Dietetic Advice for Immunodeficiency
by Siro Passi and
Chiara De Luca
Cell Aging Center, Istituto
Dermopatico dell'Immacolata (IDI) Rome, Italy .
Note: The information on this website is
presented for educational purposes and
is not a substitute for the advice of and treatment by a qualified professional.
This document was provided by
Continuum Magazine
Dr. Siro Passi graduated in biochemistry from the University
of Rome in 1969. He is head of the Cell Aging Center of the IDI Research Institute (Rome).
Over the past two decades he has investigated in vivo natural defence mechanisms of
living cells against reactive oxygen and nitrogen species and other toxic radicals, and
has published many papers on oxidative stress and its consequences in different
pathologies. On the basis of his studies of patients diagnosed HIV positive and/or with
AIDS in the early '90s, he asserted that HIV phenomena are the outcome of oxidative
stress, not vice versa. In 1995 he published with Prof. Ferdinando Ippolitono, a
'heretic' book, AIDS - new frontier, ed. G. Lombardo, Rome.
Chiara De Luca graduated in Biology in 1985, and
Pathology in 1989. Her research has included oxidative stress in animals and plant models, inhibition of
aflatoxin induced tumor development and studies on the role of lipoperoxidation in
cutaneous aging. At the Cell Aging Center, she works on the role of antioxidants and
polyunsaturated fatty acids in blood and tissues, and oxidative mechanisms in the
induction and development of infectious, pigmentary and neoplastic pathologies. Since 1991
she has collaborated with the National Institute for Nutrition, on the prevention of
mycotoxin contamination of the main components of the national diet, the determination of
additives in special foods and total diets, the study of antioxidants in food and the
benefits of antioxidant supplementation by the use of 'functional foods'.
| Diet, by definition, is not only the food in
regular use, but also a prescribed course of food designed for the treatment and
prevention of diseases. Physicians of antiquity, first of all Hippocrates in Greece and
Rhases in Iran, taught: "If a diet can cure, prescribe no other remedy". |
With the growth of scientific knowledge, dietetics
has become an applied science, and today there is an increased understanding of the role
of nutritional factors in degenerative diseases, prolonged illness, acute injury, and
complicated surgical and medical procedures, which are all frequently accompanied by
malnutrition. The immunological disorders associated with malnutrition were named
"Nutritionally Acquired Immune Deficiency Syndrome" (NAIDS), much before the
trumpeting appearance of HIV. Nutrition must be considered a fundamental intervention in
the early and ongoing treatment of immunodeficiency; in particular, micronutrients
represent important cofactors for the optimal functioning of the immune system and are
able to enhance disease resistance in humans and animals. As a consequence, a plethora of
commercial dietary products and practices purporting to enhance well being or reduce
weight is in vogue, mainly in advanced countries. In addition, several companies have
manufactured vitamin E, b-carotene, selenium, vitamin C, superoxide dismutase capsules,
Chinese herbs, multivitamin tablets, and many other microelements as a panacea for all
diseases. This is surely a multi-million dollar business, but many claims are unlikely to
be true. And physicians and people should be alert since some of these diets and nutrients
may induce toxicity states or nutrient deficiency in individuals adhering to them. Before
getting on to the subject, we take the liberty of introducing some general considerations
on nutrition.
Nutrition: general considerations (1-5)
All natural foods, the composition of which is very
complex, yield nutrients that, on digestion, are generally classified into proteins,
lipids or fats, carbohydrates, vitamins and mineral elements. These provide the body with
the compounds necessary for the production of energy in the form of work and heat, and for
growth, repair and reproduction of every living cell. Carbohydrates, lipids and proteins
are considered macronutrients, and are interchangeable sources of energy: lipids yield up
to 9 kcal/g, protein and carbohydrates up to 4 kcal/g. Vitamins and mineral elements are
considered as micronutrients.
MACRONUTRIENTS
Proteins.
Human proteins are very large molecules which represent an
essential structural part of cells and are built up from the 20 "standard" amino
acids, listed in Table 1, and divided into essential and non-essential amino acids. The
variety of ways in which they combine can provide millions of different proteins, which
are "species-specific" in that their structures differ from one species to
another.
Table
1. Essential and non-essential aminoacids in humans.
Essential |
Non-essential |
Histidine |
Alanine |
Leucine |
Cysteine |
Isoleucine |
Glycine |
Lysine |
Proline |
Methionine |
Serine |
Phenylalanine |
Tyrosine |
Threonine |
Glutamine |
Valine |
Asparagine |
Tryptophan |
Aspartic
acid |
Arginine* |
Glutamic
acid |
Only 10 amino acids have been shown to be "essential
", i.e. indispensable nutrients for humans and must be obtained from diet; the
remaining ones can be synthesized by common intermediates, mainly deriving from the
breakdown products of the metabolism of essential aminoacids.
*Even though mammals synthesize arginine by the urea
cycle, the aminoacid is considered as essential, since it is required in a higher amount
than can be produced by this route, mainly during normal childhood development.
Since different proteins contain different amounts of the
essential amino acids, a balanced protein diet must contain different protein sources,
which complement each other to supply the right proportion of all the essential amino
acids. For example, milk proteins contain them in the proper proportion for a correct
human nutrition; bean proteins, in contrast to wheat proteins, are rich in lysine, but are
lacking in methionine. Any excess amino acids in the diet, beyond the effective needs of
the body, are metabolized and burnt as a source of energy, which is largely more expensive
than that deriving from fats or carbohydrates. In any case, as a general guide, it is
recommended that the protein intake should be equivalent to 11-14% of the total calories
in the diet.
Lipids or fats.
Lipids, partly deriving from diet, and partly from surplus
carbohydrates in the food, provide the main reserve of energy. The term "lipids"
includes both molecules that contain fatty acids (Table 2) - examples being triglycerides
and phospholipids - and molecules such as cholesterol and steroid hormones displaying
hydrocarbon ring structures. Recently, the terms "n-3 and n-6 polyunsaturated fatty
acids &endash; PUFA ", in contrast with saturated fatty acids, have become very
familiar to the general public. They have been associated with the concept of
"healthy fat", and oils such as "evening primrose oil" or "fish
oil", have been promoted by wide advertising. It is important to underline that there
are no pure "saturated" or "polyunsaturated" sources of dietary fats.
In fact, most food triglycerides or phospholipids contain a mixture of saturated,
monounsaturated and polyunsaturated fatty acids. Thus, for example, polyunsaturated corn
oil contains approximately 20 % saturated fatty acids, and saturated lard has
approximately equal levels of saturated and monounsaturated fatty acids.
