Monday, June 28, 2010


Apolipoprotein E (ApoE), a blood test to predict premature cardiovascular and/or Alzheimer’s disease, was prohibitively expensive until June 2010. The Atherotec corp then reduced the price to less than $100 as an add-on study to the VAP (Vertical Atherogenic Profile) which is paid for by most insurance. This would include about 50 other very helpful tests as mundane as a blood sugar to the extremely sophisticated Plac2. This examines for the plaque burden of your arteries as of the moment the blood is drawn.

Regarding the ApoE each of us are given two copies (alleles} of the ApoE at birth and they remain that way lifelong. Therefore the test never has to be repeated again. There is no ApoE e1. We have one each of 2,3, and 4. A person can have e2/e3 or e2/e4 or double of each such as e4/e4. Those with ApoE e2/e2 alleles are at a higher risk of premature vascular disease, although some may never develop disease depending on their lifestyle. Likewise, they may have the disease and not have e2/e2 alleles because it is only one of the factors involved. Our genes cannot change but they can be modified by our diet, exercise and medications. ApoE genotyping adds additional information and, if symptoms are present, e2/e2 can help confirm type III hyperlipoproteinemia a cardiovascular risk factor. This has Chylomicron (Fat/triglyceride globules) remnants and very low density lipoprotein (VLDL) particles which should be rapidly removed from the circulation by the liver. Apolipoprotein E, the main component of the chylomicron and VLDL, binds to a specific receptor on liver cells for disposal. In reference to e2 lipid abnormalities, it will improved lipids with alcohol consumption and there will be little response to diet. With e4, the lipids will improve with a low fat diet. So ApoE is an important determinant of metabolism and treatment of abnormally high lipids.

In addition to predicting age of death ApoE from cardiovascular disease, it predicts
Alzheimer’s(AD), perhaps a fate worse than dying of heart disease. AD is the most common form of dementia. This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuropathologist, Alois Alzheimer in 1906 and was named after him Generally, it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's does occur before this age. In 2010, there were 30.6 million sufferers worldwide. Alzheimer's is predicted to affect 1 in 85 people globally by 2050. And the ApoE test will go a long way to forecast it so you can do things NOW to prolong its onset and even prevent it!

The earliest observable symptoms are often mistakenly thought to be 'age-related' concerns, or manifestations of stress In the early stages, the most commonly recognized symptom is inability to acquire new memories, such as difficulty in recalling recently observed facts. As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. When AD is suspected, the diagnosis is usually confirmed with behavioral assessments and cognitive tests, such as a MMSE or a CDR and often I order a MRI looking at the hippocampus volume and if in real doubt a PET scan with a PIB contrast. Individual prognosis is difficult to assess, as the duration and severity of the disease varies much from patient to patient. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis.

Over 60% percent of those who have late onset AD have paired ApoE e4 (e4/e4) alleles. While genetic mutations of the PSEN1, PSEN2, and APP genes are associated with AD in a very small number of specific family lines, they are associated with early onset AD, rather than late onset. The E4 variant is the largest known genetic risk factor for late-onset AD in a variety of ethnic groups. Caucasian and Japanese carriers of 2 E4 alleles have between 10 and 30 times the risk of developing AD by 75 years of age, as compared to those not carrying any E4 alleles. Research suggests an interaction with amyloid. AD is characterized by plaques consisting of amyloid. Apolipoprotein E enhances proteolytic break-down of this peptide, both within and between cells. ApoE-4 is not as efficient as others at catalyzing these reactions resulting in increased vulnerability to Alzheimer's in individuals with this gene. Among ApoE4 carriers, another gene, GAB2, is thought to further influence the risk of getting AD. However, the relationship does not appear as strong as e4, since in the Japanese population, gab2 is not a risk factor. There is also evidence that the ApoE2 allele may serve a protective role in AD. Thus, the genotype most at risk for Alzheimer's disease is ApoE e4/4. The ApoE 3,4 genotype is at increased risk, though not to the degree that those homozygous for ApoE 4 are. The genotype ApoE 3/3 is considered at normal risk for Alzheimer's disease. The genotype ApoE 2/3 is considered at less risk for Alzheimer's disease. Interestingly, people with both a copy of the 2 allele and the 4 allele, ApoE 2/4, are at normal risk similar to the ApoE 3/3 genotype. Other than e4, the other “e s” do get better with Medium Chain Triglyceride Therapysuch as Coconut Oil. Knowing if you are in harms way for either Vascular or Alzheimers disease early in life should give the impetus to change lifestyle. “An enemy known is better than one unknown!”

Tuesday, June 22, 2010


It had been thought for 20 years that microwaved food may not have all its nutrients. According to most studies, however, the reality is quite the opposite. Every cooking method can destroy vitamins and other nutrients in food. The factors that determine the extent are how long the food is cooked, how much liquid is used and the cooking temperature.

