Caballero B. (ed.) Encyclopaedia of Food Science, Food Technology and Nutrition. Ten-Volume Set

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The Nature of Malnutrition in CF

0003 A wide range of nutritional deficits causing many

deleterious effects have been described in CF. The

heights and weights of many CF patients are markedly

skewed towards the lower centile bands, particularly

with increasing age. Body composition studies have

suggested that underweight CF children have a deficit

in body cell mass and body fat, with a reduction in

mass, muscle mass, and an excess in extracellular

water compared to controls. Whole-body protein

turnover studies have suggested that many malnour-

ished patients with severe lung disease are catabolic

with a reduction in whole-body protein turnover

synthesis occurring during pulmonary exacerbations.

The deficit of the body cell mass observed in CF from

total body potassium counting can be present from

the first few weeks of life, as judged by studies of

newborn CF infants diagnosed by neonatal screening.

Prior to neonatal screening, which has allowed the

earlier introduction of preventive therapy, overt hypo-

proteinemia was a common presenting symptom. Spe-

cific deficiencies of essential fatty acids, fat-soluble

vitamins, some water-soluble vitamins, and specific

micronutrients, including zinc, iron, and selenium,

are well described. Another important consideration,

particularly in tropical climates, is continuing specific

loss of sodium chloride resulting from the sweat gland

defect. Some patients develop CF-related diabetes or

CF-related hepatobiliary disease, which can both fur-

ther contribute to nutritional failure.

0004The range of nutritional abnormalities occurring in

CF seems likely to be caused by a combination of

inadequate absorbed intake, nutrient losses, and in-

creased requirements (Figure 2). Although many text-

books describe voracious appetites in CF children, in

reality, objective measurements often show an inad-

equate energy supply compared to recommended

intakes, and such patients with apparent excessive

appetites may often be attempting to compensate in-

adequately for requirements and excessive losses. A

poor appetite may be due to malnutrition per se, but

also appears to occur where there is poor pulmonary

function and during active pulmonary infection. This

latter problem may have a cumulative effect on nutri-

tional status over years as lung disease progresses. (See

Energy: Energy Expenditure and Energy Balance.)

0005Nutrient losses occur mainly from malabsorption,

but in some cases excessive nitrogen loss in sputum,

and excessive sodium losses from the sweat gland

abnormality (Figure 1) are also important. Fat and

protein malabsorption are present in approximately

85% of patients because of pancreatic exocrine

deficiency. The pancreatic abnormality involves

both water-electrolyte (mainly bicarbonate) secretion

as well as lipase, trypsin, and amylase deficiency.

Inadequate absorbed intake

Excessive requirements

Energy, fat, essential fatty acids

Fat, protein, fat-soluble

vitamins, micronutrients

e.g., sweat, electrolytes,

sputum, nitrogen

Deficient intake

Malabsorption

Other nutrient losses

Basal metabolic rate

Pulmonary disease

(infection, hypoxemia)

Liver disease

Protein

Essential fatty acids

Insulinopenia

Other growth factors

Altered utilization

Altered metabolism

Endocrine factors

fig0002 Figure 2 Factors affecting energy balance in cystic fibrosis. Reproduced from Cystic Fibrosis. Encyclopaedia of Food Science, Food

Technology and Nutrition, Macrae R, Robinson RK and Sadler MJ (eds), 1993, Academic Press.

1716 CYSTIC FIBROSIS

Reduced bicarbonate secretion is universal, but a

functional level of digestive enzyme capacity is

retained in 10–15% of patients termed pancreatic-

sufficient. These individuals may develop recurring

pancreatitis and some may eventually become defi-

cient. In untreated cases where enzyme outputs are

less than 10% of normal, steatorrhea, azotorrhea,

starch intolerance, and malabsorption of fat-soluble

vitamins, some minerals, and vitamin B

occur.

0006 There has been a growing interest in the nature of

energy and protein metabolism in CF since the

recognition of an apparent maladaptation to under-

nutrition, and the suggestion that there may be an

energy-requiring basic cellular defect in this disease.

There is good evidence that resting energy expend-

iture is elevated in CF irrespective of age and gender

but is genotype-specific. The energy cost of activity

is increased in those with more severe lung disease.

These factors play an incremental role in elevating

total energy expenditure and the high energy require-

ment observed in CF patients (up to 150% recom-

mended dietary intake or RDI).

The Consequences of Malnutrition in CF

0007 The major effects include nutritional growth retard-

ation, delayed puberty, adverse effects on pulmonary

disease, particularly lung growth and, ultimately, a

poorer prognosis. Patients dying of CF have marked

nutritional failure in the 1–2 years prior to their

death. Malnutrition per se can compromise absorp-

tive and immune function, and all of the specific

deficiencies mentioned above can have a wide range

of secondary adverse effects.