Table
2. Natural fatty acids occurring in common foods, as triglycerides or phospholipids.
| Common name |
Main Sources |
| Palmitic acid (C16:0) |
Palm oil, butter, cheese and other animal fats and oils |
| Stearic acid (C18:0) |
Tallow, butter, cheese, and other animal fats and oils |
| Oleic acid (C18:1 n-9) |
Olive and hazel oils |
| Linolenic acid (C18:2 n-6) |
Many seed oils |
| a-linolenic acid (C18:3 n-3) |
Linseed and rapeseed oils |
| g-linolenic acid (C18:3 n-6) |
Borago and evening primrose oils |
| di-homo-g-linolenic acid (C20:3 n-6) |
Human milk |
| Arachindonic acid (C20:4 n-6) |
Animal membranes (phospholipids) |
| Eicosapentaenoic acid (C20:5 n-3) |
Fish oils |
| Docosahexaenoic acid (C22:6 n-3) |
Fish oils, nervous system (phospholipids) |
Linoleic acid and a-linolenic acid are thought to be
essential in the human diet and are known as essential fatty acids (EFA). Our cells are
unable to synthesize them, and therefore they must be obtained mainly by food of vegetable
origin. EFA, in the organism, can both supply energy by means of their oxidation and
undergo biochemical transformations by means of desaturase and elongase enzymes to produce
n-6 or n-3 polyunsaturated fatty acids (PUFA) with a higher number of double bonds, such
as C20:3 n-6, C20:4 n-6, C20:5 n-3, C22:6 n-3, etc.
From a physio-pathological point of view, it has been
suggested that:
n-6 PUFA may play an aetiological role in heart diseases,
and cancer cells thrive on them;
n-3 PUFA may reduce the risk of both cancer and
cardiovascular diseases;
monounsaturated fatty acids may help against
cardiovascular diseases;
saturated fatty acids may be partly responsible for the
degenerative changes in the arteries, sometimes resulting in coronary thrombosis;
trans-unsaturated fatty acids, i.e. unsaturated fatty
acids with double bond in trans position, artificially generated during the process of
hydrogenation of PUFA, and found in packaged snacks, may be involved in cardiovascular
diseases and breast cancer.
Carbohydrates
Carbohydrates provide most of the energy (up to 90%) in
almost all human diets; in any case, a well-balanced diet normally contains enough
carbohydrates to provide 55-65% of total calories. The main carbohydrate in most natural
foodstuff is starch that, during digestion and metabolism, is finally converted into
glucose. This is carried by the blood to tissues, where it is either oxidized at once or
converted to fat, since the body has a very limited capability for storing it as glycogen
in muscles and liver.
MICRONUTRIENTS: vitamins and mineral
elements (Table 3)
Vitamins.
Vitamins are classified as fat soluble (A, D, E and K) or
water soluble (B group and C). The former ones are mainly derived from animal or vegetable
fats; the vitamin B group from whole grain cereals, and vitamin C from fresh fruits and
green vegetables.
Mineral elements.
The main mineral elements occurring in the body at
concentration >0.005% are calcium, phosphorus, and potassium. Other elements such as
iron, magnesium, sodium, zinc, iodine, copper, selenium, fluorine, cobalt, chromium occur
in much lower concentrations (< 0.005 %).
Elements such as gold and silver found in the body do not
appear to play a recognized metabolic role, while other elements such as barium and
strontium are only suspected of being essential.
Table 3. The principal micronutrients.
THE PRINCIPAL MICRONUTRIENTS (VITAMINS &
MINERALS)
| Micronutrients |
Main natural sources (µg /100 g) |
Main Functions |
Recommended dietary allowances (RDA)
for healthy adults (19-50 yr), males. |
Recommended dietary allowances (RDA)
for healthy adults (19-50 yr), males. |
| .. |
. |
. |
MALES |
FEMALES |
| . |
. |
FAT SOLUBLE VITAMINS |
. |
. |
| Vitamin A (Retinol) |
Cow and pigs livers 5,000-10,000
Cod liver oil
15,000-20,000
Shark liver oil
600,000-10,000,000
Egg yolk
300-450
Parmesan cheese
300-350
Milk
30-50 |
Photoreceptor mechanism of retina;integrity of
epithelia;glycoprotein synthese... antioxidant? |
1,000 ug |
800 ug |
| b-carotene |
Carrots 5,000-12,000
Fennel
4,000-5,000
Broccoli, Cabbages
1,900-5,000
Apricots
1,000-4,000 |
Provitamin A; scavenger of singlet oxygen, suggested
antioxidant in vivo... |
See vitamin A 6 ug
b-carotene=1 retinol equivalent (RE) |
See vitamin A 6 ug
b-carotene=1 retinol equivalent |
| Lycopene |
Fresh ripe tomatoes 1,800-2,500 |
Scavenger of singlet oxygen; Suggested antioxidant in
vivo |
Non set |
Non set |
| Vitamin D |
UV irradiation of the skin Cod liver oil
250-750
Tuna liver oil
5,000-10,000
Egg yolk
4-10 |
Calcium and phosphorus absorbtion; Reabsorption
mineralisation and collagen maturation of bone... |
10-5 ug 1 IU
vitamin D = 0.025 ng cholecalcipherol |
10-5 ug 1 IU
vitamin D = 0.025 ng cholecalcipherol |
| Vitamin E (d-RRR-a
tocopherol) |
Wheat germ oil 150,000-500,000
Cereal germs
12,000-14,000
Soya bean oil
120,000-160,000
Olive oil
10,000-20,000
Peanut oil
14,000-30,000
Egg yolk
1,000-1,500 |
Chain breaking anti-oxidant in vivo |
10mg (USA) 4mg (UK)
1 mg d-RRR a tocopherol = 1.49IU = 1.49mg synthetic d, 1-a
tocopherol acetate |
8 mg (USA) 3 mg
(UK)
1 mg d-RRR a tocopherol = 1.49IU = 1.49mg synthetic d, 1-a
tocopherol acetate |
| Vitamin K (group) |
Spinach leaves 500-600
Cabbages
350-400
Carrots
0,80-100
Broccoli
120-140
Lettuce
180-200
Pork liver
400-800 |
Normal blood coagulation; formation of coagulation
factors (prothrombin, etc)... |
70-80 mg |
60-65 mg |
| . |
. |
WATER SOLUBLE
VITAMINS |
. |
. |
| Vitamin C |
Citrus fruits 40,000-60,000
Spinach leaves
70,000-90,000
Potatoes
10,000-30,000
Cabbages
30,000-1,000
Broccoli
100,000-120,000 |
Collagen formation, vascular function; wound healing;
antioxidant in vivo... |
