I won't take more than 10,000 IU, unless a doctor tells me to.  A
recommendation I've seen is to use beta carotene if you want more
because vitamin A is derived from it, and it's far less likely to
cause an overdose.

Out of curiosity, how much vitamin C is in I-Caps?

Laura

There have been a couple recent posts in this group on nerve regeneration.
Here is another one related to vitamin C. This info is relevant to this
group because we know vitamin C can have a positive effect on IOP also.
March 22, 2004

Vitamin C treats neurologic condition

The April 2004 issue of the journal Nature Medicine published an article by
French researchers who discussed the finding that vitamin C could help
alleviate the symptoms of Charcot-Marie-Tooth disease (CMT), the most common
inherited peripheral neuropathy, which affects one out of every 25,000
individuals. Approximately half of CMT patients have the CMT-1A form which
is characterized by abnormal peripheral nerve myelination, leading to nerve
damage and muscle atrophy.

Michel Font?s and colleagues used a mouse model of the disease to determine
the effects of ascorbic acid, which has been shown to be necessary for the
promotion of myelination in vitro and, when deficient, has been linked with
femoral neuropathies. In a series of experiments, the mice were fed the
equivalent of approximately four grams ascorbic acid for a 70 kilogram adult
male, which approaches the maximal amount approved for ascorbic acid
deficiency treatment, or a placebo. The researchers found substantial
improvements in movement in the mice treated with vitamin C after three
months. The males were treated with the vitamin until their natural deaths.
Males of this genetic strain who received placebos or no treatment lived an
average of six months compared to male mice who received ascorbic acid who
survived an average of 19.7 months, which approaches the lifespan of normal
mice.

When the sciatic nerves of the experimental mice were examined, ascorbic
acid was found to be associated with remyelination , demonstrating nerve
repair.

A further finding was that the gene that is overexpressed in CMT-1A was
inhibited by ascorbic acid to a level below that which is necessary to
induce the disease's effects in the body. The authors propose that the
effects of ascorbic acid are due not only to its antioxidant properties, but
to a direct control of specific gene expression. They plan to initiate
future trials in humans.

I just read one more interesting snippet. Here it is:

     Vitamin C
     Fortunately, history provides significant therapeutics in regard to
managing glaucoma. Conventional medications and interventions are the most
widely used methods of treatment, but nutritional protocols have produced
convincing evidence of benefit.

     Vitamin C is an effective adjunct in stabilizing IOP. Some individuals
respond to as little as 2 grams a day of vitamin C, although others respond
to only extremely high doses, for example, 35 grams a day. Because of the
variance in the amount of vitamin C required to exert a positive effect,
careful monitoring by a physician is required. Intravenous administration of
vitamin C results in an even greater initial reduction. The
pressure-lowering action of vitamin C is long-lasting if supplementation is
continued, frequently showing an average reduction of 16 mmHg. Nearly normal
tension levels have been achieved in some patients using vitamin C, when
acetazolamide and pilocarpine therapy failed. The beneficial mechanisms by
which vitamin C lowers inner eye pressure include (1) increased blood
osmolarity, a process that draws fluid from the eye and into the blood, (2)
diminished production of eye fluid, and (3) improved fluid outflow.

     Many of the benefits of vitamin C are likely attributable to collagen
formation, an important function of this water-soluble vitamin. Collagen is
the most abundant protein in the body, including the eye, giving strength
and integrity to ocular tissue. Vitamin C helps preserve the collagen in the
eyes' drainage tubes, the very tubes that malfunction in glaucoma. Credits
directed to vitamin C appear justified when considering reduced IOP and the
improved structural health of the eye.

     Bioflavonoids: What Can They Accomplish?
     All nutrients that support collagen metabolism, particularly at the
back of the eye where the optic nerve exits and in the tissues that drain
the eye, are important in glaucoma treatment. One such nutrient
bioflavonoid, known as the proanthocyanidins (found in grape seeds and pine
bark), cooperates with vitamin C in achieving collagen integrity. In the
eye, collagen provides tensile strength and stability to the tissue. Another
major function of vitamin C is the preservation of capillary integrity, a
task made easier with the assistance of a bioflavonoid. The bioflavonoids
work not only with vitamin C but also on behalf of vitamin C, preventing the
breakdown of ascorbate. The proanthocyanidin bioflavonoids work by binding
to collagen, increasing elasticity and flexibility. The proanthocyanidins
are considered a powerful antioxidant, defending the collagen matrix against
free-radical attack and guarding it against enzymatic breakdown through the
enhanced delivery of oxygen and blood to the eye.

     Rutin, a bioflavonoid from the citrus family, has demonstrated the
ability to lower IOP when used in conjunction with standard drugs. Pansy
(Viola) contains up to 23% rutin on a dry-weight basis. Naturopaths, for the
treatment of glaucoma, often recommend sources of rutin, including pansy.

