EFFECTS OF PROLONGED FASTING IN PATIENTS

1. EFFECTS OF PROLONGED
FASTING IN PATIENTS.
DR. LANDO ELVIS. O
KIKUYU PCEA IMED PRESENTATION

2. INTRODUCTION
• FASTING IS THE WILLFUL REFRAINMENT FROM EATING AND DRINKING.
• FASTING MAY REFER TO THE METABOLIC STATUS OF A PERSON WHO HAS NOT
EATEN OVERNIGHT, OR TO THE METABOLIC STATE ACHIEVED AFTER COMPLETE
DIGESTION AND ABSORPTION OF A MEAL.

3. FEATURES OF STARVED BODY
• NO ENTRY OF EXOGENOUS FOOD CONSTITUENTS
• BODY IN STARVATION IS DEPRIVED OF:
• CALORIES (CARBS AND LIPIDS)
• BUILDING BLOCKS (PROTEINS)
• GROWTH FACTORS(VITAMINS AND MINERALS)
• PROTECTORS (ANTIOXIDANTS)

4. .
• DURING STARVATION
THE BODY
IS UNDER
METABOLIC STRESS
• DURING STARVATION THE BODY IS IN AN EMERGENCY CONDITION
• STARVED BODY HAS TO GET ADAPTED AND MANAGE WITH ENDOGENEOUS
RESERVE STORES.

5. SURVIVAL PERIOD DURING STARVATION
• SURVIVAL PERIOD DURING STARVATION
DEPENDS UPON THE:
• RESERVE FAT STORES IN ADIPOSECYTES.
• MORE CONTENT OF TAG IN ADIPOSECYTES
• MORE IS THE DURATION OF SURVIVAL IN
STARVATION AND VICE A VERSA.

6. LENGTH OF SURVIVAL IN STARVATION
• DUE TO DEPRIVATION OF ONLY FOOD:
• 3 TO 4 WEEKS
• LONGER UP TO 65 DAYS
• DEPRIVATION OF WATER ALONE THEN SURVIVAL IS
ONLY FOR FEW DAYS
• LESS THAN A WEEK

7. OCCURRENCE OF
FOUR STAGES DURING STARVATION
OR
METABOLIC ALTERATIONS DURING STARVATION
• FIRST STAGE
INCREASED GLYCOGENOLYSIS
• SECOND STAGE
INCREASED GLUCONEOGENESIS
• THIRD STAGE
INCREASED LIPOLYSIS/FATTY ACID BETA OXIDATION
• FOURTH STAGE
INCREASED KETOGENESIS

8. .
• 6-24 HOURS AFTER LAST MEAL/FAST
- FIRST PHASE IS K/A POST-
ABSORPTIVE PHASE
• INSULIN DECREASES
• GLYCOGEN BREAKDOWN —-
GLUCOSE
• THIS CONTINUES FOR APPROX. 24
HOURS
• SECOND PHASE STARTS AFTER 24
HOURS AND LASTS UPTO 2 DAYS
• GLUCONEOGENESIS = SOURCE OF
ENERGY (AA TO GLUCOSE)
• FALL IN BLOOD GLUCOSE LEVEL BUT
WITHIN RANGE OF NORMAL
• THIRD PHASE - KETOSIS
• BEGINS AFTER 2-3 DAYS OF FASTING
• LOW INSULIN LEVELS NOW HELPS IN
LIPOLYSIS TO GAIN ENERGY
• TRIGLYCERIDES (STORED FORM OF FAT) IS
BROKEN DOWN INTO GLYCEROL AND 3 FFA
CHAINS
• AGAIN GLYCEROL INITIATES
GLUCONEOGENESIS TO PRODUCE GLUCOSE
• TISSUE OTHER THAN BRAIN CAN DERIVE
ENERGY FROM FFA DIRECTLY
• ALTHOUGH KETONE BODIES DERIVED FORM
FFA CAN CROSS BLOOD-BRAIN-BARRIER &
CAN BE
• UTILISED BY BRAIN
• KETONE BODIES - BETA HYDROXY
BUTYRATE,ACETOACETATE, ACETONE

9. .
• FOURTH PHASE -PROTEIN CONSERVATION
• STARTS AFTER 5 DAYS
• ENERGY SOURCE - FFA & KETONES
• INCREASED LEVELS OF GH (TO MAINTAIN MUSCLE MASS)
• INCREASED ADRENALIN/NOREPINEPHRINE (PREVENTS FALL IN BMR)

