Modification (3-22-22): If
your weight loss greatly diminishes, usually around 2-months, cut backn on net
carbs (fiber). The gut bacteria--like
with a cow--metabolize the fiber extracellularly (outside the cell) and about
60% of the digested fiber (glucose) will be absorbed by the intestines, the
remaining by the bacteria. With lots of
fiber the insulin level could rise, then the fat tissue hormone leptin will in
about 2 months lower metabolism and increase hunger. Insulin besides regulating
uptake of glucose
from the blood, the conversion of fatty acids to the storage form of
triglycerides, it also regulates leptin, the leptin that increases appetite and
diminishes metabolism. Thus, if you
metabolize 2,500 calories a day, metabolism will slow to 2,000 calories a
day.
Part 12: Diets
for health, with all the related
topics www./healthfully.org/rh/id8.html 1/13/17
Sections #1Western
diet health disaster; 2 Definitions, body and food basics; 3 Dietary recommendation
and 4 healthful diets; 4 Tables: net
carbs and Insulin Index; 5 Energy, sugar and fats the good and the bad; 6
Fructose alcohol without the buzz; 7 NAFLD and IR are the gateway to MeS and
its comorbidities; 8 Why fasting with low-net
carbs diet for obesity and T2D; 9 Fasting is easy and essential; 10 Why some
don’t get fat; 11 Myth busters; 12 Pathogens causes of CVD; 13 Other cofactors
for CVD; 14 How did we get here—Historical; 15 Free will won’t; 16 Outline on
metabolic dysfunction; 17 Review and recommendations; 18 Videos and books on
diet, bad pharma, and
CVD; 19 Conclusion
AS Atherosclerosis
|
|
KD Ketogenic diet, very low carbs
|
ATP Adenosine triphosphate-energy molecule
|
|
KOL Key
opinion leader
|
CER
Caloric energy restricted diet
|
|
MeS Metabolic syndrome
|
CVD Cardiovascular disease
|
|
NALFD Non-alcoholic fatty liver disease
|
IR Insulin resistance
|
|
T2D Type 2 Diabetes
|
1.
Western diet health disaster
The rate of
mature adult obesity is over 50%[1],
cardiovascular disease (CVD) deaths
over 60%, and dementia 47% of those over 84 years, diabetes among seniors over 26%. Not 1 in 7 by the age of 60 has their slim
youthful figure. Something is much
different than a century ago, and much different than those paleo peoples
eating a traditional diet. It started in
1978 when the FDA influenced by commercial interests vilified saturated fats
and cholesterol as heart unhealthy. This
resulted in a shift to the cheaper grains, sugars, and polyunsaturated oils
from grains. At the food manufacturers
gradually increased the amount of sugars and aggressive advertised sugar
drinks. It starts with fructose (one
half of the disaccharide sucrose); we have gone from 15 grams of fructose daily
average to over 80 grams in 2010. Our
liver, where it is metabolized, cannot handle the overload.[2] Fructose’s adverse effects upon the liver
causes fatty liver disease (NAFLD)
and insulin resistance (IR). This
abnormally high level of insulin send a
signal to cells to burn glucose and thus to stop burning fat and store it. This
is why we get fat! We are getting fat because of the abnormally
high insulin is causing weight gain.
This system is why those who are long-term
overweight can’t keep it off; because of increased appetite and reduced
metabolism they will gradually regain the weight they have lost. Businesses
which profit from illness and
manufactured foods promote blaming the victim of the Western diet, thus we get
from our corporate media and our physician the message to eat less and exercise
more. That doesn’t fix the
weight-regulatory system; thus we have yo-yo dieting. Like all mammals we have
a weight-regulatory
system. What follows is about that
system, what science has discovered
about it including fructose, the consequences of that damage, and how to
fix that system including type-2 diabetes (T2D).
Yes, it can be fixed.
2.
Definitions: body & food basics 9/23/16
Adipocytes (fat cells) for fat storage; they
secrete the hormones resistin, adiponectin, leptin and apelin.
Amino acids
from proteins: the 20 building different
blocks of protein. Digestion converts
proteins to amino acids.
ATP, Adenosine Triphosphate (adenosine
with 3 phosphate molecules (PO4) attached):
the body’s main energy molecule. ATP transfers chemical energy within
the cell through the loss of one or two of its phosphate groups. ATP
returns to the high state of energy 3(PO4) through absorbing energy from the
metabolism of carbohydrates & fats in the mitochondria. ATP
provides the energy for over 90% of biosynthesis (hormones, collagen, etc.),
for muscle contraction, and for intra & intercellular active
transport. GTP, NADP, NAD and others
also function as energy molecules.
Cardiovascular
disease (CVD) causes, cigarettes
and a high fructose diet. By causing endothelial
dysfunction those cells permit
pathogens
to colonize in the artery walls to cause
inflammation that results in
atherosclerosis, and CVD.
Carbohydrate
(carb): fiber, fructose, glucose, glycogen,
starch, sucrose, lactose, net carbs
(total carbs minus fiber):
Fiber,
vegetable fiber, roughage, the carbohydrate component not broken down
by digestive
enzymes, but some is by gut bacteria.
Fiber has more than ten sugar units.
It lowers the insulin spike when consumed with refined carbs.
Fructose (fruit sugar) a monosaccharide;
main sources are fruits, the disaccharide sucrose, and high fructose corn
syrup. Fructose is only metabolized in
the liver. Fructose is a net 15 more reactive then glucose and by glycation damages proteins
throughout the body to cause age related
chronic diseases. In the liver it
causes IR and NAFLD. This process is
accelerated when insulin is high as the liver’s mitochondria clears first the
excess glucose.
Glucose a monosaccharide is the main energy
storage molecule for plants; in humans 1-2-lbs is stored as long-chain glycogen
a backup energy source stored in muscles, fat, and liver cells. Glucose
is as one half of sucrose, and is
also obtained from the hydrolysis of the digestible starches. Glucose and fat
are the main sources for
production of ATP.
Glycation: a process where a monosaccharide
(simple
sugar mostly fructose) randomly attaches to proteins or lipid; this adversely
affects their functions, thus glycation is a major cause of our
chronic
age-related diseases.
Starch is long chains of glucose units. This polysaccharide is produced mostly by
green plants, seeds, tubers, and other parts of plants. It is the molecule for
energy storage of
plants.
Sucrose, table sugar, produced by
plants; it is the readily hydrolyzed disaccharide consisting of fructose and
glucose.
Diabesity:
the
combination of diabetes and obesity;
they afflicts those on the Western diet—a recently coined term.
Fat
(Free Fatty acids and triglycerides): up to 24 carbon molecules with an organic acid or glycerol
molecule on end.
Glycation:
The
non-enzymatic attachment of a monosaccharide
(mostly fructose) to a protein which through changing its structure thus often
diminishes the protein’s functions It is thus a causal factor for most age
related conditions.
Incretins: a class of hormones secreted by the
stomach
and intestines into the blood in response to bulky foods to cause satiety and insulin
secretion. They are particular
responsive to the
presence of proteins and amino acids.
Insulin: a gateway
hormone produced by the pancreas. Its
main function is to have cells absorb
glucose and store fat, this causes the body to switch from metabolizing fat to
that of glucose. Insulin also regulates
other enzymes and hormones including leptin.
Low production of insulin is the cause of type 1 and 2 diabetes. Insulin
also promotes the storage in amino
acid, and thus we secret insulin by the incretin system in response to proteins
in the stomach.
Insulin
resistance (IR): Since excess glucose is toxic, cells when full
resist the signal by insulin to absorb more glucose. Thus to lower blood sugar,
the pancreas releases even more insulin, and thereby cause in a person with IR
a higher than normal amount of blood insulin.
IR occurs in the liver cells, and causes fat to accumulate
there. Later the muscle and fat cells
develop IR. As IR
progresses, fat storage increases to cause obesity and NAFLD. Fat also
increases in the pancreas to a point
which hinders (reduces) the production of insulin to become T2D. Over
50% of Americans have IR.
Ketogenic diet (KD, very low carbohydrate diet): the Atkins type diet,
a very low carbohydrate diet that causes the body because of lack of glucose to
metabolize fatty acids to produce ATP
and substances that are collectively known as ketone bodies. Most KD
doesn’t limit calories, only carbohydrates.
Ketogenesis also occurs
during fasting. Moderate protein
& fasting hasten progress. The New
Atkins diet limits protein so as to avoid the insulin stimulants leptins.
Ketone bodies: 3
water-soluble molecules (acetoacetate, beta-hydroxybutrate, and their breakdown
product acetone) are produced by cells throughout the body that have
mitochondria. Ketone bodies are produced
during periods of low food intake (sleeping, fasting, intense exercise, some
diets, and starving) and also by those with untreated type-1 (insulin
dependent) diabetes. The
beta-hydroxybutrate has been shown to have a number of healthful benefits.
Key Opinion Leaders (KOLs): people who rise to
top positions in their area of expertise.
In fields relevant to business nearly all of the KOLs violate the
standards of science to produce business-favorable spin, and are handsome
rewarded for their services. The term cenotes
bad conduct. Pharma and food industry have
used KOLs along with regulatory capture to produce a drug/diet disaster, then
sells it to medical students, physicians, politicians, and the public twaddle as
cutting- edge science.
Leptin: produced by fat cells and functions
to
maintain a fix level of fat. Leptin does
this by a 25-40% reduction in the rate of metabolism and by creating the
feeling that by eating that energy will increase and mood improve, thus the
desire to eat more. Thus leptin
functions to maintain fat storage and to restore weight even years later.
Lipids
are a
group of naturally occurring fat like molecules including waxes, sterols, fats,
phospholipids, and others.
Metabolic
syndrome (MeS) “is a is a clustering of at least three of the five following
medical conditions: abdominal (central) obesity, elevated blood pressure, elevated fasting plasma glucose, high serum triglycerides, and low high-density lipoprotein (HDL) levels”, wiki. It is
associated with development of cardiovascular disease and type two-diabetes. Pharma
has framed
the discussion of causes of CVD to
promote ineffective drug treatments—see cholesterol myth.
A more appropriate list—as its name metabolic
denotes--would be insulin resistance, non-alcoholic fatty liver disease,
obesity, and type-2 diabetes. I am using
the metabolic list.
Metabolism in
reference to diet refers to the metabolic conversion of mainly either fat or
carbohydrate into the energy molecule ATP
mostly in the mitochondria. Under conditions of starvation proteins also
can be used to make ATP.
NAFLD (Non-Alcoholic Fatty Liver
Disease): the accumulation of fat by liver cells
sufficient to significantly downgrade their various functions. The NHANES survey
2011 found NAFLD in 30% of adult population—similar % for
Europe.
Tobacco
science: generated by tobacco ethics,
industry funded studies which are by design
positively distorted to sell products, or for other business objectives such as
deflect criticism, attack off patent drugs, to promote diseases, etc.
Type-2
diabetes (T2D): occurs
when the pancreas fails to produce enough insulin to lower glucose to its
normal range; it results from chronic IR
and the accumulation of fat in the pancreas which eventually causes the decline
in insulin.
Western
diet:
one in which there is over 20% of calories from sugar, under 35% of
calories from fat, of which over half of that fat is polyunsaturated. The most
common diet of developed countries
and the cause of the diabesity pandemic.
3. Dietary Recommendations and 5 healthful
diets
Increase
|
Decrease
|
Avoid/Limit
|
Saturated and
monounsaturated fats (animal
fats, lard, & butter are best, followed by palm kernel, coconut, and
olive oils), fiber, leafy vegetables, egg, peanuts,, fish, free-ranging beef,
nuts, whole milk dairy products including cheese, plain yogurt, and cottage
cheese, breakfast protein mix, whole grain products[3],
beans.
|
Meats &
poultry unless free ranging[4],
large portions of fruits especially melons, bananas, grapes, raisins, and
dates[5]. Wanting to lose weight, limit daily to 45
grams of protein male, 35 female--for those of average stature.
|
Fructose, sugar
added foods[6],
fruit juices,[7]
polyunsaturated and trans-fats, most vegetable oil [8],
refined carbohydrates, whole wheat4, large portions of carbs and
fruits, potatoes, rice, instant breakfast cereals, alcoholic drinks,
artificial sweeteners[9]
|
Vinegar,[10]
high fiber cereal,[11], tomatoes
juice, Karo corn syrup or sorbitol as sweeteners.
|
Fried foods
(unless high in saturated fat),
large portions of food with high glycemic
index.
|
Lunch meats
unless cooked[12],
all GMOs12, corn[13],
soy products,[14]
most crackers, chain restaurants.
|
Sugars without fructose: barley
malt, corn syrup (Karol), corn syrup
solids, dextran, dextrose, diastatic
malt, diatase, ethyl maltol, galactose,
glucose, glucose solids, lactose,
malt syrup, maltodextrin, maltose, & rice syrup. For extensive foods recommendations see Fat
Chance, pages 199-205 by Prof. Robert
Lustig.
FIVE DIETS 9/13/16
1) Healthy diet: For those in good health and
normal weight without IR or
abdominal; fat. The goal is to keep fructose
low, thus avoid added sugar, juices, & limit fruits. Increase saturated
fats, therefore lower
starches. Increase physical excursion to
keep serum glucose lower and thus insulin low.
Low rate of glycation requires very low fructose (see section 6) and taking
antioxidant supplements. The short fast
at least once a week promotes a healthy liver.
2) Fatty
liver (abdominal fat) but no
major weight issue:
follow the above but do the
short-term fast every morning. This must
continue until the few extra abdominal pounds are lost, and your middle has
that youthful look, then gradually go off the daily fast and see if your weight
has stabilized at the lower point; if not than go back to short-term
fasting. Expect to be fasting for 4
months or longer. Longer fasts speed
cleansing of the liver and other organs-- section 8.
3) Weight loss diet of more than 15%:
Daily
the jk short fast and 20% calories from carbs
or less. If progress is
slow, then add the New
Atkins Diet
(ketogenic) with moderate proteins, and/or alternate day fasting. See section 9,
below.
4) T2D diet on 1 or 2 drugs,
or obesity: Daily JK
short fast and
the new
Atkins type diet
with moderate protein. Monitor plasma
glucose so as to reduce dependence on drugs.
If after 6 month this hasn’t cured T2D
then switch to full
alternate-day fasting.
Watch Dr. Jason Fung explain the
issues on insulin
and diabetes and
alternate day fasting diet.
5) Severe
T2D and morbid obesity: Follow a
very low carb diet with alternate-day
fasting. T2D is a progressive disease treated with drugs to lower
glucose,
then more drugs, & then insulin injections.
It is caused by diet and can be cured by diet. The fast following bariatric
surgery cures
over 80% of T2D in the first few
weeks, before major weight loss.
JK short fast: go on a 16 hour fast (7 PM
until 11:00 AM) or longer, thus extending nighttime fat burning to produce ATP
(the energy molecule) to
midday. At night because of not eating
there is low glucose and thus low insulin.
If hunger becomes an issue than eat green vegetables, bone broth, black
coffee or tea with lemon. Maximize saturated
fat, low protein, very low carbs. Keep
lowering carbs if progress slows and extend the fast.
Atkins maintenance phase: Once weight target is reached, the
daily intake of carbs is increased by 10 grams per day to find the level where
weight is gained, then drop below that level.
Continue to limit refined carbs and foods with high glycemic index to
small portions, limit sweets with fructose, & use the JK short fast weekly
to maintain a healthy liver. Vigorous
exercise is a general health tonic and mood elevator. For seniors the addition
of natural hormone replacement therapy
might be also required, click on estradiol and testosterone; they play
a role in fat storage, muscle tone, will to exercise, and general
health--things pharma is against.
4. Tables:
Net Carbs and Insulin Index
Net Carbs = total carbohydrates
minus fiber
content.
Egg
1 = 0.4 grams
Seafood
6 oz. = 0
Meats
6 oz. = 0
Poultry
6 oz. = 0
Oils
6 oz. = 0
|
Dairy
American processed
1 slice 1.5 grams
Cheeses 1 oz. = 0.7
Cottage cheese ½ c = 5
Cream 1 T
= 0.4
Cream cheese 2 T = 1.2
Milk 1 c = 11.7
to 15
Yogurt plain
1 c = 11.6
Greek Yogurt
plain 1 c = 9
|
Raw
Vegetables
Avocado ½ = 2 grams
Bell pepper green ½ c= 2.2
Bell pepper red ½ c =3
Broccoli ½ c = 1
Cabbage shredded ½ c = 1.1
Celery stalk = 1
Cauliflower florets ½ c = 1.4
Cucumber ½ c = 1
|
Nuts
Almonds 24 = 2.5
Brazil 6 = 1.4
Cashews 2 T =
5.1
Mixed nuts 2 T = 2
Peanuts 2 T = 1.4
Pecans 1 oz. = 1.2
Walnuts 1 oz. 1.2
|
|
Green beans ½ c = 2
Lettice 1 c = 0.36Olives black 5 = 0.7
Olives green 5 = 0.0
Onion 2 tbs. = 1
Spinach 1 c = 0.2
Squash summer ½ c 2.6
Tomato 1 med = 3.0
Tomato juice 1c = 8
|
For
those off
|
the
induction
|
(ketogenic)
phase
|
Fruits
Apple med = 8
Banana med = 30
Blueberries ½ c = 9
Dates dried 1 oz = 21
Fig dried med = 6
Grapes 1 c = 26
|
Grapefruit ½ = 9
Melon cantaloupe 1 c
= 12
Orange navel med =15
Peach med = 15
Pear med = 20
Strawberry 5 lg = 5
|
Legumes
Black bean home cooked 1 c = 8
Canned baked beans 1c = 36
Kidney home cooked 1c = 11
Pinto bean home cooked = 25
Soybean white 1c =10
|
Vegetables not leafy
Beets steamed 1c = 13
Carrots steamed 1c = 8
Corn on cob med steamed 15
Eggplant 1c = 5
|
Olive cured 7= 1
Onion 1 c = 12
Peas 1 c = 14
Potato med with skin = 26
|
Snow pea ½ c cooked = 2.7
Squash acorn 1 c = 21
Squash zucchini 1c = 3
Sweet potato med = 20
|
On the Atkins website (http://files.atkins.com/1501_CarbCounter_Online.pdf) is an
extensive table of net carbs. For
simplicity the food label on products can be used, simply subtract fiber from
carbohydrates to get an approximate value.
Remember that food manufacturers add sugar to nearly every product plus
many of them have various forms of starch as filler and thickening agent
(starch is pure glucose).
Insulin
index of common foods
Each portion of food contained 240
Calories—score relative to white bread which was set at 100
Peanuts
20
|
|
Fish
59
|
|
Grapes
82
|
Eggs
31
|
|
Oranges
69
|
|
Crackers
87
|
All
bran
32
|
|
Potato
chips 61
|
|
Ice
cream
89
|
Porridge
40
|
|
Brown
rice
62
|
|
Cookies
92
|
Brown
Pasta 40
|
|
Special
K
66
|
|
Whole
Bread
96
|
White
Pasta 40
|
|
Honey
smacks 67
|
|
White
Bread
100
|
Cheese
45
|
|
Coco
Pops
71
|
|
Yogurt
sweetened 115
|
Granola
plain 46
|
|
French
Fries 74
|
|
Baked
Beans can 120
|
Beef 51
|
|
Corn
Flakes 75
|
|
Potatoes
121
|
Popcorn
54
|
|
Croissants 79
|
|
Mars
Bar 122
|
Grain
bread 56
|
|
White
Rice
79
|
|
Jelly
Beans
160
|
Lentils
58
|
|
Bananas
81
|
|
Fats
10
|
Apples
59
|
|
Cake 82
|
|
|
from http://graemethomasonline.com/wp-content/uploads/2010/06/Insulin-Index.pdf
Detail explanation of testing
http://www.janurky.sk/db/articles/20150703n0(kj_not_kj)/images/insulin_index.pdf
These figures are based on test
results for an ideal group: average age 22 and BMI of 23. Foods needing preparation such as potatoes
and pasta were boiled, stored overnight in the refrigerator then warmed the
next day in a microwave. Test score was
based on the average insulin level over 120 minutes divided by that for white
bread times 100. There were 503 tests
total test for the 36 listed foods.
Breakfast cereals were served with milk.
“Plasma insulin concentrations were measured in duplicate by using an
antibody-coated tube radio-immuonoassy kit (Coat-A-Count; Diagnostic Products
Corporation, Los Angeles)”at 1997, p. 1295. Samples of 1.5 to 2.5
mL. of blood were
obtained at 15 minute intervals over the 2 hours test period. Unfortunately
this table lacks important
foods of vegetables, milk, soda, diet soda, and fat (which I included from
another source--Dr. Fung’s book The
Obesity Code p 193).
The goal is to maximize the
rate of fat burning which requires a
low insulin diet. Insulin causes fat
storage. Since protein is needed to
maintain muscle mass, it must be restricted but only somewhat. The USDA dietary
recommendations are high. Thus I recommend cutting it to 35 grams
women, and 45 grams men--for those of average body frame size. This is sufficient
to prevent muscle loss.[15] The effect of protein
upon insulin and thus
fat storage explains why short-term and alternate day fasting make a very
significant improvement upon the low carb KD.[16] For most on a KD, after a couple of months the rate of weight loss will decline,
the effect of insulin upon leptin. Fasting prevents this phenomenon of leptin reducing the rate
of metabolism.