0008 A close relationship exists between malnutrition

and pulmonary disease in CF. Pulmonary disease ap-

parently adversely affects energy requirements and

whole-body protein metabolism. As previously men-

tioned, CF patients who have chronic but stable

pulmonary disease tend to have excessive protein

catabolism and elevated total energy expenditure,

while those malnourished patients studied during

acute pulmonary exacerbations have a significantly

reduced level of whole-body protein turnover. Thus

both acute and chronic pulmonary disease appear

to have a major effect on energy utilization. There is

also evidence that malabsorption and malnutrition

per se adversely affect the course of pulmonary dis-

ease. An improved respiratory prognosis has been

observed in those patients with pancreatic sufficiency,

and a number of specific effects of malnutrition on

the respiratory system have been documented. Mal-

nutrition can affect the central respiratory drive

mechanism, the respiratory muscles, and the growth

of the lungs. Long-term studies of nutritional

rehabilitation of malnourished patients have sug-

gested that improved nutrition may favorably affect

the course of pulmonary disease.

Nutritional Management in CF

0009Treatment of CF patients has become increasingly

specialized and is most satisfactorily performed at

major referral clinics where a comprehensive and

intensive management program is available. It

would seem likely that early diagnosis by neonatal

screening and the institution of an aggressive therapy

program, before irreversible lung damage and chronic

nutritional deficits have occurred, may prolong

survival. Studies of neonatal screening programs to

date have indicated lower morbidity and improved

nutrition in those children diagnosed by neonatal

screening compared with a clinically diagnosed

group, and one study from Denmark has indicated

that there may also be a lower mortality. The adverse

effects of chronic pulmonary disease on nutritional

status and, conversely, the adverse effects of malnutri-

tion on pulmonary status, particularly lung growth,

require an early aggressive approach to both aspects

of the disease. Pulmonary therapy is beyond the scope

of this discussion, but its importance in the preven-

tion of malnutrition in CF cannot be overstated.

Optimal nutritional therapy involves the restoration

of energy balance by regular nutritional surveillance,

and the maintenance of an adequate absorbed pro-

tein-energy intake with the prevention and manage-

ment of specific deficiencies (Table 1). Certain phases

of the disease, such as those occurring in infancy,

during and after pulmonary exacerbations, and

during puberty, may be especially important for

tbl0001Table 1 Nutrient requirements in cystic fibrosis

Nutrient Requirement

Energy 120–150% RDA

Protein 120% RDA

Essential fatty acids 5% of total energy (kJ)

Vitamin A 5000–10 000 IU per day (water-miscible)

Vitamin E 100–300 IU per day (water-miscible)

Vitamin K 5 mg twice weekly

Vitamin D 800 IU per day in temperate zones

B vitamins 200% RDA

Vitamin C 200% RDA

Iron and zinc 120% RDA

Pancreatic

supplements

(as pH-sensitive

microspheres)

Infants: 2000 units of lipase per 120 ml

of formula

Older children: 500–4000

units of lipase per g dietary fat

Maximum dose 10 000 units kg

1

day

1

RDA, recommended dietary allowance.

CYSTIC FIBROSIS 1717

optimal nutritional therapy. Overtly malnourished

patients can benefit from long-term enteral nutrition

delivered via either nocturnal nasogastric or gastro-

stomy feeding.

Surveillance

0010 An important part of the routine management pro-

gram is the regular evaluation of protein-energy bal-

ance. This involves assessment of intake, absorbed

energy, possible nutrient losses, and the recording of

anthropometric data. An example of a computerized

surveillance program at the Royal Children’s Hos-

pital, Brisbane, is given in Figure 3, showing the

benefits of longitudinal evaluation. Certain noninva-

sive research techniques are deserving of wider appli-

cation as markers of changing nutritional status in

CF. Although many of these patients are within the

normal centile bands for weight, measurements of

total body potassium (which provide a much more

sensitive indicator of growth of the body cell mass)

suggest many patients have cell mass deficits. Body

impedance, which can be measured by a simple bed-

side technique, correlates well with body potassium

in CF and may serve as a reliable clinical tool for the

surveillance of fat-free mass. The advent of measures

of total energy expenditure in free-living humans

should also help to establish an evaluation of true

nutritional requirements in this disease.

Dietary Therapy

0011Dietary counseling, and dietary and pancreatic

enzyme supplements remain mainstays in the prevent-

ive management of nutritional problems in cystic

fibrosis. To achieve an adequate absorbed protein-

energy intake (Figure 2), daily intakes > 130% of

RDI are usually necessary to compensate for stool

losses and increased requirements. In general, it

is usually possible to achieve normal growth and

nutrition in CF children with dietary counseling, pan-

creatic enzymes, and high-energy supplements. Al-

though in the past it was standard practice in many

CF clinics to prescribe low-fat, high-carbohydrate

diets, low-fat diets offer no benefit to CF patients,

impair total energy intake, and contribute to essential

fatty acid deficiency. Indeed, mortality was higher in

clinics prescribing low-fat diets, favoring the prescrip-

tion of a moderate- to high-fat diet. Since fiber has

been shown to inhibit pancreatic enzymes in vivo and

in vitro, fiber-enriched diets should be avoided.

