Gastric Bypass II
Andre Willers
14 Jun 2013
Synopsis :
Diabetes II can be cured by diet that alters gut fauna .
Discussion :
1.Existence Theorem : See appendix A
It has been done .
2. Theory :
See appendix B .
Prolactins play key
role .
Too much lactose and the lactose <-> prolactin balance
is disturbed. More than 300 cellular systems are affected . Bad things happen .
An example of an incomplete evolutionary system (ie
utilizing lactose , a mammalian food evolved only for babies .)
The fermentation removes most of the lactose .
Or drink Woolworth’s Lactose free milk .
But then other prolactin-like markers will be missing .
4.Better yet :
The Amasi cocktail : see appendix C
20% Amasi
80% Lactose free milk .
A dash of cinnamon and turmeric.
Alcohol to taste .
Coffee ad hoc .
5. Interesting aside :
The Fasting diet . Eat as you like for 5 days, then fast for
two .
Very old . Saturday and Sunday . No work , reduced food .
6.Put the diet on fast forward :
6.1 Everyday , flip a coin “Shall I decide today to
fast(Y/N)”
6.2 If N , eat what you like . If Y , flip again “ Shall I fast
today ? (Y/N)”
If N , eat . if Y , reduce calories . ie fast .
This means on average per week , 7*1/2*1/2 = 1.75 days of
fasting .
But predictably randomly fasting .
The body treats this as normal hunter-gatherer chance . It
makes the body leaner , to be more successful in the hunt .
This randomizes the fasting . Normally this would mean the
body gathering reserves (ie getting fatter) .
But , the body-mind knows this is not a long-term drought .
It needs more nimbleness , and less fat .
The whole leveraging thingie goes into reverse leveraging .
Drinking amasi or lactose free milk will accelerate the
effect .
7.Pulsations :
Pulsing an anti-acid (kidney regenerator) like a teaspoon of
sodium bicarbonate , followed by Amazi and a good pro-biotic on a fasting day
will accelerate things .
The effect is cumulative as only beneficial gut-bacteria
survive .
The memory of the gut .
Thinly yours
Andre
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Appendix C
AMASI
This proudly South
African fermented milk product has a smooth, creamy, slightly sour taste. A
much-loved tradition in most South African cultures, First Choice Amasi is made
by adding a freeze dry culture to the milk and then fermenting it until it
reaches a specific acidity level. Our Amasi comes in 1 litre and 2 litre jugs.
|
NUTRITIONAL INFORMATION (per 100ml)
|
|
|
Energy
|
289kJ
|
|
Protein
|
3.3g
|
|
Glycaemic Carbohydrate of which:
Total sugar: Total fat: |
5g 4g |
|
Calcium
|
120mg
|
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Appendix A
Gut bacteria swap is key to knifeless gastric bypass
·
18:00 27 March 2013 by Douglas Heaven
NewScientist .
·
For similar stories, visit the Micro-organisms and Food and Drink Topic
Guides
A bacterial cocktail could soon offer a
knifeless alternative to gastric bypass surgery.
The gastric bypass limits a person's food intake
by, in effect, reducing the size of the stomach – often to the size of a
walnut. The procedure is an effective treatment for obesity and associated
diseases such as type 2 diabetes, and typically leads to a loss in excess body
weight of between 65 and 75 per cent. However, it carries a high mortality
risk, especially in severely obese individuals.
Lee Kaplan at
Massachusetts General Hospital in Boston and colleagues may have discovered an
alternative to surgery. The team performed a gastric bypass on mice and then
fed microbes from their lower intestine to other healthy mice. The mice fed the
bacterial cocktail lost five per cent of their body weight in two weeks,
compared with mice on the same diet who had not been fed the bacteria.
This work is a big step towards a
"knifeless bypass", says Carel le Roux at
University College Dublin, Ireland, who was not involved in the study. He says
that although the gastric bypass cuts calorie intake, it also leads to subtle
physiological effects, such as changes in gut bacteria, hormones, bile acids
and nerve connections. "It changes how the gut talks to the brain,"
says le Roux.
