Nutrition

Topic- Diabetes Mellitus

Submitted to::. Submitted by:

R/s ma'am. Yuti Sharma
Dr.Shreya sinha BNYS III year

Reporter ： *** Date ： 2019.4

 Introduction
• Diabetes mellitus is taken from the Greek word diabetes, meaning siphon - to
pass through and the Latin word mellitus meaning sweet. A review of the
history shows that the term "diabetes" was first used by Apollonius of
Memphis around 250 to 300 BC. Ancient Greek, Indian, and Egyptian
civilizations discovered the sweet nature of urine in this condition, and hence
the propagation of the word Diabetes Mellitus came into being.
• Mering and Minkowski, in 1889, discovered the role of the pancreas in the
pathogenesis of diabetes. In 1922 Banting, Best, and Collip purified the
hormone insulin from the pancreas of cows at the University of Toronto,
leading to the availability of an effective treatment for diabetes in 1922. Over
the years, exceptional work has taken place, and multiple discoveries, as well
as management strategies, have been created to tackle this growing problem.
Unfortunately, even today, diabetes is one of the most common chronic
diseases in the country and worldwide. In the US, it remains as the seventh
leading cause of death.
 Definition
• Diabetes mellitus (DM) is a metabolic disease, involving inappropriately
elevated blood glucose levels.
• DM has several categories, including type 1, type 2, maturity-onset diabetes of
the young (MODY), gestational diabetes, neonatal diabetes, and secondary
causes due to endocrinopathies, steroid use, etc.
• The main subtypes of DM are Type 1 diabetes mellitus (T1DM) and Type 2
diabetes mellitus (T2DM), which classically result from defective insulin
secretion (T1DM) and/or action (T2DM)
• T1DM presents in children or adolescents, while T2DM is thought to affect
middle-aged and older adults who have prolonged hyperglycemia due to poor
lifestyle and dietary choices. The pathogenesis for T1DM and T2DM is
drastically different, and therefore each type has various etiologies,
presentations, and treatments.
Type 1 Diabetes Mellitus
• Type 1 diabetes mellitus (T1D) is an autoimmune disease that leads to
the destruction of insulin-producing pancreatic beta cells. Individuals
with T1D require life-long insulin replacement with multiple daily
insulin injections daily, insulin pump therapy, or the use of an
automated insulin delivery ssystem.
• Loss of insulin secretion can occur quickly or gradually.
• In T1D, there is autoimmune destruction of the beta cells in the
pancreatic islets over months or years, causing an absolute deficiency
of insulin.
 Pathophysiology of DM 1
• The development of T1D occurs in 3 stages.
• Stage 1 is asymptomatic and characterized by normal fasting glucose,
normal glucose tolerance, and the presence of ≥2 pancreatic
autoantibodies.
• Stage 2 diagnostic criteria include the presence of pancreatic
autoantibodies (usually multiple) and dysglycemia: impaired fasting
glucose (fasting glucose 100 to 125 mg/dL) or impaired glucose tolerance
(2-hour post-75 gm glucose load glucose 140 to 199 mg/dL) or an HbA1c
5.7% to 6.4%. Individuals remain asymptomatic.
• In stage 3, there is diabetes, defined by hyperglycemia (random glucose
≥200 mg/dL) with clinical symptoms, fasting glucose ≥126 mg/dL, glucose
≥200 mg/dL two hours after ingesting 75 g of glucose during an oral
glucose tolerance test and/or HbA1c ≥6.5%.
• If the individual lacks classic symptoms of hyperglycemia or
hyperglycemic crisis, it is recommended that two tests be performed
(simultaneously or at different times) to confirm the diagnosis. If
there is an acute onset of symptoms with hyperglycemia, as more
often occurs in youth-onset T1D, HbA1c may be misleading at the
time of diagnosis, and glucose criteria should be used.
• Without insulin, diabetic ketoacidosis (DKA) develops and is life-
threatening.
