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Micronutrients, Minerals And Their Diseases
VITAMINS
Definition
Vitamins are organic substances with key roles in certain metabolic
pathways
Fat-soluble (vitamins A, D, E and K)
Water-soluble (vitamins of the B complex group and vitamin C).
Reference nutrient intake (RNI)
Fat Solouble
Rich
Important
A (retinol) Liver Milk and milk products, eggs, fish oils
700 µg men -600 µg women
D (cholecalciferol) Fish oils
UV exposure to skin
10 µg if
> 65 yrs or no sunlight exposure-Egg yolks, margarine, fortified
cereals
E (tocopherol)
Sunflower oil
Vegetables, nuts, seed oils
No RNI. Safe intake:4 mg men-3 mg women
K
Green vegetables
Soya oil, menaquinones
produced by intestinal bacteria-Safei ntake: 1 µg/kg
(phylloquinone, menaquinone)
Water-soluble
B1 (thiamin)Pork Cereals, grains, beans
0.8 mg per 9.68 MJ
(2000 kcal) energy intake
B2 (riboflavin)
Milk Milk and milk products, breakfast
cereals, bread
1.3 mg men-1.1 mg women
B3 (niacin, nicotinic acid, nicotinamide)
Meat, cereals
17 mg men-13 mg women
B6 (pyridoxine) Meat, fish, potatoes, bananas Vegetables,
intestinal microflora synthesis-1.4 mg men-1.2 mg women
Folate Liver
Green leafy
vegetables, fortified breakfast cereals 200 µg
B12 (cobalamin) Animal products Bacterial colonisation
1.5 µg
2
Biotin Egg yolk
Intestinal flora
No RNI. Safe intake: 10–
200 µg
C (ascorbic acid) Citrus fruit Fresh fruit, fresh and frozen
vegetables 40 mg
Some vitamins also have pharmacological actions when given at
supraphysiological doses, e.g. the use of vitamin A for acne.
Taking vitamin supplements is fashionable in many countries,
although there is no evidence of benefit.
Toxic effects are most serious with high dosages of vitamins A,
B6 and D.
Measurements in blood should be interpreted carefully in
conjunction with the clinical presentation.
FAT-SOLUBLE VITAMINS
Vitamin A (retinol)
Sources
Pre-formed retinol is found only in foods of animal origin.
can also be derived from carotenes, which are present in green and
coloured vegetables and some fruits.
Importance Of Vit. A
Retinol is converted to 11-cis retinaldehyde is part of the
photoreceptor complex in rods of the retina.
Retinoic acid induces differentiation of epithelial cells
Retinoids are necessary for normal growth, fetal development,
fertility, haematopoiesis and immune function.
Consequence of vitamin A deficiency
Irreversible blindness in young children.
Early deficiency causes impaired adaptation to the dark (night
blindness).
3
Keratinisation of the cornea (xerophthalmia) gives rise to
characteristic Bitot’s spots, and progresses to keratomalacia, with
corneal ulceration, scarring and irreversible damage
Consequences of high vit. A intake
Repeated moderate or high doses of retinol in pregnants can cause
liver damage, hyperostosis and teratogenicity.
Acute overdose leads to
nausea and headache,
increased intracranial pressure and
skin desquamation.
Excessive intake of carotene can cause pigmentation of the skin
(hypercarotenosis); this gradually fades when intake is reduced.
Vitamin D
Sources
The natural form of vitamin D, cholecalciferol or vitamin D3, is
formed in the skin by the action of UV light on 7-
dehydrocholesterol.
Few foods contain vitamin D naturally
Vitamin D is converted in the liver to 25-hydroxy vitamin D
(25(OH)D), which is further hydroxylated in the kidneys to 1,25-
dihydroxy-vitamin D (1,25 (OH)2D), the active form of the
vitamin The synthetic form,
Ergocalciferol, or vitamin D2, is considered to be less potent than
the endogenous D3.
Action of vitamin D
1,25(OH)2D activates specific intracellular receptors which influence
Calcium metabolism,
Bone mineralisation and
Tissue differentiation.