5.
Energy: Carbs, Sugars, and Fats--the bad
and good
With the Western diet yearly
sugars consumption of added sugar has gone
from 35 lbs. in 1909 (43
gm/day) to 152 lbs. in 2000 (751 calories/per day or 189 gm/day) to cause the
diabesity (diabetes and obesity) pandemics.
Part of that increase is a result of the vilification of fats and the
official government recommendation of lowering carb intakes from a bit over 40%
of calories to 30% or less. With this
reduction in calories from fats came it replacement with mostly sugars, but
also an increase in grains, mostly wheat and corn. Starches are a fairly safe
source of energy,
but the increase of sucrose and HFCS high fructose corn syrup is a bad thing
because of the fructose—see next section.
Table sugar (sucrose) is
hydrolyzed in the stomach into fructose and glucose, starch in the stomach to
glucose. Glucose and fats are the body’s
main sources of ATP (energy molecule)—other monosaccharides such as galactose,
fructose, and amino acids contribute to the remaining 20% of the conversion of
ADP to ATP. High blood glucose (a bad
thing) is down regulated by increased insulin (also bad) which sends a message
for the body to burn glucose and thus
store fats. High insulin levels in
response to high glucose will over the decades cause insulin resistance (IR,
a reduced response to insulin) in insulin receptor on cell walls. This is a
way of cells to limit its amount of
sugar to a safe level. IR caused
high serum glucose results in
more insulin secreted by the pancreas. IR
increases fat storage. Gradually
many of those on a Western diet accumulate 2-3 extra pounds of stored fat in
the liver, nearly doubling the weight of the liver which normally weights 3.2
to 3.7 lb. This causes mild liver
inflammation and what is clinically called Non-Alcoholic Fatty Liver Disease
(NAFLD) the starting point
the comorbidities from MeS and cirrhosis
of the liver (see section 6 on NAFLD).
Excess fat in the pancreas eventually causes
a decline in insulin production that result in T2D. High insulin from IR also causes low leptin a hormone
which among many things increases appetite by stimulating the control center in
the brain, and leptin also lowers metabolism—2 causes for obesity and the yo-yo
diets. The other problem is the table sugar sucrose, a disaccharide of
fructose and
glucose. Fructose
in sucrose attaches
randomly to proteins in a process called glycation at 7.5 times the rate of glucose, however the
slower in vivo clearance doubles that
figure.[17] Glycation damages proteins—the main cause of
age related chronic conditions.[18]
Fructose
is metabolized only in the
liver where it damages the liver by glycation resulting in IR in the liver. With
the Western diet’s high carbs, some of the fat in the liver is stored
there. Some of that fat comes from the
conversion of fructose to fat and some from conversion of glucose to fat in the
liver. This fat de novo lipolysis
(synthesis of fat) plus IR in the liver causes
gradual causes NAFLD. In
other words, if more fat is made than the
liver can use, and there is high insulin due to IR and a diet high in carb glucose,
this fat accumulates
in the liver cells to cause non-alcoholic fatty
liver disease (NAFLD).
This fat
accumulates in the liver cells and reduces liver functions, as too dose
glycation by fructose and glucose; this double assault on the liver adversely
affects the many functions of the liver and thereby contributes to IR.[19] NAFLD with its IR is the main cause of a group of conditions labeled metabolic syndrome (MeS):
NAFLD, IR, and T2D, and its
sign obesity (pharma
adds the non-metabolic high
cholesterol and the resultant
hypertension and CVD—for marketing
of their drugs). Sections 6 covers
fructose, 7NAFLD.
Fructose:
The very
reactive sugar fructose is the starting point for the diabesity pandemic. As
stated above fructose, which accumulates
in the liver where it is metabolized, it damages the liver through glycation
and fat accumulation. In the US we have
gone from 15 grams per day, mainly from fruits, in 1900 to over 90 grams a day
(hh.edu at) mainly from sucrose and HFCS (high fructose corn syrup). We have not evolved a system to handle this
load since our ancestors only ate moderate amounts of fruit, and in the wild
they were smaller and far less sweet.
It isn’t the glucose half of the disaccharide sucrose that is the
problem, since grains are pure glucose and mostly paleo peoples ate a high
carbohydrate diet. The traditional
oriental diet is high in carbs (up to 75%) but low in fructose (14 grams or
less) and as expected their incidents of obesity, CVD, and T2D was and is on that
diet quite low, especially among those who don’t smoke. Fructose among
other things damages the liver
and this is the starting point for causal chain leading to obesity, MeS, T2D and NAFLD. See
section 6 for an extensive account of
harm caused by excess fructose and watch
the documentaries on the health consequences of sugar—link. Sugar us called “White Poison” because it is one-half
fructose.
2) Starches are
molecules made up of
chains of the monosaccharide glucose; their rate of absorption during digestion
varies according to their structure.
Some have a much lower rate than sucrose, and are called resistant
starch; thus not all carbohydrates are equal—for tables and more
on carbs. Fiber is a very resistant
starch, which
lowers insulin by slowing digestion, and which through bacterial action in the
intestines approximately a third of it is absorbed as glucose during the next
24 hours.[20] The portion of and type of starch in meals
affects serum glucose, as too the rate of stomach clearance. Fats, resistant
starch, and proteins in the
meal slows stomach clearance, thus extending the time in which glucose is
absorbed by the duodenum; this lowers the blood insulin spike—a good
thing. There are a number more good
things you can do: see section #12, why
some don’t get fat.
3)
Fats, like carbs, are not all equal. The
right fats are the best source of energy.
Two fats are bad: trans-fats and polyunsaturated
fats. Trans-fats are not natural, but
are man made by a process of hydrogenation of polyunsaturated fats. Their abnormal
shapes entail that they don’t
function very well in cell walls—a bad thing.
For the same reason polyunsaturated fats are a bad thing. This is because
of their multiple double
bonds in the carbon chain (why they are called polyunsaturated). These
double bonds are available to be bonded with reactive chemicals in a process
called rancidification, which changes their shapes. This oxidation can occur
on the shelf, it is
accelerated when heat is applied as when baking or frying foods, and in the
body where reactive chemicals are made during biological processes. The rancid
fats, just like trans-fats, don’t function properly in cell walls—a bad
thing. Rancid fats are casual for many,
if not most, of the maladies associated with the Western diet. Rancid fats have
been shown, for example as a
causal factor for NAFLD, and thus all the comorbidities associated with a fatty
liver. The extent of the health has,
like drug side effects, not be a priority of funding. The evidence is found
in scientific studies
published in journal: for rancidification
see #25
and for
trans-fats (from hydrogenated vegetable oil) see
#27. Another issue arise because polyunsaturated
fats
are that they are high in omega-6 fatty acids.
The omega-3
fatty acids EPA & DHA
are used to limit the immune responses, thus they lower risk for AS & CVD, but too much omega-6 competitively blocks
omega-3 usage--a bad thing. Hunter-gatherer societies averaged about 2 parts omega-6 to one of
omega-3; in the U.S. it is 16 to 1 (a bad thing). Vegetable oils (except from
palm & olive
trees) are very high in omega-6. Like
trans-fats, the body lack enzymes to metabolism them; thus both types of fat
cause AS and thus CVD.
Food manufacturers and restaurants use both of these bad fats. This leaves
us with the safe saturated and
monounsaturated fats. “Over the years, data revealed that
dietary
saturated fatty acids (SFAs) are not associated
with CAD [coronary artery disease]
and other adverse health effects” in journal.
The same in Wikipedia: ”There is s no significant evidence for concluding
that
dietary saturated fat is associated with an increased risk of CHD or CVD” which is based on a meta study of 21 journal articles--and they taste much better. Saturated fats are best source of
energy—see Prof. Miller's for
list of their 6 essential functions.
Proteins, though rated
at 6 calories per gram, under normal
conditions they are not appreciable metabolism for energy (ATP) except on a high
protein diet or during starvation. When fats stores are depleted to 4% during
starvation, the cells switch from storing to metabolizing amino acids (the
building blocks of proteins)
[1] The
worse way to find out what peoples weight and height is to ask them over the
phone; and that is how the figures are
obtained! The figure of 35.7% for
2010 does not include the morbidly obese which are 6.3%, giving a total of 42%,
at.
Adjusting for survey error, a figure of 50% obese (including morbidly obese) is
reasonable, with seniors of course have the highest rate by age.
[2]
See Abundance
of Fructose, not Good for the Liver and Heart, Harvard Medical School Heart
Letter, 2011, hh.edu at.
[3] Most whole wheat breads are comparable
to white bread as to glycemic index (GI) and insulin index (IL) (see table Part 3), plus they have phytic acid
(inositol hexaphosphate (IP6): “Phytic acid has a strong binding
affinity to
important minerals, such as calcium, iron, and zinc” Wiki that binds to and thus prevents
their absorption. Phytic acid is also in beans, peanuts, soybean, brown rice,
oat meal, corn, and nuts. White flour lacks
phytic acid. Sugars are added to mask
the rancid taste of phytic acid. Lustig,
Fat
Chance 133.
[4]
Cattle are fed a diet of GMO grains. Certified
Organic has been outsourced to companies most of whom do sham
inspections.
[5]
High sugar fruits with high glycemic index (raises insulin).
[6] In
2018 “Sugar added” is
to be listed (maybe) under sugar in food labels. For current labels, how much
has been added
depends on ingredients, vegetables have natural low levels of sugar, fruits
higher. There are 56 different sweeteners used in processed foods. If in
doubt, look at the list of ingredients for sweeteners. Ingredients are listed
in order of percentage
by weight.
[7]
Fruit juices having most of the fiber removed, thus produce a serum glucose
increase comparable to a like amount of soda.
[8]
Polyunsaturated fats undergo in the body unhealthful rancidification, and they
are high in omega-6 fatty acids which block the healthful conversion of omega-3
fatty acids. Like trans-fats they cause CVD.
US regulations are just a pseudo fix—see fats.
[9]
They raise insulin through a hormonal system found in the stomach and intestines. Studies
of the obese show that artificially
sweetened drinks do not promote weight loss because their taste stimulates
insulin which causes the body to store fat.
[10]
Vinegar reduces insulin resistance and increase satiation.
[11] These oils are lowest in
polyunsaturated fats, including omega 6 fatty acids And because they are from
trees they are GMOs free.
[12] Given the broken food-inspection
process, they pose a major risk factor, which has been grossly under reported
in our corporate media. A 2008 study in
France showed that their rate of food poisoning was 1/4th the US
rate.
[13] Avoid because of high insulin
index, and they have a GMO gene that causes corn to produces a pesticide—same
for canola, soy. and others. Testing and review is a regulatory
façade; and the companies do tobacco science to “prove” GMOs are
beneficial. There is very little science
on GMOs. There are several quality documentaries under
GMO on the video page.
[14]
Soybean has estrogen-testosterone mimic, for which there is evidence that the
mimics interfere with their healthful functions.
[15]
The science on the effects of elevated insulin due to protein when carbs are
low is very incomplete. For one thing,
with a high-protein-low carb diet (once popular in the 1920s and before) proved
successful short term. Obviously, when
there is no glucose to burn the body will continue to burn fat. Insulin also
functions to prevent the
metabolism the amino acids derived from proteins.
[16]
There is a second hormonal system, incretins, one not affected by blood
glucose, that stimulates the release of insulin.
[17]
Serum fructose is twice as high from sucrose compared to glucose, thus the 7.5
rate of glycation is multiplied by 2, at
1988. Fructose unlike glucose
exists far more in the linear form rather than the ring form like glucose. In
the ring form of these sugars the reactive
aldol or keto groups on not available.
This structural difference entails that fructose is 7.5 times more
reactive, Lustig.
[18] Attaching a sugar molecule or
its metabolite onto a protein changes its shape and thereby reduces the
protein’s biological functions (a bad thing).
Tissues and organs throughout the body gradually experience a decline
due to their glucose and fructose caused modifications. Othe r
reactive chemical such as from metabolism and the carbon monoxide from tobacco
smoke are also a bad thing.
[19] Insulin resistance in the liver entails also elevated
glucose because of a reduced production of glycogen by the liver. Insulin resistance
is where the normal level
of insulin fails to sufficiently lower serum glucose, and the pancreas thus
releases more insulin to obtain the fasting serum level of glucose. This abnormally
high level of insulin slowly
causes the body to store more than the normal level of fat. White adipose (fat)
tissue (the most common kind)
produces hormones which regulate the level of fat. With insulin resistance this
regulatory
system is reset to maintain the weight gain.
[20]
This explains in part the benefit to extended fasting, not only does it permit
the body to fully adjust to the metabolic changes for fat metabolism which take
3 to 5 day, but also lowers the level of insulin by clearing the intestines of
fiber. The fast following bariatric
surgery is why over 80% are cured of T2D
|
6. Fructose
alcohol without the Buzz and worse
Fructose
is toxic to the liver like alcohol; both are metabolized in the liver, and through various
processes compromise liver functions, see Prof. Robert Lustig’s Alcohol without the
Buzz. Like ethanol
the
quantity consumed determines its toxicity.
Fructose is 15 times net more reactive
than equal quantity of glucose to proteins in a process called glycation—unregulated
bonding to proteins, a bad
thing. Fructose and glucose exist
primarily in a ring formation, however because fructose exist to a greater
extent in a linear structure for which its carbonyl group on the molecule is
exposed, it is more likely to bond with certain amino acids such as lysine on
proteins than compared to glucose. Using fluorescence
method of analysis it is
estimated to be 7.5 times more reactive than glucose. The liver is the only significant place
for metabolism of fructose, thus fructose is actively transported into the
liver from the blood. Collecting in the
liver entails that the liver is subjected to a much greater rate of glycation
than other tissues. That is the first
blow to the liver. Among the process
affected in the liver is its major metabolic process of producing glycogen from
glucose. With the slower than normal
rate of glycogen production, the glucose accumulates to a higher than normal
level in the hepatocytes (liver cells).
Being stuffed with glucose (a bad thing) entails that the hepatocytes
are resistant to insulin’s message for to absorb more glucose. . This
is why the hepatocytes are the first cells to exhibit insulin resistance. This
damage to the hepatocytes also affects
the metabolism by the hepatocytes of fructose, thus increasing the rate of
damage through glycation. Second blow
comes from IR in the liver: it
causes excess fat storage in the
hepatocytes. In the liver when the
insulin level is high, as occurs with a meal high in easily digested carbs,
there is an excess of glucose more than the liver can use for metabolism and
production of glycogen, this excess glucose is converted through de novo lipogenesis
into fats
(triglycerides) and stored there. Glycogen.[1]storage
is limited because of builk. Thus insulin shuts down the metabolism of fats
(triglycerides), its transport from the liver as free fatty acids, and also
causes the fats to be stored in the liver.
The fructose (glycation) damage liver with a high carb diet accumulates
excessive fat storage. On a steady
typical Western diet, very
slowly this excess fat accumulates to a toxic level in the liver (2-to-3
pounds). With that amount it is known as
non-alcoholic fatty liver disease (NAFLD). The three work together, high fructose,
glucose and insulin, to cause NAFLD. (See the next section for the pathologies NAFLD causes.)
This lower rate of utilization of glucose from the blood by the liver
raises the level of blood glucose. The
muscle and fat cells being at their maximum level of glucose following a high
carb meal, they resist the message from the insulin receptors to absorb more
glucose—see Fung on protective mechanism of cells resisting more glucose from the
blood. However, these tissues are
resistant to taking up more glucose as signaled by insulin, they nevertheless
respond to the message “burn glucose
and therefore store fat”.
Thus with those developing a fatty liver, NAFLD,
they are storing more fat, typically a couple of pounds a year: the gradual
march to obesity. (See section #10, which list various things
that can be done to slow or stop the march to obesity.) This process of glycation
and fat
accumulation also occurs in the pancreas, but at a slower
rate, since the pancreas’s level of fructose is lower. After a number
of years, however, for about
24% of the seniors it will sufficiently damage the pancreas so that its insulin
production will decline about 70% over a period of about a year, and this may
become symptomatic or detected by blood work and diagnosed as T2D.
2) There is an
important point to tease out of the many studies, namely that it isn’t the high
carb diet, or refined carbs that is causal for IR and NAFLD, but the
inclusion of fructose in that diet. For
example, those on the traditional diet
of Japanese, Chinese, and Okinawans[2] have only a 1%
risk for T2D, NAFLD, and obesity,
even though they over 70% of their calories
come mainly from the quickly absorbed carbs of white rice, noodles, and/or
Oriental yams); and among those who don’t smoke their rate of CVD is low. Sugar, which came from fruits and
vegetables, amounted to an average of 15 grams a day—in America the average is
over 189 grams a day[3]. And there is
experimental evidence that fructose not glucose is the culprit. Fructose has been linked in an experiment on healthy
volunteers without IR in which 25%
of calories came from fructose sweetened drinks, compared to a control group
with 25% from glucose (corn syrup). In 2
weeks the volunteers on the fructose group developed IR, while those on the glucose
sweetened drink didn’t. Similar results have
been obtain in animal experiments. Fructose
(not
glucose) is the sand in the oil that damages the metabolic engine, the liver
leading to T2D and obesity, and in
addition more comes from glycation in other tissues.
3) The diabesity
pandemics is not the only reason why Dr. Lustig calls sugar white
poison, and state that it should be regulated like alcohol. He
and other scientist call Alzheimer’s
disease, whose incidence has increase several fold in the last 4 decades, type-3
diabetes—and there is more.
Allow me here to explain how
this reactive sugar when consumed in amounts well above the bodily mechanism
for its safe metabolism and repair of glycated proteins. Cellular damage by
glycation is not just limited to the liver.
It is a major cause of age related conditions. ”It degrades the
quality of cartilage and
affects bone metabolism” at 2013.
Thus we have an explanation for the sharp rise is sport injuries since
the 1970s, and also the osteoarthritic joint problems in the general
population. Prior to reading that
journal article, I though the increase in osteoporosis and joint problems was
driven by the chemical bath we are subject to from drugs, food additives, BPA,
and others. Especially those that are sex hormone mimics.[4]. Now it seems
that glycation by fructose is the main culprit. Glycated
substances are eliminated from the body slowly, since the renal clearance
factor is only about 30%. This occurs in
two ways through cell death (apoptosis) and through an enzyme which removes
glycated amino acids. The latter is
called proteolysis. The
slow clearance by proteolysis entails that for those on the Western diet only
about half of the glycation products within the body will be eliminated. “As a
consequence, long-lived cells (such as nerves, brain cells) and long-lasting
proteins (such as DNA, eye crystalline, and collagen) may accumulate
substantial damage over time. Metabolically-active cells such as the glomeruli
in the kidneys, retina cells
in the eyes, [epithelial cells in arteries], and beta cells (insulin-producing) in the
pancreas are also at
high risk of damage” Wiki. “Some AGEs (advanced glycation end products)
are benign, but others are more reactive than the sugars they are derived from,
and are implicated in many age-related chronic
diseases such as cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer's disease (amyloid proteins are side-products of the reactions
progressing to AGEs),[7][8] cancer (acrylamide and other side-products are
released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination). This range of
diseases is the result of the very basic level at which glycations
interfere with molecular and cellular functioning throughout the body and the release of highly oxidizing
side-products such as hydrogen peroxide. Long-lived cells (such as nerves
and different types of
brain cell), long-lasting proteins (such as crystallins of the lens and cornea), and DNA may accumulate substantial damage over time.
Cells such as the retina cells in the eyes, and beta cells (insulin-producing)
in the pancreas are also at high risk of damage“ Wiki 2015. Also
under-rated is the role of fructose
in glycation in retinopathy, nephropathy, and endothelial dysfunction[5] in diabetics, and the over attributing
to reactive oxygen species created by metabolism—see Protein
Glycation, A firm Link to Endothelial Cell Dysfunction. Endothelial
dysfunction is a starting cause for atherosclerosis and thus CVD--see section
12. And there are other ways fructose in excess
destroys health.
4) “Fructose also chelates minerals in the blood.
This effect is especially important with micronutrients such as copper, chromium and zinc. Since these solutes are
normally present in small quantities,
chelation of small numbers of ions may lead to deficiency diseases, immune system impairment and even insulin resistance, a component of type II diabetes (Higdon). Compared with consumption of
high glucose beverages, drinking high fructose beverages with meals results in
lower circulating insulin and leptin
levels, and higher ghrelin
levels after the meal.[62] Since leptin and insulin decrease
appetite and ghrelin increases appetite, some researchers suspect that eating
large amounts of fructose increases the likelihood of weight gain”[63] Wiki
2014. Fructose
has a glycemic index of 17, while corn syrup compared to pure glucose’s 100
results in a major difference is satiety, thus justifying this type of
contribution to obesity.