Diabetic ketoacidosis
• Diabetic ketoacidosis (DKA) is a serious complication of diabetes that
can be life-threatening. DKA is most common among people with type
1 diabetes
• DKA develops when our body doesn’t have enough insulin to allow
blood sugar into our cells for use as energy. Instead, our liver breaks
down fat for fuel, a process that produces acids called ketones. When
too many ketones are produced too fast, they can build up to
dangerous levels in our body.
Causes
• Type 1 diabetes is thought to be caused by an autoimmune reaction
(the body attacks itself by mistake). This reaction destroys the cells in
the pancreas that make insulin, called beta cells. This process can go on
for months or years before any symptoms appear.
• Genetic predisposition- Some people have certain genes (traits passed
on from parent to child) that make them more likely to develop type 1
diabetes. However, many of them won’t go on to have type 1 diabetes
even if they have the genes.
• Environmental triggers- A trigger in the environment, such as a virus,
may also play a part in developing type 1 diabetes. Diet and lifestyle
habits don’t cause type 1 diabetes.Causes
Signs and symptoms
• The most common symptoms of type 1 diabetes include:
• Abnormal thirst and dry mouth
• Sudden weight loss
• Frequent urination
• Lack of energy, tiredness
• Constant hunger
• Blurred vision
• Bedwetting
• Diagnosing type 1 diabetes can be difficult so additional tests may be
required to confirm a diagnosis
Diagnosis
• Diabetes is typically diagnosed by a blood test showing unusually high
blood sugar.
• The World Health Organization defines diabetes as blood sugar levels
at or above 7.0 mmol/L (126 mg/dL) after fasting for at least eight
hours, or a glucose level at or above 11.1 mmol/L (200 mg/dL) two
hours after an oral glucose tolerance test.
Differentiating Diabetes mellitus type 1 from other Diseases

• Differential diagnosis of type 1 diabetes mellitus, include:

• Type 2 DM
• MODY-DM
• Psychogenic polydipsia
• Diabetes insipidus
• Transient hyperglycemia
• Steroid therapy
• Renal tubular acidosis type-1
• Glucagonoma
• Cushing's syndrome
• Hypothyroidism
• Wolfram syndrome
• Alstrom syndrome
 Lab Investigations
• There are several ways to diagnose diabetes. It is best for the tests to be repeated on a second day
to make sure of the diagnosis.
• A1C. The hemoglobin A1C test measures your average blood glucose for the past 2 to 3 months.
Diabetes is diagnosed at an A1C of greater than or equal to 6.5%.
• Diagnosing Prediabetes or Diabetes
• Normal Below 5.7%
• Prediabetes . 5.7% to 6.4%
• Diabetes 6.5% or above
• Fasting plasma glucose (FPG). This test checks your blood glucose levels after fasting for at least 8
hours, usually overnight. You may have water before this test is done, but nothing else. Diabetes is
diagnosed at a fasting blood glucose of greater than or equal to 126 mg/dl.
• A fasting blood sugar level of 99 mg/dL or lower is normal, 100 to 125 mg/dL indicates you have
prediabetes, and 126 mg/dL or higher indicates you have diabetes
• Oral glucose tolerance test (OGTT). This is a 2-hour test that checks your blood glucose levels before
and 2 hours after you drink a sugary drink. This test tells your doctor how your body processes
glucose. Diabetes is diagnosed at a 2-hour blood glucose of greater than or equal to 200 mg/dl.
• Random glucose test. This blood test is done at any time of the day. Diabetes is diagnosed at blood
glucose of greater than or equal to 200 mg/dl with the symptoms of hyperglycemia or
hyperglycemic crisis.
• Insulin and c-peptide levels. Levels of these will be low or normal with type 1 diabetes, but
high with type 2 diabetes.
• A normal result is between 0.5 to 2.0 nanograms per milliliter (ng/mL), or 0.17 to 0.83
nanomoles per liter (nmol/L).