The effects of vitamin D deficiency
calcium deficiency, rickets and osteomalacia)
4
An analogue of vitamin D (calcipotriol) is used for treatment of skin
conditions such as psoriasis.
Excessive doses of vit D
Excessive doses of
Cholecalciferol,ergocalciferol or the hydroxylated metabolites cause
hypercalcaemia
Vitamin E
There are eight related fat-soluble substances with vitamin E
activity. The most important dietary form is α-tocopherol.
direct metabolic actions:
It prevents oxidation of polyunsaturated fatty acids in cell
membranes by free radicals.
It helps maintain cell membrane structure.
It affects DNA synthesis and cell signalling.
It is involved in the anti-inflammatory and immune systems.
Deficiency
Human deficiency is rare and has only been described in premature
infants and in malabsorption. It can cause
mild haemolytic anaemia,
ataxia
visual scotomas.
Vitamin E intakes are considered safe up to 3200 mg/day (1000-
fold greater than recommended intakes).
Randomised controlled trials have not demonstrated
cardioprotective effects of vitamin E or other antioxidants.
5
Vitamin K
Sources
Vitamin K is supplied in the diet mainly as vitamin K1
(phylloquinone) in the UK, or
as vitamin K2 (menaquinone) from fermented products in parts of
Asia.
Vitamin K2 is also synthesised by bacteria in the colon.
Action of vit K
Vitamin K is a co-factor for carboxylation reactions: in particular, the
production of γ-carboxyglutamate (gla).
Gla residues are found in four of the coagulation factor proteins
(II, VII, IX and X)
Other important gla proteins are osteocalcin and matrix gla protein,
which are important in bone mineralisation.
Vitamin K deficiency
leads to delayed coagulation and bleeding.
In obstructive jaundice, dietary vitamin K is not absorbed and it
is essential to administer the vitamin in parenteral form before
surgery.
Warfarin and related anticoagulants act by antagonising vitamin
K.
Vit K excess
Symptoms of excess have been reported only in infants, with
synthetic preparations linked to haemolysis and liver damage.
Water-soluble vitamins
Thiamin (vitamin B1)
Sources
Thiamin is widely distributed in foods of both vegetable and animal
origin.
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Action of vit. B1
Thiamin pyrophosphate (TPP) is a co-factor for enzyme reactions
involved in the metabolism of macronutrients (carbohydrate, fat and
alcohol), including:
Decarboxylation of pyruvate to acetyl-co-enzyme A, which bridges
between glycolysis and the tricarboxylic acid (krebs) cycle
Transketolase activity in the hexose monophosphate shunt pathway
Decarboxylation of α-ketoglutarate to succinate in the krebs cycle.
In thiamin deficiency, cells cannot metabolise glucose aerobically
to generate energy as ATP.
Neuronal cells are most vulnerable, since they depend almost
exclusively on glucose for energy requirements.
Impaired glucose oxidation also causes an accumulation of pyruvic
and lactic acids, which produce vasodilatation and increased
cardiac output.
B1 Deficiency
beri-beri
In the developed world, thiamin deficiency is mainly
encountered in chronic alcoholics.
1. Poor diet,
2. impaired absorption, storage and phosphorylation of thiamin in the
liver,
3. increased requirements for thiamin to metabolise ethanol
In the developing world, deficiency usually arises as a
consequence of a diet based on polished rice.
The body has very limited stores of thiamin, so deficiency is manifest
after only 1 month on a thiamin-free diet.
Clinical features
There are two forms of the disease in adults:
Dry (or neurological) beri-beri manifests with
chronic peripheral neuropathy and with wrist and/or foot drop, and
may cause Korsakoff’s psychosis and Wernicke’s encephalopathy.
Wet (or cardiac) beri-beri
causes generalised oedema due to biventricular heart failure with
pulmonary congestion.
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Management
In dry beri-beri, response to thiamin administration is not
uniformly good. multivitamin therapy seems to produce some
improvement
Wernicke’s encephalopathy and wet beri-beri should be treated
without delay with intravenous vitamin B and C mixture
Korsakoff’s psychosis is irreversible and does not respond to
thiamin treatment.