5) There are several
parallels to ethanol besides there
metabolism in the liver and the reactive products damaging the liver proteins
(glycation for fructose and the reactive aldehyde from the metabolism of
ethanol), at 1991. This can progress to end stage liver disease (cirrhosis of
the liver)—see section 7 below . Both ethanol and fructose activate pleasure
centers of the brain to produce addictive behavior. Like ethanol fructose causes
a fatty liver,
and with the continued over consumption, both can lead to end-stage cirrhosis
of the liver. And both ethanol and
fructose have little effect upon the satiety hormones, thus promoting over
consumption of food. Given all these
issues, one would assume that the experts would warn the high risk populations
of elderly, diabetics, and those with CVD to avoid fructose/sugar. However,
fructose is recommended for
diabetics because of its low insulin index, and the other at risk population
are not warned; another example of profits before people. Given the power
of advertising to create
markets, and our corporatist government, effective regulations are not coming,
or an effective program of educating the public concerning the health
consequences of sugar.[6] Both the FDA and the American Heart Association now recommend no more than 200 calories
from sugar daily, however, few Americans know of this, and given the power of
advertisement such a recommendation goes unheeded by most American. The
WHO makes the same recommendation. Those who limit their sugar are doing so
for
other reasons than official pronouncements.
7. NAFLD and IR are the gateway to MeS and its
comorbidities
NAFLD “Non-alcoholic fatty
liver disease (NAFLD) is one
of the causes of fatty liver, occurring when fat
is deposited (steatosis) in the liver due to causes other than excessive alcohol
use. NAFLD is the most
common liver disorder in developed countries….[1][2] Non-alcoholic steatohepatitis (NASH)
is the most extreme form
of NAFLD, and is regarded as a major cause of cirrhosis of the liver of unknown cause.[5] A study using the National Health and
Nutrition Examination Survey (NHANES) found a 30% rate of NAFLD in the United
States between 2011 and 2012.[7 Most people with NAFLD have few or no
symptoms [other than abdominal weight gain, and a propensity to readily put on
weight]…. Soft drinks have been linked to
NAFLD due to high concentrations of fructose, which may be
present either in high-fructose corn syrup or, in similar quantities, as a
metabolite of sucrose” Wiki. Diagnosis of NALD is commonly by ultrasound or biopsy. No pharmacological
treatment has been as of
2015 been approved by the FDA, though pharma has several drug candidates. However,
the condition is responsive to
Bariatric surgery, low carbohydrate diet, and diet with fasting.
NAFLD its development: NAFLD
requir7es both high carbs and high fructose. That it takes both is confirmed
by Japanese
and other population that eat a traditionally high-carb diet, but with very low
sugar—for the Japanese 15 grams per day, and similar amounts for the Okinawans,
and Chinese. These populations have a
low rate of CVD and the other age
related conditions associated with the Western diet. Many paleo peoples eat
a high carb diet but
the Western diseases are very rare among their elders. And there is direct
evidence: a couple of experiments done
within a hospital where young healthy volunteers were fed for 2 weeks either
high fructose or high glucose, this confirmed the role of fructose, but
absolved glucose as to the development of IR.
So how are the two sugars different? The difference is because of the
fructose
which is metabolized only in the liver
where it is converted mostly to glucose and some fat. Fructose is also 7.5 times
more reactive than
glucose through the process of glycation (see definitions section 2), and its
slow clearance from the liver compared to glucose doubles that figure to 15.
Glycation damages the liver; it causes inflammation and other signs of
liver injury such as high ALT and AST--blood markers for conditions in the
liver. ALT and AST are commonly used as
a way to screen for liver problems. A
diet high in fructose is likely high in the
sugar glucose both from sucrose. Starch
consists of long chains of pure glucose.
A diet that is high in carbs is necessarily low in fats. So depending
on needs of other tissues (fats
and cholesterol are essential for cell membranes) the liver will convert in
some of the glucose and fructose through de novo lipogenesis into fats. Because
of the high insulin from IR in the liver and a high carb diet,
the high insulin accelerates the accumulation of fat in the liver. This high
carb-sugar diet causes IR in the liver and thus the gradual
accumulation of fat in the liver. The
regulation of blood insulin which in part involves the liver, such as through
the production of glycogen, will contribute to an excess of blood glucose,
which causes other cells, principle the muscle and fat cells to become
resistant to insulin. For those who stay
on the high carbohydrate Western diet this is likely to progress to obesity, NAFLD,
MeS, and obesity. Two
studies of those with NAFLD found
that they consume 2-3 times more fructose than those without NAFLD—at, and. AGEs (advanced glycation end products) in the
liver and elsewhere are recognized as foreign substances by the immune system
and can in sufficient number produce significant inflammatory response. The
attributing of excess fat in the liver as
the primary cause for liver inflammation is questionable given the co-existence
of AGEs in the liver and the natural inflammatory response by the immune system
to AGEs. Insulin resistance is like drug resistance where the body
responds less to a given dose of a drug, for example alcohol, and a higher dose
is thus required for the desired effect.
With insulin resistance the normal level of insulin fails to
sufficiently lower serum glucose, and the pancreas thus releases more insulin
to obtain the ideal fasting serum level of glucose. This abnormally high level
of insulin slowly
causes the body to store more than the normal level of fat. White adipose (fat)
tissue (the most common
kind) produces hormones which regulate the level of fat. With insulin resistance
this regulatory
system is reset to maintain the weight gained.
High fructose and high glucose from the Western diet is what has lead to
the diabesity (obesity & diabetes) epidemic.
Fortunately there is a repair mechanism
for NAFLD IR T2D, and obesity, to
simply go on a low insulin diet. This requires fasting made more effective by
low fructose and especially the ketogenic diet.
As stated before fasting keeps insulin low and thus keeps the body in
the fat burning mode. Fasting is why
about 80% of those who have undergone bariatric surgery cure their diabetes and
insulin resistance within the first month. This is because they can’t eat
during the first couple of weeks following surgery. Follow the appropriate fasting
programs
listed in section 3 duplicates the process that cured those who had bariatric
surgery. And it gets better as weight is
lost, the body heals itself, old damaged cells from glycation are replaced with
cells whose protein haven’t been damaged.[7]
8. Why a low-net carbs diet for
obesity & T2D
There are two common general approaches to dieting,
caloric energy
restriction (CER) or carbs
restriction of which some are the extreme low carbs, the ketogenic (Atkins
type) diet without CER—and there are
of course many variations of these types of diet.[8] A third approach, fasting is growing in
popularity, mainly in Europe. Unfortunately nearly all of the long-term[9] obese have
had their weight regulatory system compromised; it functions to restore weight
loss by causing a 25% reduction in metabolism or more, and an increase
in hunger through a hormonal system involving insulin and leptin. Typically
around the end of the 2nd
month (see chart above), their progress is
greatly diminished because of the fat restoring hormone leptin. Only those with
extreme calorie restriction will continue to lose significant
weight. However, once off their diet the
weight will be gradually regained (the yo-yo diet). The main cause is the hormone
leptin which is
secreted by adipose (fat) tissue; it functions to main the normal level of fat
storage. Leptin intercedes to decrease
metabolism--typically 25%--
and through this effect increases appetite.
The dieter feels that if he eats
more, he will be mentally sharper, happier and have more energy[10].
Possible there is an approach to
solving the affects of leptin which results for the long-term overweight with
the restoration of their prior level off.
To address this the government funded a major trial, and they selected a
long-term vegetarian to run it, probably want to find evidence against the then
very popular Atkins diet, which given its low carbs was unpopular with food
manufacturers.
The trial was run to
compare the CER to the carb
restricted diets. In the funded by
government[11]
Stanford University international
A to Z Weight Loss Study which compared 4 popular diets. Its lead person
was disappointed the Atkins
had the best results both in weight loss, blood glucose, and lipid
profile. At 2 moths all 4 cohorts in the
trial experience a marked reduction in the rate of weight loss. At 1 year, the
length of the trial, Atkins
(ketogenic) cohort loss 9.9, LEARN 5.5, Ornish 5.3, and Zone Diet 3.3
pounds—see JAMA
2007. Another trial had similar
results this time using overweight volunteers:
9.4 kg lost on low carb (20 gm daily) versus the low fat 4.8 kg, at. In this trial both groups reduced calories
between 500 to 1000 calories daily. In
both of the clinical trials the lipid profile and blood pressure were much
better for the low carb (thus high fat) cohorts, and more importantly their
level of blood sugar improved on the low car diet. “Insulin levels dropped
and insulin
sensitivity was restored” (Fung p 101).
A recent journal article interviewed the 2009 group on the television
show The
Biggest Losers. A group of 13
morbidly obsess participants were in a boot camp which had an extreme energy
restriction, control of foods, and a major exercise program. They too experienced
a major reduction in the
energy expended when physically active, a 40% decline.[12]
The 5-years later journal review article found that all but one of them
regained at least most of their lost weight--see. A longer period would have produced a bleaker
picture. A large 2015 UK population
study of the obese found that 99% of
long-term obese adults who lost significant weight that at the end of nine
years they were again obese or at best overweight. The UK data bank lacks information
on type of
diet, however, it did list those who had bariatric surgery and they were
excluded from the study. But given that
the KD is sufficiently popular in
the UK, on the face of it, it seems that long-term the Atkins’ maintenance
phase was poorly adhered to. So why did
the KDers fare long term?
The
KD advocates views
obesity as a problem with fat storage, and attempts to solve it long term by
forcing the body to metabolize fat. The
most popular of these is the New Atkins which calls for moderate
protein and uses net carbs
(table section 3) instead of total carbs.
It also calls for a lifetime maintenance phase of low carbs. Its limited
success is because of moderate
protein consumption. Eating foods with
protein causes the release of insulin through the incretin system of hormones.
As stated in the definitions Section 2 above:
“Incretin: class of
hormones secreted by the stomach and intestines which case insulin secretion
and satiety.” The release of insulin interferes with the
process of cleansing the liver and pancreas of fat. Even with significant
weight loss, those with
advanced T2D are still dependent
upon medications though less. Unfortunately,
KD also has a compliance issue: like
CER,
typically have over half the dieters quit before one year. Moreover both diets
for the long-term obese,
the diets aren’t sustainable. As stated
above in the CER paragraph above,
energy drops and quality of life declines typically about the 8th
week and this occurs with the KD. “Long-term
studies of the Atkins diet failed
to confirm the much hoped-for benefits” (Fung p. 102). The failure of both
diets to have sufficiently long periods of low insulin and thus to cleanse the
liver and pancreas of excess fat and permit these organs to heal, this is why
the leptin system for maintenance of fat kicks in to restore weight. In other
words they haven’t fixed the
lipogenic system where fat tissue releases leptin to restore the level of
fat. So how can the long-term obese and
overweight reset their weight regulatory system?
Fortunately,
there is a fix:
those who have used fasting in addition to low carbs have had remarkable
success. Though not a major player, it has in the 5 years increased and at
least in the UK gained the status of a fad diet because of Dr. Michael Mosley
of the BBC, his 5-2 fast. In Europe and Australia where BBC, ABC,
and
other networks have aired programs extolling fasting, and books there have a
greater share their market, more people have tried fasting. The results from
fasting are striking. Only fasting causes extended periods of low
insulin. During these periods the body
cleanses the liver and pancreas of excess fat and thereby cures IR and T2D which drives obesity.
For example, those with bariatric surgery have low insulin because they
are fed intravenously, and most of cured of type-2 diabetes within the first 2
weeks.
There
is no drop in metabolism thus weight loss is steady,
and the weight-regulatory system is reset.[13] Once the desired weight is obtain the patient
needs merely only to limit sugars and other refined carbs. There are a number
of different approaches
from modest food intake to total near restriction of caloric foods. The most
thoroughly research fasting diet is
that of alternate day fasting with near zero carbs and proteins, thus no rise
in insulin. Compared to CER and
low carbs, its prolonged
periods of low insulin make all the difference.[14] This type of diet will typically within
3
months result in the burning of fat in the liver and pancreas and thus cure IR
and T2D and causes the weight
regulatory system to eventually adjust to the lower weight. Proof is found in
the success of Intensive Dietary
Management—a medical clinic in Toronto Canada-- in curing both obesity and
T2D. The clinic uses low
carbs and fasting. Their success, success of others and the journal
literature is convincing short-term
or alternate day fasting is the best treatment for the obese and the
diabetic.[15] The clinic’s principle scholar is
Jason Fung, a nephrologist[16]. He sees end-stage diabetics, and with the
clinic’s fasting and diet program he is able to get them off their insulin
injections and other drugs to cure their diabetes while losing significant
weight. (On October 18 of 2016 The Complete
Guide to Fasting is
going to press by Jimmy Moor and Dr. Fung.
It probably will contain some figures on the success of his dietary
approach.) The merits of low carb with
alternate day fasting is not merely a theory like calories in and calories out
but one which has supporting clinical
trials and animal experiment—see the 2014 summation article, running 16 pages
with 8 more for reference by Metabolism and Diabetes Research Group of the
University of Surrey, UK, at. To make accessible confirmation of the above
claims, excerpts from this article are pasted at link and my review article on
fasting at.
9 Fasting is easy
and essential 10/23/16
What has gone wrong: It all starts with too much
of the very
reactive sugar fructose (net 15 times more than glucose), which damages the
live. The liver is part of the glucose regulatory
system and this damage causes insulin resistance. Because of insulin functions
to cause the
cells to take up glucose and burn it; it also causes those cells to stop
burning fat and to store it. With
insulin resistance, they require a higher than normal level of insulin to lower
the blood sugar, and thus they have a higher than normal rate of fat
storage. Those people are prone to
storing more fat than they burn. Over
90% of people with excess weight have what is called insulin
resistance, and its
consequence a fatty liver (NAFLD,
Non-Alcoholic Fatty Liver Disease).
Why fasting works: The fix is to
burn the excess fat in the liver (and if diabetic in the pancreas), and to
continue in the fat burning mode by fasting.
Without a signal from blood insulin, the cells throughout the body
switch to burning the stored fat, this is what occurs while sleeping. Staying
in fat burning longer by fasting allows
the liver to gradually ship-out and metabolized the excess fat it stored. Once
the liver heals by both lowering the
sugar in the diet and by eliminating the excess fat in the liver, the liver’s
contributions to the control and metabolism of glucose normalizes and insulin
resistance is cured. A healthy liver is
essential in the long-term fix of the weight regulatory system and thus being
able to lose weight and keep it off.
The use of fasting along with a low
carb diet reverses obesity and type-2 diabetes.
This fix has been growing in popularity, though food manufacturers and
pharma ignores this fix and gives us the wrong message, that of eat less and
exercise more. This doesn’t work for the
long-term overweight because their
weight-regulatory system has been reset to their current weight, and attempting
to lose weight only results in the yo-yo diet.
I have extensively research the topics of diet and fasting. With the
insights of this research I shall
use my experiences to illustrate why fasting with reduced carbs is the fix for
insulin resistance, NAFLD, and
excess fat.
My
Experience: I never had a protracted
weight problem. By logic I had used the
short-term fast when I gained 20 pounds during the winter of 1969-70. I was
in graduate school, philosophy,
University of Manitoba. At the age of 26
during the winter my metabolism slowed down, and so I didn’t burn off rapidly
the now excessive calories. I had
developed a fatty liver, and thus was putting on abdominal pounds. It took 3
months of reduced meals and
short-term fasting to lose the weight around my middle. It stayed off
because it was short-term
weight gain; my white adipose tissue through leptin had NOT reset my weight to
178 pounds.
After that, whenever I gained 5 pounds, I simply cut back on portions,
quit eating by 7 PM, and skipped breakfast several times a week. The second
change was exercise. I moved from Winnipeg to southern California
in 1974 and became in 1975 a sports addict.
I started regularly playing volleyball, cycling, and running, In
1980 I added moderate weight training
and singles racquetball. In 1993 my diet
changed for the worse: following the
lead of a very fit friend who both weight trained and ran 7 miles a day, I went
on a very low fat (thus high carb) Western diet. Fortunately I exercised daily
and watched my
weight; thus I never went more than 5 pounds above my slim weight. Skipping
breakfast, reducing portions, and
cutting back on sweets was an easy fix.
In
2012 I watched Prof. Lustig lecture on YouTube, which had gone viral.
He explained why sugar was poison and I took
notes. A year later, I researched his
explanation of the diabesity
pandemic (obesity and diabetes); he
presented the evidence on how excess fructose harmed the liver like alcohol and
was driving the diabesity pandemic. In
the spring of 2014, I reduced by 75% sugars including fruits. I also cut back
on carbs from grains about to
about 30% of calories; thus I increased saturated and monounsaturated fats to
replace those calories. It took about 4
months before candy, fruit juices, ice cream, and melons tasted way too
sweet. Though my weight remained for
decades the same, I had 3 pounds more around the lower abdomen than when
entered college in 1962. It was a sign
of a fatty liver, so I decided in March of 2016 to experiment with daily
short-term fasting. I still ate the rest of the day whatever I desired (my
carbs had been reduced a year before and replaced with saturated and
monounsaturated fats). By July of 2016,
4 months later, I lost 4 pounds, waist shrunk 1 inch, and fasting glucose (a
measure of IR) was 10% lower. I
noticed that by skipping breakfast, I had
reduced my total consumption of food. I
was less hungry especially at dinnertime and there was no decline in metabolism
with its negative affect upon physical activity and mood. The low-insulin diet
causes a lower level of
hormone leptin, a hormone which reduces metabolism and increases hunger—it is
the main cause of the yo-yo diet.
(Leptin produced by fat tissue, functions to restore fat to its normal
level.) A big plus was that I
experienced in the morning an increase in mental and physical energy; it is a
time when I do most of my studies and writing; and I avoided the decline
following breakfast.[17] I like the short-term
fasting.
One
advantage to the lower carbs is
that while in the fat burning mode the body increases metabolic rate about
10%. Secondly neurons releases the
catechol amines (adrenalin and noradrenalin, and dopamine) which cause stimulation
and mood elevation. This combination has
been inherited because of the survival advantage when food is short—more energy
for hunting and gathering. This is why I
now like skipping breakfast. Morning
fasting and not eating at night has convinced me that weight control with
short-term fasting is easy and pleasant, much easier than an energy-restricted
diet.[18]
Literature
on Fasting: Dr. Jason Chapter 20, “When to Eat” in his Obesity Code, 2016, p
235-251 covers the history and advantages of fasting; his opening
Sentences: “LONG-TERM DIETING is
futile. After the initial weight loss,
the dreaded plateau appears, followed by the even more dreaded weight regain.
The body reacts to weight loss by trying to return to its original body set
weight… Even if we eat all the right
things, our insulin levels stay elevated…. But we fail to address the other
problem insulin resistance.” The reason
for the major drop in metabolism--25 to 40% typically at 2 months on a calorie
restricted diet--is leptin[19] (regulated by insulin)
Leptin reducing the rate of metabolism has both
physical and emotional consequences:
inactivity and a general decline in psychic energy compounded by an
increase in boredom associated with inactivity.
lack of energy with its consequences on moody and activities. The obese dieter feels that if he
eat more he will have more energy to do things and be in a better mood. Very few of the long-term obese are
capable of going on a life-long energy restricted diet—there are numerous
long-term studies which show that these obese gain back most or all of their
lost weight.[20] “Only
fasting addresses insulin resistance.”
His clinical experience (over 1,000 patients) and extensive published research
proves that fasting is both easy and works—as too my own experience, and other
whom I have consoled.
From
Fung’s Obesity Code: I shall present
what I find of most value in that chapter, sometimes quoted and my additions
will be in [brackets]. IR causes
excess fat storage and leptin
promote reduced metabolism and increased appetite. [But it is not appetite/hunger
exactly,
rather the feeling that if I eat a bit more my energy and mental clarity will
return to what it ought to be; viz., I will feel better and be in a better mode
(this is the effect of leptin on energy)].
All foods promote the release of insulin; only not eating will keep
blood insulin level low—see insulin Index table section 3. As Fung points in other
chapters, incretin
hormone system responds to digestion in the stomach and small intestine by
stimulating the release of insulin from the pancreas [fats and fructose by far
produce the least response, insulin index of 10 and 17 respectively. Incretins
explains why meat, fish, and
poultry have a higher insulin index than boiled pasta. Though Fung writes of
24 to 36 hour fasting
as curing IR, his clinic also uses
the short-term fasting.] “The term
‘breakfast’ is the meal that breaks the fast—which we do daily”--p 237. Fasting has been used in most cultures and
religions, and our ancestral hunter-gatherer was forced by circumstance. Hippocrates
of Kos (c. 460-370) wrote;
“instead of using medicine, better fast today; to eat when you are sick is to
feed your illness” p 237. Humans like
most animals do not eat when sick. Plato
and Aristotle were staunch supporters of fasting. “The body does not burn
muscle until all fat
store is gone” p 240. “Blood glucose
levels remain normal as the body switches over to burning fat for energy. This
effect occurs with fasting periods as
short as twenty-four to thirty six hours.