Patient tolerance of normal fat intakes of 40% of

total energy is satisfactory, provided that appropriate

enzyme preparations are used. Palatable and

Ht wt/date Z score

21 October 1987, 61

0 kg (best wt since 20 February 1987)

24 February 1988, 61

0 kg (no change)

Date

Age: 18 years 7 months. Predicted wt: 69

8kg

−1

−2

−3

−4

−5

24/2/88

25/11/87

21/10/87

19/8/87

20/7/87

16/3/87

20/2/87

9/2/87

15/12/86

10/11/86

1/9/86

16/6/86

14/4/86

6/1/86

14/10/85

5/8/85

26/6/85

19/6/85

17/6/85

27/5/85

20/5/85

18/2/85

10/12/84

8/10/84

30/4/84

6/2/84

19/12/83

26/9/83

9/5/83

28/3/83

23/2/83

16/2/83

9/2/83

7/2/83

20/12/82

22/11/82

6/9/82

5/7/82

10/5/82

15/3/82

22/2/82

9/11/81

3/8/81

11/5/81

16/3/81

19/1/81

24/11/80

21/7/80

2/6/80

21/4/80

25/2/80

fig0003 Figure 3 Serial height and weight standard deviation scores from the computerized clinic data records of an adolescent with cystic

fibrosis from the age of 10–18 years. Note the gradual decline in both height (H) and weight (I, weight as an inpatient; 0 or þ, weight as

an outpatient), until about the age of 14 years, when long-term enteral nutritional supplements were instituted by nocturnal intragastric

feeding. By the age of 18 there was a gradual improvement in these parameters. Reproduced from Cystic Fibrosis. Encyclopaedia of

Food Science, Food Technology and Nutrition, Macrae R, Robinson RK and Sadler MJ (eds), 1993, Academic Press.

1718 CYSTIC FIBROSIS

nutritious high-protein energy foods are encouraged

and special milk drinks with added energy sources,

such as chocolate-flavored protein-enriched powders,

glucose polymers, and other foods, represent a good

way of increasing total energy intake.

0012 A full range of vitamin and mineral supplements is

necessary to prevent vitamin and mineral deficiency.

In particular, fat-soluble vitamins presented in a

water-miscible form are required in all patients with

steatorrhea, administered in a dosage twice the RDI.

As mentioned previously, where oral intake with

supplements fails to achieve satisfactory height and

weight gain, or if the patient is overtly malnourished,

enteral supplements can be used. A metaanalysis of

18 studies of enteral supplementation have demon-

strated significant benefits in terms of weight gain,

growth, body protein accretion and stabilization,

and, perhaps, improvement of pulmonary function.

High-energy defined semielemental formulae are

most suitable for use in the nutritional rehabilitation

of malnourished CF patients, and are generally well

tolerated. As illustrated in Figure 3, surveillance of

weight gain and growth provides a reasonable clinical

indicator for nutritional intervention and the assess-

ment of benefits derived.

Pancreatic Enzyme Replacement Therapy

0013 Pancreatic enzyme replacement therapy (PERT)

needs to be tailored to individual requirements and

is required in about 85% of CF patients, according to

the amount of food (particularly fat) eaten and the

degree of malabsorption. It is appropriate to assess

quantitatively the degree of malabsorption and the

ability of the therapy to correct this. Some measures

to improve the efficacy of PERT have been a recent

area of study in CF, as conventional preparations

rarely fully optimize absorption. The objectives of

PERT include correction of maldigestion, elimination

of symptoms and signs of malabsorption, and sustain-

ing normal nutrition.

0014 A bewildering number of pancreatic enzyme prep-

arations are commercially available in the form of

tablets, capsules, enteric-coated microspheres,

granules, and powders. Some products have not

been designed specifically for the treatment of exo-

crine pancreatic insufficiency, but for patients with

unspecified abdominal pain. Some contain bile salts;

