The Fisher Clinic™

Dr. Howard W. Fisher
Podcasts |
Contact Form | Contact Info
Lecture Tour Schedule | Booking Info
subglobal8 link | subglobal8 link | subglobal8 link | subglobal8 link | subglobal8 link | subglobal8 link | subglobal8 link

The Relationship between Nutrition, Disease and Aging: A Review


The Relationship Between Nutrition, Disease and Aging: A Review

Dr. Howard W. Fisher


For centuries man has known that there are direct causal relationships between nutrition, disease and aging.  Sailors setting out to discover the new world would suffer from scurvy caused by a deficiency of Vitamin C.  Other diseases, such as rickets (Vitamin D), beriberi (Thiamin, Vitamin B1), and pellagra (Niacin, Vitamin B3) are unquestionably caused by vitamin deficiencies.  Research has linked many chronic diseases to significantly reduced intake, impaired absorption or decreased endogenous production of vital nutrients that act physiologically in our bodies to maintain a non-disease state of homeostasis when present at optimal levels.  “Inadequate intake of several vitamins has been linked to chronic diseases, including coronary heart disease, cancer and osteoporosis.”   The goal of this review is to examine the morbidity associated with aging and chronic disease to determine the potential benefits of nutritional intervention.

In the beginning of the last century, medical investigative pioneers such as Dr. Alexis Carrel, Nobel Prize winner in Physiology or Medicine for his vascular suturing and transplant techniques, had been seeking the answers to questions about aging and cellular longevity.  In 1912 while at the Rockefeller Institute, Carrel proved the virtual immortality of the cell by growing a small piece of chicken cardiac tissue in a nutritive medium solution.  The tissue was transferred to another fresh batch of nutrient medium every forty-eight hours for more than thirty-two years.   The cells expired only upon the failure of the lab technician to add proper nutrients and to detoxify the fluid that surrounded it by changing the containers.    Based on these results and understanding the experimental parameters, Carrel proclaimed that “the cell was immortal.”

Dr. Francis Pottenger, Jr, another medical pioneer who had been seeking the answers to questions about aging, chronic disease and the correlation to aspects of nutrition, conducted one of the most revealing nutritional studies regarding the effects of cooked versus raw food on the body.   In this comprehensive experiment, which ran for ten years and involved four generations of cats, Dr. Pottenger totally controlled the dietary intake of his subjects.   He separated his groups by feeding cooked foods and pasteurized milk combinations to three groups and only raw, non-pasteurized milk, and raw meat to the other. Predictably, from the information that is known today, the group of cats fed cooked food, suffered chronic degenerative diseases, developed the inability to reproduce and died prematurely. In reaching his conclusions, Dr. Pottenger was unable to deduce the causative factors to explain his conclusions, although he was certain that it was a nutritional component that was missing from the diets.  His research made us aware enough to look for factors such as cooking (enzyme denaturing), fertilizers, pesticides, preservatives, chilling, storage and reheating that could affect the bioavailability of nutrients and their subsequent absorption, potentially impairing physiological function.

The lesson to be learned from these somewhat obscure, but important researchers, is a direct statement about nutrition and disease.  The lesson from Dr. Carrel is basically that if the cell receives the proper nutrition and detoxification, then indeed the cell may truly be a lot more resilient, closer to his proclamation than we believed, and capable of a life expectancy far beyond anything we had previously considered.  The lesson to be learned from Dr. Pottenger is that we may not be absorbing the nutrition that we previously thought was available in the food we consume and this may be due to a number of factors. 

The advances of technology such as genetic modification of plants, mechanized processing, storage, and shipping modes, in conjunction with faster paced lifestyles, have altered our dietary patterns to the point where most of us are not ingesting the basic minimum nutrition.  This protocol is exposing more than half of the population to nutrient related disease risk.  The vast majority of the population consumes less than sixty-six percent (66%) of the recommended daily allowance for one or more nutrients.   An American study concluded that only nine percent (9%) of the population consumed the recommended five servings of fruit and vegetables daily and fifty percent (50%) had less than fifty percent (50%) of the RDA of vitamins A, C, E, and other nutrients.   Remember that the recommended daily allowance is the minimum quantity of a nutrient necessary to prevent a deficiency syndrome.  The correlation between nutrition and many of the chronic diseases exists and one does not have to have a deficiency status to be affected, only a sub-optimal intake. 

A great deal of investigation has gone into the aging process and chronic disease and antioxidants have been a focal point.  Free radical damage caused by electron-seeking, highly reactive, oxidative molecules has been identified as the source of these maladies.  The sources of these free radicals are both exogenous and endogenous.  Mitochondria generate the reactive oxygen species as a function of creating ATP and reducing oxygen.  Toxic chemicals and ionizing radiation are other prominent sources of free radicals.  These oxidants promote aging by attacking lipids in cellular membranes causing increased membrane rigidity, dysfunctional permeability and decreased activity of membrane receptors.  Furthermore, membrane proteins, including DNA, will be attacked causing aberrant physiological function and potential cross-linking.  Although there are many endogenous antioxidants, it is imperative to ingest dietary antioxidants to minimize the aging process damage caused by free radicals.

Researchers have been trying to determine the necessary nutrients that the body needs for optimal health and the best methods for not only their bioavailability but subsequent absorption after ingestion and maximal physiological utilization.  The facts are clear: if you ingest fruit, vegetables and/or nutritional supplements, your serum levels of vitamins, minerals and trace elements will be higher, and this will confer a protective element against chronic diseases.   This knowledge will allow an individual to formulate a nutritional plan of action.

According to the United States Department of Statistics (2004), the top causes of death are:  Cardiovascular disease (654,092), Cancer (550,270), Stroke (150,147), Accidents (108,694), Diabetes (72,815) and Alzheimer’s Disease (65,829).   These chronic diseases that shorten lives and cause death have a huge economic impact throughout their etiologies, and they can be affected by dietary and dietary supplement choices. Epidemiological findings advocate a direct relationship between nutrition, diet and chronic diseases.   Another aspect of health that has an overriding effect on all disease is the status of the immune system.  Approximately 98% of the North American population has a diminished immune function.   The correlation between nutrition and immune system enhancement is well documented in the review of scientific literature.   More direct randomized clinical trials are necessary to sort out all of the individual component, but the facts remain that our bodies require certain nutrients:  water, vitamins, minerals, and antioxidants to function at an optimal level.  Somehow we have overlooked this information in our quest for creature comforts and technological advancement.    We are approaching the time when technological advancement can reflect upon our pending nutritional crisis.  The bulk of the population is aging and being subjected, possibly quite unnecessarily, to many chronic diseases and concomitant immune system dysfunction related to nutritional shortfalls.

