the effect of a low carbohydrate diet, none of the lipid lowering drugs are effective at reliably increasing LDL particle size. Since a low carbohydrate diet does increase LDL-C size, it represents a fully rational approach to the management of Pattern B dyslipidemia. In a research study that is currently pending publication, we examined the effect of implementing a low carbohydrate diet on LDL size and other features of metabolic syndrome in previously hyperlipidemic men and postmenopausal women who had achieved a lowered LDL-C by statin treatment. After 6 weeks the low carbohydrate diet resulted in significant improvements in a number of markers while maintaining previously reduced levels of LDL-C. LDL particle size was significantly increased as measured by two separate methods (gel electrophoresis and vertical auto profile ultracentrifugation). Additionally, there were significant improvements in plasma triglycerides (reduced by 36%), insulin sensitivity (increased by 25%), systolic (-5%) and diastolic (-6%) blood pressure, and blood flow in the forearm. In summary, atherogenic dyslipidemia and other metabolic syndrome markers are prevalent in statin users despite wellcontrolled LDL-C and the anti-inflammatory effects of this drug class. Thus the addition of a very low carbohydrate diet in combination with statin therapy can significantly improve insulin sensitivity, LDL quality, and other features of metabolic syndrome.

Phinney, Stephen; Volek, Jeff (2011-07-08). The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-Saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable. Beyond Obesity LLC. Kindle Edition.

Other authors are not so "nice" about it. The "markers," such as LDL level, may not mean all that much, at least when interpreted the way they usually are. Consider the following from Primal Body, Primal Mind (Deep Nutrition contains a complimentary section).

All Cholesterol Is Exactly the Same

LDL takes cholesterol away from the liver to the extremities and other organs for various purposes, including the manufacture of important steroidal hormones and vitamin D. HDL merely returns the same spent cholesterol to the liver, where it can be recycled. LDL also serves as a transport mechanism for critical fat-soluble nutrients, including vitamin D and antioxidants as well as certain fats.

There is one undesirable variation of a certain LDL carrier molecule known as lipoprotein(a), which is smaller and denser than regular LDL. Within the arterial endothelium lie spaces between cells that serve as channels for the influx and outflow of nutrients. Lipoprotein(a) can actually lodge itself in the spaces between these vascular arterial cells and shut off those natural channels, resulting in poor nutrient flow to the endothelium and triggering a damaging inflammatory response. Lipoprotein(a) is the only lipoprotein of significant consequence. The drug companies, however, would rather you didn’t know about it at all, as statin drugs do nothing to change the size of LDL particles or reduce lipoprotein(a); only diet can do this. It is high-carbohydrate diets and the presence of excess insulin that are responsible for the production of this undesirable lipoprotein. Diets rich in natural fats and moderate protein with low carbohydrates result in normal LDL. Actual levels of regular LDL and HDL are of little actual consequence, though they can serve as a relative marker for illuminating certain dietary tendencies. High fructose diets, for instance, are known to greatly increase the production of LDL. They can also in part reflect other disorders and can be useful to look at in that regard. Note that HDL levels in excess of 70 to 75 mg/dL, in people for whom there is no inherent genetic predisposition toward very high HDL, can often imply the presence of undesirable inflammatory processes and potential autoimmune issues. This is because what is termed the inflammatory peroxidase system, when activated, can actually raise HDL in excess of normally positive indication ranges, as they are formed through related pathways. Higher HDL is not necessarily better. Excessively high HDL on your lab report may not be the “bee’s knees,” but it is still only an indicator, a clue toward other things—and not a cause of anything.

