FIOM: INTERAKSI ALKOHOL

DENGAN MAKANAN
Muhammad Hafizh Hariawan
• Pengaruh alkohol terhadap farmakokinetika
• Pengaruh alkohol terhadap malnutrisi dan zat gizi
• Pengaruh alkohol terhadap vitamin dan mineral
Kalori dalam Alkohol
• Karbohidrat : 4 kkal /gram
• Protein: 4 kkal/gram
• Lemak: 9 kkal/gram
• Alkohol (ethanol):
• 7 kkal/gram
• Konsumsi alkohol dapat memengaruhi status gizi dan
farmakoterapi
• Metabolisme alkohol menghasilkan energi sehingga
memengaruhi asupan energi total → terdapat potensi
penurunan asupan energi dari sumber lain, FENOMENA:
alkoholik asupan makanannya menurun
• Interaksi alkohol-zat gizi dan alkohol-obat terjadi pada
farmakokinetika dan farmakodinamika
• Farmakokinetika:
• Pengaruh tubuh terhadap obat
• Absorpsi, distribusi, metabolisme
• Farmakodinamika:
• Pengaruh obat terhadap sel hidup
• Cara kerja obat, efek obat terhadap fungsi organ dst.
https://www.researchgate.net/fig
ure/The-absorption-transportation-
and-deposition-of-alcohol-in-the-
body-After-oral_fig1_370524043
 Metabolisme Alkohol di Liver

Major and minor ethanol-oxidizing pathways in the liver. Ethanol (i.e., ethyl
alcohol) is oxidized principally in hepatocytes of the liver. (Middle
panel) Alcohol dehydrogenase (ADH), a major enzyme in the cytosol, and
aldehyde dehydrogenase 2 (ALDH2), which is located in the mitochondria,
catalyze sequential oxidations that convert ethanol to acetate, producing
two mole equivalents of reduced nicotinamide adenine dinucleotide
(NADH). (Right panel) Cytochrome P450 2E1 (CYP2E1) is a major inducible
oxidoreductase in the endoplasmic reticulum that oxidizes ethanol, in the
presence of molecular oxygen (O2), to acetaldehyde and converts reduced
NAD phosphate (NADPH) to its oxidized form, generating water. (Left
panel) Peroxisomal catalase is a minor hepatic pathway of ethanol oxidation
that uses hydrogen peroxide (H2O2) to oxidize ethanol to acetaldehyde and
water.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484
320/#:~:text=Alcohol%20is%20oxidized%20by%20alco
hol,converted%20to%20the%20indicated%20products.

Step 1 catalyzed by the enzyme alcohol dehydrogenase, which is present largely in the liver, and consists of a family of isoforms. A
vitamin-related cofactor, nicotinamide adenine dinucleotide ( NAD) (derived from the vitamin niacin) is required to accept reducing
equivalents (hydrogen atoms and electrons) from the alcohol. As a result, the ethanol is oxidized to the product acetaldehyde and
the vitamin cofactor, NAD+ is reduced to the product NADH + H+ (note two hydrogens are removed from alcohol). The ADH reaction is
reversible.
Step 2 is catalyzed by the enzyme aldehyde dehydrogenase. Acetaldehyde is oxidized to acetate; NAD+ is the cofactor, and is reduced
to NADH. The ALDH reaction is essentially irreversible. Much of the acetaldehyde produced from the oxidation of alcohol is oxidized
in the liver to acetate; circulating levels of acetaldehyde are low under normal conditions.
Step 3 Much of the acetate produced by the oxidation of acetaldehyde leaves the liver and circulates to peripheral tissues where it is
activated to a key Acetyl CoA. Acetyl CoA is also the key metabolite produced form all major nutrients- carbohydrate, fat and excess
protein. Thus, carbon atoms from alcohol wind up as the same products produced from the oxidation of carbohydrate, fat, and
protein, including CO2, fatty acids, ketone bodies, and cholesterol; which products are formed depends on the energy state and the
nutritional and hormonal conditions.
 General effects of alcohol consumption on the small intestine. Adapted with
permission from Butts M.R. [32]. GI, gastrointestinal; HSP, heat shock protein;
ROS, reactive oxygen species.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10096942/
 Figure 1. The effect of alcohol on the gut.
(a) The histological effects of alcohol on the
gut mucosa (cell death, mucosal erosions
and loss of epithelium at villi tips). (b)
Alcohol-induced disruption of tight
junctions, exacerbated by reduced luminal
SCFA concentrations. (c) Alcohol-induced
dysbiosis leading to reduced SCFA and amino
acid concentrations. (d) Increased
concentration of secondary bile acids, and
increased proportion conjugated with
glycine. (e) Nutrient deficiencies as a
consequence of (a–d). CTP: Connexin
transmembrane proteins; JAM: Junctional
adhesion molecule; EtOH: alcohol.

https://www.mdpi.com/2072-6643/13/9/3170
Absorpsi
• Interaksi makanan/zat gizi dan obat dengan alkohol terjadi di fase
farmakokinetika
• Penyerapan alkohol terjadi di duodenum. Faktor yang memengaruhi
absorbsi alkohol adalah laju pengosongan lambung
• Laju pengosongan lambung lambat --> lebih banyak mengonsumsi
alcohol
• Laju pengosongan lambung cepat --> absorpsi meningkat, kerusakan
lebih cepat dan lebih parah
• Alkohol menyebabkan kerusakan permukaan mukosa usus sehingga
absorpsi zat gizi terganggu (malabsorpsi)
• Alkohol mengganggu first-pass metabolism sehingga meningkatkan
bioavailabilitas obat
Interaction of alcohol’s direct toxic
effects with malnutrition
EFEK KONSUMSI ALKOHOL TERHADAP ZAT
GIZI: KARBOHIDRAT
• Ethanol consumption effects carbohydrate absorption in
multiple ways. Following a heavy dosage of ethanol,
xylose absorption was inhibited, but fructose absorption
was not altered in the small intestine. However, these
differ from ethanol’s effect on another carbohydrate:
glucose.