The current multi-billion dollar supplement industry would not sustain the substantial growth it is currently enjoying if there were no reason to supplement, and people were not deriving benefits.  Of course the question must be asked about the reasons that we can no longer derive adequate nutrition from our food supply.  By definition alone, the word supplement means to replace that which is missing and that in fact should be the key to the answer.  We have known for over half a century that our food sources have been deficient in vitamins and minerals.   Harvesting and shipping modes do not take nutrition into account and in combination with extensive processing, improper storage and soil deficiencies, it is almost impossible to get adequate nutrition from our current food supply.   There is a great deal of evidence supporting supplementation and the consequent decreased risk of diseases.  According to the Council for Responsible Nutrition, “There is ample evidence to suggest that the public will benefit from the adoption of healthy dietary patterns and healthy lifestyle habits including the regular use of nutritional supplements.”   “Antioxidants have long been linked to the prevention of degenerative diseases associated with aging.”   A review of the literature concerning the relationship between nutrition and disease confirms the need for something more than the average diet is currently providing.


According to nationally renowned Oncologist and Immunologist, Dr. Charles B. Simone, “Nutritional deficiencies decrease a person’s capacity to resist infection and its consequences and decrease the capability of the immune system.” When we combine that information with “protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (alpha carotene, beta carotene, lycopene, lutein, cryptoxanthin,” it becomes obvious that intelligent use of nutrients can, in fact, affect chronic disease.  Carotenoids such as beta-carotene, lycopene, zeaxanthin, and lutein have been singled out for their benefits on decreasing total cancer risk and prostate cancer risk specifically.

Other antioxidants, such as vitamin C and vitamin E, have also been linked to a reduction in cancer risk.   There are many other nutrients that have been shown to decrease cancer risk, that are generally considered to be part of a basic vitamin regimen such as folate,   vitamin B12,   and vitamin D, to name a few.


It is a well documented fact that fruit and vegetable consumption provides a protective relationship to heart disease, myocardial infarct and ischemic stroke (CVD). Researchers, such as Dr. Joshipura and many others, acknowledge that this protective effect can be explained by nutritional components in the fruit such as vitamins, folate, potassium, antioxidants, and fiber.   The recommended dosage is more than five servings of fruits and vegetables daily or the commensurate amount of nutrient supplementation.  A well stated consensus of opinion on the relationship between nutrition and cardiovascular disease (CAD) may be summed up by the statement in the Lewin Group report, “Mild to moderate deficiencies in antioxidant nutrients such as vitamin C, vitamin E and beta-carotene, as well as folic acid, although not severe enough to cause classic deficiency diseases, may be involved in the development of CAD.”   

The relationship of elevated serum homocysteine  as a major risk criterion for CAD has been well documented. Vitamins B6, B12 and folate are needed to convert homocysteine to methionine, however it is the amount of folate that enables this reaction to occur and is thus the reactive determining substance.     A 1999 study found beta-carotene capable of reducing the risk of myocardial infarction, contradicting the findings of some earlier studies.   Several investigators have found connections between carotenoids, lycopene and lutein and the risk of heart disease.



Age related macular degeneration (AMD) is the leading cause of irreversible blindness in developed countries.   When considering chronic disease and aging, the fact that cataracts are diagnosed in approximately eighty percent (80%) of the population over the age of seventy five (75), highly qualifies this disorder as a chronic disease of epidemic proportions.  The pathophysiology of degenerating eye health seems to involve damage done by exposure to excessive blue light.   Lutein and zeaxanthin, carotenoid antioxidants, highly concentrated in the macula, have been linked to providing protection from this potential threat.   The strong case for the decreased risk of AMD  is evidenced by the inverse relationship of decreased lutein and zeaxanthin macular content and the increased incidence of disease.   Increasing ingestion of foods high in lutein and other beta carotenoids or supplementing with lutein, beta carotene, vitamin C, vitamin E and zinc increases their density in the macular pigments and significantly decreases the risk of AMD in seniors.


Alzheimer's Disease   (AD) is a progressive, irreversible brain disorder with no known cause or cure affecting more than four and a half million Americans.  Unfortunately this disease leads to a rapid functional decline.  The clinical cause of Alzheimer’s disease is related to amyloid peptide microtubule deposits (tau), neurofibril entanglement and inflammation.  Neurodegenerative disorders such as Alzheimer’s, Parkinson’s and dementias are predominantly caused by oxidative damage.   Investigations have shown promising results with the role of antioxidants delaying the onset and progression of Alzheimer’s Disease by protecting against cerebral oxidative stress and abnormal protein metabolism.   This has been confirmed on autopsy findings that signs of oxidative damage are consistently found in patients with AD and neurodegenerative disorders.   Non-steroidal anti-inflammatory benefits of polysaccharides and triterpenoids found in ganoderma lucidum may provide the ability to reduce inflammation in the brain reducing the risk for suffering from this disorder.   Although the research was conducted using genetically modified drosphila, Dr. D. Dias-Santagata and her fellow researchers believe that antioxidants may be the therapeutic approach to delay or avoid the onset of AD and other neurodegenerative disorders.


The self-non-self protocol of the immune system is only as effective as the integrity of the various components of the immune system.  Much research has been carried out investigating the level of natural killer (NK) cells and their role in predicting disease.  Dr. Jesse Stoff, a immunologist from Arizona, found that the majority of the population (98%) is functioning with sixteen percent (16%) of the requisite number of natural killer cells considered to make up a virulent immune system.   Several researchers have found a direct relationship between the number of circulating lymphocytes and the risk of disease.    

There are various nutrients that can have a beneficial effect on enhancing immune system function.  Decreased dietary Vitamin A levels have been shown to reduce the number of circulating natural killer cells and their function, predisposing the subjects to increased infection. Long-term beta-carotene supplementation enhances natural killer cell activity in elderly men, decreasing the risk of infection and cancer.  Researchers have determined that certain proteins, polysaccharides and triterpenoids from the Reishi mushroom (ganoderma lucidum) act as immunomodulators. Any substance that can affect the cytokine system is known as an immunomodulator.  “Compounds that are capable of interacting with the immune system to upregulate or downregulate specific aspects of the host response can be classified as immunomodulators or biologic response modifiers.”