• C-peptide level is based on blood sugar level. C-peptide is a sign that your body is
producing insulin. A low level (or no C-peptide) indicates that your pancreas is producing
little or no insulin.
• Antibody levels. People with newly diagnosed type 1 diabetes will usually have high levels
of antibodies against certain proteins found in the pancreas.
• The antibodies tested for are:
• Islet cell cytoplasmic autoantibodies (ICA)
• Glutamic acid decarboxylase autoantibodies (GADA)
• Insulinoma-associated-2 autoantibodies (IA-2A)
• Insulin autoantibodies (IAA)
• If you have some combination of these antibodies in high levels, it could mean you have
type 1 diabetes. Or it could mean you are at risk of developing it. These antibodies often
show up years before symptoms begin. So this test is useful if you have a family history of
type 1 diabetes.
TYPE 2 DIABETES MELLITUS
Introduction
• Type 2 DM, adult onset diabetes, is called non- insulin dependent diabetes.
• It is the most common form of diabetes and develops slowly and is usually milder
and more stable.
• Insulin may be produced by pancreas but action is impaired. This form occurs mainly
in adults and the person is usually overweight. Acidosis is infrequent.
• The majority of patients improve with weight loss and are maintained on diet
therapy.
• Type 2 Diabetes Mellitus (T2DM) is one of the most common metabolic disorders
worldwide and its development is primarily caused by a combination of two main
factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-
sensitive tissues to respond to insulin. Insulin release and action have to precisely
meet the metabolic demand; hence, the molecular mechanisms involved in the
synthesis and release of insulin, as well as the insulin response in tissues must be
tightly regulated. Therefore, defects in any of the mechanisms involved can lead to a
metabolic imbalance that leads to the pathogenesis of T2DM.
Pathophysioloy
• Regarding the pathophysiology of the disease, a malfunctioning of the
feedback loops between insulin action and insulin secretion results in
abnormally high glucose levels in blood. In the case of β-cell
dysfunction, insulin secretion is reduced, limiting the body’s capacity
to maintain physiological glucose levels. On the other hand, IR
contributes to increased glucose production in the liver and
decreased glucose uptake both in the muscle, liver and adipose tissue.
Even if both processes take place early in the pathogenesis and
contribute to the development of the disease, β-cell dysfunction is
usually more severe than IR. However, when both β-cell dysfunction
and IR are present, hyperglycaemia is amplified leading to the
progression of T2DM.
• β-cells are responsible for insulin production, which is synthesized as pre-
proinsulin. In the maturation process, pre-proinsulin undergoes a
conformational modification carried out with the help of several proteins in the
endoplasmic reticulum (ER) to yield proinsulin [37]. Afterwards, proinsulin is
translocated from the ER to the Golgi apparatus (GA), entering into immature
secretory vesicles and being cleaved into C-peptide and insulin.
• Insulin release is primarily triggered by a response to high glucose
concentrations.When circulating glucose levels increase, β-cells take in glucose
mainly through the glucose transporter 2 (GLUT2), a solute carrier protein that
also works as a glucose sensor for β-cells. Once glucose enters, glucose
catabolism is activated, increasing the intracellular ATP/ADP ratio, which
induces the closing of ATP-dependant potassium channels in the plasma
membrane. This leads to membrane depolarization and opening of the voltage
dependant Ca2+ channels, enabling Ca2+ to enter the cell. The rise in the
intracellular Ca2+ concentration triggers the priming and fusion of the
secretory insulin-containing granules to the plasma membrane, resulting in
insulin exocytosis.
• other cell signals can also assist or enhance insulin release from β-cells.
• β-cell dysfunction has been traditionally associated with β-cell death.
However, recent evidence suggests that the dysfunction of β-cells in T2DM
might be due to a more complex network of interactions between the
environment and different molecular pathways implicated in cell biology. In
an excessive nutritional state, similar to that found in obesity, hyperglycemia
and hyperlipidemia are often present, favoring IR and chronic inflammation.