It is not yet clear exactly why giving mice gut
bacteria from mice that have had a bypass leads to weight loss. The researchers
suggest that the gut bacteria present following surgery may reduce the ability
of the intestines to absorb calories, or may alter signals regulating
metabolism. The goal is to understand what these microbes are doing and
duplicate the effects by other means, le Roux says.
Swapping gut bacteria isn't unprecedented as a
treatment. In 2010, an 89-year-old woman with a potentially fatal infection
received what is known as afaecal transplant from
her son. With 24 hours, her fever had abated and the infection soon
disappeared. Similar transplants have been successful inminimising symptoms of
Parkinson's, multiple sclerosis, chronic fatigue syndrome and rheumatoid
arthritis.
Journal reference: Science Translational Medicine, DOI:
10.1126/scitranslmed.3005687
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Appendix B
A Cure for Diabetes
Andre Willers
31 May 2012
Synopsis :
The control-system short-circuit
that causes diabetes can be interrupted in humans by a simple surgical
procedure . This cures diabetes , insulin resistance and high blood pressure .
We try to trace why .
Discussion :
1.Read Appendix I . This is a
succinct summation of the state–of-play as at May 2012 .
2.Why should bypassing the duodenum
have such drastic effects ?
Because the system outsmarted itself
. Too many vital feedback loops are being controlled by the same chemicals . (A
similar effect is observed in brain-stress and body-stress systems) .
Inappropriate responses are triggered . The system is unstable .
2.1Peristaltic action in the
duodenum is accompanied by
vasoactive intestinal peptide (VIP) release, a marker for inhibitory
neurotransmitter release . See Appendix III . (Note the effect on blood
pressure )
But this and PHI
release (see Appendix II) affect the Prolactin system ,(see http://en.wikipedia.org/wiki/Prolactin ) which is tied to at least 300 other
biochemical processes , as well as the prion system (see http://andreswhy.blogspot.com “Prions and the Amygdala” May 2012) .
This whole mess is an
unstable system , that can and does go wrong in a large number of ways . And
the original trigger can be impossible to trace .
2.2To add insult to
injury , the original trigger can cause an amygdala reaction : ie a memory
remains in the system , and there few , if any , “OFF” switches . Hence nasties
like insulin resistance . There are doubtlessly many more . Amygdala’s are
notoriously stupid . It is the function of other systems to reprogram them .
See Appendix IV for
the ratchet-effect on bloodpressure .
2.3Milk and
milk-products can be identified as one of the factors that should cause the
system to destabilise .Lactogen breakdown products interfere with some of the
feedback loops in the energy metabolism . The result will be idiosyncratic
according to individual metabolism , but insulin resistance will ratchet up .
(A calf-protection system short-circuits)
What to do ?
Surgery seems a bit
drastic . All we want to do is inhibit peristalsis in the duodenum . Food can
be massaged through to the jejenum . I can’t find a drug that does this
selectively , but I am sure there are some .
But in the meantime we
are stuck with something like Loperamide (Imodium) . It is like stopping an
enormous factory to fix some small problem at the front-end of the production
lines .
The following is not
medical advice , and you proceed at your own peril .
Use the pulse
principle .
1.Fast until the
duodenum is empty , (+-6 hours) . No water .
2.Take Loperimide
(Imodium) .. This stops peristalsis and release of neuro-markers .
3.Exercise (walking ,
jogging – this moves food without peristalsis ) . I have no idea what effect
this will have on digestion . But no lying in bed allowed .