Immune modulation is repairing the damaged cytokine communication pathways while enhancing other aspects of the immune system such as increasing production and activity levels of T cells, macrophages, natural killer cells leading to the subsequent production of interferon, interleukins and tumour necrotic factor.   These parameters are measurable indicators and the corresponding results will reveal the integrity of the cytokine pathway.  This ability to restore these proper levels holds a great deal of

promise in allowing the body to deal more favourably with hypersensitivity and autoimmune disorders.  There are many foods and supplements that contain nutrients which act as immunomodulators.    


Diabetes is a disease affecting serum glucose and both types can be affected by diet.  In type I diabetes the pancreas can no longer produce insulin and exogenous insulin is needed to control serum glucose levels.  With type II diabetes, the body no longer responds to the insulin secreted by the pancreas and thus serum glucose levels run out of control.  Diabetes affects seven percent (7%) of the U.S. population, twenty million, eight hundred thousand people.   As a result of these large numbers, much research has been done in the relationship between diet, nutrition and diabetes.  

The discussion from the research indicates that trace minerals such as potassium, magnesium, chromium and zinc deficiencies may have an affect on carbohydrate intolerance,   but researchers conclude that serum levels of chromium and zinc are difficult to detect.   Chromium has been linked to decreasing serum glucose, glucose intolerance, and other aspects of relieving symptoms of diabetes.   Overall, the investigations for vitamin and mineral benefits for diabetes have yielded mixed results, and have only shown true benefit when distinctive nutrient deficiencies were present.


Osteoporosis, a disease characterized by low bone mass and micro-architectural deterioration of bone tissue, affects more than twenty-eight million (28,000,000) people in the United States alone.   Hundreds of thousands of hip and fractures occur annually and twenty-five percent (25%) of these individuals die within a year.   Although there are many factors affecting this disease (malabsorption syndromes), the focal point of the process of calcium absorption is the dietary presence of the nutrients, calcium, magnesium, and vitamin D.


The maintenance of the integrity of all the physiological parameters necessary to ensure homeostasis with no aberrations and the consequent optimal health that would ensue cannot be broken down into minutiae of molecules of nutrients which have contributed to the causal relationships of the etiology of disease. Some of the reasons are due to the inability of past investigators to conduct accurate cost effective evaluations of ingested and or serum nutrient levels.  "Current measures of nutrient intake lack precision and specificity.  Biological measures of dietary intake, measured as a concentration in the blood at one point in time, may not reliably reflect dietary intake because the biological regulation of these measures is complex and may be influenced by levels of other nutrients."   This may in fact be the reason that conflicting studies appear in the research for many supplements.   However research has pointed us in the direction that will lead to further correlative studies that will yield a more specific result to the generalized nutritional findings linked to the major chronic diseases, immune system dysfunction and anti-aging that are predisposing the population to the adverse effects of aging and the associated decrease in the quality of life.  “The correlation of underlying nutritional problems could be a way to prevent some patterns of morbidity in elderly patients with chronic and acute diseases.”   

The current position based on the investigative findings to date places us far beyond a suggested connection between nutritional deficiencies, chronic disease, and aging.  There is now more than marginal corroboration, and new objective measurement techniques will confirm this beyond the shadow of a doubt.  The case to support nutrient supplementation is strong, based on the fact that nutrients, such as folate, and antioxidants, (carotenoids and vitamins C and E), when ingested as distinct compounds are extremely bioavailable, often more than most whole foods.   “If used consistently, supplements can ensure adequate intakes of specific nutrients in targeted groups.”

Antioxidants are leading the way in the battle of anti-aging and chronic disease.   Antioxidants provide an electron to neutralize a free radical and prevent the free radical from causing anatomical damage by removing an electron and degenerating a tissue or DNA molecule.  Researchers have known for decades that much of the cellular degeneration that leads to aging and chronic disease is caused by Reactive Oxygen Species (free radicals) that oxidize various parts of the body.     We cannot avoid these free radicals.  Aside from the fact that we come in contact with billions of the electron seeking molecules daily from external sources and pollutants, every mitochondrion in every cell produces them as a by-product of energy production.  Science has progressed to the point that antioxidant   potency or value can now be determined by two methods: ORP-oxidation-reduction potential and ORAC oxygen radical absorbance capacity.  The Agricultural Research Service’s Human Nutrition Research Center on Aging at Tufts suggests that diets containing fruits and vegetables with high ORAC values may help to slow down the aging process and therefore affect chronic disease.

One interesting difference in the nature of the carotenoid antioxidants is in the way they scavenge free radicals.  Carotenoids are found in colourful red, orange and yellow plants and there are more than six hundred, many of which are retinol precursors. Most antioxidants give up an electron to satiate the free radical before it can damage collagen, cell walls or DNA.  The free radicals then enter the electron cascade and seek another electron from some other antioxidant to replenish itself and subsequently seek another free radical.  Carotenoids function in a different manner.  They will scavenge fifteen to twenty free radicals and then degenerate, not entering the electron cascade and acting as a less vigorous free radical, similar to other antioxidants.  This makes them a vital component to the body’s antioxidant system.  Carotenoids are exceptional scavengers of oxygen singlet free radicals and with the predisposition of these antagonists to attack cellular membranes, demonstrate a high degree of protection for cellular integrity.  

Carotenoid levels can serve as a direct reflection of dietary intake of fruits and vegetables and antioxidant supplements.  “Skin carotenoid levels correlate well with blood carotenoid levels and may more accurately indicate carotenoid status, because, unlike blood, skin carotenoids are not influenced by postprandial fluctuations.”    Carotenoids are deposited into various tissues and organs in the body and provide specific biological antioxidant functions in skin, eye (lutein), liver, adrenal gland, kidney, lung, adipose tissue, ovaries, testes, prostate (lycopene), and lutein in the macular pigment of the eye and lens.