Under these circumstances, β-cells, due to differences in their genetic
susceptibility, are subject to toxic pressures including inflammation,
inflammatory stress, ER stress, metabolic/oxidative stress, amyloid stress,
with the potential of ultimately leading to a loss of islet integrity.
• An excess of FFAs and hyperglycemia lead to β-cell dysfunction by inducing
ER stress through the activation of the apoptotic unfolded protein response
(UPR) pathways. In fact, lipotoxicity, glucotoxicity and glucolipotoxicity
occurring in obesity, induce metabolic and oxidative stress that leads to β-cell
damage.
• Insulin secretion has to be finely regulated to precisely meet metabolic
demand. For that reason, proper islet integrity must be conserved in order to
allow β-cells to respond to metabolic needs. Under pathogenic conditions, the
mechanism described above can ultimately lead to disruption of islet
integrity/organization, impairing optimal cell-to-cell communication within
pancreatic islets, contributing to poor regulation of insulin and glucagon
release and ultimately exacerbating the hyperglycemia. Defects in the
synthesis of any insulin precursors, or insulin itself, as well as disruption of the
secretion mechanism, can lead to insulin secretory dysfunction, the primary
driver of β-cell failure, and a foundation of T2DM. For instance, reduced
expression in the GLUT2 glucose transporter would affect the downstream
signaling pathway, while failure in the folding of proinsulin is another finding
commonly linked to deficient insulin production and diabetes.
CAUSES
• Genetics- Genetic factors are more important in the development of this
type of diabetes than in type 1 diabetes. Type 2 DM is commonly associated
with obesity, hypertension and hyperlipidemia. In all this, insulin resistance
being the primary defect known as syndrome X or metabolic syndrome. It
seems likely that type 2DM represents a combination of major and minor
genes affecting insulin secretion, insulin action and obesity.
• Environmental - Obesity probably act as a diabetogenic factor through
increasing resistance to the action of insulin among those genetically
predisposed to develop type 2 DM.
• Higher intake of refined grains which have high glycaemic index such as
white rice, combined with sedentary activity could be a major reason for the
incedence of obesity , diabetes and cvs diseases. Recently resistin, a cysteine
rich protein has been implicated at the molecular link between obesity and
type2 DM
• Type 2DM is principally a disease of middle age and elderly.
SIGNS AND SYMPTOMS
• Symptoms may include:
• Frequent bladder infections
• Skin infections that don't heal easily
• Excess thirst
• Peeing often
• Weight loss
• Blurred vision
• Nausea and vomiting
• Extreme weakness and fatigue
• Irritability and mood changes
• Dry, itchy skin
• Tingling or loss of feeling in the hands or feet
• Some people who have type 2 diabetes don’t have symptoms. Symptoms may be
mild and you may not notice them.
DIAGNOSIS
• Diabetes can be diagnosed with several tests. It is best to repeat the tests a second
time to confirm the results. The tests include:

• A1C. This is the hemoglobin A1C test. It measures your average blood glucose for the
past 2 to 3 months. An A1C of 6.5% or higher means you have diabetes.
• Fasting plasma glucose (FPG). This test checks your blood glucose levels after 8 hours
of fasting. You usually get this test before your first meal of the day. This is called your
fasting blood glucose level. A result higher than or equal to 126 mg/dl means you
have diabetes.
• Oral glucose tolerance test (OGTT). For this test, your glucose level is measured
before and then after 2 hours after you drink a sugary drink. This shows how well
your body processes glucose. A result of 200 mg/dl or higher after 2 hours means you
have diabetes.
• Random glucose test. This blood test is done at any time of the day. Blood glucose of
200 mg/dl or higher with symptoms of high blood sugar means you have diabetes.
RISK FACTORS
• Risk factors include:
• Age. People ages 45 and older are at higher risk for diabetes.
• Family history of diabetes. The condition tends to run in families.
• Extra weight. Being overweight puts you at higher risk.
• Lack of exercise. Not enough physical activity also puts you at risk.
