Carbohydrates Related Diseases

- Diabetes Mellitus Type1

- Diabetes Mellitus Type 2

- Obesity

Protein Related Diseases

- Primary Amyloidosis
- Kwashiorkor
- Marasmus

Fats related diseases

- Skin problems
- Rheumatoid Arthritis
- Multiple Sclerosis
VOCABULARY
Coxsackie B4 virus is a virus which can trigger an autoimmune
reaction which results in destruction of the insulin-producing beta cells
of the pancreas, which is one of several different etiologies of diabetes
mellitus.

HERE ARE SOME DISEASES HELPED BY A LOW FAT DIET

ARTHRITIS
Another disease which we have come to expect with old age is
arthritis. The joints become stiff and sore, sometimes to the point where
anti-inflammatory drugs are needed. Many health authorities do not
think that there is a link between diet and arthritis, but there is evidence
to the contrary. The Wyane State University Medical School put six
rheumatoid arthritis sufferers on a fat-free diet. In seven weeks all the
symptoms of the disease were gone.
RHEUMATOID ARTHRITIS
The British Medical Journal reported on a 38 year-old woman who
had been suffering from rheumatoid arthritis for 11 years. Four months
after her doctor had removed all dairy products from her diet, her
arthritic symptoms disappeared. She remained this way until, in the
interest of science; she went back to eating dairy products. Within a day
her joints became swollen and painful. When she returned to her
abstinence of dairy products, these symptoms disappeared.
It is quite possible that animal products lead to arthritis because fat
and cholesterol coat the lining of the blood vessels leading to joint
tissues. Nodes which are composed of cholesterol are often found near
arthritic joints. Arthritis sufferers tend to have high blood cholesterol
levels.
GALLSTONES
Gallstones are made up of hardened cholesterol. Diets high in fat,
cholesterol and low in fiber lead to incidences of more gallstones. More
fiber leads to fewer gallstones. It is believed that the fiber binds the
cholesterol in the colon and helps it to exit out of the system.
SKIN PROBLEMS
Acne, blackheads, and white heads are other examples of fatty
degeneration. Sticky, thick, saturated fats and trans-fatty acids clog the
narrow pores and cause infection and pimples. It would seem as if pores
are designed for only the fluid like quality of the essential fatty acids.
DIABETES
Diabetes is the sixth leading cause of death. The Lancet reported
on the study of diet in relation to diabetes. Dr. Inder Singh put 80
diabetic patients on a very low fat diet without any sugar. After six
weeks, 60% of the patients no longer needed insulin. Diabetics create
insulin, but high levels of fat in the blood cause insulin to malfunction.
Reduce the saturated fat and the insulin can do its work. Dr. David
Snowden summarized a report on 25,000 people over 21 years of age. In
this study we looked at various levels of meat consumption, and as those
levels got lower and lower, the risk of diabetes also decreased.
MULTIPLE SCLEROSIS
This disease gradually attacks the brain, spinal cord, and the
central nervous system. Within ten years of the first attack, most MS
patients will be permanently disabled. Dr. Roy Swank, head of the
Department of Neurology at the University of Oregon, tried treating
incurable MS patients with a low-fat, low-protein diet. They were also
given vitamins A, C, D, and B-complex. The results were astounding. Of
the 146 patients on the diet, 90% of those in the early stages of MS
stopped the disease-process and improved over a twenty-year period.
ASTHMA
The University Hospital in Linkoping, Sweden, put Asthma
sufferers on a vegetarian diet. Before the test, their condition was so
severe that they needed cortisone or other types of powerful medication.
After the test, medication dosages dropped an average of 50 to 90
percent. Some stopped taking the pills altogether.
ESSENTIAL FATTY ACIDS
Life without essential fatty acids is impossible. They are crucial to
the electrical reactions of cells. Essential fatty acids heal, carry vitamins,
enhance metabolism and bring oxygen to the tissues. They are required
by brain cells, sensory organs, synapses, retinas, adrenal glands and
testes. Essential fatty acids act as solvents to remove hardened fat. They
are involved in generating the electric currents that maintain a regular
heartbeat. They appear to regulate chromosome stability and will even
help you to lose weight!