The carotenoids have been shown to demonstrate abilities that make them an area of special interest.  Their diversity in reducing risk of chronic disease, membrane dysfunction and DNA alteration, begs for an objective monitoring of their levels.  Although serum carotenoid levels fluctuate, carotenoids present in the skin are much more stable, since they respond more slowly to postprandial fluctuations. Previously serum levels were detectable by blood test or skin biopsy using high performance liquid chromatography (HPLC).  Raman spectroscopy is a non-invasive means for detecting skin carotenoids using a 490 nanometre wavelength laser and can now be safely used to determine skin carotenoid concentrations and thus reliably predict serum concentrations. This spectroscopy value will act as an indicator to the relative overall antioxidant status.  It will also serve to estimate risk factor for aging and the chronic diseases affected by them.  By demonstrating an objective value, it will be possible to motivate individuals to improve their nutrient intake either by dietary modification with whole foods or supplements.


From an epidemiological perspective, the relationships between nutrition and disease have been identified.  The findings of Drs. Carrel and Pottenger have shown us that if the cells are properly detoxified and able to absorb proper nutrition, the potential exists for profound change regarding the incidence and onset of chronic diseases.  Further investigative studies are necessary to conclusively determine the optimal nutrient-physiological function relationships.  It is easy enough to suggest that everyone eat five to ten servings of fruit and vegetables daily or a commensurate amount of nutritional supplementation, but there are inherent difficulties with individual compliance to this regimen.  With the advances in non-invasive methods of objective measurements of nutrient status, and the dynamic changes to the ratio of molecular size and surface area through nano-technology, resolution of many of these major health issues will occur.  Compliance to the nutritional requirements will be more easily facilitated.  The demographics will demonstrate significant decreases to the incidence of these diseases and the morbidity and dysfunction associated with the aging process through a program of nutrient and antioxidant monitoring, with concomitant supplementation.

CDC Publications and Products:  National Diabetes Fact Sheet.  <

Franz M J, Bantle J P, Beebe R D, Brunzell J D, et al.  Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications.  Diabetes Care.  2002; 25:p148-198.


Mooradian A D, Failla M, Hoogwerf B, Maryniuk M, et al.  Selected vitamins and minerals in diabetes. Diabetes Care.  1994; 17:p464–479.

Mooradian AD: Micronutrients in diabetes mellitus. In Drugs, Diet and Disease2. 1999; p183–200.

Anderson R A, Cheng N, Bryden N A, Polansky M M, et al. Beneficial effects of chromium for people with diabetes. Diabetes. 1997; 46:p1786–1791,

Cheng N, Zhu X, Shi H, Wu W, Chi J, et al.  Follow-up survey of people in China with type 2 diabetes mellitus consuming supplemental chromium. J Trace Elem Exp Med. 1999; (12):p55–60.

Ravina A, Slezak L, Rubal A, Mirsky N.  Clinical use of trace element chromium (III) in the treatment of diabetes mellitus. J Trace Elem Exp Med.  1995;  8:p183–190.

Cefalu WT, Bell-Farrow AD, Stegner J, Wang ZQ, King T, Morgan, Terry JG: Effect of chromium picolinate on insulin sensitivity in vivo. J Trace Elem Exp Med.  1999; (12):p71–83.

Brunader R, Shelton D K.  Radiologic Bone Assessment in the Evaluation of Osteoporosis.  Am Fam Physician.  2002; p1357-1364.

NIH Consensus Statement.  Osteoporosis Prevention, Diagnosis, and Therapy.  2000; 17(1):p1-36.

Langton C M.  Ultrasound Measurement of Cancellous Bone for the Assessment of osteoporosis.  <

Bronner F.  Calcium Absorption:  A paradigm for mineral absorption.  J Nutr.  1998; 128:p917-920

NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy.  Osteoporosis Prevention Diagnosis, and Therapy.  JAMA.  2001; 285:p785-795.

Margetts B M, Pietenin P.  European Prospective Investigation into Cancer and Nutrition:  Validity Studies on Dietary Assessment Methods.  Int J Epidemiology.  1997;(26)1: S1-5.

Vellas B J, Albarede J L, Garry P J.  Diseases and aging: patterns of morbidity and age; relationship between aging and age associated diseases.  Am J Clin Nutr.  1992; 55:p1225S-1230S.

Hannon-Fletcher M P, Armstrong N C, Scott J M, et al.  Determining bioavailability of food folates in a controlled interventions study.  Am J Clin Nutr.  2004; 80:p911-918.

Brown E D, Micozzi M S, Craft M E, et al.  Plasma carotenoids in normal men after a single ingestion of vegetables or purified beta-carotene.  Am J Clin Nutr.  1989; 49:p1258-1265.

Lichtenstein A H, Russell R M.  Essential Nutrients:  Food or Supplements?  Where Should the Emphasis Be?  JAMA.  2005; 294:p351-358.

Dizdoroglu M, Jaruga P, Birincioglu M, Rodriguez H.  Free radical induced damage to DNA: mechanisms and measurement.  Free Radical Biology and Medicine. 2002; 32:p1102-1115.

Diplock A T.  Antioxidant nutrients and disease prevention:  an overview.  Am J Clin Nutr.  1991; 53:p194S-200S.

Wickens A P.  Ageing and the free radical theory.  Respiration Physiology.  2001; 128:p379-391.

Moskovitz J, Yim M B, Chock P B.  Free radicals and disease.  Archives of Biochemistry and Biophysics.  2002; 397:p354-359.

Hensley K, Floyd R A.  Reactive oxygen species and protein oxidation in aging: A look back, a look ahead.  Archives of Biochemistry and Biophysics.  2002; 397:p373-383.

Schafer F Q, Wang H P, Kelley E E, Cuenko K L et al.  Comparing beta-carotene, vitamin E and nitric oxide as membrane antioxidants.  Biological Chemistry.  2002; 383:p671-681.

Sohal R S, Mockett R J, Orr W C.  Mechanisms of aging:  An appraisal of the oxidative stress hypothesis.  Free Radical Biology and Medicine.  2002; 33:p575-586.

Gaziano J M, Manson J E, Branch L G, Colditz G A, et al.  A prospective study of consumption of carotenoids in fruits and vegetables and decreased cardiovascular mortality in the elderly.  Ann Epidemol  1995; 5:p 225

Di Mascio p, Murphy M E, Sies H.  Antioxidant defense systems:  The role of carotenoids, tocopherols and thiols.  Am J Clin Nutr.  1991; 53:p194S-200S.

Smidt C R, Burke D S.  Nutritional significance and measurement of carotenoids.  Current Topics in Nutritional Research.  2004; 2(2):p79-91

Smidt C R, Burke D S.  Nutritional significance and measurement of carotenoids.  Current Topics in Nutritional Research.  2004; 2(2):p79-91.

