We Are All Individuals

In all my years of medical school, one of the most interesting things I learned was in gross anatomy. Our textbook for that course contained drawings illustrating the numerous anatomical differences among individuals. It was confirmation of something that I have always felt, that each of us is totally unique, not just in our minds, but in our anatomy as well as body functions. Physiologically, biochemically, anatomically, and psychically, we all are unique creations. No two brains are designed the same way or function exactly in the same way. This is why no two people think or feel the same way when faced with similar events.

The biochemist, Dr. Roger Williams, first pointed out the importance of biochemical individuality, and that we cannot use the hypothetical "normal person" to set nutritional guidelines and norms. In his many years of study, he demonstrated that we vary considerably in our ability to detoxify environmental toxins, metabolize our foods, and in our nutritional requirements. Only recently is it being appreciated that normal values for laboratory tests do not fit a specific person. Instead, we must rely on physiological or functional values, which take into account individual variability.

With the tremendous growth in the field of biochemical genetics, we have had further confirmation of this fundamental idea of individuality. The study of human genetics has demonstrated that there is a considerable biochemical variation within and between human populations, even between identical twins. Artemis P. Simopoulos, MD, a molecular geneti cist, stated that DNA sequencing has demonstrated "how unique each one of us is, and the extent to which genetic variation occurs in human beings."

This genetic uniqueness is so prevalent that we cannot really extrapolate nutritional recommendations from one population to another, because they may have significantly differing methods of metabolism of the same food chemicals; that is, a person from Alaska metabolizes food differently than a person from Mississippi. Our metabolic individuality is also determined by constitutional factors, such as age, sex, developmental size, and parental factors, as well as environmental factors, such as time, geography, climate, occupation, education, and diet. All of these factors coalesce to influence our individual chances of surviving in a hostile world.

Another important finding has been that DNA-repair enzymes can vary as much as 180-300 times among individuals. This is critically important when we consider that our ability to repair free-radical-damaged DNA can mean the difference between developing cancer, degenerative brain diseases, or other devastating disorders and enjoying good health. Recent studies have shown that people who develop certain types of cancer have an impaired ability to repair damaged DNA. Similar defects in DNA-repair enzymes have also been seen in cases of Alzheimer's dementia. Free radicals also damage DNA-repair enzymes, as do several of the toxic metals.

This genetic and biochemical individuality can either place us at a high risk of certain diseases or a very low risk. For example, persons lacking a detoxification enzyme called glutathione transferase Ml show an increased risk of developing lung and bladder cancer, especially if they smoke. People with low liver-detoxification capacity due to other enzyme defects also show a high rate of carcinogen-induced cancers because of an inability to detoxify specific cancer-causing chemicals.

Another genetic toss of the coin can play a major role in your risk of developing two particularly devastating diseases. It has been shown that persons carrying the apolipoprotein E4 gene (apoE4) are at a very high risk of developing Alzheimer's disease and heart disease. Even having one copy of the gene increases your risk. One autopsy study found that 85 percent of those diagnosed with Alzheimer's disease were positive for the apoE4 gene. People with the apoE4 gene that suffered head injury were also found to have more long-term residual neurological damage, and were more likely to become demented than those not possessing the gene. This is especially true for boxers. Even mad cow disease (Creutzfeldt-Jakob disease) is more common in individuals possessing this gene.

So, how could one gene produce such a high incidence of such diverse diseases? It appears that people with this gene have an exaggerated inflammatory response, and both diseases— Alzheimer's and heart disease—are the result of prolonged inflammation, as we shall see. In addition, individuals possessing the apoE4 gene also have lower levels of antioxidant enzymes and therefore less protection. Those lucky enough to have the apoE2 gene have a significantly lower risk of developing these inflammatory diseases.

Again, we see that although individual variation in genetic inheritance can drastically influence our risk of disease, neither is our genetic code a "Last Will and Testament." Nutrition can alter the course of high-risk genes, not only by turning these genes off but also by inhibiting the resulting bad effects produced by them, in this case increased inflammation. In such cases, it is important to start your defense as soon as possible, before irreversible injuries can occur.

A recent review of genetic influence on disease found that 50 percent of the variation in plasma cholesterol concentration, 30-60 percent of the variation in hypertension, and 75 percent of the variance in bone density is genetically determined. In the latter case, it has been found that the vitamin D receptor gene type is of particular importance for bone density in premenopausal women, since this gene controls calcium absorption.

Postmenopausal woman with the BB genotype (homozygous dominant) were found to have difficulty absorbing calcium when dietary supply was low, whereas those with the recessive bb genotype (homozygous recessive) had better calcium absorption. When the poor absorbers (BB type) were given high doses of calcium in their diets, they were able to maintain normal calcium levels. At RDA levels of 800 milligrams (mg) of calcium, women with the BB genotype will not be able to maintain normal blood calcium levels: they will require at least 1,200 mg of calcium a day.

A recent study of seventy-two elderly women with normal vitamin D levels found that those with the bb genotype had normal spinal bone densities no matter their calcium intake. This means they would not need to take calcium supplements. Those with the BB genotype lost mineral density and required higher calcium intakes to maintain their bone density. Those having one of each of the genes, noted as Bb, had bone densities that varied with calcium intake, that is, the higher the intake, the better the bone density. So, this means that some women might need additional dietary calcium intake after menopause but that a lucky few will not. Yet, it should be understood that control of bone mineralization (strength) is determined by more than calcium intake.

Many doctors, who should know better, have their patients taking 1,500 mg of calcium a day to prevent osteoporosis. They do this out of a mistaken impression that, unless supplemented with additional calcium, all women will develop osteoporosis. Ironically, these are the same doctors who think it is ridiculous to supplement the elderly with additional vitamins and other minerals.

The problem with taking a lot of excess calcium is that calcium is also associated with many destructive reactions in the cell, and these injuries can be accelerated by increasing tissue calcium levels. This is true of Alzheimer's disease, Parkinson's disease, and all other neurodegenerative diseases. It is also true with degenerative diseases of every kind. We know that as we age we lose some of our ability to regulate cellular calcium levels. This means more calcium will leak into the cell, triggering free-radical generation, release of inflammatory chemicals called cytokines, and can lead to increased cell death. We also know that elevating calcium intake can increase the excitotoxic reaction in the brain as well. Later, I will discuss the best ways to improve bone mineral density and protect you from osteoporosis.

Have you ever wondered why some people develop Parkinson's disease and others do not? There is growing evidence that those destined to develop the disease have a defect in iron metabolism within a specialized area of the brain called the striatum. One of the earliest changes in the disease is an accumulation of iron in the part of the brain called the substantia nigra, located deep within the center of the brain. Most likely, the defect is based on a defective gene. There is also evidence that Parkinson's patients have an inherited defect in mitochondrial function, which is responsible for cellular energy production. Both of these defects can lead to destruction of the neurons controlling our motor movement. It is also critical to note that the destruction is carried out by an intense generation of free radicals caused by a combination of excess iron and low energy supply. Again, all of this damage can be mitigated by the judicious use of nutraceuticals and changing one's diet.

My Life My Diet

My Life My Diet

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