60 mg (USA) 40 mg
(UK) |
60 mg (USA) 40 mg
(UK) |
| Thiamine (vit
B1) |
Dried yeast 2,500-10,000
Whole grains
300-500
Beef meat
500-5,000
Pork meat
300-1,000
Legumes
350-400
Egg yolk
300-500 |
Carbohydrate metabolism; nerve cell function; myocardial
function... |
1.2 mg |
0.9 mg |
| Riboflavin (vit
B2) |
Dried yeast 3,000-5,000
Cheese
300-700
Milk
150-170
Beef,pork meat
100-400
Cows liver, pork liver
1,700-3,200
Cereal germ
500-4,000
Wheat flour
100-200 |
Energy and protein metabolism (precursor of FMN and FAD);
integrity of mucous membrane |
1.6 mg |
1.3 mg |
| Niacin (nicotinic
acid, nicotinamide) |
Dried yeast 50,000-60,000
Whole grain cereals
1,500-5,000
Wheat flour
4,800-5,500
Legumes
2,300-5,000
Pork, beef meats and liver
5,000-12,000
Fish (cool, salmon, tinca)
2,000-10,000 |
Oxidation-reductin reactions (precursor of NAD(P)H ;
Carbohydrate metabolism... |
18 mg 1 mg niacin =
1 niacin equivalent (1NE) = 60 mg dietary tryptofan (this aminoacid is able to synthesise
endogenous niacin) |
14 mg 1 mg niacin =
1 niacin equivalent (1 NE) = 60 mg dietary trytofan (this aminoacid is able to synthesise
endogenous niacin) |
| Pyridoxine (vit
B6 group) |
Dried yeast 4,000-10,000
Cereals
300-600
Wheat flour
400-700
Liver
1,000-2,500
Beef, pork meat
300-700
Egg yolk
170-200
Vegetables
100-500 |
Pridoxal phosphate is involved in several reactions:
transamination, decaboxylation, deamination, trytophan metabolism, porphyrin and heme
biosynthesis, linoleic acid metabolism... |
2.0 mg |
1.6 mg |
| Biotin (vit
H) |
Yeast 90
Vegetables
10-20
Milk
2-5
Cheese
1,5-2
Egg yolk
15-20
Cereals products
4-12
Meat (beef, pork, sheep, chicken)
3-10
Fish
0,2-3 |
Aminoacid and fatty acid metabolism; carboxylation and
decarboxylation of oxoloacetic acid... |
150-330 mg |
150-330 mg |
| Folic acid (vit
Bc) |
Cows liver, pork liver 30-150
Beef, pork meat
10-50
Egg yolk
60-100
Legumes
35-100
Fennel
90-100
Spinach, asparagus
90-120
Cheese
10-30
Cereals
15-30 |
Maturation of erythrocytes; synthesis of purines and
pyrimidines; metabolism of some aminoacids... |
200 mg |
180 mg |
| Vitamin B12 (cobamins) |
Beef, pork liver 30-60
Beef, pork kidney
10-30
Cow milk
1-4
Fish (Tuna)
4-5 |
Maturation of erythrocytes; DNA syntheses; neural
function... |
2.0 mg |
2.0 mg |
| . |
. |
MINERALS |
. |
. |
| Sodium |
Wide distribution in foods |
Acid-base balance; blood pH; osmotic pressure; muscle
contractility; nerve sodium pump; transcription... |
575-3,500 mg |
575-3,500 mg |
| Potassium |
Wide distribution, mainly in milk and fruits (bananas,
prunes, raisins) |
Muscle activity; nerve transcription; intracellular
acid-base balance... |
3,100 mg |
3,100 mg |
| Calcium |
Milk, cheese, meat, fruit, fish, cereals, vegetables,
legumes |
Bone and tooth formation; blood coagulation;
neuromuscular irritability; muscle contractility... |
1,200-800 mg |
1,200-800 mg |
| Phosphorus |
Milk, cheese, meat, fish, cereals, legumes |
Bone and tooth formation; acid base balance; DNA and RNA
synthesis; energy production; |
1,200-800 mg |
1,200 800 mg |
| Magnesium |
Green leaves, cereals, fish. |
Bone and tooth formation, nerve contraction, muscle
contractability, enzyme activation... |
350 mg |
280 mg |
| Iron |
Wide distribution, mainly in meat, liver etc. |
Hemoglobin, myoglobin, catalase, mitochondria... |
10 mg (USA) 8.7 mg
(UK) |
10 mg (USA) 14.8 mg
(UK) |
| Zinc |
Wide distribution, mainly in vegetables |
Component of enzymes, (Cu, Zu-SOD) and insulin; skin
integrity, wound healing and growth... |
15 mg (USA) 9.5 mg
(UK) |
15 mg (USA) 7.0 mg
(UK) |
| Cobalt |
Green leafy vegetables |
Component of vitamin B12. |
Not set |
Not set |
| Copper |
Meats, oysters, legumes, whole grain cereals |
Cu, Zn-SOD; caeruloplasmin; hemopoiesis; bone formation |
2-3 mg (USA) 1-2 mg
(UK) |
2-3 mg (USA) 1-2 mg
(UK) |
| Selenium |
Meats, fish, garlic |
Component of glutathione peroxidase; thyroid function;
Detoxification of carcinogens? |
50-200 mg (USA) 75
ug (UK) |
50-200 mg (USA) 60
ug (UK) |
| Chromium |
Brewer's yeast |
Part of glucose tolerance factor; |
200 ug |
200 ug |
| Fluorine |
Mineral water, fish, egg, tea |
Tooth formation; |
1.5-4 ug |
1.5-4 ug |
| Iodine |
Seafood, iodine salt. |
Thyroxine and triiodothyroxine formation; Energy control
mechanisms... |
150 ug |
150 ug |
| . |
. |
OTHER IMPORTANT
NUTRIENTS |
. |
. |
| Ubiquinone (CoQ10) |
Heart and liver of cow, pork, sheep etc., fish |
Antioxidant (mainly in its reduced form) |
Not set |
Not set |
| Flavonoids |
Most fruits and vegetables |
Antioxidant in vivo?, directly cytotoxic to cancer
cells? anti-angiogenetic agents? |
Not set |
Not set |
| Phitic acid |
Many grains |
Bind transitional metals, decrease iron absorption; |
Not set |
Not set |
| Genistein |
Soybeans |
Anti-angiogenetic agent; |
Not set |
Not set |
| Catchetins (polyphenols) |
Green tea, black tea, many berries |
Anti-oxidant "in vivo"? directly cytotoxic to
cancer cells? |
Not set |
Not set |
| Resveratrol |
Red wine, grape juice |
Antioxidant "in vivo"? reduce the incidence of
skin tumours in mice by approximately 88%... |
Not set |
Not set |
| Allyl sulfides |
Garlic, onions |
Stimulation of enzymes able to detoxify carcinogens; |
Not set |
Not set |
| Isothiocyanates |
Mustard, radishes |
Induce protective enzymes |
Not set |
Not set |
| Fibre |
Grains, vegetables |
Increases speed of movement of faeces through colon;
diluted carcinogenic drugs and delays their formation; |
20-30g (USA) 12-14g
(UK) |
20-30g (USA) 12-14g
(UK) |
| . |
. |
. |
The UK RDA refers to total "non starch
carbohydrate polymers" |
. |
A diet for immunodeficiency and, in
particular, for diagnosed HIV seropositive (HIV+) and AIDS patients.