     The genus Vaccinium comprises nearly 200 species of berries, all
showing generous amounts of flavonoid/anthocyanidin compounds. Bilberry,
Vaccinium myrtillus fructus, has historically been used in various eye
conditions, including glaucoma, cataracts, macular degeneration, diabetic
retinopathy, and retinitis pigmentosa. Although bilberry is not considered a
curative herb in regard to glaucoma treatment, it appears to assist in
halting additional damage by bringing a good flow of blood to the eyes.

     Coleus Forskohlii
     When Coleus forskohlii was applied directly to the eye, it was shown,
in clinical studies involving both animals and humans, to reduce IOP, making
it of significant benefit in glaucoma treatment. Forskolin represents a
potentially useful class of antiglaucoma agents, differing in molecular
mechanism and action from previously used drugs (Caprioli et al. 1984;
Hartman et al. 1988). C. forskohlii appears to have a twofold approach that
delivers benefit to the glaucomatous eye by increasing intraocular
circulation and decreasing aqueous humor outflow. The outflow facility
remains unchanged, but the ciliary blood in the vascular tunic increases.
The benefits are observable about an hour after application and reach a
therapeutic peak at 2 hours. The value of C. forskohlii remains significant
for at least 5 hours after application. Because C. forskohlii eye drops are
not yet available, oral administration may be considered, with the hope that
similar results can be obtained. C. forskohlii appears to bestow its
therapeutic values without risk of major side effect.

     C. forskohlii has been used to advantage in the treatment of
hypothyroidism. Interestingly, subclinical hypothyroidism, so mild that it
produces no symptoms, has been noted as a cofactor in some glaucomatous
patients.

     Hydergine has some of the same biochemical advantages as C.
forskohlii. Hydergine may be capable of lowering IOP by decreasing hypoxia
(reduced oxygen supply) and preventing free radical damage to critical
cells.

     The Value of Minerals
     Magnesium has long been recognized as nature's physiological calcium
blocker. Previous studies had demonstrated that calcium channel-blocking
drugs offer benefits for some glaucoma patients. Armed with this revelation,
researchers at the University Eye Clinic in Basel, Switzerland, evaluated
the effect of supplemental magnesium on glaucoma patients. Magnesium (121.5
mg twice daily) was administered to 10 glaucomatous patients for 1 month. At
the conclusion of the study, results substantiated that magnesium
supplementation improved the peripheral circulation, with an accompanying
beneficial effect on the visual field in patients with glaucoma.

     Magnesium also has the ability to turn off the sympathetic nervous
system. This is a reputation that has earned magnesium credit in cardiology,
acting as an antiadrenergic. An antiadrenergic drug blocks the effects of
impulses transmitted by the adrenergic postganglionic fibers of the
sympathetic nervous system. This act would tone and modify the sympathetic
response, soothing the "fight or flight" syndrome. Recall that among the
many functions controlled by the sympathetic nervous system--those normally
not under conscious control--are dilation of the pupils and a general
stimulatory response. Stimulation of the sympathetic nervous system would be
contraindicated in glaucoma control.

     Minerals are absolutely essential to longevity and quality of life.
Individuals can survive longer with a vitamin deficiency than with a mineral
deficiency. The importance of minerals is becoming more evident as research
data amass. The trace mineral chromium has won additional credit beyond
stabilization of blood glucose levels by being able to improve focusing of
the eye and lower IOP. Selenium benefits ocular function, and zinc supports
healthy eye structure. Selection of a good multiple will provide these vital
minerals, plus additional nutrients needed for ocular health.

     --------------------------------

     The current hypothesis regarding the causative factors of glaucoma
leans toward the neurotoxicity/neuroprotection theory. Ophthalmologists
refer to neurotoxicity as the "buzz word" in their profession (i.e., the
focus of current glaucoma exploration). It appears to be more than a trendy,
ungrounded approach to explaining the causative factors and therapeutic
modalities of glaucoma. Research emanating from various prestigious
universities converges when considering the neurotoxicity theory of
glaucoma.

     The opinions of Dr. N. N. Osborne, Nuffield Laboratory of
Ophthalmology, Oxford University, echo those of many other scholars who are
studying glaucoma. Dr. Osborne believes that the visual-field loss in
glaucoma is due to the death of retinal ganglion cells. Reducing or slowing
down the loss of ganglion cells, a concept known as neuroprotection, appears
to be the "only way forward." Osborne proposes that the death of neurons (a
process referred to as apoptotic cell death) in various diseases is
fundamentally the same but varies in cause. Experimental data show that the
death rate of neuronal populations is dependent upon the impact of the
insult. Neuroprotectants are more likely to benefit a patient in which
neurons die slowly, as in glaucoma. If a reliable neuroprotector can be
administered in such a way that it reaches the retina in appropriate amounts
and has insignificant side effects, it is likely to attenuate ganglion cell
death and thus benefit the glaucoma patient. Providing a solution to
neurotoxicity appears to be the therapeutic goal for future treatment.

