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...
Red Flags Weekly.
The UK government Food Standards Agency (FSA) has published advice recommending maximum consumption levels of oily fish for different groups according to age and reproductive status. Expert advisors examined the benefits of eating oily fish against the possible risks from consuming pollutants such as dioxins. The Agency's recommendation is that men and boys, and women past childbearing age can eat up to four portions of oily fish a week. Women of childbearing age, including pregnant and breastfeeding women, and girls, can eat up to two portions of oily fish a week.
The FSA report says that there is good evidence that eating oily fish reduces the risk of death from heart disease. Some oily fish contain chemicals such as dioxins and polychlorinated biphenyls (PCBs), which accumulate over time in the body and could have adverse health effects if consumed over long periods at high levels. The levels of dioxins in oily fish vary, and some types of fish tend to have higher levels than others. The FSA recommendations are based on people eating different types of oily fish: people should eat at least two portions of fish a week, one of which should be oily. A portion = 140 g (5 oz)
White fish: no limit
Girls (under 16), breastfeeding or pregnant women and those who may become pregnant: Up to 2 portions a week
Boys (under 16), men, and women who are not intending to, or can't become pregnant: Up to 4 portions a week
Marlin, shark, swordfish (heavily contaminated due to being at the top of the food chain):
Girls and boys (under 16), pregnant women and those who may become pregnant, breastfeeding women: do not eat
Men, and women who are not intending to, or can't become pregnant: Up to 1 portion a week.
Fresh tuna counts as oily fish, but tinned tuna counts as white because the oils are lost in the canning process. There is no consumption limit for tinned tuna, except for pregnant women and those who may become pregnant: Up to 4 medium-sized cans per week [presumably the canning process also destroys the PCBs and dioxins in the tuna].
The full report can be downloaded as a PDF from the FSA web site
It also lists the types of fish considered oily, and white (non-oily) fish.
The UK Vegetarian & Vegan Foundation have, not surprisingly, produced a response to the claim that eating oily fish is healthy in a report on their web site.
Plant sources of essential fatty acids (EFAs) as an alternative to those from fish are listed in the report.
The report says to ensure an adequate intake of alpha linolenic acid, good plant sources should be included in the daily diet, including green leafy vegetables, seeds, whole grains, beans and nuts, and flaxseed oil, Minimising consumption of omega-6 rich vegetable oils (especially corn oil, sunflower oil and safflower oil) and commercial oil-based processed foods will also help increase the omega 3 to omega 6 dietary ratio. The best way to buy and store nuts, seeds and their oils is in very small quantities and to keep them in the fridge for freshness. These oils are not suitable for heating as it destroys the beneficial fatty acids. They are best used as a cold salad dressing.
The report also notes that farmed salmon can contain two to three times less omega-3 fats as well as 15% less protein. Farmed fish can also contain chemical pesticide residues as well as dangerous levels of PCBs.
Of course neither of these reports take individuality into account when examining the health benefits of EFAs in oils. Those who have a genetic tendency to cardiovascular disease are people with blood group A, who will get the benefit from eating fish instead of meat.
The potential human health effects of dioxins and PCBs may also include damage to the immune system, infertility, birth defects, and altered levels of sex hormones. These are not yet known to have blood group specificity [although the next IfHI conference may enlighten us on this].
This is an example of how difficult it is to decide whether a basic food product such as fish is going to be healthy to eat. The FSA guidelines advise those who are likely to become pregnant to avoid swordfish, for example. Should restaurants therefore restrict the sale of meals containing this popular seafood to girls and young women unless they confirm that they are not intending to have children?
The only answer is to keep as healthy as possible while avoiding industrial processes that contaminate the sea, and encouraging environmentally friendly alternatives to polluting practices. It may take generations to clean up the damage that has already been done, but at the very least we should stop making it worse.
The book Eat Right for Your Baby contains detailed information on which food to avoid before and during pregnancy according to ABO blood type, including certain types of fish high in mercury.
A UK national tabloid newspaper the ‘Daily Express’ today ran the front page story with the headline: ‘THE DNA DIET MIRACLE – Greatest medical breakthrough in 100 years could save your life’.
The story follows a presentation to the annual meeting of the British Association for the Advancement of Science by a UK company offering DNA testing. The newspaper reports how British nutritionists have apparently developed a groundbreaking diet programme based on detailed analysis of DNA, to set out exactly what each person as an individual should and should not eat for the rest of their life.
The company claims to be “the first in the world to offer a nutrigenomic diet”, and that “a person’s genes should effectively recommend exactly what he or she eats.”
These ‘revelations’ will come as no surprise to the millions of readers of Dr. Peter D’Adamo’s books, many of whom have been following a diet tailored to the information on their gene 9q37 (ABO blood group) for years. Some have looked into further refinement of this knowledge of how genetic inheritance affects interaction with food and the environment by finding their secretor status (gene 19q13.3).