It is important to emphasise that it is a nonsense to
believe that a single diet may be useful for all patients. In general, macro and
micronutrients mentioned under "general considerations" are essential for
humans, and their metabolism follows the same pathways, but the response is individual. A
relationship has been shown to exist between the quality and quantity of digested
nutrients and the nutritional state and the immunocompetence of an individual. There can
be various "degrees" of immunodeficiency, each of which can display peculiar
nutritional requirements. Therefore, we'll confine ourselves to giving dietetic advice
that, in any case, can be modified during treating immunodeficiency. In our laboratory,
such advice is monitored quarterly by blood analyses (plasma, lymphocytes, erythrocytes)
of factors we have called "cell health indicators", i.e., albumin, free and
esterified cholesterol, phospholipids and their fatty acid pattern, vitamin E, vitamin A,
b-carotene, lycopene, vitamin C, uric acid, ubiquinol/ubiquinone and reduced
glutathione/oxidized glutatione redox couples, total thiols, selenium, iron, copper,
lipoperoxidation levels, superoxide dismutase, glutathione peroxidase, catalase, etc.6-9.
These analyses, in addition to haemochrome, CD4+, and CD8+, represent the basis of our
12-year experimental observations on patients diagnosed with AIDS, pointing out that a
severe oxidative stress occurs in the blood of patients diagnosed HIV positive (HIV+) in
comparison with healthy age and sex matched controls, and increases significantly with the
degree of immunodeficiency: AIDS > symptomatic HIV+ > asymptomatic HIV+ >
controls.
The observed oxidative stress is characterized either
by the depletion of:
* lipophilic antioxidants [vitamin E (vit E), ubiquinol
(CoQ10H2), ubiquinone(CoQ10), vitamin A (vit A), and
b-carotene],
* hydrophilic antioxidants [reduced glutathione (GSH),
ascorbate, and urate],
* selenium (Se),
* phospholipids (PL) and cholesterol esters (CE), and
their polyunsaturated fatty acid (PUFA) patterns, or by an increase of:
* by-products of polyunsaturated fatty acid and protein
oxidation, or by:
* a critical imbalance ofenzymatic antioxidants
(superoxide dismutase and glutathione peroxidase).
In particular, the deficiency of ubiquinol, vitamin E,
reduced glutathione, phospholipids, cholesterol, and polyunsaturated fatty acids
represents an early marker of the condition. It is worth mentioning that deficiency of
antioxidants produces oxidative stress. When this is severe, it is able to damage cellular
macromolecules, in particular, DNA; proteins, and unsaturated lipids (Table 4), and their
functions, which are maintained and mediated by critical redox systems, thus contributing
to the physio-pathology of many diseases (Fig.1).
Table 4
| Molecule |
Type of damage |
| DNA |
Changes in adenine, guanine, cytosine, and thymine bases. Breakage of DNA backbone in single or double strand breaks of the
double helix.
Attack on the deoxyribose. |
| Unsaturated lipids |
Oxidation of PUFA (lipoperoxidation) and damage to
membrane proteins. |
| Proteins |
Breakage of proteins. Oxidation of thiol and amino residues of aminoacids .
Cross-linking of different protein molecules by aminoacid
radicals |
Table 4. Molecules
damaged by a sustained oxidative stress and type of damage. An oxidative stress can be
defined as any unbalance between antioxidant defences and generation of reactive oxygen
and nitrogen species (ROS, RNS), and other reactive radicals (R). It follows that an
oxidative stress can be induced in biological systems by the depletion of antioxidants
and/or an overload of reactive oxidant species, so that the antioxidant pool becomes
insufficient 8-11.

Fig.1. Possible
involvement of oxidative stress in numerous diseases.
This does not mean that reactive oxidant species are the
main cause of the above diseases. Certainly it cannot be denied that their production
accompanies most, and perhaps all, human diseases, and that, in several cases, they may
play a significant role in the onset of the diseases and /or contribute significantly to
their progression.
The first necessary measure is to take regard of the
reinstatement of those molecules, the levels of which are reduced when compared to normal,
and this is possible by the opportune combination of diet and integrators.
It is enlightening that many years ago, long before the
antibiotic era, there were fierce quarrels between scientists aiming to discover a drug
active against Koch tubercle bacillus and scientists who, conscious that environmental
factors such as poverty, deficient diet and poor housing can play an aet ological role in
the incidence and spread of tubercolosis, maintained that it would be better to empower
the body's defences, by reducing the influence of environmental factors. The suggestions
of the latter prevailed mainly in Northern European countries. Bed rest, plentiful diet,
sunlight, fresh air, adequate hygienic measures, and isolation of the patients became the
regime of choice. These rational and preventive treatments led to the inversion of the
spread of the disease in those countries, some decades before the discovery of
streptomycin by S. A. Waksman in 1944.
What to do?
Table 3 can be considered as a useful guide for the
physiological intake of micronutrients from the diet. Micronutrients does not mean
nutrients of less importance as compared to macronutrients: antioxidant defences, for
example, rely mainly on some vitamins and minerals from the diet. However, it is often
better to utilize one or more micronutrients in the form of pills or tablets, the
prerequisite being that they must be taken from natural sources and assimilated in proper
amounts. An apt example is given by vitamin E (vit E). Dietary vit E occurs in a variety
of forms, such as a, b, d, and g-tocopherols differing in the number of methyl groups on
the chromanol ring and having a phytyl tail. The biological activities of the four
homologues, as determined by a rat resorption test12, vary from 100% for
a-tocopherol (d-RRR-a-tocopherol), to 57% for b-tocopherol, (d-RRR-b-tocopherol), 31% for
g-tocopherol (d-RRR-g-tocopherol), to 1.4% for d-tocopherol (d-RRR-d-tocopherol). In
addition to natural homologues, synthetic vit E (d, l-a-tocopherol or all-rac
a-tocopherol), which is widely used as a supplement, contains eight different isomers
(SSR,SSS,SRS,SRR, RSS, RRS, RRR, RSR), of which only approximately 12% is
d-RRR-a-tocopherol (Fig.2). Its stereosisomers are less biologically active (21-90 %), the
biological activities of the 2-S forms being lower than the 2-R forms13.
In any case, despite the different biological activities
of homologues and stereoisomers of a-tocopherol, there is biodiscrimination, which allows
a-tocopherol to predominate in blood and tissues. Dietary or synthetic forms of vit E are
absorbed from the intestinal lumen in the presence of biliary and pancreatic secretions,
which are necessary for micelle formation. It has been observed that the different forms
do not compete with each other during absorption and secretion in chylomicrons. In other
words they are absorbed with equal affinity, and, during chylomicron catabolism, are
similarly present in all of lipoproteins, an aliquot being delivered to peripheral
tissues, and the remainder to liver under the form of chylomicron remnants. In contrast
to the intestine, the liver discriminates among the various forms of tocopherols. In
fact the hepatic tocopherol transfer protein preferentially selects and transfers
d-RRR-a-tocopherol to VLDL (very low density lipoproteins) during their assembly.
