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Summary
and Conclusions about the Vitamin Treatment of Arthritis |
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Joint Dysfunction, Part 5 |
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CHAPTER 5 To go back
to Chapter 4: http://www.doctoryourself.com/kaufman9.html
Some Inferences Concerning
Joint Dysfunction (Dr. Kaufman, writing
in 1949, shows remarkable foresight half a century into the future of
orthomolecular (megavitamin) medicine. In this chapter, he describes how the
lack of a single nutrient can cause diverse diseases; the need for a new way
of looking at arthritis, and reviews his treatment and what level of success
to expect with it.) References cited are
posted at this link: http://www.doctoryourself.com/kaufman11.html It has been shown that
the clinical diagnosis of joint dysfunction and the clinical classification
of the severity of joint dysfunction are made on the basis of an objective
criterion, the Joint Range Index, which is the weighted mean of the numerical
values obtained upon measurement of 20 specified joint ranges. Measurement of
the Joint Range Indices of an unselected, untreated population of 455
ambulatory male and female patients, 4 to 78 years of age, subsisting on the
average American diet of 1945 to 1947, demonstrated that joint dysfunction,
as defined by a Joint Range Index of less than 96, was almost universal in
occurrence, and was present in individuals with or without complaints
referable to muscles and joints, and with or without clinically obvious
rheumatoid arthritis or clinically obvious hypertrophic arthritis. The
decline of the means of the Joint Range Indices for each succeeding 5-year
age group was practically linear in the untreated population, indicating that
joint dysfunction tends to increase in severity with increasing age, although
within any 5-year age group there are individual variations in the numerical
values of the Joint Range Indices which can best be seen in Table 1G.
Usually, in the more severe clinical grades of joint dysfunction, clinically
obvious rheumatoid and hypertrophic arthritis are commonly found. It has been
observed that a person less than 40 years of age with a severe or extremely
severe clinical grade of joint dysfunction is more likely to have rheumatoid
than hypertrophic arthritis, and that a person more than 50 years of age with
a severe or extremely severe clinical grade of joint dysfunction is more
likely to have hypertrophic than rheumatoid arthritis. However, a person with
mild, moderate or severe joint dysfunction may show no evidence of either
hypertrophic or rheumatoid arthritis, or a person with slight joint
dysfunction may have local evidences of hypertrophic arthritis (Heberden's
nodes) and no other clinical evidence of arthritis. During the first month
of adequate therapy with niacinamide (alone or in combination with other
vitamins) a patient with joint dysfunction (with or without rheumatoid or
hypertrophic arthritis) will have a rise in the Joint Range Index of at least
6-12 points, and thereafter will have a rise of at least 0.5 to 1 point per
month of adequate niacinamide therapy, provided he eats the average American diet containing
adequate calories and sufficient protein, and provided he does not
mechanically injure his joints excessively. This improvement in joint
mobility occurs regardless of the age or sex of the patient, and regardless
of whatever other health problems he may have. Subsequently, with
continuously adequate niacinamide therapy, the Joint Range Index of 96-100
(no joint dysfunction) is reached, and maintenance doses of niacinamide
are required to keep the Joint Range Index at this level. The only observed
exception to the attainment in time of a Joint Range Index of 96-100
with prolonged adequate niacinamide therapy occurs in persons who have
ankylosed joints which have not regained any mobility in response to adequate
niacinamide therapy. In such persons with one or more ankylosed joints, the
rise in the Joint Range Index with adequate prolonged niacinamide therapy is
the same as the patterns described above, although in time serially rising
values of the Joint Range Index may stabilize at a level below 96, which
represents the maximal Joint Range Index attainable by the patient when the
ankylosed joints do not regain full mobility in response to prolonged
adequate niacinamide therapy, even though all the other joints measured for
computation of the Joint Range Index can be moved through their full ranges;
e.g., if one wrist joint is irreversibly ankylosed, the highest attainable
Joint Range Index is 90.9. As has been previously noted, some joints which
initially appear to be clinically ankylosed, in time regain their full ranges
of movement in response to prolonged adequate niacinamide therapy. Therapeutically induced
improvement in joint mobility, as shown by increasing values of the Joint
Range Index, cannot be maintained without continuously adequate niacinamide
therapy. When adequate niacinamide therapy is discontinued, there is a
regression in the Joint Range Index from the therapeutically improved value
to the pre-treatment value. When niacinamide intake is reduced from adequate
to inadequate levels, the Joint Range Index decreases and stabilizes at a
level above the pre-treatment level and below the maximum level
therapeutically achieved. In this study, in the
various case histories it has been shown that joint mobility of patients with
either hypertrophic arthritis or rheumatoid arthritis improves in response to
the administration of adequate niacinamide therapy. In addition, certain
other benefits have been observed from this therapy, most of which are not
susceptible of objective measurement. In both hypertrophic arthritis and
rheumatoid arthritis, these benefits include a feeling of being more alert,
more vigorous, tiring less easily, an increased sense of well-being. The patient
may lose certain minor digestive complaints such as constipation and
abdominal bloating. Aches, pains and stiffness in muscles and joints
gradually disappear, and his joints seem to be injured less easily by
mechanical trauma. Crepitus becomes less noticeable, and eventually
disappears. The physician may note that the patient appears younger, that his
color is improved, his skin is more elastic, and that his tongue shows
improvement in mucous membrane morphology. Liver tenderness and enlargement
may disappear. Hemoglobin levels tend to improve. Joint mobility improves,
joint deformities occasionally resolve, and impaired muscle strength tends to
improve (54) (141). Not all patients with
rheumatoid arthritis recover at the same rate from the signs and symptoms of
rheumatoid arthritis in response to prolonged adequate niacinamide therapy.