It is good that nutrigenomics is finally reaching the mainstream, although unfortunately no mention of blood groups in connection to diet is made in the article. Perhaps it is because people can find out this information for free by becoming a blood donor and then borrowing a book from the library, rather than having to have a relatively expensive DNA test via their doctor, that the laboratory have not promoted this important element of nutrigenomics.
Genetic testing can be useful where there is a strong family history of certain diseases, or where people want to find out more information about their risks. Testing can cover frequent polymorphisms such as:
* APO E (APOLIPOPROTEIN E), where certain variations can have a role in blood lipids abnormalities and in cardiovascular disease, Alzheimer disease, multiple sclerosis and in age-related macular degeneration. The genetic code responsible for polymorphisms of APO E is found at location 19q13.2. It is interesting how the location of this significant gene is such a close neighbour of the gene for ABH salivary secretor status mentioned above (19q13.3), and how it has been found that non-secretors tend to be more prone to many of these problems. Dr. D’Adamo has found that ABO blood group and secretor status have many genetic linkages with diseases (see Pathbase on this website for details).
The following link is for the entry in the Online Mendelian Inheritance in Man™ database on the scientific background to that gene and genetic disorder: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=107741
* GSTM1 (GLUTATHIONE S-TRANSFERASE M1): people lacking this enzyme found at 1p13.3 (and related enzyme GSTP1) have reduced ability to metabolize environmental carcinogens or toxins from the liver and kidneys. http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=138350
* MTHFR (Methylenetetrahydrofolate reductase): a defect in this enzyme located at gene 1p36.3 can lead to high levels of homocysteine, which can increase the risk of heart disease. http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=607093
A Genomic Profile can be obtained via the D’Adamo clinic in the US, or via Canterbury Osteopathic Clinic in the UK in addition to full blood grouping. This is a screening test for some of the commoner genetic polymorphisms affecting risks for specific problem areas. A consultation is required to determine which Genomic Profile is most appropriate, and a sample of blood or saliva is used for DNA analysis.
The ‘DNA Diet’ nutrigenomics story was also covered by ‘The Scotsman’, and can be read online at: http://news.scotsman.com/uk.cfm?id=1066652004
Research shows that non-secretor mothers are less able to protect their babies from infection with the Norwalk virus (NV) through breastfeeding than secretor mothers (1). Breast milk contains many secreted carbohydrates, including the blood group antigens, however non-secretors lack the ability to secrete their blood group antigens in their breast milk and other fluids.
It is already known (2) that secretors of their blood group antigen are more at risk of contracting gastroenteritis from NV infection, except for individuals of blood group B (3), who are at less risk of developing symptoms.
The Norwalk virus is the main cause of gastroenteritis “food poisoning” infection of a non-bacterial source. NV has a ligand that attaches to the A and H antigens in the saliva and digestive tract of blood groups O, A and AB to take hold and infect the host, but only in secretors. A ligand is a molecule that binds to another chemical entity to form a larger complex, like the agglutination of blood group antigens by lectins.
Symptoms of NV infection are: nausea, vomiting, diarrhoea and stomach cramps. Infected people usually recover in 2 to 3 days without serious or long-term health effects.
The new research shows that the milk of secretor mothers inhibits the attachment of NV to the receptors in their baby, but non-secretor mothers lack this protective secretion. Therefore non-secretor mothers are less likely to contract gastroenteritis from NV, but their babies may be at higher risk than babies of breastfeeding secretor mothers.
Suggested ways to limit the spread of Norwalk virus include:
• Wash hands with soap and warm water after toilet visits and before preparing or eating food;
• Cook all shellfish thoroughly before eating;
• Wash raw vegetables before eating;
• Dispose of sewage, including soiled nappies, in a sanitary manner.
Read ‘Eat Right 4 Your Baby’ to learn about ways of looking after your child while pregnant and breastfeeding.
1. Le Pendu, J
Histo-blood group antigen and human milk oligosaccharides: genetic polymorphism and risk of infectious diseases.
Adv Exp Med Biol, January 1, 2004; 554: 135-43.
2. Marionneau S, et. al.
Norwalk virus binds to histo-blood group antigens present on gastroduodenal epithelial cells of secretor individuals.
Gastroenterology. 2002 Jun;122(7):1967-77.
3. Hutson AM, et. al.
Norwalk virus infection and disease is associated with ABO histo-blood group type.
J Infect Dis. 2002 May 1;185(9):1335-7.
Dozens of new infectious diseases are likely to emerge over the next 25 years unless humans acquire an ecological perspective on infection rather than seeing microbes as simply an invading entity that should be blindly attacked with antibiotics or used as a tool for biological warfare.
According to Professor Tony McMichael, director of the National Centre for Epidemiology and Population Health at The Australian National University, Canberra, the emergence and spread of 35 new or newly diagnosed infectious diseases in the past 25 years is a product of our modern way of life.
