Bud’s Outcomes
1. Introduction
2. HIV Drugs
3. FIV Botanicals
4. Immunostimulators and Immunomodulators
5. Wasting
June, 2006, Last Update
1. Introduction
Sometime after midnight on June 2, 2006 Bud returned to the realm of the unknown from which
he came. I last saw him licking his paws after his final meal of the day on the exterior ramp of
the cat door leading to his enclosed backyard. Next morning he was gone. The gates were shut;
everything was as it had always been. His disappearance has no obvious explanation. Bud’s
yard successfully contained him for many years. I believe that he was taken from the yard, but I
will never know the truth of what happened to him. He is gone, and I know I will not see him
again. Bud was about 15 years old.
Although he had always seemed liable to unusual, often unexplainable, disturbances to his health, Bud was around nine years old when he began clearly experiencing ongoing problems rooted in deficient immunity. (See Bud's Timeline.) The first of these was a sinus and/or nasal infection that would not permanently resolve. There was never any any evidence that this was rooted in a past viral infection, such as herpes; instead, it seemed a primary bacterial rhinitis, unusual in cats generally but not in immune-suppressed cats. Around this time, Bud began to experience a gradual, persistent decline in weight that continued throughout the remainder of his life and that was generally unresponsive to increased food intake. Within a year, Bud began to experience depressed appetite and shortly thereafter bouts of diarrhea that, at first, resolved completely with metronidazole, but over time recurred with lesser intervals of normality, until finally the diarrhea became chronic. The cause of the inappetence is unclear, but was probably related, at least to some extent, to GI inflammation and perhaps bacterial overgrowth. A year later, following a brief period of anorexia, liver disease was diagnosed. It is possible, perhaps even likely, that the liver disease was related to small bowel inflammatory disease (triaditis), but clinical and white-count response to certain antibiotics indicated a bacterial component. A biopsy was never done, so not much more can be said with certainty. The steady slide in Bud's health eventually led to the decision to try to address his primary FIV infection.
Bud’s FIV therapy began with a fifteen-month period of Immunoregulin injections. This was
followed by a period of slightly more than one year on HIV antiretroviral drugs and a few
supplements. The last phase of his therapy involved intensive administration of herbal and
nonherbal supplements. The record of his response to that therapy follows. The order reflects the order of the
Medications and Supplements page and is not chronological.
In describing and assessing outcomes in particular areas of Bud’s therapy, I have tried to be as
objective as possible and as conservative in claims of benefit as the facts of a situation seem to
warrant. A cat whose health has been made better by treatment of problems secondary to his FIV
infection is going to thrive while also being treated with medications directed at his primary
illness more than one whose immediate problems are not being successfully addressed.
Laboratory findings are the most obvious objective measure, and where I have them to offer I do.
But an individual cat owner, for reasons of cost and the quality of life of his cat, cannot rise to
the standards of a formal study. And formal studies avoid treating cats with many different
medications at the same time. To put the matter bluntly, studies and owners see “outcomes”
differently; one cares about the numbers, the other about the cat.
At the end of his life Bud was feeling very good and had a fine quality of life, much better than
when his therapy began. His chronic diarrhea and inappetence (perhaps also rooted in intestinal abnormality) were a thing of the past. Because his diarrhea problems began to disappear during his period on antiretroviral drugs, it is likely that reduction of virus was a key component, although the glycyrrhizinate and ketotifen begun during that period do have potentially helpful activity in the bowels and may have played a role in improvement. Some of the supplements he later received might well impact inflammation and bacterial overgrowth; however, as noted, improvement began prior to his being given these supplements. His chronic liver ailments returned in the last month of his life, but these appear to have been
secondary to chronic pancreatitis rather than FIV-inspired low-grade infection. His chronic
upper respiratory infection never left him, but remained well-managed and caused no significant
degradation of the quality of his life. The last year of Bud’s life was plagued by a variety of
ailments, but none of them caused more than transient disruptions to his normal functioning and
sense of well-being. In early 2005 he showed signs of neuropathy of at least one cranial nerve.
He was diagnosed with chronic pancreatitis in July 2005 and with chronic lymphocytic leukemia
(CLL) in August 2005. Medical opinion was that none of these problems were directly related to
his FIV status. I am not certain of that; I have read a mention of a case of isolated neuropathy of
cranial nerves in one FIV+ cat. His leukemia was not of the B lymphocytes, which is frequently
related to FIV disease, but rather of the T lymphocytes, a disease almost unheard of in FIV+ cats.