Furthermore, cholesterol is the human body’s version of duct tape. It travels to areas where there has been arterial damage and patches up lesions. Higher serum levels of cholesterol can serve as a message that “something is going on” for which it is needed. Serum cholesterol is simply an indicator, not a diagnosis. Allegedly high cholesterol is in no way a form of a pathologic condition, in and of itself. But it may be telling you something, much like the engine warning light illuminating the dashboard of your car. Unscrewing the bulb (i.e., taking statin drugs) isn’t going to fix the engine. You need to dig deeper. What has been deemed high cholesterol by some, however (i.e., anything over 200 mg/dL) is an entirely arbitrary and unscientifically derived number fabricated solely by pharmaceutical interests. Levels approaching 250 to 300 mg/dL might be an indication to look under the hood to see why serum cholesterol seems to be going up. Rest assured, however, that cholesterol isn’t being sent there like an evil villain to cause you trouble; it’s simply trying to do its job. In my view, it is important to simply let it, while pursuing the trail of evidence to its more meaningful source.

Going in with statin drugs to stamp out cholesterol is the equivalent of preventing the firemen who arrive to put out a fire from doing their job—and blaming them for the fire. Elevated glucose or insulin levels, for instance, damage arterial walls and lead to an increased need for cholesterol to repair them.

Roughly 80 percent of what actually clogs arteries is not even composed of cholesterol or saturated fat but is composed of oxidized or rancid unsaturated fats (Enig 2001). Statistically, individuals whose blood cholesterol levels are low develop just as many plaques in their blood vessels as individuals whose cholesterol is high (Ravnskov 1998).

Cholesterol is no more a cause of heart disease than gray hair is the cause of old age

...

Gedgaudas, Nora T. (2011-06-22). Primal Body, Primal Mind: Beyond the Paleo Diet for Total Health and a Longer Life. Healing Arts Press. Kindle Edition.

It is unlikely that you will hear this from your doctor, and when you start to research for yourself you will -- we all do -- find yourself having to choose between alternative realities. If you dig around enough, you will find that the "alternative reality" problem actually exists on a grand scale in our world.

I highly recommend that you obtain some of these books and read the material in its entirety.

 

[Rick Rowe]

...it is very difficult because I am at a point where I love living and I would hate to do anything that could/would shorten whatever little bit I may have left.

Yes, it is difficult. There is evidence that statins can help certain people that are quite ill. On the other hand there is a lot of evidence that they are harming a lot of people that were not that ill. At the very least you might want to consider switching to a less toxic statin, and to investigate what you can do to improve your nutrition. You may be able, over time, be able to resolve any problems that statins may have been helping with.

While it isn't generally seen this way, Western countries (the US in particular) are malnourished, and weaker individuals (of which I am one) can find it difficult to survive. If you are in that kind of situation you may have to take dietary measures that other people you know don't have to take, just to stay alive.

Many health problems arise from various forms of inflammation. If you have these kinds of problems and want to be well, you need to find the causes of your inflammation and eliminate them. Doctors (at least here in the US) are trained to identify "diseases" and write prescriptions that do not address causes. There are financial incentives at every level to mask symptoms (using toxic drugs that create more disease) while ignoring causes, so that patients grow progressively more ill and need ever-increasing amounts of "health care."

There are a number of books you can read to help prepare to make better decisions. Here is a section of one book that may provide a useful perspective.

Statins and Low Carbohydrate Diets

Many physicians immediately turn to statins if a patient’s LDL-C level is above standard guidelines, but the decision to begin lipid lowering therapy deserves serious thought. Without question statins markedly lower LDL-C but the impact on decreasing coronary events is less clear cut. For instance, the original Lipids Research Clinics (LRC) cholesterol lowering study with binding resin (cholestyramine) reduced the number of heart attacks but not overall mortality[16]. And a recent study with a statin (the JUPITER Study) indicates that much of the benefit with this class of drug is due to reduced inflammation rather than reduced LDL-C[46]. Therefore, if a diet could reduce your level of inflammation (discussed in Chapter 14), perhaps there’s less need for the drug.

So in the big picture, the potential benefit of a statin drug needs to be weighed against the risk of side effects and cost of medication. The number of people who experience adverse side effects is not trivial, the most common being fatigue and muscle pain, and more recently there is concern with cognitive impairment and increased risk of diabetes. Furthermore, whether or not you make a personal or professional decision to begin statin therapy, there are still unique benefits associated with a low carbohydrate diet (see side bar – Restricting Carbohydrates has Benefits Beyond Statins).