A conference at the UK Royal Society exploring the factors influencing emerging infectious diseases was told that the rise in international travel, overcrowded cities, intensive food production, sexual practices, poverty, and global warming were some of the ingredients that had come together to form a suitable culture medium for the emergence, maintenance, and spread of new infectious diseases, as well as allowing the resurgence of older diseases such as cholera, tuberculosis, and malaria.
Hepatitis C was given as an example of a disease born from sociotechnological change. "The advent of illicit intravenous drug use and blood transfusion has allowed the wider spread, and now recognition, of this virus."
The impact of the massive increase in international travel has allowed the spread of new diseases such as HIV and severe acute respiratory syndrome (SARS) on an unprecedented scale.
The way in which humans have changed their environment has also influenced the spread of disease. Developments in agriculture, urbanisation, and deforestation have all changed ecosystems and allowed the emergence of infections. Lyme disease, a disease spread by ticks, was first identified in 1976, in the United States. Forest fragmentation, loss of predators, and the shift of suburbia closer to woodlands are all implicated in the appearance of this disease.
Another example is the Nipah virus. In 1999 this virus killed 100 people in peninsular Malaysia. The virus was normally carried by the forest fruit bat and had not previously seemed to pass to humans. However, because of deforestation and agricultural techniques the bat’s normal habitat and food source were changed. This forced the bats to encroach into fruit plantations, which were in close proximity to pig farms. The bats infected the pigs, which in turn infected the farmers.
Professor McMichael concluded by emphasising the need to acquire an ecological perspective on infectious diseases. "In the 1970s, eminent people were saying it was the end of the infectious disease era. We now find after the experience of the 1980s and 1990s, we are sadder and wiser."
Infection is not to be feared – bacteria are an essential part of the natural life cycle of the environment. Many bacteria are essential in the gut as they manufacture vitamins. Bacterial decomposition is a way of recycling unhealthy, dead or dying material back to its constituent elements. Pathological bacteria cannot grow on a healthy ‘soil’, or ground substance. Mucous membranes are moist warm surfaces such as the lining of the nose, sinuses, lungs, genitals, and the lining of the gut, ideal breeding ground for bacteria. All of these surfaces secrete blood group antigens (in secretors), Lewis antigens and many other protective molecules. These are our first line of defence (apart from substances introduced directly into the blood stream) – keeping the mucous membranes healthy and clean is vital to overall health, and that includes health of the intestines.
Put only the correct food into the intestines to prevent congestion and decay in the mucous membranes of the body, and use your knowledge of blood group and secretor status to choose the foods that are most suitable to you. This is, after all, the reason why each food has been classified according to its interaction with the individual intestinal environment.
Bacteria and viruses are not the cause of disease, they are a sign that a diseased organism (the body, the mind, the surrounding environment, exposure to toxic pollutants and susceptibility due to inherited weaknesses) has allowed a pathological process to bring about decay and decomposition. The symptoms that go with disease (inflammation, swelling etc.) are an indication that the natural healing processes of the body are active. Rather than poison the symptoms and suppress the cleansing mechanisms, encourage the eliminative processes and allow the internal healer to do its work.
British Naturopath Roger Newman-Turner says: “It is widely believed that healthy, well-nourished cattle will develop a natural immunity to Foot & Mouth Disease (FMD), or recover without long-term harm. In this context it should be emphasised that ‘health’ is not synonymous with ‘hygiene’ or asepsis. The antibiotic-ridden cow is the antithesis of a healthy animal. It could even be argued that an obsession with sterility has weakened the immunity by removing natural challenges to inherent defence mechanisms.
“It is high time this hypothesis was put to the test with properly conducted trials. It is not a new idea. Nearly fifty years ago, during the 1952 epidemic of FMD, my father, F. Newman Turner, invited the Ministry of Agriculture and the Animal Disease Research Centre at Pirbright to allow infected animals to mix freely with his herd of pedigree Jerseys. They had been reared organically, were never vaccinated, and were treated only with herbal medicines when the need arose.
“He based this challenge on the experiences of Sir Albert Howard, who had conducted a similar experiment with his pedigree oxen in India in the nineteen-thirties. Sir Albert had allowed his naturally reared animals to rub noses with neighbouring herds infected with FMD. None of his animals contracted the disease.
“F Newman Turner’s challenge was ignored - Pirbright did not even acknowledge his letters - but at least, fifty years later, some people are acknowledging that FMD might partly be the consequence of the intensive farming practices about which he was warning people then.”
The moral of the story is: Live peacefully with nature - any change in the environment in the name of development of human society must be ecologically sound and sustainable. To cure health problems first remove the cause.
New infectious diseases will continue to emerge. BMJ 2004;328:186 (24 January 2004)