Whether any therapeutic agents he took played a role in his neuropathy, pancreatitis, or cancer I
am in no position to say with certainty. Bud had become an old cat, and things happen to old
cats. The mean age for diagnosis of CLL, for instance, is 14, which is what Bud was when he was
diagnosed. Shortly before his disappearance, testing confirmed that his pancreatitis was chronic
and had not gone away. However, it caused neither pain nor loss of appetite, save for one brief
period when it first began. His neuropathy may have affected both hearing and vision to some
extent, but never reached the point of impacting normal functioning or good quality of life.
Because of the difficulty in knowing what was best for so many health problems without doing
harm to any one of them, Bud received only vitamin supplements and feline omega interferon
after November of 2005.
2. HIV Drugs
As of 29 May 2004, Bud’s regimen of antiretroviral drugs was suspended after 1 year and 6 days
because of significant viremia. Studies have shown that FIV mortality rates are more directly
proportional to viral load than to any immune system indicator. Viral loads for symptomatic
FIV+ cats can range from five figures into the hundreds of thousands (between 1.26 x 105 and
1.98 x 108/ml, as reported in one study-- where each power of 10 equals an additional zero),
although characteristic viral loads do vary among FIV strains. Bud had his viral load measured
four times between beginning NRTIs in May 2003 and stopping them in May 2004. His
anniversary test in May 2004 showed a load of 54,246 virus particles (RNA)/ml of plasma, which
is a significant but not an AIDS-like viral burden. How it stands in relation to Bud’s baseline
load prior to beginning NRTIs is unknown.
Unfortunately, Bud had no “baseline” measurement because my vet could locate no one to do
the work. Subsequently, I took up that task myself and located a university program to do the
testing. The first viral load test* was done 62 days after beginning the first NRTI and 13 days
after the third and last NRTI had been added on. The test was “Negative” for recognition of a
virus. The second test took place 111 days after beginning NRTIs and 61 into a full three-drug
regimen. This test recognized the presence of a virus and eventually came up with a figure of
2040 virus particles (RNA) /ml of plasma. A third test took place 203 days into NRTIs and 153
days into a full HAART regimen. For this test, a portion of Bud’s virus was successfully
sequenced for maximum accuracy and recognition by testing instruments. (At any given time,
part of the virus population, exists at the “free” RNA level, part at the “provirus” DNA level.)
The test reported 640 virus particles (RNA) /ml.
*To see results of all viral load tests, click here to go to “Bud’s Timeline”. Use your back
button to return here.
A comparison of the first three viral load tests is somewhat perplexing. A cat or a human on a
triple cocktail of antiretroviral drugs should not be showing detectable virus 2 months after a
previous finding of no detectable virus. Compliance (i.e., taking drugs on time) had been better
than found in many HIV patients. Although recent research has found that HAART regimens
composed only of NRTIs–including the TDF(PMPA)/ABC/3TC combination that Bud began with–do
not hold up as well as many mixed regimens, some doctors treating HIV patients with this
particular combination report good success over considerable periods of time. Looked at in
isolation, the test results have several possible explanations. (1) The first test was inaccurate or
inaccurately read. The second test produced a replication trace only weakly distinguishable from background “noise” that the test needed to be run a second time to confirm that there was one. In the second case the testers were looking for one because of extensive correspondence regarding interpretation of the first
result. The third test likewise gave a very weak viral signature. (2) The second test showed the drug
regimen beginning to fail, but the third test showed that some change in the drug regimen
partially reversed the process of regimen failure. In evaluation of HIV viral loads, a “rule of
three” is often used to account for natural variability factors in viral loads. A rise of viral load
greater than 3x the previous load indicates drug failure; a drop greater than 3x constitutes
improvement.
Two changes took place in Bud’s HAART regimen after the original regimen was established.