Following VLDL secretion into the plasma, a-tocopherol can be distributed to other
lipoproteins and tissues. Excess a-tocopherol and other forms of vit E are likely excreted
in the bile.
From this wide-ranging discourse on vit E and its
homologues, it is possible to assert that the best way to face the real requirements of
the vitamin is to administer, by any route, suitable amounts of d-RRR-a-tocopherol or of
its stable derivative d-RRR-a-tocopheryl acetate.
But, let us go on with our dietetic advice.
Proteins.
60-80 g daily from different sources such as red meats,
fish, whole milk, eggs, whole cereals legumes, etc. These sources must be preferentially
fresh and varied. It is important to monitor quarterly patients' plasma levels of albumin,
a protein containing high levels of thiols (0.3-0.5 mM) and able to scavenge a wide range
of reactive species and radicals, that can damage it. Contrary to several oxidized
molecules, the damaged albumin is not dangerous for the cells: it is simply removed from
circulation and replaced, so that it is considered as a very important "sacrificial
antioxidant".
Carbohydrates.
RDA for carbohydrates is not well defined. It is normally
asserted that carbohydrates, of which approximately 90% are polysaccarides and only 10%
mono and disaccarides, must provide 55-65% total body calories. In any case, at least 180g
glucose/day, whatever the metabolic origin of glucose, are indispensable to satisfy the
energetic requirements of both brain (140 g/day) and erythrocytes (40 g/day). Among
carbohydrates, of great importance is the role of fibers, i.e. the sum of undigestible
carbohydrates, such as pentosans, pectins, cellulose, emicellulose, lignine, etc. The
daily consumption of fibers should be in the order of 15-20g, and derived from foods rich
in fibers such as cereals, legumes, vegetables, and fruit, more than from concentrated
fibers.
Lipids.
The lipid metabolism is significantly impaired in AIDS
patients: phospholipids, cholesterol esters (and therefore total cholesterol), high
polyunsaturated fatty acid patterns (C20:3 n-6, C20:4 n-6, C22:6 n-3, etc.) of
phospholipids and cholesterol esters are significantly reduced, while saturated fatty acid
patterns (C14:0, C16:0, C18:0) of the same lipid fractions are significantly increased, as
compared to healthy control values (8-9). The imbalance in fatty acid patterns of n-6 and
n-3 series is probably dependent on insufficient D-6, D-5, and D-4 desaturase activities6-9,
which require, for their normal physiological activities, optimal levels of vit E,
ubiquinol/ubiquinone, and selenium8-9. Brenner14, in studying the
factors which influence the activity of the first of these enzymes, i.e. D-6 desaturase,
demonstrated that its activity is inhibited by various causes such as ageing, reactive
oxidant species, lipoperoxidation, prolonged fasting, diabetes, hypoproteic diet, alcohol,
stress due to excessive release of catecholamines, thyroxine, radiations, etc. This means
that a normal intake of essential fatty acids (C18:2 n-6 and C18:3 n-3) may not guarantee
for their functional utilization.
From a quantitative point of view, the daily lipidic
intake of fatty acids (mainly in the form of triglycerides) should be in the order of
25-30% of the total calories in the diet. Saturated fatty acids should not exceed 10%, trans-monounsaturated
fatty acids 2%, monounsaturated fatty acids 10%, essential fatty acids and
poly-unsaturated fatty acids 6-8%, with a ratio n-6/n-3 of 6-10/1. Also extremely
important is the nutritional intake of cholesterol, and phospholipids. The former is
present, mainly in free form, in cheese, milk, offal (liver, heart, kidney of beef or
pork), meat, fish etc, and its daily intake should not exceed 400-500 mg. It is claimed
that an elevated intake of cholesterol lowers its endogenous biosynthesis, but this
homeostatic mechanism is often inefficient in many diseases. As for phospholipids, that
deliver to the body not only essential fatty acids, but also fundamental molecules, such
as choline, serine, and inositol, their daily intake should be in the order of 4-6g. The
sources of phospholipids ought to be red meats, offal, raw vegetables, legumes, etc.
Micronutrients.
A large aliquot of vitamins and minerals is supplied by
fruit and vegetables, the remainder deriving from the same sources that provide
macronutrients. For example, red meats and liver from several animals, in addition to
proteins, cholesterol and PUFA, are very rich in bio-available iron, contrary to spinach
and egg yolk, which also contain high levels of iron. Among micronutrients, antioxidants
play an important role in immunodeficiency8,9,15-24. The purpose of the immune
system is to destroy invading organisms and damaged cells, bringing about recovery. For
this purpose it generates powerful substances such as cytokines and reactive oxygen
species (ROS), the excessive or non-physiological production of which can be associated
with mortality and morbidity after infections, and with inflammatory diseases. ROS enhance
the biosynthesis of interleukin-1, interleukin-6, interleukin-8, TNF-a etc., in response
to inflammatory stimuli, by activating nuclear transcription factor, NT-kB. These
cytokines are able to stimulate ROS formation, that would contribute to the depletion of
GSH and other antioxidants, which, directly and indirectly ought to protect the host
against the damaging combined effects of ROS and cytokines. The nature and the extent of
the antioxidant defences are influenced by their dietary intake or by the intake of their
precursors. In particular, we have emphasized that the deficiency of lipophilic and
hydrophilic antioxidants coupled to an imbalance of enzymatic antioxidant activities,
affects the blood, and, consequently, tissues, of HIV+diagnosed patients, and increases
significantly if the condition progresses6-9.
Antioxidant therapies have been proposed for patients
diagnosed HIV+ or with AIDS, and several clinical trials have been carried out with GSH
pro-drugs (N-acetyl cysteine, glutathione esters, and oxothiazolidine-4-carboxylate) or
vit C or vit E or ubiquinone or lipoic acid, etc. but, to our knowledge, without evident
clinical benefits25-33. As a matter of fact, the proposed antioxidant therapies
have been nothing but antioxidant mono-therapies. They follow the dictates of literature,
where it is generally reported that enzymatic and non-enzymatic antioxidants form a
dynamic integral pool, in which the deficiency of one or more constituents can be
compensated by the increased amounts of one or more molecules of the same pool, in order
to maintain a homeostatic protective system against oxidative damage towards susceptible
cell components. This may happen with a mild degree of deficiency, but not with the severe
depletions and imbalances that may be observed in individuals diagnosed HIV+. It is a
nonsense to 'fight AIDS' on the basis of results from experimental and highly questionable
in vitro measurements, showing that an antioxidant is capable of inhibiting TNF-a
synthesis or NF-kB activation and, consequently, HIV replication. Granted, for the sake of
argument, that the administration of GSH pro-drugs leads to its increased intracellular
levels, how is it possible to believe that such increase may re-balance the significant
deficiencies of CoQ10H2, CoQ10, vit E, vit A, vit C, PL,
CE, PUFA, the imbalance of enzymatic antioxidants, etc.? The same is true same for vit E,
or CoQ10, or vit C, or lipoic acid, etc.