In summary, if LDL-C is your sole intended target, a low fat diet and/or cholesterol-lowering drugs appear to make sense. But there is enough doubt to question whether LDL-C is the best target for everyone. If your target encompasses a broader range of potent biomarkers like triglycerides, HDL-C, LDL particle size, insulin resistance, or inflammatory markers, then using a low fat/high-carbohydrate diet is equivalent to dancing on the edge of a mine field, whereas a low carbohydrate diet improves all these blood borne risk markers.

Phinney, Stephen; Volek, Jeff (2011-07-08). The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-Saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable. Beyond Obesity LLC. Kindle Edition.

Here is the sidebar:

Restricting Carbohydrates has Benefits Beyond Statins

Statin therapy effectively lowers LDL-C, but if a patient presents with other risk factors the typical course of action is to prescribe additional drugs. In the case of atherogenicdyslipidemia, combining a statin with a fibrate and/or nicotinic acid is common. While this poly-pharmacy approach can be effective in reducing lipid biomarkers, there is an increased cost and greater likelihood of side effects with multiple drug use. Importantly, in contrast to the effect of a low carbohydrate diet, none of the lipid lowering drugs are effective at reliably increasing LDL particle size. Since a low carbohydrate diet does increase LDL-C size, it represents a fully rational approach to the management of Pattern B dyslipidemia. In a research study that is currently pending publication, we examined the effect of implementing a low carbohydrate diet on LDL size and other features of metabolic syndrome in previously hyperlipidemic men and postmenopausal women who had achieved a lowered LDL-C by statin treatment. After 6 weeks the low carbohydrate diet resulted in significant improvements in a number of markers while maintaining previously reduced levels of LDL-C. LDL particle size was significantly increased as measured by two separate methods (gel electrophoresis and vertical auto profile ultracentrifugation). Additionally, there were significant improvements in plasma triglycerides (reduced by 36%), insulin sensitivity (increased by 25%), systolic (-5%) and diastolic (-6%) blood pressure, and blood flow in the forearm. In summary, atherogenic dyslipidemia and other metabolic syndrome markers are prevalent in statin users despite wellcontrolled LDL-C and the anti-inflammatory effects of this drug class. Thus the addition of a very low carbohydrate diet in combination with statin therapy can significantly improve insulin sensitivity, LDL quality, and other features of metabolic syndrome.

Phinney, Stephen; Volek, Jeff (2011-07-08). The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-Saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable. Beyond Obesity LLC. Kindle Edition.

Other authors are not so "nice" about it. The "markers," such as LDL level, may not mean all that much, at least when interpreted the way they usually are. Consider the following from Primal Body, Primal Mind (Deep Nutrition contains a complimentary section).

All Cholesterol Is Exactly the Same

LDL takes cholesterol away from the liver to the extremities and other organs for various purposes, including the manufacture of important steroidal hormones and vitamin D. HDL merely returns the same spent cholesterol to the liver, where it can be recycled. LDL also serves as a transport mechanism for critical fat-soluble nutrients, including vitamin D and antioxidants as well as certain fats.

There is one undesirable variation of a certain LDL carrier molecule known as lipoprotein(a), which is smaller and denser than regular LDL. Within the arterial endothelium lie spaces between cells that serve as channels for the influx and outflow of nutrients. Lipoprotein(a) can actually lodge itself in the spaces between these vascular arterial cells and shut off those natural channels, resulting in poor nutrient flow to the endothelium and triggering a damaging inflammatory response. Lipoprotein(a) is the only lipoprotein of significant consequence. The drug companies, however, would rather you didn’t know about it at all, as statin drugs do nothing to change the size of LDL particles or reduce lipoprotein(a); only diet can do this. It is high-carbohydrate diets and the presence of excess insulin that are responsible for the production of this undesirable lipoprotein. Diets rich in natural fats and moderate protein with low carbohydrates result in normal LDL. Actual levels of regular LDL and HDL are of little actual consequence, though they can serve as a relative marker for illuminating certain dietary tendencies. High fructose diets, for instance, are known to greatly increase the production of LDL. They can also in part reflect other disorders and can be useful to look at in that regard. Note that HDL levels in excess of 70 to 75 mg/dL, in people for whom there is no inherent genetic predisposition toward very high HDL, can often imply the presence of undesirable inflammatory processes and potential autoimmune issues. This is because what is termed the inflammatory peroxidase system, when activated, can actually raise HDL in excess of normally positive indication ranges, as they are formed through related pathways. Higher HDL is not necessarily better. Excessively high HDL on your lab report may not be the “bee’s knees,” but it is still only an indicator, a clue toward other things—and not a cause of anything.