10. GOOD TO KNOW!
INSULIN
FASTING HELPS IN DECREASING
INSULIN
WITHIN 24-36 HOURS OF FAST
LEVEL STARTS DECREASING
IMPROVES INSULIN SENSITIVITY
(HELPS IN WEIGHT LOSS)
LOW INSULIN LEVEL HELPS IN
DIURESIS (REMOVAL OF EXCESS
SALT & WATER) THROUGH
KIDNEY (SIMILAR EFFECT IN ATKINS
DIET WHICH IS HELPFUL IN WEIGHT
LOSS)
DIURESIS HELPS IN BLOATING,
FEELING OF LIGHT BODY, LOWER
B.P.
0.9KG/DAY WEIGHT LOSS HAVE
BEEN REPORTED IN SOME STUDIES
GLUCAGON AND EPINEPHRINE
GROWTH HORMONE
INCREASED DURING FASTING
HELPS IN FAT AVAILABILITY FOR
ENERGY
PRESERVES MUSCLE MASS, BONE
DENSITY
KEY FACTOR OF ANTI-AGING
EFFECT (OF FASTING)- AS
DECREASES WITH AGE
ELECTROLYTE AND
NUTRIENTS
MG, CA AND P ARE STABLE DURING
FAST
THOUGH THEIR IS NO DEFICIENCY
OF MACRONUTRIENTS DURING THE
FAST
POTASSIUM LEVEL FALLS BUT NOT
BELOW 3MMOL/L (NORMAL- 3.5 -5
MMOL/L)

11. BIOCHEMICAL ADAPTATIONS DURING STARVATION
PHASE
CARBOHYDRATE METABOLISM
IN LIVER DURING STARVATION
PHASE
• GLYCOGENOLYSIS INCREASED
• GLYCOGENESIS DECREASED
• GLUCONEOGENESIS INCREASED
• GLYCOLYSIS DECREASED
• TCA OPERATION DECREASED
• HMP SHUNT DECREASED
• BLOOD GLUCOSE LEVEL
DECREASES (LATER STAGES)
• CELLULAR GLUCOSE
DEPRIVATION (IN MUSCLE CELLS)
LIPID METABOLISM DURING
STARVATION
• LIPOLYSIS IS INCREASED
MOBILIZATION OF FREE FATTY ACIDS
INCREASED
BETA OXIDATION OF FATTY ACIDS
INCREASED
• INCOMPLETE FATTY ACID
OXIDATION INCREASED
KETOGENESIS INCREASED
KETOLYSIS DECREASED
• KETOSIS NOTED (KETOACIDOSIS)-
ROTHERAS TEST +VE
LIPOGENESIS IS DECREASED
• ENZYME ACETYL CARBOXYLASE IS
INHIBITED DURING STARVATION.
ALTERATIONS IN PROTEIN
METABOLISM DURING
STARVATION
• CATABOLISM OF MUSCLE PROTEINS
INCREASED
• TRANSDEAMINATION REACTION
OF AMINO ACIDS IS INCREASED
• TO RELEASE GLUCOGENIC AMINO
ACIDS
• AMMONIA DETOXIFICATION AND
UREA PRODUCTION INCREASED
INITIALLY AND DECREASED AS
STARVATION PHASE PROLONGS.
• BODY IS IN NEGATIVE NITROGEN
BALANCE.
• CONCENTRATION OF FUNCTIONAL
PROTEINS DECREASES.

12. BIOCHEMICAL ADAPTATIONS DURING
STARVATION PHASE
• DURING STARVATION
ALTERATIONS OCCUR IN
WATER AND ELECTROLYTE
AND
ACID BASE BALANCE
• REDUCTION IN BODY WATER
• REDUCTION OF POTASSIUM IONS
• ACIDIC BLOOD PH DUE TO INCREASED KETONE
BODIES
• ON PROLONGED PHASE OF STARVATION THERE
RESULTS IN SEVERE DEHYDRATION AND ACID
BASE IMBALANCE
• GLUCOSE NITROGEN RATIO
INCREASED IN STARVATION
• IN STARVATION BMR IS DECREASED.

