Part II of a conversation of a statin lover

This advocate of the low-fat diet and use of statins says,"In the review I cited Dr. Morrison's study and Dr. Esselstyn's study where all-cause mortality was greatly reduced. Meta-analyses of various statin studies also show a significant decrease in all-cause mortality."

Yes, there are those studies that show that people with CHD can obtain a decrease in all-cause mortality when tracked for a limited time-span. There are even studies that show apparently healthy middle-aged people with high cholesterol values receiving a very limited absolute decrease in overall mortality over a limited time span. But I wonder if there would be any advantage if the study were carried out over a time span of 15-20 years. The use of statins markedly decrease more than one substance that is needed to maintain life processes. This should be no surprise since these statins are no more than subtle rearrangements of the particular statin found in red-rice yeast, which maintains a symbiotic relationship with red rice. The statin substance in the yeast tends to protect the red rice from the predations of animals that would like to feed on red rice. In effect, people that use statins are using a substance that evolved as a poison.

Long-time users of statins would have to contend with increasing incidence of muscle weakness, depression, foggy memory, increased rate of traffic accidents and awareness that one could irreversibly damage one's liver. 

The Framingham results showed that for people over fifty, high cholesterol was not a risk factor. 

A workshop hosted by the National Heart, Lung, and Blood Institute reviewed 19 studies in 1990 and found that for women, if anything, the higher the cholesterol, the longer they lived.

Part I of a conversation with a statin advocate

The statin advocate says,
"Glucose is the energy of life. You can't live without it. If it's too low you go into a coma and die. But that doesn't mean you can't have too much. LDL is also essential but you can still have too much. Just because glucose is essential doesn't mean the body always does a good job of regulating it and just because LDL is essential doesn't mean the body always does a good job of regulating it either."

The equivalency between glucose and LDL is weak. It is well established that excessive glucose causes glycation of tissues. It is not well established what harm excessive LDL levels cause. Does it directly cause plaques to form? No experiments have ever established this. Only speculation exists. Some scientists think that the cholesterol existing in plaques are byproducts of the body fighting bacteria present in the artery and also the repair process where the endothelium is injured. Granted there may be optimum LDL levels but they vary with choice of diet, exercise, presence of infection, and stress levels. The body responds by attempting to establish those optimum levels for the environmental conditions. Sometimes the body is not successful if a poor diet or chronic stress is imposed.

The body also tries to set optimum conditions for blood sugar levels under given environmental conditions. However, a high-carb diet can force these blood-sugar levels to values that cause harm to the body. The correct approach is to change the environmental conditions to bring these levels down to the normal range. This approach would be to use a low-carb diet. One would not want to use insulin to force the blood sugar to lower levels as this would only increase insulin resistance and make the underlying problem worse. Likewise LDL levels can be forced higher than the normal range by environmental factors. Again the environmental factors should usually be changed to try to bring the LDL levels back in the normal range. Sometimes this is difficult and one can only try to optimize the VAP results where triglyceride levels, fluffiness of LDL particles, etc. are all considered.

Below is an assertion that is made by the statin advocate who obviously believes that high LDL levels are a direct cause of atherosclerosis.
"What's the best way to figure out how much LDL is normal and healthy? Look at modern hunter gatherers and free living mammals. Their LDL is 50 to 70 mg/dl and they have no heart disease. The LDL level for the average American is about twice that much. If you read peer reviewed scientific articles which try not to go beyond the evidence - instead of Dr. Ravnskov's highly biased books which completely ignore evidence that doesn't support his extreme claims - it is very clear that LDL is strongly associated with atherosclerosis, heart attacks and all-cause mortality."

The statin advocate holds up the modern hunter-gatherer's (MHG's) LDL levels as ideal. The diet of MHG's varied widely. The Masai dined mostly on meat, blood and high saturated fat milk. They had little heart disease but their kin who lived in urban areas had abundant heart disease. The traditional Inuit had little heart disease but did have appreciable incidence of hemorrhagic stroke. They ate meat and less-saturated fat. There are other MHG's who had a higher carbohydrate intake but restricted calories and they also fared well. Nevertheless, most of these MHG's are infested with parasites. Most parasites excrete substances that lower the body's inflammation response to protect them. These substances may also lower the LDL levels in the body as LDL is involved in the inflammation response. The lowered inflammation response may cause less plaque buildup when the endothelium is being repaired and thereby reduce the risk for CHD. On the other hand, the lowered immune response might be a disadvantage in fighting bacterial and viral infections.

