Micro-Macronutrients Treatments

Micro-Macronutrients Treatments


Micro-Macro Nutrients – Essential Vitamins and Trace Elements Necessary for Human Health


Micro-Macronutrients Treatments (Micro – Macro-Nutrients)

It concerns the administration of special supplements, vitamins, trace elements, minerals, and amino acids, while therapy may be also combined with special nutrition.


Micro-Macro Nutrients

The treatment regimen is configured according to any deficiencies, dysfunctions and biochemical imbalances at the cellular level.

Food nutrients act as the key stimuli that determine whether cellular function is smooth or not.

At the molecular level, the interaction between nutrients and other dietary bioactive elements, affects genes, which then influence protein expression, i.e. metabolism.

This simply means that the deficiency of certain nutrients results gradually in Disease through the necessary for the organism chemical reactions, and it is the cause of chronic and autoimmune diseases.


Therapeutic Protocols of Micronutrients – Treatments.

In patients with chronic and autoimmune diseases, chemical aberration at the organism’s functional level may be restored. Following the appropriate biochemical and metabolic exams, dysfunctions are detected and existing deficiencies are identified.

There are many exams available to ultimately determine treatment, depending on the patient’s Medical History. The cost of most of them is affordable and the results are ready within two to three days.

Micronutrients protocols, according to the American Standards, are differentiated depending on the chronic or autoimmune disease, as well as many other factors. Thus, they specify strictly dosage, duration, quantity and combination of nutrients (formula) in each person.

Depending on the treatment of the disease or diseases, the extent of lesions, and the individual findings, treatment may last from three months to one year to fully restore the patient’s clinical picture.

Patients do not modify their daily life, while they gradually see their overall health status being improved.

These therapies are systematically used in clinical practice since 1997, and the country of departure was the United States of America, while they are not contradictory to any other concurrent pharmaceutical or homeopathic treatment.

The appropriate treatment is that which ultimately provides the best possible benefit, according to the clinical outcomes and the relevant exam markers.