13. DIFFERENTIATION IN
WELL FED AND FASTING STATES
OF HUMAN BODY
.

14. WELL-FED STATE FASTING STATE
Hormones  Insulin
 Glucagon,
Adrenaline, Cortisol
Response of
the body
Hyperglycemia
 Glycogenesis
 Lipogenesis
 Protein synthesis
Hypoglycemia
 Lipolysis
 Ketogenesis
 Proteolysis

15. WELL-FED STATE FASTING STATE
Source of
Glucose
from food
from stores
(Glycogen)
Gluconeogenesis
Fate of
Glucose
Glycolysis
formation of Glycogen and
TAG stores
Glycolysis

16. WELL-FED STATE FASTING STATE
Source of
Fatty acids
from food TAG from storage TAG
Fate of Fatty
acids
-oxidation
synthesis of TAG and
Store as Depot Fat
 -oxidation
(Incomplete one)
Ketogenesis

17. WELL-FED STATE FASTING STATE
Source of
Amino acids
from food From muscle Proteins
Fate of
Amino acids
Protein synthesis
Glucogenic amino
acids
Produce Glucose via
Gluconeogenesis

18. PREFERRED FUELS BY HUMAN BODY
IN THE WELL-FED AND FASTING
STATES
Organs Well-Fed Fasting
Liver Glucose & Fatty
acids
Fatty acids
Resting skeletal
Muscle
Glucose &
Fatty acids
Fatty acids & KB
Cardiac muscle Fatty acids FA,AA & KB
Adipose tissue Glucose Fatty acids
Brain Glucose Glucose ,Later KB
RBCs Glucose Glucose

19. BIOCHEMICAL PROFILE OF STARVED STATE
GLUCOSE LEVELS MORE DECREASED
40 MG/DL(2.2MMOL/L)
PROTEIN CATABOLISM INCREASED
SEQUESTERS NITROGEN AS UREA
EXCRETES 20 TO 30 GRAMS DAILY
GLUCONEOGENESIS TAKING PLACE USING PRECURSORS AS
AMINO ACIDS
LACTATE
GLYCEROL
KETONE BODIES INCREASED
ACETYL COA CONVERTED TO KETONE BODIES VIA KETOGENESIS

20. IN PROLONGED STARVATION
• AFTER 3 DAYS OF STARVATION -> LIVER FORMS LARGE AMOUNTS OF KETONE
BODIES
( DUE TO SHORTAGE OF OXALOACETATE)
• KETONE BODIES -> RELEASED INTO BLOOD
• BRAIN AND HEART START TO USE KETONE BODIES AS FUEL DURING PHASE OF
STARVATION.
• AFTER SEVERAL WEEKS OF STARVATION
• KETONE BODIES BECOME MAJOR FUEL OF BRAIN
• AFTER DEPLETION OF TAG STORES
• PROTEINS DEGRADATION ACCELERATES
• DEATH DUE TO LOSS OF HEART, LIVER, AND KIDNEY FUNCTION.

21. 2
4
Hours of Starvation
Relative
change
6. Ketone
bodies
3
.Glucose
5. Fatty acids
4.
Glycogen
1.
Insulin
2.Glucago
n
FUEL CHOICE DURING
STARVATION

22. CHANGES OF LIVER GLYCOGEN
CONTENT

23. DURING STARVATION
• FUEL CHANGES FROM GLUCOSE TO FATTY
ACIDS TO KETONE BODIES

24. 10
20
30
40
I II III IV V
Exogenous
Glycogen
Gluconeogenesis
GLUCOSE
UTILIZED
(g/hora)
Ruderman NB. Annu Rev Med 1975;26:248
I II III IV V
GLUCOSE
GLUCOSE GLUCOSE
GLUCOSE,
KETONES
GLUCOSE,
KETONES
FUEL FOR
BRAIN
LEGEND
METABOLIC RESPONSE TO
FASTING

25. FASTING – LATE STAGE
Intestine
Muscle
Liver
Brain
Kidney
Gluconeogenesis
Ketogenesis
Ureagenesis
Glutamine
Alanine / Pyruvate
Glucos
e
Ketones
Urea
NH3
Ketones
Glycerol
AGL
Fat

26. ENERGY EXPENDITURE IN
STARVATION
Long CL et al. JPEN 1979;3:452-456
0
10 20 30 40
Partial Starvation
Days
Nitrogen
Excretion
(g/day)
12
8
4
Total Starvation
Normal Range

27. CONSEQUENCES OF STARVATION

28. • SEVERE MALNUTRITION
• DAMAGES AND AFFECTS VITALITY OF IMPORTANT INTERNAL ORGANS
• DECREASED BMR
• NIGHT BLINDNESS (VITAMIN A DEFICIENCY)
• SCURVY (VITAMIN C DEFICIENCY)
• IRREGULAR MENSES
• CONSTIPATION
• LOW IMMUNITY
• BONE LOSS
• ANAEMIA (IRON AND PROTEIN DEFICIENCY)
• FATIGUE
• DEHYDRATION
• WATER ELECTROLYTE IMBALANCE
• HIGH BLOOD PRESSURE
• BRAIN DEFECTS
• DEATH

30. END
.