in general these should be avoided in patients with

pancreatic insufficiency because high concentrations

of bile salts may aggravate diarrhea. Preparations

that are protected against peptic acid inactivation

are preferable to unprotected preparations: unpro-

tected ingested enzymes are degraded to a significant

degree as a result of increased gastric acidity, and

lowered duodenal pH secondary to depressed bicar-

bonate secretion for the pancreas. The lipase content

is the most important determinant of the effectiveness

of these products. Between 80% and 90% of unpro-

tected ingested lipase and trypsin is inactivated in the

stomach. It was thought that PERT was complica-

tion-free, but excessive doses have been associated

with renal calculi, and prolonged excessive dosages

with serious fibrosing colonopathy. Guidelines for the

safe correct use of PERT have been published. In the

UK, the Committee of Safety of Medicines suggests

doses of no more than 10 000 u lipase kg

1

day

1

0015It has been calculated that, in an adult, assuming

there is no inactivation of enzymes in the stomach,

approximately 30 000 IU of lipase is required to be

delivered to the duodenum with an average meal

containing about 6 g of fat for normal digestion. In

children approximately 500–4000 IU is required per

gram of fat ingested. The distribution of fat content of

different meals and the mixing enzymes with food in

the duodenum seems to be important. Granulated

preparations or microspheres are better than tablets

in that they enable higher enzyme activities to reach

the duodenum and mix with the food. The majority

of enzyme preparations contain between 5000 and

20 000 IU of lipase. It can thus be calculated that,

for the average adult, if some defence against gastric

inactivation is provided and there is an adequate

enzyme–meal mix, between 2 and 10 capsules are

required per meal to control steatorrhea. Studies in

children comparing conventional tablet enzyme ther-

apy to enteric-coated microspheres of pancrelipase

have shown that significantly less steatorrhea and

azotorrhea occur with the use of the microsphere

preparation. In addition, there is an improvement in

compliance because significantly fewer capsules are

required. Irrespective of the preparation used, there is

good evidence that the enzymes need to be delivered

appropriately and dispersed evenly throughout a

meal, in order to achieve maximum exposure of

food to the ingested enzymes.

0016The success of enzyme therapy is assessed by bowel

symptoms, quantitative absorptive tests, such as fecal

fat analysis, and the maintenance of normal nutrition.

In children, assessment of growth is also essential.

Azotorrhea is more frequently abolished by pancreatic

enzyme supplements than is steatorrhea, possibly be-

cause trypsin secretion is better preserved than lipase

secretion in pancreatic insufficiency, and because tryp-

sin is not inactivated by acid but only by pepsin. Poor

response to pancreatic enzyme preparations may result

from poor compliance, inappropriate timing of admin-

istration, the presence of another condition causing

steatorrhea (e.g., bacterial overgrowth), or the use of

an unprotected, acid-sensitive enzyme preparation.

CYSTIC FIBROSIS 1719

Adjuncts to Pancreatic Enzyme Therapy

0017 Adjunctive treatment to neutralize or inhibit gastric

acid and help to protect pancreatic enzymes against

acid inactivation may be useful in selected cases. The

use of antacids with pancreatic supplementation to

neutralize gastric acid has achieved variable results,

probably because some antacids form calcium soaps

and precipitate glycine-conjugated bile salts. Hista-

mine H

-receptor antagonists are of theoretical value

because many causes of pancreatic insufficiency (par-

ticularly CF) are associated with gastric hypersecre-

tion. If there is adequate reduction of gastric activity,

the addition of cimetidine does appear to be effective

when used with enteric-coated, microsphere, pH-

sensitive preparations. However, these enzyme prep-

arations do not disintegrate and release their contents

until encountering an alkaline pH, and despite acid

suppression therapy, in some cases, complete correc-

tion of steatorrhea has not been possible. Recently, a

new approach to adjuvant therapy has been suggested

with the use of misoprostol, a synthetic methylated

prostaglandin E

analog, which decreases secretion

of gastric acid and increases duodenal bicarbonate

secretion. This therapy may have inherent advantages

over histamine H

-receptor antagonists as adjuvant

therapy for pancreatic insufficiency because of the

latter effect.