In our opinion, in order to re-balance the cell redox
status, it is necessary to administer the deficient antioxidants by appropriate vegetables
and fruit plus external supplements. Appropriate vegetables and fruit, i.e. oranges, kiwi,
carrots, red grapes, apples, tomatoes, broccoli, cabbages etc. have to supply vit C,
b-carotene (the precursor of vit A), lycopene, flavonoids - all antioxidants that, when
administered in the form of tablets or capsules, i.e. without their natural entourage to
buffer and protect them, may show pro-oxidant activities. As external supplements we
intend d-RRR-a-tocopherol, ubiquinone, precursors of GSH and glutathione peroxidase,
vitamin PP, the uptake of which from foods can be insufficient or not easy. In this
connection, in our Cell Aging Center we have patented and produced a multinutrient
preparation -IMMUGEN - recommended for the prevention and treatment of oxidative stress in
all its manifestations. Each gelatine capsule (or tablet) contains:
ubiquinone, 12.5 mg; RRR-a- tocopheryl acetate, 12.5 mg;
l-methionine, 50.0 mg; selenium (as selenium aspartate), 12.5 mg; soybean phospholipid
complex, 147.0 mg. The phospholipid complex contains: phosphatidyl choline, 23%;
phosphatidyl ethanolamine, 20%; phospatidyl inositol, 14%; phosphatidic acid, 8%; other
phospholipids, 8%; glicolipids, 15%; carbohydrates, 8%; neutral lipids, 3%.
Mode
of action of IMMUGEN
Reduced and oxidized ubiquinones (CoQ10H2
and CoQ10 - UBI -) are ubiquitous and essential for life, meaning they
exist in all body cells and support cellular energy production by helping generate
adenosine triphosphate (ATP). Once UBI body levels become more than 25-30% deficient, many
diseases may begin, including immunodeficiency, cancer, cardiovascular diseases, etc.
It is well known that CoQ10, in addition to its
function as an electron and proton carrier in mitochondria, acts as a powerful antioxidant
in its reduced form ubiquinol (CoQ10H2), by preventing both the
initiation and the propagation steps of lipoperoxidation in biological membranes34-35.
Furthermore, it is able to sustain efficiently the chain breaking antioxidant capacity of
Vit E, by regenerating it from a-tocopheryl radical36, which otherwise would
need the cooperation of hydrophilic antioxidants such as Vit C and/or GSH. Therefore, as
CoQ10H2 is essential to maintain Vit E status and function, decrease
of CoQ10H2 in turn contributes to further exacerbate the depletion
of Vit E. It is worth mentioning that CoQ10H2 is the only known
lipophilic antioxidant that mammalian cells can sinthesize de novo and for which
there are enzymic NAD(P)H dependent mechanisms able to (re)generate it from CoQ1037-38.
A derangement of these reductive mechanisms, due to an over production of pro-oxidant
reactive species, coupled to a reduced CoQ10 biosynthesis, represents an
important fingerprint of immunodeficiency and its progression.
RRR-a-tocopheryl acetate is a stable form of
natural vit E, a chain breaking antioxidant that works in sinergy with CoQ10/
CoQ10H2 to prevent oxidative damage to lipid membranes and plasma
phospholipids. In its antioxidant role, vit E becomes oxidized; thereafter it can be
regenerated particularly by CoQ10H2. A recent study39
suggests that high serum levels of vit E in individuals diagnmosed HIV+ is associated with
a decrease in risk of progression to AIDS and mortality, while low serum concentrations
have been correlated with higher degree of lipoperoxidation40, decreased plasma
PUFA22, and increased p24 antigenemia22. Vit E supplementation
during murine AIDS, which may be functionally similar to human AIDS modulates cytokine
release and helps to ameliorate the disorders during the disease, suggesting vit E's
usefulness in the treatment of AIDS in humans40. Dietary oxidative stress due
to either vit E or selenium deficiency allows a normally benign virus (amyocarditic
coxackievirus B3) to convert to virulence and cause heart damage in mice. The conversion
to virulence is due, according to Beck and Levander41, to a nucleotide sequence
change in the genome of the benign virus, which then resembles the nucleotide sequence of
virulent strains.
L-methionine, an essential amino acid, supplies
both the methyl group essential for the biosynthesis of phospatidyil choline, the main
membrane phospholipid, and (?) methyl transferase activity, and the sulphur atom necessary
for the biosynthesis of reduced glutathione (GSH), which is the reducing molecule of
glutathione peroxidase, an enzyme which also requires selenium (Se) for its antioxidant
activity. Apart from polyamines, which are strong chelators of transitional metals, among
the final catabolites of methionine other sulphurated molecules must also be considered,
such as taurine and sulphates, which, together with GSH, are extremely valid endogenous
detoxifying agents. A recent study has shown that methionine, threonine, valine and lysine
are rate limiting for whole body protein synthesis in AIDS patients, suggesting that there
are selective aminoacids requirements in these individuals42.
Selenoproteins discovered in mammalian cells may account
for the important role of Se not only in the body's antioxidant defence, but also in
thyroid hormone function, cellular immunity, formation of sperm, and functioning of the
prostate gland. According to Cowgil a pattern does exist between the geographical
distribution of Se and AIDS mortality, such that an inverse relationship persists between
Se amount in the soil of an area and AIDS mortality in the same area43.
Phospolipids, together with vit E, CoQ10
and CoQ10H2 are essential constituents of cellular membranes, from
which the immune response draws its origin.
Suggested treatment to prevent
immunodeficiency progression in diagnosed HIV+ patients.
We recommend 3-4 capsules daily of IMMUGEN (or similar
micronutrients) plus 50 mg of vitamin PP (the precursor of NAD(P)H) during main meals as
external supplements, plus a varied diet in the home with a high biological value (Table
5). In addition we suggest food to avoid or, at least, to reduce drastically. It is
evident that other supplements may be absolutely necessary, for example folate and/or
vitamin B12 in the case of anemia, or vitamin B6 in psychological distress, etc.
