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Obesity
2) The
Clinical Importance Of Vitamin D
3)
Menopause And The Future Of HRT (Hormone
Replacement Therapy)
4)
Heavy Metal Toxicity - Biochemical Metabolic And
Therapeutic Considerations
Obesity
Obesity can be defined as the state of being more than 20%
above what is considered to be normal weight. It can also be
defined as having a body-fat percentage greater than 30% for women
and 25% for men. Body mass index above 30 is another way to define
obesity. With both BMI and absolute weight, there are problems
because muscular athletic individuals may weigh more for their size
because muscle weighs more than fat. I recommend using a scale that
measures bioelectrical impedance and evaluation of body fat
percentage.
Obesity can further be classified as hyperplasic or hypertrophic or
a combination of the two. Hyperplasic obesity is less associated
with serious adverse health effects and is a result of a greater
number of fat cells, which depends primarily on the diet of the
mother when the child is in utero as well as early infant
nutrition. Hypertrophic obesity is characterized by an increase in
the size of each individual fat cell and is associated with
abdominal and visceral obesity and multiple adverse health
consequences.
Obesity lends to increased risk of clot formation, arterial
plaques, inflammation, elevated cholesterol, prediabetes, type 2
diabetes, hypertension, colorectal cancer and arthritis.
OBESITY PROMOTES HYPERCOAGULABILITY
The body is a marvelous balance machine. Clotting is needed to
prevent blood loss from injuries but too much of a tendency to clot
can lead to strokes, heart attacks, and deep vein thrombosis.
Obesity pushes the balance off promoting coagulation and inhibiting
clot removal.
OBESITY PROMOTES THE FORMATION OF PLAQUE IN ARTERIES
The risk of atheromas or artery plaques is also exaggerated
especially with abdominal obesity. Depending on where your body
holds its fatty tissue determines your risk also.
Visceral obesity is the most dangerous. We have heard this
described as the apple shape with abdominal fat accumulation. The
types of fat cell in the pear shape with hip and thigh fat is
safer. Fat cells are called adipocytes. The adipocytes in visceral
fat are metabolically active playing a role in the development of
atheromas and inflammation.
OBESITY PROMOTES INFLAMMATION
Some of the known molecular players are:
CRP - Cardio reactive protein
TNF - Tumor necrosis factor alpha
IL6 Interleukin 6
We have heard quite a lot about CRP. It can be measured on a blood
test. Too much is bad. Levels of CRP decrease with weight loss.
Regular exercise leads to lower resting levels of CRP. Visceral
adipocytes produce inflammatory molecules that are released and
travel directly into a blood vessel called the portal vein. Then
the CRP and other inflammatory molecules are brought to the liver
in the portal vein. In the liver even more inflammatory molecules
are produced. This is called inflammatory up regulation.
Elevated CRP is associated with increased risk of:
Cardiovascular disease
Hypertension
Elevated cholesterol
Insulin resistance
Pre diabetes
Diabetes
Fat cells, adipocytes, make hormones called adipokines. Leptin is
the first adipokine. Leptins signal the brain of the extent of the
body’s fat stores. Increased body fat leads to increased leptin
production, which in turn suppresses appetite and stimulates fat
burning. But in chronic obesity this feedback signal doesn’t work.
Instead the state of inflammation associated with chronic obesity
leads to leptin resistance. How does this happen? Inflammation
stimulates the body’s production of SOCS – Suppressors of Cytokine
Signaling in order to limit the damage of inflammation.
Unfortunately SOCS-1 and SOCS-3 interfere with the body’s ability
to respond to leptins. So a vicious cycle occurs of obesity,
inflammation, leptin resistance, more obesity, more inflammation
etc. This is again an example of up regulation of inflammation in
chronic obesity.
OBESITY PROMOTES HIGH CHOLESTEROL
Some disorders of cholesterol are:
Hyperlipidemia – High cholesterol, high LDL – low density
lipoprotein (lousy cholesterol)
Dyslipidemia - Increased triglycerides
Decreased HDL – high-density lipoproteins – good cholesterol “Happy
Cholesterol”
OBESITY PROMOTES PRE-DIABETES
Insulin is produced by the pancreas and is utilized by cells to
metabolize glucose or blood sugar. Insulin resistance is the name
given to describe the relative disability of cells to effectively
utilize insulin to accomplish blood sugar metabolism. When body
cells develop insulin resistance they require higher levels of
circulating insulin to metabolize blood sugar. This forces the
pancreas to release exaggerated amounts of insulin. Elevated blood
insulin is called hyperinsulinemia. Two negatives develop. Elevated
insulin levels promote visceral fat/abdominal fat, which further up
regulates the aforementioned inflammation in a vicious cycle. Also
the pancreas eventually wears out. At first impaired glucose
tolerance develops because insulin receptors are only partly
working and blood sugars begin to creep up. Finally diabetes
develops when insulin levels cannot keep up.