Furthermore, cholesterol is the human body’s version of duct tape. It travels to areas where there has been arterial damage and patches up lesions. Higher serum levels of cholesterol can serve as a message that “something is going on” for which it is needed. Serum cholesterol is simply an indicator, not a diagnosis. Allegedly high cholesterol is in no way a form of a pathologic condition, in and of itself. But it may be telling you something, much like the engine warning light illuminating the dashboard of your car. Unscrewing the bulb (i.e., taking statin drugs) isn’t going to fix the engine. You need to dig deeper. What has been deemed high cholesterol by some, however (i.e., anything over 200 mg/dL) is an entirely arbitrary and unscientifically derived number fabricated solely by pharmaceutical interests. Levels approaching 250 to 300 mg/dL might be an indication to look under the hood to see why serum cholesterol seems to be going up. Rest assured, however, that cholesterol isn’t being sent there like an evil villain to cause you trouble; it’s simply trying to do its job. In my view, it is important to simply let it, while pursuing the trail of evidence to its more meaningful source.

Going in with statin drugs to stamp out cholesterol is the equivalent of preventing the firemen who arrive to put out a fire from doing their job—and blaming them for the fire. Elevated glucose or insulin levels, for instance, damage arterial walls and lead to an increased need for cholesterol to repair them.

Roughly 80 percent of what actually clogs arteries is not even composed of cholesterol or saturated fat but is composed of oxidized or rancid unsaturated fats (Enig 2001). Statistically, individuals whose blood cholesterol levels are low develop just as many plaques in their blood vessels as individuals whose cholesterol is high (Ravnskov 1998).

Cholesterol is no more a cause of heart disease than gray hair is the cause of old age

...

Gedgaudas, Nora T. (2011-06-22). Primal Body, Primal Mind: Beyond the Paleo Diet for Total Health and a Longer Life. Healing Arts Press. Kindle Edition.

It is unlikely that you will hear this from your doctor, and when you start to research for yourself you will -- we all do -- find yourself having to choose between alternative realities. If you dig around enough, you will find that the "alternative reality" problem actually exists on a grand scale in our world.

I highly recommend that you obtain some of these books and read the material in its entirety.

Thank you, Megan.
That was very informative reading, is this information from online or a book that your getting this information from?.
This is definitely something I will be looking into thoroughly. I have a feeling I will have to get a nutritionist in this battle as well, my knowledge to date is minimal when it comes to low carb diets, I am learning slowly but there is so much it seems to learn about what foods are good (low carb) and also keeping track of how much I consume. Any suggestions on how to do this better? Right now I am looking things up online for what foods are low in carbs and it seems everything is carbohydrates and some may be lower, the others have to be reduced down into smaller portion sizes? Am I getting this right?

:)

 

[mcb]

That was very informative reading, is this information from online or a book that your getting this information from?.

Both are books. See the last paragraph of each quote for the title, author, etc.

This is definitely something I will be looking into thoroughly. I have a feeling I will have to get a nutritionist in this battle as well, my knowledge to date is minimal when it comes to low carb diets, I am learning slowly but there is so much it seems to learn about what foods are good (low carb) and also keeping track of how much I consume. Any suggestions on how to do this better? Right now I am looking things up online for what foods are low in carbs and it seems everything is carbohydrates and some may be lower, the others have to be reduced down into smaller portion sizes? Am I getting this right?