Might the same combined treatment produce beneficial
effects, for example by reducing the risks of opportunistic diseases, in diagnosed
symptomatic HIV+ and AIDS patients (CD4+: < 200; 180-10 cells mm3)? The
answer is undoubtedly positive in those individuals showing no serious problems of
malabsorption and whose blood levels of "health cell indicators", though
significantly reduced before treatment as compared to healthy controls, increase
significantly after 1-2 months of treatment. When, on the contrary, oxidative stress
combined with medication and recreational drug abuses, and emotional distress, have
irreversibly undermined the body, leading to a downward spiral of malabsorption, weight
loss, wasting, diarrhea, anorexia, body image disturbance etc., it is clear that our oral
combined treatment becomes insufficient: the AIDS establishment, mercenary scientific
journals and mass media can, with impunity, toast death.
Table 5. Dietetic advice for diagnosed HIV+ (and
AIDS) patients.
BREAKFAST |
|
| Whole milk (200-300ml) or yoghurts (100-150ml); cereals
(25-50g), porridge or wholemeal biscuits; soy bean lecithin (1.2 spoons); jam or honey (as
sweetener); coffee or tea (optional) |
|
MIDMORNING OR
MIDAFTERNOON |
|
| Tea, biscuits, and/or fruit juice. |
|
LUNCH OR DINNER |
|
| Pasta or rice, or soup |
100-150g, daily |
| Bread |
200-300g of whole bread or enriched bread daily |
| Red meat |
150-200g of rare/medium steaks from beef or pork (visible
fat must be removed), 2-3 times a week. |
| Offal |
100-150g of liver or heart or kidney from beef or pork,
1-2 times a week. |
| White meat |
200-250g of chicken or lamb or rabbit etc., 1-2 times a
week |
| Fish |
150-250g of fresh fish (cod or salmon or herring or
trout. etc.,) 2 times a week. |
| Egg |
3-4 whole eggs a week |
| Vegetables |
150-200g daily of fresh vegetables (broccoli, lettuce,
spinach, Brussels sprouts, potatoes etc.) |
| Legumes |
100-150g of legumes (different types of beans,lentils
etc.), 1-2 times a week. |
| Fruit |
300-400g daily of fresh seasonal fruit (oranges, kiwi,
black grapes, apricots,prunes, banana, etc.). Also dry fruits (nuts, almonds, raisins,
dates, etc) are indicated for their high content in polyunsaturated fatty acids and
potassium). |
| Cheese |
40-50g of parmesan cheese or non-excessively fat cheese,
3-4 times a week. |
| Oil |
Olive oil (10-30g) for prolonged cooking, non-peroxidized
corn or soybean or sunflower oils for raw sauces. |
In boiling vegetables, prolonged heating at high
temperatures should be avoided, and the amount of water should be kept to a minimum and
already hot, otherwise much of ascorbic acids and other vitamins and minerals will be
destroyed or dissolved away.
Don't worry about red meats and offal: it is true they
contain remarkable amounts of cholesterol (mainly free cholesterol) and iron, but
cholesterol excess is the last thing an immunodeficient person need fear, because of its
low plasma concentrations. As for iron and its role in pro-oxidative stress, we have
ascertained that the plasma levels of ferritin and NTBI in people diagnosed HIV+ and AIDS
patients are in the normal ranges (91 ± 14 ng/mL of plasma for ferritin, and 0 µg/dL for
NTBI).
Table 6. Foods to avoid or reduce drastically.
Animal fat and dairy products such as butter, shortening,
ordinary margarine, coconut oil, lard, cream, and food containing these ingredients, i.e.,
salami, sausages, wurstels, cakes, pastries, biscuits etc;
fried foods, in particular from fast foods or fish and
chips shops;
strong spices;
highly seasoned and tinned food;
alcoholic beverages.
|
Abstract
Following many years of research in vivo on HIV+ and
AIDS patients and on the basis of their effective blood deficiencies of micronutrients,
ascertained by unequivocal analytical techniques, the authors' dietary recommendations
are:
a varied diet in the home with a high biological value,
which ensures an excellent intake of proteins, polyunsaturated fatty acids under the form
of phospholipids and triglycerides, cholesterol, vitamins and minerals;
a cocktail of natural antioxidants and their precursors
such as d-RRR-a-tocopherol, ubiquinone, selenium, precursors of GSH , to assume, as
supplements, during meals.
These combined treatments, allowing a re-balancing of cell
redox status, membrane lipid constituents, and possible caloric and protein deficiencies,
may have a beneficial therapeutic value to prevent the progression of immunodeficiency.
This is possible mainly in less compromised patients, in whom the oxidative damage to
cells has not yet reached a critical threshold of no return, and can still be successfully
fought. Certainly it is much healthier than the extremely toxic DNA chain terminators,
anti-proteases, antibiotics, antifungal agents and similar dangerous molecules,
fideistically prescribed daily by the members of the orthodox AIDS establishment, and
capable of inducing a physical decline even in healthy individuals.
References
1. Recommended Dietary Allowances, IX edition by the
National Academy of Sciences, National Academy Press, Washington, DC, 1980.
2. FAO/WHO. Handbook on human nutritional requirements.
FAO, Nutritional Studies n. 28, WHO Monograph series, n. 61, 1974.
3. Recommended Nutrient Intakes for Canadians. Minister of
National Health and Welfare, 1983.
4. Apports Nutritionelles conseillés pour la population
franVaise. CNRS-CNERNA. Technique et documentation Lovoisier, 1982.
5. Tabelle di composizione degli alimenti. Istituto
Nazionale della Nutrizione, a cura di F. Carnovale - L. Marletta, 1997.
6. Passi S., Morrone A., Picardo M., De Luca C. and
Ippolito F.. Blood levels of vitamin E. polynsatured fatty acids of phospholipids,
lipoperoxides and glutathione peroxidase in patients affected with seborrheic dermatitis.
J. Dermatol. Sci. 2:171-178, 1991.
7. Passi S., Picardo M., Morrone A., De Luca C., Ippolito
F, Rossi L. and Rotilio G. Study on plasma polyunsaturated fatty acid and vitamin E, and
on erythrocyte glutathione peroxidase in high risk HIV infection categories and AIDS
patients. Clin. Chem. Enzym. Commun. 5:169-177, 1993.
8. Passi S., Ippolito F., AIDS: nuova frontiera. pp.
1-200, Lombardo Ed. Roma, 1995.
9. Passi S. Progressive increase of oxidative stress in
advancing human immunodeficiency. Continuum, vol 5 (no 4): 20-26, 1998.
10. Halliwell B., Gutteridge J.M.C. In "Free radicals
in biology and medicine", 2nd edition. Clarendon Press, Oxford, 1989, and the
references cited therein.
11. Gutteridge J.M.C. Halliwell B. Antioxidant in
nutrition, health, and disease. Oxford University Press. Oxford-New York-Tokio, 1994.
12. Weimann B. J., Weiser H. Functions of vitamin E in
reproduction and in prostacyclin and immunoglobulin synthesis in rats. Am. J. Clin
Nutr., 53: 1056 S&endash;1060 S, 1991.