Statins also lower the inflammation response but at what price? Muscle damage, depression, etc. can result

Even if one were on an MHG diet, one might not be able to achieve these low levels of LDL if the diet were combined with the modern way of life sans parasites or statins.

I am really interested in total mortality rates rather than CHD mortality rates. These cholesterol and statin people like to focus on CHD mortality rates. I would rather die of a heart attack than cancer.

The Story of Bottled Water (2010)

Risk Associated with High Cholesterol Levels

Statins are generally recommended by drug companies for people who test above a certain LDL level. These cut-off values have been lowered through the years to such an extent that a large segment of the elderly population are advised to take statins. Implicit in the recommendation is the assumption that, since lower cholesterol levels are associated with lower risk levels, a drug that lowers cholesterol would return one to the risk level for a person with lower cholesterol levels. This assumption is questionable since cholesterol levels can be correlated with cortisol levels, infection levels, etc. Rather, cholesterol may be a marker for some other condition. This assumption has been discussed in more detail in one of my prior blogs.

Statins lower the risk for only a small segment for people with higher cholesterol levels. For elderly people without coronary heart disease, there does not seem to be a basis for these recommendations. According to the Framingham study, men with high cholesterol that are older than 47 years old are as well off or better off than people with low cholesterol¹. For women of any age, high cholesterol levels are not a risk factor². In fact, for older women, the higher the cholesterol levels the less the mortality risk. High cholesterol levels are also not important in elderly Australian men³. There are other papers in agreement with these findings and they are summarized and discussed in these books^4,5.

For those people with coronary heart disease there seem to be tradeoffs. Statins lower clotting factors but they also inhibit production of COQ10, dolichol,.and pyrroloquinoline quinone (PPQ). COQ10 and PPQ are both needed to facilitate mitochondria functioning⁶. Dolichol is needed for proper brain functioning. To lessen the bad effects from taking statins, one can obtain COQ10 and PPQ as supplements. The restoration of dolichol levels to former values is more problematical.

1.      1. Anderson KM et al. JAMA 257,2176-80, 1987.

2.      2. Oliver MF. Lancet 2, 655,1982.

3.      3. Simon LA et al. Atherosclerosis 117, 107-18, 1995.

4.      4. Ravnskov U. Fat and Cholesterol are Good for You, GB Publishing, Sweden 2009.

5.      5. Kendrick, M. The Great Cholesterol Con, John Blake Publishing, London 2008.

6.      6. Graveline, D. The Statin Damage Crisis, Duane Graveline Publishing, 2009.

Framing of Cholesterol as a Cause of Heart Disease

Faulty Arguements in Assigning Cholesterol as a Cause of Heart Disease

In reviewing the book “Good Calories, Bad Calories” by Gary Taubes I found pages 62-64,which follow immediately below this discussion, very interesting and worthwhile to think about further and discuss.  On these pages Taubes discusses how little one might benefit by lowering cholesterol. 

The first graph on page 63 shows the heart-disease mortality and serum cholesterol level for men ages 35 to 57[Stamler et al.]. I assume that this population includes people who have had a pre-study heart attack along with people who have not had a heart attack.  This curve is often shown by statin proponents except it is usually shown in terms of relative risk, which makes the results seem more impressive.

The first graph can be used to argue that decreasing the cholesterol level can reduce heart disease mortality rates. The assumption is implicitly made that cholesterol is causing heart disease. Down to a certain minimum, the lower the cholesterol levels the better. Thus, one might use a drug to optimally lower the cholesterol level.

By agreeing to frame the discussion this way, Gary Taubes loses an opportunity to emphasize that the high cholesterol levels do not necessarily directly cause heart disease. Rather, high cholesterol levels are positively correlated with age, obesity, high triglyceride levels, increased stress, infection, high blood pressure, raised clotting factors, and increased visceral fat mass. These conditions may exist singly, partially or altogether with high cholesterol levels and are all risk factors, even without the accompaniment of a high cholesterol level. If a drug is given to lower cholesterol, the other risk factors remain unless the drug also lowers the presence of another risk factor. In fact, statins do lower the clotting factor levels. Thus, one cannot make the statement that by lowering the cholesterol level with a statin, heart disease mortality is lowered only by lowering the cholesterol level.