Conclusions

0018 Nutritional problems are common in CF and have an

increasingly important role in management. Malnu-

trition is a major factor influencing survival, and may

even influence the course of lung disease as there

appears to be a close bilateral relationship between

the progression of pulmonary disease and undernutri-

tion, although the factors responsible for such a rela-

tionship are incompletely defined. Although it is

widely recognized that factors such as nutrient losses

from malabsorption, a variable but often inadequate

intake, and chronic lung disease contribute to malnu-

trition, recent studies have also suggested that the

primary defect may require energy. A wide range of

nutritional deficits occurs in CF; many patients have

deficits of body fat and body cell mass, and appear to

be in a state of chronic catabolic stress. Whole-body

protein turnover would also appear to be abnormal in

many CF patients, particularly during pulmonary

exacerbations. Specific deficiencies of essential fatty

acids, fat-soluble vitamins, and some micronutrients

also occur and may compromise pulmonary function

and immunity. Optimal nutritional management in

CF includes the provision of adequate protein and

extra energy as fat and carbohydrate, and an appro-

priate dosage and administration routine with food,

of pancreatic enzyme supplements in a form which

minimizes acid–peptic inactivation. Newer adjuncts

to pancreatic enzyme therapy, such as prosta-

glandin analogs, show promise. Food supplements

should provide extra energy, essential fatty acids,

fat-soluble vitamins in a water emulsion, salt supple-

ments in hot weather, and water-soluble vitamins,

and micronutrients. Routine surveillance of nutri-

tional status and absorbed energy should be per-

formed at regular intervals. Deviations from normal

weight gain and growth may require nutritional inter-

vention. Recent studies by a number of groups con-

firm that long-term supplementation can achieve

sustained catch-up weight gain and growth, and pro-

vide support for the view that reversible nutritional

factors may have an important influence on the

course of pulmonary disease in those CF patients

who have deteriorating lung function, and who are

unable to sustain normal growth and nutrition by the

oral route. Obviously, the overall goal should be to

prevent this situation and provide the CF patient with

as normal a lifestyle as possible, with management

aimed at preventing progressive pulmonary disease,

maintaining normal growth and nutrition, and pre-

venting complications.

See also: Energy: Energy Expenditure and Energy

Balance; Immunology of Food; Metabolic Rate

Further Reading

Anthony H, Collins CE and Davidson G et al. (1999)

Pancreatic enzyme replacement therapy in cystic fibro-

sis. Journal of Paediatric Child Health 35: 125–129.

Durie PR (1993) Gastrointestinal and hepatic complication

and their management. International Seminars in

Gastroenterology and Nutrition 2: 3–9.

Hill CM (1998) Practical Guidelines for Cystic Fibrosis

Care. London: Churchill Livingstone.

Shepherd RW and Cleghorn G (1990) Nutritional and Gas-

trointestinal Problems in Cystic Fibrosis. Boca Raton,

Florida: CRC Press.

Stapleton D, Tunnecliffe L, McGuiness D, Sheriff J and Sly

P (1998) Development of a nutrition education behav-

iour intervention in children with CF. Australian Journal

of Nutrition and Dietetics 55: 130–137.

1720 CYSTIC FIBROSIS

DAHI

C D Khedkar, College of Dairy Technology,

Maharashtra, India

G D Khedkar, Dr Babasaheb Ambedkar Marathwada

University, Aurangabad (Maharashtra), India

S D Kalyankar, Marathwada Agricultural University,

Parbhani (Maharashtra), India

D N Bajad and A R Sarode, College of Dairy

Technology, Maharastra, India

Background

0001 Indian curd, known as ‘dahi,’ is a very well-known

fermented milk product consumed by large sections of

the population throughout the country, either as a part

of the daily diet or as a refreshing beverage, e.g., lassi.

Dahi is also used for the production of Shrikhand:

some whey is removed from dahi, and the concen-

trated curd is mixed with an equal weight of sucrose.

Dahi has been a very popular fermented dairy product

in the Indian subcontinent, which includes India, Paki-

stan, Bangladesh, Nepal, and Sri Lanka. The name of

this product has been found in the ancient Hindu

scriptures, and its medicinal value has also been well

documented. Dahi may be consumed directly either

sweetened or salted and spiced. It is also consumed

with other foods such as rice and wheat loaf. Dahi has

assumed a special place in the daily diet of Indian

people, who prefer to have dahi once or twice a day

at morning or evening meals. In 1999–2000, the pro-

duction of dahi was estimated to be about 7% of total

milk production in India. Since conversion of milk into

dahi is an important intermediatary step in manufac-

ture of indigenous fat-rich dairy products like butter

and ghee, it can be said that over 40% of the total milk

production in India is converted into dahi.

Definition

0002 According to the Bureau of Indian Standards, dahi is

a product obtained by lactic fermentation of cow or

buffalo milk or mixed milk through the action of

single or mixed strains of lactic acid bacteria. This

definition does not include milk coagulated by the

addition of acids or milk coagulating enzymes. As

per the Prevention of Food Adulteration Act (1988),

dahi or curd is a product obtained from pasteurized

or boiled milk by souring natural or otherwise, by

harmless lactic acid or other bacterial culture. Dahi

may contain added cane sugar. It should have the

same percentage of fat and solids-not-fat as the milk

from which it is prepared. Where dahi or curd, other

than skimmed milk dahi, is sold or offered for sale

without any indication of the class of milk, the stand-

ards prescribed for dahi prepared from buffalo milk

should apply. This is similar to yogurt made from

boiled milk after inoculation with a mixed starter

culture which consists of dahi left over from the pre-

vious lot. However, it is less acidic than yogurt.