4.Then eat and drink
mildly on low-carb foods . Appetite will be sharply decreased as alternate
demand pathways kick in (Cf Atkins , etc) . Drink when thirsty (cf Noakes) . No
milk products of any kind .Verboten
5. How often ? I
noticed when writing this that this regimen is remarkably similar to religious
regimens like Ramadan , Jewish , Christian , Hindu and Buddhist fasts . Two
weeks to a month per year seems adequate . This should reprogram some of the
systems to at least a modicum of initial states .
6.Monitor blood
glucose about 2 hours after eating .
Interesting Asides :
1.Excessive alcohol
intake paralyses the pylorus valve between the stomach and the duodenum . The
same effect as fasting , in that food does not enter the duodenum to trigger
peristalsis . Typically bloated feeling , with big “beer bellies” . Since
alcohol is a product of carbohydrates , this is a fascinating adaptation to
high carbohydrate intake .
To put it another way
, agricultural farming only took off because periodic alcoholic binges enabled
re-normalization of glycemic systems . As this dwindled , so diabetes increased
.
2.Milk and Cheese : as
use of these increased , systems increasingly crashed in the Prolactin areas .
Energy metabolisms became unstable , and auto-immune diseases increased .And
you can’t reinstate the original system simply by stopping milk products :
amygdala’s have to be reprogrammed .
These are but the a sketch of the
bare bones of complex mechanism . But at least some indication of where to go
or where not to go .
But I refuse to countenance a system
that does not allow toasted cheese sandwiches .
There must be a better way .
Andre .
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Appendix I
Cristina Iaboni had the
dubious distinction of being not quite obese enough. For all the pounds on her
5'5" frame, she did not meet the criteria for bariatric surgery to help
control her type 2
diabetes.
Yet six years of
medications and attempts at healthy living had failed to rein in her blood
glucose, leaving Iaboni terrified that she was on course to have her kidneys
fail "and my feet cut off" -- common consequences of uncontrolled
diabetes.
Then the 45-year-old
Connecticut wife, mother of two and head of human resources for a Fortune 500
company, lucked out. In 2009 she met with Dr Francisco Rubino of Weill Cornell
Medical Center in New York. He had just received approval to study experimental
surgery on diabetics with a relatively lean weight-to-height ratio, or body-mass
index (BMI). Iaboni was among his
first subjects.
Three years on, she has
dropped 50 pounds to reach a healthy 145 and has normal blood pressure without
medication. That isn't too surprising: Weight
loss is the purpose of
bariatric surgery and often reduces blood pressure. More remarkable, Iaboni no
longer has diabetes.
She is not the first
patient with diabetes, which can be triggered by obesity, to be cured by
weight-loss surgery. But she is a rarity for having it with a BMI well below 35
and over. That's the level at which the American Diabetes Association says
surgery "may be considered" and that Medicare and some private
insurers cover. And Iaboni's diabetes disappeared months before she shed much
weight.
Her experience has
raised an intriguing possibility: that some forms of bariatric surgery treat
diabetes not by making patients shed pounds. Instead, by rerouting part of the
digestive system, they change what signals the gut sends to the brain and the
brain sends to the liver, altering the underlying causes of diabetes.
If proven, bariatric
surgery may help people with type 2 diabetes who are less obese, overweight or
even of healthy weight. And it might be effective against the currently
incurable type 1,
or "juvenile," diabetes, too.
"Every textbook
says that diabetes is chronic, irreversible, and progressive," said
Rubino. "But we have thousands of patients who once had diabetes and now
do not."
"INSUFFICIENT"
EVIDENCE
Bariatric surgeons have
long been prone to declaring victory against diabetes way too soon, before
large-scale, long-term data proved their case. "The evidence for the
success of bariatric surgery in patients with a BMI below 35 is not very
strong," said Leonid Poretsky, director of the Friedman Diabetes Institute
at Beth Israel Medical Center in New York City. "Most of the studies have
been very small and not well controlled."
The American Diabetes
Association rates the evidence that bariatric surgery can cure diabetes as
"E," the lowest of four grades. It calls data on patients with a BMI
below 35 "insufficient," and says the procedure cannot be recommended
except as part of research.