The next graph on page 64 shows total mortality as a function of serum cholesterol. Here it appears that from serum levels of 170 to 260 there is very little difference and the wiggles in the curve only give an idea of the accuracy of the data. As discussed before, the graph presents results for men between 35 and 57 years of age.  However, from the Framingham study[Anderson et al] it is shown that the risk is almost independent of the cholesterol level for those men over  47 years old. The risk as a function of cholesterol level would be almost constant and the graph curve would appear as nearly a horizontal line going out to the right. For elderly women the line to the right would be downward sloping [Simon LA et al.].  In other words elderly apparently healthy people would receive no net benefits by only lowering their cholesterol levels.

Above 200, experts recommend statins. According to this graph this recommendation would appear unwarranted and, perhaps, motivated again by greed. In fact, if the cutoff were below 260, one could say the recommendation was unwarranted. Here again, Gary Taubes agrees to frame the argument in terms of  how much mortality would be reduced by lowering cholesterol by diet, etc. Again, this argument is not valid because cholesterol levels are interwoven with and sometimes is a function of other risk factors. If the cholesterol were lowered by some method that did not reduce any other risk factor, the mortality rate might even go up. Suppose that one had a chronic infection and this might also raise the cholesterol level. Because cholesterol is involved in fighting infections,  lowering the cholesterol level may result in one becoming more vulnerable to the infection.

It may be asked why cholesterol levels rise with the other risk factors, for instance, infection and stress, etc. At least part of the answer, without going into a detailed description of mechanisms (even if I could), has to do with the maintenance of homeostasis. Homeostasis is involved in regulation of levels for cholesterol, temperature and glucose, to name a few of almost innumerable levels. The most obvious manifestation of of homeostasis acting on cholesterol is the relative invariance of cholesterol levels with choice of diet. The level of cholesterol is very insensitive to the dietary intake of cholesterol.

Levels other than cholesterol are often altered by external stimuli such as, for instance, infection. The infection will cause the body temperature to rise in order to fight the infection. A raised temperature becomes the optimal temperature for increased chance of survival.  Likewise infection will cause the cholesterol level to rise to enhance the immune response for increased chance of survival. Another example is stress, which causes increased production of cortisol and in turn increased production of cholesterol. This reaction, among others, initially prepares one for fight or flight.

Statins (Lipitor, etc.) are a class of drugs that lower cholesterol levels.  Ingestion of statins may interfere with homeostasis although the use of statins may be desirable in some very limited cases, such as might occur for some atherosclerotic conditions. Even though the statin may undesirably lower the levels of cholesterol, COQ10, dolichol,.and pyrroloquinoline quinone (PPQ) [Graveline, D.], it also lowers the clotting factor levels in the blood. The possibly detrimental effect of lowering these other levels may, for people who have coronary heart disease, sometimes be outweighed by the positive effect on the clotting factor levels in the blood. However, when one has coronary heart disease with congestive heart failure the case for prescribing statins is weakened by the deleterious effect of lowering the COQ10 level, which is involved with the mitochondria activity that is needed to furnish fuel for the heart muscle.

The argument for statins to treat high cholesterol levels is somewhat analogous to that for using Tylenol to treat a fever. When infection occurs, the body temperature is raised in order to more efficiently fight the infection. However, when the body temperature goes above a maximum value, Tylenol may be needed to forestall convulsions, etc.. Likewise when the cortisol levels are high, which causes the clotting factors to rise along with cholesterol levels, statins may be prescribed to lower the clotting factors to forestall CHD from worsening even though the rise in cholesterol level may have a beneficial effect.


Below is Taubes text.

Page 62   THE FAT-CHOLESTEROL HYPOTHESIS

One striking fact about this evolution is that the low-fat diets now being recommended for the entire nation had only been tested twice, as I've said, once in Hungary and once in Britain, and in only a few hundred middle- aged men who had already suffered heart attacks. The results of those trials had been contradictory. The diets tested since then had been exclusively cholesterol-lowering diets that replaced saturated fats with unsaturated fats.

The rationale for lowering the total fat content of the diet to 30 percent was the tangential expectation that such a diet would help us control our weight. In 1984, the year of the NIH Consensus Conference, Robert Levy and Nancy. Ernst of the NHLBI had described the state of the science this way: "There has been some indication that a low-fat diet decreases blood cholesterol levels," they wrote. "There is no conclusive proof that this lowering is independent of other concomitant changes in the diet (for example, increased dietary fiber or complex carbohydrate. . . or decreased cholesterol or saturated fatty acid level).... It may be said with certainty, however, that because 1 g fat provides about 9 calories—compared to about 4 calories for 1 g of protein or carbohydrate—fat is a major source of calories in the American diet. Attempts to lose weight or maintain weight must obviously focus on the content of fat in the diet." Though this was an untested conjecture (however obvious it might seem), the official healthy diet of the nation was now a low-fat diet. A new generation of diet doctors, the most influential of whom was Dean Ornish, were even prescribing io-percent-fat diets, if not lower.