• Taking certain medicines. These include steroids, some diuretics, and antipsychotics.
• Race and ethnicity. People who have African, Hispanic, Asian, Pacific Island, or American
Indian heritage are more likely to develop type 2 diabetes.
• Gestational diabetes. Having diabetes in pregnancy puts you at higher risk of type 2
diabetes later.
• Large baby. Giving birth to a baby over 9 pounds puts you at risk.
• Low HDL. This means low levels of the "good cholesterol."
• A high triglyceride level. This is a type of blood fat.
• Smoking. Being a smoker puts you at higher risk.
• Other health conditions. Some conditions are linked with type 2 diabetes. These include
polycystic ovary syndrome, acanthosis nigricans (patches of darker skin), or being born at a
PREVENTION
• Control your weight-- Excess weight is the single most important cause of type 2 diabetes.
Being overweight increases the chances of developing type 2 diabetes seven-fold. Being obese
makes you 20 to 40 times more likely to develop diabetes than someone with a healthy
weight. Losing weight can help if your weight is above the healthy-weight range. Losing 7-10%
of your current weight can cut your chances of developing type 2 diabetes in half.
• Get moving—and turn off the televisionInactivity promotes type 2 diabetes. Working your
muscles more often and making them work harder improves their ability to use insulin and
absorb glucose. This puts less stress on your insulin-making cells. So trade some of your sit-
time for fit-time.Long bouts of hot, sweaty exercise aren’t necessary to reap this benefit.
Findings from the Nurses’ Health Study and Health Professionals Follow-up Study suggest that
walking briskly for a half hour every day reduces the risk of developing type 2 diabetes by
30%. More recently, The Black Women’s Health Study reported similar diabetes-prevention
benefits for brisk walking of more than 5 hours per week. This amount of exercise has a
variety of other benefits as well. And even greater cardiovascular and other advantages can be
attained by more, and more intense, exercise.Television-watching appears to be an especially-
detrimental form of inactivity: Every two hours you spend watching TV instead of pursuing
something more active increases the chances of developing diabetes by 20%; it also increases
the risk of heart disease (15%) and early death (13%). The more television people watch, the
more likely they are to be overweight or obese, and this seems to explain part of the TV
viewing-diabetes link. The unhealthy diet patterns associated with TV watching may also
explain some of this relationship.
• Tune Up Your Diet-- Four dietary changes can have a big impact on the risk of type 2
diabetes.
• 1. Choose whole grains and whole grain products over refined grains and other highly
processed carbohydrates.
• 2. Skip the sugary drinks, and choose water, coffee, or tea instead.
• 3. Choose healthy fats.
• 4. Limit red meat and avoid processed meat; choose nuts, beans, whole grains, poultry, or
fish instead.
• Don’t smoke-- Add type 2 diabetes to the long list of health problems linked with
smoking. Smokers are roughly 50% more likely to develop diabetes than nonsmokers, and
heavy smokers have an even higher risk.
• Light to moderate alcohol consumption-- Evidence has consistently linked moderate
alcohol consumption with reduced risk of heart disease. The same may be true for type 2
diabetes. Moderate amounts of alcohol—up to a drink a day for women, up to two drinks a
day for men—increases the efficiency of insulin at getting glucose inside cells. And some
studies indicate that moderate alcohol consumption decreases the risk of type 2 diabetes.
[1, 34-39], but excess alcohol intake actually increases the risk. If you already drink alcohol,
the key is to keep your consumption in the moderate range, as higher amounts of alcohol
could increase diabetes risk. [40] If you don’t drink alcohol, there’s no need to start—you
can get the same benefits by losing weight, exercising more, and changing your eating
NUTRITONAL MANGEMENT OF DM
• Dietary masures are an essential part of treatment of diabetic
patients, whether they are on diet alone or on sulphonylurea drug or
insulin. If a fixed daily intake is to be achieved an exchange system is
necessary.