The immediate risks of
bariatric surgery are small -- a 0.3 per cent chance of dying within 30 days of
the procedure. But a small fraction of patients develop infections, leaking
from the stomach into the abdominal cavity, or gallstones, and it can cause
nutritional deficiencies: There is less intestine to absorb vitamins and
minerals, raising the possibility of osteoporosis and anemia.
Despite these red flags,
the surgical option is attracting intense interest because the quest to cure
diabetes has become almost desperate. In type-1 diabetes, the pancreas does not
produce enough insulin, a hormone that moves the glucose in food into cells. In
type 2 diabetes, cells become resistant to insulin. In either case, glucose
remains in the blood, damaging cells and blood vessels, sometimes severely
enough to cause blindness, kidney failure, or gangrene requiring foot or limb
amputations.
In 2010, 8.3 per cent of
adults worldwide had type 2 diabetes (11.3 per cent did in the United States),
resulting in direct medical costs of $376 billion ($116 billion in the United
States). By 2030, the global incidence is projected to rise to 9.9 per cent,
partly because of the rising obesity rate, with costs reaching $490 billion.
The possibility that
bariatric surgery could cure diabetes emerged about a decade ago. A long-term
study of thousands of patients in Sweden reported in 2004 that both gastric
bypass and banding improved diabetes in many subjects. A 2008 study of 55 obese
patients found that 73 per cent of those who underwent gastric banding saw
their diabetes disappear after two years, compared to 13 per cent undergoing
standard medical treatment such as medication, diet and exercise.
In 2009, surgeons at the
University of Minnesota analyzed 621 mostly small studies of bariatric surgery
in obese, diabetic patients. Their conclusion, reported in the American Journal
of Medicine: 78 per cent no longer needed medication to control their blood
sugar. They'd been cured. Lap banding had the worst results, worsening diabetes
in some patients.
But most patients in
these studies were obese, many morbidly so. (The average BMI was 48.) The
improvement in glucose control could therefore be credited to the patients'
weight loss, which averaged 85 pounds.
CLUES FROM THE PAST
Rubino had a hunch that
something else was at work. As a research fellow in diabetes at Mount Sinai
Hospital in New York in 1999, he was reviewing the medical literature one day
for guidance on how to best perform bariatric surgery on a man with a BMI of
80. He found papers from the 1950s and earlier reporting that surgery for
peptic ulcers had cured diabetes.
Ulcer surgery removes a
portion of the stomach and reconstructs a connection to the intestine, much as
gastric bypass does. Few diabetes experts had noticed the old papers; they were
published in surgery journals, which endocrinologists seldom read.
His serendipitous find
led Rubino to other papers describing operations on the digestive tract that
cured diabetes, something that, according to medical textbooks, was
unthinkable.
"Within two weeks
of surgery and sometimes sooner, these patients were off their insulin, off
their diabetes drugs, and with normal blood glucose levels," said Rubino.
"That was too fast to explain by weight loss."
Yet that's how experts
explained bariatric surgery's effect on diabetes, especially as the procedure
took hold in the 1990s. Few surgeons focused on how quickly the condition
disappeared, said Rubino, "or they speculated that patients weren't eating
much after the surgery, and that's what cured their diabetes."
He began pursuing the
idea that surgery might improve diabetes directly, rather than through weight
loss. "I was ignorant of diabetes, so I wasn't burdened by too much
knowledge," Rubino said. "Something that might have seemed heretical
didn't seem impossible to me."
Rubino modified the
popular gastric bypass surgery, called Roux-en-Y, to test his idea on diabetic
lab rodents. In the classic operation, the stomach is pinched off so it can
hold less food. Surgical cuts keep the rest of the stomach and the top of the
small intestine, called the duodenum, from receiving any food. Instead, the
stomach empties directly into the bottom of the small intestine, the jejunum.