Longer fasts reduce insulin even more dramatically…. Regular fasting has
been shown to significantly improve insulin sensitivity.[21] This finding is the missing
piece in the
weight-loss puzzle. Most diets don’t
address insulin resistance,” p240. One
of the most potent stimuli of [human] growth hormone {HGH] secretion during
fasting. Fasting promotes the use of fat
as fuel and preserves muscle mass and bone density. Adrenalin [and noradrenalin]
levels go up
with fasting,” p 241 they are the natural amphetamines that create alertness
and physical energy. “Breakdown of
muscle tissue happens only at extremely low levels of body fat—approximately 4
percent,” p 242. “The human body has
evolved to survive episodic periods of starvation,” p 243. “Caloric
restriction diets do not allow the
evolved adaptation that occurs during fasting,” p 244. We have also like all
mammals have evolved a system to return to our normal weight when weight has
been lost through increased hunger and reduced rate of metabolism. Its main
regulatory hormone is leptin that is
produced by the adipose (fat) tissue.
“Studies of eating a single meal per day found significantly more fat
loss, compared to eating three meals per day, despite the same caloric intake”
243[22]. “Total energy
expenditure is increased during
a fast—in a 4-day fast by 12%,” p244.
“In our clinic, experience showed that appetite decreased as duration of
fasting increased. The most astonishing
aspect of this study [107 obese subjects unable to lose weight] was the ease
with which prolonged starvation was tolerated.
These experiences echoes our own clinical experience at the Intensive
Dietary Management Clinic with hundreds of patients,” p245. The more dangerous
visceral fat is
preferentially removed with fasting.
There is reference to Dr. Michael Mosley (British on BBC) 5:2 diet, 5
days of full caloric and 2 days of 25% of calories at the end of a short-term
fast. In the trial that compared the 5:2
to the Mediterranean diet with a 25% reduction in calories. At 6 months both
groups lost about the same amount
of weight, but the 5:2 group have lower insulin and less IR, at p247. This change
(though not measured) indicates that
excess liver fat had been metabolism.
The short term fasting made this important difference. For
the long-term overweight fasting reverses insulin and leptin resistance, thus
it is essential, and it is used by Dr. Fung to cure type-2 diabetes.
For
those who want to know more of the science behind fasting, I highly recommend
that you read my “Evidence of Alternate Day Fasting—Cures
Type-2 Diabetes” and Fung’s book The
Complete Guide to Fasting. On P.
204 he states that, “A major advantage of the sixteen-hour fast is that it is
fairly simple to incorporate into everyday life.” The graph on page 202
indicates the amount
and duration of the traditional 12 hour fast (7 pm to 7 AM) the 16-hour fast
and the 20 hour fast (3, 2, and 1 meals respectively as to the extent of fat
metabolism, and fat storage when eating.
My own experience and others whom I have counseled has convinced me that
short-term fasting is easy, and the scientific literature confirms that longer
periods are also easy; this is because our body has evolved a system to burn
the fat reserve and to keep us alert and full of energy so that we more likely
to hunt and gather foods. And as Fung
states, “it has a high rate of compliance.”
10. Why some don’t get fat --
11/9/16
A variety of factors work to reduce the probability of
developing a fatty liver, the starting point for IR and its comorbidities. It
is the combination of fructose and glucose (especially form both sucrose and
high glycemic index foods (thus refined carbs and other easily digestible carbs
such as potatoes). The sugar fructose is
the starting point thus eating a low sugar diet. High insulin level driven by
high carbs
drives liver fat storage. The
traditional Chinese diet though high in white rice (which is comparable to
white bread) had little effect. Experiments
have come to the same: feeding volunteers either a high level of
fructose are glucose, only the fructose cohort developed IR.
A flawed knowledge of the processes and poor recollection
makes self-analysis of limited value.
Often the year in which a fatty liver has developed is unknown but
surmised based on a gradual gain of weight; however, it is possible that the
condition had developed years before, but based on a variety of factors listed
below weight gain was minimal.
Genetics
of course make a difference, but not that
much. One authority placed it at
5%. A major cause is learnt behavior
from family, from community, from media.
Another cause for obesity is the prenatal environment. A fetus is exposed
to high level of blood
glucose will develop more insulin-secreting cells “and the more insulin the
child will secret as it get close to birth.
The baby will now be born with more fat and will become insulin
resistant as it ages,” Taubes, supra 132.
The dramatic increase in early childhood obesity, as referred to by Dr.
Lustig, is a striking result of unhealthy womb environment and the high sugar
diet. Thus what seems to be an inherited
trait is in fact due to the womb environment and the western diet. For 98% of
the obese social factors and the
western diet play a much greater role. A
classic review article on Obesity in Scientific American pointed out that while the American Pima Indians of
Arizona have the world’s highest rate of diabetes and obesity[23], those on the
Mexican side of the boarder have a very low rate. Since each are from the same
genetic pool—104
years of separation, statehood was granted Arizona in 1912—evolution cannot
have created that great a difference. “The
diversion of the water and the introduction of non-native diet had devastating
effects on the health of the people as well”—Wiki. ‘The genes caused
obesity and diabetes’ is simplification that
hides the causes, similar to that of the weak will.
Various
common ways to avoid the health disaster caused by IR while
eating a Western diet (in approximate order of importance):
Tight weight control and
not
allowing significant weight of more than 15% above thin body weight to be
carried for years (the longer the weight is on the less likely that an energy-restricted
diet will keep that weight long-term off)
Mini-fasting when dieting,
or
alternate day fasting.
Yielding
to peer-pressure to be fit and trim
Regular exercise or strenuous
lifestyle
Multiple day fasting at least
twice
a year
Daily average of less than 40 grams for male (30 grams
for a woman) of sucrose for an active average size person
Avoiding
regular consumption of high-carb alcoholic
beverages such as beer, since glucose competes with ethanol for metabolism in
the liver, thereby increasing damage to the liver by slowing the clearance of
toxic ethanol.
Major
seasonal change in fructose and carb consumption
Having
good muscle tone
Avoiding
drugs with sedative effects (drowsiness,
increasing sleeping, muscle relaxation), thus avoiding nearly all psychotropic
drugs, some hypertension drugs, high doses antihistamines, SSRIs, and other
drugs that inhibit the functions of neural transmitters. Even when weight gain
is not listed as a side
effect, often it is.
For
seniors, natural hormone replacement therapy in
sufficient dose (see my articles on testosterone and estrogen).
Getting
more than 40% of calories from fats
High
ratio of saturated fats to unsaturated fats which
become rancid in the body (see Part 4 Fats for complex reasons)
Eating a high ratio of natural foods to manufactured
foods thus limiting the sugar added foods.
Major
seasonal change in fructose consumption
Limiting
the exposure to unnatural chemicals including
drugs, food additives, pesticides, hormone mimics, and other sources such as
cosmetics.
Aspirin
325 mg or greater per day, it lowers serum glucose—see
1950 Merck Manual, and Aspirin, under
“diabetes”.
Genetics, some are more prone, others more resistant.
Probably a significant causes in about 15% of those obese.
The
lack of sex hormones has been
shown to play a significant role in weight gain. Estradiol (the best of 4 estrogens)
controls fat distribution, which is visually obvious as a girl develops during
teen years. Lack of estrogen cause women
to gain abdominal weight following menopause and she loses muscle because her
testosterone drops.[24] The two sex hormones
are structurally
identical, but for one functional group.
Testosterone makes a different for men past the age of 60 when they do
sufficient amount to restore them to a youthful level, which is what I
did. I started in 2004 with natural testosterone[25] from a compounding
pharmacy. It made my weight control
easy. I stopped weighing myself once I
realized that my weight-regulatory system kept me between 161 and 166. Only
with fasting did drop to between 155-161
pounds.
Until 2013 I ate a high carb diet, low fat diet, I avoided the weight
gain by doing the most of the above.
11. Myth
busters -- (trashing tobacco corporate science)[26]
High serum cholesterol causes CVD.
TRUTH: High serum cholesterol
has not been demonstrated to be a
cause of plaque formation. CVD’s
main cause is infective agents within artery
walls which damage LDL with toxins and cause an immune response by macrophages
that cause atherogenesis. The cholesterol deposits in the artery walls
are a byproduct of the immune response, as too are calcium crystals, foam
cells, triglycerides, and lymphocytes.
Cholesterol is a bystander not a cause; thus lowering its production
with drugs does not prevent AS or
heart attack. Autopsy studies found no
relationship between serum cholesterol and degree of AS in those died violent
deaths, see. The Australian Broadcast Corporation has a
documentary which exposes this myth, at and one on the statin scam. Avoid saturated fats because they cause CVD
by raising the serum level of
small-dense LDL which is associated with CVD.
TRUTH: Saturated fats don’t
raise cholesterol levels
or small-dense LDL. And LDL level is not
associated with CVD (see #1). A meta-analysis of 21
studies on saturated fats, “failed to find an association with CVD, Wiki,
and also Wiki. This extends to
all types of fats when “increased from 30 to 50% of total energy,” 2004.
Moreover, those on an Atkins type KD,
their so-called “bad” LDL drops and the “good” HDL rises. Vegetable oils are preferred to saturated fats
(main source animals). TRUTH:
Vegetable oils are associated with diseases because they are high in
polyunsaturated fats that become rancid
in the body, when cooking, and on the shelf--link. Since this process of oxidation changes the
shape of the molecule and they are incorporated in cell membranes, they
adversely affect the functions of these membranes. Like trans-fats (also of
unnatural shapes)
the consequences are disease promoting.
Second, polyunsaturated fats are high in omega-6 fatty acid which blocks conversion
of omega 3 oils an
anti-inflammatory agent. Our
Paleolithic ancestor averaged 2 parts omega-6 to 1 omega-3; today it’s 16 to
1. Many people wisely take a fish-oil
supplement to improve the ratio of omega-3.
Because of its effect on the immune system and rancidification vegetable
oils promote CVD, arthritis, and
Alzheimer’s disease. The more expensive
animal fats are the best source of fat followed by the palm kernel, coconut, and olive oils which are
high in monounsaturated
fats.
There are hundreds of journal articles going back 6 decades on this
process, use scholar.google to find
them. Sugar (the disaccharide sucrose is fructose and
glucose), fruit sugar (fructose), and starches (long chains of glucose) are
merely empty calories without nutritive value; viz. harmless sources of energy.
A calorie is a calorie. TRUTH:
sugars and starches (pure glucose) damage tissues. Fructose and glucose
randomly bind to proteins
(in a process called “glycation”) to damages proteins in your
cells. Thus glycation promotes
the degenerative conditions associated with old
age: CVD, atherosclerosis,
Alzheimer’s, macular degeneration, et
al. Fructose (fruit sugar and ½ of
sucrose) has a glycation rate of 7.5 times that of glucose; actual 15 times
because of its slower clearance compared to glucose; moreover, most of the
glycation occurs in the liver where it is stored prior to metabolism
there. Since 90% of fructose goes
to the liver for metabolism, the damage there through glycation is
significant. Some of the fructose is
converted in the liver to fat[27]
which can accumulate because of the Western diet with its high carbs. Damage
from glycation and fat accumulation in
the liver causes IR and a fatty
liver called non-alcoholic
fatty liver disease (NAFLD). NAFLD affect over 30%
of the US adult
population (NHANES II study). NAFLD
affects the plasma-glucose
regulatory function of the liver to cause IR.
Fructose by causing minimal insulin response, it bypasses the appetite
regulating system involving leptin and ghrelin which reduces it affect upon the
satiation system of the hippocampus to
cause weight gain. Finally, fructose
stimulates the addiction center of the
brain (see #6 below) to promote sugar addiction. Clearly, sugars are not
harmless empty
calories, nor are starches with high insulin index, and fructose is the worse. The cause of obesity is a sedentary lifestyle
& gluttony. All one needs to do is
eat less and exercise more; viz., burn more calories than one consumes; this is
the common advice given by doctors, dieticians, and accepted as the way to lose
weight. TRUTH: For all mammals
their weight is controlled by
a biological system. The Western diet
with its average of 180 grams of sugars daily causes a fatty liver and IR. Fatty
liver and IR muck up the regulatory
system and thus cause obesity. It
is not gluttony and sloth that causes the
obesity and diabetes pandemics (blaming the victims) but rather the Western
diet which is promoted by food manufacturers and corporatist governments. For the obese, a 25% reduction
or more in
calories will result in significant long-term weight loss. Truth The weight regulatory system in an effort to
maintain the set weight will reduce the rate of metabolism approximately 25%
and increase hunger. Even those he get
past this barrier which occurs typically around the end of the 2nd
month, they will once off the diet regain the weigh (yo-yo diet). The hormone
leptin intercedes to decrease
metabolism, typically 25% and at the same time increases appetite. It is secreted
by adipose (fat) tissue to
main the normal level of fat storage.
Less than 1% of long-term
obese adults at the end of nine years will obtain normal body weight
through diet. To prevent this regain of
weight, the regulatory system must be reset, and this occurs by fasting and
going on a low carb diet. Fasting will
avoid the 2-month drop in metabolism.
This type of diet will eventually result in the burning of fat in the
liver and pancreas and thus cure IR and T2D and permit the weight regulatory
system to eventually adjust to the lower weight. Hormone replacement (HRT) will not promote
weight loss. TRUTH: Estradiol among
other things regulates fat distribution[28]
and plays a role in physical well-being.
During and following menopause women experience a precipitous drop in
estradiol (the most healthful and active of the 4 human estrogens). The common
post-menopausal reduction in
physical activity and associated rate of metabolism contributes to weight gain
and abdominal fat. “Natural
HRT [estradiol plus progesterone] reduces
insulin resistance and fasting glucose in women with diabetes” at. Since some of estradiol is converted to
testosterone NHRT prevents muscle loss with aging, another contributing factor
to weight gain. Men too following
andropause experience a reduction in muscle mass and metabolism. And the heart
as a muscle gets weaker. HRT for men and women poses major health risks
which outweigh their benefits. TRUTH:
natural hormones lower risk for breast and prostate
cancers. Men in the highest 20% for
testosterone have the
lowest rate of prostate cancer and heart attacks. Estradiol moderately lowers the rate of breast
cancer. In sufficient dose NHRT
will reset the biological clock to a
younger age and thereby significantly reduce the risk of most age-related
chronic diseases. Estradiol with progesterone
lowers CVD, Alzheimer’s, cancers,
and much more. Testosterone decreases the risk of heart attack and
cancers. Current wisdom is based on
pharma’s junk science & tobacco
ethics: clinical trials that
knowingly used the worst formulate of HRT for women, Prempro. Read the section on the WHI study
which exposes pharma’s and NIH’s tobacco science and ethics. NHRT
is good for people and thus bad for
pharma. Three lies about type-2 diabetes: a life-long
progressive condition; it can’t be cured; and is best managed with drugs that
lower blood glucose to normal level. TRUTH:
that once the excess fat stored
in the pancreas is cleansed T2D is cured (at the same time the excess fat in
the liver is cleansed). Bariatric
surgery reverses often within a month T2D by post operation fasting proves that
it can be cured and that fasting is the cure.
Dr. Janson
Fung’s dietary treatment of KD
(low carb
high fat) with alternate-day fasting cures T2D for
most within 6 months. Diet is the
cure. Moreover the cohort who
has their glucose
tightly controlled has a higher mortality rate in clinical trials. Pharma is highly regulated by the FD A to
protect the public from the tobacco
ethics used by corporations to fulfill their fiduciary duties. Truth: that there is a revolving door between the
FDA and pharma, and that at the highest levels the FDA is ran by executives
from pharma and their KOLs. For
a summation of the ways in which the evidence
base has been broken—link, or YouTube Dr. Angell. Our corporatist government enacted the
Prescription Drug User Fee Act of 1992 to make the FDA dependent upon pharma
for over half of its budget. Congress
wants the FDA to serve the pharmaceutical industry. Link to Consumer Report on the FDA. Read Prof. Ben Goldacre’s Bad
Pharma. Doctors know what is best for patients. Truth: the education and sources of doctors’
information has been manipulated by pharma so as to turn them into drug
pushers. Pharma runs and owns the
results of clinical trials, thus positive bias is the norm--32%. Pharma determines who becomes a KOLs (Key
Opinion Leaders). They are the lead
authors on clinical trials, write the medical textbooks, and give continuing
education classes. The information foundation
is thus distorted. For an insightful
explanation of how this has occurred click on link—you need to know. Pharma
and
food manufacturers through junk tobacco science, corporate media, and misinformed
doctors cause cognitive
dissonance and reliance on their KOLs by both the public and
physicians. Pharma has framed the
discussions to promote the sales of patented drugs, and food manufacturers to
promote the obesity and diabetes pandemics.
What has been said about pharma applies to the manufactured food and
tobacco industries—profits before people.
There is a struggle going by leading men in the medical field who have
broken rank over the corruption worked by pharma, but you won’t squarely hear
of it in our corporate media. But you
can watch them on YouTube
& read their journal articles.
12 Pathogens in artery walls is the main
cause of CVD
The tobacco-science
based claim that
saturated fats and cholesterol cause CVD;
this has been decisively refuted by scientific
evidence: “Atherosclerosis (AS)
is now recognised as a chronic
inflammatory disease occurring within the artery wall and ultimately
responsible for myocardial infarction, stroke & peripheral vascular disease.”
“There are approximately ten times as many bacterial
cells in
the human flora as there are
human cells in the body”, Wiki, Not surprisingly some of them are in the
interior of the artery walls, the tunica
intima. The inflammatory process starts with white
blood cells attempting to eliminate certain bacteria. They produce an inflammation
in response to
the virus and
bacteria colonies within the
artery walls. A typical study found Chlamydia
pneumonia in those with
CVD 79% vs 4% without CVD in coronary
artery specimens. LDL functioning as part of the immune system
absorb the toxic chemicals produced aby these pathogens. The “monocytes replenish
resident macrophages” (a scavenger white-blood cell) that dispose of the
products of the LDL’s immune response--see. Thus pathogens
damage to LDL is part of the process leading to the development of CVD; not high
blood cholesterol and high
fat diet which are bystanders found within the LDL. Lesser contributing factors include oxidation & glycation (sugar
bonding)
which damaging endothelial cells lining the coronary artery
walls. Pharma wants us to believe that
the inflammation response is to oxidized LDL in the artery walls. Wrong again,
the contents of LDL is cholesterol
and triglycerides which the body needs to grow new cells to promote healing in
the artery wall and to replace damage white bloods cells both of which have
been damaged by the pathogens. This
explains cogently why atherosclerosis is brought on by an inflammation
response. Pharma says this response is a
result of damage to the LDL in the inner layer of the artery; no mention of
pathogens. Pharma has ignored a century of artopsy studies of those who died
from a heart attack; these studies find pathogens. But pharma makes billions
treating hypercholesterolemia--see. Then they make billions more hypertension and heart attacks—but not
the pathogens that cause AS. Prevention
is not in their business model.
Moreover pharma is very good at marketing--see how. The scientists who are critics of pharma’s
junk science are ignored by corporate media.
Physicians hear pharma’s key opinion leaders (KOLs) at the required
continuing education classes funded by
pharma. Having said this, my concern here
is with diet’s role of insulin
resistance (IR) in obesity, fatty
liver disease, diabetes, age-related diseases, and CVD; and also about healthful
choices. Sugars through glycation damage the
endothelia cells which line the artery walls, and so damage they increase the
risk for pathogens colonizing the inner layer of the arteries—2 links see and more.
LDL is a
lipoprotein-phospholipid wrapped sphere containing
about 1500 cholesterol molecules and
3,000 to 6,000 fat molecules
including triglycerides, see
illustration. Cholesterol has several essential functions including forming the cell walls, neurons
coating, and its conversion into the sex hormones. The liver produces
cholesterol--about 70%--and sends it wrapped inside LDL through the blood to
cells in need of fats & cholesterol.
Inhibiting the synthesis of cholesterol with a statin
drug has many
side effects, and it doesn’t
prevent CVD. Numerous books and
documentaries expose the
cholesterol myth & statin horrors.
But pharma in the production and dissemination of information frames the
debate; thus only those who de-nova examine the journal evidence and adjust for
their tobacco science can come to the best evidence based answers.
13.
Other cofactors for CVD
Pathogens
play the key role in the formation of atheroma leading to AS and CVD. However, excesses in reactive blood-borne
chemicals including simple sugars (especially fructose) are contributory. Their
main pathological mechanism is through endothelial
dysfunction. Endothelial cells
function as a single layer membrane that lines all the blood vessels and act as
the gatekeeper. These cells have
receptors which allow certain chemicals to pass through. Lymphocytes, for example
have a compound
which counters adhesiveness that join the endothelial cells together to form a
membrane, thus lymphocytes can slip between them. Various chemicals and foods
adversely affect
the function of endothelial cells as gatekeepers.[29]
Trans-fats and rancid polyunsaturated
fats are statistically associated with CVD.
The abnormal shape of these fats is cause
functional issues when they are included in cell membranes. For example,
transfats induce platelet aggregation, .… inhibit activities of Na+
, K+-ATPase and adenylate cyclase and reduce density of
B-adrenergic receptors in rat heart membranes [raise blood pressure]…. Recent
evidence indicates that trans-fats promote
inflammation…. Increased tumor necrosis factor (TNF) system, levels of
interleukin-6 and C-reactive protein…. Several studies suggest that trans-fats
cause endothelial dysfunction” in the 1984 thorough review by the Department of Agriculture. Similar affects occur with
polyunsaturated
fats which are in vivo subject to oxidation.