Peng Y M, Peng Y S, Lin Y, Moon T, et al.  Concentrations and plasma-tissue-diet relationships of carotenoids, retinoids, and tocopherols in humans.  Nutrition and Cancer.  1995; 23:p233-246.

Bone R A, Landrum J T, Friedes L M, Gomez C M, et al.  Distribution of lutein and zeaxanthin in the eyes, serum, and diet of human subjects.  Experimental Eye Research.  1997; 64:p211-218.

Stahl W, Schwarz W, Sundquist A R, Sies H.  Cis-trans isomers of lycopene and beta-carotene in human serum and tissues.  Archives of Biochemistryand Biophysics.  1992; 294: p173-177.

Clinton S K, Emenhiser C, Schwartz S J, Bostwick D G, et al.  Cis-trans lycopene isomers, carotenoids, and retinol in the human prostate.  Cancer Epidemiology Biomarkers & Prevention.  1996; 5:p823-833.

Bone R A, Landrum J T, Fernandez I, Tarsis S I.  Analysis of the macular pigment by HPLC:  retinal distribution and age study.  Investigative Ophthalmology and Visual Science.  1988; 29:p843-849.

Yeum K J, Taylor R A, Tang G W, and Russel R M. Measurement of carotenoids, retinoids, and tocopherols in human lenses.  Investigative Ophthalmology and Visual Science.  1995; 36:p2756-2761. 

Ribaya-Mercado  J D, Garmyn M, Gilcrest B A, Russell R M.  Skin lycopene is destroyed preferentially over b-carotene during ultraviolet irradiation in humans.  J of Nutr.  1995; 125:p1854-1859.

Heinrich U, Gartner C, Wiebusch M, Eichler O, et al.  Supplementation with b-carotene or a similar amount of mixed carotenoids protects humans from UV-induced erythema.  J of Nutr.  2003; 133:p98-101.

Hata, T R, Scholz T A, Emakov I V, McClane R W, et al.  Non-invasive Raman spectroscopic detection of carotenoids in human skin.  J Invest Dermatology.  2000; 115:p441-448.

Cook N R, Stampfer M J, Ma J, et al.  Beta-carotene supplementation for patients with low baseline levels and decreased risks of total and prostate carcinoma.  Cancer.  1999; 86:p1783-1792.

Zhang S, Hunter D J, Forman M R, et al.  Dietary carotenoids and vitamins A, C, E and risk of breast cancer.  J Natl Cancer Inst.  1999; 91:p547-556.

Schuurman A G, Goldbohm R A, Brants H A, van den Brandt P A.  A prospective cohort study on intake of retinol, vitamins C and E, and carotenoids and prostate cancer risk (Netherlands).  Cancer Causes Control.  2002; 13:p573-582.

Wu K, Erdman J W Jr, Schwartz S J, Platz E A, Leitzmann M, et al.  Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study.  Cancer Epidemiol Biomarkers Prev. 2004; 13:p260-269.

Kucuk O, Sarkar F H, Sakr W, Djuric Z,Pollak M N, et al.  Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy.  Cancer Epidemiol Biomarkers Prev.  2001; 10:p886-893.

Giles G, Ireland P.  Diet, nutrition and prostate cancer.  Int  J Cancer.  1997; 72:p13-17.

Jacobs E J, Connell C J, Patel  A C, Chao A, et al.  Multivitamin use and colon cancer mortality in the Cancer Prevention Study II cohort (United States).  Cancer Causes Control.  2001; 12(10):p.927-934.

Byers T, Guerrero N.   Epidemiologic evidence for vitamin C and vitamin E in cancer prevention.  Am J Clin Nutr.  1995; 62:p1385S-1392S.

Negri E, Franceschi S, Bosetti C, et al. Selected micronutrients and oral and pharyngeal cancer.  Int J Cancer.  2000; 86:p122-127.

You W C, Zhang L, Gail M H, et al.  Gastric dysplasia and gastric cancer:  Helicobacter pylori, serum vitamin C, and other risk factors.  J Natl Cancer Inst.  2000; 92:p1607-1612.

Gandini S, Merzenich H, Robertson C, Boyle P.  Meta-analysis of studies on breast cancer risk and diet: the role of fruit and vegetable consumption and the intake of associated micronutirents.  Eur J Cancer.  2000; 36:p636-646.

Lee K W, Lee H J, Surh Y J, Lee C Y.  Vitamin C and cancer chemoprevention: reappraisal.  Am J Clin Nutr.  2003; 78: p1074-1078.

Kim Y I.  Folate and cancer prevention:  a new medical application of folate beyond hyperhomocysteinemia and neural tube defects.  Nutr Rev.  1999; 57:p314-321.

Wu K, Helzlsouer K J, Comstock G W, Hoffman S C, Nadeau M R, Selhub J, Mason J B.  A prospective study on folate, B12, and pyridoxal 5’-phosphate (B6) and breast cancer. Cancer Epidemiol Biomarkers Prev.  1999; 8:p209-217.

Zhang S M, Willet W C, Selhub J, Hunter D J, Giovannucci E L, Holmes M D, Colditz G A, Hankinson S E.  Plasma folate, B6, vitamin B12, homocysteine, and risk of breast cancer.  J Natl Cancer Inst.  2003; 95:p373-380.

Hollick M F, Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease and osteoporosis.  Am J Clin Nutr.  2004; 79:p362-371.

Joshipura K J, Ascherio A, Manson J E, et al.  Fruit and vegetable intake in relation to risk of ischemic stroke.  JAMA.  1999; 282:p1233-1239.

Joshipura K J, Hu F B, Manson J E, et al.  The effect of fruit and vegetable intake on risk for coronary heart disease.  Ann Intern Med. 2001; 134:p1106-1114.

Knekt P, Reunanen A, Jarvinen R, Seppanen R, et al.  Antioxidant vitamin intake and coronary mortality in a longitudinal population study.  Am J Epidemiol.  1994; 139:p1180-1189.

Hodis H N, Mack W J, LaBree L, et al.  Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis.  JAMA.  1995; 273: p1849-1854.

Rimm E B, Willet W C, Hu F B, et al.  Folate and Vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women.  JAMA.  1998; 279:p.359-364.

Evans R W, Shaten B J, Day B W, Kuller L H.  Prospective association between lipid soluble antioxidants and coronary heart disease in men: the Multiple Risk Factor Intervention Trial.  Am J Epidemiol.  1998; 147:p180-186.