Riboflavin (vitamin B2)
Function of vit. B2
Riboflavin is required for the flavin co-factors involved in
oxidation–reduction reactions.
It is widely distributed in animal and vegetable foods.
Deficiency
Deficiency is rare in developed countries.
affects the tongue and lips and manifests as glossitis, angular
stomatitis and cheilosis.
The genitals may be affected,
the skin areas rich in sebaceous glands, causing nasolabial or facial
dyssebacea.
Rapid recovery usually follows administration of riboflavin 10 mg daily
by mouth
Niacin (vitamin B3)
Function of vit B3
Niacin encompasses nicotinic acid and nicotinamide.
Nicotinamide is an essential part of the two pyridine nucleotides,
which play a key role as hydrogen acceptors and donors for many
enzymes.
Niacin can be synthesised in the body in limited amounts from the
amino acid tryptophan.
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Vit B3 Deficiency
Pellagra
Pellagra can develop in only 8 weeks in individuals eating diets that are
very deficient in niacin and tryptophan. Seen in
Alcoholics
Chronic small intestinal disease .
Hartnup’s disease (a genetic disorder with impaired absorption of
amino acids)
Carcinoid tumour
Clinical features
Pellagra has been called the disease of the three Ds:
Dermatitis. Characteristically, there is erythema resembling severe
sunburn, appearing symmetrically over the parts of the body
exposed to sunlight, particularly the limbs and especially on the
neck, but not the face (Casal’s necklace),
Diarrhoea. This is often associated with anorexia, nausea, glossitis
and dysphagia,
Dementia. In severe deficiency, delirium occurs acutely and
dementia develops
Treatment
Nicotinamide, given in a dose of 100 mg 3 times daily orally or
parenterally.
The response is usually rapid. Within 24 hours.
Toxicity
Excessive intakes of niacin may lead to reversible
hepatotoxicity.
Nicotinic acid is a lipid-lowering agent, but at doses above
200 mg a day gives rise to vasodilatory symptoms (‘flushing’
and/or hypotension).
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Pyridoxine (vitamin B6)
Pyridoxine, pyridoxal and pyridoxamine are different forms of
vitamin B6 that undergo phosphorylation to produce pyridoxal 5-
phosphate (PLP).
PLP is the co-factor for a large number of enzymes involved in the
metabolism of amino acids.
Vitamin B6 is available in most foods.
Deficiency
Drugs, such as isoniazid and penicillamine, act as chemical
antagonists to pyridoxine.
Uses of vit B6
Effective in isoniazid-induced peripheral neuropathy
Some cases of sideroblastic anaemia.
Large doses of vitamin b6 have an antiemetic effect in
radiotherapy-induced nausea.
Very high doses of vitamin B6 taken for several months can cause a
sensory polyneuropathy
hydroxycobalamin (vitamin B12)
Function of vit B12
Vitamin B12 is a co-factor in folate co-enzyme recycling and nerve
myelination.
Vitamin B12 and folate are particularly important in DNA
synthesis in red blood cells
Causes of B12 deficiency
In older people and chronic alcoholics, vitamin B12 deficiency arises
from
Insufficient intake and/or
From malabsorption.
Drugs, including neomycin, can render vitamin B12 inactive.
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Clinical features of B12 deficiency
In severe deficiency there is insidious, diffuse and uneven
demyelination. manifest as
Neurological consequences
peripheral neuropathy or spinal cord degeneration ‘subacute
combined degeneration of the spinal cord’, cerebral manifestations
(resembling dementia) or optic atrophy.
The haematological disorders (macrocytic or megaloblastic
anaemias)
Vitamin C (ascorbic acid)
Functions of vit C
Ascorbic acid is the most active reducing agent in and is involved
in intracellular electron transfer.
It takes part in the hydroxylation in mature collagen.