     Aminoguanidine may help preserve the vision of refractory glaucoma
patients by inhibiting the build-up of nitric oxide synthase-2 (NOS-2), a
substance believed to degrade neuroprotection. NOS-2 stimulates the emission
of nitric oxide, a compound implicated in retinal nerve damage (Morgan et
al. 1999). Reduction of nitric oxide through nitric oxide synthase
inhibition provides partial but significant protection against the lethal
effects of oxygen deprivation and the action of excitatory amino acids, such
as glutamate and aspartate, upon retinal ganglion cells.

     Interest in knowing exactly what aminoguanidine could accomplish in
regard to glaucoma spurred researchers at Washington University to look at
the drug more closely. Two glaucomatous groups of animals were selected for
aminoguanidine research. All animals initially displayed elevated IOP, with
cupping and pallor of the optic disc. One group remained untreated, and the
other group was treated with aminoguanidine. At the conclusion of the
6-month study, the untreated group displayed the original benchmark
symptoms, whereas the eyes of the aminoguanidine-treated group appeared
normal but with continued elevations in IOP.

     The Washington University study also quantified retinal ganglion cell
loss in a group receiving aminoguanidine compared to a control group void of
treatment. The untreated group displayed a 36% loss of retinal ganglion
cells, compared to less than 10% in the treated group. To realize the
importance of this latter finding, visualize the retina being composed of
ten layers of various types of cells. Retinal ganglion cells are large,
flask-shaped cells composing one of the ten layers. The degradation of the
ganglion cells pathologically compromises the delicate nervous tissue
membrane of the retina. The final consensus of the study was that
aminoguanidine might prove useful as a pharmacological neuroprotector in the
treatment of glaucoma, contributing to a healthier eye, with less neuronal
death.

     Some patients have normal (or low) tension glaucoma. Even though the
eye pressure is within normal range, the optic nerve continues to be
injured. Despite efficient control of IOP, retinal ganglion cell loss will
continue, resulting in further visual impairment if the causative factor is
not determined and treated. This revelation was considered valuable, for it
exonerated IOP as being the sole antagonist in retinal degradation.
Researchers at University Hospital of Wales determined that neuroprotective
agents might play a role in patients with glaucoma who have progressive
visual-field loss despite satisfactory control of IOP.

     Glutamate's Role in Glaucoma
     Agreement on the importance of preventing the death of retinal
ganglion cells has been established, but the cause of ganglion cell death
remains speculative. Present information supports the hypothesis that
ganglion cell death may result from a form of ischemia (decreased blood flow
to a body organ or part). During ischemia, glutamate is released in
excessive amounts, initiating the death of neurons. Glutamate is a salt of
glutamic acid, a nonessential amino acid occurring in a wide number of
proteins. Glutamate is considered a good guy/bad guy. Because brain cells
use glutamate as a neurotransmitter, it may rightly be termed a "great
communicator" as signals leap from neuron to neuron. Effective communication
also means the controlled release of glutamate, as precise amounts are
delivered to the proper cells. It is when glutamate occurs in excessive
amounts that trouble begins. Communication between cells fails, and
exorbitant amounts of glutamate attach to cells having glutamate receptors.
This bonding or attachment spells doom to the ganglion cell, resulting in
eventual cell death. Excesses of glutamate have, in effect, poisoned the
cell.

     Elevated glutamate levels can also exist in the vitreous humor of
patients with glaucoma (27 m M as compared to 11 m M in controls) (Vorwerk
et al. 1999a). The vitreous humor fills the posterior compartment of the
eye, assisting in holding the retina and lens in place. An increased
concentration of glutamate in the vitreous humor is sufficient to induce
retinal ganglion cell death (Vorwerk et al. 1999b). The rise in IOP is
probably the initial insult, which enhances the increase or release of
glutamate. Supplements that protect against glutamate toxicity will be
discussed later in this protocol.

Natural therapies for ocular disorders, part two: cataracts and glaucoma.

