Since being diagnosed with
Type 2 Diabetes in November 2000, I've been asking myself quite
a few questions. What causes diabetes? What is the best treatment
method? What is the best medication to use? What is the best diet
to follow? What is the best exercise? Should I use supplements and
if so which ones? Why hasn't a cure been found?
The most frequent answers I've
been given can be summarized as take your
pills, eat less,
exercise more, use
your meter more, and do whatever
works for you! I'm currently in the process of discovering
what works for me. See topical index
for my discoveries to date. Also see Reference
Links and Diabetes Books & Articles.
The search for the cause of
diabetes has being going on for a long time and many research projects
are currently underway. The fruits of all this research seems to
be better ways to control and treat the symptoms of diabetes rather
than a cure for it. Could research results be interpreted differently?
Could such interpretation lead to a cure? What do I need to learn
to interpret results? It is my intent to explore current research
results and to document my findings. My focus will be on learning
what offers the best chance of leading to a cure and, at the very
least, to learn what may work best in the treatment of diabetes.
Initially, my explorations are documented in a free-form style under
a series of unconnected topic headings.
My interest in Glutathione
was triggered when I received an email
in early September 2001 from someone who had read my story at http://diabetestype2.ca/.
The email suggested
a connection between Paxil
and the onset of diabetes. I decided to investigate further and
posted a message on
newsgroup asking if anyone was aware of a connection between Paxil
and diabetes. This query led to the exchange of a series of newsgroup
postings that didn't lead, as is often the case within the newsgroup
(where some see me as a person on the fringe, a spammer,
and someone who likes spam)
to any useful data but which did enable me to clarify my own thoughts.
Based on my personal experience,
I also believe that there is a connection between taking Paxil and
the onset of Type 2 Diabetes. Now I'm looking for the evidence.
For example, I was diagnosed within 6 months of starting Paxil and
my HbA1c indicated that I had high blood glucose levels for at least
3 months earlier. A year earlier my HbA1c was fine. So the indications
in my case are that the onset of Type 2 Diabetes was within 3 months
of starting Paxil! Coincidence? Maybe! At the very least, coincidence
or not, more investigation is warranted. Also note that I can also
personally attest that the withdrawal symptoms from Paxil are very
severe. I plan to stop taking Paxil following the protocol advocated
(which involve increasing my glutathione levels), I'm seeing my
doctor on September 10 to talk about what I'm planning, to initiate
a glutathione level test, and to get her advice. To date, January
2002, I haven't been able to find anyone who can conduct a glutathione
test; none of the local labs have even heard of it! I'm in the process
of identifying an endocrinologist working in a hospital (who could
conduct a glutathione test) with research interests that I'm also
interested in. At present, I've identified three possibilities working
at the Ottawa Civic Hospital.
The Paxil prescribing
information sheet (see page 4 and the lines I've highlighted
in red: "reported adverse events"
"rare events are those occurring in fewer
than 1/1000 patients" and "Endocrine
System: rare: diabetes mellitus, goiter, hyperthyroidism,
hypothyroidism, thyroiditis") indicates that a possible
side effect of Paxil is Type 2 Diabetes! When I mentioned this to
my doctor on September 10, she was unaware that the Paxil prescribing
information sheet even mentioned diabetes! She immediately contacted
the Paxil manufacturer's representative for clarification and received
a letter (see page1
from the manufacturer
the following day! I was surprised at the fast response! And this
immediately piqued my interest further. The letter does not address
why the Paxil prescribing information sheet indicates that diabetes
is a possible side effect, but rather seeks to show that there is
no connection. So why is diabetes shown as a possible side effect?
What is the source of the data that led the manufacturer to state
that there was a connection? I would like to see the data that led
the manufacturer to conclude that there was a negligible chance
(less than 1 in 1000 "rare event")
that Paxil might affect the endocrine
system and cause diabetes. I've started collecting experiences
of people who, like me, are seeing an adverse
relationship between Paxil and diabetes. Also of interest is
the link being made by Dr Ana Sawka at the Mayo Clinic between Paxil
and its effect upon blood glucose levels.