(1) His dosage of ABC was cut in half in mid-October after 99 days on the 30mg dosage out of
concern for persistently unresponsive hepatitis. Subsequently, with improvement of his liver,
dosage was raised from 1/20th of a tablet (15mg) to 1/18th (Dec 03), and several months later to
1/16th(Feb 04). Though counterintuitive, it is possible that a smaller dose of ABC relative, say,
to TDF is better. (2) FTC replaced 3TC in early September 04 after almost 100 days on the
latter. The change was made purely on the basis of early comparative testing that indicated less
likelihood of viral mutation occurring with FTC. The change was made 6 days before the second
viral load test. Although research has shown that viral load may rise after discontinuing 3TC, six
days are not much to account for the difference between the first and second test; however, it is at
least conceivable that the spike in the second test registered the change but that the lower viral
load on the third test represented acclimation to the change. This explanation seems unlikely to
me, but I would not wish to discount it.
The significance of the fourth test seems beyond dispute. A nearly 100 fold rise in viral level can only mean that the wild virus mutated under the selective pressure of the NRTIs and now is
now longer sensitive to them. When Bud’s HAART therapy was begun, the hope was that it
would last for at least 1 ½, possibly 2 years. One year was a minimum criterion for judging the
experiment worthwhile, but is still a disappointing figure. There are a number of possible
explanations for the HAART regimen’s loss of potency. A drug interaction with some other
element of Bud’s therapy is possible, e.g., the piperine used as a delivery agent for the chrysin or
the lecithin in which amino acids for wasting were incorporated. Some or all dosages may have
been too low, particularly the low dosage of ABC because of liver inflammation. Perhaps the low dosage of ABC encouraged development of mutations that undermined the other drugs. Or perhaps
raising the dosage of ABC from an even lower level was a mistake. The likeliest cause,
however, is the combination itself. Several months into the regimen news began to appear of
disappointing results in tests of regimens composed entirely of NRTIs. HAART regimens are
typically composed of mixed drug types; e.g., two NRTIs and one protease inhibitor. For a time
it was thought that a mix of NRTIs alone would also work This is seeming less and less the case,
at least with some combinations. One suspect combination was TDF + 3TC + ABC. There
was a suspicion that TDF and ABC are somehow noncomplementary, at least when part of an
NRTI-only cocktail. I am now inclined to think that this is so. Evidence has accumulated from
HIV therapy that NRTI-only combinations not containing AZT are vulnerable to a particular
point mutation on the virus that can lead to virologic failure. This may be only part of the story,
yet still a significant part. If I had the NRTI portion of this experiment in Bud’s therapy to do
over again, I would content myself with a two-drug combination (e.g., TDF + 3TC or FTC), with high-dose olive leaf extract added for integrase inhibition. Until a drug effective against FIV from another class of HIV drugs becomes available for use, HAART for a cat is probably (not certainly, but probably) not a good idea. The protease inhibitor Tipranavir may be that crucial third drug from another class, though its safety is an unknown quantity.
I say “not certainly” because Martina Menz, whose cat also took this combination of drugs, had
its virus genotyped around the one-year mark . The report was that the virus was “wild type,”
that is, unaffected by HIV drugs. The viral load in Menz’s cat declined modestly over a twelve-month period while the cat was on triple combination-therapy and somewhat more dramatically
between month 12 and month 15. The last, particularly, is a strange result since HIV drugs
would be expected to show a gradually diminishing level of success over time. Click here to
view details.) Menz’s experience leaves open the possibility that the TDF/3TC/ABC
combination has more staying power than Bud’s experience with it might suggest. It is,
unfortunately, difficult to generalize from the experience of only two cats, particularly when a
variety of therapeutic agents are being used at the same time.
>>>Bud’s Medications and Supplements: HIV Drugs>>>
3. FIV Botanicals
First Round. (While on HIV drugs) Bud began taking chrysin and glycyrrhizinate after his second viral load test. I regarded both as a long shot. However, a third possible explanation for the drop in viral load between the second and third viral load tests is an added antiviral effect by
one or both botanicals. The results of that test left me with little choice but to continue both as
parts of Bud’s treatment program. Subsequently, however, DNA viral counts were supplied
showing higher DNA counts (3,856 virus/million cells) on the third test than on the second
(1,197 virus/mil). So it is possible that no significant difference exists between the overall viral burdens at the time of the two tests. The fourth test (showing a sharp rise) may be interpreted in
one of three ways: (1) one or both botanicals had an impact for a time, but then lost it due to
viral mutation; (2) never had an impact; (3) continued having an impact because the viral load
would have been higher without them. I had no way of choosing among these possibilities, but
suspended use of chrysin because I felt that the third test had not made a strong enough case for
its continued use. After 7+ months on chrysin and glycyrrhizinate, Bud showed no clinical or
laboratory evidence of side effects. Later experience showed that zinc could have been 4mg twice
daily without a problem. The common worry about licorice products proved to have no basis in Bud’s case. Despite a relatively high dosage, serum chemistries never registered any abnormalities in his electrolytes. His blood pressure was taken on several occasions and was normal. I believe that the Jarrow product obviated this issue, and regret that it is no longer available.