Since microwave ovens often use less heat than conventional methods and involve shorter cooking times, they generally have the least destructive effects. The most heat-sensitive nutrients are water-soluble vitamins, like folic acid and vitamins B and C, which are common in vegetables.

In studies at Cornell University, scientists looked at the effects of cooking on water-soluble vitamins in vegetables and found that spinach retained nearly all its folate when cooked in a microwave, but lost about 77 percent when cooked on a stove. They also found that bacon cooked by microwave has significantly lower levels of cancer-causing nitrosamines than conventionally cooked bacon.

When it comes to vegetables, adding water can greatly accelerate the loss of nutrients. One study published in The Journal of the Science of Food and Agriculture in 2003 found that broccoli cooked by microwave — and immersed in water — loses about 74 percent to 97 percent of its antioxidants. When steamed or cooked without water, the broccoli retained most of its nutrients.

Some scientists feel that much of the benefit of food is due to vibration of energy. Microwaves cause isomerization which is the rearrangement of electrons which morphs into another form such an amino acid going from L. lysine to D lysine. Living tissue recognizes the L. but not the D form. This is much more in theory than proof.

However, microwaved heating of banked blood has reportedly caused at least one death. Also, people who were given microwaved foods were shown to have depletion of some vital enzymes. It may be years before the truth is known. But for now I use the microwave mostly to heat water and not food. I am still moderately concerned about the devitalization of the micronutrients in food. Study after study has shown that the more any food is cooked by any method, the less nutrition it has "if it's not raw don’t eat it at all".

Tuesday, June 8, 2010


For several decades, I’ve been interested in chocolate. Is it anything more than a delicious, but fattening treat? There are over 80 chemicals in chocolate that have been shown to be beneficial to man. There are also some negative ones. The beneficial ones include Minerals (particularly magnesium), vitamins (B6, niacin, thiamine, riboflavin), hormone-like chemicals (ferulic acid and phosphatidylcholine), stimulants (caffeine and theobromine), amino acids (threonine), pain relievers (nicotinamide), aspirin-like anti platelet compounds as well as several other chemicals that have antiseptic, antioxidant and anti parasite properties.

Chocolate comes from the cacao tree, a small evergreen that grows as high as 25 feet in the wild, but when cultivated, is only five feet for convenient hand picking. One inch long, reddish brown beans are imbedded in a white. pulp. The chocolate nuts were taken from this and by a simple fermenting process, such as burying them under leaves for several days, they were ready for use. In the New World, chocolate was consumed in a bitter, spicy drink called xocoatl, and was often flavored with vanilla and chili pepper.

Until the 16th century, no European had ever heard of the popular drink from the Central and South American peoples. It was after the Spanish conquest of the Aztecs that chocolate was imported to Europe. The first chocolate house opened in London in 1657. In 1689, noted physician and collector Hans Sloane developed a milk chocolate drink in Jamaica which was initially used by apothecaries, but later sold to the Cadbury brothers in 1897. Chocolate in its solid form was invented in 1847. Joseph Fry & Son discovered a way to mix some of the cocoa butter back into the dutched chocolate, and added sugar, creating a paste that could be moulded. The result was the first modern chocolate bar.

One ounce of dark chocolate contains the same amount of antioxidants as a 5 ounce glass of red wine. Even the fat (cocoa butter), which was once thought to be bad, is now known to be mostly stearic acid, which is far better for our arteries than other saturated fats.

The smooth rich taste of chocolate has to do with palate pleasing physical property as well as with almost 300 aromas and flavors to tease the taste buds and tweak the brain. The dark chocolate has far less fat and more of the “good stuff’ than the light chocolate. White chocolate has none of this. I would advise reading the label to make sure there are no hydrogenated oils, excessive sugar and artificial flavors that are sometimes used in less expensive forms of chocolate. Hopefully, xylitol and/or stevia will be used as a sweetener.

Chocolate has been shown to be positive in human health. Panamanian Indians who consumed a cocoa-ladened drink (xocoatl) had one-third less incidence of cancer and cardiovascular disease. The first epidemiological study that proved increased cocoa (chocolate) intake, improved the cardiovascular system with a decrease of all-cause mortality, took place in Holland. The Zutphen Elderly Study published several years ago in The Archives of Internal Medicine revealed that men who ate the most cocoa had a significant drop in blood pressure and a 50 percent lower risk of cardiovascular death.

In a more recent study of 44,489 people, those who ate one serving of chocolate per week had a 22% reduction in the likelihood of stroke. Another study found that people who ate 50 gms of chocolate a week were 46% less likely to die following a stroke.