Claims that high-dose vitamin C improves immune function
It is very easily destroyed by heat, increased pH and light, and is very
soluble in water)
Vit C Deficiency
scurvy
Vitamin C deficiency causes
defective formation of collagen with impaired healing of wounds,
capillary haemorrhage and reduced platelet adhesiveness (normal
platelets are rich in ascorbate)
Causes of vit.C deficiency
Increased requirement
Trauma, surgery, burns, infections
Smoking
Drugs (corticosteroids, aspirin, indometacin, tetracycline)
dietary deficiency
Lack of dietary fruit and vegetables for > 2 mths
Infants fed exclusively on boiled milk
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Clinical features
Swollen gums which bleed easily
Perifollicular and petechial haemorrhages
Ecchymoses
Haemarthrosis
Gastrointestinal bleeding
Anaemia
Poor wound healing
Treatment of vit C deficiency
A dose of 250 mg vitamin C 3 times daily by mouth.
The deficiencies of the patient’s diet to be corrected and other
vitamin supplements given if necessary.
Toxicity
Daily intakes of more than 1 g/day have been reported to cause
Diarrhoea
Formation of renal oxalate stones.
Inorganic micronutrients
— A number of inorganic elements are essential dietary constituents
for humans
— Deficiency is seen when there is inadequate dietary intake of
minerals or excessive loss from the body.
— Toxic effects have also been observed from self-medication and
disordered absorption or excretion
Clinically Important Minerals
Rich
Important
— Calcium
Milk and milk products,
Milk, boned
fish, green vegetables, beans
— Phosphorus Most foods contain phosphorus
Marmite® and
dry-roasted peanuts,Milk, cereal products, bread and meat
— Magnesium Whole grains, nuts Unprocessed and wholegrain
foods
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— Iron Liver, red meat (haem iron) Non-haem iron from
vegetables, whole meal bread
— Zinc Red meat, seafood
Dairy
produce, wholemeal bread
— Iodine
Edible seaweeds Milk and
dairy products
— Selenium Fish, wheat grown in selenium-rich soils
Fish
— Copper
Shellfish, liver
Bread, cereal
products, vegetables
— Fluoride
Drinking water, tea
— Potassium Dried fruit, potatoes, coffee Fresh fruit,
vegetables, milk
— Sodium
Table salt, anchovies
Processed foods, bread, bacon
Calcium and phosphorus
— Calcium is the most abundant cation in the body
— Powerful homeostatic mechanisms control circulating ionised
calcium levels .
— Between 20 and 30% of calcium in the diet is absorbed, depending
on vitamin D status and food source.
— Calcium requirements depend on phosphorus intakes, with an
optimum molar ratio (Ca : P) of 1 : 1. Excessive phosphorus intakes
(e.g. 1–1.5 g/day) with a Ca : P of 1 : 3 have been shown to cause
hypocalcaemia and secondary hyperparathyroidism
Calcium deficiency
— Calcium absorption may be impaired in vitamin D deficiency
— Malabsorption secondary to small intestinal disease.
— Calcium deficiency causes impaired bone mineralisation and can
lead to osteomalacia in adults.
— The potential benefits of high calcium intake in osteoporosis
— Too much calcium can lead to constipation and toxicity has been
observed in ‘milk-alkali syndrome
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Deficiency Of Phosphorus
causes
— in patients with renal tubular phosphate loss
— due to prolonged high dosage of aluminium hydroxide
— sometimes when alcoholics are fed with high-carbohydrate foods
— in patients receiving parenteral nutrition if inadequate phosphate is
provided.
— Dietary deficiency of phosphorus is rare (except in older people
with limited diets)
defiency causes hypophosphataemia and muscle weakness secondary to
ATP deficiency.
Iron
Functions of iron
— Iron is involved in the synthesis of haemoglobin,
— required for the transport of electrons within cells
— Required in number of enzyme reactions.
Non-haem iron in cereals and vegetables is poorly absorbed compared
to the well-absorbed haem iron from animal products.
— The normal daily loss of iron is 1 mg, arising from desquamated
surface cells and intestinal losses.
— A regular loss of only 2 mL of blood per day doubles the iron
requirement.