Second Round. (After stopping HIV Drugs). The fifth, sixth, and seventh viral load tests (indicating little or no detectable virus) clearly validate at least some element or elements of Bud’s second-round regime. It is impossible to know which are the most effective of the supplements being given, but one or more of them was clearly very effective, and synergy among
some seems likely. The content of Bud’s regimen of supplements was variable and was never
the same in the periods between any of the viral load tests. To see which supplements have been
given when, consult the Bud’s Timeline page. The reason for variation was partly to not allow
the virus to accommodate itself to a static regime, but mostly to militate possible side-effects
with continuous long-term usage. Green tea and grape seed were added to the regimen to
provide greater flexibility. The effect of the supplements on immune parameters is an area where data is unfortunately lacking. However, a burst of unexpected weight gain back to the 10 lb level during the early months of the regimen were, I believe, related to a general improvement of health and well being.
In April 2005 SPV-30 was stopped because the situation with Bud’s abnormal white cell counts
was, at that time, unresolved. The fact that the seventh viral load test in August 2005
produced such a good result after nearly four months without using SPV-30 suggests that,
whatever its benefits, it may not be an essential component of the herbal therapy. There has
always been a concern that it might be immunosuppressive. The fact that an antibiotic
supposedly effective against his sinus pathogen did not work in February and March sparked
concern of possible immune suppression. However, the later revelation of Bud’s leukemia
weakens, perhaps eliminates, any case to be made against SPV-30 by explaining his high white
count and weakened immune response.
In July 2005 , following completion of a long period of antibiotic therapy with tetracycline, a TLI
test showed pancreatic inflammation, which subsequent tests have shown to be chronic. The
cause has never become clear. Tetracycline is notorious for causing pancreatitis in humans and
dogs, but it has not been proven to do the same in cats. A consulted internist speculated on
possible inflammation of the small bowel as a cause. I was and am doubtful. The possible
influence of herbal supplements on small bowel, pancreas, or both is something I simply cannot
assess. SPV-30 has always been a question mark. Curcumin, it has always been speculated,
might cause GI inflammation when used long term. Piperine may have as yet undocumented
long-term effects; bitter melon likewise. Perhaps long periods of “down time” are advisable with
these supplements. (See Bud’s “Second Chance”: Lifetime FIV Therapy). Or perhaps a newer
supplement, such as grape seed, had unexpected results. Or perhaps none of these were a
problem. Treating any serious illness often involves the unknown, including unknown risk.
In November 2005 an attempt was made to treat Bud’s leukemia and FIV simultaneously with
four herbs that have shown some ability to inhibit both. Chrysin, Lutein, and Quercetin were
given, mixed in mashed lecithin, oil, and the emulsifier casein. All were swirled into a dollop of
baby food. Green tea was given separately in a capsule. Either there was something about the
herbs that Bud could not handle, or (more likely) the lipid medium was too much for his still
abnormal pancreas. Vomiting dictated stopping the effort after five days. A later attempt to give
green tea alone seemed to produce a loss of appetite after only one pilling. Since the particular
brand of green tea being used all along was used prior to the onset of symptoms later to be
revealed as pancreatitis, it is possible that the green tea was somehow involved with the
pancreatitis. I just don’t know. Green tea is well established as a safe product for cats. If green
tea was, in fact, a problem, perhaps a contaminant or the potency of the particular product (Green
Tea 70) was involved. I do not believe that dosage was the problem, although I cannot entirely
eliminate the possibility. Several people of my acquaintance give a similar dosage, though only
once daily.
