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PABA vitamin b10

robinhood12345

Senior Member
Messages
151
Hey all
PABA appears in nutritional biochemistry textbooks in the 1940s, and 50s, then vanishes from them after around the 60s or 70s. It is not in any today. Was considered essential nutrient till around 1954 when FDA removed that status from it. With normal PABA levels the body can make vit d in the skin with no sunburn. Binds to melanin in the lab so plays a role in skin pigmentation. White people may have low levels of it. I started taking PABA pills a few days ago. Food sources are brewers yeast, rice bran, cabbage.

Some info from 40s and 50s textbooks

cases); it benefits asthmatic patients in certain instances; and it increases
the appetite and induces a feeling of well-being.”

Although confirmation of all of Sieve’s claims is lacking, the return of
pigmentation in human gray hair has been described by others (94-100)
referred to in the preceding chapter. Furthermore, Costello (103) published
a case of vitiligo successfully treated with PARA. DeVilbiss (99) commented
on the &timulation of libido. Banay (94, 95) mentioned a marked
increase in erotic drive as well as stimulation of appetite. Other physicians
stated in private communications that PABA therapy seems to have
*a favorable action in chronic constipation and appears to contribute to a
feeling of well-being. Most clinicians are of the opinion that asthmatics
are not benefited by PABA, although some cases were noted to be favorably
influenced (48). Doma,rus (104) found PABA to be beneficial in 4 cases
(psychotic episode with psychopathic personality ; alcoholic Korsakow
226 S. ANSDACHEIt

psychosis; chronic alcoholism; and morphine addiction). He believes
that PABA therapy should be further investigated in parasympatheticotonic
conditions and as an adjuvant to morphine withdrawal treatment.


page 215


In view of the fact that a diabetic patient went into shock as a result of
combined PABA and insulin therapy (91), it is of interest that PABA appears
to potentiate insulin (143). Insulin was injected subcutaneously
into mice in a dose (Q unit per 18 g. of body weight) which is known not
to reduce the blood sugar to convulsive levels. When PABA was given
either before, simultaneously, or after the insulin, convulsions typical of
insulin shock were produced.

At the same level of 1 g. per kg. of body
weight, the simple aromatic amine effected a mild but definite hyperglycemia
in rats. It did not alter the speed, degree, or duration of the hypoglycemia
produced in rabbits by insulin. As determined by the method of
Grattan and Jensen (144), it was noted to deplete the liver of glycogen.
Since mice treated with a cortical extract and PABA had an average liver
glycogen content of about 500 mg. per cent as contrasted with approximately
1700 mg. per cent found in the livers of animals which had received
solely the cortical extract, it may be concluded that the rate a t which the
organism is required to yield its stores of liver glycogen is augmented by the
simple aromatic amine.

Conditions favorable for insulin potentiation by
PABA ha+e not been found in clinical trials.
The above data were discussed and extended by Martin (145) who considered
the following facts:

1) PABA acts in the pseudo-potentiation of insulin (143, 145);
2) it produces a mild hyperglycemia in doses of 1 and 2 g. per kg. in
3) it depletes the glycogen reserves of the liver (113);
4) it causes a mild rise in blood pressure in the anesthetized cat, reversed
by 2-( 1)-piperidylmethyl)-] ,4-benzodioxan (146) ;
5) i t is known to inhibit various enzyme systems (142);



it produces hypertrophied thyroids with hyperthyroidism (145, 147,
7) it protects against the action of thyroxine in the intact animal (145).
Martin suggested that these actions of PARA may be motivated via the
pituitary and production of thyrotrophic hormone, as already concluded by
Astwood, et al. (148) and Mackenzie, et al. (147). Therefore, PABA may
be effective clinically in counteracting hypothyroidism and may be contraindicatecl
in cases of hyperthyroidism.

Indeed, the action of a number
of agents, including thioureas. sulfanilamide and PABA in producing
hypertrophied thyroids (147-151) has teen demonstrated. These various
substances may be considered to be inhibitors of tissue metabolism, as
firbc suggested by Cutting and Kuzell (152). The peeudo-potentiation
of insulin by these compounds as well as by others, such as e.g. saccharin
(153), can best be explained at present on the baais of the above considera
tio

C. Conclusion : Physiological Importance
From a pharmacological point of view, PABA may be considered to be a
detoxified aniline. Since it does not act like pigments do and since no
results were obtained in cases of faulty pigmentation from its local or
topical application, its physiological effect is not that of an aniline-like dye.
However, the question whether it is to be considered one of the B-vitamins,
can be answered.