Starter Cultures for Dahi

0003In the production of dahi, inoculation with a small

quantity of the desired fermenting flora, named the

starter culture, (since the culture initiates or starts

fermentation). The most important organisms in

starter cultures are the homofermentative and hetero-

fermentative lactic acid bacteria. Dahi starter cultures

can be classified into two groups, according to the

characteristics of the microorganisms: mesophilic and

thermophilic. Mesophilic starters and cultures are

used at a temperature of 16–30



C and contain meso-

philic organisms (Table 1). The most typical represen-

tatives are the homofermentative Lactococcus lactis

ssp. lactis and Lc. lactis ssp. cremoris, which are

similar, although the former is able to produce free

amino acids, which are believed to stimulate the

growth of Lc. lactis ssp. cremoris strains. Another

important species in mesophilic starters is the homo-

fermentative citrate

Lc. lactis ssp. lactis, which is

able to produce lactic acid and in the presence of

lactose to ferment citric acid into a number of other

compounds such as diacetyl and carbon dioxide.

However, at a pH below 5, carbon dioxide and a

number of compounds similar to diacetyl, but non-

aromatic, are produced. The heterofermentative Leu-

conostoc mesenteroides ssp. dextranicum and Ln.

mesenteroides ssp. plantarum are able to ferment

citric acid into carbon dioxide, diacetyl, and several

other products. Unfortunately, the Leuconostoc species

may reduce diacetyl into nonaromatic compounds. The

intensity of reduction varies between the various repre-

sentatives of the strains. Homofermentative thermo-

philic starter organisms like Lactobacillus delbrueckii

ssp. bulgaricus and Streptococcus thermophilus are

used to obtain mildly sour dahi. These starters play an

important role in producing a good-quality dahi with a

firm and uniform consistency, sweet aroma, and clean,

acidic taste.

Classification of Dahi

0004 Broadly speaking, dahi may be classified into two

types:

0005 dahi for churning into desi (indigenous) butter;

0006 dahi for direct consumption.

Dahi for direct consumption is further classified into

the following subtypes:

0007 whole-milk and skim-milk dahi;

0008 sweet (or mildly sour), sour, and sweetened dahi.

Technology of Sweet and Sour Dahi

Manufacture

0009 The steps involved in the manufacture of sweet (or

mildly sour) and sour dahi are shown in Figure 1. The

manufacture is as follows:

Preliminary Treatment of Milk

0010 The preparation of the basic mix involves selection of

milk, preheating, filtration/clarification, and stand-

ardization of milk. The different methods for stand-

ardizing the milk indicate the possibilities that exist

for either increasing or reducing the various milk

constituents, especially the fat content. However, the

choice of any particular method is primarily governed

by the following factors:

0011cost and availability of the raw materials;

0012scale of production.

The composition of dahi varies considerably. The

composition of dahi made from buffalo milk is

detailed in Table 2. Commercial dahi tends to contain

around 14% milk solids; the use of ultrafiltration

to concentrate the solids in cows’ milk and skim

Selection of milk

Preheating (40 8C)

Filtration/clarification

Standardization (3% fat

+ 10% milk solids not fat)

Heat treatment (60 8C)

Homogenization (7 MPa)

Final heat treatment (80−90 8C for 20 min)

Cooling to 22−25 8C

Inoculation with active starter culture @ 1−1.5%

(For sweet dahi Lactococcus

lactis ssp. lactis

+ Lactococcus

lactis ssp. cremoris

+ Leuconostoc

mesenteroides ssp. dextranicum)

(For sour dahi Lactobacillus delbrueckii ssp.

bulgaricus

+ Streptococcus thermophilus)

Incubation at 27−30 8C/18 h (for preparation of sweet dahi)

and 37−38 8C/10−12 h (for preparation of sour dahi)

Cooling to 5 8C or below

Storage and distribution

Distribution in the packages of desired size

fig0001Figure 1 Flow diagram for preparation of dahi.

tbl0001 Table 1 Designation of dahi based on the type of starter culture

Designation Cultures used Remarks

Sweet dahi Lactococcus lactis ssp.

lactis, Lactococcus

lactis ssp. cremoris,

Single or in combination

with or without aroma

producers like

Leuconostoc

mesenteroides ssp.

dextranicum, Leuconostoc

mesenteroides ssp.

plantarum

Sour dahi Lactobacillus

delbrueckii ssp.

bulgaricus and

Streptococcus

thermophilus

Single or in combination

with or without aroma

producers

1722 DAHI

milk is being considered as a feasible alternative. The

importance of total solids stems from the improved

consistency imparted to the dahi coagulum, an im-

provement that is carried further by the homogeniza-

tion stage by employing a pressure of 17 MPa.

Homogenization of milk improves the texture of the

coagulum and also reduces the likelihood of whey

separation. Homogenization is followed by a final

heat treatment of 80–90



C for a prolonged period

of 20 min. The effect of this drastic heat treatment can

be summarized as follows:

0013 The bacterial load in the milk is reduced, and

hence the starter culture has less competition

from the contaminating organisms.

