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tom, I wonder if you could help with a question on borderline-high cholesterol. Results of a recent blood test showed; TC: 5.8 mmol/L; HDL: 1.67mmol/L; LDL: 3.86mmol/L; Triglycerides: 0.6 mmol/L. I am 95% compliant to the BTD and eat no grains. Is elevated cholesterol a warning in every case? Is this level within the bounds of acceptability for type ‘O’ Non-sec? Thanks for your time, Regards, Keith
High cholesterol has been associated with cardiovascular disease risk, and the American Heart Association is committed to increasing public awareness of the significance of cholesterol levels (1) A telephone survey of Americans over 40 found that 91% of respondents stated that it was "important to them personally to have a healthy cholesterol level", 51% did not know their own level. Only 40% were aware of national guidelines for cholesterol management, and 53% either did not know or overestimated the correct desirable total cholesterol level for a healthy adult.
The American Heart Association states that “Public awareness and understanding of risk factors for atherosclerotic vascular disease are essential for successful primary and secondary prevention”. The researchers concluded that “public understanding of cholesterol management is suboptimal. Physicians have a unique opportunity, on the basis of public attitudes and access, to improve cholesterol education”.
It is worth looking more closely at “cholesterol education”, and generally accepted risk factors for prevention of cardiovascular disease.
Cholesterol is a hormone providing the basis for all steroids made in the body, including adrenal
hormones and vitamin D. It is found in the blood and in every cell, where it forms part of the cell membrane. The liver, intestines and skin usually provide about 60-80% of the body’s cholesterol, the rest comes from the diet.
Total cholesterol (TC) measurement includes HDL, LDL and Triglycerides (from which VLDL can be estimated). TC Levels are influenced by metabolic rate, and thus can be affected by changes in thyroid or adrenal function.
High cholesterol is not a disease in itself unless genetically high due to a lipoprotein disorder, such as familial hypercholesterolaemia: this is an autosomal dominant disorder of chromosome 19, the heterozygous (more common) form occurs in one in 500 people, making it the most common human genetic disorder.
Other common genetic factors that can affect cholesterol levels are polymorphisms of APO E (Apolipoprotein E), CETP (Cholesterol ester transfer protein), SELE (E-Selectin). A CardioGenomic Profile is available as a screening for these commoner genetic polymorphisms affecting cardiovascular risk, and also includes methylation, coagulation risk and redox balance.
In terms of blood group associations, it is well documented that blood groups A and AB are at higher risk of death from elevated cholesterol levels (2). Blood groups B and O are at higher risk from heart disease as a result of carbohydrate intolerance, rather than from high cholesterol. A higher protein diet will protect blood groups B and O from hypercholesterolaemia, as it increases levels of fat-digesting intestinal alkaline phosphatase enzyme (IAP). IAP may be inactivated by the blood group A antigen, hence the reduced inability of A and AB to metabolise fats. Blood group O, and especially O non-secretors are at highest risk of disease as a result of having elevated triglycerides and obesity along with poor blood lipid profiles (3). In fact non-secretors of all blood groups are likely to have higher cholesterol levels due to lower intestinal alkaline phosphatase (4).
In terms of cholesterol itself, it is therefore important to take blood group and secretor status into account to get a more meaningful idea of cardiovascular risk.
The blood group O diet is designed to be effective in improving cardiovascular parameters in blood group O, “a variance from the conventionally accepted idea that high carbohydrate, low fat diets are the only manner in which to improve cardiovascular parameters” (5). The reduction of dietary lectin ingestion allows better glucose tolerance, which improves the important triglyceride levels.
The MN subgroup can also be a factor in evaluating cholesterol and triglyceride levels: there is an association between MN group with environmentally induced (diet-linked) hyperlipidaemia, with NN more easily able to lower cholesterol levels through diet than MN (6), (7) (8).
Blood tests for cholesterol measurement should be done after a 12-hour fast.
The blood results above (SI units) convert to the following (US):
TC = 224 mg/dL (150-220)
HDL = 64 mg/dL (40-90)
LDL = 149 mg/dL (60-130)
Trigs = 53 mg/dL (30-150)
VLDL [Trigs/5] = 10.6 mg/dL (estimated)
Chol/HDL ratio: 3.5 (<4)
The figures in brackets indicate the standard laboratory reference ranges. It can be seen from these reference ranges that TC is only slightly over the recommended maximum range of 220. This TC is fine, and your HDL and Chol/HDL ratio are also OK if you are otherwise healthy and your BMI is normal, as contrary to popular belief blood group O tends to function better with a cholesterol of over 200. If one wanted to be picky your LDL is a little high, which could be reduced by substituting fish for meat, as DHA, the ‘heart-healthy’ fatty acid found in oily fish actually raises LDL (9) (This apparently contradictory fact shows how unimportant cholesterol levels are without looking at the big picture). Moderate alcohol intake will increase HDL cholesterol. Finally your triglycerides are slightly on the low side (although within the reference range), which is not normally a problem, and could in fact be a result of your high dietary compliance level, but depending on symptoms you could check your thyroid function to be certain.