By definition, a vitamin B complex factor is
a) a natural constituent of yeast, liver, and/or cereals.
b) water-soluble.
c) a growth-promoting substance for bacteria, yeasts, fungi, and/or
molds
d) a co-enzyme or activator of enzymstic prozesses.
e) physiologically effective in minute amounts.
f) a substance which causes a deficiency diseage when laoking in the diet.

The data presented in the preceding chapters seem to justify the conclusion
that PABA is one of the vitamin B complex factors: i t occurs in
nature as universally as and side by side with most of the B-vitamins; it
is about thirty times more soluble in water than riboflavin; i t is a growth
factor for a variety of microorganisms; its r61e as a phenolase activator has
been suggested; i t has been claimed to bz clinically effective in amounts
comparable to those employed in choline and inositol therapy; deficiency
sjrlnptoms resulting from its absence in the diet have been described.

However, it may be argued that PABA per se is not a vitamin, since the
amounts necessary to show effectiveness experimentally and clinically
are by far greater than the ones ingested in a normal diet. Nevertheless,
it has been suggested (VII, 2) that PABA as found in natural products
may possibly be more efficacious than the simple aromatic amine by
itself. The PABA-peptide, p-aminobenzoyl-2-glutamic acid, although
not known to occur in nature, has been reported (294) to have 8 to 10 times
more anti-sulf onamide activity than equimolecular amounts of PABA
per se.

To date, the high potency of the peptide could not be confirmed
experimentally, but further work will undoubtedly yield PABA derivatives
with more clinical effectiveness than has the simple aromatic amine.
As recently as April 1943, Hogan and Kamm (295) remarked that the
status of PABA as a vitamin still is indefinite. Nevertheless, the American
Medical Association (102) commented on PABA as a vitamin in relation
to humangray hair in July of the same year. In a 1044 review of the present
status of the vitamin B complex, Elvehjem (296) stated that the vitaminlike
property of PABA has been demonstrated and that the simple aromatic
amine can undoubtedly produce certain effects in the human, but he is
inclined to believe that its action is indirect.

Although the U. S. Food
and Drug Administration (297) prescribed in 1941 that a product designated
as a “vitamin B complex preparation” should furnish demonstrable
amounts of PABA, the same administrative agency (298) made known
about two years later that there was no convincing evidence for PABA to
be a food essential for animals or humans. Indeed, PABA occupies as
peculiar a position as do some of the B-vitamins, such as choline (299).
It may not be classified as a vitamin for animals capable of synthesizing it.
It may be considered to be a vitamin for all species for which it must be
supplied preformed in the diet in order to satisfy tissue demands. According
to Williams’ (300) thesis on vitamins, the significance of PABA
in the intestinal physiology of the animal is just as great whether it is an
indispensable food constituent or is manufactured within body tissues.

Oops didnt copy paste properly- the first part is

p-Aminobenzoic Acid Deficiency. Relatively little is known about
p-aminobenzoic acid (PABA) deficiency and its incidence in man, or
about the relationship of this vitamin to another in which it is contained,
folic acid. There is good evidence to indicate, however, that it is effective
in the treatment of certain types of hair graying in man. Folic and
pantothenic acids have been reported to have similar effects, and it has
been suggested that p-aminobenzoic acid may act through folic acid
synthesis.

There is some reason to believe that pantothenic acid functions
with PABA in hair pigmentation. The effect of PABA ultimately is involved
in melanin formation however, and the oxidation of tyrosine to
melanin may in some manner be related to the apparent relationship
between tyrosine and folic acid (p. 415).

PABA stimulates the growth of rats and chicks on a deficiency diet,
and is a growth requirement for certain microorganisms. In the black or
piebald rat, deficiency results in graying of the hair (nutritional achromotrichia)—
a condition which, like hydroquinone-induced achromotrichia,
can be cured by PABA administration. Female albino rats have been
reported to have lactation disturbances when fed a PABA-deficient diet.