Harman, Aging: prospects for further increases ίη the functionallife span. Age 17: 19-146,1994.
Kohn, R. Aging and age-related diseases: normal processes. Ια: Relation Between Normal Aging and Disease. Johnson,H.A. Ed., New York: Raven Press, ρρ.Ι -44, 1985.
Upton, A. Pathobiology. Ιε: The Biology οf aging. Finch, C. Ε., Hayflick, L. Eds., New York: Van Nostrand, ρρ. 513-535, 1977.
Sveήges officiella statistik. ΒefοlkίηgsfοrandήgaLίvslangstabelΙer, 1951- Ι 993.
Statistiska centralbyran, Stockhlom, Sweden, ρρ. 114-115,
Jones, Η. R. The relation of human health το age, place and ti Ιn: Handbook ΟΙ Aging and the Individual. Βίπen, J. Ε. Ed., Chicago: Chicago University Press, ρρ. 333-363, 1955.
Woodhall, Β., Joblon, S. Prospects for future increases ία average Iongevity.Geήatήcs 12:586-591, 1957.
Fήes, F. Aging, natural death, and the compression of morbidity. Ν Engl J Med 303:130-135,1988.
Olshansky, S. J., Carnes, Β. Α., Cassel, C. Ια search of Methuselah: estimating the upper limits to human longevity. Science 250:634-640, 1990.
Nationa! Center for Health Statistics. Vital Statistics of the United States. 1985.
Life Tab!es, Υοl. 2 (6).Hyattsville, M (U.S. Dept. Hea!th & Human Serv.) PHS Publ. Νο. 88-1104, ρ.9, 1988
Rockstein, Μ., Sussman, Μ. , Chesky, J., Eds., Theoretical Aspects ΟΙ Aging. New York: Academic Press, 1974.
Wamer, Η. , Butler, R. Ν., Sprott, R. L., Schneider, Ε. L., Eds., Modem Biological Theories ΟΙ Aging. NewYork: Raven Press, 1987.
Medvedev, Ζ. Α. Αα attempt at a rationa! classification of theοήes of agi
Biological Review 65:375-398,
Harman, D. Aging: a theory based οα free radical and radiation chemistr J Gerontolll:298300, 1956.
Harman, D. Role of free radicals ίη mutation, cancer, aging, and the maintenance of
!ife. Rad Res 16:753-763, 1962.
Harman, D. The aging process. Proc Natl Acad Sci USA 78:7124-7128, 1981.
Bjorksten, Ι. The crosslinkage theory of J Amer Geriatr Soc 16:408-427, 1968..
Hayflick, Οήgίns of longevity. Ιn: Modern Biological Τheοήes of Aging. Warner, Η. R., Butler, R. Ν., Sprott, R. L., Schneider, Ε. L., Eds., New York: Raven Press, ρρ. 21-34,1987.
Wa!ford, R. The Immunologic Theory ΟΙ Aging. Copenhagen: Munksgaard,1969.
Harman, D. Free radical theory of aging: history. Ιτι: Free Radicals and AginΕπισίι, Ι., Chance, Β., Eds.,Basel: Birkhauser, ρρ. 1-10, 199
Haπnan, D. The bio!ogical clock: the mitochondήa? J Amer Geriαtr Soc 20:145-147,1972.
Haπnan, D. Free radical theory of aging; consequences of mίtochοηdήal aging. Age 6:86-94, 1983.
Haπnan, D. Free radical theory of aging: ro!e of free radicals ίη the οήgίηatίοn and evolution of life, aging, and disease processes. Ια: Free Radicals, Aging, and Degenerative Diseases. Johnson, Jr., J. Ε., Walford, R., Haπnan, υ., Miquel, J.,
,New York: Alan R. Liss, ρρ. 3-49, 1986.
Haπnan, D. Free radical involvement ίη aging: pathophysiology and therapeutic imp!ications. Drugs & Aging 3:60-80,
Bandy, Β., Davison, Α. Μίtσchσndήa! mutations may increase oxidative stress:imp!ications for carcinogenesis and aging? Free Radical Βίο! Med 8:523-539, 1990.
F!eming, J. Ε., Mique!, , Cottrell, S. F., Yengoyan, L. ε., Economos, Α. C. Is celI aging caused by respiratorydependent injury to the mίtochοndήa! genome? Gerontology 28: 44-53, 1982.
Miquel, , Economos, Α. C., F1eming, J., Johnson, Jr., J. Ε. Μίtochοndήal role ίn cel1 aging. Exper Gerontol 15:575-591, 1980.
Noh!, Η., Hegner, D. Do mίtοchοndήa produce oxygen radica!s ίη vίvο? Eur J Biochem 82:863-867, 1978.
Sohal, S., Ku, Η.-Η., Agarwa!, S.; Forster, Μ. J., La!, Η. Oxidative damage, mitochondria! oxidant generation and antioxidant defenses during aging and ίn response to food restriction ίn the mouse. Mech Ageing Develop 74:121-133, 1994.
Sohal, R.S., Soha!, Β. Η. Hydrogen peroxide release by mitochondria increases during aging. MechAgeing Dev 57:187-202,1991.
Κυ., Η.-Η., Brunk, U. Τ., Soha!, S. Relationship between mitochondria! superoxide and hydrogen peroxide production and 10ngevity of mammalian species. Free Rad Βίο! Med 15:621-627, 1993.
Halliwell, Β., Gutteridge, J. Μ. C. Free radicals in biology and medicine, 2nd edition, Oxford: Clarendon Press,
Yu, Β. Ρ., Masoro, Ε. , Murata, Ε. J., Bertrand, Η. Α., Lynd, F. Τ. Life span study of SPF Fischer 344 male rats fed ad libitum or restricted diets: longevity, growth, lean body mass and disease. J GerontoI37:130l41, 1982.