In the early stage of rheumatoid arthritis (prodromal period), there is
prompt resolution of the patient's symptoms and signs. In the intermediate
stage of rheumatoid arthritis (active acute rheumatoid arthritis) there is a
slower resolution of the symptoms and clinical signs of this disorder, not
unlike that described in Case E, page 46. In the late stages of rheumatoid
arthritis (advanced chronic rheumatoid arthritis), there may be so much
retrogressive tissue alteration in nonarticular as well as articular tissues,
that complete functional and structural recovery may not be possible, even
with prolonged niacinamide therapy. Resolution of the clinical signs and
symptoms of late rheumatoid arthritis is exceedingly slow, and not unlike
that described in Case V, page 39. Especially noticeable in
patients with rheumatoid arthritis who are receiving adequate niacinamide
therapy is improvement in appetite, with concomitant gain in weight, recovery
from many nervous and mental symptoms, gradual disappearance of muscle
atrophy, and improvement of muscular strength; usually, also, the anemia is
corrected, the sedimentation rate index decreases to the normal range, and
subcutaneous nodules tend to disappear.
At the present time, no
explanation can be given to account for the biodynamic mechanism of
niacinamide4nduced improvements in persons with joint dysfunction. However,
in both hypertrophic arthritis and rheumatoid arthritis, articular and
non-articular improvements continue for as long as the patient's niacinamide
intake remains adequate, and they tend to fade away when inadequate
niacinamide therapy is substituted for adequate niacinamide therapy, or when
niacinamide therapy is discontinued. Most writers have
considered hypertrophic arthritis and rheumatoid arthritis to be two distinct
clinical entities (147) (33) (121) (195) (196) (197) (198) (161) (79) (12).
Hypertrophic arthritis has been considered to be a degenerative joint disease,
and rheumatoid arthritis has been considered to be a generalized disease of
the entire body, of unknown etiology (57) (58) (132) (134) (145) (227) (228)
(229) (230) (231) (28) (77) (140). From this work, no proof can be given for
or against the theory that niacinamide tissue deficiency disease is a prime
mover in the evolution of both hypertrophic arthritis and rheumatoid
arthritis. It should be realized, however, that merely because
hypertrophic arthritis and rheumatoid arthritis are different clinical
entities, one cannot exclude the possibility that they may be caused by the
same etiologic agent, acting in different ways. For example, in
experimental animals, it has been shown that the lack of a single
essential nutriment can produce a variety of dissimilar clinical disorders in
different individuals of the same species. However, without knowledge of
the animals previous nutritional history, one might not suspect that the same
etiologic factor, lack of a specific essential nutrient, was responsible for
each of the various clinical syndromes of the same tissue deficiency disease
which is permitted to develop at different rates in different individuals of
the same species. For example, "two distinct syndromes of ascorbic acid
deficiency have been observed in the Rhesus monkey depending on whether the
deficiency was acute or chronic. An acute deficiency was characterized by a
precipitous weight loss and tenderness in the joints of the legs but no
gingival lesions. A chronic deficiency was characterized by severe gingival
lesions and skeletal changes but no rapid decrease in weight" (192).