The high efficacy of the sulfonamides in inhibiting bacterial growth indicates
that PABA plays an unusually critical role in cellular metabolism,
particularly since analogues of many other metabolites have not proved
effective therapeutic agents. It would seem, therefore, that PABA occupies
some key metabolic position, which when blocked causes the breakdown
of a number of metabolic sequences.

The reversal of sulfanilamide
by folic acid and vitamin B12 indicates indeed that PABA is intimately
related to these substances (see Chapter HID). In view of these considerations
it is remarkable that the physiological effects of PABA and
its deficiency in the higher animals are not more pronounced.

Friedgood (98) reviewed the attributes that Sieve has ascribed to PABA:
“it darkens gray hair; it intensifies the normal pigmentation of the nipples
and mucous membranes of the mouth, vagina, and anus; it eradicates areas
of vitiligo; it induces a return of color and ‘changes the hypertrophy’ d
areas of leukoplakia in the mouth; it causes a decrease or almost complete
disappearance of hyperpigmentation of nevi and freckles; it stimulates
.libido; it re-establishes the menstrual cycle in amenorrhea and increases the
amount of flow in oligomenotrhea; it cures female sterility (12 out of 22
cases); it benefits asthmatic patients in certain instances; and it increases
the appetite and induces a feeling of well-being.”

From: Vitamin and Hormones volume 2 1946 (textbook)
THE ANTI GREY HAIE VITAMIN, A NEW FACTOR
IN THE VITAMIN B COMPLEX lunde et al 1939 (study)

The biochemistry of b vitamins 1950 (textbook)

The vitamins volume 3 1954 (textbook)

textbooks are on libgen
 
Last edited by a moderator:

pattismith

Senior Member
Messages
3,946
it produces hypertrophied thyroids with hyperthyroidism (145, 147,
7) it protects against the action of thyroxine in the intact animal (145).
Martin suggested that these actions of PARA may be motivated via the
pituitary and production of thyrotrophic hormone, as already concluded by
Astwood, et al. (148) and Mackenzie, et al. (147). Therefore, PABA may
be effective clinically in counteracting hypothyroidism and may be contraindicatecl
in cases of hyperthyroidism.

Indeed, the action of a number
of agents, including thioureas. sulfanilamide and PABA in producing
hypertrophied thyroids (147-151) has teen demonstrated. These various
substances may be considered to be inhibitors of tissue metabolism, as
firbc suggested by Cutting and Kuzell (152). The peeudo-potentiation
of insulin by these compounds as well as by others, such as e.g. saccharin
(153), can best be explained at present on the baais of the above considera
tio
warning:
Thiouracil and PABA are anti-thyroid compounds.

PABA has anti-TPO properties and promotes thyroid cancer in rats:

2005
Promotion of thyroid carcinogenesis by para-aminobenzoic acid in rats initiated with N-bis(2-hydroxypropyl)nitrosamine.

Abstract
Sulfonamide analogues of para-aminobenzoic acid (PABA), a precursor of folate synthesis, have beneficial effects as antifolate, but thyroid peroxidase inhibition has been reported as a side effect that results in promotion of rat thyroid carcinogenesis. In the present study, effects of PABA itself on F344 rat thyroid carcinogenesis after initiation with N-bis(2-hydroxypropyl)nitrosamine (DHPN) were evaluated. In experiment 1, rats in groups 1-4 received a single subcutaneous injection of DHPN at 2800 mg/kg, and groups 5 and 6 received vehicle saline alone. From 1 week after DHPN initiation, rats in groups 2, 3, 4, and 6 were fed basal diet containing 0.25%, 0.5%, 1.0%, and 1.0% PABA, respectively, for 40 weeks. Rats in groups 1 and 5 received basal diet alone throughout the experiment. The final incidence of thyroid follicular cell adenomas and adenocarcinomas was significantly (p < 0.05 or 0.01) increased in groups 3 and 4 as compared to group 1. No thyroid tumors were found in groups 5 and 6. In experiment 2, animals in group 1 were fed basal diet alone, while groups 2 and 3 were given 0.5% and 1.0% PABA in the diet, respectively, for 2 weeks. Thyroid weights in group 3, and serum thyroid stimulating hormone level and proliferative activity of follicular cells in groups 2 and 3 were significantly (p < 0.05 or 0.01) elevated.