How could Paxil affect the
endoctrine system and lead to Type 2 Diabetes? Based on what I've
read so far, I'm leaning towards the idea that Paxil reduces the
level of glutathione (GSH) in body cells and that this may contribute
to, or even cause, Type 2 Diabetes. I suspect that this may only
be the case for people already at a high risk of contracting Type
2 Diabetes. What percentage of the North American population are
in the high-risk category? Is it less than 1 in 1000? Probably significantly
higher! For more information on the side-effects of Paxil I'm currently
reading Prozac Backlash by Joseph
Glenmullen, MD and Beyond
Prozac by Michael Norden, MD.
There is evidence that in order
to minimize the withdrawal symptoms associated with stopping Paxil
that the body's GSH levels have to be increased with the use of
a Whey protein product; for example, Immunocal/HMS90
(which is rather expensive). Could the continued use of a Whey protein
make it easier to control blood glucose levels? I'm continuing my
research and am currently reading Breakthrough
in Cell-Defense by Dr. Bounous and Dr. Somersall; Glutathione:
Your Body's Most Powerful Healing Agent by Dr. Gutman and Stephen
Schettini; and The
Immune System Cure by Lorna Vanderhaeghe and Patrick Bouic
It seemed prudent to get myself
off Paxil as quickly as possible! On September 8 2001, I reduced
my Paxil dosage from 20mg to 10mg (1/2 pill) each day; at the same
time, I increased my Whey protein intake by 20g/day taken in a glass
of 1% milk at around 10:00pm each night. I decided to take the Whey
protein just before bed in order to address another problem I've
been having with high morning fasting blood glucose levels, which
are typically 8mmol (144mg/dL) or more. Due to dizziness and lightheadedness
I worked at home from September 10 to 14; otherwise, I had no other
major withdrawal symptoms. On September 22, I reduced my Paxil dosage
to 10mg (1/2 pill) every other day. For about a week, later in the
day, usually between 3 to 5pm, I've been feeling very irritable
for no apparent reason and my sense of balance seemed out-of-whack.
My blood glucose levels were fine. My fasting blood glucose levels
have been the lowest since I started recording them in January 2001.
So the Whey protein seems to be effective in lessening the Paxil
widthrawal symptoms (compared to my attempt early this year) and
in reducing my fasting blood glucose levels.
Stopped Paxil completely on
October 8 2001. For the past week I've been coughing, sneezing,
and have a runny nose. Just coincidence? Probably! During the week,
I've been feeling more nervous, jumpy and easily startled. I've
also been feeling more irritable and emotional. For example, while
watching For Love of the Game I felt like crying throughout
the movie! And I'm not even very fond of baseball! I'm also finding
my wife's attitudes towards me very annoying (I usually just quietly
accept her attempt to control everything; her habit of minimizing
the importance of my personal feelings, opinions, and advice; and
her general overall negativity). Is this indicative that my normal
feelings are returning after being suppressed for the past 15 months
by Paxil? I also think I may also be overreacting to any attempts
to control me and any kind of negative reactions towards me; both
areas in which I have a past history of being particularly sensitive
Paxil was prescribed by my
MD (Dr Christina Mundi) on June 14 2000 to treat mood swings after
I'd seen theraphist Sandra Slover, April 26 and May 11 2000, who
recommended I take an anti-anxiety drug. Paxil belongs to a group
of drugs known as selective serotonin reuptake inhibitors (SSRI).
These medicines are thought to work by increasing the activity of
the chemical serotonin in the brain. Takes a few weeks to
work, can be very addictive, and should be stopped by reducing dose
by 10%/week while supplementing with a high-bioavailable Whey Isolate
protein such as Immunocal/HMS90
(which is very expensive). Side effects (experienced by
me): decreased sexual desire; delayed ejaculation; increased
sweating; trouble in sleeping; unusual tiredness and weakness. Withdrawal
symptoms (experienced by me): easily agitated; dizziness and
lightheadedness; headaches; inability to focus and concentrate;
and inexplicable emotional outbursts. Feb01: Reduced from
20mg to 10mg. Feb12: Stopped. Experienced withdrawal symptoms
listed above. Feb16: At the insistent promptings of my wife,
and my own state of misery, started again at 20mg/day. Sep08:
Reduced to 10mg/day (1/2 pill) while increasing ingestion of unsweetened
SISU Body Elite Whey Protein Isolate from about 20 to 40mg/day.
