Refusing to take statins. What can my doctor do?

I suggested he asked the surgery what his levels were. He came the figure of 5.4!!

From what I have read that is in the "optimum" level of between 5 and 7 mmol/l.

He called the surgery again to check the numbers and they confirmed the 5.4. He then asked why, as he had dieted away a stone in weight and the level appeared quite normal, was he being advised to double the dose. Surgery replied: " We want to get everyone below 5."

Seems to me there could be what may be called a scandal here. People are being asked to take a drug which can have all sorts of side effects with little evidence of benefit so that, according to Dr Phil Hammond in "Trust me I'm still a doctor" the surgery can claim the government payment for reaching the target of 60% of patients below the arbitrary level of 5.

How can constantly making holes in my vein in same area be wise? How do we know what happens when the vein heals? Is there any protrusion inside the vessel? And all because they are treating folks who are not sick.

She said my readings had gone up from 7.3 to 7.4 but eventually removed statins from my prescription. I was speaking with another medical professional at the practice about this and she said that she wouldn't take them either!!

BTW, I did take Benecol for several weeks in an effort to please the doctor with lower levels ( coward that I am ) but it does not seem to have worked in my case.

The fact is, no published studies have tested the impact of stanols or sterols on human health in the long term. One may argue that this is not an issue because we know that cholesterol reduction is beneficial and, so the benefits are almost assured and, anyway, what harm can they do?

Well, the evidence shows that when we take dietary steps to reduce cholesterol through reducing fat in the diet or substituting saturated fat for ‘healthier’ fats, it does not reduce the risk of heart attack or stroke or overall risk of death. This, obviously, casts some doubt on the validity of the assumption that dietary reduction of cholesterol is necessarily a good thing.

The other issue though concerns safety. How do we know if we do not have the long-term studies of the use of stanols and sterols in humans that are even safe? Again, one may argue what’s the harm, seeing as they’re ‘plant-derived’. Well, it turns out there is quite a body of evidence which suggests far from being the wonder-chemicals we’ve been lead to believe them to be, stanols and sterols may pose real and significant risks to health.

The research was summarized in a 2009 paper published in the European Heart Journal.

Several studies link the presence of higher levels of sterols in the blood stream with raised risk of cardiovascular disease. This evidence is epidemiological, which means we cannot conclude from it that sterols actually increase the risk of cardiovascular disease (only that the two are associated with each other). However, more incriminating evidence comes of studies in which the effects of sterols have been tested on tissues or animals in the lab.

In one study, feeding animals with sterols increased what is known as ‘endothelial dysfunction’ – unhealthy changes on the inside of blood vessels associated increased cardiovascular disease risk. The sterols also led to animals having strokes bigger in size than when no sterols were consumed.

In another study, sterols led to an increased level of damaging oxidation and release of free oxygen radicals (oxidative stress) compared to cholesterol, which suggests a greater capacity to induce chronic disease (including cardiovascular disease). Sterols have also been shown to induce cell death (what is known as ‘apoptosis’), including in the cells which line human blood vessels (endothelial cells). In another experiment, giving plant sterols to rats (with high blood pressure and prone to stroke) shortened their life spans.

In summary, there is no evidence that stanols and sterols benefit human health, and quite a few lines of evidence that suggest these substances have potential for harm. Yet, this is the stuff that is marketed on the basis of their assumed value for heart health.

1. Weingartner O, et al Controversial role of plant sterol esters in the management of hypercholesterolaemia. Europlean Heart Journal 2009;30:404-409

2. Relationships of serum plant sterols (phytosterols) and cholesterol in 595 hypercholesterolemic subjects, and familial aggregation of phytosterols, cholesterol, and premature coronary heart disease in hyperphytosterolemic probands and their first-degree relatives. Metabolism 1991;40:842–848

3. Independent association of serum squalene and noncholesterol sterols with coronary artery disease in postmenopausal women. J Am Coll Cardiol 2000;35:1185–1191

4. Association of plasma noncholesterol sterol levels with severity of coronary heart disease. Nutr Metab Cardiovasc Dis 1998;8:386–391

5. Baseline serum cholestanol as predictor of recurrent coronary events in subgroup of Scandinavian simvastatin survival study. Finnish 4S Investigators. BMJ 1998;316:1127–1130

6. Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Munster (PROCAM) study. Nutr Metab Cardiovasc Dis 2006;16:13–21

7. Abstract 4099: elevated campesterol serum levels–a significant predictor of incident myocardial infarction: results of the population-based MONICA/KORA follow-up study 1994–2005. Circulation 2006;114:II_884

8. Vascular effects of diet supplementation with plant sterols. J Am Coll Cardiol 2008;51:1553–1561

9. Oxidized plant sterols in human serum and lipid infusions as measured by combined gas-liquid chromatography-mass spectrometry. J Lipid Res 2001;42:2030–2038

10. Beneficial or harmful influence of phytosterols on human cells? Br J Nutr 2008;100:1183–1191

11. Vegetable oils high in phytosterols make erythrocytes less deformable and shorten the life span of stroke-prone spontaneously hypertensive rats. J Nutr 2000;130:1166–1178