— On average, an additional 20 mg of iron is lost during
menstruation, so pre-menopausal women require about twice as
much iron as men (and more if menstrual losses are heavy).
consequence of iron deficiency
— The major consequence of iron deficiency is anaemia .
iron overload
— Dietary iron overload is occasionally observed and results in iron
accumulation in the liver and, rarely, cirrhosis.
— Haemochromatosis results from an inherited increase in iron
absorption
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Iodine
— Iodine is required for synthesis of thyroid hormones .
— It is present in sea fish, seaweed and most plant foods grown near
the sea.
— Iodine is lacking in the highest mountainous areas of the world
Iodine Deficiency
— Goitre is the most common manifestation,
— In those areas where most women have endemic goitre, 1% or
more of babies are born with cretinism
— There is a higher than usual prevalence of deafness,
— slowed reflexes and
— poor learning in the remaining population.
Zinc
— Zinc is present in most foods of vegetable and animal origin.
— It is an essential component of many enzymes, including carbonic
anhydrase, alcohol dehydrogenase and alkaline phosphatase.
Zinc Deficiency
Acute zinc deficiency
Reported in patients receiving prolonged zinc-free parenteral nutrition
— Diarrhoea,
— Mental apathy,
— A moist, eczematoid dermatitis, especially around the mouth, and
— Loss of hair.
Chronic zinc deficiency
Occurs In Dietary Deficiency, Malabsorption Syndromes, Alcoholism
And Its Associated Hepatic Cirrhosis.
— It Causes The Clinical Features Seen In The Very Rare Congenital
Disorder Known As Acrodermatitis Enteropathica (Growth
Retardation, Hair Loss And Chronic Diarrhoea).
— Dwarfism And Hypogonadism.
— In Starvation, Zinc Deficiency Causes Thymic Atrophy,
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zinc supplements
— accelerate the healing of skin lesions,
— promote general well-being,
— improve appetite and
— reduce the morbidity associated with the under-nourished state,
— lower the mortality associated with diarrhoea and pneumonia in
children.
Selenium
The family of seleno-enzymes includes
— glutathione peroxidase, which helps prevent free radical damage to
cells
— monodeiodinase, which converts thyroxine to triiodothyronine
— Selenium deficiency can cause hypothyroidism, cardiomyopathy in
children (Keshan’s disease) and myopathy in adults.
— Excess selenium can cause heart disease.
Fluoride
— Fluoride helps prevent dental caries, since it increases the
resistance of the enamel to acid attack.
— It is a component of bone mineral and some studies have shown
anti-fracture effects at low doses, but excessive intakes may
compromise bone structure.
— If the local water supply contains more than 1 part per million
(ppm) of fluoride, the incidence of dental caries is low.
— Soft waters usually contain no fluoride, whilst very hard waters
may contain over 10 ppm.
— The addition of traces of fluoride (at 1 ppm) to public water
supplies is now a widespread practice
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Chronic fluoride poisoning
— is occasionally seen where the water supply contains > 10 ppm
fluoride.
— occur in workers handling cryolite (aluminium sodium fluoride),
used in smelting aluminium.
— Pitting of teeth is a result of too much fluoride as a child.
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اروى طب
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OBESITY
Definition
Obesity is a condition characterised by an excess of body fat, with
BMI of more han 30 kg/m2. Result from an imbalance between the
amount of energy consumed in the diet and the amount of energy
expended through exercise and bodily functions.
Complications of obesity
Metabolic syndrome
Type 2 diabetes, Hypertension, Hyperlipidaemia
Coronary heart disease
Stroke
Diabetes complications
Liver fat accumulation
Non-alcoholic steatohepatitis
Cirrhosis
Restricted ventilation
Exertional dyspnoea
Obstructive sleep apnoea
Obesity hypoventilation syndrome (Pickwickian syndrome)
Mechanical effects of weight
Urinary incontinence
Osteoarthritis
Varicose veins
Increased peripheral steroid interconversion in adipose tissue
Hormone-dependent cancers (breast, uterus)
Polycystic ovarian syndrome (infertility, hirsutism)
Others
Psychological morbidity (low self-esteem, depression)
Socioeconomic disadvantage (lower income, less likely to be
promoted)
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Gallstones
Colorectal cancer
Skin infections (groin and submammary candidiasis; hidradenitis)
Body fat distribution
obesity, the distribution rather than the absolute amount of excess
adipose tissue appears to be important.
