Our greatest source of energy coming from food is the
carbohydrates, which are transformed in glucose. Glucose is stored in the liver,
for future use, in the form of glycogen. Under the effect of a hormone called
glucagon (produced in the alpha cells of pancreas), glycogen is transformed in
glucose, released in the blood stream. Another hormone called insulin (produced
in the beta cells of pancreas) pushes glucose inside the cells. Glucose inside
of a cell is used to produce energy to keep the cell alive and perform its
duties, such as substance production, reproduction and so on. Notice that
glucose can not go inside the cell without insulin. Although some other cells
can eventually use other raw materials to produce energy, such as protein or
fat, the cells of nerve tissue can only use glucose as fuel. Thus, lack of
insulin means irreversible damage for the nerves and brain. Consequently,
insulin is of vital importance for a healthy body.
The lack of insulin is called Diabetes. In this case, patient has
glucose in the blood, however due to lack of insulin, the same glucose does not
go inside the cell and two phenomena happen: too much glucose in the blood and
lack of glucose inside the cell. The latter makes the cells suffer from lack of
energy so they need to use other mechanisms to generate energy, causing many
side effects on the body.
There are 2 types of Diabetes:
Diabetes Type 1
-
It is characterized by the total failure of the pancreas in producing
insulin. The cause is the autoimmunity, that is, patient produces antibodies
that destroy beta cells (which produce insulin) of pancreas. In other words,
patient produces an antibody that attacks his/her own body.
-
Patient's body does not produce insulin, so he/she needs to take "external"
insulin. No surgery can repair the pancreas. The pathology diagnosis is
complex and a good parameter is a lab test called C-peptide. If the test
result is less than 1, it suggests Diabetes Type 1. Another lab test used is
the verification of low levels of proinsulin.
Diabetes Type 2
-
It is different from Diabetes Type 1. In this
case, pancreas works and produces insulin, however it does not get to do its
job (for example, due to obesity or other situation in which there is
peripheral insulin resistance). If patient loses weight, pancreas is able to
do its job and, sometimes, the cure for Diabetes Type 2 happens. This is the
sort of patient whom lab tests present C-peptide greater than 1 and normal
proinsulin. In this case, there are ways to stimulate the pancreatic
production of insulin or turn the body cells more responsive to the insulin
action.
The question is:
What factors could improve pancreas performance and insulin action?
The intra-abdominal visceral fat produces a hormone called
adiponectin, which betters the insulin action in the body cells; that is, it
diminishes the peripheral insulin resistance. However, the same fat produces
inflammatory cytokines that increase the peripheral insulin resistance. So, fat
has a mechanism that controls insulin, sometimes it can better its action, but
sometimes it can worsen it. The problem is that obese patient produces little
adiponectin and his/her visceral fat contributes to worsen the insulin action.
Perhaps, this feature of obesity contributes for the great incidence of Diabetes
Type 2 in obese people.
Note: When obese people lose weight, their bodies go back producing
adiponectin, and maybe this is one of the reasons why Diabetes Type 2 is
improved after weight loss.
Another breakthrough
When food gets at the end of small intestine, it stimulate the
production of some hormones:
§
PYY - GLP1 - Oxintomodulina hormones
They stimulate the
hypothalamus to produce the "fullness sensation", which makes us lose appetite.
Besides, they cause anti-peristaltic movements, taking the food backwards to the
stomach, which causes nausea. These actions together are called
ileal brake. Intestine tells the body
to stop eating.
There are also hormones that warn pancreas that the body had a meal
and the sugar level in the blood will increase soon, and insulin must be
produced to move the glucose inside the cells. The insulin production stimulus
is called incretin effect and these
hormones are classified as incretins,
as follows:
§
B1 - GLP1
Produced in the
terminal ileum and colon. It stimulates pancreatic beta cells to produce
insulin. This hormone is so powerful that it reactivates lazy cells. The hormone
inhibits alpha cell, the producer of glucagon, which increases glycemia. It is
an anorexigen and also ileal brake, which betters Diabetes Type 2. It does not
improve Diabetes Type 1, since beta cells have already failed;
§
B2 - GIP
Same effect as
GLP1. It is mostly produced in the duodenum and jejunum.
Notice that if food goes throughout intestine and gets in the final
portion of the small intestine, hormones are released and they inhibit more
ingestion, improve insulin production by pancreas and they also improve the
action of insulin in the body cells. The problem lies in modern food. It is
fiberless, therefore easily and quickly absorbed in the initial part of small
intestine, but no residues get in the rest of intestine. Consequently, there are
no stimuli for the production of right amounts of hormones that would prevent
Diabetes Type 2. Furthermore, we already know that obese and type 2 diabetic
patients have less amount of GLP1 and PYY than non-obese and non-diabetic
people. At this point, we understand that if food gets in the terminal ileum
(Hindgut Theory), there will be a hormone response from intestine (incretin
action) and thus, there will be relief from Diabetes Type 2.
Francesco Rubino, an Italian researcher, believes that when the
food goes through duodenum, there is the production of one certain hormone that
inhibits the incretin effect, i.e., the hormone inhibits the intestine stimulus
to produce insulin secretion. He explain it as "anti-incretin theory", called as
"Rubino Factor".
Note: Probably, this hormone aims to counterbalance the incretinic
action of intestine to avoid severe hypoglycemia, due to an excessive and
abnormal discharge of incretins. This mechanism, in modern times, is likely
unnecessary, considering hyperglycemia being infinitely more often than
hypoglycemia
According to this theory, it would be interesting if food would not
go through duodenum. A nourished duodenum would release hormones that block
incretin action, and thus, it would prevent the intestine hormones from cure
Diabetes Type 2. The procedure that aims preventing food from going into the
duodenum is called Duodenal Exclusion (Foregut Theory).