The inflammation associated with obesity leads to the production of
SCOS – Suppressors of Cytokine Signaling.
SOCS-3 leads to insulin resistance the same way that SOCS-1 and
SOCS-3 lead to leptin resistance. Insulin resistance decreases the
ability of cell receptors to utilize sugar and promotes greater
deposition of fat. Again the vicious cycle is seen. Obesity
promotes inflammation with insulin resistance leading to further
obesity and inflammation.
There is a special term called metabolic syndrome which describes a
constellation of effects:
Central/visceral/abdominal obesity
Impaired glucose tolerance
Dyslipidemia – Elevated triglycerides
Low HDL (good cholesterol)
Metabolic syndrome can precede frank diabetes.
ELEVATED LEVELS OF TNF ALSO LEADS TO INFLAMMATION, PLAQUE IN
ARTERIES, INCREASED RISK OF HEART ATTACKS
TNF in particular can lead to increases in insulin resistance in
adipocytes. TNF also encourages adipocytes to produce another pro
inflammatory molecules like IL-6 interleukin –6. Additionally IL-6
released into the circulation increases central abdominal obesity
by its affect on the hypothalamic pituitary adrenal axis.
TNF also decreases activity of an enzyme called lipoprotein lipase.
This causes accumulation of foam cells in artery plaques by
decreasing breakdown of lipoproteins.
Adipocytes make a protein called adiponectin. Levels of adiponectin
are inversely associated with heart attacks; that is the higher the
level of adiponectin, the lower the risk of myocardial infarctions
or heart attacks. TNF inhibits the production of adiponectin by
adipocytes thus increasing the risk of myocardial infarctions
(heart attacks).
TNF also plays a role in repeat heart attacks. After a myocardial
infarction, elevated levels of TNF are associated with increase
risk of repeat MI’s (heart attack).
OBESITY PROMOTES HYPERTENSION
Obesity is associated with elevated levels of angiotensinogen and
angiotensin II – AT II. These molecules cause the muscles in artery
walls to constrict or tighten leading to high blood pressure. AT II
also leads to increases in inflammation in the lining of blood
vessels. AT II activates molecules called endothelial adhesion
proteins. These molecules attract inflammation at the level of
blood vessel walls. It is likely that inflammation as well as
clotting is a major contributor to heart attacks and strokes.
The blood pressure medicines called ACE inhibitors and ARBS lower
levels of AT II and decrease the effects of AT II on blood vessel
linings.
OBESITY LEADS TO INCREASED COLORECTAL CANCER
Obesity leads to increased risk of colorectal cancer. Physical
activity leads to decreased risk of colon cancer. Suppression of
inflammation in patients with inflammatory bowel disease leads to
decreased rates of colorectal cancer. High fiber diets from fruits
and vegetables lead to decreased risk of colorectal cancer.
OBESITY IS ASSOCIATED WITH OSTEOARTHRITIS
Obesity is associated with osteoarthritis of weight bearing joints.
Osteoarthritis is generally considered to be from wear and tear on
cartilage. Cartilage is the cushion between bones at a joint. The
gristle on the end of a chicken bone is cartilage. Chondrocytes are
the cells that produce and maintain cartilage in joints. The sheer
wear and tear of the burden of additional weight leads to damage to
cartilage and joints. Osteoarthritis is becoming known to be
variably related to inflammation. The relative contribution of
inflammation varies from time to time within an individual patient
as well as between patients. TNF and IL1-B (interleukins) 1-B can
decrease the ability of chondrocytes (cartilage cells) to repair
damaged cartilage. TNF and IL –1B are inflammatory molecules. As if
this is not bad enough other molecules released during inflammation
called angiogenesis factors, introduce sensory verve cells into the
joint space. Usually cartilage lacks these nerves that sense pain.
Cartilage is aneural does not have sensory nerves. So now the
damaged cartilage senses and “feels” increased pain.
THIS IS TERRIBLE WHAT CAN I DO?
Obesity especially abdominal obesity has many serious adverse
health consequences.
Weight loss and maintance is crucial to your health. There are
nutrition and pharmacologic interventions that may be appropriate
to your individual needs. Exercise where appropriate is also
helpful. Regular physical activity decreases production of
inflammatory cytokines, improves metabolic rate and sense of well
being. Loss of abdominal fat begins to reverse the generalized
inflammation, hypercoagulability, dyslipidemia, leptin resistance,
glucose intolerance, insulin resistance and atheromatous changes.
We use a wholistic design to help promote appetite suppression to
allow more appropriate choices. The type of “diet” is
individualized. Appetite suppression is achieved using amino acids,
vitamins and minerals that increase the individuals production of
the neurotransmitters which also help promote a sense of natural
well being.
A weekly support group and/or individual spiritually oriented
sessions help reinforce adherence and improve outcomes.
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