THE HIGHS AND LOWS OF CARBOHYDRATES

How do foods affect blood sugar levels? The old myth that a
sugary snack will cause a dramatic rise, and then a fall, in blood sugar
levels has been overturned as researchers find out more about the
physiological effects of foods on blood sugar levels. New ways to
measure just how our blood sugar will react to various foods has
provided insights into the prevention and control of conditions such as
obesity, diabetes and heart disease and has also revolutionized diet in
sport and the foods eaten in the hours before physical exertion in sport.

GASTROINTESTINAL SURPRISES
The finding of the glycemic index resulted in a few surprises.
Originally it was believed that "complex" carbohydrate foods, such as
bread, rice and potatoes, were digested slowly, causing a gradual
increase in blood sugar levels. However, it is now known that many
starchy foods are digested very rapidly and absorbed quickly. They are
high G.I. foods. On the other hand, moderate amounts of many “sugary”
foods (those high in sucrose), such as confectionery, do not generally
produce dramatic increases in blood sugar as has always been thought.
Foods containing sucrose actually show quite low-to-moderate blood
sugar (glucose) responses - lower than foods like rice.

DIABETES MELLITUS TYPE 1

ETIOLOGY
Diabetes Mellitus Type 1, or Insulin Dependent Diabetes Mellitus
(IDDM), is a disease characterized by "auto-destruction" of the
pancreatic beta cells that produce insulin. Overtime, your body silently
destroys these cells creating an insulin deficiency. IDDM appears to
stem from an inherited defect in the immune system, triggered by some
environmental stimuli. The exact cause of the disease is still unknown;
however, scientists have isolated a few factors that may be related to
development of the disease. The purpose of this review is to provide
insight on where research is headed and what we already know about the
progression of IDDM.

SIGNS AND SYMPTOMS

The classical symptoms of type 1 diabetes include: polyuria
(frequent urination), polydipsia (increased thirst), polyphagia (increased
hunger), and weight loss.

PATHOPHYSIOLOGY
Type I Diabetes Mellitus (insulin- dependent diabetes mellitus,
IDDM) is due to destruction of pancreatic B cells. The cause of B cell
destruction in type I diabetes is unknown. A few cases have followed
viral infections, most commonly with coxsakie virus B or mumps virus.
Autoimmunity is believed to be the major mechanism involved. Islet cell
autoantibodies are present in the serum of 90% of newly diagnosed
cases. Such antibodies are directed against several cell components,
including cytoplasmic and membrane antigens or against insulin itself
(IgG and IgE antibodies). Sensitized T lymphocytes with activity against
B cells have also been demonstrated in some patients.
The cause of type 1 diabetes is not fully understood. Some theorize
that type 1 diabetes is a virally triggered autoimmune response in which
the immune system's attack virus infected cells along with the beta cells
in the pancreas. The Coxsackie virus family or German measles is
implicated, although the evidence is inconclusive. In type 1, pancreatic
beta cells in the Islets of Langerhans are destroyed decreasing
endogenous insulin production. This distinguishes type 1's origin from
type 2 DM. The type of diabetes a patient has is determined only by the
cause—fundamentally by whether the patient is insulin resistant (type 2)
or insulin deficient without insulin resistance (type 1).
This vulnerability is not shared by everyone, for not everyone
infected by the suspected organisms develops type 1 diabetes. This has
suggested presence of a genetic vulnerability and there is indeed an
observed inherited tendency to develop type 1. It has been traced to
particular HLA genotypes, though the connection between them and the
triggering of an auto-immune reaction is still poorly understood.