• Food Exchange lists-- The diet for the diabetic patient is prescribed in
terms of excahnge lists. Food exchange lists are groups of measured
foods of the same calorific value and similar protein, fat and
carbolhydrate and can be substituted one for another in a meal plan.
All foods of exchange make a specific coontribution to a good diet.
None of the exchange groups can itself supply all the nutrrients
needed for a well balanced diet. The food exchange list helps the
patient to:
1. Restrict the food intake according to the insulin prescription so that both
hyperglycaemia and hypoglycaemia can be prevented.
2. Have a variety in the diet so that he can adhere to it always
3. Easy learnning of the principles of diet.
Since diabetes is a chronic disease patient need to be educated regarding diet
prescription and food exchange list helps in this. By following the food
exchange list, the ptient can also maintain body weight.
DIET and INSULIN
• The philosophy of diet therapy for the juvenile diabetic is that while in a
healthy child, the insulin secretion matches the food intake, in a diabetic
child the food intake has to match the injected insulin.A child unlike an adult,
is still in the process of growth and development and is bound to have more
activity.
• Dietary measures should be used to control blood glucose and to minimize
the risk of hypoglycaemia and to reduce the long-term complications.
• The doctor will decide the type of insulin that patient requires. A person who
is on short acting insulin has to be more careful with the timing of his meals.
• The quantity of calories/carbohydrates also should match the dose of insulin
given.
• Measured diets using household measures or weighing scales are used by
type 1 diabetes patients.
• In addition to a regular schedule of breakfast, two meals and evening tea,
patients with type 1 diabetes may require bedtime snacks to prevent
hypoglycaemia during the night.
• The use of acarbose in combination with the insulin reduces the post prandial
blood glucose level in patients with type 1 diabetes who are not satisfactorily
controlled by the use of insulin alone. It prevents long term diabetic
complications. It is safe and effective agent.
• Insulin dose needs to be adjusted according to the patient’s physical activity.The
patient has to maintain a set patterrn for the quality and quantity of meals,
timing of the meals andtype of physical activity he does to control the blood
sugar level.
• NUTRITIONAL REQUIREMENTS:
• ENERGY:- hospitalised patients are given 25 kcal/kg body weight
• CARBOHYDRATES:- crbohydrate restriction impairs insulin sensitivity and reversed
by high carbohydrate diet.High carbohydrate and high fiber diet improve insulin
binding and increase in insulin receptor binding. Carbohydrate is maintained
about 45-60% of total calories.Most carbohydrates should be in the form of
polysaccahrides such as whole grains. Rapidly absorbed mono and disaccharides
such as sweets, chocolates and sweeetened drinks should be avoided.
High fiber and low glycemic index foods are preferred.
several studies have shown that raising the carbohydrate intake does not
adversely affect the fasting blood glucose levels, glucose tolerance or insulin
reqirements provided that total calories are not increased. insulin needs
aremore closely related to the carbohydrate intake than with the total calorie
intake. Only comlex carbohydrates should be included in the diet.
Carbohydrate should be distributed in accordance with the one’s daily needs,
particularly type1 diabetics, who are on short acting insulin. One carbohydrate
exchange is equal to 15 g of carbohydrate.
• PROTEINS:- A diet high in protein (15-20% of total intake) is good for the
health of diabetics because it supplies the essential amino acids needed for
tissue repair. Protein does not rasise blood sugar during absorption as do
carbohydrates and it does not supply as many calories as fats.
In patient’s with type 2DM, consumption of proteiin along with carbohydrate
will lower the blood glucose concentration due to amino acid stimulation of
insulin secretion. Proteins also promotes satiety and helps both types of
diabetic patients to adhere to the carbohydrate allowance.
• VITAMINS AND MINERALS:-- Diabetics who consume <1200kcal/day require
supplementation of micronutrients. Supplementation of vitamin B12, calcium and iron can
be given to vegans, pregnant and lactating patients. Consumption of diet rich in vitamiin C
and E antioxidants should be encouraged. Foods rich in minerals especially magnesium and
zinc need to be taken. Vitamin D deficiency should be taken in the elderly or
institutionalised.