Sep29: Reduced to 10mg (1/2 pill) every other day. Oct08:
Stopped Paxil completely but continued with Whey protein twice /day.
What is glucokinase?
This question was raised when I was trying to learn the potential
benefits of using a Biotin supplement. I couldn't find a
satisfactory answer and ended up being confused. However, I let
my intuition guide me to add Biotin to my supplement regime and
to investigate later why it might be beneficial. My investigation
led me to glucokinase. According to my Gage Canadian Dictionary,
"kinase is an enzyme able to activate the inactive form of
another enyzme." So glucokinase is an enzyme. But what is an
enzyme? I guess I need to bone up on words used by doctors and biochemists.
controls the rate of metabolism of glucose in pancreatic beta cells,
and the metabolism rate is related the the amount of insulin
secreted. A glucokinase gene mutation could cause
the secretion of less insulin. Why? The first step in glucose metabolism
is the phosphorylation of glucose to glucose 6-phosphate. In most
tissues (for example, muscles), this first step is catalysed by
hexokinase (HK), which has a low Km for glucose, and is inhibited
allosterically by its product glucose 6-phosphate. In turn, inhibitation
of HK suppresses glucose uptake. In the liver and pancreatic beta
cells, phosphorylation of glucose to glucose 6-phosphate is catalysed
by glucokinase. Glucokinase has a high Km for glucose and
is not inhibited by glucose 6-phosphate. Glucokinase phosphorylates
glucose only when blood glucose levels are high. Glucokinase plays
a key role in the regulation of glucose-induced insulin secretion
and it also determines the "set point" for insulin secretion.
into cells involves a family of glucose transporter proteins (GLUTs)
which are structurally related but encoded by different genes.
- GLUT1 is used in
many tissues; for example, muscle, brain, kidney, and colon
- GLUT2 is used in
liver and pancreatic beta cells
- GLUT3 is used in
- GLUT4 is used in
skelital muscle and adipose tissue
- GLUT5 is the small
intestine fructose transporter
Using my Webster's
9th Collegiate Dictionary for all definitions.
is "any of numerous complex proteins that are produced by
living cells and catalyze specific biochemical reactions at body
is "a hexokinase found especially in the liver that catalyzes
the phosphorylation of glucose."
is "any monosacchoride (eg, glucose) containing six carbon
atoms in the molecule." Hexokinase is "any of a group
of enzymes that accelerate the phosphorylation of hexoses (as
in the formation of glucose-6-phosphate from glucose and ATP)
in carbohydrate metabolism."
is "to cause (an organic compound) to take up or combine
with phosphoric acid or a phosphorus-containing group."
is "the process of phosphorylating a chemical compund either
by reaction with inorganic phosphate or by transfer of phosphate
from another organic phosphate; especially the enzymatic conversion
of carbohydrates into their phosphoric esters in metabolic processes."
is "a phosphorylated nucleoside ... of adenine that supplies
energy for many biochemical cellular processes by undergoing enzymatic
hydrolysis especially to ADP."
is "any class of often fragrant compounds formed by the reaction
between an acid and an alcohol usually with elimination of water."
Nucleoside? Adenine? Hydrolysis?
is "an ester of adenosine that is reversibly converted to
ATP for the storage of energy by the addition of a high-energy
phosphate group-called also adenosine diphosphate."
is "a compound (as guanosine or adenosine) that consists
of a purine or pyrimidine base combined with deoxyribose or ribose
and is found especially in DNA or RNA."
is "a nucleoside...that is a constitituent of RNA yielding
adenine and ribose on hydrolysis."
is "a chemical process of decomposition involving splitting
of a bond and addition of the elements of water."
Pyrimidine? Deoxyribose? Ribose?
is "a purine base ... that codes hereditary information in
the genetic code in DNA and RNA."
is "a crystalline base...that is the parent of compounds
of the uric-acid group ... a derivative of purine: especially
a base (as adenine or guanine) that is a constituent of DNA or
is "a pentose suger ...that is a structural element of DNA."
is "a type of suger made up of five carbon atoms to the molecule,
instead of the six that make up glucose."
is ribose + nucleic acid that helps promote the synthesis of cell
is "any monosaccharide...(as ribose) that contains five carbon
atoms in the molecule."
Planned future area of investigation...