Increased intra-abdominal fat causes ‘central’ (‘abdominal’,
‘visceral’, ‘android’ or ‘apple-shaped’) obesity, more common in
men and is more closely associated with type 2 diabetes, the
metabolic syndrome and cardiovascular disease.
subcutaneous fat accumulation causing ‘generalised’ (‘gynoid’ or
‘pear-shaped’) obesity
fat deposition within specific organs, especially the liver, is an
important determinant of metabolic risk in the obese.
Aetiology
Accumulation of fat results from a discrepancy between energy
consumption and energy expenditure that is too large to be
defended by the hypothalamic regulation of BMR.
A continuous small daily positive energy balance of only 0.2–
0.8 MJ (50–200 kcal; < 10% of intake) would lead to weight gain
of 2–20 kg over a period of 4–10 years. Given the cumulative
effects of subtle energy excess,
body fat content shows ‘tracking’ with age such that obese children
usually become obese adults.
Weight tends to increase throughout adult life, as BMR and
physical activity decrease.
Increasing prevalence of obesity
The ‘obesogenic’ environment
Increasing energy intake
•↑ Portion sizes
•↑ Snacking and loss of regular meals
•↑ Energy-dense food (mainly fat)
•↑ Affluence
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Decreasing energy expenditure
•↑ Car ownership
•↓ Walking to school/work
•↑ Automation; ↓ manual labour
•↓ Sports in schools
•↑ Time spent on computer games and watching TV
•↑ Central heating
Susceptibility to obesity
Genetic
(polygenic disorder), account for less than 5% of the variation in
body weight
few rare single-gene disorders have been identified that lead to
severe childhood obesity
Reversible causes of obesity and weight gain
Endocrine factors
•Hypothyroidism
•Cushing’s syndrome
•Insulinoma
•Hypothalamic tumours or injury
Drug treatments
•Atypical antipsychotics (e.g. olanzapine)
•Sulphonylureas, thiazolidinediones, insulin
•Pizotifen
•Corticosteroids
•Sodium valproate
•β-blockers
Clinical assessment and investigations
In assessing obesity, the aims are :
•Quantify the problem
•Exclude an underlying cause
•Identify complications
•Reach a management plan.
20
Quantifying obesity with body mass index
(weight/height2)
BMI (kg/m2)
Classification*
Risk of obesity comorbidity
18.5–24.9 Reference range
Negligible
25.0–29.9 Overweight Mildly increased
30.0 Obese
30.0–34.9 Class I
Moderate
35.0–39.9 Class II
Severe
> 40.0 Class III
Very severe
A dietary history
• ‘pathological’ eating behaviour (such as binge eating, nocturnal
eating or bulimia)
• Alcohol is an important source of energy intake
history of weight gain
• A patient who has recently gained substantial weight or has gained
weight at a faster rate than previously, and is not taking relevant
drugs), is more likely to have an underlying disorder such as
hypothyroidism or Cushing’s syndrome).
Lab tests
• thyroid function tests performed on one occasion,
• overnight dexamethasone suppression test or 24-hour urine free
cortisol if Cushing’s syndrome is suspected.
• Monogenic and ‘syndromic’ causes of obesity are usually only
relevant in children presenting with severe obesity.
Assessment of the diverse complications of obesity
• thorough history, examination and screening investigations.
The impact of obesity on the patient’s life and work
Assessment of other cardiovascular risk factors.
• Blood pressure should be measured with a large cuff,
• Associated type 2 diabetes and dyslipidaemia are detected by
measuring blood glucose or HbA1c and a serum lipid profile,
ideally in a fasting morning sample.