Should you however still wish to reduce your cholesterol-related risk of heart disease, exercise may be useful. The link with obesity and poor blood lipid profile is well-documented (10), particularly for those with intra-abdominal fat. A 10 kg weight loss can produce a 15% decrease in LDL cholesterol levels and an 8% increase in HDL cholesterol. Apart from reducing refined carbohydrates and hydrogenated fats, the best way to improve your cholesterol score as a group O is vigorous physical exercise according to current fitness levels and individual ability (for those of blood group A it may also be worth looking out for liver/gall bladder congestion). A thyroid blood test will exclude raised cholesterol secondary to hypothyroidism.
[Note: don’t think that if your levels of cholesterol are very low that it means you are super-healthy – a sudden drop in cholesterol can be a sign of disease onset. Kidney problems, some diuretics and pregnancy can also increase cholesterol levels, and high dose vitamin C can make cholesterol appear lower.]
Other tests that can give a more complete picture of possible risk of atherosclerosis are levels of apolipoprotein A and B, plasma homocysteine, and high-sensitivity C-reactive protein.
Other Risk Factors
It must be remembered that many of the connections between risk factors and actual disease have multiple causes. Blood group connections for example should not be interpreted as ‘certain’. There are certainly other lifestyle issues which can erode any statistical correlation. What we should get from the information are ‘trends’ which may be useful as a preventive.
The Cardiac risk calculator (11) will estimate your risk of developing heart disease over the next 5-10 years based on your age, sex, blood group, secretor status, cholesterol levels and other relevant factors. You will find from this that although your non-secretor status puts you at higher risk than a blood group O secretor, you are still at less risk than if you were blood group A or AB if all other variables remain the same.
In terms of orthodox medicine, the preventative treatment of choice for high cholesterol is HMG CoA Reductase Inhibitor medication (statins). These have been so ‘effective’ in reducing cholesterol that they are now on sale over the counter in the UK, and the US is considering following suit. Side-effects include gastro-intestinal disturbances, e.g. abdominal pain, constipation and flatulence, headache and musculoskeletal symptoms, muscle breakdown and death. Not generally listed is the fact that statins decrease the body’s production of Co-enzyme Q10, and long-term exposure to statins may substantially increase the risk of polyneuropathy (12). Why not trade one risk for another!
Alternative Views on Cholesterol
Not everyone sees a clear connection between high cholesterol and coronary heart disease (CHD). Dr. D’Adamo shows evidence that: “there is no clear relationship between the blood cholesterol level and the degree of atherosclerosis in the vessels” (13).
Dr. Malcom Kendrick appears to have made a similar discovery. He interpreted data from an international study of cholesterol and heart disease and found the results directly contradictory to the hypothesis that high cholesterol is related to CHD:
“For myself, all I can see is a French ‘paradox’ and Swiss ‘paradox’ a Russian ‘paradox’ a Lithuanian ‘paradox…My interpretation is that there is absolutely no connection between cholesterol levels and CHD rates in these nineteen different countries” (14).
For those who still feel they may be at risk of heart disease due to long term blood lipid readings, the thickness of the carotid artery may be measured using ultrasound to estimate damage to the heart vessels. When in doubt, evidence of preclinical vascular disease can be found by non-invasive means, such as CAT scanning for coronary calcification, before resorting to potentially harmful pharmaceuticals for which there are many natural alternatives.
1. Nash I.S, Mosca L, Blumenthal RS, Davidson MH, et. al.
Contemporary Awareness and Understanding of Cholesterol as a Risk Factor
Results of an American Heart Association National Survey
Arch Intern Med. 2003;163:1597-1600.
2. Pathbase: Cardiovascular Disease.
3. Pathbase: Hypertriglyceridemia.
4. Blomstrand R, Werner B.
Alkaline phosphatase activity in human thoracic duct lymph.
Acta Chir Scand. 1965 Feb;129:177-91
In Disease Knowledge Base.
5. Clinical Outcomes.
6. Berg K, Borresen AL, Nance WE.
Clin Genet. 1981 Jan;19(1):67-70.
Apparent influence of marker genotypes on variation in serum cholesterol in monozygotic twins.
7. Martin NG, Rowell DM, Whitfield JB.
Clin Genet. 1983 Jul;24(1):1-14.
Do the MN and Jk systems influence environmental variability in serum lipid levels?
8. Birley AJ, MacLennan R, Wahlqvist M, Gerns L, et. al.
Clin Genet. 1997 May;51(5):291-5.
MN blood group affects response of serum LDL cholesterol level to a low fat diet.
9. Theobald HE, Chowienczyk PJ, Whittall R, Humphries SE, Sanders TA.
LDL cholesterol-raising effect of low-dose docosahexaenoic acid in middle-aged men and women.
Am J Clin Nutr. 2004 Apr;79(4):558-63.
10. Dattilo, A.M. and P.M. Kris-Etherton,
Effects of weight reduction on blood lipids and lipoproteins: a meta analysis.
American Journal of Clinical Nutrition, 1992. 56: p. 320-328.
11. Cardiac Risk Calculator.
12. D. Gaist, et. al.
Statins and risk of polyneuropathy.
13. Pathbase: Hypercholesterolemia.
14. Kendrick M.
Cholesterol And The French Paradox, The Swiss Paradox, The Russian Paradox, The Lithuanian Paradox...Etc...
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