Kushi L H, Folsom A R, Prineas R J, Mink P J, et al.  Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women.  N Eng J Med.  1996; 334(18):p1156-1162.

Rimm E B, Stampfer M J, Ascherio A,  et al.  Vitamin E consumption and the risk of coronary heart disease in men.  N Engl J Med.  1993; 328:p1450-1456.

Ward M, McNulty H, McPartlin J, Strain J J, et al.  Plasma homocysteine, a risk factor for cardiovascular disease is lowered by physiological doses of folic acid.  QJM. 1997; 90:p519-524.

Committee on Diet and Health.  Diet and Health: Implications for Reducing Chronic Disease Risk.  Washington DC.  National Academy Press.  1989.

Dobson A, DaVanzo J, Consunji M, Gilani J, et al.  A Study of the Cost Effects of Daily Multivitamins for Older Adults.  The Lewin Group.   Falls Church, VA.  2004.

Selhub J, Jacques P F, Rosenberg I H et al.  Serum total homocysteine concentrations in the third National Health and Nutrition Examination Survey (1991-1994); population reference ranges and contribution of vitamin status to high serum concentrations.  Ann Intern Med. 1999; 131: p331-339.

Eikelboom J W, Lonn E, Genest J Jr, Hankey G, Yusuf S.  Homocysteine and cardiovascular disease: a critical review of the epidemiological evidence.  Ann Intern Med.  1999; 131:p363-375.

Graham I M, Daly  L E, Refsum H M, et al.  Plasma homocysteine as a risk factor for vascular disease:  the European Concerted Action Project.  JAMA.  1997; 277:p1775-1781.

Welch G N, Loscalzo J.  Homocysteine and atherothrombosis.  N Engl J Med.  1998; 338:p1042-1050.

Robinson K, Arheart K, Refsum H et al for the European COMAC Group.  Low circulating folate and vitamin B6 concentrations: risk factors for stroke, peripheral vascular disease, and coronary artery disease.  Circulation.  1998; 97:p437-443.

Nygard O, Refsum H, Ueland P M, Vollset S E.  Major lifestyle determinants of plasma total homocysteine distribution: the Hordaland Homocysteine Study.  Am J Clin Nutr.  1998; 67:p263-270.

Selhub J, Jacques PF, Rosenberg IH et al.  Serum total homocysteine concentrations in the third National Health and Nutrition Examination Survey (1991-1994); population reference ranges and contribution of vitamin status to high serum concentrations.  Ann Intern Med. 1999; 131: p331-339.

Klipstein-Grobusch K, Geleijnse J M, den Breeijen J H, Boeing H et al.  Dietary antioxidants and risk of myocardial infarction in the elderly: the Rotterdam Study.  Am J Clin Nutr.  1999; 69(2):p261-266.

Sesso H D, Buring J E, Norkus E P, Gaziano J M.  Plasma lycopene, other carotenoids and retinol and the risk of cardiovascular disease in women.  Am J Clin Nutr.  2004; 79:p47-53.

Cardinault N, Gorrand j M, Tyssandier V, Grolier P, et al.  Short term supplementation with lutein affects biomarkers of lutein status similarly in young and elderly subjects.  Experimental Gerontology. 2003; 38:p573-582.

Van Leeuwen R, Boekhoorn S, Vingerling J R, Witteman C M, et al.  Dietary intake of antioxidants and risk of age-related macular degeneration.  JAMA.  2005; 294:p3101-3107.

Deming D M, Boileau T, Heintz K H, Arkinson C A, Erdman J W  Jr.  Carotenoids:  Linking chemistry, absorption, and metabolism to potential roles in human health and disease.  In Cadenas E, and Packer L, (Eds).  Handbook of Antioxidants.  Marcel-Dekker.  New York.  2002; p189-221.

Bone R A, Landrum J T, Guerra L H, Ruiz C A.  Lutein and zeaxanthin dietary dietary supplements raise macular pigment density and serum concentrations of these carotenoids in humans.  J of Nutr. 2003; 133:p992-998.

Bone R A, Landrum J T, Friedes L M, Gomez C M, et al.  Distribution of lutein and zeaxanthin stereoisomers in the human retina.  Experimental Eye Research.  1997; 64:p211-218.

Sies H, Stahl W.  Non-nutritive bioactive constituents of plants:  lycopene, lutein and zeaxanthin.  Intl J for Vitamin and Nutritional Research.  2003; 73:p95-100.

Krinsky N I, Landrum J T, Bone R A.  Biologic mechanisms of the protective role of lutein and zeaxanthin in the eye.  Annual Review of Nutrition.  2003; 23:p171-201.

Bone R A, Landrum J T, Dixon Z, Chen Y, Lierena C M.  Lutein and zeaxanthin in the eyes, serum and diet of human subjects.  Experimental Eye Research.  2000; 71:p239-245

Bernstein P S, Zhao D Y, Wintch S W, Ermakov I V, et al.  Resonance Raman measurement of macular carotenoids in normal subjects and in age-related macular degeneration.  Ophthalmology.  2002; 109:p1780-1787.

Bone R A, Landrum J T, Guerra L H, Ruiz C A.  Lutein and zeaxanthin dietary dietary supplements raise macular pigment density and serum concentrations of these carotenoids in humans.  J of Nutr. 2003; 133:p992-998.

Mares-Perlman JA, Fisher AI, Klein R, et al. Lutein and zeaxanthin in the diet and serum and their relation to age-related maculopathy in the third National Health and Nutrition Examination Survey.  Am J Epidemiol. 2001; 153:p424–432

van Leeuwen R, Boekhoorn S, Vingerling J R, Witteman C M, et al.  Dietary intake of antioxidants and risk of age-related macular degeneration.  JAMA.  2005; 294:p3101-3107.

Mares J A.  Potential value of antioxidant-rich foods in slowing age-related macular degeneration.  Arch Ophthamol.  2006; 124(9):p1339-1340.

Mayo J C, Sainz R M, Tan D X, Antolin I, Rodriguez C, Reiter R J.  Melatonin and parkinson’s disease.  Endocrine.  2005; 27:p169-178.

Calabrese V, Butterfield D A, Stella A M.  Nutritional antioxidants and the heme pathway of stress tolerance:  novel targets for neuroprotection in Alzheimer’s disease.  Ital J Biochem.  2003; Dec: (52)4:p177-181.