Chromimum : Most diabetics are not chromium deficient but severe chromium deficiency
can lead to glucose intolerance and insulin resistance. Chromium prevents loss of lean
muscle, promotes weight loss and lower cholesterol and triglycerides. Chromium
supplementation decreases the requirement for insulin or oral hypoglycaemic agents in
patients with type 2 diabetes.
Zinc : zinc deficiency is associated with reduced insulin secretion and increased insulin
resistance. Very high or very low plasma levels impair the secretion of insulin. Pregnancy
related diabetic complications are seen more often in women with zinc deficiency compared
to women with normal zinc levels.
Sodium and Potassium: Dietary sodium may have a role in the development of insulin
resistance apart from its role in maintaining blood pressure. Moderate sodium restriction is
beneficial. A new study claimed that consuming diet rich in potassium may help protect the
heart and kidney health of patients with type 2 diabetes.
When hyperglycaemia is present, protein intake may be >0.8g/kg body weight.
In type 1 DM children, 1-1.5g/kg body weight is recommended. In dibetes with renal
problems, protein is restricted to 0.6g/kg body weight.
Pulses like beans, peas and lentils are high in protein and fiber, low in fat foods and have
low GI and GL. Proteins from vegetarian sources are better than from flesh foods.
Vegetarian sources do not contribute to cholesterol and rich in fiber.
• FAT:- Low fat diet increases insulin binding and also reduces LDL and VLDL levels and
reduce the incidence of atherosclerosis which is more common in diabetics. Fat content
in the diet should be 15-25% of total calories and higher in polyunsaturated fatty acids,
saturated fats should be <7% of total calories.
Diabetics can take 20-25g/d visible fat. Total quantity as well as the type of fat influence
the serum lipids and could increase the risk for heart diseases. Diabetics can consume fish
or chicken without skin, instead of mutton, liver and brain. Diabetics should also focus on
taking protective fats from nuts, seeds, cold pressed oils and fatty fish. Omega-3 fatty acids
are anti-inflammatory, antithrombotic, hypolipidemic and vasodilatory. Fish, mustard,
soyabean, walnuts, flaxseeds, greenleafy vegetables, fenugreek seeds and spirulina are rich
in omega-3 fatty acids and should be included in the diet of diabetics. Trans fats should be
avoided , blended vegetable oils should be consumed.
• Dietary fiber :- Dietary fiber and complex carbohydrate benefit type 1 and
type 2 DM. Such diets lower insulin reqirements, increase insulin sensitivity,
decrease cholesterol, helps in weight control and lower B.P.
Soluble fibres such as pectin, gums, hemicellulose(in fruits) increase intestinal
transit time, delay gastric emptying, slow glucose absorption and low serum
cholesterol. About 20-30 g of soluble fibre should be taken.
Insoluble fibres such as cellulose and lignin( vegetables, grains) decrease
intestinal transit time, increase faecal bulk, delay glucose absorption and slow
starch hydrolysis.
Consumption of brown rice in place of white rice can help reduce 24h glucose
and fasting insulin responses among overweight indians. Processed foods
should be avoided.
• FLUIDS:- fluids are essential for diabetics who are at a higher risk of
dehydration. Soft drinks, sweetened fruit juices and energy and sports drinks
are to be avoided.
WHAT TO EAT AND WHAT NOT:
FOODS TO BE AVOIDED
• Simple sugars(glucose, honey, syrups), sweets, dried fruits, cake,
candy, fried foods , alcohol, jaggery, brown sugar,sweetened juices,
roots and tubers, banana, pineapple.
EATEN IN MODERATION
• Fats, cereals, pulses, meat, eggs, nuts, fruits .
PERMITTED FOODS
• Green leafy vegetables, fruits containing more than 10g/100g total
free sugar content lemon, clear soups, onion, mint, spices, salads,
plain coffee or tea, skimmed milk, fenugreek seeds and powder.
THANK YOU