In addition the high ration of omega-6 to omega-3 fatty acids has been
shown to be atherogenic. Similar
association with CVD is associated
with a diet high in fructose (but not other carbs).[30]
Hyperinsulinemia, IR, NAFLD, T2D[31] are contributory to endothelial
dysfunction. Like so much that goes on
in the body, the causal mechanisms of these condition in the development of
endothelia dysfunction is complex and thus process leading to pathology are
tentative. The associations with sugars,
smoking, trans and polyunsaturated fats to endothelia dysfunction and CVD are
firmly established. These are the main culprits explaining strong
association of CVD to the Western
diet, they all promote endothelia dysfunction.
So what about
the standard
explanation for atherogenesis? Pharma’s
case for LDL undergoing oxidative damage from metabolites within the tunica
intima, and this being the most principle cause of CVD, this is suspect.
Suspect because it ignores pathogens, suspect because it ignores the
immune role of LDL, suspect because it fails to explain cogently why LDL is
actively transported in large numbers through the epithelial cells into the
tunica intima; and downright misleading because it uses the dual meaning of
“oxidative” to imply that the products of metabolism is causing the oxidative
damage to LDL while in fact it is the toxins that are latching onto the
external protein shell of LDL. Their
explanation fails to explain why there is LDL in the intima medial, and to
explain cogently why the immune system is involved in the process. Pharma’s
KOLs state that the lymphocytes and
macrophages are there to clean up the oxidized LDL—no mention of pathogens. The
debris of this process results from the macrophages engulfing large numbers of
the oxidized LDL and resultantly undergoing apoptosis that results in the
formation of plaque. Are we to believe
in an atypical process involving pathogens, or to think the worse of pharma? Given
pharma’s repeated examples of tobacco
science being generated by pharma to promote profits, the plausible conclusion
is that this is one more example of bad conduct by pharma. Pharma has already
been proven to have
generated the cholesterol and triglyceride myth (see Cholesterol Myth and 2nd
article) and to support it pharma
has created a factitious modus operandi.
Given the totality of evidence, the healthful choice is to ignore the
recommendations of pharma’s KOLs and those, whom they have educated, the majority
of physicians.
14.
How Did We Get Here--Historical
The prima facie evidence is
that the diet adopted by the FDA and Department of Agriculture in the 1977
brought on the health pandemics. The
switch to low fat, low cholesterol, which entails higher carbs, just so
happened to favor the products of the food manufactures and the cholesterol
lowering drugs of pharma. In 1977 our
government, and later those around the world, ignored over 60 years of dietary science
and switched its position as to what is heart healthy. Based on weak evidence,
high serum
cholesterol and triglycerides (3-fat
molecules joined to 1-glycerol molecule)
were accused of being the leading cause
of CVD.
Somehow the Senate panels
(McGovern Commission) and their experts on CVD
missed cigarettes which at a pack a day doubles the deaths from heart attacks. The
Surgeon General only warned about lung cancer and emphysema in The
1964 Report on
Smoking and Health. Over three times as many deaths are caused by tobacco induced heart attacks and strokes than from
lung cancer and emphysema, yet the Surgeon General missed it and a large body
of journal literature going back to the turn of the century. Dr.
Kellogg, of cereal fame, published in 1922
a 171 page concise compendium on the published research on tobacco’s known
health consequences, including its destructive action on blood vessels, at. Kellogg’s book has hundreds of scientific
citations. In 1965, 42% of the adult population smoked, yet the McGovern Commissioned missed
tobacco. So why was the evidence on
tobacco distorted by the Surgeon in 1964 and ignored by our government in 1977,
and why were saturated fats and cholesterol blamed?
Simply
follow the dollars. Once you realize that serving
the public is cloak worn by our corporatist state, than it
makes sense, and when we review the details we find that this is standard
operating procedure: serve big dollars
while advertising serving the public.
This method explains why our government fingered tobacco for lung
cancer, but missed the much bigger killer from CVD:
they were doing
damage control for tobacco. The connection with lung cancer was too
obvious, and too well known. The Surgeon
General had done damage control dressed as science in the public’s
interest. So why finger cholesterol and
saturated fats? Animal (saturated) fats
cost twice that of vegetable oils; and sugars and refined starches are cheap
and addictive. And most of the products
made by food manufacturers are loaded with refined carbs including sugars. Moreover,
pharma doesn’t have drugs to treat
the pathogens living inside the artery walls which are the principle
cause of AS and CVD, but with
drugs they could modestly lower cholesterol and triglycerides in 1977.[32] Thus pharma
was by 1972 (and before) promoting hyperlipidemia and hypertension as causes
for CVD and MI. For example in the 1972,
12th
edition of Merck Manual p.374 recommends restrict fats to 30-40 gm/day
to lower CVD risk. And the role
of pharma gets more
insidious. If the patient believes X is
a risk factor and he tries a cheap fix that must fail, then he is likely to go
back to his physician and try patented drugs to fix X. This is a standard business
practice for
pharma. Diet does not significantly
lower cholesterol, because the liver makes cholesterol to serve vital
needs. Only about 30% is from diet,
lower it and the liver makes more on a need basis. Moreover, saturated fats
don’t raise
cholesterol or cause CVD--see Dr. Miller’s lecture. Thus the low fat and low cholesterol diet
fails, so the patient with elevate cholesterol and/or CVD then tries drugs. This
plus the food manufacturers favor their high sugar and starch products over eggs,
meats, poultry, and fish, because these foods are a very small part of their
product line. Secondly the vegetable
oils are about half the price of animal fats.
The McGovern Committee and the US Department of Agriculture followed the
bucks.[33] The
government’s inaction and at times support for tobacco[34] that permits harm from cigarettes is one more
example of the power of tobacco (dollar) ethics in a pseudo-democracy, our
corporatist state. The science behind
healthy diet was turned upside down by big money and we have a health epidemic.
15. Free will won’t, rational control of
behavior will
On
how to deal with food addiction
which seems to trump rational control?
In 1985 applying the standard behavioral analysis for dieting: I set
down various types of behavior that
would result in weight loss including food selection. Small portions, peer support,
visualization, etc. I held that thoughts
(silent whispers) are merely epiphenomenon that accompanies behavior like a
shadow. Eloquent proof came 2 decades
later; one was an experiment that was published in American Scientist (2004, Free Will, Free Won’t).
Electroencephalography was used to measure brain activity and a button
was pressed by the participant to indicate when the thought occurred. The deep
brain activity occurred a half-second
before the thought of his arm movement.
The thought of the action came after preparatory subconscious neural
activity, like the thunder following lightening. Neurological science has since
established that thoughts are generated by deep brain processes and accompany
an action like a shadow. To begin with neuroscience has demonstrated
that the brain is modular, each of the hundreds of sections has a specific
function. One of these modules functions
to create an image of man as being guided by thought.[35]
But rather in the verbal sections of the brain is not aware of what goes
on in the motor sections of the cerebellum which acts as a traffic cop
coordinating behavior. In other words the
brain has hundreds of specialized modules I call the analytic portions (AP) that function to produce verbal behavior
including thoughts. Thoughts has been by
B.F. Skinner labeled as silent whispers. Consider the behavior process similar to
vector algebra (see graphs above on website) where several different forces are acting
simultaneously on an object at a point, the result of which will be movement of
the object in only one direction. The
deep brain operates according to the diverse force to produce behavior,
sometimes contrary to the input from AP.
For diet, based on a complex collection of
evidence, the AP has determined that
sugars and starches need to be avoided.
At home the AP opposes the
eating of refined carbs and sugars, but its contribution to eating choices
isn’t sufficient to consistently throughout the day bypass the grapes and
candies. Thus I must influence the
arrows of forces in my brain so that at home there aren’t foods high in refined
starches and sugars. The explanation
from behavioral psychology: the closer
in time and space to a reinforcer, the greater is the probability that it will
affect behavior. The AP plots that
I need to stock the
kitchen with items that aren’t high in refined carbs and high sugars. I
also enlisted my wife to use social
reinforcers such as praise and she too has changed her diet. We watch the video
Sugar White Poison and other like videos every
week. The AP has set out a program
by which I can change my eating behavior
life-long. Moreover, given my extensive
education and application of academic skills, my AP is stronger than the norm.
If it were true that the will (mind,
AP) could decide independent of the
deep brain process, then there wouldn’t be smokers, drunks, and an obesity
epidemic, and certainly there wouldn’t be so many morbidly obese (about 10%
with a body mass index, BMI, over 40).
Today I saw a women under the age of 30 whose weight forced her to rely
upon a wheel chair. Does she have a
defect in her will (mind)? Or is it a
confluence of genes coupled with dietary causes that have reset her normal
weight to a BMI of over 50? She can
think of losing weight, swear that she will, go on a diet, but the deep brain
is committed to 400 lbs. and gaining.
The low fat, low calories diet is not her long-term answer. A bariatric
operation is one way, but her
stomach will expand sufficiently to accompany many small meals and about half
will regain most of their former weight—as two of my friends have done over a
period of 6 years. The wrong expert
information spread by doctors and the media has the AP applying a low fat diet
with more exercise as the healthful
program, and they gained back their weight.
16
Outline on metabolic
dysfunction
This
page 6/9/16, is on http://healthfully.org/rc/id23.html
All
mammals have a complex regulatory system for appetite, rate of metabolism, and
fat storage. There are over eighty
hormones involved in the system. The
Western diet is high carbs fructose and glucose that causes a fatty liver (NAFLD)
which mucks up the regulatory systems leading to the IR that causes obesity,
T2D, CVD, etc. Glucose raises insulin
level, and insulin causes cells to STORE FAT and
burn glucose. IR
causes excess fat storage. Causes: The
carb fructose--a simple sugar--goes
to the liver where some is converted to fat, and when insulin is high this fat
is stored in the liver. The low fat,
thus high-sugar, high-carb Western diet will for most cause excess fat storage
in the liver. Gradual over the
years/decades 2 to 3 pounds of fat is stored in the liver (NAFLD). This causes IR first in the liver then in other tissues. IR mucks-up
the complex metabolic systems. With IR
comes a gradual gain in weight. If you
have T2D then you have excess fat in the pancreas, and your beta cells no
longer produce sufficient insulin to manage your glucose. When on an energy-restricted
diet the fat
tissue through the 4 hormone it produces functions to maintain current weight
by increasing appetite and reducing metabolism.
Even after losing weight, the system works to restore the fat—the yo-yo
diet. Goals: to stay in fat
burning (low insulin) mode and thus to metabolize the excess fat in the liver
and pancreas to reverse IR and T2D. Once
fatty liver & IR are cured than carbs can be moderately increased and weight
will
still be lost. Once ideal weight is
obtained remain on moderate
carb-sugar diet. Follow the dollars and
you will find out why we have the Western diet and the wrong advice—click on link for a list of the
misinformation, and much more.
Fix: Short-term fasting with low carb diet to
stay in fat burning to cleanse the liver and cure NAFLD & IR.
Fructose converted to fat in
the liver and high glucose via
insulin causes fat storage in liver (a 1-2 punch)
Fatty liver >>>>
IR in liver >>>> IR
in muscle and fat tissues
>>>> IR causes abnormal
high insulin >>>> excess fat storage
T2D can be cured with diet. For
example in the first 2-weeks following bariatric
surgery over 80% with T2D are cured
before major weight loss. With very low
carb diet and alternate day-fasting the cure takes from 2-6
months.
Simple fix: it starts with supermarket.
For B) & C) just
buy wholesome, very low net-carb foods (on food label, carbs
minus fiber) with low glycemic (table). The goal is to stay in the fat burning
mode
by not eating easily digestible carbs.
17.
Review and recommendations
Glycation cause tissue
damage especially in the liver from fructose which leads to IR, fatty liver, &
chronic age-related
conditions. High blood glucose
causes a 2-hour spike in insulin contributes to IR and NAFLD. The
Western diet with its combination of sugars and refined carbs causes obesity. Fructose,
one-half of sucrose, is the worse
sugar (see #4 above). The traditional
Japanese diet is high in carbs but has almost no sugar (15 gm, compared to U.S. 162 gm daily average). Their
carbs from white rice are slowly
absorbed because of the large portion of vegetables (fiber) in their meals, and
they have a low (healthful) omega-6-to-3
ratio. The Western diet is also high in polyunsaturated
fats, another bad thing. Their obesity,
diabetes, and CVD rates are very low
for those following a traditional diet, though many smoke. The Western high
sugar-starches diet is a
deadly combo that eventually upset the mechanism that controls appetite,
metabolism, and fat storage, and it creates a craving for sweets and other
carbs.
Size of portion, rate
of absorption, and the amount of exercise
prior to and subsequently,
these determine the blood sugar
and insulin levels. Avoid large meals
and
refined carbs to keep insulin low. Eat
frequent-wholesome snacks. Increase
fiber, protein, and the good fats because they delay clearance from the
stomach of the carbs; thereby reducing the spike in both glucose and insulin. Low
insulin is for fat burning; low sugar for
healthy liver. Check nutrition labels
for the percentage and grams of sugar.
Four grams of sugar equals one teaspoon of sugar. Avoid manufactured
foods with their refined
carbs, added sugar, and polyunsaturated fats. The cure is to go on a very strict low-sugar-low-carb diet (20% of
calories from carbs) with small portion (thus low insulin), and also include
JK’s 16 hour short fast. Select
the appropriated diet program in
Section #2. You should take better care
of your body than your car!
Besides diet, exercise and physical
activity contribute to controlling weight and remaining healthy. In addition
there are supplements and drugs
that reduce damage from reactive chemical.
Best are Aspirin, CoQ10, vitamin
C, &
omega-3 fatty acids fish oil—in that order.
Aspirin 325 mg has
an assortment of health benefits including reducing the risk of most
cancers over 30% by
enhancing the action of our body’s system for the destruction of abnormal
cells, and aspirin also inhibits the development
of AS. Natural
hormone replacement therapy (NHRT) for women and elderly men testosterone in sufficient dose is highly recommended. These hormones promote weight
control and the
motivation to be physically active. Go
to their links above for the best usage and their benefits, and you will
understand why pharma has with junk science opposed their usage. For more info,
there are links to statins, cholesterol
myth, CVD, carbs, fats, and a video
library. The video
page has links
to documentaries and books confirm my claims.
Watch on YouTube CBC
on sugar and Australian
Broadcast corp. I Google Chromecast the
documentaries to my television which has a stereo connected. The recommended
healthfully section
has over 1,000 pages involving
over 10,000 hours of research and studies of subjects, and counting. To check
my research, the articles I wrote have links to medical journals, and a number
of their articles are pasted on the website.
The site covers a number of family of drugs, diet, and some very
healthful drugs that pharma opposes. The
research exposes a very flawed corporate information system; on point are Marketing
Science and Junk
treatments. The global corporate
profits-first system produces perverse results including regulatory capture. Pharma,
alcohol, tobacco, manufactured-food,
and GMO companies such as Monsanto, cause the greatest harm. Knowledge is the
starting point to better
health. You should take better care of
your body than your
18.
Videos & books On diet, bad pharma, and CVD
The
page is at http://healthfully.org/rc/id22.html,
rg/4, and rh/id7 for the complete, current
collection
Videos are
the best method for teaching and reinforcing the lessons within this
article. I have collected with
summations a list of over 130 videos on health related topics, the largest
section is on diet. Please view them.
For a
list of books on diet, bad pharma, and related topics click on link. You
should take better care of your health than your car.
[1]
“f
the human body relied on carbohydrates to store energy, then a person would
need to carry 31 kg (67.5 lb) of
hydrated glycogen to have the energy equivalent to 4.5 kg (10 lb) of fat” Wiki.
[2] It is not just the race of Mongoloids,
for a
number of tribal societies consume a high-carb diet without Western consequences.
[3]
In 2000 the USDA placed added sugar at 152 lbs/year, that doesn’t count sugar
from fruits and vegetables, thus about 200 lbs. yearly. Being an average half
the people are above
average. Nearly half that figure is
fructose.
[4]
Estradiol and testosterone both promote bone remodeling, and thus are the most
effective way to prevent osteoporosis and stop its progression. The older
medical literature confirms see estradiol and Testosterone.
[5]
A high glycemic index diet with its sugars: ”Consuming
higher GI diets was associated with > 3 fold higher accumulation of
advanced glycation end products (AGEs) in retina, lens, liver, and brain in the
age-matched mice, suggesting that higher GI diets induce systemic glycative
stress that is etiologic for lesions” at
2011.
[7]
The DNA is housed within a membrane in the nucleus to protect it from reactive
chemicals such as fructose. Another
layer of protection is the mitochondria, a vessula for metabolism and the
reactive chemical produced in the process.
[8]
NutraSweet for example uses low carb (not extreme) with energy restriction and
weekly counseling—a bit like Weight Watchers.
[9] Long-term makes a different for
after several years it is likely that their weight control system has reset to
the obese level of fat. Unfortunately,
this conclusion is observational; viz., I have been unable to find significant
research on this issue, as of now.
[10]
This is an important difference from the normal hunger, which with our Western
diet is the up down blood glucose cycle caused by insulin clearing the high
carb meal. This type of hunger occurs
even when at full energy. It causes the
Western graving phenomena: 3 meals a day
with snacking in between meals. Fasting
with merely low carbs eliminates that phenomenon.
[11]
The government clearly on the side of food manufactures and grain grower,
expected that the Atkins low card diet would fare worse than the others (at
least on cardiac measurements of lipids and blood pressure, it came out best);
therefore the lead person selected for the study, Christopher Gardner, a
long-term vegetarian, was clearly on the low fat energy restricted camp. The
results disappointed both. In measurements of LDL, HDL where higher is
better, blood pressure triglycerides and weight Atkins was best. See Gary Taubes,
Why We Get Fat and What to Do
About It, 2009, p 190-192.
[12] “Energy expenditure attributed to physical activity
increased by 10.2 ± 5.1 kcal/kg.d at wk
6 and 6.0 ± 4.1 kcal/kg.d
at wk
30 [10.2 – 6.0 = 4.2 less energy expenditure when physically active (i.e.,
awake)] …. CONCLUSIONS: Despite relative preservation of FFM, exercise did
not prevent
dramatic slowing of resting metabolism out of proportion to weight loss. This
metabolic adaptation may persist during weight maintenance and predispose to
weight regain unless high levels of physical activity or caloric restriction
are maintained.”
Journal of Clinical Endocrinology
Metabolism
2012
[13]
There is an evolutionary reason why fasting doesn’t kick in the drop in
metabolism. Our ancestors when out of
food need the energy to search and hunt for food. Thus there is an increase
in HGH and catechol
amines to increase energy, improve mood, and mental activity. People feel
good when fasting because of
these biological mechanisms..
[14]
See my development of the topic at
link, Dr. Jason Fung’s blogs,
his book The Obesity Code 2016, and
in October 2016 The complete Guide
to Fasting
[15]
In a testimonial (Richard’s Story) of Richard’s, his wife who is only obese
states that she uses the short term fasting.
I then wrote Dr. Fung, and he replied that the clinic also uses the
short-term fasting and the results are similar.
[16]
Kidney failure is one of the 4 major comorbidities caused by late stage T2D,
the others being cardiovascular disease, and two related to leaking
capillaries, namely blindness and leg amputation.
[17]
Seniors, much more than people under the age of 60, experience postprandial a
major decline in energy because of the major reduction in metabolism by the
mitochondria as it switches to glucose metabolism to produce the energy
molecule ATP. The lower store and
reduced rate of
production of ATP has profound
effects upon seniors.
[18]
As I age (73 years in 2016), the diversion of energy and blood to promote
digestion entails a low point after eating a full meal.
[19]
Leptin is produces by the fat (adipose) cells and among its functions is the
restoration of fat to the set level.
[20]
This topic is masterfully covered in the two books of Dr. Jason Fung, The
Obesity Code, part 2, p 29-66, and The
Complete Guide to Fasting, 97 to
109. Repeated failures accounts for the
reluctance of seniors to try one more time.
[21]
This could well make a daily skipping of breakfast equal or better than
alternate day fasting. There is journal
evidence to decide this possibility.
[22]
I two friends have lost significant weight on one meal a day. One a Dr. Evans
lost over 150 pounds, and
both kept the w eight off.
[23]
See Gary Taubes, Why We Get Fat and What
to Do About It, 2009 pgs. 19-24.
[24]
Part of the estradiol produced is converted to testosterone, and testosterone
maintains muscle. Reduced muscles are
replaced by increased fat. Less muscles
increase the sedentary lifestyle of women who aren’t exercise addicts. A
similar issue for elderly men and testosterone.
Both hormones significantly reduce the risk atherosclerosis and its
comorbidities, osteoporosis, arthritis, dementia, some cancers. This explains
why pharma is against hormone
replacement therapy. .
