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International Journal of Human Nutrition and Functional Medicine

www.IntJHumNutrFunctMed.Org

2014 Final PDF

based on their genetics, lifestyle, and environmental

exposure to various stresses.

Dr. Roger Williams contributed to the

understanding of the molecular origin of disease with the

development of the concept of biochemical individuality

(

4

). He described anatomical and physiological variations

among people and how they related to their individual

responses to the environment. He was the first to gain

recognition for the term biochemical individuality and

how this related to differing nutritional needs for optimal

function among different people. He pointed out that even

identical twins could be different in their needs for optimal

function based upon the fact that they developed in

different environments in utero. Although identical twins

share the same genes, their differing nutrition and

developmental environments can result in different

expression of the genes as they grow older. The second

important concept we need to understand is the

recognition that nutritional status can influence the

expression of genetic characteristics. It is now well

recognized that our genotype gets transformed into our

phenotype as a consequence of nutritional, lifestyle and

environmental factors which are important in determining

our eventual health patterns.

Dr. Williams coined the term genetotrophic

disease to describe diseases which resulted from

genetically determined nutritional metabolic needs not

being met by the individual and which result in faulty gene

expression. Motulsky explained that many the common

degenerative diseases are the result of the imbalance

nutritional intake with genetically determined needs for

good health (

5

).

The principle can explain some of these

discrepancies since every individual organism has a

distinctive genetic background and therefore distinctive

nutritional needs. Although all human beings operate on

the same general physical mechanisms and the same

metabolic processes, the individual physical structures

and genetically determined enzyme efficiencies vary

sufficiently between individuals so that the effect of all the

combined reactions in one body may be completely

different from that in another individual, even if of the

same age, sex, and body size (

4

). These concepts can

irreversibly change the way medicine is practiced and may

result in the extension of both life expectancy and health

span, or disease-free years of life.

A person’s particular genetics influences on how

much of a specific nutrient they need. For example, folic

acid is a B-vitamin that is relevant for cardiovascular and

neurological health. One important role of folic acid is to

decrease the amount of homocysteine that may

accumulate as a normal part of metabolism. Homocysteine

is an amino acid by product of methionine that plays a role

in the development of heart disease, osteoporosis,

dementia, and cancer. Folic acid is required to break down

homocysteine. In order for folic acid to do this, it must be

activated by the enzyme methylenetetrahydrofolate

reductase (MTHFR). MTHFR is produced by the body

and coded for by a specific gene. People can have different

variations of this gene, which slightly changes the

structure of MTHFR. This structural change can reduce its

function by 30–65%, meaning that it may not be able to

activate folic acid as easily. People who have the gene that

de- creases the MTHFR activity require higher doses of

folic acid or an activated form of the vitamin to effectively

push the reaction forward and decrease homocysteine. The

requirement for folic acid is greater in people with this

genetic variation.

G6PD (Glucose-6-phosphate dehydrogenase)

human polymorphism, is a cytosolic enzyme in the

pentose phosphate pathway, a metabolic pathway that

supplies reducing energy to cells (such as erythrocytes) by

maintaining the level of the co-enzyme nicotinamide

adenine dinucleotide phosphate (NADPH). G6PD

deficiency is the most common human enzyme defect. .

Individuals with the disease may exhibit non-immune

hemolytic anemia in response to a number of causes, most

commonly infection or exposure to certain medications or

chemicals. The NADPH in turn maintains the level of

glutathione in these cells that helps protect the red blood

cells against oxidative damage. Patients with this

deficiency should not receive vitamin C infusions because

it can cause hemolytic anemia. The regulation of gene

expression gives the cell control over the versatility and

adaptability of any organism and serves as a substrate for

evolutionary change. This is profound since our diet has

impact on our genetic code which is passed on to the next

generation. The more nutritious our diet, the stronger will

be the gene pool.

The Km concept

Approximately 50 different human genetic diseases are

due to a poor binding affinity (Km) of the mutant enzyme

for its coenzyme. This can be remedied by feeding high-

dose B vitamins, which raise levels of the corresponding

coenzyme. Many polymorphisms also result in a lowered

affinity of the enzyme for the coenzyme (

6

).This should

be of interest since it seems that a considerable percentage

of the population is affected by polymorphisms (

6

).

The Weakest Link

Every element of your physiology must be addressed in

order for your body to perform at peak efficiency. Michael

Zumpano coined the term Metabolic Optimization in the

early eighties to describe his systematic approach to

training and nutrition. You can view the metabolic

processes as links in a chain. The strength of the entire

chain can be compromised by only one weak link.