>>>Bud’s Medications and Supplements: Botanicals>>>
4. Immunostimulators and Immunomodulators
The only specialized testing of Bud’ immune system took place in April 2003. That is, the T-Cell and B-Cell lymphocytes most directly impacted by FIV were quantified relative to one
another and the total number of lymphocytes. The test showed CD4+ lymphocytes at a very low
7% of total lymphocytes. 20% or more is normal; 15% the very bottom end of normal. Bud’s
CD4:CD8 ratio was 0.3. This ratio is one of the benchmarks of FIV/HIV infection. As CD4+
cells decline as a result of cell death, CD8+ cells increase in response to the immune system’s
attempt to deal with the cause. A normal ratio favors CD4+ cells. 0.3 stands about on the
borderline of severe immune deficiency. This test was one factor in the decision to begin giving
antiviral drugs. However, it was not been repeated, so no basis of comparison exists to test the
impact of any therapeutic agent in this particular area. It must also be kept in mind that the
damage done by FIV to the immune system goes beyond lymphocyte numbers and ratios.
● Immunoregulin. During the twelve-month period preceding Bud’s treatment with
Immunoregulin his average white cell count was 6840; the percentage of lymphocytes to
total white cells averaged 25.6%. During the fifteen-month period Bud was treated with
ImmunoRegulin, his average white count was 16600; the average lymphocyte to white
cell ratio was 42.8%. In the four months or so from discontinuation of ImmunoRegulin
to the last tabulated count in November 2003, Bud’s average white count was 9125, his
lymphocyte to white cell average, 33.25%. The numbers suggest a decided impact on
white counts generally and on lymphocyte ratios. A variety of factors can affect white
and lymphocyte counts, but many counts during cyclical bouts of illness followed by
temporary recovery should do much to even out the impact of transient influences. Of
particular note is the fact that at the time of Bud’s T-cell and B-cell test his lymphocyte
count was so high (9344) that the 7% CD4+ figure (dismal in isolation) yielded an
absolute count of 654 cells mm3, a very substantial number for a cat with advanced FIV
disease. Whether all of these cells were acting efficiently is impossible to know. There is
also the question of whether white counts on the order Bud generated are necessary or
beneficial. Another matter as well is whether activation of the lymphocytes by
ImmunoRegulin left them vulnerable to attack by the virus, thereby resulting in higher
viral loads. It is worth noting, however, that if Bud’s first viral load test was accurate in
suggesting a suppression below detectable limits by HIV drugs, then Immunoregulin did
not in any way prejudice the later use of antivirals. Even if it was not, subsequent viral
load tests show that nothing irremediable occurred. Whether giving ImmunoRegulin in
the absence of antivirals is a good idea remains to be discovered. *Note: A detailed,
graphed record of Bud’s experience with Immunoregulin (including analysis) is available
for viewing in pdf. form. Click here.
● Thymus Peptide. No firm conclusions can be drawn about the efficacy of thymus
peptide as an element of Bud’s therapy. Although some researchers claim a beneficial
impact on CD4+ numbers, the general view of proponents is that thymus peptides work
primarily by activating chemical messengers (chemokines) that direct CD8+ cells in
fighting the virus. I have no way of tracking anything related to this action. I have seen
nothing to suggest side-effects.
● Moducare. No firm conclusions can be drawn about the efficacy of this particular blend
of sterols and sterolins. Viral load both rose and fell, but no clinical changes for the
worse occurred during the period when Moducare was given, and I am aware of no side-effects. In June 2004 I doubled the initial dosage to parallel that specified for children
under 5 and to reflect the dosage given in trials with FIV+ cats.
● Dimethylglycine. No firm conclusions can be reached about the efficacy of DMG based
on Bud’s experience with it. It is tasteless (slightly sweet) and easy to give. I have seen
nothing to suggest side effects. Because of its broad immune-stimulating effect, Bud’s
original daily dosage was halved, except when his immune system was being stressed by
infection. An FIV+ cat in good health does not require stimulus to the humoral (B Cell)
response and to TNF-α production that accompanies the supplement’s other more
relevant effects.
● Melatonin. Caused no visible disruption of sleep patterns or general behavior. To draw
any conclusions about neural-protective or immunomodulating qualities is difficult to do.
● Feline Omega Interferon. Following one five-shot course of injections with omega
interferon, Bud had no observable side effects. Use of interferon was suspended after
that series because changes in Bud’s health status showed no good reason to continue
giving it. There was also a fear of risk to his eyesight since in human medicine
interferons are not administered when there is preexisting neuropathy. Starting in
February 2005, Bud showed clear evidence of poor pupillary reflexes (PLRs), suggesting
neuropathy in the cranial nerves. It now seems that his leukemia may have been the
cause, though FIV cannot be ruled out. At the time there was no information supporting
the use of the interferon as a treatment for Bud’s leukemia. A second series of injections
was completed in November 2005, and monthly injections followed until the supply ran
out in March 2006. I have given the injections of interferon myself, and most pet owners,
I believe, could do the same.