• Elevated serum transaminases occur in patients with non-alcoholic
fatty liver disease
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Management
most guidelines focus resources on short-term interventions in those who
have high health risks and comorbidities associated with their obesity,
and who have demonstrated their capacity to alter their lifestyle to
achieve weight loss
The management plan will vary according to
severity of the obesity
associated risk factors
complications.
availability of resources and health-care providers
Lifestyle advice
Behavioural modification to avoid some of the effects of the
‘obesogenic’ environment
Regular eating patterns
maximising physical activity
Alternative exercise (e.g. swimming) may be considered if
musculoskeletal complications prevent walking.
Changes in eating behaviour (including food selection, portion
size control, avoidance of snacking, regular meals to encourage
satiety, and substitution of sugar with artificial sweeteners)
.Regular support from a dietitian or attendance at a weight loss
group may be helpful
39GwAQ7PeH7fJTFa4DXguurfn7GULq2pTs
Diet % carbohydrate % fat % protein Comments
Normal
50 30
15
Moderate fat 60 25
15 Maintains balance
in
macronutrients and micronutrients
while reducing energy-dense fats
Low carbohydrate
10
60
30 Induction of ketosis
may suppress hunger
22
High protein
43
30
27 Protein has greater
satiety effect
than other macronutrients Low
low fat
70
13
17
The composition of the diet should ensure a minimum of
50 g of protein each day for men and 40 g for women to minimise
muscle degradation.
Energy content should be a minimum of 1.65 MJ (400 kcal) for
women of height < 1.73 m, and 2.1 MJ (500 kcal) for all men and
for women taller than 1.73 m.
Side-effects are a problem in the early stages and include orthostatic
hypotension, headache, diarrhoea and nausea.
There is no role for starvation diets, which risk
profound loss of muscle mass
development of arrhythmias (and even sudden death) secondary to
elevated free fatty acids, ketosis and deranged electrolytes.
Recommended weight loss
0.5 kg/week on conventional regimens
Very-low-calorie diets (VLCDs) are recommended for short-term
rapid weight loss, producing losses of 1.5–2.5 kg require the
supervision of an experienced physician and nutritionist.
Drugs
only one drug, orlistat, is currently licensed for long-term use.
Orlistat inhibits pancreatic and gastric lipases, reducing dietary fat
absorption by approximately 30%.
The drug is not absorbed and adverse side-effects relate to the
effect of the resultant fat malabsorption on the gut: loose stools,
oily spotting, faecal urgency, flatus and the potential for
malabsorption of fat-soluble vitamins.
Orlistat is taken with each of the three main meals of the day and
the dose can be adjusted (60–120 mg) to minimise side-effects.
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Surgery
‘Bariatric’ surgery
most effective long-term treatment for obesity
is the only anti-obesity intervention that has been associated with
reduced mortality.
should be contemplated in motivated patients who have very high
risks of complications of obesity in whom extensive dietary and
drug therapy has been insufficiently effective.
usually reserved for those with severe obesity (BMI > 40 kg/m2),
or those with a BMI > 35 kg/m2 and significant complications,
such as type 2 diabetes or obstructive sleep apnoea.
Several approaches are used and all can be performed
laparoscopically.
Diabetes may improve rapidly after surgery, particularly after
gastric bypass, this may be attributed to severe energy restriction in
the perioperative period, increased release of incretin hormones
such as glucagon-like peptide (GLP)-1 may contribute to the
improvement in glucose control.
Laparoscopic bariatric surgical procedures
Gastric banding
Sleeve gastrectomy
Roux-en-Y gastric bypass
Duodenal switch
Complications
depend upon the approach.
Mortality is low in experienced centres,
post-operative respiratory problems, wound infection and
dehiscence, staple leaks, stomal stenosis, marginal ulcers and
venous thrombosis may occur.
later stage, pouch and distal oesophageal dilatation, persistent
vomiting, ‘dumping’ and micronutrient deficiencies, particularly of
folate, vitamin B12 and iron
24
Treatment of additional risk factors
including smoking,
excess alcohol consumption,
diabetes mellitus,
hyperlipidaemia,
hypertension and
obstructive sleep apnoea