In Rubino's variation, called duodenal-jejunal bypass (DJB), the stomach is
untouched, but the rest of the procedure is the same.
The rats that Rubino
operated on beginning in 2000 were cured of diabetes much more quickly than
their weight fell. It was the first rigorous evidence, from a well-controlled
study, that gut surgery has an anti-diabetes effect.
In 2006, Rubino was
ready to move from rats to people. Two patients, with BMIs of 29 and 30,
underwent his procedure. Their blood sugar levels returned to normal within
days, though they lost no weight. In his most recent trial, reported in March
in the New England Journal of Medicine, Rubino and colleagues at Catholic
University in Rome performed standard gastric bypass surgery or a procedure
similar to DJB on people with type 2 diabetes. After two years, 15 of 20 bypass
patients and 19 of 20 DJB patients no longer had diabetes.
Curiously, although
patients shed pounds, there was no correlation between weight loss and blood
glucose, the key marker of diabetes. "Bariatric surgery is more effective
on diabetes than obesity," said Rubino. "Patients don't become lean,
but they do not have diabetes anymore."
FROM GUT TO BRAIN
Research from the
University of Toronto, reported online this month in Nature Medicine, may
finally explain why. It examined the effects of bypass surgery on rats with
type-1 diabetes, which is considered even harder to treat than type 2. Normally
the jejunum receives only digested mush, as nutrients have already been
absorbed in the duodenum, explained lead researcher Tony Lam.
Bypassing the duodenum
allows the jejunum to receive an influx of nutrients for the first time, said
Lam. Sensing them, the jejunum sends a "got glucose!" signal to the
brain. The brain interprets that as a sign of glucose overabundance and orders
the liver to decrease glucose production. Result: The rats no longer have
diabetes.
"I believe that
similar mechanisms are taking place in surgery for type 2 diabetes," said
Lam. "It strengthens the case for the surgery treating diabetes
independent of weight loss."
His rat study shows why
lap banding and stomach stapling are less effective against diabetes than
gastric bypass. Banding causes diabetes to go into remission in about 50 per
cent of patients, probably due to weight loss, said endocrinologist Dr Allison
Goldfine of the Joslin Diabetes Center in Boston.
In contrast, the
diabetes-remission rate after Roux-en-Y is 80 to 85 per cent. "The
improvements in blood glucose with Roux-en-Y appear to occur very early, by day
three after surgery, so patients are being discharged with no medication,"
she said. Something other than weight loss "must be going on."
Goldfine has launched a
study of diabetics with BMIs of 30 to 42 to compare outcomes after lap band
surgery, Roux-en-Y, and intense medical management.
A year ago, Rubino began
the first large study for type 2 diabetes patients with a BMI as low as 26,
where "overweight" begins. The cost of the bypass surgery is covered
by a grant from Covidien Plc, which makes laparoscopic instruments and surgical
staplers. He aims to enroll at least 50 patients, following them for five
years; he has operated on 20 so far.
© Copyright (c) Reuters
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Appendix II
1. peptide
phi
A 27-amino acid peptide with histidine at the N-terminal and isoleucine amide at the C-terminal. The exactamino acid composition of the peptide is species dependent. The peptide is secreted in the intestine, but is foundin the nervous system, many organs, and in the majority of peripheral tissues. It has a wide range of biological actions, affecting the cardiovascular, gastrointestinal, respiratory, and central nervous systems.
A 27-amino acid peptide with histidine at the N-terminal and isoleucine amide at the C-terminal. The exactamino acid composition of the peptide is species dependent. The peptide is secreted in the intestine, but is foundin the nervous system, many organs, and in the majority of peripheral tissues. It has a wide range of biological actions, affecting the cardiovascular, gastrointestinal, respiratory, and central nervous systems.