PREVALENCE
It is estimated that about 5%–10% of North American diabetes
patients have type 1. The fraction of type 1 in other parts of the world
differs; this is likely due to both differences in the rate of type 1 and
differences in the rate of other types, most prominently type 2. Most of
this difference is not currently understood. Variable criteria for
categorizing diabetes types may play a part. The longest surviving Type
I diabetes patient is Gladys Dull, who has lived with the condition for
over 83 years.

MANAGEMENT
- Blood Sugar Monitoring
- Islet Cell Transplantation
- Pancreas Transplant
o Pancreas transplants are generally performed together with or
some time after a kidney transplant. One reason for this is
that introducing a new kidney requires taking
immunosuppressive drugs such as cyclosporin. Nevertheless
this allows the introduction of a new, functioning pancreas to
a patient with diabetes without any additional
immunosuppressive therapy. However, pancreas transplants
alone can be wise in patients with extremely labile type 1
diabetes mellitus
- Insulin Pump
o The insulin pump is a medical device used for the
administration of insulin in the treatment of diabetes mellitus,
also known as continuous subcutaneous insulin infusion
therapy. The device includes:
 the pump itself (including controls, processing module,
 and batteries)
 a disposable reservoir for insulin (inside the pump)
 a disposable infusion set, including a cannula for
subcutaneous insertion (under the skin) and a tubing
system to interface the insulin reservoir to the cannula.

o An insulin pump is an alternative to multiple daily injections

of insulin by insulin syringe or an insulin pen and allows for
intensive insulin therapy when used in conjunction with
blood glucose monitoring and carbohydrates counting.

DIABETES MELLITUS TYPE 2

Diabetes mellitus type 2 or type 2 diabetes (formerly called non-
insulin-dependent diabetes mellitus (NIDDM), or adult-onset diabetes)
is a disorder that is characterized by high blood glucose in the context of
insulin resistance and relative insulin deficiency.

SIGNS AND SYMPTOMS

- Early symptoms may be nothing more than chronic fatigue,
generalized weakness and malaise (feeling of unease)
- Excessive urine production
- Excessive thirst and increased fluid intake
- Blurred vision (typically from lens shape alterations, due to
osmotic effects, e.g., high blood glucose levels
- Unexplained weight loss
- Lethargy
- Itching of external genitalia
- Excessive bowel movements

PATHOPHYSIOLOGY
Type 2 diabetes is characterized by peripheral insulin resistance
with an insulin-secretory defect that varies in severity. For type 2
diabetes mellitus to develop, both defects must exist: all overweight
individuals have insulin resistance, but only those with an inability to
increase beta-cell production of insulin develop diabetes. In the
progression from normal glucose tolerance to abnormal glucose
tolerance, postprandial glucose levels first increase. Eventually, fasting
hyperglycemia develops as inhibition of hepatic gluconeogenesis
declines.
Insulin resistance means that body cells do not respond
appropriately when insulin is present. Unlike type 1 diabetes mellitus,
insulin resistance is generally "post-receptor", meaning it is a problem
with the cells that respond to insulin rather than a problem with the
production of insulin.

Other important contributing factors:

- increased hepatic glucose production (e.g., from glycogen ->
glucose conversion), especially at inappropriate times (typical
cause is deranged insulin levels, as those levels control this
function in liver cells)
- decreased insulin-mediated glucose transport in (primarily) muscle
and adipose tissues (receptor and post-receptor defects)
- Impaired beta-cell function—loss of early phase of insulin release
in response to hyperglycemic stimuli.
-
MANAGEMENT
- Lifestyle Modifications
- Exercise
- Dietary Management
- Blood glucose Monitoring
- Medications
o Metformin 500mg tablets

There are several drugs available for type 2 diabetics—most are

unsuitable or even dangerous for use by type 1 diabetics.

One of the most widely used drugs now used for type 2 diabetes is
the biguanide metformin; it works primarily by reducing liver release of
blood glucose from glycogen stores and secondarily by provoking some
increase in cellular uptake of glucose in body tissues. Both historically,
and currently, the most commonly used drugs are in the Sulfonylurea
group, of which several members (including glibenclamide and
gliclazide) are widely used.