0014 The whey proteins (albumins and globulins) are

denatured and interact with the casein molecules,

which form a three-dimensional network on acid-

ification. The network traps the whey proteins,

and the dahi coagulum subsequently produced is

rendered more viscous.

0015 There is a reduction in the amount of oxygen in

the milk, and as the normal dahi cultures are

microaerophilic, the lowered oxygen tension en-

courages their growth.

0016 Some limited damage to the milk proteins may

occur during heating, and the breakdown prod-

ucts can stimulate starter activity.

0017 The heat treatment imparts a cooked flavor for

misti dahi.

Fermentation of Milk

0018 The acidification of milk during the manufacture of

dahi is an important biochemical process which must

be carried out under controlled conditions in special

incubators and/or fermentation tanks. Fermentation

tanks are used as incubators only, and they are usually

insulated in order to maintain the appropriate tem-

perature. The processing of the milk and the cooling

of the dahi are carried out in other equipment in the

production line. Cabinets are also used for this pur-

pose. These comprise a small insulated room which

is divided into compartments, and most incubators

of this type are multipurpose chambers capable of

circulating hot or cold air. Hot air is circulated during

the fermentation period, followed by cold air during

the cooling stage. Sometimes, these cabinets are used as

incubators only, and the dahi can be cooled in refriger-

ated cold storage. In the case of mildly sour (sweet)

dahi manufacture, the temperature is maintained at

27–30



C, while for sour dahi, it is 37–38



Cooling of Dahi

0019After the incubation period, dahi is cooled in order

to control the level of lactic acid in the product. The

rate of cooling can affect the structure of the coagu-

lum. Thus, very rapid cooling can lead to whey separ-

ation, if the protein filaments are concentrated

too rapidly, which in turn affects their hydrophilic

properties.

Microbiological Quality of Dahi

0020An examination of the microbiological quality of a

product is usually concerned with two aspects,

namely: protection of the consumers from exposure

to any health hazard and ensuring that the material

does not suffer microbiological deterioration during

its anticipated shelf-life. Both these aims are of im-

portance to the consumer and producer alike. Thus,

over and above any moral responsibility that a com-

pany accepts for the integrity of its product, the finan-

cial losses that follow a public health incident, or even

a high level of consumer complaints, provides a very

strong incentive for a manufacturer to give quality

assurance a high priority. The type of hazard that may

be encountered depends on the nature of the product,

and in general terms, dahi can be regarded as ‘hygien-

ically safe.’ The reason for this confidence stems from

the level of acidity present (around 0.7–1.0% lactic

acid), for this situation, potential pathogens such as

Salmonella spp. will be largely inactive. Similarly,

‘coliforms’ will be unable to survive the low pH en-

countered, and this inhibition is reinforced by the

production of antibiotic substances by the dahi starter

organisms. Microbiological standards for dahi are

given in Table 3. Typically, the shelf-life of dahi is

2–4 days at 4



tbl0003Table 3 Indian Standard Institute specifications for dahi

Characteristics Requirement

Sweet dahi Sour dahi

Acidity, lactic (% wt) (max.) 0.70 1.0

Yeast and mold count g

1

(max.) 100 100

Coliform count g

1

(max.) 10 10

Phosphatase test Negative Positive

From Indian Standards Institution (1973) ISI Document No. 7035. New Delhi:

Manak Bhavan.

tbl0002 Table 2 Composition of buffalo milk dahi

Constituents Level (%)

Moisture 85–88

Fat 5–8

Protein 3.2–3.4

Lactose 4.6–5.2

Ash 0.7–0.75

Lactic acid 0.5–1.0

Calcium 0.12–0.14

Phosphorus 0.09–0.11

DAHI 1723

Technology of Sweetened Dahi (Misti

Dahi) Manufacture

0021 Misti dahi (syn. sweetened dahi, red dahi, payodhi) is

a traditional sweetened fermented milk product of the

Eastern region of India. It is prepared on a cottage

scale by sweetmeat makers everyday to meet local

demands. Traditionally, milk with added cane sugar

is continuously heated in an open pan at a simmering

temperature (68–70



C) for 6–7 h to concentrate and

develop the intense cooked flavor and brown color,

increase the viscosity, and induce other physicochem-

ical changes. After cooling to about 40



C, the mix

is inoculated with a commercial misti dahi starter

culture, which is generally a mixed lactic culture like

LF-40 or Lb. delbrueckii ssp. bulgaricus, St. thermo-

philus, and some aroma-producing organisms, as in

mildly sour and sour dahi. Wide variations in total

solids content (27–43%), milk-solids-not fat (11–

16%) and sucrose (13–19%) in market samples of

misti dahi sold in Calcutta city have been reported.