Similarly, marked differences exist between the clinical manifestations of
acute and subacute athiaminosis. When monkeys were made
completely deficient in thiamin, an acute athiaminosis was produced, and
"death occurred before any outstanding clinical symptoms or marked histological
degeneration of nerves set in.” When monkeys were given about one-half
of the needed thiamin, subacute athiaminosis ensued, and there were
"clinical signs of polyneuritis and cardiac failure, autopsy findings of
peripheral nerve degeneration and
Although it may appear
from this study that niacinamide has a high degree of specificity in the reversal
of the metabolic processes which permit joint dysfunction to evolve, it may
well be that a number of other therapeutic agents may influence these
metabolic processes in the same direction and to the same extent that
niacinamide does. Future clinical studies may indicate that there exist
substances other than niacinamide which can produce therapeutic effects which
equal or surpass those obtained in response to prolonged adequate niacinamide
therapy in the treatment of persons with joint dysfunction. (Editor’s note:
Vitamin C is one such substance.) In the treatment of joint
dysfunction in the future there may be clinical applicability of the findings
of recent studies concerning the metabolism of niacin under a variety of
experimental conditions and in different species of experimental animals
(238) (178) (176) (177) (90) (69) (70) (44) (45) (112) (120). (In most of
these laboratory studies, niacin rather than niacinamide was administered to
experimental animals. While there are certain differences in the biologic
utilization of niacin and niacinamide (71) (82) (69) (70), there are
sufficient similarities to suggest that biologic utilization of niacin and
niacinamide for many metabolic purposes might not be dissimilar, and thus
many of the findings that hold true for niacin may also hold true for
niacinamide.) In these studies, certain
metabolic interrelationships between niacin, tryptophane, protein, amino
acids, pyridoxine and 3-hydroxyanthranilic acid have been discovered (201)
(202) (188) (186) (179) (173) (162) (129) (101) (102) (103) (72) (92) (76)
(42) (24) (1). It has been found
that when a niacin-deficient animal is fed a sufficient amount of
tryptophane, the animal is cured of its niacin deficiency, and increased
amounts of niacin-containing molecules appear in the animal's urine. For this
reason, naturally occurring tryptophane is thought to be a biological
precursor of niacin. In the rat, 50 mg. of tryptophane is the equivalent of
1.0 to 1.5 mg of niacin or niacinamide. In the biotransformation of
tryptophane to niacin, 3-hydroxyanthranilic acid is an intermediary compound
which is capable of replacing tryptophane in the biosynthesis of niacin and
niacinamide (129). It has been found that the amount and type of protein the
animal is fed determine the amount of niacin or tryptophane needed by the
animal to prevent a niacin deficiency disease, and that a naturally occurring
protein (gelatin) (20) and certain naturally occurring amino acids
(especially threonine) can inhibit or nullify the effect of niacin or
tryptophane in the diet; similarly, other naturally occurring materials
(especially corn) (247) (205) and certain synthetic molecules (244) (245)
(246) may effectively block the metabolic action of niacin or tryptophane.
The level of pyridoxine nutrition also influences the metabolic pathways by
which niacin and tryptophane are utilized (204) (185) (187) (163) (146) (116)
(119) (7) (11). Many diverse types of
investigation in humans and in suitable experimental animals remain to be
carried out in order to determine the exact nature of the biochemical,
metabolic and morphologic changes occurring as a result of the ingestion of
different amounts of niacinamide for short or long periods of time. Such
studies could evaluate (a) any differences which might exist in the
biochemistry of persons with different grades of joint dysfunction, (b) the
effect of adequate niacinamide ingestion on the biochemistry of persons with
joint dysfunction who are eating a standard diet and are performing a
standard daily amount of physical exercise; (c) any sex differences which
might exist in biochemical reactivity to niacinamide therapy; (d) the maximal
safe doses of niacinamide therapy which would cause optimal improvement in
joint dysfunction; (e) various therapeutic agents which have been shown to be
capable of replacing niacinamide in animal studies; (f) various conditions
which have been found to enhance the effectiveness of niacinamide in animals;
and (g) various nutritional conditions which have been found to inhibit the
action of niacinamide in animals. In addition, it would be
desirable (a) to study the effects of continuous niacinamide therapy on the
biochemical, metabolic and morphologic properties of articular structures in
various animal species including bovine animals which are subject to
spontaneously occurring hypertrophic arthritis with increasing age (225); (b)
to study the distribution of niacinamide in articular structures of
experimental animals through the use of tagged molecules (isotopic and radioactive)
(85) (17) (212) (164); and (c) to produce graded sub-acute and chronic
aniacinamidosis in experimental animals and to study articular structures at
various time intervals (244). While such animal studies
and specialized chemical and metabolic studies in humans may prove fruitful
in elucidating the mechanisms which permit joint dysfunction to evolve in an
untreated population, and to be corrected by niacinamide therapy, from a
practical point of view it has been demonstrated that the progressive
impairment in joint mobility with advancing age, which has been accepted in
the past as an inevitable concomitant of the normal aging process, can be
corrected or ameliorated by prolonged adequate niacinamide therapy. In
addition, it seems not unreasonable to suppose that the evolution of the
common form of joint dysfunction can be prevented by adequate niacinamide
supplementation of an adequate diet throughout the lifetime of an individual. (End of Chapter 5, and of the book. 248 references follow in the Bibliography, which is posted at this link: http://www.doctoryourself.com/kaufman11.html )
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