[25]
Pharma is against hormone replacement, and thus too are most doctors. You must
tell your doctor that a friend (me)
has great success by raising his testosterone to a youthful level (above 700
ng/dl) and you want to do the same. From
a compounding pharmacy ¼ tsp. of 15% lotion (60 gm/mo.). Tell him that you are
willing to be at
greater risk of prostate cancer and heart attacks which is what your doctor
believes. Both are false, and the
opposite is the case, but pharma is against health and has generated junk
science with the support of our government.
Androgel, the strongest of pharma’s testosterone products is less than
half the dose required for significant benefits. See Gary Taubes Why We Get Fat, his
account of Wades rat, p 89-94, and elsewhere, where he discusses sex hormones’
roles in fat distribution. Testosterone
improves muscle tone, mass, and mood, for active lifestyle.
[26] "’Science’ done on
behalf of an interest defending its cash cow from overwhelming credible science
that shows it is harmful or detrimental to public benefit in some way at”. Through the use of KOLs and supported
by
government and corporate media the industry or corporation can frame the
discussion of the subject and discredited or worse critics.
[27]
“Like ethanol, fructose increases de novo lipogenesis
(DNL), inhibits fatty acid oxidation, and has been implicated in NAFLD” at
[28]
Girls during menarche put fat on their buttock; and women abdominal fat
following menopause—like men. Steatopygia
(huge butt) is a sexually selected trait among African pygmy women, which
occurs following menarche. It is an
extreme example of the effect of estradiol—see Gary Taubes Why We Get Fat, and What to Do
About It, p 63, also read Wades experiments on rats.
[29]
Why veins are immune to formation of plaque and endothelial dysfunction is due
to the much lower blood pressure in the veins.
Just how the higher arterial blood pressure effect endothelial cell
functions remains a mystery. Evidence
for the role of increased blood pressure resides in the fact that when a
section of vein is transplanted to a artery in a bypass operation approximately
half of them will be subject to atherogenesis.
[30]
The traditional diet of the Japanese which is very low in sugar, though high in
carbs, has a far lower incidence of CVD.
Some primitive tribes have a high fruit diet,
yet they too have very low rates of CVD.
The likely reason is the seasonal nature of fruits, which thereby entail
that those peoples do not develop IR
and NAFLD which requires years to
develop. The body thus has time to burn
the excess liver fat before it accumulates to a pathological level.
[31]
T2D affects the adhesion between
adjacent endothelial cells thus causing them to leak. This phenomena results
from the high the
leaking of blood, especially in the lower legs & feet, the eyes, and
kidneys. T2D is the leading cause
of amputation of legs, and major cause of
kidney failure, and blindness.
[32]
Moreover cholesterol and triglycerides are not causal associated with CVD,
and pharma doesn’t profits from preventing disease, thus they with their KOLs created the lipid hypothesis for
CVD.
Worth reading is chapter 3 of Good
Calories, Bad Calories by Gary
Taubes, 2008, which goes describes 2 major clinical trials and McGovern
Commission’s agenda.
[33]
The
Soft Science of Dietary Fat, Science Vol.
291, 3/30/01, Gary Taubes; and also in his 2 books Why we get fat & Good
Calories.
[34]
One example was that during WWII there was a program for the distribution of
free cigarettes to the fighting soldiers.
[35] Chapter 3 and 4 of Who’s In charge?: Free
Will and the Science of the Brain,
by Michael Gazzaniga, is on how “the interpreter” part of the brain gives us
the story of thoughts leading actions.
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
5. On
sources of energy, sugars and fats the bad and good
With the Western diet yearly sugars
consumption all sources has gone from 35 lbs. in 1909 (43 gm/day) to 151
lbs. in 2010 (751 calories/per day or 188 gm/day) to cause the diabesity
(diabetes and obesity) pandemics. Table
sugar (sucrose) is hydrolyzed in the
stomach into fructose and glucose, starch in the stomach to glucose. Glucose
and fats are the body’s main sources
of ATP (energy)—other monosaccharides such as galactose and amino acids the remaining
10%. High blood glucose (a bad thing) is
down regulated by increased insulin (also bad) which sends a message for the
body to burn glucose and thus store fats.
High insulin levels in response to high
glucose will over the decades cause insulin
resistance (IR, a reduced
response to insulin) in insulin receptor on cell walls. This is a way of cells
to limit its amount of
sugar to a safe level. IR caused
high serum glucose results in
more insulin secreted by the pancreas. IR
increases fat storage. Gradually
many of those on a Western diet accumulate 2-3 extra pounds of stored fat in
the liver, nearly doubling the weight of the liver which normally weights 3.2
to 3.7 lb. This causes mild liver
inflammation and what is clinically called Non-Alcoholic Fatty Liver Disease
(NAFLD) the starting point
the comorbidities from MeS and cirrhosis
of the liver (see section 6 on NAFLD).
excess fat in the pancreas eventually causes a decline in insulin
production that result in T2D. High
insulin from IR also causes low leptin a hormone which among many things
increases appetite by stimulating the control center in the brain, and leptin also
lowers metabolism—2 causes for obesity and the yo-yo diets. The other
problem is the table sugar sucrose, a disaccharide of fructose and
glucose. Fructose in sucrose attaches
randomly to proteins in a process called glycation at 7.5 times the rate of glucose.[1] Glycation damages proteins—the main cause of
age related chronic conditions.[2] Fructose
is
metabolized only in the liver where it damages the liver by glycation resulting
in IR in the liver. With the Western
diet’s high carbs, some of the fat in the liver is stored there. Some
of that fat comes from the conversion of
fructose to fat and some from conversion of glucose to fat in the liver. This
fat de novo synthesized fat driven by
high insulin causes a gradual accumulation to cause NAFLD. In other words, if
more fat is made than the liver can use, and there is high insulin due to
glucose, this fat
accumulates in the liver cells to cause
non-alcoholic fatty
liver disease (NAFLD). This fat in cells reduces liver functions, as
too dose glycation by fructose and glucose; this double assault on the liver
adversely affects the many functions of the liver and thereby contributes to IR.[3] NAFLD
with its IR is the main cause of a
group of conditions labeled metabolic syndrome
(MeS): NAFLD,
IR, and T2D, and its sign obesity (pharma
adds the non-metabolic high
cholesterol and the resultant
hypertension and CVD—for marketing
of their drugs).
Fructose: The
very reactive sugar fructose is the starting point for the diabesity
pandemic. As stated above fructose,
which accumulates in the liver where it is metabolized, it damages the liver
through glycation and fat accumulation. In
the US we have gone from 15 grams per day, mainly from fruits, in 1900 to over
90 grams a day (hh.edu at) mainly from
sucrose and HFCS (high fructose corn syrup).
We have not evolved a system to handle this load since our ancestors
only ate moderate amounts of fruit, and in the wild they were smaller and far
less sweet. It isn’t
the glucose half of the disaccharide
sucrose that is the problem, since grains are pure glucose and mostly paleo
peoples eat a high carbohydrate diet. Paleo
peoples on a traditional diet have a fasting glucose level that is much lower
than our norm; for example, the Tokelau off of New Zealand their average is
lower than the bottom 10% of the Swedes.
It isn’t the carbs but the fructose.
The Western diet overwhelms the repair system for damage proteins by
glycation. The traditional oriental diet
is high in carbs (up to 75%) but low in fructose (14 grams or less) and as
expected their incidents of obesity, CVD,
and T2D is quite low, especially
among those who don’t smoke. Fructose
among other things damages the liver (see next section) and this is the
starting---watch the documentaries on the health consequences of sugars—link.
2) Starches
are molecules made up of chains of the
sugar glucose; their rate of absorption during digestion varies according to
their structure. Some have a much lower
rate than sucrose, and are called resistant starch; thus not all carbohydrates are equal—for tables and more on
carbs. Fiber is a very resistant starch,
which lowers insulin by slowing digestion.
The portion of and type of starch in meals affects serum glucose, as too
the rate of stomach clearance. Fats,
resistant starch, and proteins in the meal, they slow stomach clearance, thus
extending the time in which glucose is absorbed by the duodenum; this lowers
the blood insulin spike—a good thing.
There are a number more good things you can do: see section #12, why some don’t get fat.
3) Fats,
like carbs, are not all
equal. The
right fats are the best source of energy. Two fats are bad: trans-fats and polyunsaturated fats. Trans-fats are not
natural, but are man made
by a process of hydrogenation of polyunsaturated fats. Their abnormal shapes
entail that they don’t
function very well in cell walls—a bad thing.
For the same reason polyunsaturated fats are a bad thing. This is because
of their multiple double
bonds in the carbon chain (why they are called polyunsaturated). These
double bonds are available to be bonded with reactive chemicals in a process
called rancidification, which changes their shapes. This oxidation can occur
on the shelf, it is
accelerated when heat is applied as when baking or frying foods, and in the
body where reactive chemicals are made during biological processes. The rancid
fats, just like trans-fats, don’t function properly in cell walls—a bad
thing. Rancid fats are casual for many,
if not most, of the maladies associated with the Western diet. Rancid fats has
been shown, for example as a
causal factor for NAFLD, and thus all the comorbidities associated with a fatty
liver. The extent of the health has,
like drug side effects, not be a priority of funding. The evidence is found
in scientific studies
published in journal: for
rancidification see #25 and
for trans-fats (from hydrogenated vegetable oil) see #27. Another
issue arise
because polyunsaturated fats are that they are high in omega-6 fatty
acids. The omega-3 fatty acids
EPA & DHA are used to limit the immune responses, thus they lower risk for AS
& CVD, but too much omega-6 competitively blocks omega-3 usage--a bad
thing. Hunter-gatherer
societies averaged about 2 parts omega-6 to one of omega-3; in the U.S. it
is 16 to 1 (a bad thing). Vegetable oils
(except from palm & olive trees) are very high in omega-6. Like
trans-fats, the body lack enzymes to
metabolism them; thus both types of fat cause AS and thus CVD. Food manufacturers and restaurants use both
of these bad fats. This leaves us with
the safe saturated and monounsaturated fats.
“Over the years, data revealed that dietary
saturated fatty acids (SFAs) are not associated
with CAD [coronary artery disease]
and other adverse health effects” in
journal. The same in Wikipedia: ”There is s no
significant evidence for concluding that dietary saturated fat is associated
with an increased risk of CHD or CVD”
which is based on a meta study of
21 journal articles--and they taste much better. Saturated fats are best source of energy—see Prof. Miller's for list of their 6 essential
functions.
Proteins,
though rated at 6 calories per
gram, under normal conditions they are not appreciable metabolism for energy (ATP).
However during starvation they are used in the production of ATP.
The cells switch from storing to metabolism amino acids (the building
blocks of proteins) when fats stores are depleted to 4%.
6. Fructose
alcohol without the Buzz
Fructose is
toxic to the liver like
alcohol: Prof. Lustig a leading research on childhood obesity in his The Complete Skinny on
Obesity states: “fructose is a
poison like alcohol.” He then explains
why it is addicting and how it damages the liver. The same is repeated in a
series of lectures
and documentaries of his on YouTube, and UCTV—link to list. Both
are metabolized in the liver, and through various processes compromise liver
functions. And like ethanol the quantity
consumed determines the toxicity. (For
detailed review of the scientific evidence on how fructose causes insulin resistance) Fructose
is 15 times more reactive than glucose, and through the unregulated attachment to proteins it
damages protein. Over a 2 hour period of bolus
of
fructose compared to a bolus of glucose will result in 15 times more bonding to
proteins.[4] Science
it accumulates in the liver where it is metabolized the liver more than other
organs are damaged. This process is called glycation (see section 2,
definitions). That is the first blow to
the liver. In the liver when the insulin
level is high, and there is an excess fructose from sweets, some of the excess
is converted through de novo lipogenesis to fat along with lipogenesis of the
excess glucose and this excess fat because of insulin is stored in the
liver. Very slowly this fat on a typical
Western diet accumulates to a toxic level (2-to-3 pounds), and becomes a
clinical condition known as non-alcoholic fatty liver disease (NAFLD).
The two work together, fructose and insulin (in response to blood
glucose) to cause NAFLD. See the
next section for the pathologies NAFLD causes.
An important point to tease out of the many
studies is that it is not the high
carb diet itself that is causal for IR
and NAFLD, but the inclusion of
fructose in that diet. A proof is that
those on traditional diet of Japanese, Chinese, and Okinawans diet all of which are above 70% calories
from quickly absorbed carbs from white rice, noodles, and/or Oriental yams,
they have about a 1% risk for type-2 diabetes, NAFLD, and obesity, and a low
rate among those who don’t smoke of CVD.
Sugar, which came from fruits and
vegetables, amounted to an average of just 14 grams a day. It was the addition
of fructose from sucrose to
their diet that has changed all that, their rates of obesity and T2D has soared. Numerous
lab experiments have shown that
fructose causes liver changes leading to IR.
High fructose sugar diet is the cause for the diabetes pandemic.
Number can be misleading: USDA chart: The per-capita yearly consumption of ADDED sweeteners was 109 lbs.
in 1950
and 152 lbs. in 2000.[5] With the major reduction in corn syrup (pure
glucose), which has been replaced with HFCS (high fructose corn syrup) our
fructose consumption has doubles. Thus
the harm done is far greater than the increase in 43 pounds of added sweeteners
would indicate.[6]
But this is only the picture of why Dr. Lustig calls
sugar white poison,
and should be regulated like alcohol.
Glycation is not just limited to the liver. It is a major cause of age
related
conditions. I just found an article describing how it degrades the quality of
cartilage and affects bone metabolism, at 2013.
Prior to that I though the increase in osteoporosis and joint problems
was driven by the chemical bath we are subject to in drugs and food additives.
Now it seems that glycation by fructose is the main culprit. Glycated
substances are eliminated from the body slowly. On a high sugar diet, the renal
clearance is
only about 30%. This implies that the half-life of a glycation within the body
is about double the average cell life. Red blood cells are the shortest-lived
cells in the body (120 days), so, the half-life is about 120 days. (This fact
is used in monitoring blood sugar control in diabetes by monitoring the glycated hemoglobin level.) As a consequence, long-lived cells (such
as nerves, brain cells) and long-lasting proteins (such as DNA, eye
crystalline, and collagen) may accumulate substantial damage over time.
Metabolically-active cells such as the glomeruli in the kidney, retina cells in the eyes, and beta cells (insulin-producing) in the pancreas are also at high
risk of damage” Wiki. “It appears that
fructose and galactose have approximately ten times the glycation activity of
glucose, the primary body fuel.[7] Glycation is the first step in the evolution of these
molecules through a complex series of very slow reactions in the body known as Amadori reactions, Schiff base
reactions,
and Maillard reactions;
which lead to advanced glycation end products
(AGEs) Some AGEs (advanced glycation end products)
are benign, but
others are more reactive than the sugars they are derived from, and are
implicated in many age-related chronic
diseases such as cardiovascular
diseases (the endothelium,
fibrinogen, and collagen are damaged), Alzheimer's
disease (amyloid proteins
are side-products of the reactions progressing to AGEs),[7][8] cancer (acrylamide and other side-products
are released), peripheral
neuropathy (the myelin is
attacked), and other sensory losses such as deafness (due to demyelination). This range of diseases is the result of the
very basic level at which glycations interfere with molecular and cellular
functioning throughout the body and the release of highly oxidizing
side-products such as hydrogen
peroxide. Long-lived cells (such
as nerves and different types of brain cell), long-lasting proteins (such as crystallins of
the lens and cornea),
and DNA may accumulate substantial damage over time. Cells such as the retina cells
in the eyes, and beta cells (insulin-producing)
in the pancreas are also at high risk of damage“ Wiki
2015. Also under-rated is the role of glycation in retinopathy, nephropathy,
and endothelial dysfunction[7]
in diabetics, and the over attributing to reactive oxygen species created by
metabolism—see Protein Glycation, A firm
Link to Endothelial Cell Dysfunction. Endothelial
dysfunction is the immediate cause of
CVD, see section 12. Fructose
also chelates
minerals in the blood. This effect is especially important with micronutrients
such as copper, chromium and zinc. Since these solutes are normally present in
small quantities, chelation of small numbers of ions may lead to deficiency
diseases, immune system impairment and even
insulin
resistance, a component of type II diabetes
(Higdon)” Wiki
2012.[8] Yes,
the lipid (cholesterol and fats) hypothesis another example of pharma and the
food manufacturers
framing the discussion to promote their profits.
7. NAFLD and IR are the gateway to MeS and its
comorbidities
NAFLD its development: NAFLD requires both high carbs
and high fructose. That it takes
both is confirmed by Japanese and other population that eat a traditionally
high-carb diet, but with very low sugar—for the Japanese 15 grams per day, and
similar amounts for the Okinawans, and Chinese . These populations have a low
rate of CVD and
the other age related conditions associated with the Western diet. And there
is direct evidence: a couple of experiments done within a
hospital where young healthy volunteers were fed for 2 weeks either high
fructose or high glucose, this confirmed the role of fructose, but absolved
glucose as to the development of IR. So
how are the two sugars different? The difference is because of the fructose
which is metabolized only in the liver
where it is converted mostly to glucose and some fat. Fructose is also 7.5 times
more reactive than
glucose through the process of glycation (see definitions section 2), and its
slow clearance from the liver compared to glucose doubles that figure to 15. Glycation
damages the liver, and too much
fructose causes inflammation and other signs of liver injury such as high ALT,
a blood marker for conditions of the liver.
ALT is commonly used as a way to screen for liver problems. AST another
liver marker is commonly also
tested for in blood work, and it too test high from a diet with excessive
fructose. A diet high in fructose is
likely high in the sugar glucose both from sucrose. Starch consists of long
chains of pure
glucose. A diet that is high in carbs is
necessarily low in fats. So depending on
needs of other tissues (fats and cholesterol are essential for cell membranes)
the liver will convert in some of the glucose and fructose through de novo
lipogenesis into fats. Because of the
high insulin from IR in the liver
and a high carb diet, the high insulin accelerates the accumulation of fat in
the liver. This high carb-sugar diet
causes IR in the liver and thus the
gradual accumulation of fat in the liver.
The regulation of blood insulin which in part involves the liver, such
as through the production of glycogen, will contribute to an excess of blood
glucose, which causes other cells, principle the muscle and fat cells to become
resistant to insulin. For those who stay
on the high carbohydrate Western diet this is likely to progress to obesity, NAFLD,
MeS, and obesity. Two
studies of those with NAFLD found
that they consume 2-3 times more fructose than those without NAFLD—at, and. AGEs (advanced glycation end products) in the
liver and elsewhere are recognized as foreign substances by the immune system
and can in sufficient number produce significant inflammatory response. The
attributing of excess fat in the liver as
the primary cause for liver inflammation is questionable given the co-existence
of AGEs in the liver and the natural inflammatory response by the immune system
to AGEs. Insulin resistance
is like drug resistance where the body responds less to a given dose of a drug,
for example alcohol, and a higher dose is thus required for the desired
effect. With insulin resistance the
normal level of insulin fails to sufficiently lower serum glucose, and the
pancreas thus releases more insulin to obtain the ideal fasting serum level of
glucose. This abnormally high level of
insulin slowly causes the body to store more than the normal level of fat. White
adipose (fat) tissue (the most common
kind) produces hormones which regulate the level of fat. With insulin resistance
this regulatory
system is reset to maintain the weight gained.
High fructose and high glucose from the Western diet is what has led to
the diabesity (obesity & diabetes) epidemic.
Fortunately
there is a repair mechanism for NAFLD
IR T2D, and obesity, to simply go on
a low insulin diet. This requires
fasting made more effective by low fructose and other carbs. As stated before
fasting keeps insulin low
and thus keeps the body in the fat burning mode. Fasting is why about 80% of
those who have
undergone bariatric surgery cure their diabetes and insulin resistance within
the first month. This is because they can’t eat during the first couple of
weeks following surgery. Follow the
appropriate fasting programs listed in section 3 duplicates the process that
cured those who had bariatric surgery.
And it gets better as the weight goes away the body heals itself, old
damaged cells from glycation are replaced with cells whose protein haven’t been
damaged.[9]
8. Why fasting with low-net carbs diet
for obesity & T2D
There are two common general
approaches
to dieting, caloric energy restriction (CER)
or carbs restriction of which some are the extreme low carbs, the ketogenic
(Atkins type) diet without CER—and
there are of course many variations of these types of diet.[10] A third
approach, fasting is growing in popularity, mainly in Europe. Unfortunately
nearly all of the long-term[11]
obese have had their weight regulatory system
compromised; it functions to restore weight loss by causing a 25% reduction in metabolism or more,
and an increase in hunger through a hormonal system involving insulin and
leptin. Typically around the end of the
2nd month (see chart above), their
progress is greatly diminished because of the fat restoring hormone leptin. Only
those with extreme calorie restriction will continue to lose significant
weight. However, once off their diet the
weight will be gradually regained (the yo-yo diet). The main cause is the hormone
leptin which is
secreted by adipose (fat) tissue; it functions to main the normal level of fat
storage. Leptin intercedes to decrease
metabolism--typically 25%--
and through this effect increases appetite.
