Vitamin C. Mythical Rebound effect.

[Sheri Nakken]

FYI

From "Hilary Butler"
in response to myth of rebound effect

The gold standard textbook on the topic is a three volume text by CRC
press, called Vitamin C, written by Professor C. Alan B. Clemetson.
Everyone has to find their own baseline.. that level which suits their
metabolism, and whatever toxic factors they encounter every day.
THEN, when the person gets sick, or something goes wrong, they increase the
dose to meet the need.
Given that the "human" animal is incapable of MAKING vitamin C, the rebound
effect is a mythical phenomenon, made up by people who have no
understanding of vitamin C.

This is the current stupid explanation of rebound effect (DOESN"T EXIST)
(comments after)
http://www.vitamincfoundation.org/faq.html
Q., What is the rebound effect?
A., It is our understanding that most humans are in a state of sub clinical
scurvy (vitamin C deprivation).
In this state "non critical " body functions (enzyme systems) that use up
vitamin C (vitamin C acts as a co-enzyme) are 'switched off' - for survival.
Pauling explained that these enzymes reactions, in the presence of
adequate vitamin C, have beneficial effects, including possible anti-cancer
effects.
When you begin taking adequate amounts of vitamin C (amounts that approach
normal serum levels in animals) the blood concentration reaches a level
where these "normal" enzyme reactions are turned back on, and the body
begins using the vitamin C in the blood for other metabolic functions. This
is the normal nonscorbutic state for most animals.
The rebound effect is then when you suddenly discontinue vitamin C after a
high sustained dosage.
The enzyme reactions continue for 24-48 hours, and use up what little
vitamin C there is in the blood, tehreby lowering the concentration for a
few hours, and depriving cells of vitamin C. This is the rebound effect.
Soon the enzyme systems, lacking vitamin C, "turn themselves off" and you
are back to the normal unhealthy "survival "state without vitamin C.
As you can see, there is no such thing as "rebound effect." above

You are either in a sub-acute state of scurvy, or you are not.

If you have enough vitamin C, all the enzyme pathways will work properly.

If you don't have enough vitamin C, the enzyme pathways won't work. They
will switch back off.

It has nothing to do with "high sustained doses" actually. You either
have enough, or you don't. It's as simple as that.

FACT. The human can only use the vitamin C that is put into it.
FACT. The human cannot store excess vitamin C.
FACT. If a human being stops eating vitamin C, depending on the level of
exerctise or stress, the body will run out of vitamin C. In the early
days, with sailors, that number of days was around 90. Under other
circumstances, the longest a human can last until the need for vitamin C
becomes critical is 140 days.
The problem IMO is with the words "rebound"
Rebound from what, to what?
My opinion is forget a rebound anything, and concentrate on working out
what is the baseline whereby all essential enzyme functions work smoothly.
Then factor in the various biochemical processes that the body goes through
in abnormal states.
For those who don't know what is in these three volumes, here are the
chapter headings of each volume.

Volume 1
Vitamin C Deficiency.
Classical Scurvy : A Historic Review
Chronic Subclinical Ascorbic Acid Deficiency.
Factors Affecting the Economy of Ascorbic Acid.
Inadequate Ascorbic Acid Intake.
Smoking
Aging
Sex
Menstrual Cycle, Estrus Cycle, Ovulation
Infection
Trauma, Surgery and Burns
Heavy Metals, Water Supplies: copper, Iron, Manganese, Mercury, and Cobalt.
Biofavonoids.
Dietary Protein
Hormone Administration: Birth Control Pills.
Pregnancy
Hemolysis
Stress and the Pituitary - Adrenal System
Lack of Sleep
Time of Day
Season
Achlorhydria
Ionizing Radiation
Aspirin and Salicylates.
Alcohol
Other Factors affecting Ascorbic Acid needs.
Volume II
Clinical and Pathological Findings in Ascorbic Acid Deficiency
Vascular Changes
Diabetes Mellitus
Anemia
Defective Wound Healing
Bone Changes
Joint Lesions
Dental and Periodontal Changes
Atherosclerosis
Mental Depression
Amyloid
Venous Thrombosis
Decreased REsistance to Infection
Liver Bile and Gallstones.
Volume III
Chemical Changes Associated with Vitamin C Deficiency.
Histamine Metabolism
Proline and Lysine Metabolism
Carbohydrate Metabolism
Folic Acid Metabolism
Cholesterol Metabolism
Tyrosine and Phenylalanine Metabolism
Tryptophan Metabolism
Adrenal Corticoid Metabolism
Uric Acid Clearance
Clinical Conditions Associated with Disorders of Ascorbic Acid Metabolism
Rheumatic Fever
Monorrhagia
Wound Dehiscence
Habitual Abortion
Abruptio Placentae
Prematurity and Premature rupture of the Fetal Membranes
Megaloblastic Anemia of Infancy, Pregnancy, and Steatorrhea
Gastrointestinal Ulcers and Hemorrhage
Ocular Lesions
Cerebral Hemorrhage and Thrombosis'
Coronary Thrombosis and Myocardial Infarction.

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~```
Those heading are very simplistic. The books actually cross reference back
and forth, and though you might be reading about pregnancy in one place,
you will find it interrelated in others as well...the chapters are very
comprehensive and the headings don't do them a service really...
The chapter on ocular lesions, is compulsory reading for anyone involved in
SBS cases... but see the occular chapter also includes in it the
implications of vitamin C levels...
to give an example.
Here is one paragraph:
Page 204:
A. Hemorrhagic Lesions.
There is plenty of evidence that retinal hemorrhage is associated with
skin "capillary fragility" in hypertensives, in diabetics, in nondiabetic
nonhypertensives, and also in Eales' disease (recurrent hemorrhages into
the retina and vitreous humor). Moreoever there is evidence that treatment
with bioflavinoid rutin, or with rutin and ascorbic acid corrects or
improves the "capillary fragility" in the majority of such patients, as
seen in Figure 1, , which is based on work by Donegan and Thomas (1948).
Objective evidence of improvement in the retinal picture is less frequent,
espcecially in diabetics. Few investigators have felt justified in
observing an untreated control group of people who are gradually losing
their vision. However, Beardwood et al. (1948) did report an excellent
controlled study. Amonst 321 consecutive clinic patients receiving
treatment for diabetes mellitus, they found that 46% showed increased
capilary fragility, and that 24% of the total number 77 subjects) showed an
associated retinopathy. Another 46 patients with capillary fragility and
retinitus were added from the private practice of the authors. Successive
patients were given rutin, hesperidin, or placebo. The initial dose of
rutin was 20 mg t.i.d, increased to 50 mg t.i.d. if the capillary fragility
did not return to normal in 4 or 5 weeks. The dose of hesperidin was 50 mg
twice a day. After 6 months of treatment, a definit improvement in the
retinal picture was observed in 25% of each of the two test groups, and in
only 11% of the control group receiving the placebo. The capillary
strength returned to normal in 80% of the flavonoid treated patients. In
the other 20%, the capillary fragility was more refractory to treatment
and, in some cases, remained abnormal at the end of 6 months of study
(Table 5).

Obviously, not all references are this old. But I deliberately chose this
paragraph to show that much of the foundation work was done a long time
ago. And anyone working with pregnant women today, and dealing with babies
with SBS, should be nodding their heads away, if they understand the whole
sub-scorbutic bit.
Hilary.
--------------------------------------------------------------------
Sheri Nakken, R.N., MA, Classical Homeopath
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