:)

Join us in theLife Without Bread topic (you might want to start at the end). We're trying to figure it out too. I don't think most nutritionists are going to be able to help much. They are caught in the system like the doctors are, trained in and dispensing "standard advice."

The books we have been reading stand out as containing objective, scientifically-based information, although each has its peculiar strengths and weaknesses. I think there is a list of them mentioned somewhere in the topic. The New Atkins For A New You is quite detailed about what to do, although it doesn't take into account all of the anti-nutrient issues that we know about. It offers a flexible approach, though, and can be easily adapted to avoid unhealthy low-carb foods. Just don't dive directly into "induction." The book doesn't warn people sufficiently about possible reactions to suddenly lowering carbs steeply, I don't think.

 

[Rick Rowe]

That was very informative reading, is this information from online or a book that your getting this information from?.

Both are books. See the last paragraph of each quote for the title, author, etc.

This is definitely something I will be looking into thoroughly. I have a feeling I will have to get a nutritionist in this battle as well, my knowledge to date is minimal when it comes to low carb diets, I am learning slowly but there is so much it seems to learn about what foods are good (low carb) and also keeping track of how much I consume. Any suggestions on how to do this better? Right now I am looking things up online for what foods are low in carbs and it seems everything is carbohydrates and some may be lower, the others have to be reduced down into smaller portion sizes? Am I getting this right?

:)

Join us in theLife Without Bread topic (you might want to start at the end). We're trying to figure it out too. I don't think most nutritionists are going to be able to help much. They are caught in the system like the doctors are, trained in and dispensing "standard advice."

The books we have been reading stand out as containing objective, scientifically-based information, although each has its peculiar strengths and weaknesses. I think there is a list of them mentioned somewhere in the topic. The New Atkins For A New You is quite detailed about what to do, although it doesn't take into account all of the anti-nutrient issues that we know about. It offers a flexible approach, though, and can be easily adapted to avoid unhealthy low-carb foods. Just don't dive directly into "induction." The book doesn't warn people sufficiently about possible reactions to suddenly lowering carbs steeply, I don't think.

Thanks Megan, I have started to read the threads now on "Life without Bread". I will post any further question now there about this topic.
I wanted to know if you knew the names of the other 3 staten drugs that were better more efficient then "Crestor" so I could look them up as well?
Thanks again.

 

[mcb]

Thanks Megan, I have started to read the threads now on "Life without Bread". I will post any further question now there about this topic.
I wanted to know if you knew the names of the other 3 staten drugs that were better more efficient then "Crestor" so I could look them up as well?
Thanks again.

worstpills.org has this:

Rosuvastatin joins fluvastatin (LESCOL, LESCOL XL) as the statins that have not been approved by the FDA to confer a health benefit in terms of reducing the serious cardiovascular consequences of high cholesterol, such as a first or second heart attack or stroke. Lovastatin, pravastatin, atorvastatin and simvastatin have shown such benefits to patients in addition to their cholesterol-lowering properties, and this is reflected in the professional product labels and advertising for these drugs.

If you live in the US and are taking prescription drugs or live with someone who does, worstpills.org can be well worth the $15/year subscription. It may be worth it even if you live elsewhere and cannot find a similar service.

 

[Rick Rowe]

Thanks Megan, I have started to read the threads now on "Life without Bread". I will post any further question now there about this topic.
I wanted to know if you knew the names of the other 3 staten drugs that were better more efficient then "Crestor" so I could look them up as well?
Thanks again.

worstpills.org has this:

Rosuvastatin joins fluvastatin (LESCOL, LESCOL XL) as the statins that have not been approved by the FDA to confer a health benefit in terms of reducing the serious cardiovascular consequences of high cholesterol, such as a first or second heart attack or stroke. Lovastatin, pravastatin, atorvastatin and simvastatin have shown such benefits to patients in addition to their cholesterol-lowering properties, and this is reflected in the professional product labels and advertising for these drugs.

If you live in the US and are taking prescription drugs or live with someone who does, worstpills.org can be well worth the $15/year subscription. It may be worth it even if you live elsewhere and cannot find a similar service.