OBESITY
Obesity is a medical condition in which excess body fat has
accumulated to the extent that it may have an adverse effect on health,
leading to reduced life expectancy and/or increased health problems.
At an individual level, a combination of excessive caloric intake
and a lack of physical activity are thought to explain most cases of
obesity. A limited number of cases are due primarily to genetics,
medical reasons, or psychiatric illness. In contrast, increasing rates of
obesity at a societal level are felt to be due to an easily accessible and
palatable diet, increased reliance on cars, and mechanized
manufacturing.

CAUSES
A 2006 review identified ten other possible contributors to the
recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors
(environmental pollutants that interfere with lipid metabolism), (3)
decreased variability in ambient temperature, (4) decreased rates of
smoking, because smoking suppresses appetite, (5) increased use of
medications that can cause weight gain (e.g., atypical antipsychotics),
(6) proportional increases in ethnic and age groups that tend to be
heavier, (7) pregnancy at a later age (which may cause susceptibility to
obesity in children), (8) epigenetic risk factors passed on generationally,
(9) natural selection for higher BMI, and (10) assertive mating leading to
increased concentration of obesity risk factors (this would not
necessarily increase the number of obese people, but would increase the
average population weight)

MAJOR FACTORS:
- Diet
- Sedentary lifestyles
 - Medications

PATHOPHYSIOLOGY
Two white mice both with similar sized ears, black eyes, and pink
noses. The body of the mouse on the left, however, is about three times
the width of the normal sized mouse on the right.
A comparison of a mouse unable to produce leptin thus resulting in
obesity (left) and a normal mouse (right)
Flier summarizes the many possible pathophysiological
mechanisms involved in the development and maintenance of obesity.
This field of research had been almost unapproached until leptin was
discovered in 1994. Since this discovery, many other hormonal
mechanisms have been elucidated that participate in the regulation of
appetite and food intake, storage patterns of adipose tissue, and
development of insulin resistance. Since leptin's discovery, ghrelin,
insulin, orexin, PYY 3-36, cholecystokinin, adiponectin, as well as many
other mediators have been studied. The adipokines are mediators
produced by adipose tissue; their action is thought to modify many
obesity-related diseases.

PREVALENCE
A map of the world with countries colored to reflect the percentage
of men who are obese. Obese males have higher prevalence (above
30%) in the U.S. and some Middle Eastern countries, medium
prevalence in the rest of North America and Europe, and lower
prevalence (<5%) in most of Asia and Africa.
Before the 20th century, obesity was rare; in 1997 the WHO
formally recognized obesity as a global epidemic. As of 2005 the WHO
estimates that at least 400 million adults (9.8%) are obese, with higher
rates among women than men. The rate of obesity also increases with
age at least up to 50 or 60 years old and severe obesity in the United
States, Australia, and Canada is increasing faster than the overall rate of
obesity. Once considered a problem only of high-income countries,
obesity rates are rising worldwide and affecting both the developed and
developing world. These increases have been felt most dramatically in
urban settings. The only remaining region of the world where obesity is
not common is sub-Saharan Africa.

MANAGEMENT
The main treatment for obesity consists of dieting and physical
exercise. Diet programs may produce weight loss over the short term,
but keeping this weight off can be a problem and often requires making
exercise and a lower calorie diet a permanent part of a person's lifestyle.
Success rates of long-term weight loss maintenance are low and range
from 2–20%. In a more structured setting, however, 67% of people who
lost greater than 10% of their body mass maintained or continued to lose
weight one year later. An average maintained weight loss of more than 3
kg (6.6 lbs.) or 3% of total body mass could be sustained for five years.