In addition, the serum thyroxine level in group 3 was significantly (p < 0.05) depressed.

These results clearly indicate that PABA exerts promotion/progression effects on rat thyroid carcinogenesis as a result of hypothyroidism followed by negative-feedback via the thyroid-pituitary axis
.
 

robinhood12345

Senior Member
Messages
151
They gave the rats something that causes thyroid cancer first. One of the groups given PABA at the highest dose with DHPN was no different than a non DHPN group. One group was. Sample size was too small was one of the problems with the study leading to someone not skilled in the art to interpret a co incidence as something more serious.

These results clearly indicate that PABA exerts promotion/progression effects on rat thyroid carcinogenesis as a result of hypothyroidism followed by negative-feedback via the thyroid-pituitary axis.

The results clearly indicate the sample size was too small to draw any firm conclusions. Therefore there is no evidence to state that PABA exerts promotion/progression effects on rat thyroid carcinogenesis as a result of hypothyroidism followed by negative-feedback via the thyroid-pituitary axis.

Yeast, rice bran, cabbage, milk, meat and multiple other foods all contain the essential nutrient PABA aka vitamin b 10. And some b complex pills contain it too. So if you really believed PABA was a scary poison you would never eat cabbage, rice, milk, meat or anyone of the other multiple foods that contain it.

I have been taking 10g a day PABA for 5 days with no side effects.

On another forum someone said they have been taking it for 9 years with no side effects, and they no longer get sunburned at the beach.
 

pamojja

Senior Member
Messages
2,398
Location
Austria
On another forum someone said they have been taking it for 9 years with no side effects, and they no longer get sunburned at the beach.

That was me. :) However, my verbatim reply to you on that other forum in your PABA thread was:

pamojja said:
Made the experience with Pauling therapy and comprehensive supplementation since now more than 9 year, that I don't get sun-burns anymore. Not that I didn't tried: Since 2013 I'm every Jan/Feb for 6 weeks on a South-Indian beach, each day between 10-12 AM and 3:30-5:30 with whole-body sun-exposure (of course, without sun-cream).

Did anyone else here had the same experience?

robinhood12345 said:
Wow that's amazing. That's awesome. I can't wait to take it, and also to see how I go in the hot sun with it as I normally get burned pretty quickly. In one of the patents on it they give up to 20 grams a day for cancer so it is good to know it is safe even at high doses. I was planning to take 2-3 grams a day of it. What dosage of it do you take each day?

pamojja said:
Have to disappoint you. PABA was long one of the neglected nutrients in my stack, only got what tiny amount there was in the 2-per-day Multi and B-complex (LEF), recently increasing a bid. But still not more than 220 mg/d in average for 9 years.

In my case can't pin it down to any one single nutrient, but guess the synergistic effects of many, especially antioxidants (vitamin C, A, E, lutein, lycopene, astaxanthin...).
 

robinhood12345

Senior Member
Messages
151
I'm day 6 on PABA getting better rapidly. In bed for 17 years. Must have a genetic disease of it- transport problem or enzyme defect. Genes, and enzymes for it have never been identified- well at least not published in the literature. So even whole exome sequencing would not of picked it up. Urine organic acid, plasma amino acids all normal. Lactate/pyruvate ammonia, all normal. I suspected for a long time it was a genetic disease of a b vitamin, and tried all the other ones but was never really aware of PABA though had heard of it.

Early deficiency signs-
Weird skin rash/unhealthy skin on face
Greying of the hair/decrease healthiness of hair
Conjunctivitis for months/years
Crippling fatigue which progresses to fully disabled in bed fatigue
Slight neuro degeneration that progresses to severe over time
In later stages paralysis/stiffening/rigidity of the muscles worse on right side of body than left
In later stages personality change with aggression, very negative attitude, kind if paranoia, kind of delusional.

So that is what PABA deficiency looks like. Of course one from diet would be treatable just with yeast. Genetic PABA diseases will require life long supplementation with PABA. If a scientist reads this why not study PABA metabolism in man, identify the genes, enzymes, and their function, then publish it. I will eventually if someone else doesn't.