I am now looking into maybe using the pill called "UIBIQUINOL" I was reading some very good stuff on here with regards to how it strengthens the muscles around the heart which aids and helps increase the blood flow to the heart. It was listed to be a great suppliment either for people who were on "Staten" drugs and also for people who were not on it.

I signed up onto worsrpills.org, here is the continuation to our discussion from there website we had earlier...

Do Not Use! Rosuvastatin (Crestor) - A New But More Dangerous Cholesterol Lowering 'Statin' Drug

Worst Pills Best Pills Newsletter article October, 2003


Rosuvastatin (CRESTOR) became the sixth cholesterol lowering "statin" drug on the U.S. market when it was approved by the Food and Drug Administration (FDA) on August 13, 2003. The other members of the statin family are atorvastatin (LIPITOR), fluvastatin (LESCOL), lovastatin (MEVACOR), pravastatin (PRAVACHOL), and simvastatin (ZOCOR). These drugs are only approved to be used along with a low-cholesterol diet and an exercise program to lower cholesterol.

One of the statins, cerivastatin (BAYCOL), was removed from the market because of at least 31 reports of fatal rhabdomyolysis, an adverse reaction involving the destruction of muscle tissue that can lead to kidney failure (see Worst Pills, Best Pills News October 2001). We had warned patients not to use this drug more than three years before it was removed from the market.

Rosuvastatin will be sold by AstraZeneca of Wilmington, DE under license from Shionogi & Co., Ltd., of Osaka, Japan.

AstraZeneca originally filed its application with the FDA to market rosuvastatin in June 2001. The application was delayed when the company halted clinical trials worldwide after reports of kidney damage and muscle weakness (an early signal for rhabdomyolysis) in clinical trials in patients taking 80 milligrams of the drug per day and the FDA asked AstraZeneca for more data. The company stopped development of the 80 milligram dose because of the safety problems, and rosuvastatin will only be sold in 5, 10, 20, and 40 milligram strengths. Because of safety concerns there will be special restrictions on the distribution of the 40 milligram strength that will be discussed further below.

The Health Research Group made a formal presentation before the FDA's Endocrinologic and Metabolic Drugs Advisory Committee on July 9, 2003 strongly opposing the approval of rosuvastatin because of its unique kidney toxicity. We were also seriously concerned because of seven cases of rhabdomyolysis that were common enough to have shown up in the pre-approval clinical trials of rosuvastatin in which the 80 milligram dose was used. Not one case of rhabdomyolysis appeared in any of the pre-approval studies of the previously approved statins, including cerivastatin, which was removed from the market because of rhabdomyolysis.

As we said in our testimony before the advisory committee, a major factor that distinguishes rosuvastatin from the other five statins remaining on the market is the drug's potential to cause kidney toxicity. In the FDA review documents posted on the agency's web site before the Endocrinologic and Metabolic Drugs Advisory Committee it was noted "In contrast to currently approved statins, rosuvastatin was also associated with renal [kidney] findings not previously reported with other statins."

A number of patients taking primarily the 80 and 40 milligram doses of rosuvastatin had an increased frequency of persistent protein in the urine (proteinuria) and blood in the urine (hematuria), that in some subjects was also associated with another abnormal test result that is an early signal for kidney toxicity known as the serum creatinine level. The FDA documents pointed out that there were two cases of kidney failure and one case of kidney insufficiency with 80 milligrams of rosuvastatin in which these patients also had experienced both protein and blood in the urine.

An FDA medical officer reviewing rosuvastatin had sobering comments on the cases of kidney problems with the drug:

These three cases of renal insufficiency of unknown etiology are of concern because they present with a clinical pattern, which is similar to the renal disease seen with rosuvastatin in these clinical trials. There is mild proteinuria associated with hematuria and the suggestion of tubular inflammation or necrosis [death of cells]. All cases occurred at the 80 mg dose which was also associated with the greatest number of patients with abnormal renal findings in these clinical trials. Proteinuria and hematuria could be potentially managed with regular urinalysis screening. However, if they are the signals for the potential progression to renal failure in a small number of patients, this may represent an unacceptable risk since currently approved statins do not have similar renal effects.