EXERCISE
With use, muscles consume energy derived from both fat and
glycogen. Due to the large size of leg muscles, walking, running, and
cycling are the most effective means of exercise to reduce body fat.
Exercise affects macronutrient balance. During moderate exercise,
equivalent to a brisk walk, there is a shift to greater use of fat as a fuel.
To maintain health the American Heart Association recommends a
minimum of 30 minutes of moderate exercise at least 5 days a week.

PRIMARY AMYLOIDOSIS
Primary amyloidosis is a disorder in which protein fibers are
deposited in tissues and organs, harming them.
In medicine, amyloidosis refers to a variety of conditions in which
amyloid proteins are abnormally deposited in organs and/or tissues. A
protein is described as being amyloid if, due to an alteration in its
secondary structure, it takes on a particular aggregated insoluble form
similar to the beta-pleated sheet. Symptoms vary widely depending upon
the site of amyloid deposition. Amyloidosis may be inherited or
acquired.

CAUSES
 The cause of primary amyloidosis is unknown, but the condition is
related to abnormal production of antibodies by a type of immune cell
called plasma cells.
The symptoms depend on the organs affected by the deposits.
These organs can include the tongue, intestines, skeletal and smooth
muscles, nerves, skin, ligaments, heart, liver, spleen, and kidneys.
Primary amyloidosis can result in conditions that include:
- CARPAL TUNNEL SYNDROME
o Carpal tunnel syndrome is pressure on the median nerve --
the nerve in the wrist that supplies feeling and movement to
parts of the hand. It can lead to numbness, tingling,
weakness, or muscle damage in the hand and fingers.
- GASTROINTESTINAL REFLUX DISEASE (GERD)
o Gastroesophageal reflux disease (GERD) is a condition in
which the stomach contents (food or liquid) leak backwards
from the stomach into the esophagus (the tube from the
mouth to the stomach). This action can irritate the esophagus,
causing heartburn and other symptoms.
- HEART MUSCLE DAMAGE (Cardiomyopathy)
o Cardiomyopathy is a weakening of the heart muscle or a
change in heart muscle structure. It is often associated with
inadequate heart pumping or other heart function problems.
- KIDNEY FAILURE
o Acute (sudden) kidney failure is the sudden loss of the ability
of the kidneys to remove waste and concentrate urine without
losing electrolytes.
- MALABSORPTION
o Malabsorption is difficulty digesting or absorbing nutrients
from food.

The deposits build up in the affected organs, causing them to become

stiff, which decreases their ability to function.

Risk factors have not been identified. Primary amyloidosis is rare. It is

similar to multiple myeloma, and is treated the same way.

SYMPTOMS
- Enlarged tongue
- Fatigue
- Irregular heart rhythm
- Numbness of hands and feet
- Shortness of breath
- Skin changes
- Swallowing difficulties
- Swelling in the arms and legs
- Weak hand grip loss

ADDITIONAL SYMPTOMS THAT MAY BE ASSOCIATED

WITH THIS DISEASE:
- Clay-colored stools
- Urine output
- Diarrhea
- Hoarseness or changing voice
- Joint pain
- Other tongue problems
- Weakness

EXAMINATION AND TESTS

Your doctor may discover that you have an enlarged liver or
spleen.
If specific organ damage is suspected, your doctor may order tests
to confirm amyloidosis of that organ. For example:
- Abdominal ultrasound may reveal a swollen liver or spleen.
- An abdominal fat pad biopsy, rectal mucosa biopsy, or a bone
marrow biopsy can help confirm the diagnosis.
- A heart evaluation, including an ECG,may reveal arrhythmias,
abnormal heart sounds, or signs of congestive heart failure. An
echocardiogram shows poor motion of the heart wall, due to a stiff
heart muscle.
 - A carpal tunnel syndrome evaluation may show that hand grips
are weak.Nerve conduction velocity shows abnormalities.
- Kidney function tests may show signs of kidney failure or too
much protein in the urine ( nephrotic syndrome).
o BUN level is increased.
o Serum creatinine is increased.
o Urinalysis shows protein, casts, or fat bodies.