The dieter feels that if he eats
more, he will be mentally sharper, happier and have more energy[12]. A trial was run to compare the CER to the carb restricted diets. In the funded by government[13]
Stanford University international
A to Z Weight Loss Study which compared 4 popular diets, Atkins had
the best results both in weight loss, blood glucose, and lipid profile. At 2
moths all 4 cohorts in the trial
experience a marked reduction in the rate of weight loss. At 1 year, the length
of the trial, Atkins
(ketogenic) cohort loss 9.9, LEARN 5.5, Ornish 5.3, and Zone Diet 3.3
pounds—see JAMA
2007. Another trial had similar
results this time using overweight volunteers:
9.4 kg lost on low carb (20 gm
daily) versus the low fat 4.8 kg, at. In this trial both groups reduced calories
between 500 to 1000 calories daily. In
both of the clinical trials the lipid profile and blood pressure were much
better for the low carb (thus high fat) cohorts, and more importantly their
level of blood sugar improved on the low car diet. “Insulin levels dropped
and insulin
sensitivity was restored” (Fung p 101). A
recent journal article interviewed the 2009 group on the television show The
Biggest Losers. A group of 13
morbidly obsess participants were in a boot camp which had an extreme energy
restriction, control of foods, and a major exercise program. They too experienced
a major reduction in the
energy expended when physically active, a 40% decline.[14]
The 5-years later journal review article found that all but one of them
regained at least most of their lost weight--see. A longer period would have produced a bleaker
picture. A large 2015 UK population
study of the obese found that 99% of
long-term obese adults who lost significant weight that at the end of nine
years they were again obese or at best overweight. The UK data bank lacks information
on type of
diet, however, it did list those who had bariatric surgery and they were
excluded from the study. But given that
the KD is sufficiently popular in
the UK, on the face of it, it seems that long-term the Atkins’ maintenance
phase was poorly adhered to. So why did
the KDers fare long term?
The KD views obesity as a problem with fat
storage, and attempts to solve it long term by forcing the body to metabolize
fat. The most popular of these is the
New Atkins which calls for moderate protein and uses net carbs (table
section 3) instead of total carbs. It
also calls for a lifetime maintenance phase of low carbs. Its limited success
is because of moderate
protein consumption. Eating foods with
protein causes the release of insulin through the incretin system of hormones. As
stated in the definitions Section 2 above:
“Incretin: class of hormones
secreted by the stomach and intestines which case insulin secretion and
satiety.” The release of insulin interferes with the
process cleansing the excess fat in the pancreas and
liver.
Even with significant weight loss, those with advanced T2D are still dependent
upon medications
though less. Unfortunately,
KD also has a compliance issue:
like CER, typically have over
half the dieters quit before one year. Moreover
both diets for the long-term obese, the diets aren’t sustainable. As stated
above in the CER paragraph above, energy drops and quality of life declines
typically about the 8th week and this occurs with the KD.
“Long-term studies of the Atkins diet failed to confirm the much
hoped-for benefits” (Fung p. 102). The failure of both diets to have
sufficiently long periods of low insulin and thus to cleanse the liver and
pancreas of excess fat and permit these organs to heal, this is why the leptin
system for maintenance of fat kicks in to restore weight. In other words they
haven’t fixed the
lipogenic system where fat tissue releases leptin to restore the level of
fat. So how can the long-term obese and
overweight reset their weight regulatory system?
Fortunately,
there is a fix: those who have used
fasting in addition to low carbs have had remarkable success. Though not a
major player, it has in the 5 years increased and at least in the UK gained the
status of a fad diet because of Dr. Michael Mosley of the BBC, his 5-2 fast. In Europe and Australia where BBC, ABC, and
other networks have aired programs extolling fasting, and books there have a
greater share their market, more people have tried fasting. The results from
fasting are striking. Only fasting causes extended periods of low
insulin. During these periods the body cleanses
the liver and the pancreas of excess and thereby
cures IR and T2D which drives obesity. For
example, those with bariatric surgery have low insulin because they are fed
intravenously, and most of cured of type-2 diabetes within the first 2
weeks.
There is no
drop in metabolism thus weight loss is steady, and the weight-regulatory system
is reset.[15] Once the desired weight is obtain the patient
needs merely only to limit sugars and other refined carbs. There are a number
of different approaches
from modest food intake to total near restriction of caloric foods. The most
thoroughly research fasting diet is
that of alternate day fasting with near zero carbs and proteins, thus no rise
in insulin. Compared to CER and
low carbs, its prolonged
periods of low insulin make all the difference.[16] This type of diet will typically within 3
months result in the burning of fat in the liver and pancreas and thus cure IR
and T2D and causes the weight
regulatory system to eventually adjust to the lower weight. Proof is found in
the success of Intensive Dietary
Management—a medical clinic in Toronto Canada-- in curing both obesity and
T2D. The clinic uses low
carbs and fasting. Their success, success of others and the journal
literature is convincing short-term
or alternate day fasting is the best treatment for the obese and the
diabetic.[17] The clinic’s principle scholar is Jason Fung, a nephrologist[18]. He sees end-stage diabetics, and with the
clinic’s fasting and diet program he is able to get them off their insulin
injections and other drugs to cure their diabetes. The merits of low carb with
alternate day
fasting is not merely a theory like calories
in and calories out but one which has supporting clinical trials and animal
experiment—see the 2014 summation article, running 16 pages with 8 more for
reference by Metabolism and Diabetes Research Group of the University of
Surrey, UK, at. To make accessible confirmation of the above
claims, excerpts from this article are pasted at link and my review article on
fasting at.
9. Fasting
is easy and essential
I never had a protracted
weight
problem. By chance I had used the
short-term fast when I gained 20 pounds during the winter of 1969-70. At the
age of 26 my metabolism slowed down,
and so I didn’t burn off rapidly the excess glucose and fructose. I had
developed a fatty liver, and thus was
putting the pounds on. It took 3 months
of reduced meals and fasting to lose it.
It stayed off because it was short-term weight gain: my white adipose
tissue through leptin had not rest my weight to 170. After that, whenever I gained 5 pounds, I
simply cut back on portions, quit eating by 7 PM, and skipped breakfast several
times a week. The second change was
exercise. I moved from Winnipeg to Southern
California and became in 1975 a sports addict.
I started playing volley ball and cycling, then over the next 7 years I
added moderate weight training and singles racquet ball. In 1993 my diet changed
for the worse: following the lead of a very fit friend
Robert Fischer, I went on a very low fat (thus high carb) Western diet. Fortunately
I watched my weight, thus I never
went more than 5 pounds above my youthful weight. Skipping breakfast is easy. In 2012 I watched Prof. Lustig lecture on YouTube, which had gone
viral. He explained why sugar was poison
and I took notes. In 2013 I researched
his explanation of the diabesity epidemic.
In the spring of 2014, I reduced sugars including fruits, and carbs from
grains, thus I increased fats. It took 4
months before candies, fruit juices, ice creams, and sweet melons tasted way
too sweet. Though my weight remained for
decades the same, I had 3 pounds more around the lower abdomen than when I was 25.
It probably was a sign of a fatty liver, so I
decided in the spring of 2016 to experiment with daily short fasting. By July
of 2016, 4 months later, I lost
4 pounds, waist shrunk 1 inch, and
fasting glucose (a measure of IR)
was lower. I noticed that by skipping
breakfast, I had reduced my total consumption of food. I was less hungry especially
at dinner
time. A big plus was that I experienced
no decline in mental or physical energy in the morning, and avoided the decline
following breakfast.[19] After a couple of months of adjusting,
I now
like skipping breakfast. I stopped
eating a handful of nuts or some celery mind morning, and now I have just 16
ounces of tea with a teaspoon of lime juice. Morning fasting and not eating at
night has convinced me that weight control with short-term fasting is easy and
pleasant, easier than an energy-restricted diet.[20]
The lack of sex hormones
has been
shown to play a significant role in weight gain. Estradiol (the best of 4 estrogens)
controls
fat distribution, which is visually obvious as a girl develops during teen
years. The low estradiol causes women to
gain abdominal weight following menopause.
The natural estradiol
with progesterone from a compounding pharmacy has many benefits including
helping avoid abdominal weight. The two
sex hormones are nearly structurally identical, but for on functional group. Testosterone
makes a different for men past
the age of 60 when they do sufficient amount to restore them to a youthful
level, which is what I did. Starting in
2004 was the use of natural testosterone[21] from a compounding
pharmacy. It made my weight control
easy. I stopped weighing myself once I
realized that my weight regulatory system kept me between 161 and 165. Again
we have an example of why corporations
should not be allowed to dominate medical science; and those who know of the
benefits of hormone replacement therapy are marginalized.[22]
Dr. Jason Chapter 20 “When to Eat” in his Obesity Code, 2016, p
235-251 covers the history and advantages of fasting; his opening words
“LONG-TERM DIETING is futile”. The
reason is the major drop in metabolism due to leptin and it physical and
emotional consequences; thus few are capable of going on a life-long energy
restricted diet—there are numerous long-term studies which show that the obese
gain back most or all of their lost weight.
“The body reacts to weight loss by trying to return to its original body
set weight… [because] our insulin level
stays elevated” which is due to insulin resistance; thus leptin also is
elevated. Only fasting addresses IR.
His clinical experience and extensive research proves that fasting is
both easy and works. Here I stand upon
his shoulders: I shall present what I
find of most value in that chapter, sometimes quoted and my additions will be
in [brackets]. IR causes excess
fat storage and leptin promote reduced metabolism
and increased appetite. [But it is not
appetite/hunger exactly, rather the feeling that if I eat a bit more my energy
and mental clarity will return to what it ought to be; this is the effect of
leptin on energy.] All foods promote
the release of insulin; only not eating will keep blood insulin level low. As
Fung points in other chapters, incretin
hormone system responds to digestion in the stomach and small intestine by
stimulating the release of insulin from the pancreas [fats and fructose by far
produce the least leptin response]. It
explains why meat, fish, and poultry have a higher insulin index than boiled
pasta. Though Fung writes of 24 to 36
hour fast as curing IR, his clinic also uses the short-term fast. “The
term ‘breakfast’ is the meal that breaks
the fast—which we do daily”--p 237.
Fasting has been involved used in most cultures and religions, and among
the hunter-gatherer was forced by circumstance.
Hippocrates of Kos (c. 460-370) wrote; “instead of using medicine,
better fast today; to eat when you are sick is to feed your illness” p
237. Humans like most animals do not eat
when sick. Plato and Aristotle were
staunch supporters of fasting. “The body
does not burn muscle until all fat store is gone” p 240. “Blood
glucose levels remain normal as the
body switches over to burning fat for energy.
This effect occurs with fasting periods as short as twenty-four to
thirty six hours. Longer fasts reduce
insulin even more dramatically…. Regular fasting has been shown to
significantly improve insulin sensitivity.
This finding is the missing piece in the weight-loss puzzle. Most diets
don’t address insulin resistance,”
p240. One of the most potent stimuli of
growth hormone {HGH] secretion is fasting.
Fasting promotes the use of fat as fuel and preserves muscle mass and
bone density. Adrenalin [and
noradrenalin] levels go up with fasting,” p 241 they are the natural
amphetamines- that create alertness and physical energy. “Breakdown of
muscle tissue happens only at
extremely low levels of body fat—approximately 4 percent,” p242. “The
human body has evolved to survive
episodic periods of starvation,” p 243.
“Caloric restriction diets do not allow the evolved adaptation that
occurs during fasting,” p 244. “Studies
of eating a single meal per day found significantly more fat loss, compared to
eating three meals per day, despite the same caloric intake” 243[23]. “Total energy expenditure is increased
during
a fast—in a 4-day fast by 12%,” p244.
“In our clinic experience showed that appetite decreased as duration of
fasting increased. The most astonishing
aspect of this study [107 obese subjects unable to lose weight] was the ease
with which prolonged starvation was tolerated.
These experiences echo our own clinical experience at the Intensive
Dietary Management Clinic with hundreds of patients,” p245. The more dangerous
visceral fat is
preferentially removed with fasting. There is reference to Dr. Michael Mosley
(British on BBC) 5:2 diet, 5 days of full caloric and 2 days of 25% of calories
at the end of a short-term fast. In the
trial that compared the 5:2 to the Mediterranean diet with a 25% reduction in
calories. At 6 months both groups lost
about the same amount of weight, but the 5:2 group have lower insulin and less IR,
at p247. The short term fasting made this important
difference. Fasting because it corrects
insulin resistance is essential for
long-term dieting success.
For those
who want to know more of the science behind fasting, I
highly recommend that you read my “Evidence
of Alternate Day Fasting—Cures Type-2 Diabetes” and Fung’s book on Fasting that is scheduled
for release October 2016. For a concise
refresher as to the details of what has caused the weight control system to
crash click on link. My own experience, an others whom I have
talked to and counseled, this has convinced me that short-term fasting is easy,
and the scientific literature confirms that longer periods are also easy; this
is because our body has evolved a system to burn the fat reserve and to keep us
alert and full of energy so that we more likely to hunt and gather foods.
10. Why some don’t get fat
A variety
of factors work to reduce the probability of developing a fatty liver, the
starting point for IR and its comorbidities.
It is the combination of fructose and glucose (especially form both
sucrose and high glycemic index foods (thus refined carbs and other easily
digestible carbs such as potatoes). The
sugar fructose is the starting point thus eating a low sugar diet. High insulin
level driven by high carbs
drives liver fat storage. The
traditional Chinese diet though high in white rice (which is comparable to
white bread) had little effect. Experiments
have come to the same: feeding volunteers either a high level of
fructose are glucose, only the fructose cohort developed IR.
Recollection
of events prior and imperfect knowledge of causes makes self-analysis of
limited value. Often the year in which a
fatty liver has developed is unknown but surmised based on a gradual gain of
weight; however, it is possible that the condition had developed years before,
but based on a variety of factors listed below weight gain was minimal. Moreover,
given the typical imperfect method
of diagnosis (ultra sound or biopsy) there might be a false negative, or the
test was ran during a period were the amount of fat stored in the liver had
decreased to a temporary subclinical level.
Genetics
of course make a difference, but not that much.
One authority placed it at 5%. A
major cause is learnt behavior from family, from community, from media. Another
cause for obesity is the prenatal
environment. A fetus is exposed to high level
of blood glucose will develop more insulin-secreting cells “and the more
insulin the child will secret as it get close to birth. The baby will now be
born with more fat and
will become insulin resistant as it ages,” Taubes, supra 132. The dramatic
increase in early childhood
obesity, as referred to by Dr. Lustig, is a striking result of unhealthy womb
environment and its effect upon the weight regulatory system. Thus what seems
to be an inherited trait is in fact due to the womb environment. This is not
to deny the relevance of genes,
only clear examples of a specific gene cause a group or sizeable subgroup to
have the debilitating biological disadvantages genes is contra evolution,
except when promoted by sexual selection.
A classic review article on Obesity in Scientific American pointed out that while the American Pima Indians of
Arizona have the world’s highest rate of diabetes and obesity[24], those on the Mexican side of the boarder have a very
low rate. Since each come from the same
genetic pool—104 years of separation, statehood was granted Arizona in
1912—evolution cannot have created that great a difference. “The diversion of the
water and the introduction of non-native diet had devastating effects on the
health of the people as well”—Wiki. ‘The genes caused
obesity and diabetes’ is simplification that hides the causes: it is like
saying, “god made the earth”: explains
everything and nothing.
Childhood
malnourishment results in adjustments made that promote fat storage. Such children
have a greater response to the
refined carbs including sugars. Thus
countries with high childhood soda consumption coupled by poor nutrition (lack
of protein), there is a high rate of childhood and young adult obesity and
diabetes. Three noted examples are the
poor in Mexico, India, and China.
Steady
high fructose childhood diet of sodas, fruits, table sugar along with plenty of
carbs will—all things being average—cause obesity. Note native peoples
on a traditional diet
don’t become obese. And the Japanese,
and Chinese on the traditional diet high in high carbs (over 70% of calories)
yet less than 20 grams of fructose don’t have an issue with either obesity or
diabetes—see Dr. Fung 160-65 for more evidence.
Various common ways
to avoid the health disaster caused by IR while eating a Western diet
(in approximate order of importance):
Daily average of less than 40 grams for male (30 grams
for a woman) of fructose for an active average size person
Regular exercise or strenuous
lifestyle
Tight weight control and not
allowing significant weight of more than 5% above lean body weight. The longer
the excess fat is carried the less
likely is it that an energy-restricted diet will keep that weight long-term off.
Mini-fasting when dieting
Yielding to peer-pressure to be fit and trim
Major seasonal change in fructose and carb consumption
Limiting high sugar beverages
Natural hormone replacement therapy (testosterone or
estradiol with progesterone from a compounding phamacy.
Having good muscle tone
Getting more than 40% of calories from fats of which over
half is saturated fats
High ratio of saturated fats to unsaturated fats (see Part 4 Fats for complex reasons)
Eating a high ratio of natural foods to manufactured
foods thus limiting the sugar added foods and polyunsaturated fats.
Choosing fruits and pure dark chocolates as a desert or
snack over items high in sucrose such as fruit juices, candies, cookies, sodas,
and like.
11. Myth busters
-- (trashing tobacco corporate science)[25]
High serum cholesterol causes CVD.
TRUTH: High serum
cholesterol has not been
demonstrated to be a cause of plaque formation. CVD’s
main cause is infective agents
within artery walls which damage LDL with toxins and cause an immune response
by macrophages that cause atherogenesis. The cholesterol deposits in the artery walls
are a byproduct of the immune response, as too are calcium crystals, foam cells,
triglycerides, and lymphocytes.
Cholesterol is a bystander not a cause; thus lowering its production
with drugs does not prevent AS or
heart attack. Autopsy studies found no
relationship between serum cholesterol and degree of AS in those died violent
deaths, see. The Australian Broadcast Corporation has a
documentary which exposes this myth, at and one on the statin scam. Avoid saturated
fats because they cause CVD by raising the serum level of
small-dense LDL which is associated with CVD.
TRUTH: Saturated fats don’t
raise cholesterol levels
or small-dense LDL. And LDL level is not associated with CVD (see #1). A meta-analysis
of 21
studies on saturated fats, “failed to find an association with CVD, Wiki, and also Wiki. This extends to all types of fats when
“increased from 30 to 50% of total energy,” 2004.
Moreover, those on an Atkins type KD,
their so-called “bad” LDL drops and the “good” HDL rises. Vegetable oils are preferred to saturated fats (main
source animals). TRUTH: Vegetable oils are
associated with diseases because they are high in polyunsaturated fats that
become rancid in the body, when cooking,
and on the shelf--link. Since this process of oxidation changes the
shape of the molecule and they are incorporated in cell membranes, they
adversely affect the functions of these membranes. Like trans-fats (also of
unnatural shapes)
the consequences are disease promoting. Second,
polyunsaturated fats are high in omega-6 fatty acid which blocks conversion of
omega 3 oils an anti-inflammatory agent. Our Paleolithic
ancestor averaged 2 parts
omega-6 to 1 omega-3; today it’s 16 to 1.
Many people wisely take a fish-oil supplement to improve the ratio of
omega-3. Because of its effect on the
immune system and rancidification vegetable oils promote CVD, arthritis, and
Alzheimer’s disease. The more expensive animal fats are the best source of fat followed by the palm kernel, coconut, and olive oils which are high in
monounsaturated fats. There
are hundreds of journal articles
going back 6 decades on this process, use scholar.google
to find them. Sugar (the disaccharide sucrose is fructose and
glucose), fruit sugar (fructose), and starches (long chains of glucose) are
merely empty calories without nutritive value; viz. harmless sources of energy.
A calorie is a calorie. TRUTH:
sugars and starches (pure glucose) damage tissues. Fructose and glucose
randomly bind to
proteins (in a process called “glycation”) to damages proteins in your cells.
Thus glycation
promotes the degenerative conditions associated with old age: CVD,
atherosclerosis, Alzheimer’s, macular degeneration, et al. Fructose (fruit
sugar and ½ of sucrose) has a
glycation rate of 7.5 times that of glucose; actual 15 times because of its
slower clearance compared to glucose; moreover, most of the glycation occurs in
the liver where it is stored prior to metabolism there. Since 90% of fructose goes
to the liver for metabolism, the damage there through glycation is
significant. Some of the fructose is
converted in the liver to fat[26]
which can accumulate because of the Western diet with its high carbs. Damage
from glycation and fat accumulation in
the liver causes IR and a fatty
liver called non-alcoholic
fatty liver disease (NAFLD). NAFLD affect over 30%
of the US adult
population (NHANES II study). NAFLD
affects the plasma-glucose
regulatory function of the liver to cause IR.