AstraZeneca attempted to "spin" the drug's potential for causing elevated protein levels in the urine by claiming that it was due to a previously unobserved effect of the statin family of drugs. However, the research submitted by AstraZeneca to the FDA did not show a similar degree urine protein elevation with any of the other statins.

The Endocrinologic and Metabolic Drugs Advisory Committee recommended that kidney monitoring be required for patients taking 40 milligrams of rosuvastatin per day. The FDA failed to take this advice, rather, the agency approved this puzzling statement in the Laboratory Tests section of the drug's professional product labeling or package insert:

In the rosuvastatin clinical trial program, dipstick-positive proteinuria and microscopic hematuria were observed among rosuvastatin treated patients, predominantly in patients dosed above the recommended dose range (i.e., 80 mg). However, this finding was more frequent in patients taking rosuvastatin 40 mg, when compared to lower doses of rosuvastatin or comparator statins, though it was generally transient and was not associated with worsening renal function. Although the clinical significance of this finding is unknown, a dose reduction should be considered for patients on rosuvastatin 40 mg therapy with unexplained persistent proteinuria during routine urinalysis testing.

The problem with this statement is that it is very unlikely that the average patient would routinely receive urine testing for protein. National guidelines only recommend the periodic urine testing of people without symptoms who have diabetes or for pregnant women. At a minimum the FDA should have required routine urine testing for all dosages of rosuvastatin.

Any elevation of protein in the urine beyond a trace is abnormal and is a possible signal of more serious kidney problems, even more so if there is also blood in the urine.

A popular buzz word frequently used by the FDA these days is Risk Management - assessing public health risks, analyzing methods for reducing them, and taking appropriate action. The FDA's Risk Management strategy for the safety problems associated with rosuvastatin can hardly be called "appropriate." The 40 milligram tablet will not be stocked in retail pharmacies and the pharmacy would need to go through a wholesaler to obtain the 40 milligram tablets. This would take an extra day before the tablets arrived at the pharmacy. Somehow the FDA believes that "These steps will help to ensure that the 40-mg dose is available only to patients who truly need this dose." To easily beat this restriction, there is nothing to prevent a physician from writing a prescription for 20 milligram tablets and instructing the patient to take two tablets of rosuvastatin daily.

Clearly, the only "appropriate" and safe Risk Management strategy for rosuvastatin would have been not to have approved the drug in the first place.

Rosuvastatin's professional labeling also carries warnings about elevated liver enzymes, an early signal for possible liver toxicity, and muscle pain and weakness that may be precursors to rhabdomyolysis. These warnings appear in the labeling for all statin drugs:

It is recommended that liver function tests be performed before and at 12 weeks following both the initiation of therapy and any elevation of dose, and periodically (e.g., semiannually) thereafter.

Rare cases of rhabdomyolysis with acute renal failure secondary to myoglobinuria [a protein from muscle] have been reported with rosuvastatin and with other drugs in this class.

The professional product labeling goes on to instruct physicians to tell patients "... to promptly report unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever."

The risk of muscle damage leading to rhabdomyolysis during treatment with rosuvastatin may be increased when it is used together with other cholesterol-lowering drugs and cyclosporine (NEORAL, SANDIMMUNE), a drug used after transplantation to prevent organ rejection.

A single rosuvastatin dose given to healthy volunteers on the cholesterol-lowering drug gemfibrozil (LOPID) resulted in a significant increase in the amount of rosuvastatin in the body. There is a bolded statement in the Warnings section of rosuvastatin's labeling stating that "Combination therapy with rosuvastatin and gemfibrozil should generally be avoided." The risk of muscle problems possibly leading to rhabdomyolysis is also increased when niacin is used to lower cholesterol in combination with rosuvastatin.

When rosuvastatin was given together with cyclosporine in heart transplant patients, the amount of rosuvastatin increased significantly in the blood compared with healthy volunteers. This increase is considered to be clinically significant.