Many flavor defects such as fruity, alcoholic, highly

acidic, flat, etc., and textural defects like gassiness,

weak body, wheying off, and a thick crust on the top

surface have been observed in most of the market

samples. In view of the increasing nationwide

demand for this product and the growing interest in

organized dairy plants for large-scale manufacture,

the technology has been developed to suit industrial-

scale production. The manufacturing technology for

the industrial production of misti dahi is outlined in

Figure 2. Fresh buffalo milk is standardized to 3.5%

fat and 9% milk-solids-not fat, heated to 65



Cina

plate heat exchanger, and homogenized at a pressure

of 56 kg cm

2

(one stage). Milk is concentrated to

1.44-fold in a vacuum evaporator. After adding cane

sugar (7–15%), the milk is heated at 85



C for 10 min

to generate a cooked flavor. The mix is water-cooled

to 40



C before inoculation with the mixed culture,

LF-40. In some cases, sugar, caramel, jaggery, and

artificial colors are added to impart a brown color.

The inoculated mix is aseptically distributed into pre-

sterilized polystyrene containers of the desired size

and mechanically transferred to an incubation cham-

ber at 40



C. During curd formation, the milk must

remain stationary. In all postfermentation activities,

the gel should be subjected to minimal external influ-

ences. Diacetyl is the predominant flavor component,

but microquantities of acetoin, acetic acid, and car-

bonyls are also present. Off-flavors in this product

can be traced back to poor-quality raw milk, use of

contaminated cultures, a high incubation tempera-

ture, and contaminated packages.

Food and Nutritive Value and Therapeutic

Benefits of Dahi

0022Indian literature has described in detail the import-

ance of dahi in human nutrition. Scientific invest-

igations have proved that dahi is digested and

assimilated more easily by virtue of its buffering

action and supplies more nutrients than milk. Trical-

cium phosphate is converted into monocalcium phos-

phate, and some insoluble minerals are rendered

more soluble due to lactic acid production. Many

researchers have found an increase in the levels of

Receiving buffalo milk

Standardization (Fat, 3.5%

+ SNF, 9.0%)

Preheating (65 8C−70 8C)

Homogenization (56 kg/cm

at 65 8C)

Concentration to 1.44 fold by heating under vacuum

Addition of cane sugar (approx. 6−7%)

Heating at 85−90 8C for 10 min.

Cooling to 37−40 8C

Inoculation with active starter culture @ 2%

(LF-40 or Lactobacillus delbrueckii ssp.

bulgaricus

+ Streptococcus thermophilus)

Aseptic packaging in the pre-sanitized retail packs

Incubation at 37−40 8C for 12−13 h

Storage at 5 8C or below

Distribution

fig0002 Figure 2 Flow diagram for the preparation of misti dahi

(sweetened dahi). The temperature of homogenization is differ-

ent for both types.

1724 DAHI

riboflavin (vitamin B

) and thiamin (vitamin B

)in

dahi.

0023 Converting milk into dahi also tends to stabilize the

vitamin C potency more than fresh milk, which is

vitally important for the growth and repair of tissues

in bones, teeth, and blood vessels, health of gums and

teeth, overall body growth, and resistance to infec-

tion. Lactose-fermenting bacteria have been found to

synthesize vitamin B, present only in small quantities

in milk. The mineral and vitamin contents in dahi are

listed in Table 4.

0024 Dahi obtained from cows’ milk has been found to

cure dysentery, diarrhea, thirst, coughs and colds,

indigestion, headache, weakness, and many other dis-

eases and ailments. It improves the digestibility of

food and allays the fear of diseases of any nature by

checking the undesirable putrefactive fermentations

in the alimentary canal. The putrefying bacteria in-

habiting the human intestines are harmful, because

they poison the food with the products of their me-

tabolism. Since the bacterial flora of the intestines live

in an alkaline medium, the best thing would be to

create an acid medium in the lower intestine. For this

reason, the introduction of regular use of dahi is

advocated. Its palatability and pleasant flavor have

an appetizing effect. Those who do not relish milk

like dahi. It is beneficial to youngsters and pregnant

and lactating females. It is a good dietary item for all

and deserve a high priority in our daily menu for

healthful living.

0025Industrial methods have been developed during the

last decade to mechanize the production, packaging,

and storage of dahi, and it is now produced regularly

on a factory scale. The need for more promising

mechanization and upgrading of production tech-

nologies, packaging, preservation, and distribution

of dahi has now been recognized. Attempts to develop

any large-scale process for dahi-based sweets must

aim at using the existing processes in dairy plants

rather than relying on a new plant design and fabri-

cation, which carry limitations of available engineer-

ing skill, high costs, and time loss. In view of the

growing market demands for dahi and its derivatives,

there is a great scope for modernizing the existing

technology for industrial production.

See also: Fermented Milks: Dietary Importance