Head KA. Thorne Research, Inc., P.O. Box 25, Dover, ID 83825,USA.
kathi@thorne.com

Altern Med Rev 2001 Apr;6(2):141-66

Pathophysiological mechanisms of cataract formation include deficient
glutathione levels contributing to a faulty antioxidant defense system
within the lens of the eye. Nutrients to increase glutathione levels and
activity include lipoic acid, vitamins E and C, and selenium. Cataract
patients also tend to be deficient in vitamin A and the carotenes, lutein
and zeaxanthin. The B vitamin riboflavin appears to play an essential role
as a precursor to flavin adenine dinucleotide (FAD), a co-factor for
glutathione reductase activity. Other nutrients and botanicals, which may
benefit cataract patients or help prevent cataracts, include pantethine,
folic acid, melatonin, and bilberry. Diabetic cataracts are caused by an
elevation of polyols within the lens of the eye catalyzed by the enzyme
aldose reductase. Flavonoids, particularly quercetin and its derivatives,
are potent inhibitors of aldose reductase. Glaucoma is characterized by
increased intraocular pressure (IOP) in some but not all cases. Some
patients with glaucoma have normal IOP but poor circulation, resulting in
damage to the optic nerve. Faulty glycosaminoglycan (GAG) synthesis or
breakdown in the trabecular meshwork associated with aqueous outflow has
also been implicated. Similar to patients with cataracts, those with
glaucoma typically have compromised antioxidant defense systems as well.
Nutrients that can impact GAGs such as vitamin C and glucosamine sulfate may
hold promise for glaucoma treatment. Vitamin C in high doses has been found
to lower IOP via its osmotic effect. Other nutrients holding some potential
benefit for glaucoma include lipoic acid, vitamin B12, magnesium, and
melatonin. Botanicals may offer some therapeutic potential. Ginkgo biloba
increases circulation to the optic nerve; forskolin (an extract from Coleus
forskohlii) has been used successfully as a topical agent to lower IOP; and
intramuscular injections of Salvia miltiorrhiza have shown benefit in
improving visual acuity and peripheral vision in people with glaucoma.

Ascorbic acid in the treatment of alkali burns of the eye.

Pfister RR, Paterson CA.

Ophthalmology 1980 Oct;87(10):1050-7

Severe ocular alkali burns in rabbits result in a decrease in aqueous humor
ascorbate levels to one-third normal levels. If this deficiency is reversed
by immediate treatment with parenteral or topical ascorbate, there is a
significantly decreased incidence of subsequent corneal ulceration and
perforation. The morphologic changes in these ulcerating corneas are typical
of those noted in scorbutus (scurvy). It is concluded that alkali injury to
the ciliary epithelial transport processes or ciliary body vasculature
results in localized deficiency of ascorbic acid in the aqueous humor and
cornea. The development of corneal ulceration is thought to be based on this
deficiency which results in the failure of fibroblasts to produce sufficient
collagen for repair. A randomized clinical trial of ascorbic acid in the
treatment of human alkali burned eyes is now underway.

Abnormal formation of collagen cross-links in skin fibroblasts cultured from
patients with Ehlers-Danlos syndrome type VI.

Pasquali M, Still MJ, Vales T, Rosen RI, Evinger JD, Dembure PP, Longo N,
Elsas LJ. Department of Pediatrics, Emory University, Atlanta, GA 30322,
USA.

Proc Assoc Am Physicians 1997 Jan;109(1):33-41

Ehlers-Danlos syndrome type VI (EDS VI) is an autosomal recessive disorder
of connective tissue characterized by hyperextensible, friable skin and
joint hypermobility. Severe scoliosis and ocular fragility are present in
some patients. This disease is caused by defective collagen lsyl
hydroxylase, a vitamin C-dependent enzyme that converts lysyl residues to
hydroxylysine on procollagen peptides. Hydroxylysine is essential for the
formation of the covalent pyridinium cross-links pyridinoline (Pyr) and
deoxypyridinoline (Dpyr), among mature collagen molecules. Pyr derives from
three hydroxylysyl residues, whereas Dpyr derives from one lysyl and two
hydroxylysyl residues. Patients with EDS VI have high urinary excretion of
Dpyr, resulting in a high ratio of Dpyr-Pyr. In this study, we evaluate
content and production of pyridinium cross-links in the skin and cultured
fibroblasts from patients with EDS VI. The skin of normal controls contained
both Pyr and Dpyr, with a marked predominance of Pyr as observed in normal
urine. The skin of patients with EDS VI had reduced total content of
pyridinium cross-links, with the presence of Dpyr but not Pyr. Long-term
cultures of control fibroblasts produced both Pyr and Dpyr, with a pattern
resembling that of normal skin. By contrast, cross-links were not detected
in dermal fibroblasts cultured from patients with EDS VI. Vitamin C, which
improves the clinical manifestations of some patients with EDS VI, decreased
Dpyr accumulation though only minimally affecting Pyr content in control
cells. By contrast, addition of vitamin C to fibroblasts from patients with
EDS VI stimulated the formation of Dpyr more than that of Pyr and greatly
increased total pyridinium cross-link formation. These results indicate that
qualitative and quantitative alterations of pyridinium cross-links occur in
skin and in cultured dermal fibroblasts of patients with EDS VI and may be
responsible for their abnormal skin findings. The vitamin C-stimulated
production of Dpyr and Pyr in fibroblasts from patients with EDS VI may
explain at least in part the therapeutic effects of this vitamin in EDS VI.