Dias-Santagata D, Fulga T A, Duttaroy A, Feany M B.  Oxidative stress mediates tau-induced neurodegeneration in Drosophila.  J. Clin. Invest. 2007; 117:p236-245

Fisher H W.  Reishi Rescue: R & R for Your Immune System.  Wood Publishing.  Toronto.  2005; p31.

Dias-Santagata D, Fulga T A, Duttaroy A, Feany M B.  Oxidative stress mediates tau-induced neurodegeneration in Drosophila.  J. Clin. Invest. 2007; 117:p236-245.

Stoff J. An Examination of Immune Response Modulation in Humans by Antigen Infused Dialyzable Bovine Colostrum/Whey Extract Using A Double Blind Study.  Tucson. Immune Consultants. 2001.

Imai K, Matsuyama S, Miyake S, Suga K, et al.  Natural cytotoxic activity of peripheral-blood lymphocytes and cancer incidence: an 11 year follow-up study of a general population.  Lancet.  2000; 9244:p1795-1799.

Whiteside T, Herberman R.  The role of natural killer cells in human disease.  Clin Immunology Immunopathology.  1989; 53:p1-23.

Dawson H D, Li N Q, Decicco K L, Nibert J A, Ross A C.  Chronic marginal vitamin A status reduces natural killer cell number and function in aging Lewis rats.  J Nutr. 1999; 129:p1510-1517.

Bowman T A, Goonewardene M, Pasatiempo A M G, Ross A C, Taylor C E.  Vitamin A deficiency decreases natural killer cell activity and interferon production in rats. J. Nutr. 1990; 120:p1264-1273.

Santos M S, Meydani S N, Leka L, Wu D, Fotouli M et al.  Natural killer cell activity in elderly men is enhanced by beta-carotene supplementation.  Am J Clin Nutr.  1996; 64:p772-777.

Wasser S P, and Weis A L.  Therapeutic effects of substances occurring in higher Basidiomyte mushrooms: a modern perspective.  Critical Reviews in Immunology. 1999. 19; p65-96.

Wang S Y, Hsu M L, Hsu H C, Tzeng S S, Lee S S, Shiao M S, and Ho C R.  The antitumour effect of Ganoderma lucidum is mediated by cytokines released from activated macrophages and T-lymphocytes.  Intl J Cancer.  1997; 70(6); p669-705.

van der Hem L G, van der Vliet J A, Bocken C F, et al.  Ling Zhi-8; studies of qa new immunomodulatring agent.  Transplantation.  1995; 60(5): p438-443.

Chen H S et al. Studies on the immunomodulating and antitumor activities of Ganoderma lucidum (Reishi) polysaccharides. Bioorg Med Chem. 2004.  Nov 1;12(21): p.5595-5601.

Ooi V E, Liu F.  Immunomodulation and anti-cancer activity of polysaccharide-protein complexes.  Curr Med Chem.  2000; Jul: 7(7): p.715-729.

Tzianabos A O.  Polysaccharide Immunomodulators as Therapeutic Agents:  Structural Aspects and Biologic Function.  Clinical Microbiology Reviews. October 2000;  13;p523-533.

Smith J E, Rowan N J, Sullivan R.  Medicinal mushrooms: their therapeutic properties and current medical usage with special emphasis on cancer treatments.  University of Strathclyde. 2002.

Herder R, Demmig-Adams B.  The power of a balanced diet and lifestyle in preventing cardiovascular disease.  Nutr Clin Care.  2004; 7(2):46-55.

Gaziano J M, Manson J E.  Diet and heart disease.  The role of fat, alcohol, and antioxidants.  Cardiol Clin.  1996; 14(1):p69-83.

Eyre H, Kahn, R, Robertson R M.  American Cancer Society, American Diabetes Association, and American Heart Association Collaborative Writing Committees.  Preventing Cancer, cardiovascular disease, and diabetes: a common agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association.  Diabetes Care.  2004; 27(7):p1812-24.

Donaldson M S.  Nutrition and Cancer: A review of the evidence for an anti-cancer diet.  Nutrition Journal.  2004; 3(19).

Key T J, Schatzkin A, Willett W C, Allen N E, Spencer E A et al.  Diet, nutrition, and the prevention of cancer.  Public Health Nutr.  2004; 7(1A):p187-200.

Stoff J. An Examination of Immune Response Modulation in Humans by Antigen Infused Dialyzable Bovine Colostrum/Whey Extract Using A Double Blind Study.  Tucson. Immune Consultants. 2001.

Chandra R K. Effect of vitamin and trace-element supplementation on immune responses and infection in elderly subjects.  Lancet.  1992; 340:p1124-7.

Fawzi W, Stanpfer MJ.  A role for multivitamins in infection?  Ann Int Med.  2003; 138(5):p430-431.

Meydani S N, Meydani M, Blumberg J B, et al.  Vitamin E supplementation and in vivo immune response in healthy elderly subjects: a randomized controlled trial.  JAMA.  1997; 277:p1380-1386.

Chandra R K.  Nutrition and the immune system from birth to old age.   Eur J Clin Nutr.  2002; 131:p2192-2196.

Chandra R K.  Influence of multinutrient supplement on immune responses and infection-related illness in 50-65 year old individuals.  Nutr Res.  2002; 22:p5-11.

Beach R.  Modern Miracle Men.  Washington.  United States Government Printing Office Document No. 264. 1941.

Balch J, Balch P.  Prescription for Nutritional Healing.  New York.  Avery Publishing Group.  2000; p14.

Dickinson A, Ed.  The Benefits of Nutritional Supplements.  Washington.   Council for Responsible Nutrition.  1998; p61.

Hallfrisch J H,  Muller D C, Singh D M.  Vitamin A and E intake plasma concentration   of retinol, beta.carotene, alpha-tocophero in men and women of the Baltimore longitudinal study of aging.  Am J Clin Nutr.  1992; 1994; 60:p176-182.

Fletcher R H,  Fairfield K M.  Vitamins for chronic disease prevention in adults: scientific review.  JAMA.  2002; 287(23):p3116-26.

Simone C.  Cancer and Nutrition.  Garden City Park, New York.  Avery Publishing Group.  1992; p46.

Donaldson M S.  Nutrition and Cancer: A review of the evidence for an anti-cancer diet.  Nutrition Journal.  2004; 3(19).