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Appendix III
Neurotransmitters
Mediating the Intestinal Peristaltic Reflex in the Mouse
- Departments of Physiology and Medicine,
Medical College of Virginia Campus, Virginia Commonwealth University,
Richmond, Virginia
- Address correspondence to:
Dr. J. R. Grider, Department of Physiology, P.O. Box 980551, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298. E-mail: jgrider@hsc.vcu.edu
Abstract
The motor, modulatory,
and sensory neurotransmitters that mediate the peristaltic reflex in the mouse
colon were identified by direct measurement, and their involvement in various
pathways was determined by selective receptor antagonists. Mucosal stimulation
in the central compartment of a three-compartment flat sheet preparation of
mouse colon elicited ascending contraction and descending relaxation in the
orad and caudad compartments, respectively. Ascending contraction was
accompanied by substance P release, a marker for excitatory neurotransmitter
release, into the orad compartment and was partly inhibited by atropine and
spantide, and abolished by a combination of the two antagonists.
Descending relaxation
was accompanied by vasoactive intestinal peptide (VIP) release, a marker for
inhibitory neurotransmitter release, into the caudad compartment,
and was partly
inhibited by VIP10-28 and NG-nitro-L-arginine, and abolished by a combination of
the two agents. Somatostatin release increased during descending relaxation:
immunoneutralization of somatostatin or blockade of its effect with a selective
somatostatin type 2 receptor antagonist inhibited descending relaxation. The
δ-opioid receptor antagonist naltrindole augmented descending relaxation and
ascending contraction. Calcitonin gene-related peptide (CGRP) release increased
in the central compartment and was mediated by concurrent release of
5-hydroxytryptamine (5-HT) because its release was blocked by a 5-HT4 receptor antagonist. Both the latter and the CGRP
antagonist CGRP8-37, inhibited ascending contraction and
descending relaxation. Thus, the reflex in mouse like that in rat and human
intestine is initiated by mucosal release of 5-HT and activation of 5-HT4 receptors on CGRP sensory neurons and is relayed via
somatostatin and opioid interneurons to VIP/nitric-oxide synthase inhibitory
motor neurons and via cholinergic interneurons to acetylcholine/tachykinin
excitatory motor neurons.
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Appendix IV
Co-existence of peptide HI (PHI) and VIP in
nerves regulating blood flow and bronchial smooth muscle tone in various
mammals including man.
Abstract
By
immunohistochemistry it was found that PHI- and VIP-like immunoreactivity (-IR)
occurred in the same autonomic neurons in the upper respiratory tract, tongue
and salivary glands with associated ganglia in rat, guinea-pig, cat, pig and
man. VIP- and PHI-like immunoreactivity was also found in similar locations in
the human heart. The N-terminally directed, but not the C-terminally directed,
PHI antiserum or the VIP antiserum stained endocrine cells in the pig duodenum.
This suggests the existence of an additional PHI-like peptide. Ligation of
nerves acutely caused marked overlapping axonal accumulations of PHI- and VIP-IR
central to the lesion. Two weeks after transection of the nerves, both types of
immunoreactivities were still observed in accumulations both in the axons as
well as in the corresponding cell bodies. The levels of PHI- and VIP-IR in
normal tissues from the cat were around 10-50 pmol/g with a molar ratio of
about 1 to 2. Systemic administrations of PHI and VIP induced hypotension,
probably due to peripheral vasodilation in both guinea-pig and cat.
Furthermore, both PHI and VIP caused an inhibition of the vagally induced
increase in respiratory insufflation pressure in guinea-pig. PHI and VIP
relaxed the guinea-pig trachea in vitro, suggesting a direct action on
tracheobronchial smooth muscle. VIP was about 5-10 times more potent than PHI
with regard to hypotensive effects and 2-3-fold, considering respiratory smooth
muscle-relaxant effects in the guinea-pig. PHI was about 50-fold less potent to
induce hypotension in the cat than in the guinea-pig. Although species
differences seem to exist as regards biological potency, PHI should also be
considered when examining the role of VIP as an autonomic neurotransmitter.
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