TREATMENT
Some patients with primary amyloidosis respond to chemotherapy
directed at the abnormal plasma cells. Stem cell transplantation may be
used, as in multiple myeloma.
In secondary amyloidosis, aggressive treatment of the underlying
disease can improve symptoms and/or slow progression of disease.
Complications such as heart failure, kidney failure, and other problems
can sometimes be treated as necessary.

KWASHIORKOR
Kwashiorkor is an acute form of childhood protein-energy
malnutrition characterized by edema, irritability, anorexia, ulcerating
dermatoses, and an enlarged liver with fatty infiltrates. The presence of
edema caused by poor nutrition defines kwashiorkor.[1] Kwashiorkor
was thought to be caused by insufficient protein consumption but with
sufficient calorie intake, distinguishing it from marasmus. More
recently, micronutrient and antioxidant deficiencies have come to be
recognized as contributing to kwashiorkor as well. Cases in the
developed world are rare.
Jamaican pediatrician Dr. Cicely D. Williams introduced the name
into the medical community in her 1935 Lancet article. The name is
derived from the Ga language of coastal Ghana, translated "the sickness
the baby gets when the new baby comes", and reflecting the
development of the condition in an older child who has been weaned
from the breast when a younger sibling comes. Breast milk contains
proteins and amino acids vital to a child's growth. In at-risk populations,
kwashiorkor may develop after a mother weans her child from breast
milk and replaces the diet with foods high in starches and carbohydrates
and deficient in protein.

SIGNS AND SYMPTOMS

The defining sign of kwashiorkor in a malnourished child is pedal
edema (swelling of the feet). Other signs include a distended abdomen,
an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin
depigmentation and dermatitis. Children with kwashiorkor often develop
irritability and anorexia.

SYMPTOMS
- Changes in skin pigment
- Coma (late stage)
- Decreased muscle mass
- Diarrhea
- Failure to gain weight and grow
- Fatigue
- Hair changes (change in color or texture)
- Increased and more severe infections due to damaged immune
system
- Irritability
- Large belly that sticks out (protrudes) or apathy
- Loss of muscle mass
- Rash (dermatitis)
- Shock (late stage)
- Swelling (edema)

Victims of kwashiorkor fail to produce antibodies following

vaccination against diseases, including diphtheria and typhoid.
Generally, the disease can be treated by adding food energy and protein
to the diet; however, it can have a long-term impact on a child's physical
and mental development, and in severe cases may lead to death.

CAUSES
 Kwashiorkor is most common in areas where there is:
- Famine
- Limited food supply
- Low levels of education (when people do not understand how to
eat a proper diet)

This disease is more common in very poor countries. It often occurs

during a drought or other natural disaster, or during political unrest.
These conditions are responsible for a lack of food, which leads to
malnutrition.

PATHOPHYSIOLOGY
The unifying pathophysiological concept of kwashiorkor is that
cell membranes are damaged throughout the body. This damage results
in the egress of potassium and water from cells and dysfunction of most
major organ systems. It is not a condition of water retention but one
where intracellular water moves to the extracellular space resulting in
oedema. There is a profound reduction in whole body potassium to
about 35 mmol/kg (44 mmol/kg is normal). This corresponds to the loss
of intracellular potassium.

TREATMENT
Getting more calories and protein will correct kwashiorkor, if
treatment is started early enough. However, children who have had this
condition will never reach their full height and growth.
Treatment depends on the severity of the condition. People who
are in shock need immediate treatment to restore blood volume and
maintain blood pressure.
Calories are given first in the form of carbohydrates, simple sugars,
and fats. Proteins are started after other sources of calories have already
provided energy. Vitamin and mineral supplements are essential.
Since the person will have been without much food for a long
period of time, eating can cause problems, especially if the calories are
too high at first. Food must be reintroduced slowly. Carbohydrates are
given first to supply energy, followed by protein foods.