13. Weiser H., Vecchi M., Schlachter M. Stereoisomers of
alpha-tocopheryl acetate. IV. USP units and alpha-tocopherol equivalents of all- rac-,
2-ambo- and RRR-alpha-tocopherol evaluated by simultaneous determination of
resorption-gestation, myopathy and liver storage capacity in rats. Int. J. Vit. Nutr.
Res., 56:45-56, 1986.
14. Brenner RR. Nutritional and hormonal factors
influencing desaturation of essential fatty acids. Prog. Lipid Res. 20:41-47, 1982.
15. Halliwell B., Cross C. Reactive oxygen species,
antioxidants, and acquired immunodeficiency syndrome. Arch. Intern. Med. 151:29-31,
1991.
16. Eck H.P., Grumder H., Hartmann M.L., et al. Low
concentration of acid soluble thiol (cystein) in the blood plasma of HIV-1 infected
patients. Biol. Chem. Hoppe Seyler 370:101-8, 1989.
17. Staal F.J.T., Roederer M., Israelski D.M., et al.
Intracellular glutathione levels in T-cell subsets decrease in HIV infected individuals.
AIDS Res. Human Retrovirus 8:305-11, 1992.
18. Javier J.J., Fordyce-Baun M.K., Beach R.S., et al.
Antioxidant micronutrients and immune function in HIV-1 infection. FASEB Proc. 4A:940-945,
1990.
19. Folkers K., Langajoen P., Nara Y., et al.
Biomedical deficiencies of coenzyme Q10 in HIV infection and exploratory treatment. Biochem.
Biophys. Res. Commun. 153:888-96, 1988.
20. Buhl R., Holroyd K.J., Cantin A.M., et al.
Systemic glutathione-deficiency in symptom-free seropositive individuals. Lancet
2:1294-1298, 1989.
21. Dworkin B.M. Selenium deficiency in HIV infection and
the acquired immune deficiency syndrome (AIDS). Chem. Biol. Interact. 91:181-186,1994.
22. Semba R.D., Graham N.M.H., Caiaffa W.T. Increased
mortality associated with vitamin A deficiency during human immunodeficiency virus type 1
infection. Arch. Intern. Med. 153:2149-2154, 1993.
23. Constants J., Peuchant E., Pellegrin J.L. et al.
Fatty acids and plasma antioxidants in HIV-positive patients: correlation with nutritional
and immunological status. Clin Biochem 28:421-6, 1995.
24. Coodley G.O., Nelson H.D., Loveless M.O., Folk C. Beta
carotene in HIV infection. AIDS 6:272-276, 1993.
25. Mihm S., Ennen J., Pessara U., et al.
Inhibition of HIV-1 replication and NF-kB activity by cysteine and cysteine derivatives. AIDS
5:497-503, 1991.
26. Kalebic T., Kinter A., Poli G., et al.
Suppression of human immunodeficiency virus expression in chronically infected monocytic
cells by glutathione, glutathione ester, and N-acetylcysteine. Proc Natl Acad Sci
USA 88:986-990, 1991.
27. Delmas-Beauvieux M.C., Peuchant E., Couchouron A., et
al. The enzymatic antioxidant system in blood and glutathione status in human
immunodeficiency virus (HIV)-infected patients: effects of supplementation with selenium
or b-carotene. Am. J. Clin. Nutr. 64:101-107,1996.
28. Olivier R., Dragic T., Lopez O. et al. An
antioxidant prevents apoptosis and early cell death in lymphocytes from HIV-infected
individuals. International Conference on AIDS 1: A 65, 1992.
29. Harakeh S., Jariwalla R.J. Comparative study of the
anti HIV activities of ascorbate and thiol-containing reducing agents in chronically
HIV-infected cells. Am. J. Clin. Nutr. 54:1231S-1235S, 1991.
30. Suzuki Y.J., Aggarwal B.B., Packer L. Lipoic acid is a
potent inhibitor of NF-kB activation in human T cells. Biochem. Biophys. Res. Commun. 189:1709-1715,
1992.
31. Gogu S.R., Beckman B.S., Rangan S.R.S. et al. Increased
therapeutic efficacy of zidovudine in combination with vitamin E. Biochem. Biophys.
Res. Commun. 165:401-407, 1989.
32. Makonkawkeyoon S., Limson-Pobre R.N., Moreira A.L., et
al. Thalidomide inhibits the replication of human immunodeficiency virus type 1. Proc.
Natl. Acad. Sci. USA, 90(13):5974-5978, 1993.
33. Hersh E.M., Brewton G., Abrams D. et al.
Dithiocarb sodium (diethyldithiocarbamate) therapy in patients with symptomatic HIV
infection and AIDS. JAMA 265: 538-1544, 1991.
34. Frei, B., Kim M.C., Ames B.N. Ubiquinol-10 is an
effective lipid-soluble antioxidant at physiological concentrations. Proc. Natl. Acad.
Sci. USA., 87:4878-48831990
35. Mohr, D., Bowry V.W., Stocker R. Dietary
supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within
circulating lipoproteins and increased resistance of human low-density lipoprotein to the
initiation of lipid peroxidation. Biochim. Biophys. Acta., 1126: 247-254,1992.
36. Ernster, L., Forsmark P., and Nordenbrand K. The mode
of action of lipid-soluble antioxidants in biological membranes: relationship between the
effects of ubiquinol and vitamin E as inhibitors of lipid peroxidation in submitochondrial
particles. BioFactors., 3: 241-248,1992.
37. Cadenas, E., Hochstein P., Ernster L. Pro- and
antioxidant functions of quinones and quinone reductases in mammalian cells. Adv.
Enzymol., 65:97-146,1992.
38. Crane, F.L., Sun I.L., Clark M.G. et al.
Transplasma membrane redox system in growth and development. Biochim. Biophys. Acta.,
811:233-264, 1985.
39. Tang M.A., Graham N.M.H., Semba R., Saah A.J.
Association between vitamin A and E levels and HIV-1 disease progression. AIDS
11:613-620,1997.
40. Wang Y., Watson R.R. Vit E supplementation at various
levels alters cytokine production by thymocytes during retrovirus infection causing murine
AIDs. Thymus 22(3):153-165, 1994.
41. Beck M. A., Levantčs O. A. Dietary oxidative stress
and the potentiation of viral infection. Am. Rev. Nutr., 18:93-116, 1998.
42. Laurichesse A., Tauveron I., Gourdon F., et al.
Threonine and methionine are limiting amino acids for protein synthesis in patients with
AIDS. J. Nutrition, 12(8):1342-8, 1998.
43. Congil U. M. The distribution of selenium and
mortality owing to acquired immunodeficiency syndrome in the continental United States. Biol.
Trace Elem. Res. 56 (1):43-61, 1997.
44. N. Y. Times, Aug. 20, 1994.
Click here for More About CONTINUUM
|