Christen W G, Gaziano M, Hennekens C H.  Design of  Physicians’ Health Study II- A Randomized Trial of Beta-Carotene, Vitamins E and C, and Multivitamins, in Prevention of Cancer, Cardiovascular Disease, and Eye Disease, and Review of Results of Completed Trials.  Annals of Epidemiology.  2000; 10(2):p125-134

Deming D M, Boileau T, Heintz K H, Arkinson C A, Erdman J W  Jr.  Carotenoids:  Linking chemistry, absorption, and metabolism to potential roles in human health and disease.  In Cadenas E, and Packer L, (Eds).  Handbook of Antioxidants.  Marcel-Dekker.  New York.  2002; p189-221.

Giovannucci E, Stampfer M J, Colditz G A, Hunter D J, Fuchs C, et al.  Multivitamin use, folate and colon cancer in women in the Nurses’ Health Study.  Ann Intern Med. 1998; 129(7):p517-24.

Giovannucci E, Ascherio A, Rimm E B, Stampfer M J, Colditz G A, Willett W.  Intake of carotenoids and retinol in relation to risk of prostate cancer.  J Natl Cancer Inst.  1995; 87: p1767-1776.

Giovannucci E, Rimm E B, Stampfer M J,  Willett W.  A prospective study of tomato products, lycopene and prostate cancer risk..  J Natl Cancer Inst.  2002; 94: p391-398.

Chan J M, Stampfer M J, Ma J, Rimm E B, Willett W C, Giovannucci E L.  Supplemental Vitamin E intake and prostate cancer risk in a large cohort of men in the United States.  Cancer Epidemiol Biomarkers Prev.  1999; 8:p893-899.

Alpha-Tocopherol Beta-Carotene Cancer Prevention Study Group.  The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers,  N Engl J Med. 1994; 330:p1029-1035.

Speizer F E, Colditz G A, Hunter D J, Rosner  B, et al.  Prospective study of smoking, antioxidant intake, and lung cancer in middle-aged women (USA).  Cancer Causes Control.  1999; 10:p475-482.

Michaud D S, Feskanich D, Rimm E B, et al.  Intake of specific carotenoids and the risk of lung cancer in 2  prospective US cohorts.  Am J Clin Nutr.  2000; 72:p990-997.

Hsing A W, Comstock G W, Abbey H, Polk B F.  Serologic precursors of cancer.  Retinol, carotenoids and tocopherol and risk of prostate cancer.  J Natl Cancer Inst.  1990; 82:p941-946.

Knekt P, Jarvinen, Teppo L, Aromaa A, Seppanen R.  Role of various carotenoids in lung cancer prevention.  J Natl Cancer Inst.  1999; 91:p182-184.

Pottenger Francis Jr, Pottenger’s Cats: A Study in Nutrition.Price-Pottenger Foundation, Inc., La Mesa, CA, 1995.

Fairfield K M, Fletcher R H.  Vitamins for chronic disease prevention in adults: scientific review.  JAMA.  2002; 287(23):p3116-3126.

Murphy SP et al.    Demographic and economic factors associated with dietary quality for adults in 1987-1988 Nationwide Food Consumption Survey.  J Am Diet Assn. 1992; 92:1352-1357.

Challem, Jack.  10 Reasons to take supplements.  Aloha, Ore.  The Nutrition Reporter.  October/November 1996; p7-9.

Schafer F Q, Wang H P, Kelley E E, Cuenko K L et al.  Comparing beta-carotene, vitamin E and nitric oxide as membrane antioxidants.  Biological Chemistry.  2002; 383:p671-681.

Sies H, Menck C F.  Singlet oxygen induced DNA damage.  Mutation Research. 1992; 275:p367-375.

Mckay D L, Perrone G, Rasmussen H, Dallal G, et al.  The effects of a multivitamin/mineral supplement on micronutrient status, antioxidant capacity and cytokine production in healthy older adults consuming a fortified diet.  J Am Coll Nutr.  2000; 19(5):p613-621.

Preziosi P, Galan P, Herbeth B, Valeix P, et al.  Effects of supplementation with a combination of antioxidant vitamins and trace elements at nutritional doses, on biochemical indicators and markers of the antioxidant system in adult subjects.  J Am Coll Nutr. 1998; 17(3):p244-249.

Block G, Patterson B, Subar A.  Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence.  Nutr Cancer.  1992; 18:p1-29.

Steinmetz K A, Potter J D.  Vegetables, fruit, and cancer protection:  a review.  J Am Diet Assoc.  1996: 96:p1027-1039.

U.S. Department of Health and Human Service Centers for Disease Control and Prevention.  National Center for Health Statistics.  Deaths – Leading Causes 2004.

Fairfield K M, Fletcher R H.  Vitamins for chronic disease prevention in adults: scientific review.  JAMA.  2002; 287(23):p3116-26.

Selhub J, Jacques PF, Rosenberg IH et al.  Serum total homocysteine concentrations in the third National Health and Nutrition Examination Survey (1991-1994); population reference ranges and contribution of vitamin status to high serum concentrations.  Ann Intern Med. 1999; 131: p331-339.

Chandra RK.  Influence of multinutrient supplement on immune responses and infection-related illness in 50-65 year old individuals.  Nutr Res.   2002;22;p5-11.

Knekt P, Reunanen A, Jarvinen R, Seppanen R, et al Antioxidant vitamin intake and coronary mortality in a longitudinal study.  Am J Epidemiol.  1994; 139:p180-189.

Ness A R, Powles J W.  Fruit and vegetables, and cardiovascular disease: a review.  Int J Epidemiol.  1997; 26:p1-13.

Fletcher R H,  Fairfield K M.  Vitamins for chronic disease prevention in adults: scientific review.  JAMA.  2002; 287(23):p3116-26.

Vellas B J, Albarede J L, Garry P J.  Diseases and aging: patterns of morbidity and age; relationship between aging and age associated diseases.  Am J Clin Nutr.  1992; 55:p1225S-1230S.

Alexis Carrel. The Columbia Electronic Encyclopedia, 6th ed. Copyright 2007, Columbia University Press.  <

Lindsten  J, Ed. Nobel Lectures, Physiology or Medicine 1901-1921.  Elsevier Publishing Company.  Amsterdam.  1967.

Disclaimer | Site Map | Privacy Policy | Contact Us | ©2007 The Fisher Clinic