Fructose by causing minimal insulin response, it bypasses the appetite
regulating system involving leptin and ghrelin which reduces it affect upon the
satiation system of the hippocampus to
cause weight gain. Finally, fructose
stimulates the addiction center of the
brain (see #6 below) to promote sugar addiction. Clearly, sugars are not
harmless empty
calories, nor are starches with high insulin index, and fructose is the worse. The cause of obesity is a sedentary lifestyle &
gluttony. All one needs to do is eat
less and exercise more; viz., burn more calories than one consumes; this is the
common advice given by doctors, dieticians, and accepted as the way to lose
weight. TRUTH: For all mammals
their weight is controlled by
a biological system. The Western diet
with its average of 180 grams of sugars daily causes a fatty liver and IR. Fatty
liver and IR muck up the regulatory
system and thus cause obesity. It
is not gluttony and sloth that causes the
obesity and diabetes pandemics (blaming the victims) but rather the Western
diet which is promoted by food manufacturers and corporatist governments. For the obese, a 25% reduction or more in calories will
result in significant long-term weight loss.
Truth The weight regulatory
system in an effort to
maintain the set weight will reduce the rate of metabolism approximately 25%
and increase hunger. Even those he get
past this barrier which occurs typically around the end of the 2nd
month, they will once off the diet regain the weigh (yo-yo diet). The hormone
leptin intercedes to decrease
metabolism, typically 25% and at the same time increases appetite. It is secreted
by adipose (fat) tissue to
main the normal level of fat storage. Less
than 1%
of long-term obese adults at the end of nine years will obtain normal body
weight through diet. To prevent this
regain of weight, the regulatory system must be reset, and this occurs by fasting
and going on a low carb diet. Fasting
will avoid the 2-month drop in metabolism.
This type of diet will eventually result in the burning of fat in the
liver and pancreas and thus cure IR and T2D and permit the weight regulatory
system to eventually adjust to the lower weight. Hormone replacement (HRT) will not promote weight
loss. TRUTH: Estradiol among
other things regulates fat distribution[27]
and plays a role in physical well-being.
During and following menopause women experience a precipitous drop in
estradiol (the most healthful and active of the 4 human estrogens). The common
post-menopausal reduction in
physical activity and associated rate of metabolism contributes to weight gain
and abdominal fat. “Natural
HRT [estradiol plus progesterone] reduces insulin resistance and
fasting glucose in women with diabetes”
at. Since some of estradiol is converted to
testosterone NHRT prevents muscle loss with aging, another contributing factor
to weight gain. Men too following
andropause experience a reduction in muscle mass and metabolism. And the heart
as a muscle gets weaker. HRT for men and women poses
major health risks which
outweigh their benefits. TRUTH:
natural hormones lower risk for breast and prostate
cancers. Men in the highest 20% for
testosterone have the
lowest rate of prostate cancer and heart attacks. Estradiol moderately lowers the rate of breast
cancer. In sufficient dose NHRT
will reset the biological clock to a
younger age and thereby significantly reduce the risk of most age-related
chronic diseases. Estradiol with progesterone
lowers CVD, Alzheimer’s, cancers,
and much more. Testosterone decreases the risk of heart attack and
cancers. Current wisdom is based on
pharma’s junk science & tobacco
ethics: clinical trials that
knowingly used the worst formulate of HRT for women, Prempro. Read the section on the WHI study
which exposes pharma’s and NIH’s tobacco science and ethics. NHRT
is good for people and thus bad for pharma. Three lies about type-2 diabetes:
a life-long progressive condition;
it can’t be cured; and is best managed with drugs that lower blood glucose to
normal level. TRUTH: that once
the excess fat stored in the pancreas is cleansed
T2D is cured (at the same time the excess fat in the liver is cleansed). Bariatric
surgery reverses often within a
month T2D by post operation fasting proves that it can be cured and that
fasting is the cure. Dr. Janson
Fung’s dietary treatment of KD
(low carb
high fat) with alternate-day fasting cures T2D for most
within 6 months. Diet is the cure. Moreover
the cohort who has their glucose tightly controlled has a higher mortality rate
in clinical trials. Pharma is highly regulated
by the FD A to protect the
public from the tobacco ethics used
by corporations to fulfill their fiduciary duties. Truth: that there is a revolving door between the
FDA and pharma, and that at the highest levels the FDA is ran by executives
from pharma and their KOLs. For
a summation of the ways in which the
evidence base has been broken—link,
or YouTube Dr. Angell. Our corporatist government enacted the
Prescription Drug User Fee Act of 1992 to make the FDA dependent upon pharma
for over half of its budget. Congress
wants the FDA to serve the pharmaceutical industry. Link to Consumer Report on the FDA. Read Prof. Ben Goldacre’s Bad
Pharma. Doctors know what is best for patients. Truth:
the education and sources of doctors’
information has been manipulated by pharma so as to turn them into drug
pushers. Pharma runs and owns the
results of clinical trials, thus positive bias is the norm--32%. Pharma determines who becomes a KOLs (Key
Opinion Leaders). They are the lead
authors on clinical trials, write the medical textbooks, and give continuing
education classes. The information
foundation is thus distorted. For an
insightful explanation of how this has occurred click on link—you need to know. Pharma
and
food manufacturers through junk tobacco science, corporate media, and
misinformed doctors cause cognitive dissonance
and reliance on their KOLs by both the public and physicians. Pharma has framed
the discussions to promote
the sales of patented drugs, and food manufacturers to promote the obesity and
diabetes pandemics. What has been said
about pharma applies to the manufactured food and tobacco industries—profits
before people. There is a struggle going
by leading men in the medical field who have broken rank over the corruption
worked by pharma, but you won’t squarely hear of it in our corporate
media. But you can watch them on YouTube & read their journal articles.
12 Pathogens in artery walls is the main
cause of CVD
The tobacco-science based
claim that
saturated fats and cholesterol cause CVD;
this has been decisively refuted by scientific
evidence: “Atherosclerosis
(AS)
is now recognised as a chronic
inflammatory disease occurring within the artery wall and ultimately
responsible for myocardial infarction, stroke & peripheral vascular disease.”
“There are approximately ten times as many bacterial
cells in
the human flora as there are
human cells in the body”, Wiki, Not surprisingly some of them are in the
interior of the artery walls, the tunica intima. The inflammatory process starts with white
blood cells attempting to eliminate certain bacteria. They produce an inflammation
in response to
the virus and bacteria colonies within the
artery walls. A typical study found Chlamydia pneumonia in those with
CVD 79% vs 4% without CVD in coronary
artery specimens. LDL functioning as part of the immune system
absorb the toxic chemicals produced aby these pathogens. The “monocytes replenish
resident macrophages” (a scavenger white-blood cell) that dispose of the
products of the LDL’s immune response--see. Thus
pathogens damage to LDL is part of the process leading to the development of CVD;
not high blood cholesterol and high
fat diet which are bystanders found within the LDL. Lesser contributing factors include oxidation & glycation (sugar bonding)
which damaging endothelial cells lining the coronary artery
walls. Pharma wants us to believe that
the inflammation response is to oxidized LDL in the artery walls. Wrong again,
the contents of LDL is
cholesterol and triglycerides which the body needs to grow new cells to promote
healing in the artery wall and to replace damage white bloods cells both of which
have been damaged by the pathogens. This
explains cogently why atherosclerosis is brought on by an inflammation
response. Pharma says this response is a
result of damage to the LDL in the inner layer of the artery; no mention of
pathogens. Pharma has ignored a century of autopsy studies of those who died
from a heart attack; these studies find pathogens. But pharma makes billions
treating hypercholesterolemia--see. Then they make billions more hypertension and heart attacks—but not
the pathogens that cause AS. Prevention
is not in their business model.
Moreover pharma is very good at marketing--see how. The
scientists who are critics of pharma’s junk science are ignored by corporate media.
Physicians hear pharma’s key opinion leaders
(KOLs) at the required continuing
education classes funded by pharma. Having
said this, my concern here is with
diet’s role of insulin resistance (IR)
in obesity, fatty liver disease, diabetes, age-related diseases, and CVD; and
also about healthful choices. Sugars through glycation damage the
endothelia cells which line the artery walls, and so damage they increase the
risk for pathogens colonizing the inner layer of the arteries—2 links see and more.
LDL is a
lipoprotein-phospholipid wrapped sphere containing
about 1500 cholesterol molecules and
3,000 to 6,000 fat molecules
including triglycerides, see
illustration. Cholesterol has several essential functions including forming the cell walls, neurons
coating, and its conversion into the sex hormones. The liver produces
cholesterol--about 70%--and sends it wrapped inside LDL through the blood to
cells in need of fats & cholesterol.
Inhibiting the synthesis of cholesterol with a statin drug has many
side effects, and it doesn’t
prevent CVD. Numerous books and documentaries expose the
cholesterol myth & statin horrors.
But pharma in the production and dissemination of information frames the
debate; thus only those who de-nova examine the journal evidence and adjust for
their tobacco science can come to the best evidence based answers.
13.
Other cofactors for CVD
Pathogens
play the key role in the formation of atheroma leading to AS and CVD. However, excesses in reactive blood-borne
chemicals including simple sugars (especially fructose) are contributory. Their
main pathological mechanism is through endothelial
dysfunction. Endothelial cells
function as a single layer membrane that lines all the blood vessels and act as
the gatekeeper. These cells have
receptors which allow certain chemicals to pass through, others such as
lymphocytes posses a compound which effects the adhesiveness that join the
endothelial cells to form a membrane and thereby permit the lymphocytes to slip
between them. harm the gateway cells
that line blood vessels.[28]
Trans-fats and rancid polyunsaturated
fats are statistically associated with CVD.
The abnormal shape of these fats is thought
to contribute to various disposal issues that are pathological. For example,
transfats induce platelet
aggregation, .… inhibit activities of Na+ ,
K+-ATPase
and adenylate cyclase and reduce density of B-adrenergic receptors in rat heart
membranes [raise blood pressure]…. Recent evidence indicates that trans-fats promote
inflammation…. Increased tumor
necrosis factor (TNF) system, levels of interleukin-6 and C-reactive protein….
Several studies suggest that trans-fats cause endothelial dysfunction” in the
1984 thorough review
by the Department of Agriculture. Similar affects occur with polyunsaturated
fats which are in vivo subject to oxidation.
In addition the high ration of omega-6 to omega-3 fatty acids has been
shown to be atherogenic. Similar
association with CVD is associated
with a diet high in sugars (but not carbs).[29]
Hyperinsulinemia, IR, NAFLD, T2D[30]
are contributory to endothelial
dysfunction. Like so much that goes on
in the body, the causal mechanisms of these condition in the development of
endothelia dysfunction is complex and thus tentative. The associations with
sugars, smoking, trans
and polyunsaturated fats to endothelia dysfunction and CVD are firmly established.
The strong association of CVD
with Western diet is based on carbs with sugar causing IR and IR’s role in
endothelia dysfunction.
So what about the standard
explanation for atherogenesis? Pharma’s
case for LDL undergoing oxidative damage from metabolites within the tunica
intima, and this being the most principle cause of CVD, this is suspect.
Suspect because it ignores pathogens, suspect because it ignores the
immune role of LDL, suspect because it fails to explain cogently why LDL is
actively transported in large numbers through the epithelial cells into the
tunica intima; and downright misleading because it uses the dual meaning of
“oxidative” to imply that the products of metabolism is causing the oxidative
damage to LDL while in fact it is the toxins that are latching onto the
external protein shell of LDL. Their
explanation fails to explain why there is LDL in the intima medial, and to
explain cogently why the immune system is involved in the process. Pharma’s
KOLs state that the lymphocytes and
macrophages are there to clean up the oxidized LDL—no mention of pathogens. The
debris of this process results from the macrophages engulfing large numbers of
the oxidized LDL and resultantly undergoing apoptosis that results in the
formation of plaque. Are we to believe
in an atypical process involving pathogens, or to think the worse of
pharma? Given pharma’s repeated examples
of tobacco science being generated by pharma to promote profits, the plausible
conclusion is that this is one more example of bad conduct by pharma. Pharma
has already been proven to have
generated the cholesterol and triglyceride myth (see Cholesterol
Myth
and 2nd article)
and to support it pharma has
created a factitious modus operandi.
Given the totality of evidence, the healthful choice is to ignore the
recommendations of pharma’s KOLs and those, whom they have educated, the
majority of physicians.
14. How Did We Get Here--Historical
The prima
facie evidence is that the diet adopted by the FDA and Department of Agriculture
in the 1977 brought on the health pandemics.
The switch to low fat, low cholesterol, which entails higher carbs, just
so happened to favor the products of the food manufactures and the cholesterol
lowering drugs of pharma. In 1977 our government,
and later those
around the world, ignored over 60 years of dietary science and switched its
position as to what is heart healthy.
Based on weak evidence, high serum cholesterol and triglycerides (3-fat molecules joined
to 1-glycerol
molecule)
were accused of being the leading cause of CVD.
Somehow
the Senate panels (McGovern Commission) and their experts on CVD missed cigarettes
which at a pack a
day doubles the deaths from heart attacks.
The Surgeon General only
warned about lung cancer and emphysema in The 1964 Report on
Smoking and Health. Over three times as many deaths are caused by tobacco induced heart attacks and
strokes than from lung cancer and emphysema, yet the Surgeon General missed it
and a large body of journal literature going back to the turn of the century. Dr.
Kellogg, of cereal fame, published in 1922 a 171 page concise compendium on the
published research on tobacco’s known health consequences, including its
destructive action on blood vessels, at. Kellogg’s book has hundreds
of scientific citations. In 1965, 42% of
the adult population smoked, yet the McGovern Commissioned
missed tobacco. So why was the evidence
on tobacco distorted by the Surgeon in 1964 and ignored by our government in
1977, and why were saturated fats and cholesterol blamed?
Simply
follow the dollars. Once you realize that serving
the public is cloak worn by our corporatist state, than it
makes sense, and when we review the details we find that this is standard
operating procedure: serve big dollars
while advertising serving the public.
This method explains why our government fingered tobacco for lung
cancer, but missed the much bigger killer from CVD:
they were
doing damage control for tobacco. The
connection with lung cancer was too obvious, and too well known. The Surgeon
General had done damage control
dressed as science in the public’s interest.
So why finger cholesterol and saturated fats? Animal (saturated) fats
cost twice that of
vegetable oils; and sugars and refined starches are cheap and addictive. And
most of the products made by food
manufacturers are loaded with refined carbs including sugars. Moreover,
pharma doesn’t have drugs to treat
the pathogens living inside the artery walls which are the principle
cause of AS and CVD, but with drugs they could modestly lower cholesterol and
triglycerides in 1977.[31]
Thus pharma was by 1972 (and before) promoting hyperlipidemia and
hypertension as causes for CVD and MI.
For example in the 1972, 12th
edition of Merck Manual
p.374 recommends restrict fats to 30-40 gm/day to lower CVD risk. And the role of
pharma gets more insidious. If the
patient believes X is a risk factor and he tries a cheap fix that must fail,
then he is likely to go back to his physician and try patented drugs to fix
X. This is a standard business practice
for pharma. Diet does not significantly
lower cholesterol, because the liver makes cholesterol to serve vital
needs. Only about 30% is from diet,
lower it and the liver makes more on a need basis. Moreover, saturated fats
don’t raise
cholesterol or cause CVD--see Dr. Miller’s lecture. Thus
the low fat and low cholesterol diet fails, so the patient with elevate
cholesterol and/or CVD then tries
drugs. This plus the food manufacturers
favor their high sugar and starch products over eggs, meats, poultry, and fish,
because these foods are a very small part of their product line. Secondly the
vegetable oils are about half
the price of animal fats. The McGovern
Committee and the US Department of Agriculture followed the bucks.[32] The government’s inaction and at times
support
for tobacco[33] that permits harm from cigarettes is
one more example of the power of tobacco (dollar) ethics in a pseudo-democracy,
our corporatist state. The science
behind healthy diet was turned upside down by big money and we have a health
epidemic.
15. Free will won’t, rational control of
behavior will
On how
to deal with food
addiction which seems to trump rational control? In 1985 applying the standard
behavioral
analysis for dieting: I set down various
types of behavior that would result in weight loss including food selection.
Small portions, peer support, visualization, etc. I held that thoughts (silent
whispers) are
merely epiphenomenon that accompanies behavior like a shadow. Eloquent proof
came 2 decades later; one was
an experiment that was published in American Scientist (2004, Free Will, Free Won’t).
Electroencephalography was used to measure brain activity and a button
was pressed by the participant to indicate when the thought occurred. The deep
brain activity occurred a half-second
before the thought of his arm movement.
The thought of the action came after preparatory subconscious neural
activity, like the thunder following lightening. Neurological science has since
established that thoughts are generated by deep brain processes and accompany
an action like a shadow. To begin with neuroscience has demonstrated
that the brain is modular, each of the hundreds of sections has a specific
function. One of these modules functions
to create an image of man as being guided by thought.[34] But rather in the verbal sections of the
brain is not aware of what goes on in the motor sections of the cerebellum
which acts as a traffic cop coordinating behavior. In other words the brain
has hundreds of
specialized modules I call the analytic
portions (AP) that function to produce
verbal behavior including
thoughts. Thoughts has been by B.F.
Skinner labeled as silent whispers.
Consider the behavior process similar to vector algebra (see graphs
above on website) where several different forces are acting
simultaneously on an object at a point, the result of which will be movement of
the object in only one direction. The
deep brain operates according to the diverse force to produce behavior,
sometimes contrary to the input from AP.
For diet, based on a complex collection of
evidence, the AP has determined that
sugars and starches need to be avoided.
At home the AP opposes the
eating of refined carbs and sugars, but its contribution to eating choices
isn’t sufficient to consistently throughout the day bypass the grapes and
candies. Thus I must influence the
arrows of forces in my brain so that at home there aren’t foods high in refined
starches and sugars. The explanation
from behavioral psychology: the closer
in time and space to a reinforcer, the greater is the probability that it will
affect behavior. The AP plots that
I need to stock the
kitchen with items that aren’t high in refined carbs and high sugars. I
also enlisted my wife to use social
reinforcers such as praise and she too has changed her diet. We watch the video
Sugar White Poison and other like videos every
week. The AP has set out a program
by which I can change my eating behavior
life-long. Moreover, given my extensive
education and application of academic skills, my AP is stronger than the norm.
If it were
true that the
will (mind, AP) could decide
independent of the deep brain process, then there wouldn’t be smokers, drunks,
and an obesity epidemic, and certainly there wouldn’t be so many morbidly obese
(about 10% with a body mass index, BMI, over 40). Today I saw a women under
the age of 30 whose
weight forced her to rely upon a wheel chair.
Does she have a defect in her will (mind)? Or is it a confluence of genes
coupled with
dietary causes that have reset her normal weight to a BMI of over 50? She can
think of losing weight, swear that
she will, go on a diet, but the deep brain is committed to 400 lbs. and gaining. The
low fat, low calories diet is not her
long-term answer. A bariatric operation
is one way, but her stomach will expand sufficiently to accompany many small
meals and about half will regain most of their former weight—as two of my
friends have done over a period of 6 years.
The wrong expert information spread by doctors and the media has the AP
applying a low fat diet with more
exercise as the healthful program, and they gained back their weight.
16
Outline on metabolic
dysfunction
This
page 6/9/16, is on http://healthfully.org/rc/id23.html
All
mammals have a complex regulatory system for appetite, rate of metabolism, and
fat storage. There are over eighty
hormones involved in the system. The
Western diet is high carbs fructose and glucose that causes a fatty liver (NAFLD)
which mucks up the regulatory systems leading to the IR that causes obesity,
T2D, CVD, etc. Glucose raises insulin
level, and insulin causes cells to STORE FAT and
burn glucose. IR
causes excess fat storage. Causes: The
carb fructose--a simple sugar--goes
to the liver where some is converted to fat, and when insulin is high this fat
is stored in the liver. The low fat,
thus high-sugar, high-carb Western diet will for most cause excess fat storage
in the liver. Gradual over the
years/decades 2 to 3 pounds of fat is stored in the liver (NAFLD). This causes IR
first in the liver then in other tissues. IR mucks-up
the complex metabolic systems. With IR
comes a gradual gain in weight. If you
have T2D then you have excess fat in the pancreas, and your beta cells no
longer produce sufficient insulin to manage your glucose. When on an energy-restricted
diet the fat
tissue through the 4 hormone it produces functions to maintain current weight
by increasing appetite and reducing metabolism.
Even after losing weight, the system works to restore the fat—the yo-yo
diet. Goals: to stay in fat
burning (low insulin) mode and thus to metabolize the excess fat in the liver
and pancreas to reverse IR and T2D. Once
fatty liver & IR are cured than carbs can be moderately increased and weight
will
still be lost. Once ideal weight is
obtained remain on moderate
carb-sugar diet. Follow the dollars and
you will find out why we have the Western diet and the wrong advice—click on link for a list of the
misinformation, and much more.
Fix: Short-term fasting with low carb diet to
stay in fat burning to cleanse the liver and cure NAFLD & IR.
Fructose converted to fat in
the liver and high glucose via
insulin causes fat storage in liver (a 1-2 punch)
Fatty liver >>>> IR in liver >>>> IR in muscle and fat tissues
>>>> IR causes abnormal
high insulin >>>> excess fat storage
T2D can be cured with diet. For example
in the first 2-weeks following bariatric
surgery over 80% with T2D are cured
before major weight loss. With very low
carb diet and alternate day-fasting the cure takes from 2-6
months.
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