When rosuvastatin was given to patients on stable warfarin (COUMADIN) treatment to prevent blood clots, there was a clinically significant rise in the International Normalized Ratio (INR), the laboratory test used to monitor warfarin therapy that can increase the risk of bleeding.

A number of factors went into our decision to list rosuvastatin as a DO NOT USE drug:

1. Rosuvastatin joins atorvastatin and fluvastatin as the statins that have not demonstrated a health benefit to the patients that use them in terms of reducing the serious cardiovascular consequences of high cholesterol such as a first or second heart attack or stroke. Lovastatin, pravastatin, and simvastatin have shown such benefits to patients in addition to their cholesterol-lowering properties and this is reflected in the professional product labels and advertising for these drugs.

The only reliable, valid indicator that consumers can use that a drug has a demonstrated health benefit is if that information is contained in the drug's FDA approved product labeling. Advertising claims for drugs can not be made unless research has been submitted to and approved by the FDA that the drug will actually do what a manufacturer claims it will do.

2. Rosuvastatin causes abnormal elevations in urine protein and blood that are signals for serious kidney toxicity; other statins are not associated with this risk of kidney toxicity.

3. Rosuvastatin is the only statin that has shown life-threatening rhabdomyolysis in pre-approval clinical trials.

In summary, rosuvastatin has no proven health benefit as discussed above, it can cause potentially serious kidney toxicity that is not seen with the other statins, it is the only statin that caused rhabdomyolysis, a life-threatening adverse drug reaction, in pre-approval clinical trials, and there are already three statins on the market that are safer than rosuvastatin and have demonstrated a health benefit to patients.

What You Can Do

There is no medical reason for you to be taking rosuvastatin when there are three safer and more effective statins, in terms of reducing cardiovascular events, on the market.

 

[anart]

Hi Hellfire, I think the ultimate goal here will be to get off medication all together, not to find a 'better pill'. This can be accomplished through diet. Have you had a chance to read the "Life without Bread' thread in the diet and health section?

 

[Nienna]

Hi Hellfire, I think the ultimate goal here will be to get off medication all together, not to find a 'better pill'. This can be accomplished through diet. Have you had a chance to read the "Life without Bread' thread in the diet and health section?

I was about to write something similar, Hellfire. There is no problem with cholesterol. It does not cause heart attacks. Actually, high-carbohydrate diets cause heart attacks, among many other things. Cholesterol is needed in the body.

It really is important to read Life Without Bread, and get the book, along with Primal Body, Primal Mind, and The Art and Science of Low Carbohydrate Living. Pills usually just lead to you needing more pills. That's what the pharmaceutical companies are all about.

 

[mcb]

I am now looking into maybe using the pill called "UIBIQUINOL" I was reading some very good stuff on here with regards to how it strengthens the muscles around the heart which aids and helps increase the blood flow to the heart. It was listed to be a great suppliment either for people who were on "Staten" drugs and also for people who were not on it.

Ubiquinol is a form of coenzyme Q10 (CoQ10) and I have often seen it recommended for people that have been taking statins, to help with healing from the heart damage that statins cause. I do not know if it would be wise to take it concurrently with a statin.

I agree with Anart that it would be better to eliminate the statin rather than replace it with a "better" one, but I don't know your current health status and wouldn't be able to interpret it if I did. The obvious path toward health (eliminate bad things; replace them with good things) doesn't always work when your health has already deteriorated and/or you have become dependent upon medications (which is exactly what "the system" is seeking). I don't want to encourage you to make changes that seem to be for the better but that actually can make things worse.

Ubiquinol, however, is a naturally occurring form of CoQ10 that, once you are off of statins, could help your heart and other organs to recover from the statin side effects.

I have some experience with statins through someone close to me. I can't go into any details without compromising that person's privacy but the bottom line is that if you educate yourself first, you can work with your doctor (or some other doctor if that one proves to be a knucklehead) to withdraw from statin "therapy." You will most likely also have to understand cholesterol and LDL/HDL/trigliceride levels, because it goes against their training to do the right thing. So start reading. :D