Until 2007, it was not possible to know which theory would be the
best one for Diabetes Type 2 treatment (perhaps they are complementary). Many
studies are still going on, though.
In the last 30 years, the most performed bariatric surgery in the
world is Gastric Bypass. This technique results in the duodenal exclusion, that
is, food does not passes through great portion of stomach, does not reach
duodenum or the initial portion of small intestine. Duodenum and initial jejunum
have great capability to absorb food into the blood (like a sponge). Through
exclusion technique, food is not absorbed in the duodenum, but ileum is fed, so
food stays in the intestine and then conducted to the distal intestine, which
unchains incretin production. Consequently, Bypass increases the incretin
production and completely blocks the anti-incretin one. That's why there is
improvement of Diabetes Type 2, sometimes cure, few days after Gastric Bypass
Surgery.
So, during these years, we realized that morbid obese patients,
with Diabetes Type 2, who underwent Gastric Bypass Surgery, would improve their
condition in relation to Diabetes, even before the weight loss. In theory,
bariatric surgery would better Diabetes Type 2 because patient had lost weight,
however in practice, the improvement, sometimes cure, would happen soon after
surgery, independently from the weight loss. From this observation, scientists
learnt about incretin and anti-incretin, and bariatric surgery is also seen as
an endocrinological approach, and
nowadays we call it as "Metabolic and Bariatric Surgery".
In 2007, there were 220 million people with Diabetes Type 2
worldwide, besides another 350 million people with Metabolic Syndrome, a disease
close to Diabetes Type 2 (see our
website forum).
The world statistics show that only 40% of patients with Diabetes
Type 2 take treatment seriously, 50% of patients with Diabetes Type 2 have BMI
between 30 and 35 and 20% type 2 diabetic patients are thin.
Diabetes brings damages to the arteries, so it diminishes the
arterial amount of blood in the body cells. That causes cell hypoxia (inadequate
oxygen supply), and according to an old aphorism "A man is as old as his
arteries". Besides, it hardens the process of glucose entrance in the cells, and
then occurs the cellular malfunction due to lack of energy. In addition,
Diabetes causes production of toxins, such as sorbitol, that cause general
damages.
Those consequences together bring cardiovascular damages, which
diminishes the quantity and quality of life of the diabetic patient. There is a
blood test called Glycohemoglobin that evaluates in what level diabetes has been
affecting the cardiovascular system. Levels higher than 7 indicate poor diabetes
control and a level higher than 7.5 indicates high risk to the cardiovascular
system. Such damages are irreversible and most frequently the cause of mortality
(heart attack, stroke and so on). That's why patient must hurry to treat
diabetes.
The big question is: "When surgery approach should be indicated to
treat Diabetes Type 2?" The answer has been elaborated over the years, and only
time will bring a conclusive one. The fact is that we know Gastric Bypass can
help this sort of patient. We also know that diabetes harms the cardiovascular
system irreversibly, and we need to do something before it is too late. The best
answer, until 2007, is the clinical treatment for diabetes, however, in some
very selected cases, we indicate surgery (Gastric Bypass).
The criteria include:
-
Diabetes Type 2, characterized by C-peptide greater than 1, normal
Proinsulin;
-
Unsuccessful clinical treatment from 3 to 5 years, with rising levels of
Glycohemoglobin;
-
Glycohemoglobin greater than 7.5 (even under adequate clinical treatment);
-
Clinical indicia of systemic vascular lesion;
-
Presence of Metabolic Syndrome;
-
Weight - it is the greatest doubt.
For the past 30 years, we have learned that Gastric Bypass has been
easing and usually curing Diabetes Type 2 in
obese patients with BMI > 35. This is an unquestionable fact in any
age, gender, country or social condition. We also know that this is a
long-lasting benefit. We have learned that part of the benefit comes from
incretins, another comes from the weight loss. We wonder if the incretin action
is the responsible for curing Diabetes Type 2 in the first months right after
surgery, and after this period, the weight loss turns into the great agent for
the cure. Unfortunately, we still do not have the answer, because no non-obese,
type 2 diabetic patient has undergone Gastric Bypass just yet.
The American endocrinologist Christopher Sorli thinks that weight
is not important to indicate surgery for patient with Diabetes Type 2. The
decision is individual, according to each case.
Another American endocrinologist, Dr. Lee Kaplan, indicates surgery
for type 2 diabetic patients whenever the clinical treatment has not been
efficient from 3 to 5 years, with rising levels of Glycohemoglobin. He thinks
that some patients with Diabetes Type 2 do not respond well to the medication.
Once again, it is an individual decision, according to each case.
Dr. Eric de Maria, also an American endocrinologist, considers that
it would be great if doctors could predict which patients "will not respond well
to the treatment in the future", so these patients could undergo surgery soon
enough, in order to avoid irreversible cardiovascular damages. However,
unfortunately, at this moment, this sort of prediction is not possible.
Alert signals to possible candidates to the Bypass, would be type 2
diabetic patients, with Metabolic Syndrome (see website
Forum):
BMI greater than 28, waist circumference greater than 110 cm, diastolic pressure
reading greater than 8.5, rising triglyceride levels (mainly in young people)
and Glycohemoglobin greater than 7
Some studies show that patients who developed Diabetes Type 2 after
they become obese, have a clinical evolution less serious than non-obese type 2
diabetic patients, that is, thin type 2 diabetic patients can present more
serious disease than an obese one. Maybe, in the future, this is the path that
would lead thin patients with Diabetes Type 2 to surgery.
Anyway, we should perform surgery in obese patients with Diabetes
Type 2 and wait for new studies to indicate whether surgical treatment is the
best approach for the non-obese patients with Diabetes Type 2.