• Konsumsi alcohol menurunkan absorpsi glukosa

EFEK KONSUMSI ALKOHOL TERHADAP ZAT
GIZI
• Asam Amino
• Konsumsi alkohol meningkatkan nitrogen loss di urin.
• konsumsi etanol jangka pendek menghambat transport aktif asam
amino di mukosa usus
• Lipid
• Konsumsi etanol jangka pendek menghambat transport lipid melewati
mukosa usus.
• Alkohol meningkatkan lipogenesis di hepar
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513682/
EFEK KONSUMSI ALKOHOL TERHADAP
VITAMIN DAN MINERAL
• Thiamin
• Asupan alkohol akut
menurunkan absorpsi thiamin di
usus
• Rendahnya absorpsi thiamin
disebabkan karena kerusakan
receptor sites akibat dari
konsumsi alkohol dalam jangka
panjang, atau defisiensi zat gizi
tersebut, atau kombinasi
• Wernicke-Korsakoff syndrome →
toksisitas alkohol atau defisiensi
thiamin sekundeR
EFEK KONSUMSI ALKOHOL TERHADAP
VITAMIN DAN MINERAL
• Riboflavin
• 17% alkoholik kronis mengalami defisiensi riboflavin
• Alkohol menghambat aborpsi riboflavin di sel epitel usus dan
reabsorpsi di ginjal
• Defisiensi riboflavin: gangguan sistem syaraf, anemia, gagal tumbuh,
lesi kulit dan peningkatan kerentanan terhadap karsinogen
• Biotin
• Alkohol menghambat absorpsi biotin di usus dengan cara menekan
transkripsi gen Slc5a6
EFEK KONSUMSI ALKOHOL TERHADAP
VITAMIN DAN MINERAL
• Folat
• Alkohol menghambat transport folat melewati lumen GI
• Diet seimbang → tidak muncul reaksi merugikan terhadap folat
• Anemia megaloblastik pada alkoholik kemungkinan besar disebabkan oleh
defisiensi folat
• Vitamin B6
• Vitamin B6 → penting untuk aktivitas ALT (alanine transaminase) sehingga
defisiensi vitamin B6 berkontribusi pada rendahnya ALT di alcoholic liver
disease
• Penyebab defisiensi vitamin B6 pada alkoholik kronis → acetaldehyde
menggantikan bentuk aktif vitamin B6 (pyridoxal phosphate) di albumin
sehingga meningkatkan ekskresi vitamin via urin
• Defisiensi → anemia sideroblastik
EFEK KONSUMSI ALKOHOL TERHADAP
VITAMIN DAN MINERAL
• Vitamin C
• Absorpsi asam askorbat menurun jika dikonsumsi bersamaan dengan
etanol, meskipun penyebab utama defisiensi vitamin C pada alkoholik
adalah asupan vitamin C inadekuat, malarbsorpsi, dan ekskresi
berlebih akibat dari konsumsi alcohol
• Vitamin A
• Pasien alcoholic liver disease memiliki kadar vitamin A hepatik yang
rendah
• Penyebab: malabsorpsi → alcohol menghambat abosrpsi lemak
sehingga mengganggu absorpsi vitamin larut lemak (A,E,D)
EFEK KONSUMSI ALKOHOL TERHADAP
VITAMIN DAN MINERAL
• Kalsium
• Konsumsi alkohol jangka panjang menghambat absorpsi kalsium di
duodenum.
• Risiko osteoporosis meningkat karena absorpsi kalsium dan vitamin D
menurun
• Zinc dan Zat Besi
• Zinc: kofaktor retinol dehydrogenase. Defisiensi zinc terjadi karena
gangguan absorpsi dan peningkatan ekskresi melalui urin → rabun
senja dan hipogonadisme
• Faktor-faktor penyebab defisiensi zat besi pada alkoholik: asupan
makan inadekuat, absorpsi di usus menurun, peningkatan ekskresi
melalui urin.
EFEK KONSUMSI ALKOHOL TERHADAP
VITAMIN DAN MINERAL
• Fosfor dan Magnesium
• Asupan fosfor yang tidak cukup → risiko refeeding syndrome
(hipofosfatemia)
• Defisiensi magnesium: kram otot, hipertensi, vasospasme otak dan
jantung.
• Mekanisme → Secara akut, alkohol bersifat diuretik terhadap
magnesium sehingga ekskresi magnesium dan elektrolit melalui urin
meningkat. Secara kronis, seiring dengan perkembangan alkoholisme
menyebabkan simpanan Magnesium menurun
Interaksi Alkohol dengan Obat
Nama Obat Kelas dan Aksi Efek Samping Dampak terhadap Zat
Gizi
Fluoxetine Selektif serotonin Alkohol dapat Hindari alcohol
Prozac reuptake inhibitor meningkatkan depresi
Isocarboxazid Antidepressant Alkohol meingkatkan efek Hindari alcohol
Marplan Monoamine Oxidase depresan
Inhibitor (MAOI)
Phenelzine Antidepressant Alkohol meingkatkan efek Hindari alcohol
Nardil Monoamine Oxidase depresan
Inhibitor (MAOI)
Sertraline Antidepressant Alkohol meingkatkan efek Hindari alcohol
Zoloft Selektif serotonin depresan
reuptake inhibitor
Trancylpromine Antidepressant Alkohol meingkatkan efek Hindari alcohol
Parnate Monoamine Oxidase depresan
Inhibitor (MAOI)
Terima kasih