Another striking aspect of the low-fat diet recommendations is how little any individual might benefit from lowering his cholesterol.* Keys and others had argued that heart disease had to be prevented because its first symptom was often a fatal heart attack. But in twenty-four years of observation, the Framingham Heart Study had detected no relationship between cholesterol and sudden cardiac death. The likelihood of suffering a fatal first heart attack was no less for those with a cholesterol level of 18o mg/dl than for those with 250. "The lack of association between serum cholesterol level and the incidence of sudden death suggests that factors other than the atherosclerotic process may be of major importance in this manifestation of coronary artery disease," explained Thomas Dawber.

* Though women were clearly meant to adhere to the low-fat guidelines, they had not been included in any of the clinical trials. The evidence suggested that high cholesterol in women is not associated with more heart disease, as it might be in men, with the possible exception of women under fifty, in whom heart disease is exceedingly rare.


Page 63

                 

  

There is also little to gain from lowering cholesterol even in less catastrophic manifestations of the disease. This was made clear in 1986, when Stamler published a reanalysis of his MRFIT data in JAMA. As Stamler reported it, the MRFIT investigators had continued to track the health of the 362,000 middle-aged men who had originally been screened as potential candidates for MRFIT, including death certificates. Stamler reported that the cholesterol/heart-disease association applied at any level of cholesterol, and so anyone would benefit from lowering cholesterol.

Using the MRFIT data, however, it is possible to see how large or small that benefit might be (see chart, below). For every one thousand middle- aged men who had high cholesterol—between, say, 240 and 250 mg/dlight could expect to die of heart disease over any six-year period. For every housand men with cholesterol between 210 and 220, roughly six could expect to die of heart disease. These numbers suggest that reducing choesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand). If we were to stick rigorously to a cholesterol-lowering diet for thirty years—say, from age forty to seventy, at which point

The health effects of drinking soda - quotes from the experts

The health effects of drinking soda - quotes from the experts

Plumpy'nut - Wikipedia, the free encyclopedia

Plumpy'nut

A recent report by 60-minutes examines this “miracle food”:

Every year, 5 million children die worldwide from malnutrition. That’s one child every six seconds. Now, the relief group Doctors Without Borders says it has something that can save millions of these children. It’s called “Plumpy’nut” – a ready to eat and cheap to produce food that might be the most important advance ever in the fight against malnutrition. Anderson Cooper saw the benefits of plumpy’nut firsthand in the African nation of Niger.

Here are the food specifications provided by the World Food Programme:

Plumpy’Nut [Nutriset] Formula:

• Peanut Butter
• Dry Skim Milk
• Lactoserum
• Malto-dextrine
• Sugar
• Minerals & Vitamins

Composition (per 100g):

• Energy 545 kcal
• Proteins: 13.6g
• Fat: 35.7g

Minerals (per 100g):

• Sodium: <290>
• Calcium: 300 mg
• Phosphorus: 300 mg
• Magnesium: 92 mg
• Zinc: 14 mg
• Iodine: 100 mcg
• Potassium: 1,111 mg
• Copper: 1.8 mg
• Selenium: 30 mcg
• Iron: 11.5 mg

Vitamins (per 100g):

• Vit A: 910 mcg
• Vit D: 16 mcg
• Vit E: 20 mg
• Vit K: 21 mcg
• Vit C: 53 mg
• Vit B1: 0.6 mg
• Vit B2: 1.8 mg
• Niacin: 5.3 mg
• Vit B6: 0.6 mg
• Ac. Folic: 210 mcg
• Vit B12: 1.8 mcg
• Biotin : 65 mcg
• Ac. Panto: 3.1 mg

Oddly enough, this formulation is patented. One cannot make this food to sell or, I think, to even be given away by a nonprofit corporation. The amount of milk powder in each packet is made from a glass of milk. The total energy content of a serving is 500 kcal.

This is also an interesting link concerning Plumpy'Nut. In this link and other links, it is claimed that the recipe uses vegetable oil. Another link claims it is soybean oil. This might not be the best choice of oil, since soybean oil consumption tends to lower thyroid activity. A better choice might be coconut oil since it will not lower thyroid activity but also has antibacterial and antivirus activity. Also coconut oil will be more effective against spoilage and will not go rancid.

Plumpy'nut - Wikipedia, the free encyclopedia