>>>Bud’s Medications and Supplements: Immunostimulators . . .>>>
5. Wasting
● Cyproheptadine. During the 6+ months that Bud took cypro for inappetence he gained a
prodigious amount of weight, nearly two pounds–this at a time when he was still capable
of gaining substantial amounts of weight as a result of increased food consumption. Near
the end of his time on cypro the drug lost its efficacy as an appetite stimulant because of
the onset of serious hepatitis. The down side of using the drug was that it caused severe
depression and lassitude that (for an unconscionably long time) I mistook as a primary
effect of his disease. Vets tend not to warn of cypro’s side effects; mine seemed doubtful
about my contention even after I discovered a description in some drug literature–after I
had already stopped using the drug. A subsequent attempt to restart confirmed that cypro
was the cause of the altered behavior. (I will never again feel quite the trust in
veterinarians that I had prior to that time.) Still, in my view cypro should at least be tried
and the severity of side effects observed; it is too effective an appetite stimulant to be
discounted. Although some cat owners have claimed effectiveness at lower dosage, I
found a half tablet once a day to be more effective than a quarter tablet twice a day.
● Ketotifen. During the first 1 ½ months of its use, Bud gained 9 oz. of body weight.
However, this period coincided with improvement from his latest bout of hepatitis;
hepatitis makes weight gain impossible for him regardless of food intake. So ketotifen’s
role is impossible to ascertain. An even more notable development than his weight gain
was improvement in the normality of bowel function. (Chronic diarrhea and malabsorption
frequently accompany FIV infection.) Ketotifen, in humans, is said to have value in
reducing certain kinds of bowel inflammation and in promoting absorption of nutrients.
Again, I cannot conclusively credit ketotifen for the change, but for the first time in over
two years, Bud produced nearly normal stools without metronidazole as part of his
treatment regimen. Since metro cannot be eliminated as an exacerbating factor in Bud’s
liver problems, ketotifen may have been a useful substitute. After a brief period of
discontinuation, I reinstituted ketotifen in Bud’s treatment regimen after the viral load
report of May 2004 in order to counter possible effects of viremia. After discontinuation
Bud lost 1/4+ pound of body weight. After reinstitution, he gained back the weight, plus
an additional half to three-quarters of a pound during the period when his viral load was
falling as a presumed result of herbal supplementation. Ketotifen’s value as an
immunomodulator is impossible for me to ascertain. I began use again in July 2005 out of
a belief that Bud’s virus might have been responsible for his weight loss; since that did
not prove to be the case, I discontinued its use.
● Anabolic Steroids. Bud tolerated only two injections of nandrolone decanoate. A lull in
his liver problems led me, probably ill-advisedly, to try it. Although he registered 4oz. Of
weight gain between week two and four of use, by week 5 Bud had stopped gaining, and
by week 6 he was losing. Lab work confirmed a sharp spike in ALT, the primary
enzymatic indicator of liver inflammation. Since Bud’s recurrent hepatitis often had a
component of low-grade bacterial infection, it is possible that nandrolone was not the
cause of the spike; antibiotic therapy was eventually followed by improvement.
● Amino Acids. In 2003 Amino acid supplementation preceded ketotifen use by 23 days;
no significant weight gain occurred during that period. During the period of subsequent
weight gain described previously Bud was receiving amino acids and ketotifen
concurrently, so either, both, or neither may have been responsible. I should point out that
my original plan was to give minimally 500mg of both arginine and glutamine, 100mg of
HMB–perhaps twice the dosage of each. However, because of Bud’s age and liver
condition, I reluctantly settled on the lower dosage. In humans, the whole point of this
regimen is to megadose in order to spur production of growth hormone. The dosages I
gave were probably not adequate for this purpose. After a period off this amino
combination, Bud went back on it at higher dosage closer to my original plan because of a
healthier liver and a small weight loss in May. Results were encouraging. (See
“ketotifen” above.) Again, administration was term-limited.
[Page Top]
>>>Bud’s Medications and Supplements: Wasting>>>
